From b9ec138a80f7168c914973cabc86fa38735c2909 Mon Sep 17 00:00:00 2001
From: sigven <sigven@ifi.uio.no>
Date: Sat, 9 Mar 2024 18:02:24 +0000
Subject: [PATCH] =?UTF-8?q?Deploying=20to=20gh-pages=20from=20@=20sigven/p?=
 =?UTF-8?q?harmOncoX@708a3a5f79e02997f7b815ee29727a602b6cc7f1=20?=
 =?UTF-8?q?=F0=9F=9A=80?=
MIME-Version: 1.0
Content-Type: text/plain; charset=UTF-8
Content-Transfer-Encoding: 8bit

---
 404.html                          |   2 +-
 CODE_OF_CONDUCT.html              |   2 +-
 LICENSE-text.html                 |   2 +-
 articles/index.html               |   2 +-
 articles/pharmOncoX.html          | 199 +++++++++++++++---------------
 authors.html                      |   6 +-
 index.html                        |   2 +-
 news/index.html                   |   6 +-
 pkgdown.yml                       |   2 +-
 reference/get_biomarkers.html     |   2 +-
 reference/get_drug_records.html   |   2 +-
 reference/get_drugs.html          |   2 +-
 reference/get_targeted_drugs.html |   2 +-
 reference/index.html              |   2 +-
 reference/tidyeval.html           |   2 +-
 search.json                       |   2 +-
 16 files changed, 118 insertions(+), 119 deletions(-)

diff --git a/404.html b/404.html
index c1d80dc..7bc8639 100644
--- a/404.html
+++ b/404.html
@@ -36,7 +36,7 @@
     
     <a class="navbar-brand me-2" href="https://sigven.github.io/pharmOncoX/index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/CODE_OF_CONDUCT.html b/CODE_OF_CONDUCT.html
index c8b92ba..81034a6 100644
--- a/CODE_OF_CONDUCT.html
+++ b/CODE_OF_CONDUCT.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/LICENSE-text.html b/LICENSE-text.html
index 1aadb18..2e96a65 100644
--- a/LICENSE-text.html
+++ b/LICENSE-text.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/articles/index.html b/articles/index.html
index 7c99eb9..3d350e5 100644
--- a/articles/index.html
+++ b/articles/index.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/articles/pharmOncoX.html b/articles/pharmOncoX.html
index 0adc0aa..4f2a949 100644
--- a/articles/pharmOncoX.html
+++ b/articles/pharmOncoX.html
@@ -38,7 +38,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
@@ -103,24 +103,19 @@ <h2 id="installation">Installation<a class="anchor" aria-label="anchor" href="#i
 <span><span class="kw">if</span> <span class="op">(</span><span class="op">!</span><span class="op">(</span><span class="st">"remotes"</span> <span class="op"><a href="https://rdrr.io/r/base/match.html" class="external-link">%in%</a></span> <span class="fu"><a href="https://rdrr.io/r/utils/installed.packages.html" class="external-link">installed.packages</a></span><span class="op">(</span><span class="op">)</span><span class="op">)</span><span class="op">)</span> <span class="op">{</span></span>
 <span> <span class="fu"><a href="https://rdrr.io/r/utils/install.packages.html" class="external-link">install.packages</a></span><span class="op">(</span><span class="st">"remotes"</span><span class="op">)</span></span>
 <span><span class="op">}</span></span>
-<span><span class="co">#&gt; Installing package into '/home/runner/work/_temp/Library'</span></span>
-<span><span class="co">#&gt; (as 'lib' is unspecified)</span></span>
 <span></span>
 <span><span class="fu">remotes</span><span class="fu">::</span><span class="fu"><a href="https://remotes.r-lib.org/reference/install_github.html" class="external-link">install_github</a></span><span class="op">(</span><span class="st">'sigven/pharmOncoX'</span><span class="op">)</span></span>
 <span><span class="co">#&gt; Using github PAT from envvar GITHUB_PAT</span></span>
 <span><span class="co">#&gt; Downloading GitHub repo sigven/pharmOncoX@HEAD</span></span>
-<span><span class="co">#&gt; cpp11 (NA -&gt; 0.4.7) [CRAN]</span></span>
-<span><span class="co">#&gt; Installing 1 packages: cpp11</span></span>
-<span><span class="co">#&gt; Installing package into '/home/runner/work/_temp/Library'</span></span>
-<span><span class="co">#&gt; (as 'lib' is unspecified)</span></span>
+<span><span class="co">#&gt; </span></span>
 <span><span class="co">#&gt; <span style="color: #00BBBB;">──</span> <span style="color: #00BBBB;">R CMD build</span> <span style="color: #00BBBB;">─────────────────────────────────────────────────────────────────</span></span></span>
-<span><span class="co">#&gt; * checking for file ‘/tmp/RtmpsVdIol/remotes192d6fcd8dac/sigven-pharmOncoX-f93bff7/DESCRIPTION’ ... OK</span></span>
+<span><span class="co">#&gt; * checking for file ‘/tmp/Rtmp1n8MHG/remotes189d4fa6d09/sigven-pharmOncoX-708a3a5/DESCRIPTION’ ... OK</span></span>
 <span><span class="co">#&gt; * preparing ‘pharmOncoX’:</span></span>
 <span><span class="co">#&gt; * checking DESCRIPTION meta-information ... OK</span></span>
 <span><span class="co">#&gt; * checking for LF line-endings in source and make files and shell scripts</span></span>
 <span><span class="co">#&gt; * checking for empty or unneeded directories</span></span>
 <span><span class="co">#&gt; Omitted ‘LazyData’ from DESCRIPTION</span></span>
-<span><span class="co">#&gt; * building ‘pharmOncoX_1.5.10.tar.gz’</span></span>
+<span><span class="co">#&gt; * building ‘pharmOncoX_1.6.0.tar.gz’</span></span>
 <span><span class="co">#&gt; Installing package into '/home/runner/work/_temp/Library'</span></span>
 <span><span class="co">#&gt; (as 'lib' is unspecified)</span></span>
 <span></span>
@@ -171,24 +166,24 @@ <h3 id="get-braf-targeted-drugs-list-records-per-indication">Get BRAF-targeted d
 <span>  treatment_category <span class="op">=</span>  <span class="fu"><a href="https://rdrr.io/r/base/c.html" class="external-link">c</a></span><span class="op">(</span><span class="st">"targeted_therapy_classified"</span>,</span>
 <span>                          <span class="st">"targeted_therapy_unclassified"</span><span class="op">)</span>,</span>
 <span>    drug_target <span class="op">=</span> <span class="fu"><a href="https://rdrr.io/r/base/c.html" class="external-link">c</a></span><span class="op">(</span><span class="st">'BRAF'</span><span class="op">)</span><span class="op">)</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Object 'drug_map_name' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Retrieved n = 31451 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Object 'drug_map_alias' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Retrieved n = 677295 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Object 'drug_map_basic' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Retrieved n = 31486 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Object 'drug_map_target' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Retrieved n = 39369 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Object 'drug_map_indication' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:54] Retrieved n = 62752 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:57] Record set satisfying user-defined criteria: n = 279</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:57] Collapsing record set - providing output on a 'per_drug_target_indication' resolution</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:57:57] Final record set: n = 237 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Object 'drug_map_name' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Retrieved n = 31451 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Object 'drug_map_alias' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Retrieved n = 677295 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Object 'drug_map_basic' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Retrieved n = 31486 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Object 'drug_map_target' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Retrieved n = 39369 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Object 'drug_map_indication' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:36] Retrieved n = 62752 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:39] Record set satisfying user-defined criteria: n = 279</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:39] Collapsing record set - providing output on a 'per_drug_target_indication' resolution</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:39] Final record set: n = 237 records</span></span>
 <span></span>
 <span><span class="co">## Number of drug records</span></span>
 <span><span class="fu"><a href="https://rdrr.io/r/base/nrow.html" class="external-link">nrow</a></span><span class="op">(</span><span class="va">drugs</span><span class="op">$</span><span class="va">records</span><span class="op">)</span></span>
@@ -249,8 +244,8 @@ <h3 id="get-ras-targeted-drugs-list-per-drug-target">Get RAS-targeted drugs, lis
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
-<div id="htmlwidget-0fab9ea84c9792498ec0" style="width:100%;height:auto;" class="datatables html-widget"></div>
-<script type="application/json" data-for="htmlwidget-0fab9ea84c9792498ec0">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20","21","22","23","24","25","26","27","28","29","30","31","32","33","34","35","36","37"],[27330,837,22100,11354,26452,26452,26452,14987,15212,17712,25292,25292,25292,25293,25293,25293,17718,17717,17721,17716,17814,22882,17713,17719,17720,17723,17724,17726,17727,17722,17731,22881,17714,17715,17732,2670,2671],["Sotorasib","Adagrasib","Opnurasib","Divarasib","Salirasib","Salirasib","Salirasib","Garsorasib","Glecirasib","KRAS G12C Inhibitor","Ras Inhibitor LUNA18","Ras Inhibitor LUNA18","Ras Inhibitor LUNA18","Ras Inhibitor RSC-1255","Ras Inhibitor RSC-1255","Ras Inhibitor RSC-1255","KRAS G12C Inhibitor GH35","KRAS G12C Inhibitor GEC255","KRAS G12C Inhibitor IBI351","KRAS G12C Inhibitor D3S-001","Kras G12C Inhibitor MK-1084","Pan-KRAS Inhibitor YL-17231","KRAS G12C Inhibitor BEBT-607","KRAS G12C Inhibitor HBI-2438","KRAS G12C Inhibitor HS-10370","KRAS G12C Inhibitor RMC-6291","KRAS G12C Inhibitor YL-15293","KRAS G12D Inhibitor HRS-4642","KRAS G12D Inhibitor MRTX1133","KRAS G12C Inhibitor LY3499446","KRAS-G12C Inhibitor LY3537982","Pan-KRAS Inhibitor BI 1701963","KRAS G12C Inhibitor BI 1823911","KRAS G12C Inhibitor BPI-421286","KRASG12C Inhibitor JNJ-74699157","Anti-K-RAS G12D mTCR-transduced Autologous Peripheral Blood Lymphocytes","Anti-K-RAS G12V mTCR-transduced Autologous Peripheral Blood Lymphocytes"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Antibody","Antibody"],["CHEMBL4535757","CHEMBL4594350","CHEMBL5077861","CHEMBL5095236","CHEMBL23293","CHEMBL23293","CHEMBL23293",null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null],["INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR"],["An orally available inhibitor of the specific KRAS mutation, p.G12C, with potential antineoplastic activity. Upon oral administration, sotorasib selectively targets, binds to and inhibits the activity of the KRAS p.G12C mutant. This may inhibit growth in KRAS p.G12C-expressing tumor cells. The KRAS p.G12C mutation is seen in some tumor cell types and plays a key role in tumor cell proliferation.","An orally available, small molecule inhibitor that targets the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration adagrasib covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon administration, opnurasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, divarasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, garsorasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, glecirasib selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Any agent that inhibits the oncogenic KRAS substitution mutation G12C.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable irreversible inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GH35 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GEC255 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor IBI351 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor D3S-001 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor MK-1084 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of various KRAS mutations, such as the oncogenic KRAS substitution mutations G12C, G12D and G12V, with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor YL-17231 targets, binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BEBT-607 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in KRAS G12C mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HBI-2438 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HS-10370 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable, covalent inhibitor of the active, guanosine triphosphate (GTP)-bound form of the oncogenic KRAS substitution mutation G12C, KRAS G12C(ON), with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor RMC-6291 forms a tri-complex with the intracellular chaperone protein and immunophilin cyclophilin A (CypA) and KRAS G12C(ON). This tri-complex inhibits KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor YL-15293 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon administration, KRAS G12D inhibitor HRS-4642 specifically targets and binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable reversible inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor MRTX1133 specifically targets and noncovalently binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, LY3499446 targets and covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS-G12C inhibitor LY3537982 selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available protein-protein interaction (PPI) inhibitor that targets the guanine nucleotide exchange factor Son of sevenless homolog 1 (SOS1), with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor BI 1701963 selectively targets and binds to SOS1, thereby preventing the interaction of SOS1 with Kirsten rat sarcoma viral oncogene homolog (KRAS) in the guanosine diphosphate (GDP)-bound 'off' state, which is the inactivated state of KRAS. This abrogates the exchange of RAS-bound GDP for guanosine triphosphate (GTP) and prevents the formation of GTP-loaded KRAS, which is the activated 'on' state of KRAS. This prevents activation of downstream RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway by GTP-loaded KRAS. This inhibits mutant KRAS-dependent signaling and may inhibit growth and survival of KRAS-expressing tumor cells. KRAS is a member of the RAS family of oncogenes that is mutated in many cancer cell types. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, survival, invasion, and metastasis. SOS1 regulates the KRAS GDP-GTP cycle and promotes nucleotide exchange and formation of 'active' KRAS-GTP.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BI 1823911 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BPI-421286 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available, small molecule inhibitor of the oncogenic Kirsten rat sarcoma virus homolog KRAS glycine-to-cysteine substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration JNJ-74699157 targets and binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding for an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine (Gly, G) to aspartic acid (Asp, D) point mutation at position 12 (G12D) variant of K-RAS (KRAS), with potential immunomodulating and antineoplastic activities. HLA-A1101-positive PBLs are harvested from a K-RAS G12D-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12D mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12D mTCR-expressing PBLs target and bind to K-RAS G12D-overexpressing tumor cells, which results in both cytokine secretion, including interferon-gamma (IFN-g), and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Autologous peripheral blood lymphocytes (PBLs) transduced with an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine to valine point mutation at position 12 (G12V) variant of K-RAS, with potential antineoplastic activity. HLA-A1101 positive PBLs are harvested from a K-RAS G12V-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12V mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12V mTCR-expressing PBLs target and bind to K-RAS G12V-overexpressing tumor cells, which results in both cytokine secretion and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and 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class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>target_symbol<\/th>\n      <th>target_entrezgene<\/th>\n      <th>target_genename<\/th>\n      <th>target_ensembl_gene_id<\/th>\n      <th>target_type<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,15,19,21,22,23]},{"orderable":false,"targets":0},{"name":" 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+<script type="application/json" data-for="htmlwidget-05dc8f37c0e094b296ac">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20","21","22","23","24","25","26","27","28","29","30","31","32","33","34","35","36","37"],[27330,837,22100,11354,26452,26452,26452,14987,15212,17712,25292,25292,25292,25293,25293,25293,17718,17717,17721,17716,17814,22882,17713,17719,17720,17723,17724,17726,17727,17722,17731,22881,17714,17715,17732,2670,2671],["Sotorasib","Adagrasib","Opnurasib","Divarasib","Salirasib","Salirasib","Salirasib","Garsorasib","Glecirasib","KRAS G12C Inhibitor","Ras Inhibitor LUNA18","Ras Inhibitor LUNA18","Ras Inhibitor LUNA18","Ras Inhibitor RSC-1255","Ras Inhibitor RSC-1255","Ras Inhibitor RSC-1255","KRAS G12C Inhibitor GH35","KRAS G12C Inhibitor GEC255","KRAS G12C Inhibitor IBI351","KRAS G12C Inhibitor D3S-001","Kras G12C Inhibitor MK-1084","Pan-KRAS Inhibitor YL-17231","KRAS G12C Inhibitor BEBT-607","KRAS G12C Inhibitor HBI-2438","KRAS G12C Inhibitor HS-10370","KRAS G12C Inhibitor RMC-6291","KRAS G12C Inhibitor YL-15293","KRAS G12D Inhibitor HRS-4642","KRAS G12D Inhibitor MRTX1133","KRAS G12C Inhibitor LY3499446","KRAS-G12C Inhibitor LY3537982","Pan-KRAS Inhibitor BI 1701963","KRAS G12C Inhibitor BI 1823911","KRAS G12C Inhibitor BPI-421286","KRASG12C Inhibitor JNJ-74699157","Anti-K-RAS G12D mTCR-transduced Autologous Peripheral Blood Lymphocytes","Anti-K-RAS G12V mTCR-transduced Autologous Peripheral Blood Lymphocytes"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Antibody","Antibody"],["CHEMBL4535757","CHEMBL4594350","CHEMBL5077861","CHEMBL5095236","CHEMBL23293","CHEMBL23293","CHEMBL23293",null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null],["INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR"],["An orally available inhibitor of the specific KRAS mutation, p.G12C, with potential antineoplastic activity. Upon oral administration, sotorasib selectively targets, binds to and inhibits the activity of the KRAS p.G12C mutant. This may inhibit growth in KRAS p.G12C-expressing tumor cells. The KRAS p.G12C mutation is seen in some tumor cell types and plays a key role in tumor cell proliferation.","An orally available, small molecule inhibitor that targets the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration adagrasib covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon administration, opnurasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, divarasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","A salicylic acid derivative with potential antineoplastic activity. Salirasib dislodges all Ras isoforms from their membrane-anchoring sites, thereby preventing activation of RAS signaling cascades that mediated cell proliferation, differentiation, and senescence. RAS signaling is believed to be abnormally activated in one-third of human cancers, including cancers of the pancreas, colon, lung and breast.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, garsorasib selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, glecirasib selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Any agent that inhibits the oncogenic KRAS substitution mutation G12C.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable cyclic peptide and Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor LUNA18 selectively targets, binds to and inhibits Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable pan-mutant and wild-type Ras inhibitor, with potential antineoplastic activity. Upon oral administration, Ras inhibitor RSC-1255 selectively targets, binds to and inhibits both wild-type and mutated forms of Ras, thereby inhibiting Ras-dependent signaling and inhibits proliferation of tumor cells in which Ras is overexpressed and/or mutated. Ras serves an important role in cell signaling, division and differentiation. Mutations of Ras may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable irreversible inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GH35 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor GEC255 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor IBI351 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor D3S-001 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor MK-1084 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of various KRAS mutations, such as the oncogenic KRAS substitution mutations G12C, G12D and G12V, with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor YL-17231 targets, binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BEBT-607 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in KRAS G12C mutated tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HBI-2438 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable small molecule inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor HS-10370 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable, covalent inhibitor of the active, guanosine triphosphate (GTP)-bound form of the oncogenic KRAS substitution mutation G12C, KRAS G12C(ON), with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor RMC-6291 forms a tri-complex with the intracellular chaperone protein and immunophilin cyclophilin A (CypA) and KRAS G12C(ON). This tri-complex inhibits KRAS G12C(ON)-mediated signaling, which may inhibit tumor cell proliferation. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor YL-15293 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon administration, KRAS G12D inhibitor HRS-4642 specifically targets and binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally bioavailable reversible inhibitor of the oncogenic KRAS substitution mutation G12D, with potential antineoplastic activity. Upon oral administration, KRAS G12D inhibitor MRTX1133 specifically targets and noncovalently binds to KRAS G12D. This prevents KRAS G12D-mediated signaling and activation of downstream survival pathways. This leads to an inhibition of the growth of tumor cells that overexpress KRAS G12D. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, LY3499446 targets and covalently binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS-G12C inhibitor LY3537982 selectively targets the KRAS G12C mutant and inhibits KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally available protein-protein interaction (PPI) inhibitor that targets the guanine nucleotide exchange factor Son of sevenless homolog 1 (SOS1), with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor BI 1701963 selectively targets and binds to SOS1, thereby preventing the interaction of SOS1 with Kirsten rat sarcoma viral oncogene homolog (KRAS) in the guanosine diphosphate (GDP)-bound 'off' state, which is the inactivated state of KRAS. This abrogates the exchange of RAS-bound GDP for guanosine triphosphate (GTP) and prevents the formation of GTP-loaded KRAS, which is the activated 'on' state of KRAS. This prevents activation of downstream RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway by GTP-loaded KRAS. This inhibits mutant KRAS-dependent signaling and may inhibit growth and survival of KRAS-expressing tumor cells. KRAS is a member of the RAS family of oncogenes that is mutated in many cancer cell types. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, survival, invasion, and metastasis. SOS1 regulates the KRAS GDP-GTP cycle and promotes nucleotide exchange and formation of 'active' KRAS-GTP.","An orally available inhibitor of the oncogenic KRAS substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BI 1823911 selectively targets, binds to and inhibits the activity of the KRAS G12C mutant, thereby inhibiting KRAS G12C mutant-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","An orally bioavailable inhibitor of the oncogenic KRAS substitution mutation G12C, with potential antineoplastic activity. Upon oral administration, KRAS G12C inhibitor BPI-421286 selectively targets the KRAS G12C mutant and inhibits KRAS G12C-mediated signaling. This may halt proliferation and metastasis in susceptible tumor cells. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, invasion, and metastasis.","An orally available, small molecule inhibitor of the oncogenic Kirsten rat sarcoma virus homolog KRAS glycine-to-cysteine substitution mutation, G12C, with potential antineoplastic activity. Upon oral administration JNJ-74699157 targets and binds to cytosine 12 within the switch II pocket of GDP-bound KRAS G12C, thereby inhibiting mutant KRAS-dependent signaling. KRAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Autologous peripheral blood lymphocytes (PBLs) transduced with a retroviral vector encoding for an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine (Gly, G) to aspartic acid (Asp, D) point mutation at position 12 (G12D) variant of K-RAS (KRAS), with potential immunomodulating and antineoplastic activities. HLA-A1101-positive PBLs are harvested from a K-RAS G12D-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12D mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12D mTCR-expressing PBLs target and bind to K-RAS G12D-overexpressing tumor cells, which results in both cytokine secretion, including interferon-gamma (IFN-g), and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. Mutation of K-RAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.","Autologous peripheral blood lymphocytes (PBLs) transduced with an HLA class I histocompatibility antigen A*11:01 (HLA-A1101)-restricted murine T-cell receptor (mTCR) that recognizes the glycine to valine point mutation at position 12 (G12V) variant of K-RAS, with potential antineoplastic activity. HLA-A1101 positive PBLs are harvested from a K-RAS G12V-expressing cancer patient and transfected with a retroviral vector that encodes anti-K-RAS G12V mTCR. The transduced PBLs are then expanded in culture. When reintroduced to the patient, these anti-K-RAS G12V mTCR-expressing PBLs target and bind to K-RAS G12V-overexpressing tumor cells, which results in both cytokine secretion and tumor cell lysis. K-RAS, a member of the RAS family of oncogenes, serves an important role in cell signaling, division and differentiation. 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GTPase"],["ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000174775","ENSG00000133703","ENSG00000213281","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000174775","ENSG00000133703","ENSG00000213281","ENSG00000174775","ENSG00000133703","ENSG00000213281","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703","ENSG00000133703"],["single_protein","single_protein","single_protein","single_protein","protein_family","protein_family","protein_family","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein","single_protein"],[0.857,0.667,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0],[false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false,false],[7,3,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0,0],[2021,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null],[4,3,3,2,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null,null],["cancer, colorectal adenocarcinoma, lung adenocarcinoma, lung cancer, non-small cell lung carcinoma, pancreatic carcinoma","cancer, non-small cell lung carcinoma","non-small cell lung carcinoma, small cell lung carcinoma","non-small cell lung carcinoma","","","","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer","cancer"],["1|2|3|4","1|3","1|3","2","","","","","","","","","","","","","","","","","","","","","","","","","","","","","","","","",""],["L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01","L01"],["ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS"],["L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X"],["OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS"],["L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC","L01XXC"],["RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS inhibitors","RAS 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inhibitors"],["cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>target_symbol<\/th>\n      <th>target_entrezgene<\/th>\n      <th>target_genename<\/th>\n      <th>target_ensembl_gene_id<\/th>\n      <th>target_type<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,15,19,21,22,23]},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"drug_id","targets":1},{"name":"drug_name","targets":2},{"name":"drug_type","targets":3},{"name":"molecule_chembl_id","targets":4},{"name":"drug_action_type","targets":5},{"name":"nci_concept_definition","targets":6},{"name":"opentargets","targets":7},{"name":"drug_cancer_relevance","targets":8},{"name":"inhibition_moa","targets":9},{"name":"is_salt","targets":10},{"name":"is_adc","targets":11},{"name":"drug_blackbox_warning","targets":12},{"name":"nci_t","targets":13},{"name":"target_symbol","targets":14},{"name":"target_entrezgene","targets":15},{"name":"target_genename","targets":16},{"name":"target_ensembl_gene_id","targets":17},{"name":"target_type","targets":18},{"name":"drug_frac_cancer_indications","targets":19},{"name":"drug_approved_noncancer","targets":20},{"name":"drug_n_indications","targets":21},{"name":"drug_year_first_approval","targets":22},{"name":"drug_max_ct_phase","targets":23},{"name":"disease_indication","targets":24},{"name":"disease_indication_max_phase","targets":25},{"name":"atc_code_level1","targets":26},{"name":"atc_level1","targets":27},{"name":"atc_code_level2","targets":28},{"name":"atc_level2","targets":29},{"name":"atc_code_level3","targets":30},{"name":"atc_level3","targets":31},{"name":"atc_treatment_category","targets":32}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
 </div>
 <div class="section level3">
 <h3 id="get-mek-inhibitors-list-per-drug-only">Get MEK inhibitors, list per drug only<a class="anchor" aria-label="anchor" href="#get-mek-inhibitors-list-per-drug-only"></a>
@@ -285,8 +280,8 @@ <h3 id="get-mek-inhibitors-list-per-drug-only">Get MEK inhibitors, list per drug
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
-<div id="htmlwidget-d189155130bcb5cc3111" style="width:100%;height:auto;" class="datatables html-widget"></div>
-<script type="application/json" data-for="htmlwidget-d189155130bcb5cc3111">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20"],[26696,5231,8779,29481,29479,19071,19060,23725,25530,20194,29940,31265,19068,19065,19059,417,19066,25079,4534,4132],["Selumetinib","Binimetinib","Cobimetinib","Trametinib Dimethyl Sulfoxide","Trametinib","E-6201","CI-1040","Pimasertib","Refametinib","Mirdametinib","Tunlametinib","Zunsemetinib","WX-554","TAK-733","AZD-8330","As-703988","RO-4987655","Rg-7167","Balamapimod","Avutometinib"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule"],["CHEMBL1614701","CHEMBL3187723","CHEMBL2146883","CHEMBL2105741","CHEMBL2103875","CHEMBL1097999","CHEMBL105442","CHEMBL2107832","CHEMBL1236682","CHEMBL507361","CHEMBL5095241","CHEMBL3704901","CHEMBL3545145","CHEMBL1615025","CHEMBL3182621","CHEMBL3545243","CHEMBL1614766","CHEMBL3545383","CHEMBL2104954","CHEMBL3264002"],["INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR"],["An orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.","An orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2 dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.","NA","An orally bioavailable inhibitor of mitogen-activated protein kinase kinase (MAP2K; MAPK/ERK kinase; MEK) 1 and 2, with potential antineoplastic activity. Upon oral administration, trametinib specifically binds to and inhibits MEK 1 and 2, resulting in an inhibition of growth factor-mediated cell signaling and cellular proliferation in various cancers. MEK 1 and 2, dual specificity serine/threonine and tyrosine kinases often upregulated in various cancer cell types, play a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth.","A synthetic, fungal metabolite analogue inhibitor of mitogen-activated protein kinase kinase 1 (MEK-1) and mitogen-activated protein kinase kinase kinase 1 (MEKK-1) with potential antipsoriatic and antineoplastic activities. MEK-1/MEKK-1 inhibitor E6201 specifically binds to and inhibits the activities of MEK-1 and MEKK-1, which may result in the inhibition of tumor cell proliferation. MEK-1 and MEKK-1 are key components in the RAS/RAF/MEK/MAPK signaling pathway, which regulates cell proliferation and is frequently activated in human cancers.","An agent that inhibits both mitogen-activated protein kinase kinases 1 and 2 (MEK1 and MEK2), substrates of Raf and phosphorylates extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), preventing phosphorylation and activation of the Mitogen-Activated Protein Kinase (MAPK) pathways, involved with signal transduction pathways and tumor proliferation.","An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally bioavailable selective MEK inhibitor with potential antineoplastic activity. Refametinib specifically inhibits mitogen-activated protein kinase kinase 1 (MAP2K1 or MAPK/ERK kinase 1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","An orally bioavailable, synthetic organic molecule targeting mitogen-activated protein kinase kinase (MAPK/ERK kinase or MEK) with potential antineoplastic activity. Upon administration, mirdametinib selectively binds to and inhibits MEK, which may result in the inhibition of the phosphorylation and activation of MAPK/ERK and the inhibition of tumor cell proliferation. The dual specific threonine/tyrosine kinase MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors.","An orally bioavailable inhibitor of mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK), with potential antineoplastic activity. Upon administration, tunlametinib selectively binds to and inhibits the activity of MEK, preventing the activation of MEK-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a threonine/tyrosine kinase, plays a key role in the activation of the RAS/RAF/MEK/ERK pathway that regulates cell growth. This pathway is often dysregulated in a variety of tumor cell types through BRAF, KRAS and NRAS mutations.","An orally bioavailable, small molecule inhibitor of mitogen-activated protein (MAP) kinase-activated protein kinase 2 (MAPKAPK2; MK2), with potential anti-inflammatory activity. Upon oral administration, zunsemetinib targets and binds to the p38MAPK-MK2 complex, thereby inhibiting the p38MAPK phosphorylation and activation of MK2. This inhibits p38MAPK/MK2-mediated inflammatory signaling pathway. This may result in the inhibition of the production of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1-alpha, IL-1-beta and IL-6.","An orally available small molecule mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK) inhibitor, with potential antineoplastic activity. MEK inhibitor WX-554 selectively binds to and inhibits the activity of MEK, thereby preventing the activation of MEK-dependent effector proteins including some transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual-specificity threonine/tyrosine kinase that plays a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway, is frequently upregulated in a variety of tumor cell types.","An orally bioavailable, non-ATP-competitive, allosteric, small-molecule inhibitor of mitogen-activated protein kinase kinase (MAP2K; MAPK/ERK kinase; MEK) 1 and MEK2, with potential antineoplastic activity. Upon oral administration, MEK inhibitor REC-4881 selectively binds to and inhibits the activity of MEK1/2. This prevents the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally active, selective MEK inhibitor with potential antineoplastic activity. MEK inhibitor AZD8330 specifically inhibits mitogen-activated protein kinase kinase 1 (MEK or MAP/ERK kinase1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","NA","An orally active small molecule, targeting mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. MEK inhibitor RO4987655 binds to and inhibits MEK, which may result in the inhibition of MEK-dependent cell signaling and the inhibition of tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","NA","NA","An orally bioavailable inhibitor of the serine/threonine protein kinases Raf and mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK), with potential antineoplastic activity. Upon oral administration, avutometinib specifically targets, binds to and inhibits the kinase activities of Raf and MEK, resulting in the inhibition of Raf/MEK-mediated signal transduction pathways. This results in the inhibition of Raf/MEK-dependent tumor cell proliferation and survival. The RAS/RAF/MEK/extracellular signal-regulated kinase (ERK) signaling pathway is often dysregulated in human cancers and plays a key role in tumor cell proliferation, differentiation and 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<th>nci_t<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"drug_id","targets":1},{"name":"drug_name","targets":2},{"name":"drug_type","targets":3},{"name":"molecule_chembl_id","targets":4},{"name":"drug_action_type","targets":5},{"name":"nci_concept_definition","targets":6},{"name":"opentargets","targets":7},{"name":"drug_cancer_relevance","targets":8},{"name":"inhibition_moa","targets":9},{"name":"is_salt","targets":10},{"name":"is_adc","targets":11},{"name":"drug_blackbox_warning","targets":12},{"name":"nci_t","targets":13},{"name":"drug_frac_cancer_indications","targets":14},{"name":"drug_approved_noncancer","targets":15},{"name":"drug_n_indications","targets":16},{"name":"drug_year_first_approval","targets":17},{"name":"drug_max_ct_phase","targets":18},{"name":"disease_indication","targets":19},{"name":"disease_indication_max_phase","targets":20},{"name":"atc_code_level1","targets":21},{"name":"atc_level1","targets":22},{"name":"atc_code_level2","targets":23},{"name":"atc_level2","targets":24},{"name":"atc_code_level3","targets":25},{"name":"atc_level3","targets":26},{"name":"atc_treatment_category","targets":27}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
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+<script type="application/json" data-for="htmlwidget-6ce5a4724c28d6dcbdb5">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20"],[26696,5231,8779,29481,29479,19071,19060,23725,25530,20194,29940,31265,19068,19065,19059,417,19066,25079,4534,4132],["Selumetinib","Binimetinib","Cobimetinib","Trametinib Dimethyl Sulfoxide","Trametinib","E-6201","CI-1040","Pimasertib","Refametinib","Mirdametinib","Tunlametinib","Zunsemetinib","WX-554","TAK-733","AZD-8330","As-703988","RO-4987655","Rg-7167","Balamapimod","Avutometinib"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule"],["CHEMBL1614701","CHEMBL3187723","CHEMBL2146883","CHEMBL2105741","CHEMBL2103875","CHEMBL1097999","CHEMBL105442","CHEMBL2107832","CHEMBL1236682","CHEMBL507361","CHEMBL5095241","CHEMBL3704901","CHEMBL3545145","CHEMBL1615025","CHEMBL3182621","CHEMBL3545243","CHEMBL1614766","CHEMBL3545383","CHEMBL2104954","CHEMBL3264002"],["INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR"],["An orally active, small molecule with potential antineoplastic activity. Selumetinib is an ATP-independent inhibitor of mitogen-activated protein kinase kinase (MEK or MAPK/ERK kinase) 1 and 2. MEK 1 and 2 are dual specificity kinases that are essential mediators in the activation of the RAS/RAF/MEK/ERK pathway, are often upregulated in various cancer cells, and are drivers of diverse cellular responses, including proliferation. Inhibition of both MEK1 and 2 by selumetinib prevents the activation of MEK1/2 dependent effector proteins and transcription factors, thereby leading to an inhibition of cellular proliferation in various cancers.","An orally available inhibitor of mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) with potential antineoplastic activity. Binimetinib, noncompetitive with ATP, binds to and inhibits the activity of MEK1/2. Inhibition of MEK1/2 prevents the activation of MEK1/2 dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling. This may eventually lead to an inhibition of tumor cell proliferation and an inhibition in production of various inflammatory cytokines including interleukin-1, -6 and tumor necrosis factor. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally bioavailable small-molecule inhibitor of mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a B-RAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases.","NA","An orally bioavailable inhibitor of mitogen-activated protein kinase kinase (MAP2K; MAPK/ERK kinase; MEK) 1 and 2, with potential antineoplastic activity. Upon oral administration, trametinib specifically binds to and inhibits MEK 1 and 2, resulting in an inhibition of growth factor-mediated cell signaling and cellular proliferation in various cancers. MEK 1 and 2, dual specificity serine/threonine and tyrosine kinases often upregulated in various cancer cell types, play a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth.","A synthetic, fungal metabolite analogue inhibitor of mitogen-activated protein kinase kinase 1 (MEK-1) and mitogen-activated protein kinase kinase kinase 1 (MEKK-1) with potential antipsoriatic and antineoplastic activities. MEK-1/MEKK-1 inhibitor E6201 specifically binds to and inhibits the activities of MEK-1 and MEKK-1, which may result in the inhibition of tumor cell proliferation. MEK-1 and MEKK-1 are key components in the RAS/RAF/MEK/MAPK signaling pathway, which regulates cell proliferation and is frequently activated in human cancers.","An agent that inhibits both mitogen-activated protein kinase kinases 1 and 2 (MEK1 and MEK2), substrates of Raf and phosphorylates extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), preventing phosphorylation and activation of the Mitogen-Activated Protein Kinase (MAPK) pathways, involved with signal transduction pathways and tumor proliferation.","An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally bioavailable selective MEK inhibitor with potential antineoplastic activity. Refametinib specifically inhibits mitogen-activated protein kinase kinase 1 (MAP2K1 or MAPK/ERK kinase 1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","An orally bioavailable, synthetic organic molecule targeting mitogen-activated protein kinase kinase (MAPK/ERK kinase or MEK) with potential antineoplastic activity. Upon administration, mirdametinib selectively binds to and inhibits MEK, which may result in the inhibition of the phosphorylation and activation of MAPK/ERK and the inhibition of tumor cell proliferation. The dual specific threonine/tyrosine kinase MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors.","An orally bioavailable inhibitor of mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK), with potential antineoplastic activity. Upon administration, tunlametinib selectively binds to and inhibits the activity of MEK, preventing the activation of MEK-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a threonine/tyrosine kinase, plays a key role in the activation of the RAS/RAF/MEK/ERK pathway that regulates cell growth. This pathway is often dysregulated in a variety of tumor cell types through BRAF, KRAS and NRAS mutations.","An orally bioavailable, small molecule inhibitor of mitogen-activated protein (MAP) kinase-activated protein kinase 2 (MAPKAPK2; MK2), with potential anti-inflammatory activity. Upon oral administration, zunsemetinib targets and binds to the p38MAPK-MK2 complex, thereby inhibiting the p38MAPK phosphorylation and activation of MK2. This inhibits p38MAPK/MK2-mediated inflammatory signaling pathway. This may result in the inhibition of the production of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1-alpha, IL-1-beta and IL-6.","An orally available small molecule mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK) inhibitor, with potential antineoplastic activity. MEK inhibitor WX-554 selectively binds to and inhibits the activity of MEK, thereby preventing the activation of MEK-dependent effector proteins including some transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK, a dual-specificity threonine/tyrosine kinase that plays a key role in the activation of the RAS/RAF/MEK/ERK signaling pathway, is frequently upregulated in a variety of tumor cell types.","An orally bioavailable, non-ATP-competitive, allosteric, small-molecule inhibitor of mitogen-activated protein kinase kinase (MAP2K; MAPK/ERK kinase; MEK) 1 and MEK2, with potential antineoplastic activity. Upon oral administration, MEK inhibitor REC-4881 selectively binds to and inhibits the activity of MEK1/2. This prevents the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.","An orally active, selective MEK inhibitor with potential antineoplastic activity. MEK inhibitor AZD8330 specifically inhibits mitogen-activated protein kinase kinase 1 (MEK or MAP/ERK kinase1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","NA","An orally active small molecule, targeting mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), with potential antineoplastic activity. MEK inhibitor RO4987655 binds to and inhibits MEK, which may result in the inhibition of MEK-dependent cell signaling and the inhibition of tumor cell proliferation. MEK, a dual specificity threonine/tyrosine kinase, is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.","NA","NA","An orally bioavailable inhibitor of the serine/threonine protein kinases Raf and mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK), with potential antineoplastic activity. Upon oral administration, avutometinib specifically targets, binds to and inhibits the kinase activities of Raf and MEK, resulting in the inhibition of Raf/MEK-mediated signal transduction pathways. This results in the inhibition of Raf/MEK-dependent tumor cell proliferation and survival. The RAS/RAF/MEK/extracellular signal-regulated kinase (ERK) signaling pathway is often dysregulated in human cancers and plays a key role in tumor cell proliferation, differentiation and 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inhibitors"],["cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy","cancer_targeted_therapy"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"drug_id","targets":1},{"name":"drug_name","targets":2},{"name":"drug_type","targets":3},{"name":"molecule_chembl_id","targets":4},{"name":"drug_action_type","targets":5},{"name":"nci_concept_definition","targets":6},{"name":"opentargets","targets":7},{"name":"drug_cancer_relevance","targets":8},{"name":"inhibition_moa","targets":9},{"name":"is_salt","targets":10},{"name":"is_adc","targets":11},{"name":"drug_blackbox_warning","targets":12},{"name":"nci_t","targets":13},{"name":"drug_frac_cancer_indications","targets":14},{"name":"drug_approved_noncancer","targets":15},{"name":"drug_n_indications","targets":16},{"name":"drug_year_first_approval","targets":17},{"name":"drug_max_ct_phase","targets":18},{"name":"disease_indication","targets":19},{"name":"disease_indication_max_phase","targets":20},{"name":"atc_code_level1","targets":21},{"name":"atc_level1","targets":22},{"name":"atc_code_level2","targets":23},{"name":"atc_level2","targets":24},{"name":"atc_code_level3","targets":25},{"name":"atc_level3","targets":26},{"name":"atc_treatment_category","targets":27}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
 </div>
 <div class="section level3">
 <h3 id="get-immune-checkpoint-inhibitors-list-per-drug-target">Get immune checkpoint inhibitors, list per drug target<a class="anchor" aria-label="anchor" href="#get-immune-checkpoint-inhibitors-list-per-drug-target"></a>
@@ -333,8 +328,8 @@ <h3 id="get-immune-checkpoint-inhibitors-list-per-drug-target">Get immune checkp
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
