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|Therapy Name||Defactinib + Gemcitabine + Pembrolizumab|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Defactinib||VS-6063|PF-04554878||FAK inhibitor 13||Defactinib (VS-6063) inhibits FAK, resulting in decreased downstream signaling, and potentially leading to reduced tumor cell proliferation and survival (PMID: 31739184).|
|Gemcitabine||Gemzar||Difluorodeoxycytidine Hydrochlorothiazide|LY-188011||Chemotherapy - Antimetabolite 11||Gemzar (gemcitabine) is converted in cells to difluorodeoxycytidine di- and triphosphate (dFdCDP, dFdCTP), which act to inhibit ribonucleoside reductase and as a deoxynucleotide analog respectively, resulting in DNA strand termination and apoptosis (NCI Drug Dictionary).|
|Pembrolizumab||Keytruda||MK-3475||Immune Checkpoint Inhibitor 94 PD-L1/PD-1 antibody 63||Keytruda (pembrolizumab) is an antibody against PD-1 that activates T-cell mediated anti-tumor immune response (PMID: 25977344). Keytruda (pembrolizumab) is approved in melanoma, SCLC, HNSCC, classical Hodgkin Lymphoma, primary mediastinal large B-cell lymphoma, urothelial carcinoma, HCC, Merkel cell carcinoma, NMIBC, cutaneous squamous cell carcinoma, MSI-H or dMMR or TMB high advanced solid tumors, PD-L1 expressing NSCLC, gastric and GEJ adenocarcinoma, squamous esophageal carcinoma, and cervical cancer, in combination with pemetrexed and platinum in non-squamous NSCLC with no EGFR or ALK mutations, with carboplatin and paclitaxel/nab-paclitaxel in squamous NSCLC, with axitinib in RCC, and with Lenvatinib in endometrial carcinoma that is not MSI-H or dMMR (FDA.gov).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status|
|NCT02546531||Phase I||Defactinib + Gemcitabine + Pembrolizumab||Defactinib Combined With Pembrolizumab and Gemcitabine in Patients With Advanced Cancer||Active, not recruiting|