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human IgG2 monoclonal antibody directed against the T-cell receptor protein cytotoxic T-lymphocyte-associated protein 4 (CTLA4). Tremelimumab binds to CTLA4 and blocks the binding of the antigen-presenting cell ligands B7-1 and B7-2 to CTLA4, resulting in inhibition of B7-CTLA4-mediated downregulation of T-cell activation; subsequently, B7-1 or B7-2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA4-mediated inhibition.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; programmed death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, dostarlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T-cells, functions as an immune checkpoint protein that negatively regulates T-cell activation and T-cell-mediated immune responses when activated by its ligands programmed cell death receptor ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cemiplimab binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.","A monoclonal antibody directed against B7H1 (B7 homolog 1; programmed cell death ligand 1) with potential immunostimulating activity. Upon intravenous administration, durvalumab binds to the cell surface antigen B7H1, thereby blocking B7H1 signaling. This may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7H1-expressing tumor cells. B7H1, a member of the B7 protein superfamily and a negative regulator of cytokine synthesis, is overexpressed on certain tumor cell types.","A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T-cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","A fully human immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, nivolumab binds to and blocks the activation of PD-1, an immunoglobulin superfamily (IgSF) transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T-cells and cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.","A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.","A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A monoclonal antibody directed against the inhibitor receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, relatlimab binds to LAG-3 on tumor infiltrating lymphocytes (TILs). This may activate antigen-specific T-lymphocytes and enhance cytotoxic T cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3 is a member of the immunoglobulin superfamily (IgSF) and binds to major histocompatibility complex (MHC) class II. LAG-3 expression on TILs is associated with tumor-mediated immune suppression.","NA","NA","NA","NA","NA","NA","An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sasanlimab targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.","A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PDCD1; PD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sintilimab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","A proprietary humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, retifanlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tislelizumab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","NA","NA","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, spartalizumab binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.","NA","A recombinant antibody prodrug composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) programmed cell death 1 ligand 1 (PD-L1; B7-H1; CD274) that is linked to a proprietary masking peptide through a protease-cleavable linker on the amino terminus of the light chain domain of the antibody, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of pacmilimab, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment, the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the tumor microenvironment, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables binding of the unmasked, fully active monoclonal antibody moiety of CX-072 to PD-L1, which is over expressed on certain cancer cells. This blocks the binding to and activation of its receptor programmed cell death 1 (PD-1) on T-lymphocytes, thereby enhancing the T-cell-mediated anti-tumor immune response and reversing PD-L1/PD-1-mediated T-cell suppression. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. Compared to the unmodified PD-L1 antibody, peptide masking of CX-072 minimizes binding to PD-L1 in normal tissues, thereby decreasing autoimmune-based side effects while retaining anti-tumor activity.","An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","A humanized monoclonal antibody directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. Pidilizumab blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues.","NA","NA","A recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, zalifrelimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A recombinant B7-DC Fc-fusion protein composed of the extracellular domain of the PD-1 ligand programmed cell death ligand 2 (PD-L2, B7-DC) and the Fc region of human immunoglobulin (Ig) G1, with potential immune checkpoint inhibitory and antineoplastic activities. Anti-PD-1 fusion protein AMP-224 specifically binds to PD-1 on chronically stimulated T-cells and reduces their proliferation. This may restore immune function and may result in the activation of cytotoxic T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein of Ig superfamily and inhibitor receptor expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. AMP-224 does not bind normal activated T-cells.","NA","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1 , PCD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody Sym021 binds to and inhibits PD-1 activation and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF), is expressed on T-cells and functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2). Activated PD-1 plays an important role in tumor evasion from host immunity.","A fully human, immunoglobulin G4 (IgG4) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody ASP8374 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A fully human monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Anti-PD-L1 monoclonal antibody MDX-1105 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","NA","NA","A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, lodapolimab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T-cells.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,encelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, manelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A humanized, Fc-engineered bispecific monoclonal antibody directed against both the human negative immunoregulatory checkpoint receptor, programmed cell death protein 1 (PD-1; PCD-1; CD279), and inducible T-cell co-stimulator (ICOS; CD278), with potential immunomodulating and antineoplastic activities. Upon administration, izuralimab targets and binds to both PD-1 and ICOS expressed on certain T-cells, including tumor-infiltrating lymphocytes (TILs). This prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2), and stimulates ICOS-mediated signaling, which promotes the activation of T-cells and enhances T-cell-mediated immune responses against tumor cells. Combined PD-1 blockade and ICOS stimulation may enhance T-cell activation and proliferation more than targeting each receptor individually. The engineered Fc domain increases the stability and half-life of the antibody.","A recombinant human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, opucolimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","An immunoglobulin G4 (IgG4), humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, adebrelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody (MAb) directed against the inhibitory receptor lymphocyte activation gene-3 protein (LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, favezelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized, pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, gotistobart targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. As gotistobart is dissociated from CTLA-4 under low pH, it does not cause lysosomal degradation of CTLA-4, preserving CTLA-4 and allowing the recycling of CTLA-4. This may result in more efficient and selective CTLA-4-targeted regulatory T-cell (Treg) depletion within the tumor microenvironment (TME) while preserving CTLA-4 functions outside the TME, thereby reducing toxicities. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor, programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, lipustobart binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands, programmed cell death-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways, leading to the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1 is a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells that negatively regulates T-cell activation and effector function when activated by its ligands. PD-1 plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, prolgolimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,rulonilimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, tamgiblimab targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A human monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, zeluvalimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, caldonirimab targets and binds to both PD-1 and CTLA4 expressed on tumor-infiltrating T lymphocytes (TILs), and inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity.","An immunoglobulin G4 (IgG4) humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PD1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, geptanolimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,miptenalimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, negalstobart targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, nofazinlimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, renvistobart binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T-lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells, and leads to CD226 dimerization and CD226-mediated signaling. This activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tagitanlimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A Fc-engineered immunoglobulin G1-kappa (IgG1k) monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, tuparstobart targets and binds to human LAG-3 on tumor-infiltrating  lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, which leads to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both proliferation and activation of T-cells. Its expression on  TILs is associated with tumor-mediated immune suppression.","An immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, tuvonralimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A second-generation, humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Betifisolimab contains a unique, not as of yet elucidated, pH-dependent antigen binding property allowing the antibody to only bind to PD-L1 within the acidic tumor microenvironment (TME), while it is not able to bind to PD-L1 in normal, healthy tissue. Upon administration, once able to bind to PD-L1 in the TME, betifisolimab blocks the binding of PD-L1 to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on activated T-cells suppresses the immune system and results in immune evasion. PD-1 negatively regulates T-cell activation.","An agent designed to interfere with the activity of programmed cell death protein 1 (PD1). PD1 inhibitors block T-cell apoptosis and act as non-specific activators of the immune system.","An agent designed to interfere with the activity of programmed death ligand 1 (PD-L1; CD274), a ligand for the receptor programmed cell death protein 1 (PD-1; PD1).","A humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pradusinstobart targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Any agent that targets lymphocyte-activation gene 3 protein (LAG-3; CD223).","Any agent that binds to any of the ligands for the receptor programmed cell death protein 1 (PD-1; PD1); programmed death ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273).","A self-delivering small-interfering RNA (siRNA) targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, anti-PD-1 siRNA PH-762 binds to and destroys mRNA PD-1, thereby preventing the expression of PD-1. As PD1-mediates the downregulation of T-cell activation and proliferation, PH-762 is able to restore immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This may lead to an inhibition of tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 (cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","Any agent that targets cytotoxic T-lymphocyte-associated protein 4 (CTLA-4; CTLA4; CD152).","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor AN4005 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding of PD-L1 to and subsequent activation of its receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor ABSK043 specifically targets and binds to PD-L1 expressed on tumor cells, leading to internalization and preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, anti-viral and antineoplastic activities. Upon administration, PD-L1 inhibitor GS-4224 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. It may also enhance hepatitis B virus (HBV)-specific CD8+ T-cell function, thereby killing HBV-infected cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells. It is also upregulated in HBV-positive patients and contributes to immune dysfunction against HBV infection.","A mixture of the two engineered monoclonal antibodies iparomlimab, which is an immunoglobulin G4 (IgG4) monoclonal antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and tuvonralimab, which is an IgG1 monoclonal antibody directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of iparomlimab/tuvonralimab, iparomlimab and tuvonralimab target and bind to PD-1 and CTLA4 expressed on tumor-infiltrating lymphocytes (TILs), respectively. This inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor BPI-371153 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, PD-L1 inhibitor INCB086550 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099280 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099318 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","A monoclonal antibody directed against programmed cell death protein 1 (PD-1; PD1; CD279).","A probody composed of a modified version of ipilimumab, a recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 probody BMS-986288, the masking peptide is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to CTLA-4, which is expressed on certain T-cells. This inhibits the CTLA4-mediated downregulation of T-cell activation, and leads to both activation of tumor infiltrating T-effector cells and a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily expressed on activated effector T-cells (Teffs) and regulatory T-cells (Tregs), plays a key role in the inhibition of T-cell activity and downregulation of the immune system. The peptide masking of BMS-986288 minimizes binding to CTLA-4 in normal tissues and may reduce systemic toxicity, when compared to ipilimumab. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.","A monoclonal antibody directed against programmed death-ligand 1 (PD-L1; CD274).","A recombinant immunoglobulin G4 (IgG4) kappa monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody 609A targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MW11 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody TY101 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody RC98 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A preparation of T-lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-PD-L1 CAR-T cells target and bind to CLDN18.2- and PD-L1-expressing tumor cells, thereby inducing selective toxicity in CLDN18.2- and PD-L1-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity.","A recombinant monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody HLX26 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A recombinant monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody PE0105 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody QL1604 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SYN125 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune functions through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody LP002 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, by binding to PD-L1, LP002 also prevents binding of this ligand to B7.1 expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A recombinant, humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody YH001 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A recombinant, human Fc-inert monoclonal antibody targeting lymphocyte-activation gene 3 protein (LAG-3; LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, monoclonal antibody Sym022 binds to human LAG-3 and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHCII) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHCII binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Additionally, Sym022 decreases LAG-3 surface levels through internalization and shredding. LAG-3 plays a key role in the activation of T-cells and natural killer (NK) cells.","A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1306 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized  immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1308 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody GNR-051 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody OSE-279 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1), with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody FAZ053 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated anti-tumor immune response and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T-cells.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody GR1405 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to the immunostimulatory cytokine interleukin-15 (IL-15), with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein KD033, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","An immunoglobulin G4 (IgG4) monoclonal antibody targeting the poliovirus receptor (PVR; CD155; nectin-like protein 5; NECL-5), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PVR monoclonal antibody NTX-1088 targets and binds to PVR expressed on tumor cells, thereby preventing its interactions with the human cell surface glycoprotein CD226 (DNAX accessory molecule-1; DNAM-1), the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the negative immunoregulatory human cell surface receptor CD96 (Tactile; T cell activation increased late expression). The binding of NTX-1088 to CD226 prevents the internalization of CD226 and restores its expression on the surface of immune cells. This promotes CD226-dependent signaling pathways, which may trigger the activation of antigen-presenting cells (APCs) and activate T-cells and natural killer (NK) cells, and result in an enhanced cytotoxic T-lymphocyte (CTL)-mediated and NK cell-mediated immune response against tumor cells. The binding of NTX-1088 to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands and promotes the interaction of its ligands with the costimulatory receptor CD226 expressed on immune cells. This leads to CD226 dimerization and further promotes CD226-mediated signaling and anti-tumor immune responses. The binding of NTX-1088 to CD96 expressed primarily on T-cells and NK cells prevents its downstream signaling pathways. This may abrogate CD96-mediated inhibition of T-cell and NK cell effector function and may further restore immune function and anti-tumor immune responses through the activation of T-cells and NK cells. PVR, a key regulator of immune activation through multiple mechanisms, is overexpressed in a variety of tumor cell types while minimally or not expressed in normal tissues.","A fully human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody COM902 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody PM1021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody TAB006 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody IBI310 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody KD6001 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A fully humanized, Fc-engineered monoclonal antibody with masked antigen-binding regions directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration and the activation of the antigen-binding regions via cleavage by proteases that are upregulated in the tumor microenvironment (TME), anti-CTLA-4 monoclonal antibody XTX101 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody GLS-012 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody LBL-007 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A recombinant humanized monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody TQB2223 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MEDI0680 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1901 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2). PD-1 plays an important role in tumor evasion from host immunity.","An immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6005 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A nonfucosylated human immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody SGN-TGT targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T-lymphocytes (TILs). This prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5), and enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This enhances depletion of TIGIT-positive regulatory T-cells (Tregs) and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), fused with potency reduced interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) sushi domain complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein SIM0237, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, the IL-15/IL-15Ra complex stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. The attenuated IL-15 prevents the overstimulation of CD8+ T and NK cells.","A fusion protein composed of an antibody moiety targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a mutein of the immunostimulatory cytokine interleukin-15 (IL-15), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD1/IL-15 fusion protein SAR445877, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. The IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the tumor microenvironment (TME), and induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. The IL-15 mutein form lowers the systemic toxicity of IL-15.","A preparation of autologous engineered red blood cells (RBCs) conjugated with pembrolizumab, an antibody against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of the RBCs-anti-PD1 antibody conjugate WTX212, the RBCs primarily and directly distribute to the spleen and vascular system. The anti-PD1 antibodies target, bind to and inhibit PD-1, leading to the abrogation of PD1-mediated downregulation of T-cell activation and proliferation. This restores immune function, decreases programmed cell death-1 ligand 1 (PD-L1)-positive myeloid-derived suppressor cells (MDSCs) and regulatory T-cells (Tregs) and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 (cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","A humanized immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody ADU-1604 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A fully human immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody REGN4659 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A tetravalent bispecific fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta receptor II (TGFbRII) fusion protein LBL-015 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocyte; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A Fc-enhanced bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and an as of yet undisclosed receptor expressed specifically on T-cells and natural killer (NK) cells, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, the anti-TIGIT bispecific antibody BMS-986442 simultaneously targets and binds to TIGIT and the undisclosed receptor. Upon binding to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), BMS-986442 blocks the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as NK cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. In addition, binding of BMS-986442 to the undisclosed target expressed on T-cells and NK cells may further enhance anti-tumor immune responses. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant, humanized fusion protein consisting of a cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) single domain antibody linked to a Fc domain, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA4 antibody Fc fusion protein KN044 targets and binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A bispecific antibody directed against both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the cell surface antigen CD27, with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PD-L1/CD27 bispecific antibody CDX-527 targets and binds to both PD-L1 expressed on tumor cells and CD27 expressed on a variety of immune cell types, including most T-lymphocytes. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling and induces CD27-mediated signaling. This inhibits the PD-1-mediated downregulation of T-cell activation and proliferation, and enhances CD27-mediated responses, including the expansion of antigen-activated T-cells and the cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity. CD27, a co-stimulatory molecule and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T-lymphocytes, memory B-cells and natural killer (NK) cells. It plays an important role in NK cell-mediated cytolytic activity and T- and B-lymphocyte proliferation and activation.","An antibody-drug conjugate (ADC) composed of an antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), conjugated to the cytotoxic agent monomethyl auristatin E (MMAE) via a protease-cleavable peptide linker, with potential antineoplastic activity. Upon administration of the anti-PD-L1 ADC SGN-PDL1V, the anti-PD-L1 antibody specifically targets and binds to PD-L1 expressed on tumor cells. Following internalization, enzymatic cleavage and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on the surface of certain immune cells and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","A human immunoglobulin G1 (IgG1) Fc-silenced bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279; programmed death 1) and lymphocyte activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3/PD-1 bispecific antibody INCA32459 targets and binds to both PD-1 and LAG-3 expressed on T-cells and inhibits PD-1- and LAG-3-mediated downregulation of T-cell activation and proliferation. This may lead to cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1 and LAG-3 play key roles in suppressing T-cell activation and proliferation.","A recombinant humanized bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody JS207 simultaneously targets and binds to both PD-1 expressed on T-cells and VEGF expressed on tumor cells. The binding of JS207 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of JS207 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.","A bispecific antibody targeting the immunosuppressive ligand programmed death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/4-1BB bispecific antibody QLF31907 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. Upon 4-1BB binding, QLF31907 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, QLF31907 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A full-length, Fc-silenced immunoglobulin G1 (IgG1) bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/CD137 bispecific antibody MCLA-145 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T-lymphocytes. Through CD137 binding, MCLA-145 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, MCLA-145 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. Crosslinking of PD-L1-expressing tumor cells and activated T-lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells.","Fc-engineered bispecific monoclonal antibody targeting both immune checkpoint regulatory proteins human programmed death-ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/PD-L2 bispecific antibody IMGS-001 simultaneously targets and binds to PD-L1 and PD-L2 expressed on tumor cells, immunosuppressive stromal cells and endothelial cells. PD-L1 and PD-L2 binding by IMGS-001 prevents both PD-L1 and PD-L2 from binding to and activating their receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates PD-1-mediated signaling in T-cells and PD-1-mediated T-cell inhibition. This activates cytotoxic T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. In addition, IMGS-001 induces antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), thereby killing PD-L1 and PD-L2-expressing cells in the tumor microenvironment (TME), and further abrogating the immunosuppressive nature of the TME. PD-L1 and PD-L2 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","A fusion protein composed of a recombinant human monoclonal antibody targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a prodrug for the immunostimulatory cytokine interleukin-15 (IL-15), composed of a potency reduced, mutein form of interleukin (IL)-15 complexed with the high-affinity IL-15 receptor alpha (IL-15Ra) binding sushi domain, that is masked by a protease-cleavable masking protein, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD-1-IL-15 prodrug fusion molecule ASKG915, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and a T-cell-mediated immune response against tumor cells. Upon cleavage of the protease-cleavable linker by proteases overexpressed in the tumor environment (TME), the IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, and further induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. The IL-15 mutein form lowers systemic toxicity of IL-15. Protease-dependent activation of IL-15 increases its efficacy and decreases systemic toxicity. IL-15Ra complexed with IL-15 domain improves stability and increases the half-life of IL-15.","A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the T-cell surface antigen CD3, with potential immunomodulatory and antineoplastic activities. Upon administration, anti-PD-1/anti-CD3 bispecific antibody ONO-4685 binds to both PD-1 expressed on activated T- and B-cells and certain malignant T-cells and CD3 antigen on cytotoxic T-lymphocytes (CTLs). This may activate and redirect CTLs to PD-1-expressing cells, resulting in CTL-mediated killing of these cells. This may lead to anti-tumor activity in some T-cell lymphomas, and immunomodulatory activity in some autoimmune diseases.","A preparation of autologous human T-lymphocytes engineered to express a chimeric antigen receptor (CAR) composed of a modified from of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1), in which the intracellular signal domain of PD-1 is transformed to allow for stimulatory signaling but with an intact extracellular ligand binding domain that specifically binds the tumor-associated antigen (TAA) programmed cell death-1 ligand 1 (PD-L1), and a modified form of the T-cell inhibitory receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with a transformed intracellular signal domain to allow for stimulatory signaling, which specifically binds the B7 proteins CD80 (B7-1) and CD86 (B7-2), with potential immunostimulating and antineoplastic activities. Usually, ligand binding to PD-1 and CTLA-4 inhibits T-cell activity; however, these modified forms of PD-1 and CTLA-4 promote T-cell stimulatory signaling. Upon administration, the autologous PD-L1/CD80/CD86-targeted CAR-T cells target and bind to PD-L1 expressed on certain tumor cells and to CD80/CD86 expressed on antigen-presenting cells (APCs). This stimulates T-cell activation, T-cell proliferation and enhanced cytokine production, which induces selective toxicity in tumor cells expressing PD-L1. PD-1, found on activated T-cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PD-L1 is often overexpressed on tumor cell types and plays a key role in immune evasion. The co-stimulatory molecules CD80 and CD86 play a key role in T-lymphocyte activation upon binding to CD28 upon antigen recognition; however, binding of CD80 and CD86 to wild-type CTLA-4 inhibits T-cell activity and results in T-cell exhaustion.","A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-4-1BB bispecific antibody IBI-319 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes in the tumor microenvironment (TME), and 4-1BB, which is expressed on activated T-lymphocytes and natural killer (NK) cells. This crosslinks PD-1- and 4-1BB-expressing T cells. Through 4-1BB binding, IBI-319 acts as a conditional 4-1BB agonist, resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, PD-1 binding prevents PD-L1 from binding to and activating its receptor PD-1 and inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A bispecific antibody composed of a Fc-silenced human immunoglobulin G1 (IgG1) monoclonal antibody targeting human programmed death-ligand 1 (PD-L1) fused with a single chain variable fragment (scFv) targeting 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/anti-4-1BB bispecific antibody ABL503 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. Upon PD-L1 binding, the 4-1BB activation signal is induced and ABL503 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, ABL503 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A fusion protein composed of a pentameric immunoglobulin M (IgM) antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1 antibody/IL-15 fusion protein IGM-7354, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cancer cells and antigen presenting cells (APCs) in the tumor microenvironment (TME), thereby delivering IL-15 to PD-L1-expressing tumor cells. In turn, the IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally, and reverses T-cell exhaustion. This induces an anti-tumor immune response in the TME against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on APCs and on various cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. The immunostimulatory cytokine IL-15 regulates CD8+ T- and NK cell development, activation, and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. By binding to PD-L1-expressing cells in the TME, IGM-7354 enhances its IL-15-mediated activity on the immune system locally and increases its efficacy while reducing systemic toxicities.","A bispecific antibody targeting both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and vascular endothelial growth factor A (VEGF-A), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF-A bispecific antibody PM8002 targets and simultaneously binds to both PD-L1 and VEGF-A expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. The binding of PM8002 to VEGF-A prevents the binding of VEGF-A to VEGF receptor (VEGFR), thereby preventing the activation of VEGF-A/VEGFR-mediated signaling pathways. This prevents angiogenesis and may halt tumor cell proliferation. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF-A is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis.","A fixed-dose co-formulation composed of pembrolizumab, a humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against human cell surface receptor PD-1 (programmed death-1; programmed cell death-1; cluster of differentiation 279; CD279), and MK-5180, a recombinant form of human hyaluronidase, with potential immune checkpoint inhibitory and antineoplastic activities. Upon subcutaneous administration of recombinant human hyaluronidase and pembrolizumab, the hyaluronidase reversibly depolymerizes the polysaccharide hyaluronan in the subcutaneous tissue. This increases the permeability of the subcutaneous tissue and enhances the absorption of pembrolizumab into the systemic circulation. In turn, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T-cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1; cluster of differentiation 274; CD274), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity. When administered subcutaneously, hyaluronidase, an endoglycosidase, increases the dispersion and absorption of co-administered drugs.","A bispecific antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta) receptor II (TGFbRII), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/anti-TGFbRII bispecific antibody INCA33890 targets and binds to both PD-1 and TGFbRII and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). The binding of INCA33890 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of INCA33890 to TGFbRII prevents the binding of TGF-beta to TGFbRII, thereby preventing the activation of the TGF-beta-mediated signaling pathway. This abrogates TGF-beta-mediated immunosuppression in the TME, increases natural killer (NK) cell and CTL activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A bispecific antibody fusion protein composed of a monoclonal antibody targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and fused to a mutated form of the endogenous cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/IL-2 bispecific antibody fusion protein IBI363 targets and binds to PD-1 expressed on PD-1-expressing T-cells, thereby inhibiting PD-1-mediated signaling. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. IL-2 targets and binds to the IL-2 receptor IL2R and activates IL-2/IL-2R-mediated signaling, which further activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). This further enhances T-cell-mediated cytotoxic immune responses against tumor cells. By selectively activating PD-1 positive T-cells by IL-2, but not PD-1 negative bystander or na\u001a\u001ave T cells, the activity of tumor specific T-cells is specifically enhanced while IL-2-induced systemic toxicity is decreased. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A bifunctional fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating, immunomodulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta RII bifunctional fusion protein JS201 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression and the suppression of the immune response.","A genetically modified oncolytic virus (OV) composed of a replication competent orthopoxviral chimera engineered to express the human sodium iodine symporter (hNIS) and a human monoclonal antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential oncolytic, immunostimulating and antineoplastic activities that can be used for radioimaging upon positron emission tomography (PET) and radiotherapeutic applications. Upon subcutaneous (SC) intratumoral (IT) administration of the oncolytic virus CF33-expressing hNIS/anti-PD-L1 antibody, the oncolytic virus specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, the anti-PD-L1 antibody produced by the infected tumor cells targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), a transmembrane protein and negative regulator of the immune system, expressed on activated T-cells. This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the CTL-mediated anti-tumor immune response against PD-L1-expressing tumor cells, thereby further killing tumor cells. Upon subsequent administration of certain iodine-containing imaging agents, hNIS expression by the infected tumor cells allows visualization and tracking of viral biodistribution, and analysis and quantification of CF33-infected tumor cells by PET. Also, administration of iodine I 131 results in its uptake by hNIS-expressing tumor cells, which may result in the selective accumulation of a cytotoxic dose of radiation in tumor cells while sparing adjacent normal tissue.","A bifunctional fusion protein directed against both the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TGF-beta bifunctional fusion protein TQB2868  targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A bifunctional fusion protein directed against both human programmed death ligand 1 (PD-L1) and transforming growth factor beta (TGF-beta), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, anti-PD-L1/anti-TGF-beta bifunctional fusion protein TQB2858 targets, binds to and neutralizes TGF-beta on tumor cells and simultaneously targets, binds to, and inhibits the activity of PD-L1 on the tumor cells. This prevents both TGF-beta- and PD-L1-mediated immunosuppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This also restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. TGF-beta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.","A fixed dose combination of two monoclonal antibodies of which one is directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the other one is directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217 targets and binds to both PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","A fixed dose combination of two monoclonal antibodies of which one is directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the other one is directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217 targets and binds to both PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","A bispecific antibody fusion protein composed of an immunoglobulin G1 (IgG1) monoclonal antibody targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and fused to anti-vascular endothelial growth factor (VEGF) protein, with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF bispecific antibody fusion protein B1962 targets and simultaneously binds to both PD-L1 and VEGF expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against VEGF-expressing tumor cells. The binding of B1962 to VEGF prevents the binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.","A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 promotes the secretion of IL-12 and anti-PD-1 antibody by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant fusion protein consisting of a human monoclonal antibody directed against cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) fused to the immunostimulatory cytokine interleukin-15 (IL-15) cross-linked with the sushi domain of IL-15 receptor alpha (IL-15Ra), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 monoclonal antibody-IL-15/IL-15Ra fusion protein JK08, the monoclonal antibody domain targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. The IL-15/IL-15Ra complex targets and binds to CD8+ T and natural killer (NK) cells, thereby increasing their activation and proliferation. Altogether, this leads to an inhibition of regulatory T-cell (Tregs)-mediated immunosuppression, induces antibody-dependent cellular cytotoxicity (ADCC), increases memory T-cells and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration into the glioma, oHSV-1 expressing IL-12 and anti-PD-1 antibody MVR-C5252 specifically infects and replicates in glioma cells causing viral-mediated glioma cell lysis. The released virus particles, in turn, infect and replicate in neighboring glioma cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected glioma cells. In addition, as MVR-C5252 carries exogenous genes, it is also able to express IL-12 and anti-PD-1 antibody and are released by the infected cells, both of which are able to promote an immune response in the tumor microenvironment (TME). IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against uninfected glioma cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. The anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Autologous human T-lymphocytes that are genetically engineered to express a chimeric switch receptor (CSR) composed of the extracellular ligand binding domain of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1) fused to the transmembrane and cytoplasmic co-stimulatory signaling domains of CD28 (PD1CD28; PD-1:CD28 switch receptor), with potential immunomodulating and antineoplastic activities. Upon reintroduction of autologous PD-1-targeted CSR-modified T-lymphocytes into the patient, the switch receptor expressed by the engineered T-cells targets and binds to the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2) expressed, on tumor cells. The nature of the PD-1/CD28 switch receptor fusion protein prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T-lymphocytes. This induces enhanced toxicity against PD-L1-expressing tumor cells. PD-1 protein, found on activated T-cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. Exchanging the transmembrane and intracellular domain of PD-1 with that of CD28 converts PD-L1 into a co-stimulation ligand of primary human CD8+ cytotoxic T-lymphocytes (CTLs). CD28, is a molecule expressed by T-cells that stimulates increased T-lymphocyte proliferation and activity.","An oncolytic vaccinia virus (VV; VACV) genetically engineered to express 4-E03, an immunoglobulin G1 (IgG1) antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4) and the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential oncolytic, immunostimulating and antineoplastic activities. Upon intra-tumoral administration, the oncolytic VV expressing anti-CTLA-4 antibody and GM-CSF BT-001 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oncolytic virus BT-001 promotes the secretion of anti-CTLA-4 antibody 4-E03 and GM-CSF by the tumor cells. GM-CSF attracts dendritic cells (DCs) and may further stimulate a CTL-mediated immune response against tumor cells. Anti-CTLA-4 antibody 4-E03 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This enhances the CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A preparation of autologous T-lymphocytes that have been activated and genetically modified to express immune checkpoint antibodies against the negative immunoregulatory receptors human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR), with potential immunomodulating and antineoplastic activities. After isolation, activation, transduction, expansion in culture and reintroduction into the patient, the T-cells in the autologous EGFR specific CAR-T-cells expressing anti-PD-1/CTLA4 antibodies  specifically target and kill EGFR-expressing tumor cells. The anti-PD-1 antibody secreted from the CAR-T cells binds to PD-1 expressed on T-cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion. The anti-CTLA4 expressed by the CAR-T cells targets and binds to CTLA4 expressed on T-cells, and inhibits the CTLA4-mediated downregulation of T-cell activation. Both antibodies enhance T-cell activation, improve immunosuppression in the tumor microenvironment (TME) and improve the T-cell mediated immune response against and toxicity in EGFR-expressing tumor cells. Both PD-1 and CTLA-4 negatively regulate T-cell activation and proliferation, and play a key role in immunosuppression within the TME. EGFR, a receptor tyrosine kinase that is overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation.","A preparation of autologous T-lymphocytes that have been activated and genetically modified to express immune checkpoint antibodies against the negative immunoregulatory receptors human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR), with potential immunomodulating and antineoplastic activities. After isolation, activation, transduction, expansion in culture and reintroduction into the patient, the T-cells in the autologous EGFR specific CAR-T-cells expressing anti-PD-1/CTLA4 antibodies  specifically target and kill EGFR-expressing tumor cells. The anti-PD-1 antibody secreted from the CAR-T cells binds to PD-1 expressed on T-cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion. The anti-CTLA4 expressed by the CAR-T cells targets and binds to CTLA4 expressed on T-cells, and inhibits the CTLA4-mediated downregulation of T-cell activation. Both antibodies enhance T-cell activation, improve immunosuppression in the tumor microenvironment (TME) and improve the T-cell mediated immune response against and toxicity in EGFR-expressing tumor cells. Both PD-1 and CTLA-4 negatively regulate T-cell activation and proliferation, and play a key role in immunosuppression within the TME. EGFR, a receptor tyrosine kinase that is overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation.","A preparation of autologous, engineered T-lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T-lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.","A preparation of autologous, engineered T-lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T-lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.","A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, expressing an antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), CD40 ligand (CD40L; CD154; TRAP; TNFSF5) and the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-1 expressing anti-CTLA-4 Antibody/CD40L/4-1BBL RP3 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Oncolytic virus RP3 expresses a fusogenic protein, GALV-GP R-, for optimal tumor cell infection and killing. In addition, Oncolytic virus RP3 promotes the expression of anti-CTLA-4 antibody, CD40L and 4-1BBL by the tumor cells. Anti-CTLA-4 antibody targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. CD40L specifically binds to and activates CD40, a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor family and is expressed on various immune cells, such as B-lymphocytes, monocytes, and dendritic cells (DCs). Activation of CD40 induces proliferation and activation of B-lymphocytes, shifts the induction of suppressive macrophages towards immunostimulatory macrophages, activates monocyte-derived DCs (moDCs), and leads to the secretion of inflammatory cytokines, which activates the immune system to induce the proliferation and activation of CTLs against tumor cells. 4-1BBL binds to and subsequently induces the proliferation and activation of natural killer (NK) cells and T-cells. This enhances the secretion of cytokine interferon-gamma (IFN-g) and further induces an anti-tumor immune response.","A 1:1 fixed dose combination formulation composed of the two monoclonal antibodies AI-025, a monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), and gotistobart, a pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061, AI-025 targets, binds to and inhibits PD-1 and ONC-392 targets, binds to and inhibits CTLA-4. This inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A 1:1 fixed dose combination formulation composed of the two monoclonal antibodies AI-025, a monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), and gotistobart, a pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061, AI-025 targets, binds to and inhibits PD-1 and ONC-392 targets, binds to and inhibits CTLA-4. This inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex virus type 2 (HSV-2), derived from the HG52 strain and encoding a bispecific antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the T-cell surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, oncolytic HSV-2 expressing anti-PD-L1/CD3 bispecific antibody BS-006 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, BS-006 promotes the secretion of anti-PD-L1/CD3 bispecific antibody by the infected tumor cells. The bispecific antibody targets and binds to both the CD3 on T-cells and the PD-L1 expressed on tumor cells. This results in the cross-linking of T-cells and tumor cells and may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against PD-L1-expressing tumor cells. At the same time, BS-006 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances CTL-mediated tumor cell lysis, which may further lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Deletion of ICP47 also leads to an increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and the oncolysis of tumor cells.","A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, expressing the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) and an antibody-like molecule directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-1 expressing anti-CTLA-4 antibody-like molecule and GM-CSF RP2 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Oncolytic virus RP2 expresses a fusogenic protein, GALV-GP R-, for optimal tumor cell infection and killing. In addition, Oncolytic virus RP2 promotes the secretion of GM-CSF and anti-CTLA-4 antibody-like molecule by the tumor cells. GM-CSF attracts dendritic cells (DCs) and may further stimulate a CTL-mediated immune response against tumor cells. Anti-CTLA-4 antibody-like molecule targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune 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human IgG2 monoclonal antibody directed against the T-cell receptor protein cytotoxic T-lymphocyte-associated protein 4 (CTLA4). Tremelimumab binds to CTLA4 and blocks the binding of the antigen-presenting cell ligands B7-1 and B7-2 to CTLA4, resulting in inhibition of B7-CTLA4-mediated downregulation of T-cell activation; subsequently, B7-1 or B7-2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA4-mediated inhibition.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; programmed death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, dostarlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T-cells, functions as an immune checkpoint protein that negatively regulates T-cell activation and T-cell-mediated immune responses when activated by its ligands programmed cell death receptor ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cemiplimab binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.","A monoclonal antibody directed against B7H1 (B7 homolog 1; programmed cell death ligand 1) with potential immunostimulating activity. Upon intravenous administration, durvalumab binds to the cell surface antigen B7H1, thereby blocking B7H1 signaling. This may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7H1-expressing tumor cells. B7H1, a member of the B7 protein superfamily and a negative regulator of cytokine synthesis, is overexpressed on certain tumor cell types.","A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T-cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","A fully human immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, nivolumab binds to and blocks the activation of PD-1, an immunoglobulin superfamily (IgSF) transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T-cells and cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.","A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.","A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A monoclonal antibody directed against the inhibitor receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, relatlimab binds to LAG-3 on tumor infiltrating lymphocytes (TILs). This may activate antigen-specific T-lymphocytes and enhance cytotoxic T cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3 is a member of the immunoglobulin superfamily (IgSF) and binds to major histocompatibility complex (MHC) class II. LAG-3 expression on TILs is associated with tumor-mediated immune suppression.","NA","NA","NA","NA","NA","NA","An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sasanlimab targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.","A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PDCD1; PD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sintilimab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","NA","A proprietary humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, retifanlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tislelizumab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","NA","NA","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, spartalizumab binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.","NA","A recombinant antibody prodrug composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) programmed cell death 1 ligand 1 (PD-L1; B7-H1; CD274) that is linked to a proprietary masking peptide through a protease-cleavable linker on the amino terminus of the light chain domain of the antibody, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of pacmilimab, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment, the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the tumor microenvironment, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables binding of the unmasked, fully active monoclonal antibody moiety of CX-072 to PD-L1, which is over expressed on certain cancer cells. This blocks the binding to and activation of its receptor programmed cell death 1 (PD-1) on T-lymphocytes, thereby enhancing the T-cell-mediated anti-tumor immune response and reversing PD-L1/PD-1-mediated T-cell suppression. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. Compared to the unmodified PD-L1 antibody, peptide masking of CX-072 minimizes binding to PD-L1 in normal tissues, thereby decreasing autoimmune-based side effects while retaining anti-tumor activity.","An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","A humanized monoclonal antibody directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. Pidilizumab blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues.","NA","NA","A recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, zalifrelimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A recombinant B7-DC Fc-fusion protein composed of the extracellular domain of the PD-1 ligand programmed cell death ligand 2 (PD-L2, B7-DC) and the Fc region of human immunoglobulin (Ig) G1, with potential immune checkpoint inhibitory and antineoplastic activities. Anti-PD-1 fusion protein AMP-224 specifically binds to PD-1 on chronically stimulated T-cells and reduces their proliferation. This may restore immune function and may result in the activation of cytotoxic T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein of Ig superfamily and inhibitor receptor expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. AMP-224 does not bind normal activated T-cells.","NA","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1 , PCD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody Sym021 binds to and inhibits PD-1 activation and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF), is expressed on T-cells and functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2). Activated PD-1 plays an important role in tumor evasion from host immunity.","A fully human, immunoglobulin G4 (IgG4) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody ASP8374 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A fully human monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Anti-PD-L1 monoclonal antibody MDX-1105 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","NA","NA","A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1) with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, lodapolimab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T-cells.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,encelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, manelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A humanized, Fc-engineered bispecific monoclonal antibody directed against both the human negative immunoregulatory checkpoint receptor, programmed cell death protein 1 (PD-1; PCD-1; CD279), and inducible T-cell co-stimulator (ICOS; CD278), with potential immunomodulating and antineoplastic activities. Upon administration, izuralimab targets and binds to both PD-1 and ICOS expressed on certain T-cells, including tumor-infiltrating lymphocytes (TILs). This prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2), and stimulates ICOS-mediated signaling, which promotes the activation of T-cells and enhances T-cell-mediated immune responses against tumor cells. Combined PD-1 blockade and ICOS stimulation may enhance T-cell activation and proliferation more than targeting each receptor individually. The engineered Fc domain increases the stability and half-life of the antibody.","A recombinant human monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, opucolimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","An immunoglobulin G4 (IgG4), humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, adebrelimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody (MAb) directed against the inhibitory receptor lymphocyte activation gene-3 protein (LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, favezelimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized, pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, gotistobart targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. As gotistobart is dissociated from CTLA-4 under low pH, it does not cause lysosomal degradation of CTLA-4, preserving CTLA-4 and allowing the recycling of CTLA-4. This may result in more efficient and selective CTLA-4-targeted regulatory T-cell (Treg) depletion within the tumor microenvironment (TME) while preserving CTLA-4 functions outside the TME, thereby reducing toxicities. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor, programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, lipustobart binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands, programmed cell death-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways, leading to the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1 is a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells that negatively regulates T-cell activation and effector function when activated by its ligands. PD-1 plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, prolgolimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,rulonilimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, tamgiblimab targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A human monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, zeluvalimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PDCD1; CD279) and cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, caldonirimab targets and binds to both PD-1 and CTLA4 expressed on tumor-infiltrating T lymphocytes (TILs), and inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity.","An immunoglobulin G4 (IgG4) humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PD1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, geptanolimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the inhibitory receptor lymphocyte activation gene 3 protein (LAG3; LAG-3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration,miptenalimab binds to LAG3 expressed on tumor-infiltrating lymphocytes (TILs) and blocks its binding with major histocompatibility complex (MHC) class II molecules expressed on tumor cells. This activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG3, a member of the immunoglobulin superfamily (IgSF), is expressed on various immune cells, and negatively regulates both proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, negalstobart targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized, immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, nofazinlimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, renvistobart binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T-lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells, and leads to CD226 dimerization and CD226-mediated signaling. This activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tagitanlimab specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A Fc-engineered immunoglobulin G1-kappa (IgG1k) monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, tuparstobart targets and binds to human LAG-3 on tumor-infiltrating  lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, which leads to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both proliferation and activation of T-cells. Its expression on  TILs is associated with tumor-mediated immune suppression.","An immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, tuvonralimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A second-generation, humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Betifisolimab contains a unique, not as of yet elucidated, pH-dependent antigen binding property allowing the antibody to only bind to PD-L1 within the acidic tumor microenvironment (TME), while it is not able to bind to PD-L1 in normal, healthy tissue. Upon administration, once able to bind to PD-L1 in the TME, betifisolimab blocks the binding of PD-L1 to and activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on activated T-cells suppresses the immune system and results in immune evasion. PD-1 negatively regulates T-cell activation.","An agent designed to interfere with the activity of programmed cell death protein 1 (PD1). PD1 inhibitors block T-cell apoptosis and act as non-specific activators of the immune system.","An agent designed to interfere with the activity of programmed death ligand 1 (PD-L1; CD274), a ligand for the receptor programmed cell death protein 1 (PD-1; PD1).","A humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pradusinstobart targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Any agent that targets lymphocyte-activation gene 3 protein (LAG-3; CD223).","Any agent that binds to any of the ligands for the receptor programmed cell death protein 1 (PD-1; PD1); programmed death ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273).","A self-delivering small-interfering RNA (siRNA) targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, anti-PD-1 siRNA PH-762 binds to and destroys mRNA PD-1, thereby preventing the expression of PD-1. As PD1-mediates the downregulation of T-cell activation and proliferation, PH-762 is able to restore immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This may lead to an inhibition of tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 (cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","Any agent that targets cytotoxic T-lymphocyte-associated protein 4 (CTLA-4; CTLA4; CD152).","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor AN4005 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding of PD-L1 to and subsequent activation of its receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor ABSK043 specifically targets and binds to PD-L1 expressed on tumor cells, leading to internalization and preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, anti-viral and antineoplastic activities. Upon administration, PD-L1 inhibitor GS-4224 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. It may also enhance hepatitis B virus (HBV)-specific CD8+ T-cell function, thereby killing HBV-infected cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells. It is also upregulated in HBV-positive patients and contributes to immune dysfunction against HBV infection.","A mixture of the two engineered monoclonal antibodies iparomlimab, which is an immunoglobulin G4 (IgG4) monoclonal antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and tuvonralimab, which is an IgG1 monoclonal antibody directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of iparomlimab/tuvonralimab, iparomlimab and tuvonralimab target and bind to PD-1 and CTLA4 expressed on tumor-infiltrating lymphocytes (TILs), respectively. This inhibits the PD-1- and CTLA4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor BPI-371153 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, PD-L1 inhibitor INCB086550 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099280 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099318 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T-cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.","A monoclonal antibody directed against programmed cell death protein 1 (PD-1; PD1; CD279).","A probody composed of a modified version of ipilimumab, a recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), linked to a proprietary masking peptide that covers the active antigen-binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 probody BMS-986288, the masking peptide is cleaved by tumor-associated proteases upon extravasation into the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to CTLA-4, which is expressed on certain T-cells. This inhibits the CTLA4-mediated downregulation of T-cell activation, and leads to both activation of tumor infiltrating T-effector cells and a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily expressed on activated effector T-cells (Teffs) and regulatory T-cells (Tregs), plays a key role in the inhibition of T-cell activity and downregulation of the immune system. The peptide masking of BMS-986288 minimizes binding to CTLA-4 in normal tissues and may reduce systemic toxicity, when compared to ipilimumab. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.","A monoclonal antibody directed against programmed death-ligand 1 (PD-L1; CD274).","A recombinant immunoglobulin G4 (IgG4) kappa monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody 609A targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MW11 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody TY101 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody RC98 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A preparation of T-lymphocytes that have been genetically modified to express chimeric antigen receptors (CARs) targeting the tumor-associated antigen (TAA) Claudin18.2 (CLDN18.2; A2 isoform of claudin-18) and the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immunostimulating and antineoplastic activities. Upon administration, anti-CLDN18.2/anti-PD-L1 CAR-T cells target and bind to CLDN18.2- and PD-L1-expressing tumor cells, thereby inducing selective toxicity in CLDN18.2- and PD-L1-expressing tumor cells. CLDN18.2, a tight junction protein and stomach-specific isoform of claudin-18, is expressed on a variety of tumor cells, but its expression in healthy tissues is strictly confined to short-lived differentiated epithelial cells of the gastric mucosa. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity.","A recombinant monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody HLX26 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A recombinant monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody PE0105 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody QL1604 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SYN125 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune functions through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody LP002 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. In addition, by binding to PD-L1, LP002 also prevents binding of this ligand to B7.1 expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A recombinant, humanized immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody YH001 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A recombinant, human Fc-inert monoclonal antibody targeting lymphocyte-activation gene 3 protein (LAG-3; LAG3), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, monoclonal antibody Sym022 binds to human LAG-3 and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHCII) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHCII binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Additionally, Sym022 decreases LAG-3 surface levels through internalization and shredding. LAG-3 plays a key role in the activation of T-cells and natural killer (NK) cells.","A recombinant, humanized monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1306 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A humanized  immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody BAT1308 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody GNR-051 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A human immunoglobulin G4 (IgG4) monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody OSE-279 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1), with immune checkpoint inhibitory and potential antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody FAZ053 binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated anti-tumor immune response and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T-cells.","A monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-L1 monoclonal antibody GR1405 specifically targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279). This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein belonging to the immunoglobulin superfamily (IgSF) expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8-positive T-cells.","A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to the immunostimulatory cytokine interleukin-15 (IL-15), with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein KD033, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","An immunoglobulin G4 (IgG4) monoclonal antibody targeting the poliovirus receptor (PVR; CD155; nectin-like protein 5; NECL-5), with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PVR monoclonal antibody NTX-1088 targets and binds to PVR expressed on tumor cells, thereby preventing its interactions with the human cell surface glycoprotein CD226 (DNAX accessory molecule-1; DNAM-1), the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and the negative immunoregulatory human cell surface receptor CD96 (Tactile; T cell activation increased late expression). The binding of NTX-1088 to CD226 prevents the internalization of CD226 and restores its expression on the surface of immune cells. This promotes CD226-dependent signaling pathways, which may trigger the activation of antigen-presenting cells (APCs) and activate T-cells and natural killer (NK) cells, and result in an enhanced cytotoxic T-lymphocyte (CTL)-mediated and NK cell-mediated immune response against tumor cells. The binding of NTX-1088 to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), prevents the interaction of TIGIT with its ligands and promotes the interaction of its ligands with the costimulatory receptor CD226 expressed on immune cells. This leads to CD226 dimerization and further promotes CD226-mediated signaling and anti-tumor immune responses. The binding of NTX-1088 to CD96 expressed primarily on T-cells and NK cells prevents its downstream signaling pathways. This may abrogate CD96-mediated inhibition of T-cell and NK cell effector function and may further restore immune function and anti-tumor immune responses through the activation of T-cells and NK cells. PVR, a key regulator of immune activation through multiple mechanisms, is overexpressed in a variety of tumor cell types while minimally or not expressed in normal tissues.","A fully human monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody COM902 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody PM1021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized immunoglobulin G4 kappa (IgG4k) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody TAB006 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized immunoglobulin G1 (IgG1) monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody IBI310 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4; CTLA4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4 monoclonal antibody KD6001 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A fully humanized, Fc-engineered monoclonal antibody with masked antigen-binding regions directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration and the activation of the antigen-binding regions via cleavage by proteases that are upregulated in the tumor microenvironment (TME), anti-CTLA-4 monoclonal antibody XTX101 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells, thereby killing cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody GLS-012 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody LBL-007 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A recombinant humanized monoclonal antibody targeting the co-inhibitory receptor lymphocyte-activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3 monoclonal antibody TQB2223 targets and binds to LAG-3 expressed by tumor infiltrating lymphocytes (TILs) and blocks the interaction between LAG-3 and major histocompatibility complex class II (MHC II) molecules on the surface of antigen-presenting cells (APCs) and tumor cells. This prevents the negative regulation of T-cell activity that occurs via LAG-3-MHC II binding and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells, leading to a reduction in tumor growth. LAG-3, a member of the immunoglobulin superfamily (IgSF), negatively regulates both the proliferation and activation of T-cells. Its expression on TILs is associated with tumor-mediated immune suppression.","A humanized immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody MEDI0680 binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1 monoclonal antibody SHR-1901 targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2). PD-1 plays an important role in tumor evasion from host immunity.","An immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6005 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant humanized monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory and immunostimulating activities. Upon administration, anti-TIGIT monoclonal antibody BAT6021 targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), thereby preventing the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A nonfucosylated human immunoglobulin G1 (IgG1) monoclonal antibody targeting the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT), with potential immune checkpoint inhibitory activity. Upon administration, anti-TIGIT monoclonal antibody SGN-TGT targets and binds to TIGIT expressed on various immune cells, particularly on tumor-infiltrating T-lymphocytes (TILs). This prevents the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5), and enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as natural killer (NK) cells and CD8+ T-cells. This enhances depletion of TIGIT-positive regulatory T-cells (Tregs) and activates the immune system to exert a T-cell-mediated immune response against cancer cells. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A fusion protein composed of a monoclonal antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), fused with potency reduced interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) sushi domain complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1/IL-15 fusion protein SIM0237, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cells in the tumor microenvironment (TME). In turn, the IL-15/IL-15Ra complex stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, which induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-L1, a transmembrane protein, is expressed on the surface of antigen presenting cells (APCs) and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. The attenuated IL-15 prevents the overstimulation of CD8+ T and NK cells.","A fusion protein composed of an antibody moiety targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a mutein of the immunostimulatory cytokine interleukin-15 (IL-15), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD1/IL-15 fusion protein SAR445877, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. The IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the tumor microenvironment (TME), and induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. The IL-15 mutein form lowers the systemic toxicity of IL-15.","A preparation of autologous engineered red blood cells (RBCs) conjugated with pembrolizumab, an antibody against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of the RBCs-anti-PD1 antibody conjugate WTX212, the RBCs primarily and directly distribute to the spleen and vascular system. The anti-PD1 antibodies target, bind to and inhibit PD-1, leading to the abrogation of PD1-mediated downregulation of T-cell activation and proliferation. This restores immune function, decreases programmed cell death-1 ligand 1 (PD-L1)-positive myeloid-derived suppressor cells (MDSCs) and regulatory T-cells (Tregs) and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 (cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity.","A humanized immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody ADU-1604 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A fully human immunoglobulin G1 (IgG1) antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intravenous administration, anti-CTLA-4 monoclonal antibody REGN4659 targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A tetravalent bispecific fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta receptor II (TGFbRII) fusion protein LBL-015 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocyte; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A Fc-enhanced bispecific antibody directed against both the co-inhibitory molecule and immune checkpoint inhibitor T-cell immunoreceptor with immunoglobulin (Ig) and immunoreceptor tyrosine-based inhibitory motif (ITIM) domains (TIGIT) and an as of yet undisclosed receptor expressed specifically on T-cells and natural killer (NK) cells, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration, the anti-TIGIT bispecific antibody BMS-986442 simultaneously targets and binds to TIGIT and the undisclosed receptor. Upon binding to TIGIT expressed on various immune cells, particularly on tumor-infiltrating lymphocytes (TILs), BMS-986442 blocks the interaction of TIGIT with its ligands CD112 (nectin-2; poliovirus receptor related-2; PRR2; PVRL2) and CD155 (poliovirus receptor; PVR; nectin-like protein 5; NECL-5). This enhances the interaction of CD112 and CD155 with the costimulatory receptor CD226 (DNAX Accessory molecule-1; DNAM-1), which is expressed on immune cells, such as NK cells and CD8+ T-cells. This leads to CD226 dimerization and CD226-mediated signaling and activates the immune system to exert a T-cell-mediated immune response against cancer cells. In addition, binding of BMS-986442 to the undisclosed target expressed on T-cells and NK cells may further enhance anti-tumor immune responses. TIGIT, a member of the Ig super family (IgSF) and an immune inhibitory receptor, plays a key role in the suppression of T-cell proliferation and activation; it is involved in tumor cell immune evasion, and the inhibition of antiviral immune responses.","A recombinant, humanized fusion protein consisting of a cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) single domain antibody linked to a Fc domain, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA4 antibody Fc fusion protein KN044 targets and binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A bispecific antibody directed against both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the cell surface antigen CD27, with potential immune checkpoint inhibitory, immunostimulatory and antineoplastic activities. Upon administration, anti-PD-L1/CD27 bispecific antibody CDX-527 targets and binds to both PD-L1 expressed on tumor cells and CD27 expressed on a variety of immune cell types, including most T-lymphocytes. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling and induces CD27-mediated signaling. This inhibits the PD-1-mediated downregulation of T-cell activation and proliferation, and enhances CD27-mediated responses, including the expansion of antigen-activated T-cells and the cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. This restores immune function and activates a sustained cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-L1, which is overexpressed in many human cancer cell types, plays an important role in the downregulation of the immune system and tumor evasion from host immunity. CD27, a co-stimulatory molecule and member of the tumor necrosis factor receptor superfamily (TNFRSF), is expressed on T-lymphocytes, memory B-cells and natural killer (NK) cells. It plays an important role in NK cell-mediated cytolytic activity and T- and B-lymphocyte proliferation and activation.","An antibody-drug conjugate (ADC) composed of an antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), conjugated to the cytotoxic agent monomethyl auristatin E (MMAE) via a protease-cleavable peptide linker, with potential antineoplastic activity. Upon administration of the anti-PD-L1 ADC SGN-PDL1V, the anti-PD-L1 antibody specifically targets and binds to PD-L1 expressed on tumor cells. Following internalization, enzymatic cleavage and release of MMAE, MMAE targets and binds to tubulin, and inhibits microtubule polymerization. This results in G2/M phase cell cycle arrest and apoptosis in PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on the surface of certain immune cells and on many cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","A human immunoglobulin G1 (IgG1) Fc-silenced bispecific antibody directed against the human negative immunoregulatory checkpoint receptors programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279; programmed death 1) and lymphocyte activation gene 3 protein (LAG-3; LAG3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-LAG-3/PD-1 bispecific antibody INCA32459 targets and binds to both PD-1 and LAG-3 expressed on T-cells and inhibits PD-1- and LAG-3-mediated downregulation of T-cell activation and proliferation. This may lead to cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. PD-1 and LAG-3 play key roles in suppressing T-cell activation and proliferation.","A recombinant humanized bispecific antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the human vascular endothelial growth factor (VEGF), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-1/anti-VEGF bispecific antibody JS207 simultaneously targets and binds to both PD-1 expressed on T-cells and VEGF expressed on tumor cells. The binding of JS207 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of JS207 to VEGF prevents binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands PD-L1 and/or PD-L2; it plays an important role in tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.","A bispecific antibody targeting the immunosuppressive ligand programmed death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/4-1BB bispecific antibody QLF31907 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. Upon 4-1BB binding, QLF31907 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, QLF31907 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A full-length, Fc-silenced immunoglobulin G1 (IgG1) bispecific antibody targeting both the human programmed death-ligand 1 (PD-L1) and CD137 (4-1BB; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/CD137 bispecific antibody MCLA-145 simultaneously targets and binds to CD137, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells, thereby crosslinking PD-L1-expressing tumor cells and T-lymphocytes. Through CD137 binding, MCLA-145 acts as a conditional CD137 agonist, resulting in T-cell co-stimulation and enhanced anti-tumor activity. At the same time, MCLA-145 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. CD137, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. Crosslinking of PD-L1-expressing tumor cells and activated T-lymphocytes may enhance T-lymphocyte-mediated lysis of PD-L1-expressing tumor cells.","Fc-engineered bispecific monoclonal antibody targeting both immune checkpoint regulatory proteins human programmed death-ligand 1 (PD-L1; CD274) and 2 (PD-L2; CD273), with potential immune checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/PD-L2 bispecific antibody IMGS-001 simultaneously targets and binds to PD-L1 and PD-L2 expressed on tumor cells, immunosuppressive stromal cells and endothelial cells. PD-L1 and PD-L2 binding by IMGS-001 prevents both PD-L1 and PD-L2 from binding to and activating their receptor programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates PD-1-mediated signaling in T-cells and PD-1-mediated T-cell inhibition. This activates cytotoxic T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. In addition, IMGS-001 induces antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), thereby killing PD-L1 and PD-L2-expressing cells in the tumor microenvironment (TME), and further abrogating the immunosuppressive nature of the TME. PD-L1 and PD-L2 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion.","A fusion protein composed of a recombinant human monoclonal antibody targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a prodrug for the immunostimulatory cytokine interleukin-15 (IL-15), composed of a potency reduced, mutein form of interleukin (IL)-15 complexed with the high-affinity IL-15 receptor alpha (IL-15Ra) binding sushi domain, that is masked by a protease-cleavable masking protein, with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of anti-PD-1-IL-15 prodrug fusion molecule ASKG915, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and a T-cell-mediated immune response against tumor cells. Upon cleavage of the protease-cleavable linker by proteases overexpressed in the tumor environment (TME), the IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15-mediated signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally in the TME, and further induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T and NK cell development, activation and proliferation. The IL-15 mutein form lowers systemic toxicity of IL-15. Protease-dependent activation of IL-15 increases its efficacy and decreases systemic toxicity. IL-15Ra complexed with IL-15 domain improves stability and increases the half-life of IL-15.","A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the T-cell surface antigen CD3, with potential immunomodulatory and antineoplastic activities. Upon administration, anti-PD-1/anti-CD3 bispecific antibody ONO-4685 binds to both PD-1 expressed on activated T- and B-cells and certain malignant T-cells and CD3 antigen on cytotoxic T-lymphocytes (CTLs). This may activate and redirect CTLs to PD-1-expressing cells, resulting in CTL-mediated killing of these cells. This may lead to anti-tumor activity in some T-cell lymphomas, and immunomodulatory activity in some autoimmune diseases.","A preparation of autologous human T-lymphocytes engineered to express a chimeric antigen receptor (CAR) composed of a modified from of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1), in which the intracellular signal domain of PD-1 is transformed to allow for stimulatory signaling but with an intact extracellular ligand binding domain that specifically binds the tumor-associated antigen (TAA) programmed cell death-1 ligand 1 (PD-L1), and a modified form of the T-cell inhibitory receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with a transformed intracellular signal domain to allow for stimulatory signaling, which specifically binds the B7 proteins CD80 (B7-1) and CD86 (B7-2), with potential immunostimulating and antineoplastic activities. Usually, ligand binding to PD-1 and CTLA-4 inhibits T-cell activity; however, these modified forms of PD-1 and CTLA-4 promote T-cell stimulatory signaling. Upon administration, the autologous PD-L1/CD80/CD86-targeted CAR-T cells target and bind to PD-L1 expressed on certain tumor cells and to CD80/CD86 expressed on antigen-presenting cells (APCs). This stimulates T-cell activation, T-cell proliferation and enhanced cytokine production, which induces selective toxicity in tumor cells expressing PD-L1. PD-1, found on activated T-cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PD-L1 is often overexpressed on tumor cell types and plays a key role in immune evasion. The co-stimulatory molecules CD80 and CD86 play a key role in T-lymphocyte activation upon binding to CD28 upon antigen recognition; however, binding of CD80 and CD86 to wild-type CTLA-4 inhibits T-cell activity and results in T-cell exhaustion.","A bispecific antibody targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/anti-4-1BB bispecific antibody IBI-319 simultaneously targets and binds to PD-1, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes in the tumor microenvironment (TME), and 4-1BB, which is expressed on activated T-lymphocytes and natural killer (NK) cells. This crosslinks PD-1- and 4-1BB-expressing T cells. Through 4-1BB binding, IBI-319 acts as a conditional 4-1BB agonist, resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, PD-1 binding prevents PD-L1 from binding to and activating its receptor PD-1 and inhibits the PD-L1/PD-1-mediated downregulation of T-cell activation and proliferation. This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A bispecific antibody composed of a Fc-silenced human immunoglobulin G1 (IgG1) monoclonal antibody targeting human programmed death-ligand 1 (PD-L1) fused with a single chain variable fragment (scFv) targeting 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. Upon administration, anti-PD-L1/anti-4-1BB bispecific antibody ABL503 simultaneously targets and binds to 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. Upon PD-L1 binding, the 4-1BB activation signal is induced and ABL503 acts as a conditional 4-1BB agonist in the tumor microenvironment (TME), resulting in T-cell co-stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, ABL503 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity.","A fusion protein composed of a pentameric immunoglobulin M (IgM) antibody directed against the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) fused to interleukin (IL)-15/IL-15 receptor alpha (IL-15Ra) complex, with potential immunostimulatory and antineoplastic activities. Upon administration of the anti-PD-L1 antibody/IL-15 fusion protein IGM-7354, the anti-PD-L1 antibody moiety specifically targets and binds to PD-L1 expressing cancer cells and antigen presenting cells (APCs) in the tumor microenvironment (TME), thereby delivering IL-15 to PD-L1-expressing tumor cells. In turn, the IL-15 stimulates the proliferation of natural killer (NK) cells, cytotoxic T-lymphocytes (CTLs) and memory T-cells locally, and reverses T-cell exhaustion. This induces an anti-tumor immune response in the TME against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein, is expressed on APCs and on various cancer cell types. PD-L1 binding to PD-1, a negative regulator of the immune system on activated T-cells, limits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. The immunostimulatory cytokine IL-15 regulates CD8+ T- and NK cell development, activation, and proliferation. IL-15Ra complexed with IL-15 increases the half-life of IL-15. By binding to PD-L1-expressing cells in the TME, IGM-7354 enhances its IL-15-mediated activity on the immune system locally and increases its efficacy while reducing systemic toxicities.","A bispecific antibody targeting both the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and vascular endothelial growth factor A (VEGF-A), with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF-A bispecific antibody PM8002 targets and simultaneously binds to both PD-L1 and VEGF-A expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. The binding of PM8002 to VEGF-A prevents the binding of VEGF-A to VEGF receptor (VEGFR), thereby preventing the activation of VEGF-A/VEGFR-mediated signaling pathways. This prevents angiogenesis and may halt tumor cell proliferation. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF-A is upregulated in a variety of cancer cell types and plays a crucial role in angiogenesis.","A fixed-dose co-formulation composed of pembrolizumab, a humanized immunoglobulin G4 (IgG4) monoclonal antibody directed against human cell surface receptor PD-1 (programmed death-1; programmed cell death-1; cluster of differentiation 279; CD279), and MK-5180, a recombinant form of human hyaluronidase, with potential immune checkpoint inhibitory and antineoplastic activities. Upon subcutaneous administration of recombinant human hyaluronidase and pembrolizumab, the hyaluronidase reversibly depolymerizes the polysaccharide hyaluronan in the subcutaneous tissue. This increases the permeability of the subcutaneous tissue and enhances the absorption of pembrolizumab into the systemic circulation. In turn, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T-cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1; cluster of differentiation 274; CD274), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity. When administered subcutaneously, hyaluronidase, an endoglycosidase, increases the dispersion and absorption of co-administered drugs.","A bispecific antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PD1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta) receptor II (TGFbRII), with potential immune checkpoint modulating and antineoplastic activities. Upon administration, anti-PD-1/anti-TGFbRII bispecific antibody INCA33890 targets and binds to both PD-1 and TGFbRII and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). The binding of INCA33890 to PD-1 prevents the activation of PD-1 by its ligands, programmed cell death-1 ligand 1 (PD-L1; CD274) and/or 2 (PD-L2; CD273). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-lymphocyte (CTL)-mediated tumor cell lysis, which may lead to a reduction in tumor growth. The binding of INCA33890 to TGFbRII prevents the binding of TGF-beta to TGFbRII, thereby preventing the activation of the TGF-beta-mediated signaling pathway. This abrogates TGF-beta-mediated immunosuppression in the TME, increases natural killer (NK) cell and CTL activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A bispecific antibody fusion protein composed of a monoclonal antibody targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and fused to a mutated form of the endogenous cytokine interleukin-2 (IL-2), with potential immunostimulating and antineoplastic activities. Upon administration, anti-PD-1/IL-2 bispecific antibody fusion protein IBI363 targets and binds to PD-1 expressed on PD-1-expressing T-cells, thereby inhibiting PD-1-mediated signaling. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. IL-2 targets and binds to the IL-2 receptor IL2R and activates IL-2/IL-2R-mediated signaling, which further activates cytotoxic T-lymphocytes (CTLs) and natural killer (NK) cells, and induces expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). This further enhances T-cell-mediated cytotoxic immune responses against tumor cells. By selectively activating PD-1 positive T-cells by IL-2, but not PD-1 negative bystander or na\u001a\u001ave T cells, the activity of tumor specific T-cells is specifically enhanced while IL-2-induced systemic toxicity is decreased. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A bifunctional fusion protein targeting both the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint modulating, immunomodulating and antineoplastic activities. Upon administration, anti-PD-1/TGF-beta RII bifunctional fusion protein JS201 targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates the PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression and the suppression of the immune response.","A genetically modified oncolytic virus (OV) composed of a replication competent orthopoxviral chimera engineered to express the human sodium iodine symporter (hNIS) and a human monoclonal antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential oncolytic, immunostimulating and antineoplastic activities that can be used for radioimaging upon positron emission tomography (PET) and radiotherapeutic applications. Upon subcutaneous (SC) intratumoral (IT) administration of the oncolytic virus CF33-expressing hNIS/anti-PD-L1 antibody, the oncolytic virus specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, the anti-PD-L1 antibody produced by the infected tumor cells targets and binds to PD-L1, blocking its binding to and activation of its receptor programmed cell death 1 (PD-1; cluster of differentiation 279; CD279), a transmembrane protein and negative regulator of the immune system, expressed on activated T-cells. This reverses T-cell inactivation caused by PD-1/PD-L1 signaling and enhances the CTL-mediated anti-tumor immune response against PD-L1-expressing tumor cells, thereby further killing tumor cells. Upon subsequent administration of certain iodine-containing imaging agents, hNIS expression by the infected tumor cells allows visualization and tracking of viral biodistribution, and analysis and quantification of CF33-infected tumor cells by PET. Also, administration of iodine I 131 results in its uptake by hNIS-expressing tumor cells, which may result in the selective accumulation of a cytotoxic dose of radiation in tumor cells while sparing adjacent normal tissue.","A bifunctional fusion protein directed against both the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and transforming growth factor beta (TGF-beta; TGFb), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-PD-1/anti-TGF-beta bifunctional fusion protein TQB2868  targets and binds to PD-1 and TGF-beta and prevents the activation of PD-1 and TGF-beta-mediated signaling pathways in the tumor microenvironment (TME). This abrogates PD-1- and TGFb-mediated immunosuppression in the TME, increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities, and inhibits tumor cell proliferation in susceptible tumor cells. PD-1, an inhibitory receptor belonging to the immunoglobulin superfamily (IgSF), is expressed on activated T-lymphocytes; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands and plays an important role in tumor evasion from host immunity. TGF-beta, a pro-inflammatory mediator, is upregulated in certain types of cancers and is involved in cancer cell proliferation, tumor progression, migration and invasion, and the suppression of the immune response.","A bifunctional fusion protein directed against both human programmed death ligand 1 (PD-L1) and transforming growth factor beta (TGF-beta), with potential antineoplastic and immune checkpoint modulating activities. Upon administration, anti-PD-L1/anti-TGF-beta bifunctional fusion protein TQB2858 targets, binds to and neutralizes TGF-beta on tumor cells and simultaneously targets, binds to, and inhibits the activity of PD-L1 on the tumor cells. This prevents both TGF-beta- and PD-L1-mediated immunosuppressive pathways signaling, and increases natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activities. This also restores and enhances anti-tumor responses and inhibits tumor cell proliferation in susceptible tumor cells. TGF-beta and PD-L1 are both upregulated in certain types of cancers; their overexpression is associated with increased evasion of immune surveillance and contributes to poor prognosis.","A fixed dose combination of two monoclonal antibodies of which one is directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the other one is directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217 targets and binds to both PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","A fixed dose combination of two monoclonal antibodies of which one is directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and the other one is directed against the cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, anti-CTLA-4/anti-PD-1 monoclonal antibody combination BCD-217 targets and binds to both PD-1 and CTLA-4 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone.","A bispecific antibody fusion protein composed of an immunoglobulin G1 (IgG1) monoclonal antibody targeting the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and fused to anti-vascular endothelial growth factor (VEGF) protein, with potential immune checkpoint inhibitory, anti-angiogenic and antineoplastic activities. Upon administration, anti-PD-L1/anti-VEGF bispecific antibody fusion protein B1962 targets and simultaneously binds to both PD-L1 and VEGF expressed on tumor cells. This prevents the binding of PD-L1 to its receptor, programmed cell death protein 1 (PD-1, CD279), inhibits the PD-1-mediated signaling, and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. This restores and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against VEGF-expressing tumor cells. The binding of B1962 to VEGF prevents the binding of VEGF to its receptor VEGFR, abrogates VEGF/VEGFR-mediated signaling and may lead to the inhibition of vascular endothelial cell proliferation. The inhibition of tumor angiogenesis may further decrease tumor cell proliferation and prevent metastasis. PD-L1 is overexpressed in many human cancer cell types and plays an important role in the downregulation of the immune system and tumor evasion from host immunity. VEGF is overexpressed in a variety of cancers and is associated with increased invasiveness and decreased survival.","A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oHSV-1 expressing IL-12 and anti-PD-1 antibody T3011 promotes the secretion of IL-12 and anti-PD-1 antibody by the tumor cells. IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against the tumor cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. Anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","A recombinant fusion protein consisting of a human monoclonal antibody directed against cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) fused to the immunostimulatory cytokine interleukin-15 (IL-15) cross-linked with the sushi domain of IL-15 receptor alpha (IL-15Ra), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-CTLA-4 monoclonal antibody-IL-15/IL-15Ra fusion protein JK08, the monoclonal antibody domain targets and binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. The IL-15/IL-15Ra complex targets and binds to CD8+ T and natural killer (NK) cells, thereby increasing their activation and proliferation. Altogether, this leads to an inhibition of regulatory T-cell (Tregs)-mediated immunosuppression, induces antibody-dependent cellular cytotoxicity (ADCC), increases memory T-cells and enhances a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A genetically engineered oncolytic herpes simplex virus type 1 (oHSV-1) expressing the human immunostimulating cytokine interleukin-12 (IL-12) and an antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon intratumoral administration into the glioma, oHSV-1 expressing IL-12 and anti-PD-1 antibody MVR-C5252 specifically infects and replicates in glioma cells causing viral-mediated glioma cell lysis. The released virus particles, in turn, infect and replicate in neighboring glioma cells, thereby further killing tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected glioma cells. In addition, as MVR-C5252 carries exogenous genes, it is also able to express IL-12 and anti-PD-1 antibody and are released by the infected cells, both of which are able to promote an immune response in the tumor microenvironment (TME). IL-12 promotes the activation of natural killer cells, which induces both the secretion of interferon-gamma and a cytotoxic T-lymphocyte (CTL) response against uninfected glioma cells. This results in both immune-mediated tumor cell death and further inhibition of tumor cell proliferation. The anti-PD-1 antibody targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","Autologous human T-lymphocytes that are genetically engineered to express a chimeric switch receptor (CSR) composed of the extracellular ligand binding domain of the human inhibitory receptor programmed cell death protein 1 (PD-1; PDCD1) fused to the transmembrane and cytoplasmic co-stimulatory signaling domains of CD28 (PD1CD28; PD-1:CD28 switch receptor), with potential immunomodulating and antineoplastic activities. Upon reintroduction of autologous PD-1-targeted CSR-modified T-lymphocytes into the patient, the switch receptor expressed by the engineered T-cells targets and binds to the PD-1 ligands, programmed cell death ligand 1 (PD-L1) and 2 (PD-L2) expressed, on tumor cells. The nature of the PD-1/CD28 switch receptor fusion protein prevents the normal PD1/PD-L1-mediated T-cell suppression and, instead, promotes signaling through the CD28 domain, which results in the stimulation of T-lymphocytes. This induces enhanced toxicity against PD-L1-expressing tumor cells. PD-1 protein, found on activated T-cells, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. Exchanging the transmembrane and intracellular domain of PD-1 with that of CD28 converts PD-L1 into a co-stimulation ligand of primary human CD8+ cytotoxic T-lymphocytes (CTLs). CD28, is a molecule expressed by T-cells that stimulates increased T-lymphocyte proliferation and activity.","An oncolytic vaccinia virus (VV; VACV) genetically engineered to express 4-E03, an immunoglobulin G1 (IgG1) antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4) and the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential oncolytic, immunostimulating and antineoplastic activities. Upon intra-tumoral administration, the oncolytic VV expressing anti-CTLA-4 antibody and GM-CSF BT-001 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. In addition, oncolytic virus BT-001 promotes the secretion of anti-CTLA-4 antibody 4-E03 and GM-CSF by the tumor cells. GM-CSF attracts dendritic cells (DCs) and may further stimulate a CTL-mediated immune response against tumor cells. Anti-CTLA-4 antibody 4-E03 targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This enhances the CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A preparation of autologous T-lymphocytes that have been activated and genetically modified to express immune checkpoint antibodies against the negative immunoregulatory receptors human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR), with potential immunomodulating and antineoplastic activities. After isolation, activation, transduction, expansion in culture and reintroduction into the patient, the T-cells in the autologous EGFR specific CAR-T-cells expressing anti-PD-1/CTLA4 antibodies  specifically target and kill EGFR-expressing tumor cells. The anti-PD-1 antibody secreted from the CAR-T cells binds to PD-1 expressed on T-cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion. The anti-CTLA4 expressed by the CAR-T cells targets and binds to CTLA4 expressed on T-cells, and inhibits the CTLA4-mediated downregulation of T-cell activation. Both antibodies enhance T-cell activation, improve immunosuppression in the tumor microenvironment (TME) and improve the T-cell mediated immune response against and toxicity in EGFR-expressing tumor cells. Both PD-1 and CTLA-4 negatively regulate T-cell activation and proliferation, and play a key role in immunosuppression within the TME. EGFR, a receptor tyrosine kinase that is overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation.","A preparation of autologous T-lymphocytes that have been activated and genetically modified to express immune checkpoint antibodies against the negative immunoregulatory receptors human cell surface receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) and human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), and are transduced with a gene encoding a chimeric antigen receptor (CAR) specific for the human tumor-associated antigen (TAA) epidermal growth factor receptor (EGFR), with potential immunomodulating and antineoplastic activities. After isolation, activation, transduction, expansion in culture and reintroduction into the patient, the T-cells in the autologous EGFR specific CAR-T-cells expressing anti-PD-1/CTLA4 antibodies  specifically target and kill EGFR-expressing tumor cells. The anti-PD-1 antibody secreted from the CAR-T cells binds to PD-1 expressed on T-cells and prevents the interaction of PD-1 with its ligand programmed cell death 1 ligand 1 (PD-L1, PD-1L1; CD274) expressed on cancer cells, which prevents PD-1-mediated signaling and T-cell exhaustion. The anti-CTLA4 expressed by the CAR-T cells targets and binds to CTLA4 expressed on T-cells, and inhibits the CTLA4-mediated downregulation of T-cell activation. Both antibodies enhance T-cell activation, improve immunosuppression in the tumor microenvironment (TME) and improve the T-cell mediated immune response against and toxicity in EGFR-expressing tumor cells. Both PD-1 and CTLA-4 negatively regulate T-cell activation and proliferation, and play a key role in immunosuppression within the TME. EGFR, a receptor tyrosine kinase that is overexpressed in a variety of cancer cell types, plays a key role in tumor cell proliferation.","A preparation of autologous, engineered T-lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T-lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.","A preparation of autologous, engineered T-lymphocytes that express both a second-generation chimeric antigen receptor (CAR) specific for the human gastric carcinoma-associated antigen MG7, and the co-stimulatory molecule 4-1BB (CD137), with potential antineoplastic activity. Upon intratumoral injection, the autologous anti-MG7-CAR T-lymphocytes target and attach to cancer cells expressing MG7. This induces selective toxicity in and causes lysis of MG7-expressing tumor cells. MG7, a glycosylated protein sequence from the tumor-associated antigen (TAA) carcinoembryonic antigen (CEA), plays a key role in the development of certain tumor cell types. 4-1BB enhances T-cell activation and signaling after recognition of MG7.","A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, expressing an antibody directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), CD40 ligand (CD40L; CD154; TRAP; TNFSF5) and the co-stimulatory molecule tumor necrosis factor ligand superfamily (TNFSF) member 9 (TNFSF9; 4-1BBL) with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-1 expressing anti-CTLA-4 Antibody/CD40L/4-1BBL RP3 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Oncolytic virus RP3 expresses a fusogenic protein, GALV-GP R-, for optimal tumor cell infection and killing. In addition, Oncolytic virus RP3 promotes the expression of anti-CTLA-4 antibody, CD40L and 4-1BBL by the tumor cells. Anti-CTLA-4 antibody targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system. CD40L specifically binds to and activates CD40, a cell surface receptor that belongs to the tumor necrosis factor (TNF) receptor family and is expressed on various immune cells, such as B-lymphocytes, monocytes, and dendritic cells (DCs). Activation of CD40 induces proliferation and activation of B-lymphocytes, shifts the induction of suppressive macrophages towards immunostimulatory macrophages, activates monocyte-derived DCs (moDCs), and leads to the secretion of inflammatory cytokines, which activates the immune system to induce the proliferation and activation of CTLs against tumor cells. 4-1BBL binds to and subsequently induces the proliferation and activation of natural killer (NK) cells and T-cells. This enhances the secretion of cytokine interferon-gamma (IFN-g) and further induces an anti-tumor immune response.","A 1:1 fixed dose combination formulation composed of the two monoclonal antibodies AI-025, a monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), and gotistobart, a pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061, AI-025 targets, binds to and inhibits PD-1 and ONC-392 targets, binds to and inhibits CTLA-4. This inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A 1:1 fixed dose combination formulation composed of the two monoclonal antibodies AI-025, a monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), and gotistobart, a pH-sensitive immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4; CD152), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of anti-PD-1 antibody AI-025/anti-CTLA-4 antibody ONC-392 combination formulation AI-061, AI-025 targets, binds to and inhibits PD-1 and ONC-392 targets, binds to and inhibits CTLA-4. This inhibits the PD-1- and CTLA-4-mediated downregulation of T-cell activation and proliferation. This restores immune function and activates a cytotoxic T-lymphocyte (CTL)-mediated immune response against tumor cells. Both PD-1 and CTLA-4 are selectively expressed on TILs in the tumor microenvironment (TME) and negatively regulate the activation and effector functions of T-cells. They play key roles in the downregulation of the immune system and tumor evasion from host immunity. Dual checkpoint blockade of PD-1 and CTLA-4 enhances T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2; CD273); it plays an important role in tumor evasion from host immunity. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune system.","A genetically engineered, ICP34.5- and ICP47-deleted oncolytic human herpes simplex virus type 2 (HSV-2), derived from the HG52 strain and encoding a bispecific antibody directed against the immunosuppressive ligand and immune checkpoint inhibitor programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) and the T-cell surface antigen CD3, with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, oncolytic HSV-2 expressing anti-PD-L1/CD3 bispecific antibody BS-006 selectively infects and replicates in tumor cells, thereby inducing tumor cell lysis. In addition, BS-006 promotes the secretion of anti-PD-L1/CD3 bispecific antibody by the infected tumor cells. The bispecific antibody targets and binds to both the CD3 on T-cells and the PD-L1 expressed on tumor cells. This results in the cross-linking of T-cells and tumor cells and may induce a cytotoxic T-lymphocyte (CTL)-mediated immune response against PD-L1-expressing tumor cells. At the same time, BS-006 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances CTL-mediated tumor cell lysis, which may further lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T-cells inhibits the expansion and survival of CD8-positive T-cells, suppresses the immune system and results in immune evasion. Deletion of the gene encoding for ICP34.5 provides tumor selectivity and prevents replication in healthy cells. As ICP47 blocks antigen presentation in HSV-infected cells, deletion of this gene may induce a more potent antitumor immune response in the tumor cells. Deletion of ICP47 also leads to an increased expression of the HSV US11 gene and allows US11 to be expressed as an immediate early and not a late gene. This further enhances the degree of viral replication and the oncolysis of tumor cells.","A genetically modified oncolytic viral strain of the herpes simplex type 1 (HSV-1) virus, expressing the immunostimulatory cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) and an antibody-like molecule directed against the human inhibitory T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4;CTLA4), with potential oncolytic, immunostimulating and antineoplastic activities. Upon administration, the oncolytic HSV-1 expressing anti-CTLA-4 antibody-like molecule and GM-CSF RP2 specifically infects and replicates in tumor cells causing viral-mediated tumor cell lysis. The released virus particles, in turn, infect and replicate in neighboring tumor cells. Tumor antigens released from the lysed tumor cells also activate the immune system to induce a tumor-specific systemic immune and cytotoxic T-lymphocyte (CTL) response, thereby killing nearby non-infected tumor cells. Oncolytic virus RP2 expresses a fusogenic protein, GALV-GP R-, for optimal tumor cell infection and killing. In addition, Oncolytic virus RP2 promotes the secretion of GM-CSF and anti-CTLA-4 antibody-like molecule by the tumor cells. GM-CSF attracts dendritic cells (DCs) and may further stimulate a CTL-mediated immune response against tumor cells. Anti-CTLA-4 antibody-like molecule targets and binds to CTLA-4 expressed on T-cells, and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a CTL-mediated immune response against tumor cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily (IgSF), plays a key role in the downregulation of the immune 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class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>target_symbol<\/th>\n      <th>target_genename<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>target_entrezgene<\/th>\n      <th>target_ensembl_gene_id<\/th>\n      <th>target_type<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,16,19,21,22,23]},{"orderable":false,"targets":0},{"name":" 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 </div>
 <div class="section level3">
 <h3 id="get-immune-checkpoint-inhibitors-indicated-for-lung-cancer-conditions-list-per-drug-target-entry">Get immune checkpoint inhibitors indicated for lung cancer
@@ -382,8 +377,8 @@ <h3 id="get-immune-checkpoint-inhibitors-indicated-for-lung-cancer-conditions-li
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
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-<script type="application/json" data-for="htmlwidget-0fab9523224a357edaca">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20","21","22","23","24","25","26","27","28","29","30","31","32","33","34","35","36","37","38","39","40","41","42"],[7499,3581,23189,17332,9053,26787,27060,29167,11508,12794,12794,25749,30571,31136,11855,21527,29621,4102,23245,26960,21785,6653,29184,25627,11573,12615,23744,24772,31005,27354,26296,27667,29388,19117,6520,6520,24907,393,16222,26563,4555,5875],["Cemiplimab","Atezolizumab","Pembrolizumab","Ipilimumab","Cosibelimab","Serplulimab","Socazolimab","Tiragolumab","Domvanalimab","Erfonrilimab","Erfonrilimab","Retifanlimab","Vibostolimab","Zimberelimab","Durvalumab","Nivolumab","Tremelimumab","Avelumab","Penpulimab","Sintilimab","Ociperlimab","Camrelizumab","Tislelizumab","Relatlimab","Dostarlimab","Envafolimab","Pimivalimab","Pucotenlimab","Zalifrelimab","Spartalizumab","Shr-1316","Sugemalimab","Toripalimab","Mk-4280","Cadonilimab","Cadonilimab","Quavonlimab","Apl-501","Ibi-939","Sasanlimab","Balstilimab","Budigalimab"],["Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Antibody","Unknown","Antibody","Antibody","Unknown","Antibody","Antibody","Antibody","Unknown","Unknown","Antibody","Antibody","Antibody"],["PDCD1","CD274","PDCD1","CTLA4","CD274","PDCD1","CD274","TIGIT","TIGIT","CD274","CTLA4","PDCD1","TIGIT","PDCD1","CD274","PDCD1","CTLA4","CD274","PDCD1","PDCD1","TIGIT","PDCD1","PDCD1","LAG3","PDCD1","CD274","PDCD1","PDCD1","CTLA4","PDCD1","CD274","CD274","PDCD1","LAG3","CTLA4","PDCD1","CTLA4","PDCD1","TIGIT","PDCD1","PDCD1","PDCD1"],["programmed cell death 1","CD274 molecule","programmed cell death 1","cytotoxic T-lymphocyte associated protein 4","CD274 molecule","programmed cell death 1","CD274 molecule","T cell immunoreceptor with Ig and ITIM domains","T cell immunoreceptor with Ig and ITIM domains","CD274 molecule","cytotoxic T-lymphocyte associated protein 4","programmed cell death 1","T cell immunoreceptor with Ig and ITIM domains","programmed cell death 1","CD274 molecule","programmed cell death 1","cytotoxic T-lymphocyte associated protein 4","CD274 molecule","programmed cell death 1","programmed cell death 1","T cell immunoreceptor with Ig and ITIM domains","programmed cell death 1","programmed cell death 1","lymphocyte activating 3","programmed cell death 1","CD274 molecule","programmed cell death 1","programmed cell death 1","cytotoxic T-lymphocyte associated protein 4","programmed cell death 1","CD274 molecule","CD274 molecule","programmed cell death 1","lymphocyte activating 3","cytotoxic T-lymphocyte associated protein 4","programmed cell death 1","cytotoxic T-lymphocyte associated protein 4","programmed cell death 1","T cell immunoreceptor with Ig and ITIM domains","programmed cell death 1","programmed cell death 1","programmed cell death 1"],["CHEMBL4297723","CHEMBL3707227","CHEMBL3137343","CHEMBL1789844","CHEMBL4297729","CHEMBL4594550","CHEMBL4802221","CHEMBL4298050","CHEMBL4650392","CHEMBL4650483","CHEMBL4650483","CHEMBL4298037","CHEMBL4297785","CHEMBL4297856","CHEMBL3301587","CHEMBL2108738","CHEMBL2108658","CHEMBL3833373","CHEMBL4297571","CHEMBL4297829","CHEMBL4650411","CHEMBL4297715","CHEMBL4297840","CHEMBL3990044","CHEMBL4298124","CHEMBL4298006","CHEMBL4650482","CHEMBL4650472","CHEMBL4297876","CHEMBL4297831","CHEMBL4297828","CHEMBL4594535","CHEMBL4297843","CHEMBL4297784","CHEMBL4594456","CHEMBL4594456","CHEMBL4650419","CHEMBL4594355","CHEMBL4650473","CHEMBL4298191","CHEMBL4297877","CHEMBL4297858"],["INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","ANTAGONIST","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","ANTAGONIST","ANTAGONIST","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","OTHER","INHIBITOR","ANTAGONIST","INHIBITOR","ANTAGONIST","INHIBITOR","INHIBITOR","ANTAGONIST","BINDING AGENT","INHIBITOR","INHIBITOR","INHIBITOR","ANTAGONIST","INHIBITOR","BINDING AGENT","ANTAGONIST","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","ANTAGONIST","ANTAGONIST","INHIBITOR"],["A human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1) protein, with potential immune checkpoint inhibitory and antineoplastic activity. Upon administration, cemiplimab binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T-cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.","A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","NA","NA","NA","NA","NA","NA","NA","A proprietary humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, retifanlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","NA","NA","A monoclonal antibody directed against B7H1 (B7 homolog 1; programmed cell death ligand 1) with potential immunostimulating activity. Upon intravenous administration, durvalumab binds to the cell surface antigen B7H1, thereby blocking B7H1 signaling. This may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7H1-expressing tumor cells. B7H1, a member of the B7 protein superfamily and a negative regulator of cytokine synthesis, is overexpressed on certain tumor cell types.","A fully human immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, nivolumab binds to and blocks the activation of PD-1, an immunoglobulin superfamily (IgSF) transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T-cells and cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.","A human IgG2 monoclonal antibody directed against the T-cell receptor protein cytotoxic T-lymphocyte-associated protein 4 (CTLA4). Tremelimumab binds to CTLA4 and blocks the binding of the antigen-presenting cell ligands B7-1 and B7-2 to CTLA4, resulting in inhibition of B7-CTLA4-mediated downregulation of T-cell activation; subsequently, B7-1 or B7-2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA4-mediated inhibition.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.","NA","A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PDCD1; PD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sintilimab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","NA","NA","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tislelizumab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the inhibitor receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, relatlimab binds to LAG-3 on tumor infiltrating lymphocytes (TILs). This may activate antigen-specific T-lymphocytes and enhance cytotoxic T cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3 is a member of the immunoglobulin superfamily (IgSF) and binds to major histocompatibility complex (MHC) class II. LAG-3 expression on TILs is associated with tumor-mediated immune suppression.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; programmed death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, dostarlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T-cells, functions as an immune checkpoint protein that negatively regulates T-cell activation and T-cell-mediated immune responses when activated by its ligands programmed cell death receptor ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","NA","A recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, zalifrelimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, spartalizumab binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.","NA","NA","NA","NA","NA","NA","NA","NA","NA","An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sasanlimab targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host 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<th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,16,19,21,22,23]},{"orderable":false,"targets":0},{"name":" 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Upon administration, cemiplimab binds to PD-1, inhibits its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host immunity.","A humanized, Fc optimized, monoclonal antibody directed against the protein ligand PD-L1 (programmed cell death-1 ligand 1; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1; PDCD1) expressed on activated T-cells, which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. In addition, by binding to PD-L1, atezolizumab also prevents binding of this ligand to B7.1 (CD80) expressed on activated T cells, which further enhances the T-cell-mediated immune response. PD-L1 is overexpressed on many human cancer cell types and on various tumor-infiltrating immune cells. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in increased immune evasion. PD-1, a transmembrane protein, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells. The Fc region of atezolizumab is modified in such a way that it does not induce either antibody-dependent cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC).","A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.","A recombinant human immunoglobulin (Ig) G1 monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4), with immune checkpoint inhibitory and antineoplastic activities. Ipilimumab binds to CTLA4 expressed on T-cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","NA","NA","NA","NA","NA","NA","NA","A proprietary humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, retifanlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T-cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","NA","NA","A monoclonal antibody directed against B7H1 (B7 homolog 1; programmed cell death ligand 1) with potential immunostimulating activity. Upon intravenous administration, durvalumab binds to the cell surface antigen B7H1, thereby blocking B7H1 signaling. This may activate the immune system to exert a cytotoxic T-lymphocyte (CTL) response against B7H1-expressing tumor cells. B7H1, a member of the B7 protein superfamily and a negative regulator of cytokine synthesis, is overexpressed on certain tumor cell types.","A fully human immunoglobulin (Ig) G4 monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1) with immune checkpoint inhibitory and antineoplastic activities. Upon administration, nivolumab binds to and blocks the activation of PD-1, an immunoglobulin superfamily (IgSF) transmembrane protein, by its ligands programmed cell death ligand 1 (PD-L1), which is overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen-presenting cells (APCs). This results in the activation of T-cells and cell-mediated immune responses against tumor cells. Activated PD-1 negatively regulates T-cell activation and plays a key role in tumor evasion from host immunity.","A human IgG2 monoclonal antibody directed against the T-cell receptor protein cytotoxic T-lymphocyte-associated protein 4 (CTLA4). Tremelimumab binds to CTLA4 and blocks the binding of the antigen-presenting cell ligands B7-1 and B7-2 to CTLA4, resulting in inhibition of B7-CTLA4-mediated downregulation of T-cell activation; subsequently, B7-1 or B7-2 may interact with another T-cell surface receptor protein, CD28, resulting in a B7-CD28-mediated T-cell activation unopposed by B7-CTLA4-mediated inhibition.","A human immunoglobulin G1 (IgG1) monoclonal antibody directed against the human immunosuppressive ligand programmed death-ligand 1 (PD-L1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, avelumab binds to PD-L1 and prevents the interaction of PD-L1 with its receptor programmed cell death protein 1 (PD-1). This inhibits the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-lymphocytes (CTLs) targeted to PD-L1-overexpressing tumor cells. In addition, avelumab induces an antibody-dependent cellular cytotoxic (ADCC) response against PD-L1-expressing tumor cells. PD-1, a cell surface receptor belonging to the immunoglobulin superfamily expressed on T-cells, negatively regulates T-cell activation and effector function when activated by its ligand, and plays an important role in tumor evasion from host immunity. PD-L1, a transmembrane protein, is overexpressed on a variety of tumor cell types and is associated with poor prognosis.","NA","A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; PDCD1; PD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sintilimab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","NA","NA","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, tislelizumab binds to PD-1 and inhibits the binding of PD-1 to the PD-1 ligands programmed cell death-1 ligand 1 (PD-L1), and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of both T-cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin (Ig) superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the inhibitor receptor lymphocyte activation gene-3 (LAG-3), with potential immunomodulating and antineoplastic activities. Upon administration, relatlimab binds to LAG-3 on tumor infiltrating lymphocytes (TILs). This may activate antigen-specific T-lymphocytes and enhance cytotoxic T cell-mediated tumor cell lysis, which leads to a reduction in tumor growth. LAG-3 is a member of the immunoglobulin superfamily (IgSF) and binds to major histocompatibility complex (MHC) class II. LAG-3 expression on TILs is associated with tumor-mediated immune suppression.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1; programmed death-1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, dostarlimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T-cells. PD-1, a transmembrane protein in the Ig superfamily expressed on T-cells, functions as an immune checkpoint protein that negatively regulates T-cell activation and T-cell-mediated immune responses when activated by its ligands programmed cell death receptor ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.","An injectable formulation of a monoclonal antibody directed against programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with immune checkpoint inhibitory and potential antineoplastic activities. Upon subcutaneous administration, envafolimab binds to PD-L1, blocking its binding to and activation of its receptor programmed death 1 (PD-1), which may enhance the T-cell-mediated immune response to neoplasms and reverse T-cell inactivation. PD-L1 is overexpressed by many human cancer cell types. PD-L1 binding to PD-1 on T-cells suppresses the immune system and results in immune evasion. PD-1, a transmembrane protein expressed on activated T-cells, is a negative regulator of the immune system that limits the expansion and survival of CD8+ T cells.","NA","NA","A recombinant human monoclonal antibody directed against the human T-cell receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, zalifrelimab binds to CTLA-4 expressed on T-cells and inhibits the CTLA-4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA-4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.","A humanized monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed death-1 (PD-1, PCD-1), with immune checkpoint inhibitory and antineoplastic activities. Upon administration, spartalizumab binds to PD-1 expressed on activated T-cells and blocks the interaction with its ligands, programmed cell death 1 ligand 1 (PD-L1, PD-1L1) and PD-1 ligand 2 (PD-L2, PD-1L2). The inhibition of ligand binding prevents PD-1-mediated signaling and results in both T-cell activation and the induction of T-cell-mediated immune responses against tumor cells. PD-1, an immunoglobulin (Ig) superfamily transmembrane protein and inhibitory receptor, negatively regulates T-cell activation.","NA","NA","NA","NA","NA","NA","NA","NA","NA","An inhibitor of the human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, sasanlimab targets and binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family, is expressed on activated T-lymphocytes, B-cells and NK cells; it functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, and plays an important role in tumor evasion from host immunity.","A monoclonal antibody directed against the negative immunoregulatory human cell surface receptor programmed cell death 1 (PD-1, PCD-1; PDCD1) protein, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, balstilimab binds to PD-1, and thereby blocks its binding to the PD-1 ligand programmed cell death-1 ligand 1 (PD-L1), and prevents the activation of its downstream signaling pathways. This may restore immune function through the activation of cytotoxic T-cells. PD-1, a transmembrane protein in the immunoglobulin superfamily expressed on activated T-cells, negatively regulates T-cell activation and effector function when activated by its ligand; it plays an important role in tumor evasion from host 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class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>target_symbol<\/th>\n      <th>target_genename<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>target_entrezgene<\/th>\n      <th>target_ensembl_gene_id<\/th>\n      <th>target_type<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,16,19,21,22,23]},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"drug_id","targets":1},{"name":"drug_name","targets":2},{"name":"drug_type","targets":3},{"name":"target_symbol","targets":4},{"name":"target_genename","targets":5},{"name":"molecule_chembl_id","targets":6},{"name":"drug_action_type","targets":7},{"name":"nci_concept_definition","targets":8},{"name":"opentargets","targets":9},{"name":"drug_cancer_relevance","targets":10},{"name":"inhibition_moa","targets":11},{"name":"is_salt","targets":12},{"name":"is_adc","targets":13},{"name":"drug_blackbox_warning","targets":14},{"name":"nci_t","targets":15},{"name":"target_entrezgene","targets":16},{"name":"target_ensembl_gene_id","targets":17},{"name":"target_type","targets":18},{"name":"drug_frac_cancer_indications","targets":19},{"name":"drug_approved_noncancer","targets":20},{"name":"drug_n_indications","targets":21},{"name":"drug_year_first_approval","targets":22},{"name":"drug_max_ct_phase","targets":23},{"name":"disease_indication","targets":24},{"name":"disease_indication_max_phase","targets":25},{"name":"atc_code_level1","targets":26},{"name":"atc_level1","targets":27},{"name":"atc_code_level2","targets":28},{"name":"atc_level2","targets":29},{"name":"atc_code_level3","targets":30},{"name":"atc_level3","targets":31},{"name":"atc_treatment_category","targets":32}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
 </div>
 <div class="section level3">
 <h3 id="get-antimetabolite-drugs">Get antimetabolite drugs<a class="anchor" aria-label="anchor" href="#get-antimetabolite-drugs"></a>
@@ -394,24 +389,24 @@ <h3 id="get-antimetabolite-drugs">Get antimetabolite drugs<a class="anchor" aria
 <span>  cache_dir <span class="op">=</span> <span class="va">cache_dir</span>, </span>
 <span>  treatment_category <span class="op">=</span> <span class="fu"><a href="https://rdrr.io/r/base/c.html" class="external-link">c</a></span><span class="op">(</span><span class="st">"chemo_therapy_classified"</span><span class="op">)</span>,</span>
 <span>  output_resolution <span class="op">=</span> <span class="st">"drug"</span><span class="op">)</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:17] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:17] Object 'drug_map_name' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:17] Retrieved n = 31451 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Object 'drug_map_alias' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Retrieved n = 677295 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Object 'drug_map_basic' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Retrieved n = 31486 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Object 'drug_map_target' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Retrieved n = 39369 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Object 'drug_map_indication' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:18] Retrieved n = 62752 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Record set satisfying user-defined criteria: n = 16534</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Collapsing record set - providing output on a 'per_drug' resolution</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Final record set: n = 170 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Object 'drug_map_name' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Retrieved n = 31451 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Object 'drug_map_alias' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Retrieved n = 677295 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Object 'drug_map_basic' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Retrieved n = 31486 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Object 'drug_map_target' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Retrieved n = 39369 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Object 'drug_map_indication' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:01:59] Retrieved n = 62752 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:02] Record set satisfying user-defined criteria: n = 16534</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:02] Collapsing record set - providing output on a 'per_drug' resolution</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:02] Final record set: n = 170 records</span></span>
 <span></span>
 <span><span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">&lt;-</span> <span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">|&gt;</span></span>
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@@ -439,8 +434,8 @@ <h3 id="get-antimetabolite-drugs">Get antimetabolite drugs<a class="anchor" aria
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-<div id="htmlwidget-5479e9e1fc98bb379014" style="width:100%;height:auto;" class="datatables html-widget"></div>
-<script type="application/json" data-for="htmlwidget-5479e9e1fc98bb379014">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20","21","22","23","24","25","26","27","28","29"],[24318,10341,21161,23196,4149,8606,3291,6702,15044,8489,14057,9695,16168,28844,14198,19639,28426,25250,12541,26512,14532,29235,28709,29874,3382,28677,5003,14536,7166],["Pralatrexate","Decitabine","Nelarabine","Pemetrexed","Azacitidine","Clofarabine","Arsenic Trioxide","Capecitabine","Gemcitabine","Cladribine","Floxuridine","Cytarabine","Hydroxyurea","Thioguanine","Fluorouracil","Mercaptopurine","Tegafur","Raltitrexed","Eniluracil","Sapacitabine","Fosgemcitabine Palabenamide","Tocladesine","Tezacitabine","Troxacitabine","Aspacytarabine","Tetrahydrouridine","2'-DEOXYTHIOGUANOSINE","Fosifloxuridine Nafalbenamide","Carmofur"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule"],["CHEMBL1201746","CHEMBL1201129","CHEMBL1201112","CHEMBL225072","CHEMBL1489","CHEMBL1750","CHEMBL2362016","CHEMBL1773","CHEMBL888","CHEMBL1619","CHEMBL917","CHEMBL803","CHEMBL467","CHEMBL727","CHEMBL185","CHEMBL1425","CHEMBL20883","CHEMBL225071","CHEMBL355200","CHEMBL2105681","CHEMBL3126004","CHEMBL2107085","CHEMBL2105467","CHEMBL359164","CHEMBL4297599","CHEMBL1236475","CHEMBL3250476","CHEMBL2181367","CHEMBL460499"],["INHIBITOR","INHIBITOR","NA","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","NA","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","NA","NA","NA","INHIBITOR","INHIBITOR","INHIBITOR","NA","NA","NA","NA"],["A folate analogue inhibitor of dihydrofolate reductase (DHFR) exhibiting high affinity for reduced folate carrier-1 (RFC-1) with antineoplastic and immunosuppressive activities. Pralatrexate selectively enters cells expressing RFC-1; intracellularly, this agent is highly polyglutamylated and competes for the folate binding site of DHFR, blocking tetrahydrofolate synthesis, which may result in depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death. Efficient intracellular polyglutamylation of pralatrexate results in higher intracellular concentrations compared to non-polyglutamylated pralatrexate, which is more readily effuxed by the MRP (multidrug resistance protein) drug efflux pump. RFC-1, an oncofetal protein expressed at highest levels during embryonic development, may be over-expressed on the cell surfaces of various cancer cell types.","A cytidine antimetabolite analogue with potential antineoplastic activity. Decitabine incorporates into DNA and inhibits DNA methyltransferase, resulting in hypomethylation of DNA and intra-S-phase arrest of DNA replication. (NCI04)","An arabinonucleoside antimetabolite with antineoplastic activity. Nelarabine is demethoxylated by adenosine deaminase to become biologically active 9-beta-D-arabinosylguanine (ara-G); ara-G incorporates into DNA, thereby inhibiting DNA synthesis and inducing an S phase-dependent apoptosis of tumor cells. (NCI04)","A synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS), which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.","A pyrimidine nucleoside analogue of cytidine with antineoplastic activity. Azacitidine is incorporated into DNA, where it reversibly inhibits DNA methyltransferase, thereby blocking DNA methylation.  Hypomethylation of DNA by azacitidine may activate tumor suppressor genes silenced by hypermethylation, resulting in an antitumor effect. This agent is also incorporated into RNA, thereby disrupting normal RNA function and impairing tRNA cytosine-5-methyltransferase activity. (NCI04)","A second generation purine nucleoside analog with antineoplastic activity. Clofarabine is phosphorylated intracellularly to the cytotoxic active 5'-triphosphate metabolite, which inhibits the enzymatic activities of ribonucleotide reductase and DNA polymerase, resulting in inhibition of DNA repair and synthesis of DNA and RNA. This nucleoside analog also disrupts mitochondrial function and membrane integrity, resulting in the release of pre-apoptotic factors, including cytochrome C and apoptotic-inducing factors, which activate apoptosis.","A small-molecule arsenic compound with antineoplastic activity.  The mechanism of action of arsenic trioxide is not completely understood. This agent causes damage to or degradation of the promyelocytic leukemia protein/retinoic acid receptor-alpha (PML/RARa) fusion protein; induces apoptosis in acute promyelocytic leukemia (APL) cells and in many other tumor cell types; promotes cell differentiation and suppresses cell proliferation in many different tumor cell types; and is pro-angiogenic. (NCI04)","A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites.  As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. (NCI04)","A broad-spectrum antimetabolite and deoxycytidine analogue with antineoplastic activity. Upon administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA.  This locks DNA polymerase thereby resulting in \"masked termination\" during DNA replication. On the other hand, dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis. The reduction in the intracellular concentration of dCTP potentiates the incorporation of dFdCTP into DNA.","A purine nucleoside antimetabolite analogue. Cladribine triphosphate, a phosphorylated metabolite of cladribine, incorporates into DNA, resulting in single-strand breaks in DNA, depletion of nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP), and apoptosis.  Because this agent is resistant to adenosine deaminase, an enzyme that inactivates some antineoplastic agents, it is selectively toxic to lymphocytes and monocytes which exhibit little deoxynucleotide deaminase activity. (NCI04)","A fluorinated pyrimidine monophosphate analogue of 5-fluoro-2'-deoxyuridine-5'-phosphate (FUDR-MP) with antineoplastic activity. As an antimetabolite, floxuridine inhibits thymidylate synthase, resulting in disruption of DNA synthesis and cytotoxicity. This agent is also metabolized to fluorouracil and other metabolites that can be incorporated into RNA and inhibit the utilization of preformed uracil in RNA synthesis. (NCI04)","An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA.  Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle.  This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. (NCI04)","A monohydroxyl-substituted urea (hydroxycarbamate) antimetabolite. Hydroxyurea selectively inhibits ribonucleoside diphosphate reductase, an enzyme required to convert ribonucleoside diphosphates into deoxyribonucleoside diphosphates, thereby preventing cells from leaving the G1/S phase of the cell cycle.  This agent also exhibits radiosensitizing activity by maintaining cells in the radiation-sensitive G1 phase and interfering with DNA repair. (NCI04)","A synthetic guanosine analogue antimetabolite. Phosphorylated by hypoxanthine-guanine phosphoribosyltransferase, thioguanine incorporates into DNA and RNA, resulting in inhibition of DNA and RNA syntheses and cell death. This agent also inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase, thereby inhibiting purine synthesis. (NCI04)","An antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Fluorouracil and its metabolites possess a number of different mechanisms of action. In vivo, fluoruracil is converted to the active metabolite 5-fluoroxyuridine monophosphate (F-UMP); replacing uracil, F-UMP incorporates into RNA and inhibits RNA processing, thereby inhibiting cell growth. Another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP), inhibits thymidylate synthase, resulting in the depletion of thymidine triphosphate (TTP), one of the four nucleotide triphosphates used in the in vivo synthesis of DNA. Other fluorouracil metabolites incorporate into both RNA and DNA; incorporation into RNA results in major effects on both RNA processing and functions.","A thiopurine-derivative antimetabolite with antineoplastic and immunosuppressive activities.  Produced through the metabolism of mercaptopurine by hypoxanthine-guanine phosphoribosyltransferase (HGPRT), mercaptopurine metabolites 6-thioguanosine-5'-phosphate (6-thioGMP) and 6-thioinosine monophosphate (T-IMP) inhibit nucleotide interconversions and de novo purine synthesis, thereby blocking the formation of purine nucleotides and inhibiting DNA synthesis.  This agent is also incorporated into DNA in the form of deoxythioguanosine, which results in the disruption of DNA replication. In addition, mercaptopurine is converted to 6-methylmercaptopurine ribonucleoside (MMPR) by 6-thiopurine methyltransferase; MMPRs are also potent inhibitors of de novo purine synthesis. (NCI04)","A congener of the antimetabolite fluorouracil with antineoplastic activity. Tegafur is a prodrug that is gradually converted to fluorouracil in the liver by the cytochrome P-450 enzyme. Subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by inhibiting thymidylate synthase and reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate. (NCI04)","A quinazoline folate analogue with antineoplastic activity.  After transport into cells via the reduced folate carrier, raltitrexed undergoes intracellular polyglutamation and blocks the folate-binding site of thymidylate synthase, thereby inhibiting tetrahydrofolate activity and DNA replication and repair and resulting in cytotoxicity. (NCI04)","An orally-active fluoropyrimidine analogue. Eniluracil inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil (5-FU) in the liver. Co-administration of ethynyluracil permits the oral administration of 5-FU.","An orally bioavailable pyrimidine analogue prodrug with potential antineoplastic activity. Sapacitabine is hydrolyzed by amidases to the deoxycytosine analogue CNDAC (2'-Cyano-2'-deoxyarabinofuranosylcytosine), which is then phosphorylated into the active triphosphate form. As an analogue of deoxycytidine triphosphate, CNDAC triphosphate incorporates into DNA strands during replication, resulting in single-stranded DNA breaks during polymerization due to beta-elimination during the fidelity checkpoint process; cell cycle arrest in the G2 phase and apoptosis ensue. The unmetabolized prodrug may exhibit antineoplastic activity as well.","A pyrimidine analogue and a proprietary prodrug based on an aryloxy phosphoramidate derivative of gemcitabine with potential antineoplastic activity. Upon intravenous administration and cellular uptake, fosgemcitabine palabenamide is converted into the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually induction of apoptosis. With the phosphoramidate moiety on the gemcitabine monophosphate group, NUC-1031 has improved properties over its parent molecule: 1) is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, 2) as the agent is delivered in the monophosphate form, the first phosphorylation step by deoxycytidine kinase is not required, 3) this agent is not susceptible to deactivation by cytidine deaminase cleavage of the monophosphorylated form. Altogether, this may help overcome resistance to gemcitabine.","An antimetabolite and a chlorine derivative of the intracellular secondary messenger, cyclic adenosine 3,5-monophosphate (cAMP), with potential antineoplastic activity. Tocladesine appears to be converted to 8-chloro-adenosine by phosphodiesterases and subsequently phosphorylated to 8-chloro-ATP, which functions as a purine analogue and competes with ATP in transcription. In addition, generation of 8-chloro-ATP depletes endogenous ATP pool that is essential for many biological reactions in intracellular energy transfer. As a result, this agent causes RNA synthesis inhibition, blocks cellular proliferation, and induces apoptosis.","A synthetic pyrimidine nucleoside analogue with potential antineoplastic activity. Phosphorylated by cellular kinases, tezacitabine is converted into its active diphosphate and triphosphate metabolites. Tezacitabine diphosphate binds to and irreversibly inhibits the activity of the enzyme ribonucleotide reductase (RNR), which may result in the inhibition of DNA synthesis in tumor cells and tumor cell apoptosis. Tezacitabine triphosphate acts as a substrate for DNA polymerase, further compromising DNA replication. This agent is relatively resistant to metabolic deactivation by cytidine deaminase. RNR catalyzes the conversion of ribonucleoside 5'-diphosphates to deoxyribonucleoside 5'-diphosphates necessary for DNA synthesis and is overexpressed in many tumor types.","A dioxolane derivative and a novel L-configuration deoxycytidine analogue with potent antineoplastic activity. When incorporated into growing chain during DNA replication, troxacitabine stops DNA polymerization due to its unnatural L-configuration, in contrast to the normal nucleotides with D-configuration. As a result, this agent terminates DNA synthesis upon incorporated into DNA molecules, and consequently interrupts tumor cell proliferation.","A small molecule pro-drug consisting of cytarabine, an antimetabolite analog of cytidine with a modified arabinose sugar moiety, covalently bonded to asparagine, with potential antineoplastic activity. Upon intravenous administration, aspacytarabine targets cancer cells, which often lack asparagine synthetase and are dependent on an external source of amino acids due to their high metabolic rate. Once the prodrug is inside target cells, the cytarabine component is cleaved and competes with cytidine for incorporation into DNA. The arabinose sugar moiety of cytarabine sterically hinders the rotation of the molecule within DNA, resulting in cell cycle arrest, specifically during the S phase of replication. Cytarabine also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Because BST-236 specifically targets cancer cells, it may spare normal tissues from cytarabine-related toxicities.","A synthetic pyrimidine nucleoside analogue with biomodulating activity. Tetrahydrouridine increases the efficacy of the radiosensitizer cytochlor (5-chloro-2'-deoxycytidine) by inhibiting the enzyme deoxycytidine monophosphate (dCMP) deaminase and preventing the premature deamination of the cytochlor metabolite 5-chloro-2'-deoxycytidine monophosphate (CldCMP) to 5-chloro-2'-deoxyuridine monophosphate (CldUMP); in turn, this increases tumor concentrations of CldUMP which is then further anabolized and incorporated selectively into tumor DNA as CldU (5-chloro-2'-deoxyuridine). (NCI04)","A thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication.  This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo.  Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells. (NCI04)","A phosphoramidate-based prodrug of the monophosphate (MP) form of 5-fluoro-2'-deoxyuridine (FUdR; FUDR), the active metabolite of fluorouracil (5-FU), an antimetabolite fluoropyrimidine analog of the pyrimidine nucleoside, with potential antineoplastic activity. Upon administration of the nucleotide analog prodrug fosifloxuridine nafalbenamide, fosifloxuridine nafalbenamide is readily taken up by tumor cells. In the tumor cell, the phosphoramidate moiety is removed and fosifloxuridine nafalbenamide is converted to its active form FUDR-MP. In turn, FUDR-MP binds to and inhibits thymidylate synthase (TS), resulting in the depletion of thymidine triphosphate (TTP) and thus DNA synthesis. With the phosphoramidate moiety attached to FUDR-MP, fosifloxuridine nafalbenamide, compared to 5-FU, is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, thereby generating higher intracellular concentrations. In addition, compared to 5-FU, once inside the cell FUDR-MP does not need to be phosphorylated and is already in its active form. Unlike 5-FU, fosifloxuridine nafalbenamide does not get deactivated or converted into toxic metabolites by dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP), which leads to both a longer half-life and less toxicity.","An antimetabolite (pyrimidine analogue) antineoplastic derivative of 5-fluorouracil. 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t-cell leukemia/lymphoma, anaplastic large cell lymphoma, breast carcinoma, cancer, fallopian tube cancer, head and neck malignant neoplasia, lung cancer, lymphoma, mature t-cell and nk-cell non-hodgkin lymphoma, multiple myeloma, mycosis fungoides, non-small cell lung carcinoma, ovarian cancer, peritoneum cancer, sezary's disease, t-cell non-hodgkin lymphoma","acute myeloid leukemia, acute promyelocytic leukemia, adult lymphoma, blast phase chronic myelogenous leukemia, bcr-abl1 positive, breast neoplasm, burkitts lymphoma, cancer, childhood acute lymphoblastic leukemia, chronic myelomonocytic leukemia, chronic myeloproliferative disorder, cutaneous melanoma, diffuse large b-cell lymphoma, esophageal squamous cell carcinoma, extranodal nasal nk/t cell lymphoma, fallopian tube cancer, follicular thyroid carcinoma, head and neck malignant neoplasia, hodgkins lymphoma, leukemia, lymphoid neoplasm, lymphoma, mantle cell lymphoma, mature t-cell and nk-cell non-hodgkin lymphoma, medulloblastoma, melanoma, metastatic melanoma, multiple myeloma, myelodysplastic syndrome, myeloproliferative disorder, neoplasm of mature b-cells, neuroblastoma, non-hodgkins lymphoma, non-small cell lung carcinoma, ovarian cancer, papillary thyroid carcinoma, pediatric lymphoma, peritoneum cancer, prostate carcinoma, refractory anemia with excess blasts, renal cell carcinoma","cancer, chronic myeloproliferative disorder, leukemia, lymphoblastic lymphoma, lymphoid leukemia, lymphoma, multiple myeloma, mycosis fungoides, myelodysplastic syndrome, sezary's disease, t-cell acute lymphoblastic leukemia, t-lymphoblastic lymphoma","biliary tract cancer, breast carcinoma, breast neoplasm, cancer, cervical cancer, chordoma, colorectal adenocarcinoma, colorectal carcinoma, cutaneous melanoma, diffuse large b-cell lymphoma, endometrial cancer, esophageal cancer, esophageal carcinoma, fallopian tube cancer, fallopian tube carcinoma, gastric cancer, gastric carcinoma, gestational trophoblastic neoplasm, head and neck malignant neoplasia, head and neck squamous cell carcinoma, large cell lung carcinoma, leptomeningeal metastasis, liver cancer, lung adenocarcinoma, lung cancer, lymphoma, male breast carcinoma, malignant glioma, malignant pleural mesothelioma, medulloblastoma, mesothelioma, metastatic melanoma, nasopharyngeal neoplasm, non-hodgkins lymphoma, non-small cell lung carcinoma, osteosarcoma, ovarian cancer, ovarian carcinoma, pancreatic carcinoma, pancreatic neoplasm, peritoneum cancer, prostate cancer, renal cell carcinoma, salivary gland carcinoma, sarcoma, small cell lung carcinoma, squamous cell carcinoma, squamous cell lung carcinoma, stomach neoplasm, thymic carcinoma, thymoma, thymus cancer, thyroid cancer, urethra cancer, urinary bladder cancer, urothelial carcinoma","acute myeloid leukemia, angioimmunoblastic t-cell lymphoma, brain neoplasm, breast neoplasm, cancer, chronic lymphocytic leukemia, chronic myelomonocytic leukemia, classic hodgkin lymphoma, colorectal carcinoma, cutaneous melanoma, diffuse large b-cell lymphoma, ependymoma, esophageal cancer, follicular lymphoma, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hematopoietic and lymphoid cell neoplasm, hodgkins lymphoma, leukemia, liposarcoma, lymphoid leukemia, lymphoid neoplasm, lymphoma, male breast carcinoma, malignant colon neoplasm, mature t-cell and nk-cell non-hodgkin lymphoma, metastatic melanoma, multiple myeloma, myelodysplastic syndrome, myeloproliferative disorder, nasopharyngeal neoplasm, non-hodgkins lymphoma, non-small cell lung carcinoma, osteosarcoma, ovarian cancer, pancreatic carcinoma, prostate adenocarcinoma, prostate cancer, refractory anemia with excess blasts, renal cell carcinoma, squamous cell carcinoma, t-cell acute lymphoblastic leukemia, t-cell large granular lymphocyte leukemia","acute myeloid leukemia, acute promyelocytic leukemia, cancer, chronic lymphocytic leukemia, chronic myelomonocytic leukemia, hodgkins lymphoma, langerhans cell histiocytosis, leukemia, lymphoblastic lymphoma, lymphoma, multiple myeloma, myelodysplastic syndrome, neoplasm of mature b-cells, non-hodgkins lymphoma, t-cell non-hodgkin lymphoma","acute myeloid leukemia, acute promyelocytic leukemia, cancer, cervical cancer, chronic lymphocytic leukemia, colorectal carcinoma, endometrial carcinoma, essential thrombocythemia, gliosarcoma, hepatocellular carcinoma, kidney cancer, leukemia, liver cancer, lung cancer, lymphoma, metastatic melanoma, multiple myeloma, myelodysplastic syndrome, neuroblastoma, non-small cell lung carcinoma, pancreatic carcinoma, polycythemia vera, prostate cancer, skin basal cell carcinoma, small cell lung carcinoma, ureter cancer, urethra cancer, urinary bladder carcinoma","anus cancer, biliary tract cancer, biliary tract neoplasm, breast carcinoma, breast neoplasm, cancer, cervical cancer, cholangiocarcinoma, colon adenocarcinoma, colonic neoplasm, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, cutaneous melanoma, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, fallopian tube cancer, fallopian tube carcinoma, gallbladder cancer, gallbladder carcinoma, gastric adenocarcinoma, gastric cancer, gastric carcinoma, glioblastoma multiforme, glioma, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hepatocellular carcinoma, hypopharyngeal carcinoma, inflammatory breast carcinoma, intrahepatic cholangiocarcinoma, kidney cancer, kidney neoplasm, laryngeal squamous cell carcinoma, liver cancer, lung cancer, male breast carcinoma, malignant colon neoplasm, malignant glioma, melanoma, merkel cell skin cancer, mesothelioma, metastatic melanoma, nasopharyngeal neoplasm, non-hodgkins lymphoma, non-small cell lung carcinoma, oropharyngeal carcinoma, ovarian cancer, ovarian carcinoma, pancreatic carcinoma, pancreatic endocrine carcinoma, pancreatic neoplasm, pancreatic neuroendocrine tumor, peritoneum cancer, prostate cancer, rectal carcinoma, rectal neoplasm, renal cell carcinoma, skin cancer, skin carcinoma, squamous cell carcinoma, stomach neoplasm, thyroid cancer, triple-negative breast cancer, urothelial carcinoma","acute myeloid leukemia, adult t-cell leukemia/lymphoma, anaplastic large cell lymphoma, angioimmunoblastic t-cell lymphoma, bile duct cancer, biliary tract cancer, biliary tract neoplasm, bladder tumor, bone sarcoma, breast carcinoma, breast neoplasm, cancer, cervical adenocarcinoma, cervical cancer, cervical carcinoma, cholangiocarcinoma, classic hodgkin lymphoma, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, diffuse intrinsic pontine glioma, diffuse large b-cell lymphoma, endometrial cancer, endometrioid carcinoma, esophageal cancer, ewing sarcoma, extranodal nasal nk/t cell lymphoma, fallopian tube cancer, fallopian tube carcinoma, follicular lymphoma, gallbladder cancer, gallbladder carcinoma, gallbladder neoplasm, gastric cancer, gastrointestinal stromal tumor, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hepatoblastoma, hepatocellular carcinoma, hilar cholangiocarcinoma, hodgkins lymphoma, intrahepatic cholangiocarcinoma, kidney cancer, large cell lung carcinoma, leiomyosarcoma, leukemia, liver cancer, lung adenocarcinoma, lung cancer, lymphoma, male breast carcinoma, malignant colon neoplasm, malignant epithelial tumor of ovary, malignant pleural mesothelioma, mantle cell lymphoma, mature t-cell and nk-cell non-hodgkin lymphoma, medulloblastoma, melanoma, mesothelioma, multiple myeloma, mycosis fungoides, nasopharyngeal neoplasm, neoplasm of mature b-cells, non-hodgkins lymphoma, non-small cell lung carcinoma, osteosarcoma, ovarian cancer, ovarian carcinoma, ovarian neoplasm, ovarian serous cystadenocarcinoma, pancreatic carcinoma, pancreatic neoplasm, peritoneal neoplasm, peritoneum cancer, plasma cell leukemia, plasmacytoma, prostate cancer, renal cell carcinoma, sarcoma, small cell lung carcinoma, soft tissue sarcoma, squamous cell carcinoma, squamous cell lung carcinoma, synovial sarcoma, t-cell non-hodgkin lymphoma, thyroid cancer, triple-negative breast cancer, ureter cancer, urethra cancer, urinary bladder cancer, urinary bladder carcinoma, urothelial carcinoma, uterine carcinosarcoma, uterine neoplasm","acute leukemia of ambiguous lineage, acute monocytic leukemia, acute myeloid leukemia, blast phase chronic myelogenous leukemia, bcr-abl1 positive, cancer, chronic lymphocytic leukemia, chronic myeloproliferative disorder, diffuse large b-cell lymphoma, hairy cell leukemia, histiocytosis, langerhans cell histiocytosis, leukemia, lymphoma, malt lymphoma, mantle cell lymphoma, multiple myeloma, myelodysplastic syndrome, myeloid leukemia, systemic mastocytosis","cancer, cholangiocarcinoma, colorectal adenocarcinoma, colorectal carcinoma, esophageal cancer, fallopian tube cancer, gastric adenocarcinoma, gastric cancer, gastrointestinal stromal tumor, hepatocellular carcinoma, intrahepatic cholangiocarcinoma, liver cancer, malignant colon neoplasm, ovarian cancer, peritoneum cancer","acute basophilic leukemia, acute erythroleukemia, acute leukemia of ambiguous lineage, acute megakaryoblastic leukaemia, acute monocytic leukemia, acute myeloblastic leukemia with maturation, acute myeloblastic leukemia without maturation, acute myeloid leukemia, acute myelomonocytic leukemia, acute promyelocytic leukemia, adult t-cell leukemia/lymphoma, anaplastic large cell lymphoma, b-cell acute lymphoblastic leukemia, blast phase chronic myelogenous leukemia, bcr-abl1 positive, brain neoplasm, burkitts lymphoma, cancer, childhood acute lymphoblastic leukemia, chronic lymphocytic leukemia, chronic myelomonocytic leukemia, chronic myeloproliferative disorder, classic hodgkin lymphoma, diffuse large b-cell lymphoma, essential thrombocythemia, follicular lymphoma, glioblastoma multiforme, granulocytic sarcoma, hematopoietic and lymphoid cell neoplasm, hodgkins lymphoma, juvenile myelomonocytic leukemia, langerhans cell histiocytosis, leptomeningeal metastasis, leukemia, lymphoblastic lymphoma, lymphoid leukemia, lymphoma, lymphoma, aids-related, mantle cell lymphoma, medulloblastoma, melanoma, multiple myeloma, myelodysplastic syndrome, myeloid sarcoma, myeloproliferative disorder, neoplasm of mature b-cells, non-hodgkins lymphoma, ovarian cancer, plasma cell leukemia, polycythemia vera, prostate cancer, refractory anemia, refractory anemia with excess blasts, sarcoma, t-cell acute lymphoblastic leukemia, t-lymphoblastic lymphoma","acute myeloid leukemia, acute promyelocytic leukemia, cancer, desmoid-type fibromatosis, esophageal cancer, essential thrombocythemia, gastric cancer, glioblastoma multiforme, gliosarcoma, head and neck malignant neoplasia, laryngeal neoplasm, leukemia, lung cancer, lymphoma, melanoma, meningioma, myelodysplastic syndrome, myeloproliferative disorder, oral cavity cancer, paranasal sinus neoplasm, pharynx cancer, polycythemia vera, 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colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, cutaneous melanoma, ependymoma, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, fallopian tube carcinoma, gastric adenocarcinoma, gastric cancer, gastric carcinoma, gastrointestinal stromal tumor, head and neck carcinoma, head and neck malignant neoplasia, head and neck neoplasia, head and neck squamous cell carcinoma, hepatoblastoma, hepatocellular carcinoma, hypopharyngeal carcinoma, inflammatory breast carcinoma, intrahepatic cholangiocarcinoma, kidney cancer, laryngeal carcinoma, laryngeal neoplasm, liver cancer, lymphoma, lymphoma, aids-related, malignant colon neoplasm, melanoma, merkel cell skin cancer, metastatic melanoma, mucinous carcinoma, multiple myeloma, myelodysplastic syndrome, nasopharyngeal neoplasm, neoplasm of esophagus, non-hodgkins lymphoma, non-small cell lung carcinoma, oral cavity cancer, oral squamous cell carcinoma, ovarian cancer, ovarian carcinoma, pancreatic carcinoma, pancreatic endocrine carcinoma, pancreatic neoplasm, paranasal sinus neoplasm, peritoneal neoplasm, peritoneum cancer, pharynx cancer, rectal carcinoma, renal cell carcinoma, skin carcinoma, squamous cell carcinoma, stomach neoplasm, urethra cancer, urinary bladder cancer, urinary bladder carcinoma, urothelial carcinoma, uterine neoplasm","acute leukemia of ambiguous lineage, acute myeloid leukemia, acute promyelocytic leukemia, anaplastic astrocytoma, anaplastic oligodendroglioma, b-cell acute lymphoblastic leukemia, brain neoplasm, burkitts lymphoma, cancer, childhood acute lymphoblastic leukemia, glioblastoma multiforme, langerhans cell histiocytosis, leukemia, lymphoblastic lymphoma, lymphoid leukemia, lymphoma, mixed glioma, t-cell acute lymphoblastic leukemia, t-lymphoblastic lymphoma","biliary tract cancer, biliary tract neoplasm, breast neoplasm, cancer, cervical cancer, cholangiocarcinoma, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, 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<th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" 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+<script type="application/json" data-for="htmlwidget-3c16c154854e7e2c043a">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10","11","12","13","14","15","16","17","18","19","20","21","22","23","24","25","26","27","28","29"],[24318,10341,21161,23196,4149,8606,3291,6702,15044,8489,14057,9695,16168,28844,14198,19639,28426,25250,12541,26512,14532,29235,28709,29874,3382,28677,5003,14536,7166],["Pralatrexate","Decitabine","Nelarabine","Pemetrexed","Azacitidine","Clofarabine","Arsenic Trioxide","Capecitabine","Gemcitabine","Cladribine","Floxuridine","Cytarabine","Hydroxyurea","Thioguanine","Fluorouracil","Mercaptopurine","Tegafur","Raltitrexed","Eniluracil","Sapacitabine","Fosgemcitabine Palabenamide","Tocladesine","Tezacitabine","Troxacitabine","Aspacytarabine","Tetrahydrouridine","2'-DEOXYTHIOGUANOSINE","Fosifloxuridine Nafalbenamide","Carmofur"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule"],["CHEMBL1201746","CHEMBL1201129","CHEMBL1201112","CHEMBL225072","CHEMBL1489","CHEMBL1750","CHEMBL2362016","CHEMBL1773","CHEMBL888","CHEMBL1619","CHEMBL917","CHEMBL803","CHEMBL467","CHEMBL727","CHEMBL185","CHEMBL1425","CHEMBL20883","CHEMBL225071","CHEMBL355200","CHEMBL2105681","CHEMBL3126004","CHEMBL2107085","CHEMBL2105467","CHEMBL359164","CHEMBL4297599","CHEMBL1236475","CHEMBL3250476","CHEMBL2181367","CHEMBL460499"],["INHIBITOR","INHIBITOR","NA","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","NA","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","INHIBITOR","NA","NA","NA","INHIBITOR","INHIBITOR","INHIBITOR","NA","NA","NA","NA"],["A folate analogue inhibitor of dihydrofolate reductase (DHFR) exhibiting high affinity for reduced folate carrier-1 (RFC-1) with antineoplastic and immunosuppressive activities. Pralatrexate selectively enters cells expressing RFC-1; intracellularly, this agent is highly polyglutamylated and competes for the folate binding site of DHFR, blocking tetrahydrofolate synthesis, which may result in depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death. Efficient intracellular polyglutamylation of pralatrexate results in higher intracellular concentrations compared to non-polyglutamylated pralatrexate, which is more readily effuxed by the MRP (multidrug resistance protein) drug efflux pump. RFC-1, an oncofetal protein expressed at highest levels during embryonic development, may be over-expressed on the cell surfaces of various cancer cell types.","A cytidine antimetabolite analogue with potential antineoplastic activity. Decitabine incorporates into DNA and inhibits DNA methyltransferase, resulting in hypomethylation of DNA and intra-S-phase arrest of DNA replication. (NCI04)","An arabinonucleoside antimetabolite with antineoplastic activity. Nelarabine is demethoxylated by adenosine deaminase to become biologically active 9-beta-D-arabinosylguanine (ara-G); ara-G incorporates into DNA, thereby inhibiting DNA synthesis and inducing an S phase-dependent apoptosis of tumor cells. (NCI04)","A synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS), which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.","A pyrimidine nucleoside analogue of cytidine with antineoplastic activity. Azacitidine is incorporated into DNA, where it reversibly inhibits DNA methyltransferase, thereby blocking DNA methylation.  Hypomethylation of DNA by azacitidine may activate tumor suppressor genes silenced by hypermethylation, resulting in an antitumor effect. This agent is also incorporated into RNA, thereby disrupting normal RNA function and impairing tRNA cytosine-5-methyltransferase activity. (NCI04)","A second generation purine nucleoside analog with antineoplastic activity. Clofarabine is phosphorylated intracellularly to the cytotoxic active 5'-triphosphate metabolite, which inhibits the enzymatic activities of ribonucleotide reductase and DNA polymerase, resulting in inhibition of DNA repair and synthesis of DNA and RNA. This nucleoside analog also disrupts mitochondrial function and membrane integrity, resulting in the release of pre-apoptotic factors, including cytochrome C and apoptotic-inducing factors, which activate apoptosis.","A small-molecule arsenic compound with antineoplastic activity.  The mechanism of action of arsenic trioxide is not completely understood. This agent causes damage to or degradation of the promyelocytic leukemia protein/retinoic acid receptor-alpha (PML/RARa) fusion protein; induces apoptosis in acute promyelocytic leukemia (APL) cells and in many other tumor cell types; promotes cell differentiation and suppresses cell proliferation in many different tumor cell types; and is pro-angiogenic. (NCI04)","A fluoropyrimidine carbamate belonging to the class of antineoplastic agents called antimetabolites.  As a prodrug, capecitabine is selectively activated by tumor cells to its cytotoxic moiety, 5-fluorouracil (5-FU); subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate for incorporation into the RNA strand. (NCI04)","A broad-spectrum antimetabolite and deoxycytidine analogue with antineoplastic activity. Upon administration, gemcitabine is converted into the active metabolites difluorodeoxycytidine diphosphate (dFdCDP) and difluorodeoxycytidine triphosphate (dFdCTP) by deoxycytidine kinase. dFdCTP competes with deoxycytidine triphosphate (dCTP) and is incorporated into DNA.  This locks DNA polymerase thereby resulting in \"masked termination\" during DNA replication. On the other hand, dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA synthesis. The reduction in the intracellular concentration of dCTP potentiates the incorporation of dFdCTP into DNA.","A purine nucleoside antimetabolite analogue. Cladribine triphosphate, a phosphorylated metabolite of cladribine, incorporates into DNA, resulting in single-strand breaks in DNA, depletion of nicotinamide adenine dinucleotide (NAD) and adenosine triphosphate (ATP), and apoptosis.  Because this agent is resistant to adenosine deaminase, an enzyme that inactivates some antineoplastic agents, it is selectively toxic to lymphocytes and monocytes which exhibit little deoxynucleotide deaminase activity. (NCI04)","A fluorinated pyrimidine monophosphate analogue of 5-fluoro-2'-deoxyuridine-5'-phosphate (FUDR-MP) with antineoplastic activity. As an antimetabolite, floxuridine inhibits thymidylate synthase, resulting in disruption of DNA synthesis and cytotoxicity. This agent is also metabolized to fluorouracil and other metabolites that can be incorporated into RNA and inhibit the utilization of preformed uracil in RNA synthesis. (NCI04)","An antimetabolite analogue of cytidine with a modified sugar moiety (arabinose instead of ribose). Cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA.  Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle.  This agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. (NCI04)","A monohydroxyl-substituted urea (hydroxycarbamate) antimetabolite. Hydroxyurea selectively inhibits ribonucleoside diphosphate reductase, an enzyme required to convert ribonucleoside diphosphates into deoxyribonucleoside diphosphates, thereby preventing cells from leaving the G1/S phase of the cell cycle.  This agent also exhibits radiosensitizing activity by maintaining cells in the radiation-sensitive G1 phase and interfering with DNA repair. (NCI04)","A synthetic guanosine analogue antimetabolite. Phosphorylated by hypoxanthine-guanine phosphoribosyltransferase, thioguanine incorporates into DNA and RNA, resulting in inhibition of DNA and RNA syntheses and cell death. This agent also inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase, thereby inhibiting purine synthesis. (NCI04)","An antimetabolite fluoropyrimidine analog of the nucleoside pyrimidine with antineoplastic activity. Fluorouracil and its metabolites possess a number of different mechanisms of action. In vivo, fluoruracil is converted to the active metabolite 5-fluoroxyuridine monophosphate (F-UMP); replacing uracil, F-UMP incorporates into RNA and inhibits RNA processing, thereby inhibiting cell growth. Another active metabolite, 5-5-fluoro-2'-deoxyuridine-5'-O-monophosphate (F-dUMP), inhibits thymidylate synthase, resulting in the depletion of thymidine triphosphate (TTP), one of the four nucleotide triphosphates used in the in vivo synthesis of DNA. Other fluorouracil metabolites incorporate into both RNA and DNA; incorporation into RNA results in major effects on both RNA processing and functions.","A thiopurine-derivative antimetabolite with antineoplastic and immunosuppressive activities.  Produced through the metabolism of mercaptopurine by hypoxanthine-guanine phosphoribosyltransferase (HGPRT), mercaptopurine metabolites 6-thioguanosine-5'-phosphate (6-thioGMP) and 6-thioinosine monophosphate (T-IMP) inhibit nucleotide interconversions and de novo purine synthesis, thereby blocking the formation of purine nucleotides and inhibiting DNA synthesis.  This agent is also incorporated into DNA in the form of deoxythioguanosine, which results in the disruption of DNA replication. In addition, mercaptopurine is converted to 6-methylmercaptopurine ribonucleoside (MMPR) by 6-thiopurine methyltransferase; MMPRs are also potent inhibitors of de novo purine synthesis. (NCI04)","A congener of the antimetabolite fluorouracil with antineoplastic activity. Tegafur is a prodrug that is gradually converted to fluorouracil in the liver by the cytochrome P-450 enzyme. Subsequently, 5-FU is metabolized to two active metabolites, 5-fluoro-2-deoxyuridine monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP) by both tumor cells and normal cells.  FdUMP inhibits DNA synthesis and cell division by inhibiting thymidylate synthase and reducing normal thymidine production, while FUTP inhibits RNA and protein synthesis by competing with uridine triphosphate. (NCI04)","A quinazoline folate analogue with antineoplastic activity.  After transport into cells via the reduced folate carrier, raltitrexed undergoes intracellular polyglutamation and blocks the folate-binding site of thymidylate synthase, thereby inhibiting tetrahydrofolate activity and DNA replication and repair and resulting in cytotoxicity. (NCI04)","An orally-active fluoropyrimidine analogue. Eniluracil inhibits dihydropyrimidine dehydrogenase, the rate-limiting enzyme that catabolizes and inactivates 5-fluorouracil (5-FU) in the liver. Co-administration of ethynyluracil permits the oral administration of 5-FU.","An orally bioavailable pyrimidine analogue prodrug with potential antineoplastic activity. Sapacitabine is hydrolyzed by amidases to the deoxycytosine analogue CNDAC (2'-Cyano-2'-deoxyarabinofuranosylcytosine), which is then phosphorylated into the active triphosphate form. As an analogue of deoxycytidine triphosphate, CNDAC triphosphate incorporates into DNA strands during replication, resulting in single-stranded DNA breaks during polymerization due to beta-elimination during the fidelity checkpoint process; cell cycle arrest in the G2 phase and apoptosis ensue. The unmetabolized prodrug may exhibit antineoplastic activity as well.","A pyrimidine analogue and a proprietary prodrug based on an aryloxy phosphoramidate derivative of gemcitabine with potential antineoplastic activity. Upon intravenous administration and cellular uptake, fosgemcitabine palabenamide is converted into the active metabolites difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP). dFdCDP inhibits ribonucleotide reductase, thereby decreasing the deoxynucleotide pool available for DNA replication; dFdCTP is incorporated into DNA, resulting in premature termination of DNA replication and eventually induction of apoptosis. With the phosphoramidate moiety on the gemcitabine monophosphate group, NUC-1031 has improved properties over its parent molecule: 1) is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, 2) as the agent is delivered in the monophosphate form, the first phosphorylation step by deoxycytidine kinase is not required, 3) this agent is not susceptible to deactivation by cytidine deaminase cleavage of the monophosphorylated form. Altogether, this may help overcome resistance to gemcitabine.","An antimetabolite and a chlorine derivative of the intracellular secondary messenger, cyclic adenosine 3,5-monophosphate (cAMP), with potential antineoplastic activity. Tocladesine appears to be converted to 8-chloro-adenosine by phosphodiesterases and subsequently phosphorylated to 8-chloro-ATP, which functions as a purine analogue and competes with ATP in transcription. In addition, generation of 8-chloro-ATP depletes endogenous ATP pool that is essential for many biological reactions in intracellular energy transfer. As a result, this agent causes RNA synthesis inhibition, blocks cellular proliferation, and induces apoptosis.","A synthetic pyrimidine nucleoside analogue with potential antineoplastic activity. Phosphorylated by cellular kinases, tezacitabine is converted into its active diphosphate and triphosphate metabolites. Tezacitabine diphosphate binds to and irreversibly inhibits the activity of the enzyme ribonucleotide reductase (RNR), which may result in the inhibition of DNA synthesis in tumor cells and tumor cell apoptosis. Tezacitabine triphosphate acts as a substrate for DNA polymerase, further compromising DNA replication. This agent is relatively resistant to metabolic deactivation by cytidine deaminase. RNR catalyzes the conversion of ribonucleoside 5'-diphosphates to deoxyribonucleoside 5'-diphosphates necessary for DNA synthesis and is overexpressed in many tumor types.","A dioxolane derivative and a novel L-configuration deoxycytidine analogue with potent antineoplastic activity. When incorporated into growing chain during DNA replication, troxacitabine stops DNA polymerization due to its unnatural L-configuration, in contrast to the normal nucleotides with D-configuration. As a result, this agent terminates DNA synthesis upon incorporated into DNA molecules, and consequently interrupts tumor cell proliferation.","A small molecule pro-drug consisting of cytarabine, an antimetabolite analog of cytidine with a modified arabinose sugar moiety, covalently bonded to asparagine, with potential antineoplastic activity. Upon intravenous administration, aspacytarabine targets cancer cells, which often lack asparagine synthetase and are dependent on an external source of amino acids due to their high metabolic rate. Once the prodrug is inside target cells, the cytarabine component is cleaved and competes with cytidine for incorporation into DNA. The arabinose sugar moiety of cytarabine sterically hinders the rotation of the molecule within DNA, resulting in cell cycle arrest, specifically during the S phase of replication. Cytarabine also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Because BST-236 specifically targets cancer cells, it may spare normal tissues from cytarabine-related toxicities.","A synthetic pyrimidine nucleoside analogue with biomodulating activity. Tetrahydrouridine increases the efficacy of the radiosensitizer cytochlor (5-chloro-2'-deoxycytidine) by inhibiting the enzyme deoxycytidine monophosphate (dCMP) deaminase and preventing the premature deamination of the cytochlor metabolite 5-chloro-2'-deoxycytidine monophosphate (CldCMP) to 5-chloro-2'-deoxyuridine monophosphate (CldUMP); in turn, this increases tumor concentrations of CldUMP which is then further anabolized and incorporated selectively into tumor DNA as CldU (5-chloro-2'-deoxyuridine). (NCI04)","A thiopurine nucleoside derivative with antineoplastic activity. After conversion to the triphosphate, beta-thioguanine deoxyriboside is incorporated into DNA, resulting in inhibition of DNA replication.  This agent is cytotoxic against leukemia cell lines and has demonstrated some activity against leukemia cells in vivo.  Beta-thioguanine deoxyriboside demonstrates antineoplastic activity against 6-thioguanine-resistant tumor cells. (NCI04)","A phosphoramidate-based prodrug of the monophosphate (MP) form of 5-fluoro-2'-deoxyuridine (FUdR; FUDR), the active metabolite of fluorouracil (5-FU), an antimetabolite fluoropyrimidine analog of the pyrimidine nucleoside, with potential antineoplastic activity. Upon administration of the nucleotide analog prodrug fosifloxuridine nafalbenamide, fosifloxuridine nafalbenamide is readily taken up by tumor cells. In the tumor cell, the phosphoramidate moiety is removed and fosifloxuridine nafalbenamide is converted to its active form FUDR-MP. In turn, FUDR-MP binds to and inhibits thymidylate synthase (TS), resulting in the depletion of thymidine triphosphate (TTP) and thus DNA synthesis. With the phosphoramidate moiety attached to FUDR-MP, fosifloxuridine nafalbenamide, compared to 5-FU, is more lipophilic and accumulates in cancer cells by passive diffusion and does not require a nucleoside transporter, thereby generating higher intracellular concentrations. In addition, compared to 5-FU, once inside the cell FUDR-MP does not need to be phosphorylated and is already in its active form. Unlike 5-FU, fosifloxuridine nafalbenamide does not get deactivated or converted into toxic metabolites by dihydropyrimidine dehydrogenase (DPD) and thymidine phosphorylase (TP), which leads to both a longer half-life and less toxicity.","An antimetabolite (pyrimidine analogue) antineoplastic derivative of 5-fluorouracil. 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medulloblastoma, melanoma, metastatic melanoma, multiple myeloma, myelodysplastic syndrome, myeloproliferative disorder, neoplasm of mature b-cells, neuroblastoma, non-hodgkins lymphoma, non-small cell lung carcinoma, ovarian cancer, papillary thyroid carcinoma, pediatric lymphoma, peritoneum cancer, prostate carcinoma, refractory anemia with excess blasts, renal cell carcinoma","cancer, chronic myeloproliferative disorder, leukemia, lymphoblastic lymphoma, lymphoid leukemia, lymphoma, multiple myeloma, mycosis fungoides, myelodysplastic syndrome, sezary's disease, t-cell acute lymphoblastic leukemia, t-lymphoblastic lymphoma","biliary tract cancer, breast carcinoma, breast neoplasm, cancer, cervical cancer, chordoma, colorectal adenocarcinoma, colorectal carcinoma, cutaneous melanoma, diffuse large b-cell lymphoma, endometrial cancer, esophageal cancer, esophageal carcinoma, fallopian tube cancer, fallopian tube carcinoma, gastric cancer, gastric carcinoma, gestational trophoblastic 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lymphoma, langerhans cell histiocytosis, leukemia, lymphoblastic lymphoma, lymphoma, multiple myeloma, myelodysplastic syndrome, neoplasm of mature b-cells, non-hodgkins lymphoma, t-cell non-hodgkin lymphoma","acute myeloid leukemia, acute promyelocytic leukemia, cancer, cervical cancer, chronic lymphocytic leukemia, colorectal carcinoma, endometrial carcinoma, essential thrombocythemia, gliosarcoma, hepatocellular carcinoma, kidney cancer, leukemia, liver cancer, lung cancer, lymphoma, metastatic melanoma, multiple myeloma, myelodysplastic syndrome, neuroblastoma, non-small cell lung carcinoma, pancreatic carcinoma, polycythemia vera, prostate cancer, skin basal cell carcinoma, small cell lung carcinoma, ureter cancer, urethra cancer, urinary bladder carcinoma","anus cancer, biliary tract cancer, biliary tract neoplasm, breast carcinoma, breast neoplasm, cancer, cervical cancer, cholangiocarcinoma, colon adenocarcinoma, colonic neoplasm, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, cutaneous melanoma, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, fallopian tube cancer, fallopian tube carcinoma, gallbladder cancer, gallbladder carcinoma, gastric adenocarcinoma, gastric cancer, gastric carcinoma, glioblastoma multiforme, glioma, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hepatocellular carcinoma, hypopharyngeal carcinoma, inflammatory breast carcinoma, intrahepatic cholangiocarcinoma, kidney cancer, kidney neoplasm, laryngeal squamous cell carcinoma, liver cancer, lung cancer, male breast carcinoma, malignant colon neoplasm, malignant glioma, melanoma, merkel cell skin cancer, mesothelioma, metastatic melanoma, nasopharyngeal neoplasm, non-hodgkins lymphoma, non-small cell lung carcinoma, oropharyngeal carcinoma, ovarian cancer, ovarian carcinoma, pancreatic carcinoma, pancreatic endocrine carcinoma, pancreatic neoplasm, pancreatic neuroendocrine tumor, peritoneum cancer, prostate cancer, rectal carcinoma, rectal neoplasm, renal cell carcinoma, skin cancer, skin carcinoma, squamous cell carcinoma, stomach neoplasm, thyroid cancer, triple-negative breast cancer, urothelial carcinoma","acute myeloid leukemia, adult t-cell leukemia/lymphoma, anaplastic large cell lymphoma, angioimmunoblastic t-cell lymphoma, bile duct cancer, biliary tract cancer, biliary tract neoplasm, bladder tumor, bone sarcoma, breast carcinoma, breast neoplasm, cancer, cervical adenocarcinoma, cervical cancer, cervical carcinoma, cholangiocarcinoma, classic hodgkin lymphoma, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, diffuse intrinsic pontine glioma, diffuse large b-cell lymphoma, endometrial cancer, endometrioid carcinoma, esophageal cancer, ewing sarcoma, extranodal nasal nk/t cell lymphoma, fallopian tube cancer, fallopian tube carcinoma, follicular lymphoma, gallbladder cancer, gallbladder carcinoma, gallbladder neoplasm, gastric cancer, gastrointestinal stromal tumor, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hepatoblastoma, hepatocellular carcinoma, hilar cholangiocarcinoma, hodgkins lymphoma, intrahepatic cholangiocarcinoma, kidney cancer, large cell lung carcinoma, leiomyosarcoma, leukemia, liver cancer, lung adenocarcinoma, lung cancer, lymphoma, male breast carcinoma, malignant colon neoplasm, malignant epithelial tumor of ovary, malignant pleural mesothelioma, mantle cell lymphoma, mature t-cell and nk-cell non-hodgkin lymphoma, medulloblastoma, melanoma, mesothelioma, multiple myeloma, mycosis fungoides, nasopharyngeal neoplasm, neoplasm of mature b-cells, non-hodgkins lymphoma, non-small cell lung carcinoma, osteosarcoma, ovarian cancer, ovarian carcinoma, ovarian neoplasm, ovarian serous cystadenocarcinoma, pancreatic carcinoma, pancreatic neoplasm, peritoneal neoplasm, peritoneum cancer, plasma cell leukemia, plasmacytoma, prostate cancer, renal cell carcinoma, sarcoma, small cell lung carcinoma, soft tissue sarcoma, squamous cell carcinoma, squamous cell lung carcinoma, synovial sarcoma, t-cell non-hodgkin lymphoma, thyroid cancer, triple-negative breast cancer, ureter cancer, urethra cancer, urinary bladder cancer, urinary bladder carcinoma, urothelial carcinoma, uterine carcinosarcoma, uterine neoplasm","acute leukemia of ambiguous lineage, acute monocytic leukemia, acute myeloid leukemia, blast phase chronic myelogenous leukemia, bcr-abl1 positive, cancer, chronic lymphocytic leukemia, chronic myeloproliferative disorder, diffuse large b-cell lymphoma, hairy cell leukemia, histiocytosis, langerhans cell histiocytosis, leukemia, lymphoma, malt lymphoma, mantle cell lymphoma, multiple myeloma, myelodysplastic syndrome, myeloid leukemia, systemic mastocytosis","cancer, cholangiocarcinoma, colorectal adenocarcinoma, colorectal carcinoma, esophageal cancer, fallopian tube cancer, gastric adenocarcinoma, gastric cancer, gastrointestinal stromal tumor, hepatocellular carcinoma, intrahepatic cholangiocarcinoma, liver cancer, malignant colon neoplasm, ovarian cancer, peritoneum cancer","acute basophilic leukemia, acute erythroleukemia, acute leukemia of ambiguous lineage, acute megakaryoblastic leukaemia, acute monocytic leukemia, acute myeloblastic leukemia with maturation, acute myeloblastic leukemia without maturation, acute myeloid leukemia, acute myelomonocytic leukemia, acute promyelocytic leukemia, adult t-cell leukemia/lymphoma, anaplastic large cell lymphoma, b-cell acute lymphoblastic leukemia, blast phase chronic myelogenous leukemia, bcr-abl1 positive, brain neoplasm, burkitts lymphoma, cancer, childhood acute lymphoblastic leukemia, chronic lymphocytic leukemia, chronic myelomonocytic leukemia, chronic myeloproliferative disorder, classic hodgkin lymphoma, diffuse large b-cell lymphoma, essential thrombocythemia, follicular lymphoma, glioblastoma multiforme, granulocytic sarcoma, hematopoietic and lymphoid cell neoplasm, hodgkins lymphoma, juvenile 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<th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" 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 </div>
 <div class="section level3">
 <h3 id="get-taxanes">Get taxanes<a class="anchor" aria-label="anchor" href="#get-taxanes"></a>
@@ -451,24 +446,24 @@ <h3 id="get-taxanes">Get taxanes<a class="anchor" aria-label="anchor" href="#get
 <span>  cache_dir <span class="op">=</span> <span class="va">cache_dir</span>, </span>
 <span>  treatment_category <span class="op">=</span> <span class="st">"chemo_therapy_classified"</span>,</span>
 <span>  output_resolution <span class="op">=</span> <span class="st">"drug"</span><span class="op">)</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Object 'drug_map_name' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:21] Retrieved n = 31451 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Object 'drug_map_alias' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Retrieved n = 677295 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Object 'drug_map_basic' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Retrieved n = 31486 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Object 'drug_map_target' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Retrieved n = 39369 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
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 <span><span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">&lt;-</span> <span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">|&gt;</span></span>
 <span>  <span class="fu">dplyr</span><span class="fu">::</span><span class="fu"><a href="https://dplyr.tidyverse.org/reference/filter.html" class="external-link">filter</a></span><span class="op">(</span></span>
@@ -495,8 +490,8 @@ <h3 id="get-taxanes">Get taxanes<a class="anchor" aria-label="anchor" href="#get
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
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cancer, gastric adenocarcinoma, gastric cancer, gastric carcinoma, gastrointestinal stromal tumor, gestational trophoblastic neoplasm, glioblastoma multiforme, gliosarcoma, head and neck malignant neoplasia, head and neck squamous cell carcinoma, hepatocellular carcinoma, hodgkins lymphoma, hypopharyngeal carcinoma, inflammatory breast carcinoma, intrahepatic cholangiocarcinoma, kidney cancer, large cell lung carcinoma, laryngeal squamous cell carcinoma, leukemia, liver cancer, lung adenocarcinoma, lung cancer, lymphoma, male breast carcinoma, malignant bone neoplasm, malignant epithelial tumor of ovary, malignant glioma, melanoma, merkel cell skin cancer, mesothelioma, metastatic melanoma, mouth neoplasm, multiple myeloma, nasopharyngeal neoplasm, neoplasm of esophagus, non-hodgkins lymphoma, non-small cell lung carcinoma, oral squamous cell carcinoma, oropharyngeal carcinoma, oropharynx cancer, ovarian cancer, ovarian carcinoma, ovarian neoplasm, ovarian serous cystadenocarcinoma, ovarian sex cord-stromal tumor, pancreatic carcinoma, pancreatic neoplasm, penile cancer, peritoneal neoplasm, peritoneum cancer, prostate adenocarcinoma, prostate cancer, renal cell carcinoma, salivary gland cancer, salivary gland neoplasm, sarcoma, sex cord-stromal tumor, small cell lung carcinoma, soft tissue sarcoma, squamous cell carcinoma, squamous cell lung carcinoma, stomach neoplasm, testicular neoplasm, thymic carcinoma, thymoma, thyroid cancer, thyroid carcinoma, triple-negative breast cancer, urethra cancer, urinary bladder cancer, urinary bladder carcinoma, urothelial carcinoma, uterine carcinosarcoma, uterine neoplasm, vaginal cancer, vulva cancer","bladder tumor, breast neoplasm, pancreatic neoplasm","breast neoplasm, cancer, gastric carcinoma, melanoma, prostate cancer","brain neoplasm, cancer, colorectal cancer, endometrioid carcinoma, fallopian tube cancer, lung cancer, non-small cell lung carcinoma, ovarian cancer, peritoneum cancer, prostate adenocarcinoma, prostate cancer, squamous cell carcinoma","hepatocellular carcinoma, metastatic melanoma, non-small cell lung carcinoma","glioblastoma multiforme, kidney cancer, lung cancer, lymphoma, renal cell carcinoma","cancer"],["4|2","4|3|2|1","4|3|2|1","3","3|2|1","3|2|1","3|2","2","1"],["L01","L01","L01","L01","L01","L01","L01","L01","L01"],["ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS"],["L01C","L01C","L01C","L01C","L01C","L01C","L01C","L01C","L01C"],["PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS","PLANT ALKALOIDS AND OTHER NATURAL PRODUCTS"],["L01CD","L01CD","L01CD","L01CD","L01CD","L01CD","L01CD","L01CD","L01CD"],["Taxanes","Taxanes","Taxanes","Taxanes","Taxanes","Taxanes","Taxanes","Taxanes","Taxanes"],["cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      <th>molecule_chembl_id<\/th>\n      <th>drug_action_type<\/th>\n      <th>nci_concept_definition<\/th>\n      <th>opentargets<\/th>\n      <th>drug_cancer_relevance<\/th>\n      <th>inhibition_moa<\/th>\n      <th>is_salt<\/th>\n      <th>is_adc<\/th>\n      <th>drug_blackbox_warning<\/th>\n      <th>nci_t<\/th>\n      <th>drug_frac_cancer_indications<\/th>\n      <th>drug_approved_noncancer<\/th>\n      <th>drug_n_indications<\/th>\n      <th>drug_year_first_approval<\/th>\n      <th>drug_max_ct_phase<\/th>\n      <th>disease_indication<\/th>\n      <th>disease_indication_max_phase<\/th>\n      <th>atc_code_level1<\/th>\n      <th>atc_level1<\/th>\n      <th>atc_code_level2<\/th>\n      <th>atc_level2<\/th>\n      <th>atc_code_level3<\/th>\n      <th>atc_level3<\/th>\n      <th>atc_treatment_category<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"drug_id","targets":1},{"name":"drug_name","targets":2},{"name":"drug_type","targets":3},{"name":"molecule_chembl_id","targets":4},{"name":"drug_action_type","targets":5},{"name":"nci_concept_definition","targets":6},{"name":"opentargets","targets":7},{"name":"drug_cancer_relevance","targets":8},{"name":"inhibition_moa","targets":9},{"name":"is_salt","targets":10},{"name":"is_adc","targets":11},{"name":"drug_blackbox_warning","targets":12},{"name":"nci_t","targets":13},{"name":"drug_frac_cancer_indications","targets":14},{"name":"drug_approved_noncancer","targets":15},{"name":"drug_n_indications","targets":16},{"name":"drug_year_first_approval","targets":17},{"name":"drug_max_ct_phase","targets":18},{"name":"disease_indication","targets":19},{"name":"disease_indication_max_phase","targets":20},{"name":"atc_code_level1","targets":21},{"name":"atc_level1","targets":22},{"name":"atc_code_level2","targets":23},{"name":"atc_level2","targets":24},{"name":"atc_code_level3","targets":25},{"name":"atc_level3","targets":26},{"name":"atc_treatment_category","targets":27}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
 </div>
 <div class="section level3">
 <h3 id="get-platinum-compounds">Get platinum compounds<a class="anchor" aria-label="anchor" href="#get-platinum-compounds"></a>
@@ -507,24 +502,24 @@ <h3 id="get-platinum-compounds">Get platinum compounds<a class="anchor" aria-lab
 <span>  cache_dir <span class="op">=</span> <span class="va">cache_dir</span>, </span>
 <span>  treatment_category <span class="op">=</span> <span class="st">"chemo_therapy_classified"</span>,</span>
 <span>  output_resolution <span class="op">=</span> <span class="st">"drug"</span><span class="op">)</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:25] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:25] Object 'drug_map_name' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:25] Retrieved n = 31451 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Object 'drug_map_alias' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Retrieved n = 677295 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Object 'drug_map_basic' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Retrieved n = 31486 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Object 'drug_map_target' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Retrieved n = 39369 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Object 'drug_map_indication' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:26] Retrieved n = 62752 records</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:29] Record set satisfying user-defined criteria: n = 16534</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:29] Collapsing record set - providing output on a 'per_drug' resolution</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:29] Final record set: n = 170 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:06] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:06] Object 'drug_map_name' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:06] Retrieved n = 31451 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Object 'drug_map_alias' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Retrieved n = 677295 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Object 'drug_map_basic' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Retrieved n = 31486 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Object 'drug_map_target' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Retrieved n = 39369 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Object 'drug_map_indication' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:07] Retrieved n = 62752 records</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:09] Record set satisfying user-defined criteria: n = 16534</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:09] Collapsing record set - providing output on a 'per_drug' resolution</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:10] Final record set: n = 170 records</span></span>
 <span></span>
 <span><span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">&lt;-</span> <span class="va">drugs</span><span class="op">$</span><span class="va">records</span> <span class="op">|&gt;</span></span>
 <span>  <span class="fu">dplyr</span><span class="fu">::</span><span class="fu"><a href="https://dplyr.tidyverse.org/reference/filter.html" class="external-link">filter</a></span><span class="op">(</span></span>
@@ -551,8 +546,8 @@ <h3 id="get-platinum-compounds">Get platinum compounds<a class="anchor" aria-lab
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
-<div id="htmlwidget-75846efd0ace837d43c4" style="width:100%;height:auto;" class="datatables html-widget"></div>
-<script type="application/json" data-for="htmlwidget-75846efd0ace837d43c4">{"x":{"filter":"none","vertical":false,"extensions":["Buttons","Responsive"],"data":[["1","2","3","4","5","6","7","8","9","10"],[22288,6850,8109,18633,21126,23684,26572,29546,3283,16607],["Oxaliplatin","Carboplatin","Cisplatin","Lobaplatin","Nedaplatin","Picoplatin","Satraplatin","Transplatin","Aroplatin","Imifoplatin"],["Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule","Small molecule"],["CHEMBL414804","CHEMBL1351","CHEMBL11359","CHEMBL4594256","CHEMBL3137685","CHEMBL3544907","CHEMBL3833367","CHEMBL1386","CHEMBL4297263","CHEMBL398891"],["NA","NA","NA","NA","NA","NA","NA","NA","NA","NA"],["An organoplatinum complex in which the platinum atom is complexed with 1,2-diaminocyclohexane (DACH) and with an oxalate ligand as a 'leaving group.' A 'leaving group' is an atom or a group of atoms that is displaced as a stable species taking with it the bonding electrons. After displacement of the labile oxalate ligand leaving group, active oxaliplatin derivatives, such as monoaquo and diaquo DACH platinum, alkylate macromolecules, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. The DACH side chain appears to inhibit alkylating-agent resistance. (NCI04)","A second-generation platinum compound with a broad spectrum of antineoplastic properties.  Carboplatin contains a platinum atom complexed with two ammonia groups and a cyclobutane-dicarboxyl residue.  This agent is activated intracellularly to form reactive platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, thereby inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links.  These carboplatin-induced DNA and protein effects result in apoptosis and cell growth inhibition.  This agent possesses tumoricidal activity similar to that of its parent compound, cisplatin, but is more stable and less toxic. (NCI04)","NA","A third-generation, water-soluble platinum compound with potential antineoplastic activity. Lobaplatin forms highly reactive, charged, platinum complexes that bind to nucleophilic groups such as GC- and AG-rich sites in DNA, inducing intrastrand DNA cross-links. These cross-links will ultimately result in induction of apoptosis and cell growth inhibition. Compared to first and second generation platinum compounds, lobaplatin appears to be more stable, less toxic, have a better therapeutic index and may overcome tumor resistance.","NA","A new generation organic platinum analog with an extended spectrum of antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and transcription, and the induction of apoptosis.","NA","NA","NA","A platinum (Pt)-based agent belonging to the phosphaplatin family comprised of Pt complexed to a pyrophosphate ligand, with potential antineoplastic activity. Although the exact mechanisms through which imifoplatin exerts its effect have yet to be fully elucidated, this agent, upon intravenous administration, binds to certain transmembrane proteins and activates several genes involved in tumor suppression and apoptosis. This leads to the activation of various signal transduction pathways, induces S/G2 phase cell cycle, and causes tumor cell apoptosis. In addition, imifoplatin may inhibit angiogenesis. Unlike conventional Pt-based chemotherapeutics, imifoplatin does not bind to DNA and is able to overcome drug resistance, which occurs with conventional Pt-based chemotherapeutics; it also has a more favorable side effect profile and is more stable in plasma."],[true,true,true,true,true,true,true,true,true,true],["by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp","by_cancer_condition_otp"],[false,false,false,false,false,false,false,false,false,false],[false,false,false,false,false,false,false,false,false,false],[false,false,false,false,false,false,false,false,false,false],["TRUE","TRUE","TRUE","FALSE","FALSE","FALSE","FALSE","FALSE","FALSE","FALSE"],["C1181","C1282","NA","C1434","NA","C48416","NA","NA","NA","C121375"],[0.792,0.791,0.773,0.875,0.875,0.9,0.833,0.857,0.5,0.857],[false,false,false,false,false,false,false,false,false,false],[96,182,181,8,8,10,6,7,2,7],[2002,1989,1978,null,null,null,null,null,null,null],[4,4,4,3,3,3,3,3,2,2],["acute myeloid leukemia, adult t-cell leukemia/lymphoma, anus cancer, bile duct cancer, biliary tract cancer, biliary tract neoplasm, breast carcinoma, breast neoplasm, cancer, cervical cancer, cholangiocarcinoma, colon adenocarcinoma, colonic neoplasm, colorectal adenocarcinoma, colorectal cancer, colorectal carcinoma, cutaneous melanoma, diffuse large b-cell lymphoma, endometrial cancer, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, extranodal nasal nk/t cell lymphoma, fallopian tube cancer, fallopian tube carcinoma, follicular lymphoma, gallbladder cancer, gallbladder carcinoma, gastric adenocarcinoma, gastric cancer, gastric carcinoma, gastrointestinal stromal tumor, gliosarcoma, head and neck carcinoma, head and neck malignant neoplasia, hematopoietic and lymphoid cell neoplasm, hepatoblastoma, hepatocellular carcinoma, hodgkins lymphoma, intrahepatic cholangiocarcinoma, leukemia, liver cancer, lung cancer, lymphoma, malignant colon neoplasm, malignant epithelial tumor of ovary, mesothelioma, metastatic melanoma, mucinous carcinoma, myelodysplastic syndrome, nasopharyngeal neoplasm, neoplasm of mature b-cells, neuroblastoma, non-hodgkins lymphoma, non-small cell lung carcinoma, ovarian cancer, ovarian carcinoma, pancreatic carcinoma, pancreatic endocrine carcinoma, pancreatic neoplasm, peritoneal neoplasm, peritoneum cancer, prostate cancer, rectal carcinoma, renal cell carcinoma, small cell lung carcinoma, squamous cell carcinoma, stomach neoplasm, testicular neoplasm, urinary bladder cancer, urothelial carcinoma, uterine neoplasm","acute myeloid leukemia, adrenal cortex carcinoma, adult t-cell leukemia/lymphoma, anaplastic astrocytoma, anaplastic ependymoma, anaplastic large cell lymphoma, anaplastic oligodendroglioma, anus cancer, appendix carcinoma, astrocytoma, brain neoplasm, brain stem neoplasm, breast carcinoma, breast neoplasm, burkitts lymphoma, cancer, carcinosarcoma, cervical adenocarcinoma, cervical cancer, cervical carcinoma, cholangiocarcinoma, choroid plexus neoplasm, chronic myeloproliferative disorder, classic hodgkin lymphoma, colorectal carcinoma, cutaneous melanoma, diffuse large b-cell lymphoma, digestive system neuroendocrine neoplasm, endometrial cancer, endometrial carcinoma, endometrial neoplasm, endometrioid carcinoma, ependymoma, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, fallopian tube cancer, fallopian tube carcinoma, fallopian tube neoplasm, follicular lymphoma, follicular thyroid carcinoma, gallbladder cancer, gallbladder carcinoma, ganglioneuroblastoma, gastric cancer, gastrointestinal stromal tumor, gestational trophoblastic neoplasm, glioblastoma multiforme, glioma, gliosarcoma, head and neck carcinoma, head and neck malignant neoplasia, head and neck neoplasia, head and neck squamous cell carcinoma, hepatoblastoma, hepatocellular carcinoma, hodgkins lymphoma, hypopharyngeal carcinoma, inflammatory breast carcinoma, intrahepatic cholangiocarcinoma, kidney cancer, kidney wilms tumor, large cell lung carcinoma, laryngeal carcinoma, laryngeal neoplasm, laryngeal squamous cell carcinoma, leiomyosarcoma, leukemia, liver cancer, lung adenocarcinoma, lung cancer, lymphoblastic lymphoma, lymphoma, male breast carcinoma, malignant epithelial tumor of ovary, malignant glioma, malignant pleural mesothelioma, malignant testicular germ cell tumor, malignant tumor of parathyroid gland, mantle cell lymphoma, medulloblastoma, melanoma, merkel cell skin cancer, mesothelioma, metastatic melanoma, mouth neoplasm, multiple myeloma, myelodysplastic syndrome, nasopharyngeal neoplasm, neoplasm of mature b-cells, neoplasm of oropharynx, neuroblastoma, non-hodgkins lymphoma, non-small cell lung carcinoma, oligoastrocytoma, optic nerve glioblastoma, oral squamous cell carcinoma, oropharyngeal carcinoma, oropharynx cancer, osteosarcoma, ovarian cancer, ovarian carcinoma, ovarian neoplasm, ovarian serous cystadenocarcinoma, ovarian sex cord-stromal tumor, pancreatic carcinoma, pancreatic endocrine carcinoma, papillary thyroid carcinoma, peritoneal neoplasm, 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penile cancer, peritoneal neoplasm, peritoneum cancer, pharynx cancer, prostate cancer, renal cell carcinoma, retinoblastoma, rhabdomyosarcoma, salivary gland cancer, salivary gland neoplasm, sarcoma, seminoma, skin cancer, small cell lung carcinoma, soft tissue sarcoma, squamous cell carcinoma, squamous cell lung carcinoma, stomach neoplasm, testicular choriocarcinoma, testicular neoplasm, testicular yolk sac tumor, thymic carcinoma, thymoma, thyroid cancer, tongue neoplasm, triple-negative breast cancer, urethra cancer, urinary bladder cancer, urinary bladder carcinoma, urothelial carcinoma, uterine neoplasm, vulva cancer","cancer, esophageal cancer, esophageal carcinoma, head and neck squamous cell carcinoma, hepatocellular carcinoma, nasopharyngeal neoplasm, small cell lung carcinoma","cervical cancer, esophageal cancer, esophageal carcinoma, esophageal squamous cell carcinoma, nasopharyngeal neoplasm, non-small cell lung carcinoma, squamous cell carcinoma","cancer, colorectal carcinoma, head and neck malignant neoplasia, lung cancer, ovarian cancer, pancreatic carcinoma, prostate cancer, small cell lung carcinoma, urinary bladder cancer","cancer, lung cancer, non-small cell lung carcinoma, prostate cancer","diffuse large b-cell lymphoma, malignant pleural mesothelioma, multiple myeloma, neoplasm of oropharynx, non-small cell lung carcinoma, pancreatic carcinoma","pancreatic neoplasm","biliary tract cancer, cancer, multiple myeloma, non-small cell lung carcinoma, prostate adenocarcinoma, thymoma"],["4|3|2|1","4|3|2|1","4|3|2|1|0.5","3|2|1","3|2","3|2|1","3|2|1","3|2|1","1","2|1"],["L01","L01","L01","L01","L01","L01","L01","L01","L01","L01"],["ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS","ANTINEOPLASTIC AGENTS"],["L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X","L01X"],["OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS","OTHER ANTINEOPLASTIC AGENTS"],["L01XA","L01XA","L01XA","L01XA","L01XA","L01XA","L01XA","L01XA","L01XA","L01XA"],["Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds","Platinum compounds"],["cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy","cancer_chemo_therapy"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>drug_id<\/th>\n      <th>drug_name<\/th>\n      <th>drug_type<\/th>\n      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<\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":[1,14,16,17,18]},{"orderable":false,"targets":0},{"name":" 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 </div>
 </div>
 <div class="section level2">
@@ -571,10 +566,10 @@ <h3 id="reported-associations-between-brca12-alterations-and-drug-sensitivity">R
 <code class="sourceCode R"><span></span>
 <span><span class="va">biomarkers</span> <span class="op">&lt;-</span> <span class="fu"><a href="../reference/get_biomarkers.html">get_biomarkers</a></span><span class="op">(</span></span>
 <span>  cache_dir <span class="op">=</span> <span class="va">cache_dir</span><span class="op">)</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:29] Downloading remote dataset from Google Drive to cache_dir</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:32] Reading from cache_dir = ' (/tmp/RtmpsVdIol'), argument force_download = F</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:32] Object 'biomarkers' sucessfully loaded</span></span>
-<span><span class="co">#&gt; INFO  [2024-03-09 07:58:32] md5 checksum is valid: 791bb5187dda90fb514ddd2a56ebc137</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:10] Downloading remote dataset from Google Drive to cache_dir</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:13] Reading from cache_dir = ' (/tmp/Rtmp1n8MHG'), argument force_download = F</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:13] Object 'biomarkers' sucessfully loaded</span></span>
+<span><span class="co">#&gt; INFO  [2024-03-09 18:02:13] md5 checksum is valid: 277a4cf2f80523ab3bf6d219500cc846</span></span>
 <span></span>
 <span><span class="va">brca1_biomarkers</span> <span class="op">&lt;-</span> <span class="fu"><a href="https://rdrr.io/r/base/list.html" class="external-link">list</a></span><span class="op">(</span><span class="op">)</span></span>
 <span><span class="kw">for</span><span class="op">(</span><span class="va">source</span> <span class="kw">in</span> <span class="fu"><a href="https://rdrr.io/r/base/c.html" class="external-link">c</a></span><span class="op">(</span><span class="st">'civic'</span>,<span class="st">'cgi'</span><span class="op">)</span><span class="op">)</span><span class="op">{</span></span>
@@ -627,8 +622,8 @@ <h3 id="reported-associations-between-brca12-alterations-and-drug-sensitivity">R
 <span>    dom <span class="op">=</span> <span class="st">"Bfrtip"</span><span class="op">)</span></span>
 <span><span class="op">)</span></span></code></pre></div>
 <p><br></p>
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the phase 3 POLO trial patients who had germline BRCA1/2 mutation and metastatic pancreatic adenocarcinoma that had not progressed during first-line platinum-based chemotherapy were allocated to maintenance olaparib or placebo. BRCA1/2 mutation was determine by the BRAC-Analysis CDx test. Median progression free survival was significantly longer in the olaparib group than in the placebo group (7.4 months vs. 3.8 months; hazard ratio for disease progression or death, 0.53; 95% CI, 0.35 to 0.82; p=0.004). BRCA1 mutations were present in 29/92 patients in the olaparib group and 16/62 patients in the placebo group, while one patient receiving olaparib had both BRCA1 and BRCA2 germline mutations. Responses were seen in 18 (20%) patients in the olaparib group, including two complete responses. The safety profile of olaparib was similar to that observed in other patient populations.","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo.  Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo. Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","In the phase 3 POLO trial patients who had germline BRCA1/2 mutation and metastatic pancreatic adenocarcinoma that had not progressed during first-line platinum-based chemotherapy were allocated to maintenance olaparib or placebo. BRCA1/2 mutation was determine by the BRAC-Analysis CDx test. Median progression free survival was significantly longer in the olaparib group than in the placebo group (7.4 months vs. 3.8 months; hazard ratio for disease progression or death, 0.53; 95% CI, 0.35 to 0.82; p=0.004). BRCA2 mutations were present in 62/92 patients in the olaparib group and 46/62 patients in the placebo group, while one patient receiving olaparib had both BRCA1 and BRCA2 germline mutations. Responses were seen in 18 (20%) patients in the olaparib group, including two complete responses. The safety profile of olaparib was similar to that observed in other patient populations.","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo.  Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo. Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. The olaparib arm had 191 patients with BRCA1 mutation, 66 BRCA2, and 3 patients with both BRCA1 and BRCA2, while the placebo arm had 91 BRCA1 and 40 BRCA2 mutant patients. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. Two patients were found to have somatic BRCA1/2 mutations. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","This randomized, open-label, phase 3 trial evaluated the PARP inhibitor olaparib in 387 men with metastatic castration-resistant prostate cancer (mCRPC) who had disease progression while receiving a new hormonal agent (e.g., enzalutamide or abiraterone). The study found that in men with mCRPC who had somatic or germline deleterious alterations (irrespective of zygosity) in any of the following HRR genes (BRCA1, BRCA2, ATM, BRIP1, BARD1, CDK12, CHEK1, CHEK2, FANCL, PALB2, PPP2R2A, RAD51B, RAD51C, RAD51D, and RAD54L), olaparib was associated with longer progression-free survival and better measures of response and patient-reported end points than either enzalutamide or abiraterone (PFS HR 0.49 [0.38, 0.63]). For 15 patients with BRCA1 mutations specifically, PFS HR 0.41 [0.13-1.39]. . Based on the results of this study, on May 19, 2020, the Food and Drug Administration approved olaparib (LYNPARZA) for adult patients with deleterious or suspected deleterious germline or somatic HRR gene-mutated mCRPC, who have progressed following prior treatment with enzalutamide or abiraterone.","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. The olaparib arm had 191 patients with BRCA1 mutation, 66 BRCA2, and 3 patients with both BRCA1 and BRCA2, while the placebo arm had 91 BRCA1 and 40 BRCA2 mutant patients. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","In phase 3 trial of 387 patients comparing olaparib and new hormonal agent (enzalutamide or abiraterone) therapy for patients with metastatic castration-resistant prostate cancer harboring homologous recombinant repair-related gene mutation detected from a tumor sample, olaparib showed significant PFS benefit in an ITT population (HR [95%CI] 0.49 [0.38, 0.63]). But in subgroup analysis, the treatment effect differed in each mutated genes. Among them, patients with BRCA2 mutations (olaparib: n=92, control: n=53) showed a prominent benefit of olaparib (PFS HR [95%CI] 0.21 [0.13, 0.32]).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).",null,null,null,null,null,null,null,null,null,null,"The combination of PARP inhibition (Olaparib) with BRCA mutation results in irreparable and lethal DNA damage. Response rates are higher in BRCA1 mutation positive women with high grade serous or undifferentiated ovarian cancer.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","302 patients (234 with progression events) with HER2-negative metastatic breast cancer and with a confirmed deleterious or suspected deleterious germline BRCA mutation (164 BRCA1, 129 BRCA2) had significantly improved progression-free survival and better response rate to olaparib (PARP inhibitor) than standard therapy (7.0 mo vs 4.2 mo, hazard ratio 0.58, 95% CI 0.43-0.8) in this randomized phase 3 trial (NCT02000622). For BRCA1 patients specifically, the hazard ratio was 0.54, 95% CI 0.37-0.79).","The combination of PARP inhibition (Olaparib) with BRCA mutation results in irreparable and lethal DNA damage. Response rates are higher in BRCA2 mutation positive women with high grade serous or undifferentiated ovarian cancer.","In a phase 2 trial of patients with metastatic, castration-resistant prostate cancer, treated with olaparib tablets at a dose of 400 mg twice a day, all 7 patients harbouring BRCA2 loss of function alleles (biallelic somatic loss or germline mutations in combination with somatic copy loss or copy neutral LOH) demonstrated a clinical response.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","302 patients (234 with progression events) with HER2-negative metastatic breast cancer and with a confirmed deleterious or suspected deleterious germline BRCA mutation (164 BRCA1, 129 BRCA2) had significantly improved progression-free survival and better response rate to olaparib (PARP inhibitor) than standard therapy (7.0 mo vs 4.2 mo, hazard ratio 0.58, 95% CI 0.43-0.8) in this randomized phase 3 trial (NCT02000622). For BRCA2 patients specifically, the hazard ratio was 0.68, 95% CI 0.45-0.1.07.","In this phase 1 trial, 60 patients with advanced solid tumors (ovarian, breast, colorectal, melanoma, sarcoma, prostate) were treated with PARP inhibitor olaparib. Durable antitumor activity was only observed in BRCA1/2 mutation carriers. 19 BRCA carriers had ovarian, breast, or prostate cancers; 12 of these (63%) had a clinical benefit from treatment with olaparib: radiologic or tumor-marker responses or meaningful disease stabilization (stable disease for a period of 4 months or more). Nine BRCA carriers had a response according to RECIST, with the response sustained for more than 76 weeks in one patient. No responses were seen in patients without BRCA mutation.","In a study of ovarian carcinomas, 81% of tumors with germline BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=47; N=158; P=0.01). Sensitivity was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","In a study of ovarian carcinomas, 87% of tumors with somatic BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=38; N=158; P=0.002). Sensitivity to platinum was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","46 women with platinum-sensitive, high-grade, BRCA1/2+ ovarian cancer received either olaparib monotherapy or olaparib/cediranib combination therapy.  Median PFS was increased in combination therapy (17.7 months versus 9.0 months; HR=0.42; 95%CI 0.23-0.76; p=0.005); overall response rate was increased in the combination therapy (79.6% versus 47.8%; p=0.002); and total deaths were reduced in combination therapy (6 patients versus 10 patients).","In an evaluation of 77 patients, those who had BRCA1/2 germline mutations (n=11) had an increase response rate to cisplatin when compared to those without germline mutations (54.5% versus 19.7%; P=0.022) although progression free survival and overall survival was not significantly different.","In a study of 63 patients with ovarian cancer, 17 patients had BRCA1 or BRCA2 mutations and 46 patients had no BRCA mutations.  Of the BRCA-positive patients, 7/17(41%; 95%CI 22-64) showed objective response to olaparib whereas only 11/46 BRCA-negative patients (24%; 95%CI 14-38) showed objective response to olaparib.","In a study of 26 patients with breast cancer, 10 patients were BRCA-positive and 16 patients were BRCA-negative.  Regardless of BRCA status, none showed objective response when treated with olaparib.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA mutant (BRCA1 or BRCA2) patients, 14 had homozygous somatic BRCA1 mutation or deletion. Confirmed objective response was seen in 71% (10/14) of the somatic BRCA1 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Randomized, open-label, phase 3 trial in which olaparib monotherapy was compared with standard therapy in patients with a germline BRCA mutation HER2–negative metastatic breast cancer. 205 patients were assigned to receive olaparib and 97 were assigned to receive standard therapy. Median progression-free survival was significantly longer in the olaparib group than in the standard-therapy group (7.0 months vs. 4.2 months; hazard ratio 0.58; 95%CI 0.43 to 0.80; P<0.001). A response to treatment occurred in 100 of the 167 patients who had measurable disease in the olaparib group (59.9%; 95% CI, 52.0 to 67.4) and in 19 of the 66 patients in the standard-therapy group (28.8%; 95% CI, 18.3 to 41.3). A complete response was seen in 9.0% of the patients who had measurable disease in the olaparib group and in 1.5% in the standard-therapy group.","Twenty-three patients with pancreatic cancer havoring BRCA1/2 germline mutations received olaparib. Five (21.7%) patients had a BRCA1 mutation. All but one had received prior gemcitabine, and 65% had received prior platinum. Tumor response rate was 21.7% and stable disease more than 8 weeks was 35%.","Patients with BRCA1/2 associated pancreatic adenocarcinoma were evaluated retrospectively. In patients with stage 3 and 4, the median overall survival (mOS) was 22 months for the platinum exposed (n=22), compared with 9 months for the non-platinum (n=21) treatment groups (p<0.039)","In Phase I study for pancreatic cancer patients GEM 600 mg/m2 + CDDP 25 mg/m2 + Veliparib 20 - 80 mg twice daily showed response rate of  77.8% (7/9) and mOS of 23.3 months in germline BRCA mutation-positive patients with stage IV disease.","Veliparib 400mg BID was administered to patients with germline BRCA1/2-mutated pancreatic cancer. Sixteen patients were enrolled. All except two (12.5%) had previously been treated with platinum therapy. No confirmed partial response was observed. One patient who had received prior single-agent gemcitabine only had an unconfirmed PR.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 14 had germline BRCA1 mutation, 13 of which were homozygous mutation and one with unknown zygosity. Confirmed objective response was seen in 86% (12/14) of the germline BRCA1 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","In this phase 1 trial 60 patients with advanced solid tumors (ovarian, breast, colorectal, melanoma, sarcoma, prostate) were treated with PARP inhibitor olaparib. Durable antitumor activity was only observed in BRCA1/2 mutation carriers.19 BRCA carriers had ovarian, breast, or prostate cancers; 12 of these (63%) had a clinical benefit from treatment with olaparib: radiologic or tumor-marker responses or meaningful disease stabilization (stable disease for a period of 4 months or more). Nine BRCA carriers had a response according to RECIST, with the response sustained for more than 76 weeks in one patient. No responses were seen in patients without BRCA mutation.","In a study of ovarian carcinomas, 81% of tumors with germline BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=47; N=158; P=0.01). Sensitivity was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","In a study of ovarian carcinomas, 87% of tumors with somatic BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=38; N=158; P=0.002). Sensitivity to platinum was defined by maintenance of complete response greater than 6 months post platinum therapy.","46 women with platinum-sensitive, high-grade, BRCA1/2+ ovarian cancer received either olaparib monotherapy or olaparib/cediranib combination therapy.  Median PFS was increased in combination therapy (17.7 months versus 9.0 months; HR=0.42; 95%CI 0.23-0.76; p=0.005); overall response rate was increased in the combination therapy (79.6% versus 47.8%; p=0.002); and total deaths were reduced in combination therapy (6 patients versus 10 patients).","In an evaluation of 77 patients, those who had BRCA1/2 germline mutations (n=11) had an increase response rate to cisplatin when compared to those without germline mutations (54.5% versus 19.7%; P=0.022) although progression free survival and overall survival was not significantly different.","In a study of 63 patients with ovarian cancer, 17 patients had BRCA1 or BRCA2 mutations and 46 patients had no BRCA mutations.  Of the BRCA-positive patients, 7/17(41%; 95%CI 22-64) showed objective response to olaparib whereas only 11/46 BRCA-negative patients (24%; 95%CI 14-38) showed objective response to olaparib.","In a study of 26 patients with breast cancer, 10 patients were BRCA-positive and 16 patients were BRCA-negative.  Regardless of BRCA status, none showed objective response when treated with olaparib.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 5 had somatic BRCA2 mutation, 4 of which were homozygous mutations and one had unknown zygosity. Confirmed objective response was seen in 80% (4/5) of the somatic BRCA2 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Randomized, open-label, phase 3 trial in which olaparib monotherapy was compared with standard therapy in patients with a germline BRCA mutation HER2–negative metastatic breast cancer. 205 patients were assigned to receive olaparib and 97 were assigned to receive standard therapy. Median progression-free survival was significantly longer in the olaparib group than in the standard-therapy group (7.0 months vs. 4.2 months; hazard ratio 0.58; 95%CI 0.43 to 0.80; P<0.001). A response to treatment occurred in 100 of the 167 patients who had measurable disease in the olaparib group (59.9%; 95% CI, 52.0 to 67.4) and in 19 of the 66 patients in the standard-therapy group (28.8%; 95% CI, 18.3 to 41.3). A complete response was seen in 9.0% of the patients who had measurable disease in the olaparib group and in 1.5% in the standard-therapy group.","Twenty-three patients with pancreatic cancer havoring BRCA1/2 germline mutations received olaparib. Eighteen (78%) patients had a BRCA2 mutation.  In total of patients with BRCA1/2 mutation , all but one had received prior gemcitabine, and 65% had received prior platinum. Tumor response rate was 21.7% and stable disease more than 8 weeks was 35%.","Patients with BRCA1/2 associated pancreatic adenocarcinoma were evaluated retrospectively. In patients with stage 3 and 4, the median overall survival (mOS) was 22 months for the platinum exposed (n=22), compared with 9 months for the non-platinum (n=21) treatment groups (p<0.039)","In Phase I study for pancreatic cancer patients GEM 600 mg/m2 + CDDP 25 mg/m2 + Veliparib 20 - 80 mg twice daily showed response rate of  77.8% (7/9) and mOS of 23.3 months in germline BRCA mutation-positive patients with stage IV disease.","Veliparib 400mg bid was administered to patients with germline BRCA1/2 mutated pancreatic cancer. Sixteen pts was enrolled. All except two pts (12.5%) had previously been treated with platinum therapy. No confirmed PR was observed. One patient who had received prior single-agent gemcitabine only had an unconfirmed PR.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 6 had germline homozygous BRCA2 mutation. Confirmed objective response was seen in 83% (5/6) of the germline BRCA2 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Absent/low expression of BRCA1 (IHC) was associated with improved response to chemotherapy in 292 patients with sporadic ovarian cancer compared to patients with high expression (odds ratio 2.47: 95%CI 1.10-5.55, p=0.029).","1/1 patients with BRCA1 homozygous deletion had a response to olaparib in this phase 2 study.","Patient with germline BRCA2 mutation underwent resection of pancreatic cancer. Around three years later, tumor recurrence was detected by MRI and PET-CT confirmed it. She was treated with gemcitabine plus iniparib in clinical trial. Excellent response to therapy was observed and surgery was performed but no residual tumor tissue was detected","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a case report, a 3‐year‐old girl with glioblastoma harboring a probable germline heterozygous BRCA2 Lys3326Ter (K3326*) nonsense variant. After debulking surgery, the patient received standard‐of‐care treatment with radiation and temozolomide. Nine months later the PARP inhibitor olaparib was administered in combination with temozolomide for 16 cycles. This regimen was well tolerated by the patient and serial imaging showed a reduction in tumor size.",null,null,null,null,"The authors show that in the CX-5461 and CX-3543, G-quadruplex stabilizing agents, demonstrate specific toxicity against BRCA deficient breast cancer derived cells and polyclonal patient-derived xenograft models. Xenografts harbored both a germline BRCA and a somatic BRCA mutation leading to disruption of both. The BRCA and NHEJ pathways are required for the repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.","In pancreatic cell lines PL11 (FANCC-deficient) and CAPAN1 (BRCA2-mutated), sensitivity to DNA cross-linking agents was observed compared to FANCC/BRCA2 wildtype cell lines (Su86.86, CFPAC, AsPc1, and MiaPaCa2). Mitomycin C specifically led to regression in 8/11 xenografts of the CAPAN1 cell line compared to 2/9 in the CFPAC (BRCA2 wildtype) cell line.","The authors show that in the CX-5461 and CX-3543, G-quadruplex stabilizing agents, demonstrate specific toxicity against BRCA deficient breast cancer derived cells and polyclonal patient-derived xenograft models. The BRCA and NHE J pathways are required for the repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.","Expression of BRCA1 in 6 mesothelioma cell lines was associated with sensitivity to vinorelbine in functional studies.","In an in vitro study, a SNU-251 cell line expressing BRCA1 W1815X truncating mutation demonstrated increased sensitivity to olaparib treatment with long-term exposure, compared to ovarian cell lines expressing BRCA1 wild-type. Sensitivity was determined by assessing cytotoxicity and doubling time. The authors note that the slow doubling time of SNU-251 cells was compensated for with a 2 week cytotoxicity assay as compared to the 1 week assay used for all other cell lines.",null,null],["Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Resistance","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>variant_name<\/th>\n      <th>primary_site<\/th>\n      <th>therapeutic_context<\/th>\n      <th>molecular_profile_name<\/th>\n      <th>evidence_level<\/th>\n      <th>variant_id<\/th>\n      <th>evidence_type<\/th>\n      <th>biomarker_source<\/th>\n      <th>biomarker_source_datestamp<\/th>\n      <th>evidence_id<\/th>\n      <th>variant_origin<\/th>\n      <th>literature_id<\/th>\n      <th>evidence_url<\/th>\n      <th>evidence_description<\/th>\n      <th>clinical_significance<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":6},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"variant_name","targets":1},{"name":"primary_site","targets":2},{"name":"therapeutic_context","targets":3},{"name":"molecular_profile_name","targets":4},{"name":"evidence_level","targets":5},{"name":"variant_id","targets":6},{"name":"evidence_type","targets":7},{"name":"biomarker_source","targets":8},{"name":"biomarker_source_datestamp","targets":9},{"name":"evidence_id","targets":10},{"name":"variant_origin","targets":11},{"name":"literature_id","targets":12},{"name":"evidence_url","targets":13},{"name":"evidence_description","targets":14},{"name":"clinical_significance","targets":15}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
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the phase 3 POLO trial patients who had germline BRCA1/2 mutation and metastatic pancreatic adenocarcinoma that had not progressed during first-line platinum-based chemotherapy were allocated to maintenance olaparib or placebo. BRCA1/2 mutation was determine by the BRAC-Analysis CDx test. Median progression free survival was significantly longer in the olaparib group than in the placebo group (7.4 months vs. 3.8 months; hazard ratio for disease progression or death, 0.53; 95% CI, 0.35 to 0.82; p=0.004). BRCA1 mutations were present in 29/92 patients in the olaparib group and 16/62 patients in the placebo group, while one patient receiving olaparib had both BRCA1 and BRCA2 germline mutations. Responses were seen in 18 (20%) patients in the olaparib group, including two complete responses. The safety profile of olaparib was similar to that observed in other patient populations.","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo.  Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo. Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","In the phase 3 POLO trial patients who had germline BRCA1/2 mutation and metastatic pancreatic adenocarcinoma that had not progressed during first-line platinum-based chemotherapy were allocated to maintenance olaparib or placebo. BRCA1/2 mutation was determine by the BRAC-Analysis CDx test. Median progression free survival was significantly longer in the olaparib group than in the placebo group (7.4 months vs. 3.8 months; hazard ratio for disease progression or death, 0.53; 95% CI, 0.35 to 0.82; p=0.004). BRCA2 mutations were present in 62/92 patients in the olaparib group and 46/62 patients in the placebo group, while one patient receiving olaparib had both BRCA1 and BRCA2 germline mutations. Responses were seen in 18 (20%) patients in the olaparib group, including two complete responses. The safety profile of olaparib was similar to that observed in other patient populations.","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo.  Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","Report of OlympiA (NCT02032823), a randomized, double-blind, placebo-controlled study of 1836 patients with HER2-negative breast cancer with germline pathogenic or likely pathogenic mutations in BRCA1 or BRCA2. Patients were early stage but had completed chemotherapy; ER/PR+ patients could also have concurrent hormone therapy. 82% of patients were triple negative. 72% of patients had BRCA1 germline mutations, 27% had BRCA2, and 0.4% both. 921 patients received olaparib and 915 placebo. Invasive disease-free survival (IDFS) showed improvement with olaparib treatment (86% vs 77%, HR 0.58 [0.41 to 0.82], P<0.001). For overall survival, deaths in the olaparib arm were lower (59 vs 86, HR 0.68 [0.44 to 1.05], P=0.02). The IDFS benefit was independent of whether mutation was in BRCA1 (HR=0.52, 0.39-0.70) or BRCA2 (HR 0.52, 0.30-0.86).","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. The olaparib arm had 191 patients with BRCA1 mutation, 66 BRCA2, and 3 patients with both BRCA1 and BRCA2, while the placebo arm had 91 BRCA1 and 40 BRCA2 mutant patients. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. Two patients were found to have somatic BRCA1/2 mutations. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","This randomized, open-label, phase 3 trial evaluated the PARP inhibitor olaparib in 387 men with metastatic castration-resistant prostate cancer (mCRPC) who had disease progression while receiving a new hormonal agent (e.g., enzalutamide or abiraterone). The study found that in men with mCRPC who had somatic or germline deleterious alterations (irrespective of zygosity) in any of the following HRR genes (BRCA1, BRCA2, ATM, BRIP1, BARD1, CDK12, CHEK1, CHEK2, FANCL, PALB2, PPP2R2A, RAD51B, RAD51C, RAD51D, and RAD54L), olaparib was associated with longer progression-free survival and better measures of response and patient-reported end points than either enzalutamide or abiraterone (PFS HR 0.49 [0.38, 0.63]). For 15 patients with BRCA1 mutations specifically, PFS HR 0.41 [0.13-1.39]. . Based on the results of this study, on May 19, 2020, the Food and Drug Administration approved olaparib (LYNPARZA) for adult patients with deleterious or suspected deleterious germline or somatic HRR gene-mutated mCRPC, who have progressed following prior treatment with enzalutamide or abiraterone.","In the phase 3 SOLO1 trial 390 patients with newly diagnosed advanced ovarian cancer with a mutation in BRCA1 or BRCA2 who had complete or partial response after platinum-based chemotherapy were randomized 2:1 to receive olaparib or placebo. The olaparib arm had 191 patients with BRCA1 mutation, 66 BRCA2, and 3 patients with both BRCA1 and BRCA2, while the placebo arm had 91 BRCA1 and 40 BRCA2 mutant patients. Analysis of PFS by blinded independent review found freedom from disease progression or death at 3 years was 69% in the olaparib arm compared with 35% in the placebo arm (hazard ratio for disease progression or death, 0.28; 95% CI, 0.20 to 0.39; P<0.001).","In phase 3 trial of 387 patients comparing olaparib and new hormonal agent (enzalutamide or abiraterone) therapy for patients with metastatic castration-resistant prostate cancer harboring homologous recombinant repair-related gene mutation detected from a tumor sample, olaparib showed significant PFS benefit in an ITT population (HR [95%CI] 0.49 [0.38, 0.63]). But in subgroup analysis, the treatment effect differed in each mutated genes. Among them, patients with BRCA2 mutations (olaparib: n=92, control: n=53) showed a prominent benefit of olaparib (PFS HR [95%CI] 0.21 [0.13, 0.32]).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).","Combined meta-analysis of Study 10 (NCT01482715, phase I/II) and ARIEL2 (NCT01891344, phase II), both multi-centre, open-label, single-arm trials evaluating rucaparib in ovarian cancer with BRCA1 or BRCA2 deleterious germline or somatic mutations. Mutation status was determined by local testing or by central Foundation Medicine sequencing. Of 106 patients, OR was 53.8% (95% CI, 43.8-63.5); 8.5% and 45.3% of patients achieved complete and partial responses, respectively. Median duration of response was 9.2 months (95% CI, 6.6-11.6). Response rates by gene/mutation: BRCA1/2 germline (n=88, OR 53.4); BRCA1/2 somatic (n=18, OR 55.6); BRCA1 (n=67, OR 53.7); BRCA2 (n=39, OR 53.8).",null,null,null,null,null,null,null,null,null,null,"The combination of PARP inhibition (Olaparib) with BRCA mutation results in irreparable and lethal DNA damage. Response rates are higher in BRCA1 mutation positive women with high grade serous or undifferentiated ovarian cancer.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","302 patients (234 with progression events) with HER2-negative metastatic breast cancer and with a confirmed deleterious or suspected deleterious germline BRCA mutation (164 BRCA1, 129 BRCA2) had significantly improved progression-free survival and better response rate to olaparib (PARP inhibitor) than standard therapy (7.0 mo vs 4.2 mo, hazard ratio 0.58, 95% CI 0.43-0.8) in this randomized phase 3 trial (NCT02000622). For BRCA1 patients specifically, the hazard ratio was 0.54, 95% CI 0.37-0.79).","The combination of PARP inhibition (Olaparib) with BRCA mutation results in irreparable and lethal DNA damage. Response rates are higher in BRCA2 mutation positive women with high grade serous or undifferentiated ovarian cancer.","In a phase 2 trial of patients with metastatic, castration-resistant prostate cancer, treated with olaparib tablets at a dose of 400 mg twice a day, all 7 patients harbouring BRCA2 loss of function alleles (biallelic somatic loss or germline mutations in combination with somatic copy loss or copy neutral LOH) demonstrated a clinical response.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","In part 2 of a two-part dose-escalation phase I trial (NCT01286987), 71 patients with Ewings sarcoma, breast, ovarian, small cell lung, or pancreatic cancers received 1.0 mg/day talazoparib treatment. Of patients with BRCA mutation-associated breast and ovarian cancers, confirmed responses were observed in 7 of 14 (50%) and 5 of 12 (42%) patients, respectively.","302 patients (234 with progression events) with HER2-negative metastatic breast cancer and with a confirmed deleterious or suspected deleterious germline BRCA mutation (164 BRCA1, 129 BRCA2) had significantly improved progression-free survival and better response rate to olaparib (PARP inhibitor) than standard therapy (7.0 mo vs 4.2 mo, hazard ratio 0.58, 95% CI 0.43-0.8) in this randomized phase 3 trial (NCT02000622). For BRCA2 patients specifically, the hazard ratio was 0.68, 95% CI 0.45-0.1.07.","In this phase 1 trial, 60 patients with advanced solid tumors (ovarian, breast, colorectal, melanoma, sarcoma, prostate) were treated with PARP inhibitor olaparib. Durable antitumor activity was only observed in BRCA1/2 mutation carriers. 19 BRCA carriers had ovarian, breast, or prostate cancers; 12 of these (63%) had a clinical benefit from treatment with olaparib: radiologic or tumor-marker responses or meaningful disease stabilization (stable disease for a period of 4 months or more). Nine BRCA carriers had a response according to RECIST, with the response sustained for more than 76 weeks in one patient. No responses were seen in patients without BRCA mutation.","In a study of ovarian carcinomas, 81% of tumors with germline BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=47; N=158; P=0.01). Sensitivity was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","In a study of ovarian carcinomas, 87% of tumors with somatic BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=38; N=158; P=0.002). Sensitivity to platinum was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","46 women with platinum-sensitive, high-grade, BRCA1/2+ ovarian cancer received either olaparib monotherapy or olaparib/cediranib combination therapy.  Median PFS was increased in combination therapy (17.7 months versus 9.0 months; HR=0.42; 95%CI 0.23-0.76; p=0.005); overall response rate was increased in the combination therapy (79.6% versus 47.8%; p=0.002); and total deaths were reduced in combination therapy (6 patients versus 10 patients).","In an evaluation of 77 patients, those who had BRCA1/2 germline mutations (n=11) had an increase response rate to cisplatin when compared to those without germline mutations (54.5% versus 19.7%; P=0.022) although progression free survival and overall survival was not significantly different.","In a study of 63 patients with ovarian cancer, 17 patients had BRCA1 or BRCA2 mutations and 46 patients had no BRCA mutations.  Of the BRCA-positive patients, 7/17(41%; 95%CI 22-64) showed objective response to olaparib whereas only 11/46 BRCA-negative patients (24%; 95%CI 14-38) showed objective response to olaparib.","In a study of 26 patients with breast cancer, 10 patients were BRCA-positive and 16 patients were BRCA-negative.  Regardless of BRCA status, none showed objective response when treated with olaparib.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA mutant (BRCA1 or BRCA2) patients, 14 had homozygous somatic BRCA1 mutation or deletion. Confirmed objective response was seen in 71% (10/14) of the somatic BRCA1 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Randomized, open-label, phase 3 trial in which olaparib monotherapy was compared with standard therapy in patients with a germline BRCA mutation HER2–negative metastatic breast cancer. 205 patients were assigned to receive olaparib and 97 were assigned to receive standard therapy. Median progression-free survival was significantly longer in the olaparib group than in the standard-therapy group (7.0 months vs. 4.2 months; hazard ratio 0.58; 95%CI 0.43 to 0.80; P<0.001). A response to treatment occurred in 100 of the 167 patients who had measurable disease in the olaparib group (59.9%; 95% CI, 52.0 to 67.4) and in 19 of the 66 patients in the standard-therapy group (28.8%; 95% CI, 18.3 to 41.3). A complete response was seen in 9.0% of the patients who had measurable disease in the olaparib group and in 1.5% in the standard-therapy group.","Twenty-three patients with pancreatic cancer havoring BRCA1/2 germline mutations received olaparib. Five (21.7%) patients had a BRCA1 mutation. All but one had received prior gemcitabine, and 65% had received prior platinum. Tumor response rate was 21.7% and stable disease more than 8 weeks was 35%.","Patients with BRCA1/2 associated pancreatic adenocarcinoma were evaluated retrospectively. In patients with stage 3 and 4, the median overall survival (mOS) was 22 months for the platinum exposed (n=22), compared with 9 months for the non-platinum (n=21) treatment groups (p<0.039)","In Phase I study for pancreatic cancer patients GEM 600 mg/m2 + CDDP 25 mg/m2 + Veliparib 20 - 80 mg twice daily showed response rate of  77.8% (7/9) and mOS of 23.3 months in germline BRCA mutation-positive patients with stage IV disease.","Veliparib 400mg BID was administered to patients with germline BRCA1/2-mutated pancreatic cancer. Sixteen patients were enrolled. All except two (12.5%) had previously been treated with platinum therapy. No confirmed partial response was observed. One patient who had received prior single-agent gemcitabine only had an unconfirmed PR.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 14 had germline BRCA1 mutation, 13 of which were homozygous mutation and one with unknown zygosity. Confirmed objective response was seen in 86% (12/14) of the germline BRCA1 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","In this phase 1 trial 60 patients with advanced solid tumors (ovarian, breast, colorectal, melanoma, sarcoma, prostate) were treated with PARP inhibitor olaparib. Durable antitumor activity was only observed in BRCA1/2 mutation carriers.19 BRCA carriers had ovarian, breast, or prostate cancers; 12 of these (63%) had a clinical benefit from treatment with olaparib: radiologic or tumor-marker responses or meaningful disease stabilization (stable disease for a period of 4 months or more). Nine BRCA carriers had a response according to RECIST, with the response sustained for more than 76 weeks in one patient. No responses were seen in patients without BRCA mutation.","In a study of ovarian carcinomas, 81% of tumors with germline BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=47; N=158; P=0.01). Sensitivity was defined by maintenance of complete response greater than 6 months post platinum-based therapy.","In a study of ovarian carcinomas, 87% of tumors with somatic BRCA1/2 mutations were platinum sensitive, whereas only 60% of tumors with non-BRCA1/2 mutations were platinum sensitive (N=38; N=158; P=0.002). Sensitivity to platinum was defined by maintenance of complete response greater than 6 months post platinum therapy.","46 women with platinum-sensitive, high-grade, BRCA1/2+ ovarian cancer received either olaparib monotherapy or olaparib/cediranib combination therapy.  Median PFS was increased in combination therapy (17.7 months versus 9.0 months; HR=0.42; 95%CI 0.23-0.76; p=0.005); overall response rate was increased in the combination therapy (79.6% versus 47.8%; p=0.002); and total deaths were reduced in combination therapy (6 patients versus 10 patients).","In an evaluation of 77 patients, those who had BRCA1/2 germline mutations (n=11) had an increase response rate to cisplatin when compared to those without germline mutations (54.5% versus 19.7%; P=0.022) although progression free survival and overall survival was not significantly different.","In a study of 63 patients with ovarian cancer, 17 patients had BRCA1 or BRCA2 mutations and 46 patients had no BRCA mutations.  Of the BRCA-positive patients, 7/17(41%; 95%CI 22-64) showed objective response to olaparib whereas only 11/46 BRCA-negative patients (24%; 95%CI 14-38) showed objective response to olaparib.","In a study of 26 patients with breast cancer, 10 patients were BRCA-positive and 16 patients were BRCA-negative.  Regardless of BRCA status, none showed objective response when treated with olaparib.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 5 had somatic BRCA2 mutation, 4 of which were homozygous mutations and one had unknown zygosity. Confirmed objective response was seen in 80% (4/5) of the somatic BRCA2 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Randomized, open-label, phase 3 trial in which olaparib monotherapy was compared with standard therapy in patients with a germline BRCA mutation HER2–negative metastatic breast cancer. 205 patients were assigned to receive olaparib and 97 were assigned to receive standard therapy. Median progression-free survival was significantly longer in the olaparib group than in the standard-therapy group (7.0 months vs. 4.2 months; hazard ratio 0.58; 95%CI 0.43 to 0.80; P<0.001). A response to treatment occurred in 100 of the 167 patients who had measurable disease in the olaparib group (59.9%; 95% CI, 52.0 to 67.4) and in 19 of the 66 patients in the standard-therapy group (28.8%; 95% CI, 18.3 to 41.3). A complete response was seen in 9.0% of the patients who had measurable disease in the olaparib group and in 1.5% in the standard-therapy group.","Twenty-three patients with pancreatic cancer havoring BRCA1/2 germline mutations received olaparib. Eighteen (78%) patients had a BRCA2 mutation.  In total of patients with BRCA1/2 mutation , all but one had received prior gemcitabine, and 65% had received prior platinum. Tumor response rate was 21.7% and stable disease more than 8 weeks was 35%.","Patients with BRCA1/2 associated pancreatic adenocarcinoma were evaluated retrospectively. In patients with stage 3 and 4, the median overall survival (mOS) was 22 months for the platinum exposed (n=22), compared with 9 months for the non-platinum (n=21) treatment groups (p<0.039)","In Phase I study for pancreatic cancer patients GEM 600 mg/m2 + CDDP 25 mg/m2 + Veliparib 20 - 80 mg twice daily showed response rate of  77.8% (7/9) and mOS of 23.3 months in germline BRCA mutation-positive patients with stage IV disease.","Veliparib 400mg bid was administered to patients with germline BRCA1/2 mutated pancreatic cancer. Sixteen pts was enrolled. All except two pts (12.5%) had previously been treated with platinum therapy. No confirmed PR was observed. One patient who had received prior single-agent gemcitabine only had an unconfirmed PR.","A phase 2 trial on patients with relapsed, platinum-sensitive high grade ovarian, fallopian tube or primary peritoneal carcinoma (ARIEL2 Part1, NCT01891344) was held to assess PARP inhibitor rucaparib on 3 genetically defined subsets of patients. Out of 40 BRCA (BRCA1 or BRCA2) mutant patients, 6 had germline homozygous BRCA2 mutation. Confirmed objective response was seen in 83% (5/6) of the germline BRCA2 mutant subgroup. Authors note that response rate was similar regardless of whether the BRCA mutation was somatic or germline, in BRCA 1 or BRCA 2. In a BRCA wild-type subgroup, with low levels of loss of heterozygosity (LOH), confirmed objective response was observed in 10% (7/70) of the patients. Patients with BRCA mutant tumors experienced significantly longer median progression free survival than patients with BRCA wildtype, LOH low tumors (12.8 vs 5.2 mo, HR: 0.27, P<0.0001).","Absent/low expression of BRCA1 (IHC) was associated with improved response to chemotherapy in 292 patients with sporadic ovarian cancer compared to patients with high expression (odds ratio 2.47: 95%CI 1.10-5.55, p=0.029).","1/1 patients with BRCA1 homozygous deletion had a response to olaparib in this phase 2 study.","Patient with germline BRCA2 mutation underwent resection of pancreatic cancer. Around three years later, tumor recurrence was detected by MRI and PET-CT confirmed it. She was treated with gemcitabine plus iniparib in clinical trial. Excellent response to therapy was observed and surgery was performed but no residual tumor tissue was detected","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a phase 2 study of 206 recurrent, platinum-sensitive, high-grade ovarian cancer patients, patients with germline or somatic BRCA1 or BRCA2 mutation (n=40) were associated with improved progression free survival (HR 0.27, 95% CI: 0.16-0.44, p<0.0001)  as compared to BRCA1/2 wild-type, loss of heterozygosity low patients (n=71) treated with rucaparib monotherapy; further, BRCA1/2 mutation patients achieved a longer median duration of response (9.2 months, 95% CI: 6.4-12.9, p=0.013 vs. 5.6 months, 95% CI: 4.6-8.5).","In a case report, a 3‐year‐old girl with glioblastoma harboring a probable germline heterozygous BRCA2 Lys3326Ter (K3326*) nonsense variant. After debulking surgery, the patient received standard‐of‐care treatment with radiation and temozolomide. Nine months later the PARP inhibitor olaparib was administered in combination with temozolomide for 16 cycles. This regimen was well tolerated by the patient and serial imaging showed a reduction in tumor size.",null,null,null,null,"The authors show that in the CX-5461 and CX-3543, G-quadruplex stabilizing agents, demonstrate specific toxicity against BRCA deficient breast cancer derived cells and polyclonal patient-derived xenograft models. Xenografts harbored both a germline BRCA and a somatic BRCA mutation leading to disruption of both. The BRCA and NHEJ pathways are required for the repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.","In pancreatic cell lines PL11 (FANCC-deficient) and CAPAN1 (BRCA2-mutated), sensitivity to DNA cross-linking agents was observed compared to FANCC/BRCA2 wildtype cell lines (Su86.86, CFPAC, AsPc1, and MiaPaCa2). Mitomycin C specifically led to regression in 8/11 xenografts of the CAPAN1 cell line compared to 2/9 in the CFPAC (BRCA2 wildtype) cell line.","The authors show that in the CX-5461 and CX-3543, G-quadruplex stabilizing agents, demonstrate specific toxicity against BRCA deficient breast cancer derived cells and polyclonal patient-derived xenograft models. The BRCA and NHE J pathways are required for the repair of CX-5461 and CX-3543-induced DNA damage and failure to do so leads to lethality.","Expression of BRCA1 in 6 mesothelioma cell lines was associated with sensitivity to vinorelbine in functional studies.","In an in vitro study, a SNU-251 cell line expressing BRCA1 W1815X truncating mutation demonstrated increased sensitivity to olaparib treatment with long-term exposure, compared to ovarian cell lines expressing BRCA1 wild-type. Sensitivity was determined by assessing cytotoxicity and doubling time. The authors note that the slow doubling time of SNU-251 cells was compensated for with a 2 week cytotoxicity assay as compared to the 1 week assay used for all other cell lines.",null,null],["Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Resistance","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity","Sensitivity","Sensitivity","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity/Response","Sensitivity","Sensitivity"]],"container":"<table class=\"display\">\n  <thead>\n    <tr>\n      <th> <\/th>\n      <th>variant_name<\/th>\n      <th>primary_site<\/th>\n      <th>therapeutic_context<\/th>\n      <th>molecular_profile_name<\/th>\n      <th>evidence_level<\/th>\n      <th>variant_id<\/th>\n      <th>evidence_type<\/th>\n      <th>biomarker_source<\/th>\n      <th>biomarker_source_datestamp<\/th>\n      <th>evidence_id<\/th>\n      <th>variant_origin<\/th>\n      <th>literature_id<\/th>\n      <th>evidence_url<\/th>\n      <th>evidence_description<\/th>\n      <th>clinical_significance<\/th>\n    <\/tr>\n  <\/thead>\n<\/table>","options":{"buttons":["csv","excel"],"dom":"Bfrtip","columnDefs":[{"className":"dt-right","targets":6},{"orderable":false,"targets":0},{"name":" ","targets":0},{"name":"variant_name","targets":1},{"name":"primary_site","targets":2},{"name":"therapeutic_context","targets":3},{"name":"molecular_profile_name","targets":4},{"name":"evidence_level","targets":5},{"name":"variant_id","targets":6},{"name":"evidence_type","targets":7},{"name":"biomarker_source","targets":8},{"name":"biomarker_source_datestamp","targets":9},{"name":"evidence_id","targets":10},{"name":"variant_origin","targets":11},{"name":"literature_id","targets":12},{"name":"evidence_url","targets":13},{"name":"evidence_description","targets":14},{"name":"clinical_significance","targets":15}],"order":[],"autoWidth":false,"orderClasses":false,"responsive":true}},"evals":[],"jsHooks":[]}</script><p><br><br></p>
 </div>
 </div>
 <div class="section level2">
@@ -659,7 +654,7 @@ <h2 id="session-info">Session Info<a class="anchor" aria-label="anchor" href="#s
 <span><span class="co">#&gt; [1] stats     graphics  grDevices utils     datasets  methods   base     </span></span>
 <span><span class="co">#&gt; </span></span>
 <span><span class="co">#&gt; other attached packages:</span></span>
-<span><span class="co">#&gt; [1] pharmOncoX_1.5.10</span></span>
+<span><span class="co">#&gt; [1] pharmOncoX_1.6.0</span></span>
 <span><span class="co">#&gt; </span></span>
 <span><span class="co">#&gt; loaded via a namespace (and not attached):</span></span>
 <span><span class="co">#&gt;  [1] sass_0.4.8        utf8_1.2.4        generics_0.1.3    stringi_1.8.3    </span></span>
diff --git a/authors.html b/authors.html
index 762aa53..47962d5 100644
--- a/authors.html
+++ b/authors.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
@@ -64,12 +64,12 @@ <h2>Authors</h2>
       <h2 id="citation">Citation</h2>
       <p><small class="dont-index">Source: <a href="https://github.com/sigven/pharmOncoX/blob/HEAD/inst/CITATION" class="external-link"><code>inst/CITATION</code></a></small></p>
 
-      <p>Nakken S.  (2023)  pharmOncoX: Targeted and non-targeted anti-cancer drugs and drug regimens.  R package version 1.5.10.  (https://github.com/sigven/pharmOncoX)</p>
+      <p>Nakken S.  (2023)  pharmOncoX: Targeted and non-targeted anti-cancer drugs and drug regimens.  R package version 1.6.0.  (https://github.com/sigven/pharmOncoX)</p>
       <pre>@Manual{,
   title = {pharmOncoX: Targeted and non-targeted anti-cancer drugs and drug regimens},
   author = {Sigve Nakken},
   year = {2023},
-  note = {R package version 1.5.10},
+  note = {R package version 1.6.0},
   url = {https://github.com/sigven/pharmOncoX},
 }</pre>
     </div>
diff --git a/index.html b/index.html
index 7f36609..c16fce6 100644
--- a/index.html
+++ b/index.html
@@ -54,7 +54,7 @@
     
     <a class="navbar-brand me-2" href="index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/news/index.html b/news/index.html
index 6487d73..48c7b46 100644
--- a/news/index.html
+++ b/news/index.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
@@ -52,6 +52,10 @@
       <small>Source: <a href="https://github.com/sigven/pharmOncoX/blob/HEAD/NEWS.md" class="external-link"><code>NEWS.md</code></a></small>
     </div>
 
+    <div class="section level2">
+<h2 class="pkg-version" data-toc-text="1.6.0" id="version-160-march-9th-2024">Version 1.6.0 (March 9th 2024)<a class="anchor" aria-label="anchor" href="#version-160-march-9th-2024"></a></h2>
+<ul><li>CIViC/Mitelmandb updates</li>
+</ul></div>
     <div class="section level2">
 <h2 class="pkg-version" data-toc-text="1.5.9" id="version-159-february-29th-2024">Version 1.5.9 (February 29th 2024)<a class="anchor" aria-label="anchor" href="#version-159-february-29th-2024"></a></h2>
 <ul><li>Updated CIViC</li>
diff --git a/pkgdown.yml b/pkgdown.yml
index eef94ba..184896c 100644
--- a/pkgdown.yml
+++ b/pkgdown.yml
@@ -3,7 +3,7 @@ pkgdown: 2.0.7
 pkgdown_sha: ~
 articles:
   pharmOncoX: pharmOncoX.html
-last_built: 2024-03-09T07:57Z
+last_built: 2024-03-09T18:01Z
 urls:
   reference: https://sigven.github.io/pharmOncoX/reference
   article: https://sigven.github.io/pharmOncoX/articles
diff --git a/reference/get_biomarkers.html b/reference/get_biomarkers.html
index 00b853a..175036e 100644
--- a/reference/get_biomarkers.html
+++ b/reference/get_biomarkers.html
@@ -31,7 +31,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/reference/get_drug_records.html b/reference/get_drug_records.html
index cbea565..8966b8c 100644
--- a/reference/get_drug_records.html
+++ b/reference/get_drug_records.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/reference/get_drugs.html b/reference/get_drugs.html
index fad8d15..c2aa6a9 100644
--- a/reference/get_drugs.html
+++ b/reference/get_drugs.html
@@ -27,7 +27,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/reference/get_targeted_drugs.html b/reference/get_targeted_drugs.html
index 50a748f..6728294 100644
--- a/reference/get_targeted_drugs.html
+++ b/reference/get_targeted_drugs.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/reference/index.html b/reference/index.html
index 9bc9efd..ac7493f 100644
--- a/reference/index.html
+++ b/reference/index.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/reference/tidyeval.html b/reference/tidyeval.html
index 6037ee0..8a11703 100644
--- a/reference/tidyeval.html
+++ b/reference/tidyeval.html
@@ -15,7 +15,7 @@
     
     <a class="navbar-brand me-2" href="../index.html">pharmOncoX</a>
 
-    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.5.10</small>
+    <small class="nav-text text-muted me-auto" data-bs-toggle="tooltip" data-bs-placement="bottom" title="">1.6.0</small>
 
     
     <button class="navbar-toggler" type="button" data-bs-toggle="collapse" data-bs-target="#navbar" aria-controls="navbar" aria-expanded="false" aria-label="Toggle navigation">
diff --git a/search.json b/search.json
index 7cbb652..c89cff9 100644
--- a/search.json
+++ b/search.json
@@ -1 +1 @@
-[{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"our-pledge","dir":"","previous_headings":"","what":"Our Pledge","title":"Contributor Covenant Code of Conduct","text":"members, contributors, leaders pledge make participation community harassment-free experience everyone, regardless age, body size, visible invisible disability, ethnicity, sex characteristics, gender identity expression, level experience, education, socio-economic status, nationality, personal appearance, race, religion, sexual identity orientation. pledge act interact ways contribute open, welcoming, diverse, inclusive, healthy community.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"our-standards","dir":"","previous_headings":"","what":"Our Standards","title":"Contributor Covenant Code of Conduct","text":"Examples behavior contributes positive environment community include: Demonstrating empathy kindness toward people respectful differing opinions, viewpoints, experiences Giving gracefully accepting constructive feedback Accepting responsibility apologizing affected mistakes, learning experience Focusing best just us individuals, overall community Examples unacceptable behavior include: use sexualized language imagery, sexual attention advances kind Trolling, insulting derogatory comments, personal political attacks Public private harassment Publishing others’ private information, physical email address, without explicit permission conduct reasonably considered inappropriate professional setting","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement-responsibilities","dir":"","previous_headings":"","what":"Enforcement Responsibilities","title":"Contributor Covenant Code of Conduct","text":"Community leaders responsible clarifying enforcing standards acceptable behavior take appropriate fair corrective action response behavior deem inappropriate, threatening, offensive, harmful. Community leaders right responsibility remove, edit, reject comments, commits, code, wiki edits, issues, contributions aligned Code Conduct, communicate reasons moderation decisions appropriate.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"scope","dir":"","previous_headings":"","what":"Scope","title":"Contributor Covenant Code of Conduct","text":"Code Conduct applies within community spaces, also applies individual officially representing community public spaces. Examples representing community include using official e-mail address, posting via official social media account, acting appointed representative online offline event.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement","dir":"","previous_headings":"","what":"Enforcement","title":"Contributor Covenant Code of Conduct","text":"Instances abusive, harassing, otherwise unacceptable behavior may reported community leaders responsible enforcement [INSERT CONTACT METHOD]. complaints reviewed investigated promptly fairly. community leaders obligated respect privacy security reporter incident.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement-guidelines","dir":"","previous_headings":"","what":"Enforcement Guidelines","title":"Contributor Covenant Code of Conduct","text":"Community leaders follow Community Impact Guidelines determining consequences action deem violation Code Conduct:","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_1-correction","dir":"","previous_headings":"Enforcement Guidelines","what":"1. Correction","title":"Contributor Covenant Code of Conduct","text":"Community Impact: Use inappropriate language behavior deemed unprofessional unwelcome community. Consequence: private, written warning community leaders, providing clarity around nature violation explanation behavior inappropriate. public apology may requested.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_2-warning","dir":"","previous_headings":"Enforcement Guidelines","what":"2. Warning","title":"Contributor Covenant Code of Conduct","text":"Community Impact: violation single incident series actions. Consequence: warning consequences continued behavior. interaction people involved, including unsolicited interaction enforcing Code Conduct, specified period time. includes avoiding interactions community spaces well external channels like social media. Violating terms may lead temporary permanent ban.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_3-temporary-ban","dir":"","previous_headings":"Enforcement Guidelines","what":"3. Temporary Ban","title":"Contributor Covenant Code of Conduct","text":"Community Impact: serious violation community standards, including sustained inappropriate behavior. Consequence: temporary ban sort interaction public communication community specified period time. public private interaction people involved, including unsolicited interaction enforcing Code Conduct, allowed period. Violating terms may lead permanent ban.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_4-permanent-ban","dir":"","previous_headings":"Enforcement Guidelines","what":"4. Permanent Ban","title":"Contributor Covenant Code of Conduct","text":"Community Impact: Demonstrating pattern violation community standards, including sustained inappropriate behavior, harassment individual, aggression toward disparagement classes individuals. Consequence: permanent ban sort public interaction within community.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"attribution","dir":"","previous_headings":"","what":"Attribution","title":"Contributor Covenant Code of Conduct","text":"Code Conduct adapted Contributor Covenant, version 2.0, available https://www.contributor-covenant.org/version/2/0/ code_of_conduct.html. Community Impact Guidelines inspired Mozilla’s code conduct enforcement ladder. answers common questions code conduct, see FAQ https://www.contributor-covenant.org/faq. Translations available https:// www.contributor-covenant.org/translations.","code":""},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"installation","dir":"Articles","previous_headings":"","what":"Installation","title":"Getting started","text":"","code":"if (!(\"remotes\" %in% installed.packages())) {  install.packages(\"remotes\") } #> Installing package into '/home/runner/work/_temp/Library' #> (as 'lib' is unspecified)  remotes::install_github('sigven/pharmOncoX') #> Using github PAT from envvar GITHUB_PAT #> Downloading GitHub repo sigven/pharmOncoX@HEAD #> cpp11 (NA -> 0.4.7) [CRAN] #> Installing 1 packages: cpp11 #> Installing package into '/home/runner/work/_temp/Library' #> (as 'lib' is unspecified) #> ── R CMD build ───────────────────────────────────────────────────────────────── #> * checking for file ‘/tmp/RtmpsVdIol/remotes192d6fcd8dac/sigven-pharmOncoX-f93bff7/DESCRIPTION’ ... OK #> * preparing ‘pharmOncoX’: #> * checking DESCRIPTION meta-information ... OK #> * checking for LF line-endings in source and make files and shell scripts #> * checking for empty or unneeded directories #> Omitted ‘LazyData’ from DESCRIPTION #> * building ‘pharmOncoX_1.5.10.tar.gz’ #> Installing package into '/home/runner/work/_temp/Library' #> (as 'lib' is unspecified)  library(pharmOncoX) cache_dir <- tempdir() #cache_dir <-  #  \"/Users/sigven/project_data/packages/package__pharmOncoX/pharmOncoX/data-raw/gd_local\""},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"targeted-agents","dir":"Articles","previous_headings":"Cancer drug classifications","what":"Targeted agents","title":"Getting started","text":"Plotted key statistics respect drug classification numbers targeted chemotherapy agents found pharmOncoX. Existing drug classifications retrieved ATC, extended manual addition/curation, also establishment multiple novel levels ATC tree, particularly targeted therapies. Note drugs indicated cancer conditions (harvested Open Targets platform) considered numbers plotted .","code":"p_targeted_classifications"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"chemotherapy-agents","dir":"Articles","previous_headings":"Cancer drug classifications","what":"Chemotherapy agents","title":"Getting started","text":"","code":"p_chemo_classifications"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-braf-targeted-drugs-list-records-per-indication","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get BRAF-targeted drugs, list records per indication","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,   treatment_category =  c(\"targeted_therapy_classified\",                           \"targeted_therapy_unclassified\"),     drug_target = c('BRAF')) #> INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:57:54] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 07:57:54] Retrieved n = 31451 records #> INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:57:54] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 07:57:54] Retrieved n = 677295 records #> INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:57:54] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 07:57:54] Retrieved n = 31486 records #> INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:57:54] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 07:57:54] Retrieved n = 39369 records #> INFO  [2024-03-09 07:57:54] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:57:54] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 07:57:54] Retrieved n = 62752 records #> INFO  [2024-03-09 07:57:57] Record set satisfying user-defined criteria: n = 279 #> INFO  [2024-03-09 07:57:57] Collapsing record set - providing output on a 'per_drug_target_indication' resolution #> INFO  [2024-03-09 07:57:57] Final record set: n = 237 records  ## Number of drug records nrow(drugs$records) #> [1] 237  ## Column names of drug records colnames(drugs$records) #>  [1] \"drug_id\"                      \"drug_name\"                    #>  [3] \"drug_type\"                    \"molecule_chembl_id\"           #>  [5] \"drug_action_type\"             \"drug_alias\"                   #>  [7] \"nci_concept_definition\"       \"opentargets\"                  #>  [9] \"drug_cancer_relevance\"        \"inhibition_moa\"               #> [11] \"is_salt\"                      \"is_adc\"                       #> [13] \"drug_blackbox_warning\"        \"nci_t\"                        #> [15] \"target_symbol\"                \"target_entrezgene\"            #> [17] \"target_genename\"              \"target_ensembl_gene_id\"       #> [19] \"target_type\"                  \"drug_max_phase_indication\"    #> [21] \"drug_approved_indication\"     \"drug_frac_cancer_indications\" #> [23] \"drug_approved_noncancer\"      \"drug_n_indications\"           #> [25] \"drug_year_first_approval\"     \"drug_max_ct_phase\"            #> [27] \"disease_efo_id\"               \"disease_efo_label\"            #> [29] \"primary_site\"                 \"drug_clinical_id\"             #> [31] \"drug_clinical_source\"         \"atc_code_level1\"              #> [33] \"atc_level1\"                   \"atc_code_level2\"              #> [35] \"atc_level2\"                   \"atc_code_level3\"              #> [37] \"atc_level3\"                   \"atc_treatment_category\""},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-ras-targeted-drugs-list-per-drug-target","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get RAS-targeted drugs, list per drug target","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_action_inhibition = T,   output_resolution = \"drug2target\")$records |>   dplyr::filter(atc_level3 == \"RAS inhibitors\")  drugs <- drugs |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_ras_inhibitors <- DT::datatable(   drugs,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-mek-inhibitors-list-per-drug-only","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get MEK inhibitors, list per drug only","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_action_inhibition = T,   drug_source_opentargets = T,    output_resolution = \"drug\" )$records |>   dplyr::filter(atc_level3 == \"MEK inhibitors\")  drugs <- drugs |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_mek_inhibitors <- DT::datatable(   drugs,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-immune-checkpoint-inhibitors-list-per-drug-target","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get immune checkpoint inhibitors, list per drug target","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_source_opentargets = F,   drug_classified_cancer = T,    output_resolution = \"drug2target\")  drugs$records <- drugs$records |>   dplyr::filter(     (!is.na(atc_level3) &        (atc_level3 == \"PD-1/PDL-1 inhibitors\" |      atc_level3 == \"Other immune checkpoint inhibitors\")   )) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     ) |>   dplyr::select(     drug_id,     drug_name,     drug_type,     target_symbol,     target_genename,     dplyr::everything()   )  dt_drugtable_ici <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-immune-checkpoint-inhibitors-indicated-for-lung-cancer-conditions-list-per-drug-target-entry","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get immune checkpoint inhibitors indicated for lung cancer conditions, list per drug-target entry","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    output_resolution = \"drug2target\",    treatment_category = c(\"targeted_therapy_classified\"),   drug_source_opentargets = T,   drug_indication_main = \"Lung\")  drugs$records <- drugs$records |>   dplyr::filter(     (!is.na(atc_level3) &        (atc_level3 == \"PD-1/PDL-1 inhibitors\" |      atc_level3 == \"Other immune checkpoint inhibitors\")   )) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     ) |>   dplyr::select(     drug_id,     drug_name,     drug_type,     target_symbol,     target_genename,     dplyr::everything()   )  dt_drugtable_ici_lung <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-antimetabolite-drugs","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get antimetabolite drugs","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = c(\"chemo_therapy_classified\"),   output_resolution = \"drug\") #> INFO  [2024-03-09 07:58:17] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:17] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 07:58:17] Retrieved n = 31451 records #> INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:18] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 07:58:18] Retrieved n = 677295 records #> INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:18] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 07:58:18] Retrieved n = 31486 records #> INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:18] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 07:58:18] Retrieved n = 39369 records #> INFO  [2024-03-09 07:58:18] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:18] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 07:58:18] Retrieved n = 62752 records #> INFO  [2024-03-09 07:58:21] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 07:58:21] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 07:58:21] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     !is.na(atc_level2) &     stringr::str_detect(       atc_level2, \"ANTIMETABOLITES\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_metabolites <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-taxanes","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get taxanes","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = \"chemo_therapy_classified\",   output_resolution = \"drug\") #> INFO  [2024-03-09 07:58:21] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:21] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 07:58:21] Retrieved n = 31451 records #> INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:22] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 07:58:22] Retrieved n = 677295 records #> INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:22] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 07:58:22] Retrieved n = 31486 records #> INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:22] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 07:58:22] Retrieved n = 39369 records #> INFO  [2024-03-09 07:58:22] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:22] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 07:58:22] Retrieved n = 62752 records #> INFO  [2024-03-09 07:58:25] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 07:58:25] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 07:58:25] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     stringr::str_detect(       atc_level3, \"Taxanes\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_taxanes <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-platinum-compounds","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get platinum compounds","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = \"chemo_therapy_classified\",   output_resolution = \"drug\") #> INFO  [2024-03-09 07:58:25] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:25] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 07:58:25] Retrieved n = 31451 records #> INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:26] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 07:58:26] Retrieved n = 677295 records #> INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:26] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 07:58:26] Retrieved n = 31486 records #> INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:26] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 07:58:26] Retrieved n = 39369 records #> INFO  [2024-03-09 07:58:26] Reading from cache_dir = '/tmp/RtmpsVdIol', argument force_download = F #> INFO  [2024-03-09 07:58:26] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 07:58:26] Retrieved n = 62752 records #> INFO  [2024-03-09 07:58:29] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 07:58:29] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 07:58:29] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     stringr::str_detect(       atc_level3, \"Platinum compounds\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_platins <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"reported-associations-between-brca12-alterations-and-drug-sensitivity","dir":"Articles","previous_headings":"Retrieval of biomarkers","what":"Reported associations between BRCA1/2 alterations and drug sensitivity","title":"Getting started","text":"Get evidence CIViC CGI cancer drug sensitivity BRCA1/2 alterations (somatically (tumor) inherited/germline)","code":"biomarkers <- get_biomarkers(   cache_dir = cache_dir) #> INFO  [2024-03-09 07:58:29] Downloading remote dataset from Google Drive to cache_dir #> INFO  [2024-03-09 07:58:32] Reading from cache_dir = ' (/tmp/RtmpsVdIol'), argument force_download = F #> INFO  [2024-03-09 07:58:32] Object 'biomarkers' sucessfully loaded #> INFO  [2024-03-09 07:58:32] md5 checksum is valid: 791bb5187dda90fb514ddd2a56ebc137  brca1_biomarkers <- list() for(source in c('civic','cgi')){   brca1_biomarkers[[source]] <-      biomarkers$data[[source]]$variant |>      dplyr::filter(       !is.na(symbol) & (symbol == \"BRCA1\" | symbol == \"BRCA2\")) |>     dplyr::group_by(variant_id, variant_name_primary, variant_consequence) |>     dplyr::summarise(       variant_alias = paste(variant_alias, collapse=\", \"),        .groups = \"drop\") |>      dplyr::inner_join(       biomarkers$data[[source]]$clinical, by = \"variant_id\") |>     dplyr::select(       variant_id, variant_name_primary, therapeutic_context,       evidence_type, evidence_level,        biomarker_source, biomarker_source_datestamp,       molecular_profile_name, evidence_id, variant_origin,       primary_site, evidence_id, source_id,       evidence_url,        evidence_description,        clinical_significance) |>      dplyr::distinct() |>      dplyr::rename(literature_id = source_id,                   variant_name = variant_name_primary) |>     dplyr::filter(evidence_type == \"Predictive\") |>     dplyr::select(       variant_name,        primary_site,       therapeutic_context,       molecular_profile_name,        evidence_level,       dplyr::everything()     ) }  brca1_biomarkers_all <-    dplyr::bind_rows(brca1_biomarkers[['civic']],                    brca1_biomarkers[['cgi']]) |>     dplyr::arrange(evidence_level)     dt_brca1_biomarkers <- DT::datatable(   brca1_biomarkers_all,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"session-info","dir":"Articles","previous_headings":"","what":"Session Info","title":"Getting started","text":"","code":"# set eval = FALSE if you don't want this info (useful for reproducibility)  # to appear sessionInfo() #> R version 4.3.3 (2024-02-29) #> Platform: x86_64-pc-linux-gnu (64-bit) #> Running under: Ubuntu 22.04.4 LTS #>  #> Matrix products: default #> BLAS:   /usr/lib/x86_64-linux-gnu/openblas-pthread/libblas.so.3  #> LAPACK: /usr/lib/x86_64-linux-gnu/openblas-pthread/libopenblasp-r0.3.20.so;  LAPACK version 3.10.0 #>  #> locale: #>  [1] LC_CTYPE=C.UTF-8       LC_NUMERIC=C           LC_TIME=C.UTF-8        #>  [4] LC_COLLATE=C.UTF-8     LC_MONETARY=C.UTF-8    LC_MESSAGES=C.UTF-8    #>  [7] LC_PAPER=C.UTF-8       LC_NAME=C              LC_ADDRESS=C           #> [10] LC_TELEPHONE=C         LC_MEASUREMENT=C.UTF-8 LC_IDENTIFICATION=C    #>  #> time zone: UTC #> tzcode source: system (glibc) #>  #> attached base packages: #> [1] stats     graphics  grDevices utils     datasets  methods   base      #>  #> other attached packages: #> [1] pharmOncoX_1.5.10 #>  #> loaded via a namespace (and not attached): #>  [1] sass_0.4.8        utf8_1.2.4        generics_0.1.3    stringi_1.8.3     #>  [5] digest_0.6.34     magrittr_2.0.3    evaluate_0.23     grid_4.3.3        #>  [9] fastmap_1.1.1     jsonlite_1.8.8    processx_3.8.3    pkgbuild_1.4.3    #> [13] googledrive_2.1.1 ps_1.7.6          httr_1.4.7        purrr_1.0.2       #> [17] fansi_1.0.6       crosstalk_1.2.1   scales_1.3.0      textshaping_0.3.7 #> [21] jquerylib_0.1.4   cli_3.6.2         rlang_1.1.3       crayon_1.5.2      #> [25] ellipsis_0.3.2    munsell_0.5.0     remotes_2.4.2.1   withr_3.0.0       #> [29] cachem_1.0.8      yaml_2.3.8        tools_4.3.3       gargle_1.5.2      #> [33] memoise_2.0.1     dplyr_1.1.4       colorspace_2.1-0  ggplot2_3.5.0     #> [37] DT_0.32           curl_5.2.1        assertthat_0.2.1  vctrs_0.6.5       #> [41] R6_2.5.1          lifecycle_1.0.4   stringr_1.5.1     htmlwidgets_1.6.4 #> [45] fs_1.6.3          ragg_1.2.7        pkgconfig_2.0.3   desc_1.4.3        #> [49] callr_3.7.5       pkgdown_2.0.7     pillar_1.9.0      bslib_0.6.1       #> [53] gtable_0.3.4      glue_1.7.0        lgr_0.4.4         systemfonts_1.0.6 #> [57] highr_0.10        xfun_0.42         tibble_3.2.1      tidyselect_1.2.0  #> [61] knitr_1.45        farver_2.1.1      htmltools_0.5.7   rmarkdown_2.26    #> [65] compiler_4.3.3"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/authors.html","id":null,"dir":"","previous_headings":"","what":"Authors","title":"Authors and Citation","text":"Sigve Nakken. Author, maintainer.","code":""},{"path":"https://sigven.github.io/pharmOncoX/authors.html","id":"citation","dir":"","previous_headings":"","what":"Citation","title":"Authors and Citation","text":"Nakken S.  (2023)  pharmOncoX: Targeted non-targeted anti-cancer drugs drug regimens.  R package version 1.5.10.  (https://github.com/sigven/pharmOncoX)","code":"@Manual{,   title = {pharmOncoX: Targeted and non-targeted anti-cancer drugs and drug regimens},   author = {Sigve Nakken},   year = {2023},   note = {R package version 1.5.10},   url = {https://github.com/sigven/pharmOncoX}, }"},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"pharmoncox-","dir":"","previous_headings":"","what":"Molecularly targeted cancer drugs and biomarkers","title":"Molecularly targeted cancer drugs and biomarkers","text":"pharmOncoX provides access targeted non-targeted cancer drugs, including comprehensive annotations per target, drug mechanism--action, approval dates, clinical trial phases various indications etc. data largely based drug-target-indication associations provided Open Targets Platform (Ochoa et al., Nucleic Acids Res., 2021). Associations retrieved Open Targets Platform integrated cancer-relevant indications/conditions (provided sigven/phenOncoX), allowing user retrieve drugs indicated main tumor types (e.g. Lung, Colon/Rectum etc.) Drug-target associations Open Targets Platform furthermore integrated appended drug information NCI Thesaurus, showing also non-targeted cancer drugs (chemotherapeutic agents etc.), various drug regimens. pharmOncoX provides anti-cancer drug classification existing entries Anatomical Therapeutic Chemical (ATC) Classification System, extended significantly manual curation, also establishing novel drug categories presently missing ATC classificiation tree (examples include AURK inhibitors, MET inhibitors, BET inhibitors, AKT inhibitors, PLK inhibitors, IAP inhibitors etc.) enabling filtering drugs according main mechanisms action. Currently (late February 2024), pharmOncoX built upon following releases external databases: Open Targets Platform (2023.12) ChEMBL (v33) NCI Thesaurus (24.01e)","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"getting-started","dir":"","previous_headings":"","what":"Getting started","title":"Molecularly targeted cancer drugs and biomarkers","text":"Installation instructions Usage examples","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"contact","dir":"","previous_headings":"","what":"Contact","title":"Molecularly targeted cancer drugs and biomarkers","text":"sigven ifi.uio.","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"code-of-conduct","dir":"","previous_headings":"","what":"Code of Conduct","title":"Molecularly targeted cancer drugs and biomarkers","text":"Please note project released Contributor Code Conduct. participating project agree abide terms.","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":null,"dir":"Reference","previous_headings":"","what":"Get curated cancer biomarker datasets — get_biomarkers","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"Downloads preprocessed datasets local cache directory returns curated set genomic biomarkers multiple sources (CIViC, CGI, MitelmanDB) dataset comes list object, three elements: metadata - data frame metadata regarding drug resources used data - list four elements ('civic','cgi','mitelmandb','custom_fusions') fpath - path cache file","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"","code":"get_biomarkers(cache_dir = NA, force_download = F)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"cache_dir Local directory data download force_download Logical indicating local cache force downloaded (.e. set TRUE re-download even data exists cache)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"value","dir":"Reference","previous_headings":"","what":"Value","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"entry source-specific (e.g. 'civic') entry data list contains list three data frames: variant - list biomarker variants, extensively populated according variant aliases (identifer - column variant_id) clinical - cross-references variants recorded variant data frame clinical evidence items (identifier - column evidence_id) underlying literature evidence (identifier - column source_id) literature - lists literature source_id's listed clinical data frame","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":null,"dir":"Reference","previous_headings":"","what":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"Function retrieves pharmOncoX data Google Drive","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"","code":"get_drug_records(cache_dir = NA, force_download = F)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"cache_dir Local directory data download force_download Logical indicating local cache force downloaded (.e. set TRUE re-download even data exists cache)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":null,"dir":"Reference","previous_headings":"","what":"Get antineoplastic drugs and drug regimens — get_drugs","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"Downloads preprocessed datasets local cache directory returns selected set drugs based various criteria set user. dataset comes list object, two elements: metadata - data frame metadata regarding drug resources used records - data frame drug records","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"","code":"get_drugs(   cache_dir = NA,   force_download = FALSE,   exclude_salt_forms = TRUE,   exclude_adc = FALSE,   treatment_category = c(\"targeted_therapy_classified\", \"targeted_therapy_unclassified\",     \"chemo_therapy_classified\", \"hormone_therapy_classified\",     \"immuno_suppressants_classified\", \"other\"),   drug_is_approved = FALSE,   drug_target = NULL,   drug_action_type = NULL,   drug_indication_main = NULL,   drug_source_opentargets = FALSE,   drug_cancer_indication = TRUE,   drug_classified_cancer = TRUE,   drug_has_blackbox_warning = FALSE,   drug_approval_year = 1939,   drug_minimum_phase_any_indication = 0,   output_resolution = \"drug2target2indication\",   drug_action_inhibition = F )"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"cache_dir local cache directory data retrieval force_download force download data remote repository even data exists cache exclude_salt_forms exclude salt forms drugs exclude_adc exclude antibody-drug conjugates (ADCs) treatment_category main treatment category, classified according ATC ('targeted_therapy_classified', 'targeted_therapy_unclassified','chemo_therapy_classified','hormone_therapy_classified', 'immuno_suppressants_classified','') drug_is_approved logical indicating resulting drug records contain approved drugs drug_target character vector drug targets (gene symbols) drug records included results drug_action_type character vector drug action types include drug record list - possible values \"INHIBITOR\",\"AGONIST\",\"MODULATOR\",\"ANTAGONIST\", \"BLOCKER\",\"ACTIVATOR\",\"BINDING AGENT\",\"OPENER\", \"STABILISER\",\"CROSS-LINKING AGENT\",DISRUPTING AGENT\",\"\" drug_indication_main character vector main tumor types drug(s) indicated. Possible values: \"Adrenal Gland\",\"Biliary Tract\", \"Bladder/Urinary Tract\",\"Bone\",\"Breast\",\"Cervix\",\"CNS/Brain\", \"Colon/Rectum\",\"Esophagus/Stomach\",\"Eye\",\"Head Neck\",\"Kidney\", \"Liver\",\"Lung\",\"Lymphoid\",\"Myeloid\",\"Ovary/Fallopian Tube\", \"Pancreas\",\"Penis\",\"Peripheral Nervous System\",\"Peritoneum\", \"Pleura\",\"Prostate\",\"Skin\",\"Soft Tissue\",\"Testis\",\"Thymus\", \"Thyroid\",\"Uterus\",\"Vulva/Vagina\" drug_source_opentargets logical indicating resulting drug records contain drug records Open Targets Platform/ChEMBL drug_cancer_indication logical indicating resulting drug records indicated cancer conditions (approved conditions, found clinical trials etc.) drug_classified_cancer logical indicating resulting drug records classified \"L\" class ATC ( \"ANTINEOPLASTIC IMMUNOMODULATING AGENTS\") drug_has_blackbox_warning logical indicating resulting drug records contain drugs black box warnings drug_approval_year include records drugs approved later date (year) drug_minimum_phase_any_indication include drug records clinical phase (indication) greater equal phase output_resolution dictate output record resolution ('drug','drug2target','drug2target2indication') drug_action_inhibition logical indicating return drug records inhibitory mechanism--action","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"value","dir":"Reference","previous_headings":"","what":"Value","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"records data frame contains following columns (selected columns shown based value output_resolution) drug_id - drug identifier (pharmaOncoX) drug_name - primary drug name (upper case, NCI Thesaurus) drug_type - type drug molecule (Antibody, small molecule etc) molecule_chembl_id - ChEMBL compound identifier drug_action_type - main action elicited drug (antagonist, inhibitor, stabiliser etc) drug_alias - collection unambiguous drug aliases (separated '|') nci_concept_definition - detailed description drug mechanism--action (NCI Thesaurus) opentargets - logical - drug found Open Targets Platform resource is_salt - logical - drug record represents salt form (excluded default) is_adc - logical - drug record represents antibody-drug conjugate (ADC - excluded default) drug_blacbox_warning - logical indicating drug blackbox warning nci_t - NCI thesaurus identifier target_symbol - gene symbol drug target target_entrezgene - Entrez gene identifier drug target target_genename - gene name/description drug target target_ensembl_gene_id - Ensembl gene identifier drug target target_type - type drug target (single protein, protein family etc.) drug_max_phase_indication - maximum clinical phase drug (given indication) drug_approved_indication - logical indicating drug approved indication drug_frac_cancer_indications - fraction drug indications cancers drug_approved_noncancer - logical indicating drug approved non-cancer disease drug_n_indications - number indications given drug (approved indications, clinical trials etc) drug_year_first_approval - year drug first approved drug_max_ct_phase - maximum clinical phase drug (indication) disease_efo_id - EFO (Experimental Factor Ontology) identifier drug indication disease_efo_label - EFO (Experimental Factor Ontology) label drug indication primary_site - primary tumor site/type (obtained https://github.com/sigven/oncoPhenoMap) drug_clinical_id - drug clinical identifier (clinicaltrials.gov, DailyMed, FDA etc.) drug_clinical_source - underlying source drug entry (DailyMed, clinicaltrials.gov, FDA etc.) atc_code_level1 - drug identifier ATC (level 1) atc_level1 - drug label ATC (level 1) atc_code_level1 - drug identifier ATC (level 2) atc_level2 - drug label ATC (level 2) atc_code_level3 - drug identifier ATC (level 3) atc_level3 - drug label ATC (level 3) atc_treatment_category - treatment category (targeted/chemo/hormone, cancer/etc)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":null,"dir":"Reference","previous_headings":"","what":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"Utility function get -label/-label drugs (complete)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"","code":"get_targeted_drugs(cache_dir = NA)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"cache_dir Local cache directory","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/tidyeval.html","id":null,"dir":"Reference","previous_headings":"","what":"Tidy eval helpers — tidyeval","title":"Tidy eval helpers — tidyeval","text":"https://cran.r-project.org/web/packages/dplyr/vignettes/programming.html","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-159-february-29th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.9 (February 29th 2024)","title":"Version 1.5.9 (February 29th 2024)","text":"Updated CIViC","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-158-february-6th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.8 (February 6th 2024)","title":"Version 1.5.8 (February 6th 2024)","text":"NCI Thesaurus 24.01e","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-157-february-3rd-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.7 (February 3rd 2024)","title":"Version 1.5.7 (February 3rd 2024)","text":"Fixed buggy alias PubChem","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-156-january-31st-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.6 (January 31st 2024)","title":"Version 1.5.6 (January 31st 2024)","text":"Refine possible values treatment_category argument get_drugs() function Fix anti-androgen classification Fixed bug alias type notation copy numbers expression biomarkers Filter noise rank output helper function get_targeted_drugs Include variant primary name biomarker variants","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-150-january-25th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.0 (January 25th 2024)","title":"Version 1.5.0 (January 25th 2024)","text":"Considerable improvement drug classifications (output column atc_level3), considering targeted agents chemotherapy argument drug_targeted_agent renamed treatment_category helper function get_on_off_label_drugs renamed get_targeted_drugs","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-1410-january-17th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.4.10 (January 17th 2024)","title":"Version 1.4.10 (January 17th 2024)","text":"Updated NCI Thesaurus (23.12d) Updated CIViC data (20240114) Revised manual drug classification (building upon ATC)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-148-december-12th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.8 (December 12th 2023)","title":"Version 1.4.8 (December 12th 2023)","text":"Updated NCI Thesaurus - 23.11d Updated CIViC data (20231212)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-148-november-30th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.8 (November 30th 2023)","title":"Version 1.4.8 (November 30th 2023)","text":"Updated OTP (v2023.12) Updated Mitelman database (20231016)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-147-november-3rd-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.7 (November 3rd 2023)","title":"Version 1.4.7 (November 3rd 2023)","text":"Fixed corrupt biomarker literature data frame","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-146-october-18th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.6 (October 18th 2023)","title":"Version 1.4.6 (October 18th 2023)","text":"Fixed metadata Fixed -dated version descriptions (GH site) exclude compounds missing drug action type (platins etc.)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-145-october-6th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.5 (October 6th 2023)","title":"Version 1.4.5 (October 6th 2023)","text":"Updated NCI Thesaurus - 23.09d Updated CIViC data Added drug class (ATC) get_on_off_label_drugs()","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-144-september-1st-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.4 (September 1st 2023)","title":"Version 1.4.4 (September 1st 2023)","text":"Updated NCI Thesaurus - 23.08d Updated CIViC data Updated Mitelman database (20230803) get_biomarkers() now exported main function","code":""}]
+[{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"our-pledge","dir":"","previous_headings":"","what":"Our Pledge","title":"Contributor Covenant Code of Conduct","text":"members, contributors, leaders pledge make participation community harassment-free experience everyone, regardless age, body size, visible invisible disability, ethnicity, sex characteristics, gender identity expression, level experience, education, socio-economic status, nationality, personal appearance, race, religion, sexual identity orientation. pledge act interact ways contribute open, welcoming, diverse, inclusive, healthy community.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"our-standards","dir":"","previous_headings":"","what":"Our Standards","title":"Contributor Covenant Code of Conduct","text":"Examples behavior contributes positive environment community include: Demonstrating empathy kindness toward people respectful differing opinions, viewpoints, experiences Giving gracefully accepting constructive feedback Accepting responsibility apologizing affected mistakes, learning experience Focusing best just us individuals, overall community Examples unacceptable behavior include: use sexualized language imagery, sexual attention advances kind Trolling, insulting derogatory comments, personal political attacks Public private harassment Publishing others’ private information, physical email address, without explicit permission conduct reasonably considered inappropriate professional setting","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement-responsibilities","dir":"","previous_headings":"","what":"Enforcement Responsibilities","title":"Contributor Covenant Code of Conduct","text":"Community leaders responsible clarifying enforcing standards acceptable behavior take appropriate fair corrective action response behavior deem inappropriate, threatening, offensive, harmful. Community leaders right responsibility remove, edit, reject comments, commits, code, wiki edits, issues, contributions aligned Code Conduct, communicate reasons moderation decisions appropriate.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"scope","dir":"","previous_headings":"","what":"Scope","title":"Contributor Covenant Code of Conduct","text":"Code Conduct applies within community spaces, also applies individual officially representing community public spaces. Examples representing community include using official e-mail address, posting via official social media account, acting appointed representative online offline event.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement","dir":"","previous_headings":"","what":"Enforcement","title":"Contributor Covenant Code of Conduct","text":"Instances abusive, harassing, otherwise unacceptable behavior may reported community leaders responsible enforcement [INSERT CONTACT METHOD]. complaints reviewed investigated promptly fairly. community leaders obligated respect privacy security reporter incident.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"enforcement-guidelines","dir":"","previous_headings":"","what":"Enforcement Guidelines","title":"Contributor Covenant Code of Conduct","text":"Community leaders follow Community Impact Guidelines determining consequences action deem violation Code Conduct:","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_1-correction","dir":"","previous_headings":"Enforcement Guidelines","what":"1. Correction","title":"Contributor Covenant Code of Conduct","text":"Community Impact: Use inappropriate language behavior deemed unprofessional unwelcome community. Consequence: private, written warning community leaders, providing clarity around nature violation explanation behavior inappropriate. public apology may requested.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_2-warning","dir":"","previous_headings":"Enforcement Guidelines","what":"2. Warning","title":"Contributor Covenant Code of Conduct","text":"Community Impact: violation single incident series actions. Consequence: warning consequences continued behavior. interaction people involved, including unsolicited interaction enforcing Code Conduct, specified period time. includes avoiding interactions community spaces well external channels like social media. Violating terms may lead temporary permanent ban.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_3-temporary-ban","dir":"","previous_headings":"Enforcement Guidelines","what":"3. Temporary Ban","title":"Contributor Covenant Code of Conduct","text":"Community Impact: serious violation community standards, including sustained inappropriate behavior. Consequence: temporary ban sort interaction public communication community specified period time. public private interaction people involved, including unsolicited interaction enforcing Code Conduct, allowed period. Violating terms may lead permanent ban.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"id_4-permanent-ban","dir":"","previous_headings":"Enforcement Guidelines","what":"4. Permanent Ban","title":"Contributor Covenant Code of Conduct","text":"Community Impact: Demonstrating pattern violation community standards, including sustained inappropriate behavior, harassment individual, aggression toward disparagement classes individuals. Consequence: permanent ban sort public interaction within community.","code":""},{"path":"https://sigven.github.io/pharmOncoX/CODE_OF_CONDUCT.html","id":"attribution","dir":"","previous_headings":"","what":"Attribution","title":"Contributor Covenant Code of Conduct","text":"Code Conduct adapted Contributor Covenant, version 2.0, available https://www.contributor-covenant.org/version/2/0/ code_of_conduct.html. Community Impact Guidelines inspired Mozilla’s code conduct enforcement ladder. answers common questions code conduct, see FAQ https://www.contributor-covenant.org/faq. Translations available https:// www.contributor-covenant.org/translations.","code":""},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"installation","dir":"Articles","previous_headings":"","what":"Installation","title":"Getting started","text":"","code":"if (!(\"remotes\" %in% installed.packages())) {  install.packages(\"remotes\") }  remotes::install_github('sigven/pharmOncoX') #> Using github PAT from envvar GITHUB_PAT #> Downloading GitHub repo sigven/pharmOncoX@HEAD #>  #> ── R CMD build ───────────────────────────────────────────────────────────────── #> * checking for file ‘/tmp/Rtmp1n8MHG/remotes189d4fa6d09/sigven-pharmOncoX-708a3a5/DESCRIPTION’ ... OK #> * preparing ‘pharmOncoX’: #> * checking DESCRIPTION meta-information ... OK #> * checking for LF line-endings in source and make files and shell scripts #> * checking for empty or unneeded directories #> Omitted ‘LazyData’ from DESCRIPTION #> * building ‘pharmOncoX_1.6.0.tar.gz’ #> Installing package into '/home/runner/work/_temp/Library' #> (as 'lib' is unspecified)  library(pharmOncoX) cache_dir <- tempdir() #cache_dir <-  #  \"/Users/sigven/project_data/packages/package__pharmOncoX/pharmOncoX/data-raw/gd_local\""},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"targeted-agents","dir":"Articles","previous_headings":"Cancer drug classifications","what":"Targeted agents","title":"Getting started","text":"Plotted key statistics respect drug classification numbers targeted chemotherapy agents found pharmOncoX. Existing drug classifications retrieved ATC, extended manual addition/curation, also establishment multiple novel levels ATC tree, particularly targeted therapies. Note drugs indicated cancer conditions (harvested Open Targets platform) considered numbers plotted .","code":"p_targeted_classifications"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"chemotherapy-agents","dir":"Articles","previous_headings":"Cancer drug classifications","what":"Chemotherapy agents","title":"Getting started","text":"","code":"p_chemo_classifications"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-braf-targeted-drugs-list-records-per-indication","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get BRAF-targeted drugs, list records per indication","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,   treatment_category =  c(\"targeted_therapy_classified\",                           \"targeted_therapy_unclassified\"),     drug_target = c('BRAF')) #> INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:36] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 18:01:36] Retrieved n = 31451 records #> INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:36] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 18:01:36] Retrieved n = 677295 records #> INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:36] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 18:01:36] Retrieved n = 31486 records #> INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:36] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 18:01:36] Retrieved n = 39369 records #> INFO  [2024-03-09 18:01:36] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:36] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 18:01:36] Retrieved n = 62752 records #> INFO  [2024-03-09 18:01:39] Record set satisfying user-defined criteria: n = 279 #> INFO  [2024-03-09 18:01:39] Collapsing record set - providing output on a 'per_drug_target_indication' resolution #> INFO  [2024-03-09 18:01:39] Final record set: n = 237 records  ## Number of drug records nrow(drugs$records) #> [1] 237  ## Column names of drug records colnames(drugs$records) #>  [1] \"drug_id\"                      \"drug_name\"                    #>  [3] \"drug_type\"                    \"molecule_chembl_id\"           #>  [5] \"drug_action_type\"             \"drug_alias\"                   #>  [7] \"nci_concept_definition\"       \"opentargets\"                  #>  [9] \"drug_cancer_relevance\"        \"inhibition_moa\"               #> [11] \"is_salt\"                      \"is_adc\"                       #> [13] \"drug_blackbox_warning\"        \"nci_t\"                        #> [15] \"target_symbol\"                \"target_entrezgene\"            #> [17] \"target_genename\"              \"target_ensembl_gene_id\"       #> [19] \"target_type\"                  \"drug_max_phase_indication\"    #> [21] \"drug_approved_indication\"     \"drug_frac_cancer_indications\" #> [23] \"drug_approved_noncancer\"      \"drug_n_indications\"           #> [25] \"drug_year_first_approval\"     \"drug_max_ct_phase\"            #> [27] \"disease_efo_id\"               \"disease_efo_label\"            #> [29] \"primary_site\"                 \"drug_clinical_id\"             #> [31] \"drug_clinical_source\"         \"atc_code_level1\"              #> [33] \"atc_level1\"                   \"atc_code_level2\"              #> [35] \"atc_level2\"                   \"atc_code_level3\"              #> [37] \"atc_level3\"                   \"atc_treatment_category\""},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-ras-targeted-drugs-list-per-drug-target","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get RAS-targeted drugs, list per drug target","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_action_inhibition = T,   output_resolution = \"drug2target\")$records |>   dplyr::filter(atc_level3 == \"RAS inhibitors\")  drugs <- drugs |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_ras_inhibitors <- DT::datatable(   drugs,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-mek-inhibitors-list-per-drug-only","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get MEK inhibitors, list per drug only","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_action_inhibition = T,   drug_source_opentargets = T,    output_resolution = \"drug\" )$records |>   dplyr::filter(atc_level3 == \"MEK inhibitors\")  drugs <- drugs |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_mek_inhibitors <- DT::datatable(   drugs,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-immune-checkpoint-inhibitors-list-per-drug-target","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get immune checkpoint inhibitors, list per drug target","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category =  c(\"targeted_therapy_classified\"),   drug_source_opentargets = F,   drug_classified_cancer = T,    output_resolution = \"drug2target\")  drugs$records <- drugs$records |>   dplyr::filter(     (!is.na(atc_level3) &        (atc_level3 == \"PD-1/PDL-1 inhibitors\" |      atc_level3 == \"Other immune checkpoint inhibitors\")   )) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     ) |>   dplyr::select(     drug_id,     drug_name,     drug_type,     target_symbol,     target_genename,     dplyr::everything()   )  dt_drugtable_ici <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-immune-checkpoint-inhibitors-indicated-for-lung-cancer-conditions-list-per-drug-target-entry","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get immune checkpoint inhibitors indicated for lung cancer conditions, list per drug-target entry","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    output_resolution = \"drug2target\",    treatment_category = c(\"targeted_therapy_classified\"),   drug_source_opentargets = T,   drug_indication_main = \"Lung\")  drugs$records <- drugs$records |>   dplyr::filter(     (!is.na(atc_level3) &        (atc_level3 == \"PD-1/PDL-1 inhibitors\" |      atc_level3 == \"Other immune checkpoint inhibitors\")   )) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     ) |>   dplyr::select(     drug_id,     drug_name,     drug_type,     target_symbol,     target_genename,     dplyr::everything()   )  dt_drugtable_ici_lung <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-antimetabolite-drugs","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get antimetabolite drugs","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = c(\"chemo_therapy_classified\"),   output_resolution = \"drug\") #> INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:59] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 18:01:59] Retrieved n = 31451 records #> INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:59] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 18:01:59] Retrieved n = 677295 records #> INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:59] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 18:01:59] Retrieved n = 31486 records #> INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:59] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 18:01:59] Retrieved n = 39369 records #> INFO  [2024-03-09 18:01:59] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:01:59] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 18:01:59] Retrieved n = 62752 records #> INFO  [2024-03-09 18:02:02] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 18:02:02] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 18:02:02] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     !is.na(atc_level2) &     stringr::str_detect(       atc_level2, \"ANTIMETABOLITES\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_metabolites <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-taxanes","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get taxanes","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = \"chemo_therapy_classified\",   output_resolution = \"drug\") #> INFO  [2024-03-09 18:02:02] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:02] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 18:02:02] Retrieved n = 31451 records #> INFO  [2024-03-09 18:02:03] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:03] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 18:02:03] Retrieved n = 677295 records #> INFO  [2024-03-09 18:02:03] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:03] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 18:02:03] Retrieved n = 31486 records #> INFO  [2024-03-09 18:02:03] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:03] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 18:02:03] Retrieved n = 39369 records #> INFO  [2024-03-09 18:02:03] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:03] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 18:02:03] Retrieved n = 62752 records #> INFO  [2024-03-09 18:02:06] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 18:02:06] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 18:02:06] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     stringr::str_detect(       atc_level3, \"Taxanes\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_taxanes <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"get-platinum-compounds","dir":"Articles","previous_headings":"Retrieval of drugs - examples","what":"Get platinum compounds","title":"Getting started","text":"","code":"drugs <- get_drugs(   cache_dir = cache_dir,    treatment_category = \"chemo_therapy_classified\",   output_resolution = \"drug\") #> INFO  [2024-03-09 18:02:06] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:06] Object 'drug_map_name' sucessfully loaded #> INFO  [2024-03-09 18:02:06] Retrieved n = 31451 records #> INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:07] Object 'drug_map_alias' sucessfully loaded #> INFO  [2024-03-09 18:02:07] Retrieved n = 677295 records #> INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:07] Object 'drug_map_basic' sucessfully loaded #> INFO  [2024-03-09 18:02:07] Retrieved n = 31486 records #> INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:07] Object 'drug_map_target' sucessfully loaded #> INFO  [2024-03-09 18:02:07] Retrieved n = 39369 records #> INFO  [2024-03-09 18:02:07] Reading from cache_dir = '/tmp/Rtmp1n8MHG', argument force_download = F #> INFO  [2024-03-09 18:02:07] Object 'drug_map_indication' sucessfully loaded #> INFO  [2024-03-09 18:02:07] Retrieved n = 62752 records #> INFO  [2024-03-09 18:02:09] Record set satisfying user-defined criteria: n = 16534 #> INFO  [2024-03-09 18:02:09] Collapsing record set - providing output on a 'per_drug' resolution #> INFO  [2024-03-09 18:02:10] Final record set: n = 170 records  drugs$records <- drugs$records |>   dplyr::filter(     stringr::str_detect(       atc_level3, \"Platinum compounds\"     )   ) |>   dplyr::select(     -c(\"drug_alias\",        \"disease_main_group\",        \"drug_clinical_id\")) |>   dplyr::mutate(     disease_indication = stringr::str_replace_all(       disease_indication, \"\\\\|\",\", \")     )  dt_drugtable_platins <- DT::datatable(   drugs$records,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"reported-associations-between-brca12-alterations-and-drug-sensitivity","dir":"Articles","previous_headings":"Retrieval of biomarkers","what":"Reported associations between BRCA1/2 alterations and drug sensitivity","title":"Getting started","text":"Get evidence CIViC CGI cancer drug sensitivity BRCA1/2 alterations (somatically (tumor) inherited/germline)","code":"biomarkers <- get_biomarkers(   cache_dir = cache_dir) #> INFO  [2024-03-09 18:02:10] Downloading remote dataset from Google Drive to cache_dir #> INFO  [2024-03-09 18:02:13] Reading from cache_dir = ' (/tmp/Rtmp1n8MHG'), argument force_download = F #> INFO  [2024-03-09 18:02:13] Object 'biomarkers' sucessfully loaded #> INFO  [2024-03-09 18:02:13] md5 checksum is valid: 277a4cf2f80523ab3bf6d219500cc846  brca1_biomarkers <- list() for(source in c('civic','cgi')){   brca1_biomarkers[[source]] <-      biomarkers$data[[source]]$variant |>      dplyr::filter(       !is.na(symbol) & (symbol == \"BRCA1\" | symbol == \"BRCA2\")) |>     dplyr::group_by(variant_id, variant_name_primary, variant_consequence) |>     dplyr::summarise(       variant_alias = paste(variant_alias, collapse=\", \"),        .groups = \"drop\") |>      dplyr::inner_join(       biomarkers$data[[source]]$clinical, by = \"variant_id\") |>     dplyr::select(       variant_id, variant_name_primary, therapeutic_context,       evidence_type, evidence_level,        biomarker_source, biomarker_source_datestamp,       molecular_profile_name, evidence_id, variant_origin,       primary_site, evidence_id, source_id,       evidence_url,        evidence_description,        clinical_significance) |>      dplyr::distinct() |>      dplyr::rename(literature_id = source_id,                   variant_name = variant_name_primary) |>     dplyr::filter(evidence_type == \"Predictive\") |>     dplyr::select(       variant_name,        primary_site,       therapeutic_context,       molecular_profile_name,        evidence_level,       dplyr::everything()     ) }  brca1_biomarkers_all <-    dplyr::bind_rows(brca1_biomarkers[['civic']],                    brca1_biomarkers[['cgi']]) |>     dplyr::arrange(evidence_level)     dt_brca1_biomarkers <- DT::datatable(   brca1_biomarkers_all,   escape = FALSE,   extensions = c(\"Buttons\", \"Responsive\"),    width = \"100%\",   options = list(     buttons = c(\"csv\", \"excel\"),      dom = \"Bfrtip\") )"},{"path":"https://sigven.github.io/pharmOncoX/articles/pharmOncoX.html","id":"session-info","dir":"Articles","previous_headings":"","what":"Session Info","title":"Getting started","text":"","code":"# set eval = FALSE if you don't want this info (useful for reproducibility)  # to appear sessionInfo() #> R version 4.3.3 (2024-02-29) #> Platform: x86_64-pc-linux-gnu (64-bit) #> Running under: Ubuntu 22.04.4 LTS #>  #> Matrix products: default #> BLAS:   /usr/lib/x86_64-linux-gnu/openblas-pthread/libblas.so.3  #> LAPACK: /usr/lib/x86_64-linux-gnu/openblas-pthread/libopenblasp-r0.3.20.so;  LAPACK version 3.10.0 #>  #> locale: #>  [1] LC_CTYPE=C.UTF-8       LC_NUMERIC=C           LC_TIME=C.UTF-8        #>  [4] LC_COLLATE=C.UTF-8     LC_MONETARY=C.UTF-8    LC_MESSAGES=C.UTF-8    #>  [7] LC_PAPER=C.UTF-8       LC_NAME=C              LC_ADDRESS=C           #> [10] LC_TELEPHONE=C         LC_MEASUREMENT=C.UTF-8 LC_IDENTIFICATION=C    #>  #> time zone: UTC #> tzcode source: system (glibc) #>  #> attached base packages: #> [1] stats     graphics  grDevices utils     datasets  methods   base      #>  #> other attached packages: #> [1] pharmOncoX_1.6.0 #>  #> loaded via a namespace (and not attached): #>  [1] sass_0.4.8        utf8_1.2.4        generics_0.1.3    stringi_1.8.3     #>  [5] digest_0.6.34     magrittr_2.0.3    evaluate_0.23     grid_4.3.3        #>  [9] fastmap_1.1.1     jsonlite_1.8.8    processx_3.8.3    pkgbuild_1.4.3    #> [13] googledrive_2.1.1 ps_1.7.6          httr_1.4.7        purrr_1.0.2       #> [17] fansi_1.0.6       crosstalk_1.2.1   scales_1.3.0      textshaping_0.3.7 #> [21] jquerylib_0.1.4   cli_3.6.2         rlang_1.1.3       crayon_1.5.2      #> [25] ellipsis_0.3.2    munsell_0.5.0     remotes_2.4.2.1   withr_3.0.0       #> [29] cachem_1.0.8      yaml_2.3.8        tools_4.3.3       gargle_1.5.2      #> [33] memoise_2.0.1     dplyr_1.1.4       colorspace_2.1-0  ggplot2_3.5.0     #> [37] DT_0.32           curl_5.2.1        assertthat_0.2.1  vctrs_0.6.5       #> [41] R6_2.5.1          lifecycle_1.0.4   stringr_1.5.1     htmlwidgets_1.6.4 #> [45] fs_1.6.3          ragg_1.2.7        pkgconfig_2.0.3   desc_1.4.3        #> [49] callr_3.7.5       pkgdown_2.0.7     pillar_1.9.0      bslib_0.6.1       #> [53] gtable_0.3.4      glue_1.7.0        lgr_0.4.4         systemfonts_1.0.6 #> [57] highr_0.10        xfun_0.42         tibble_3.2.1      tidyselect_1.2.0  #> [61] knitr_1.45        farver_2.1.1      htmltools_0.5.7   rmarkdown_2.26    #> [65] compiler_4.3.3"},{"path":[]},{"path":"https://sigven.github.io/pharmOncoX/authors.html","id":null,"dir":"","previous_headings":"","what":"Authors","title":"Authors and Citation","text":"Sigve Nakken. Author, maintainer.","code":""},{"path":"https://sigven.github.io/pharmOncoX/authors.html","id":"citation","dir":"","previous_headings":"","what":"Citation","title":"Authors and Citation","text":"Nakken S.  (2023)  pharmOncoX: Targeted non-targeted anti-cancer drugs drug regimens.  R package version 1.6.0.  (https://github.com/sigven/pharmOncoX)","code":"@Manual{,   title = {pharmOncoX: Targeted and non-targeted anti-cancer drugs and drug regimens},   author = {Sigve Nakken},   year = {2023},   note = {R package version 1.6.0},   url = {https://github.com/sigven/pharmOncoX}, }"},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"pharmoncox-","dir":"","previous_headings":"","what":"Molecularly targeted cancer drugs and biomarkers","title":"Molecularly targeted cancer drugs and biomarkers","text":"pharmOncoX provides access targeted non-targeted cancer drugs, including comprehensive annotations per target, drug mechanism--action, approval dates, clinical trial phases various indications etc. data largely based drug-target-indication associations provided Open Targets Platform (Ochoa et al., Nucleic Acids Res., 2021). Associations retrieved Open Targets Platform integrated cancer-relevant indications/conditions (provided sigven/phenOncoX), allowing user retrieve drugs indicated main tumor types (e.g. Lung, Colon/Rectum etc.) Drug-target associations Open Targets Platform furthermore integrated appended drug information NCI Thesaurus, showing also non-targeted cancer drugs (chemotherapeutic agents etc.), various drug regimens. pharmOncoX provides anti-cancer drug classification existing entries Anatomical Therapeutic Chemical (ATC) Classification System, extended significantly manual curation, also establishing novel drug categories presently missing ATC classificiation tree (examples include AURK inhibitors, MET inhibitors, BET inhibitors, AKT inhibitors, PLK inhibitors, IAP inhibitors etc.) enabling filtering drugs according main mechanisms action. Currently (late February 2024), pharmOncoX built upon following releases external databases: Open Targets Platform (2023.12) ChEMBL (v33) NCI Thesaurus (24.01e)","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"getting-started","dir":"","previous_headings":"","what":"Getting started","title":"Molecularly targeted cancer drugs and biomarkers","text":"Installation instructions Usage examples","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"contact","dir":"","previous_headings":"","what":"Contact","title":"Molecularly targeted cancer drugs and biomarkers","text":"sigven ifi.uio.","code":""},{"path":"https://sigven.github.io/pharmOncoX/index.html","id":"code-of-conduct","dir":"","previous_headings":"","what":"Code of Conduct","title":"Molecularly targeted cancer drugs and biomarkers","text":"Please note project released Contributor Code Conduct. participating project agree abide terms.","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":null,"dir":"Reference","previous_headings":"","what":"Get curated cancer biomarker datasets — get_biomarkers","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"Downloads preprocessed datasets local cache directory returns curated set genomic biomarkers multiple sources (CIViC, CGI, MitelmanDB) dataset comes list object, three elements: metadata - data frame metadata regarding drug resources used data - list four elements ('civic','cgi','mitelmandb','custom_fusions') fpath - path cache file","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"","code":"get_biomarkers(cache_dir = NA, force_download = F)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"cache_dir Local directory data download force_download Logical indicating local cache force downloaded (.e. set TRUE re-download even data exists cache)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_biomarkers.html","id":"value","dir":"Reference","previous_headings":"","what":"Value","title":"Get curated cancer biomarker datasets — get_biomarkers","text":"entry source-specific (e.g. 'civic') entry data list contains list three data frames: variant - list biomarker variants, extensively populated according variant aliases (identifer - column variant_id) clinical - cross-references variants recorded variant data frame clinical evidence items (identifier - column evidence_id) underlying literature evidence (identifier - column source_id) literature - lists literature source_id's listed clinical data frame","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":null,"dir":"Reference","previous_headings":"","what":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"Function retrieves pharmOncoX data Google Drive","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"","code":"get_drug_records(cache_dir = NA, force_download = F)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drug_records.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Function that retrieves pharmOncoX data from Google Drive — get_drug_records","text":"cache_dir Local directory data download force_download Logical indicating local cache force downloaded (.e. set TRUE re-download even data exists cache)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":null,"dir":"Reference","previous_headings":"","what":"Get antineoplastic drugs and drug regimens — get_drugs","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"Downloads preprocessed datasets local cache directory returns selected set drugs based various criteria set user. dataset comes list object, two elements: metadata - data frame metadata regarding drug resources used records - data frame drug records","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"","code":"get_drugs(   cache_dir = NA,   force_download = FALSE,   exclude_salt_forms = TRUE,   exclude_adc = FALSE,   treatment_category = c(\"targeted_therapy_classified\", \"targeted_therapy_unclassified\",     \"chemo_therapy_classified\", \"hormone_therapy_classified\",     \"immuno_suppressants_classified\", \"other\"),   drug_is_approved = FALSE,   drug_target = NULL,   drug_action_type = NULL,   drug_indication_main = NULL,   drug_source_opentargets = FALSE,   drug_cancer_indication = TRUE,   drug_classified_cancer = TRUE,   drug_has_blackbox_warning = FALSE,   drug_approval_year = 1939,   drug_minimum_phase_any_indication = 0,   output_resolution = \"drug2target2indication\",   drug_action_inhibition = F )"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"cache_dir local cache directory data retrieval force_download force download data remote repository even data exists cache exclude_salt_forms exclude salt forms drugs exclude_adc exclude antibody-drug conjugates (ADCs) treatment_category main treatment category, classified according ATC ('targeted_therapy_classified', 'targeted_therapy_unclassified','chemo_therapy_classified','hormone_therapy_classified', 'immuno_suppressants_classified','') drug_is_approved logical indicating resulting drug records contain approved drugs drug_target character vector drug targets (gene symbols) drug records included results drug_action_type character vector drug action types include drug record list - possible values \"INHIBITOR\",\"AGONIST\",\"MODULATOR\",\"ANTAGONIST\", \"BLOCKER\",\"ACTIVATOR\",\"BINDING AGENT\",\"OPENER\", \"STABILISER\",\"CROSS-LINKING AGENT\",DISRUPTING AGENT\",\"\" drug_indication_main character vector main tumor types drug(s) indicated. Possible values: \"Adrenal Gland\",\"Biliary Tract\", \"Bladder/Urinary Tract\",\"Bone\",\"Breast\",\"Cervix\",\"CNS/Brain\", \"Colon/Rectum\",\"Esophagus/Stomach\",\"Eye\",\"Head Neck\",\"Kidney\", \"Liver\",\"Lung\",\"Lymphoid\",\"Myeloid\",\"Ovary/Fallopian Tube\", \"Pancreas\",\"Penis\",\"Peripheral Nervous System\",\"Peritoneum\", \"Pleura\",\"Prostate\",\"Skin\",\"Soft Tissue\",\"Testis\",\"Thymus\", \"Thyroid\",\"Uterus\",\"Vulva/Vagina\" drug_source_opentargets logical indicating resulting drug records contain drug records Open Targets Platform/ChEMBL drug_cancer_indication logical indicating resulting drug records indicated cancer conditions (approved conditions, found clinical trials etc.) drug_classified_cancer logical indicating resulting drug records classified \"L\" class ATC ( \"ANTINEOPLASTIC IMMUNOMODULATING AGENTS\") drug_has_blackbox_warning logical indicating resulting drug records contain drugs black box warnings drug_approval_year include records drugs approved later date (year) drug_minimum_phase_any_indication include drug records clinical phase (indication) greater equal phase output_resolution dictate output record resolution ('drug','drug2target','drug2target2indication') drug_action_inhibition logical indicating return drug records inhibitory mechanism--action","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_drugs.html","id":"value","dir":"Reference","previous_headings":"","what":"Value","title":"Get antineoplastic drugs and drug regimens — get_drugs","text":"records data frame contains following columns (selected columns shown based value output_resolution) drug_id - drug identifier (pharmaOncoX) drug_name - primary drug name (upper case, NCI Thesaurus) drug_type - type drug molecule (Antibody, small molecule etc) molecule_chembl_id - ChEMBL compound identifier drug_action_type - main action elicited drug (antagonist, inhibitor, stabiliser etc) drug_alias - collection unambiguous drug aliases (separated '|') nci_concept_definition - detailed description drug mechanism--action (NCI Thesaurus) opentargets - logical - drug found Open Targets Platform resource is_salt - logical - drug record represents salt form (excluded default) is_adc - logical - drug record represents antibody-drug conjugate (ADC - excluded default) drug_blacbox_warning - logical indicating drug blackbox warning nci_t - NCI thesaurus identifier target_symbol - gene symbol drug target target_entrezgene - Entrez gene identifier drug target target_genename - gene name/description drug target target_ensembl_gene_id - Ensembl gene identifier drug target target_type - type drug target (single protein, protein family etc.) drug_max_phase_indication - maximum clinical phase drug (given indication) drug_approved_indication - logical indicating drug approved indication drug_frac_cancer_indications - fraction drug indications cancers drug_approved_noncancer - logical indicating drug approved non-cancer disease drug_n_indications - number indications given drug (approved indications, clinical trials etc) drug_year_first_approval - year drug first approved drug_max_ct_phase - maximum clinical phase drug (indication) disease_efo_id - EFO (Experimental Factor Ontology) identifier drug indication disease_efo_label - EFO (Experimental Factor Ontology) label drug indication primary_site - primary tumor site/type (obtained https://github.com/sigven/oncoPhenoMap) drug_clinical_id - drug clinical identifier (clinicaltrials.gov, DailyMed, FDA etc.) drug_clinical_source - underlying source drug entry (DailyMed, clinicaltrials.gov, FDA etc.) atc_code_level1 - drug identifier ATC (level 1) atc_level1 - drug label ATC (level 1) atc_code_level1 - drug identifier ATC (level 2) atc_level2 - drug label ATC (level 2) atc_code_level3 - drug identifier ATC (level 3) atc_level3 - drug label ATC (level 3) atc_treatment_category - treatment category (targeted/chemo/hormone, cancer/etc)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":null,"dir":"Reference","previous_headings":"","what":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"Utility function get -label/-label drugs (complete)","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":"ref-usage","dir":"Reference","previous_headings":"","what":"Usage","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"","code":"get_targeted_drugs(cache_dir = NA)"},{"path":"https://sigven.github.io/pharmOncoX/reference/get_targeted_drugs.html","id":"arguments","dir":"Reference","previous_headings":"","what":"Arguments","title":"Utility function to get on-label/off-label drugs (not complete) — get_targeted_drugs","text":"cache_dir Local cache directory","code":""},{"path":"https://sigven.github.io/pharmOncoX/reference/tidyeval.html","id":null,"dir":"Reference","previous_headings":"","what":"Tidy eval helpers — tidyeval","title":"Tidy eval helpers — tidyeval","text":"https://cran.r-project.org/web/packages/dplyr/vignettes/programming.html","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-160-march-9th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.6.0 (March 9th 2024)","title":"Version 1.6.0 (March 9th 2024)","text":"CIViC/Mitelmandb updates","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-159-february-29th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.9 (February 29th 2024)","title":"Version 1.5.9 (February 29th 2024)","text":"Updated CIViC","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-158-february-6th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.8 (February 6th 2024)","title":"Version 1.5.8 (February 6th 2024)","text":"NCI Thesaurus 24.01e","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-157-february-3rd-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.7 (February 3rd 2024)","title":"Version 1.5.7 (February 3rd 2024)","text":"Fixed buggy alias PubChem","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-156-january-31st-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.6 (January 31st 2024)","title":"Version 1.5.6 (January 31st 2024)","text":"Refine possible values treatment_category argument get_drugs() function Fix anti-androgen classification Fixed bug alias type notation copy numbers expression biomarkers Filter noise rank output helper function get_targeted_drugs Include variant primary name biomarker variants","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-150-january-25th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.5.0 (January 25th 2024)","title":"Version 1.5.0 (January 25th 2024)","text":"Considerable improvement drug classifications (output column atc_level3), considering targeted agents chemotherapy argument drug_targeted_agent renamed treatment_category helper function get_on_off_label_drugs renamed get_targeted_drugs","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-1410-january-17th-2024","dir":"Changelog","previous_headings":"","what":"Version 1.4.10 (January 17th 2024)","title":"Version 1.4.10 (January 17th 2024)","text":"Updated NCI Thesaurus (23.12d) Updated CIViC data (20240114) Revised manual drug classification (building upon ATC)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-148-december-12th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.8 (December 12th 2023)","title":"Version 1.4.8 (December 12th 2023)","text":"Updated NCI Thesaurus - 23.11d Updated CIViC data (20231212)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-148-november-30th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.8 (November 30th 2023)","title":"Version 1.4.8 (November 30th 2023)","text":"Updated OTP (v2023.12) Updated Mitelman database (20231016)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-147-november-3rd-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.7 (November 3rd 2023)","title":"Version 1.4.7 (November 3rd 2023)","text":"Fixed corrupt biomarker literature data frame","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-146-october-18th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.6 (October 18th 2023)","title":"Version 1.4.6 (October 18th 2023)","text":"Fixed metadata Fixed -dated version descriptions (GH site) exclude compounds missing drug action type (platins etc.)","code":""},{"path":"https://sigven.github.io/pharmOncoX/news/index.html","id":"version-145-october-6th-2023","dir":"Changelog","previous_headings":"","what":"Version 1.4.5 (October 6th 2023)","title":"Version 1.4.5 (October 6th 2023)","text":"Updated NCI Thesaurus - 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