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|Therapy Name||Decitabine + Pembrolizumab + Pralatrexate|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Decitabine||Dacogen||5-aza-2-deoxycytidine||DNMT inhibitor (Pan) 5||Dacogen (decitabine) is cytidine analog that incorporates into DNA and forms covalent bonds with DNA methyltransferases (DNMTs), resulting in decreased DNMT activity and hypomethylation, and potentially leading to reduced tumor growth (PMID: 28159832, PMID: 25130173). Dacogen (decitabine) is FDA approved for use in patients with myelodysplastic syndromes (FDA.gov).|
|Pembrolizumab||Keytruda||MK-3475||Immune Checkpoint Inhibitor 141 PD-L1/PD-1 antibody 83||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, CD274 (PD-L1)-expressing NSCLC, gastric and GEJ adenocarcinoma, squamous esophageal carcinoma, cervical cancer, and triple-negative breast 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 or lenvatinib in RCC, with Lenvatinib in endometrial carcinoma that is not MSI-H or dMMR, in combination with platinum and fluoropyrimidine-based chemotherapy for patients with esophageal or gastroesophageal carcinoma, in combination with Herceptin (trastuzumab), fluoropyrimidine- and platinum-containing chemotherapy for first-line treatment of patients with HER2-positive gastric or gastroesophageal junction adenocarcinoma, and in combination with platinum-based chemotherapy, with or without bevacizumab, for patients with CD274 (PD-L1)-expressing (CPS>=1) cervical cancer (FDA.gov).|
|Pralatrexate||FOLOTYN||Pralatrexate is folate analogue inhibitor of dihydrofolate reductase that is selective for cells expressing RFC-1 (which may be overexpressed on cancer cells). Pralatrexate causes depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death (NCI Drug Dictionary).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status||Covered Countries||Other Countries|
|NCT03240211||Phase I||Pembrolizumab + Pralatrexate Decitabine + Pembrolizumab + Pralatrexate Decitabine + Pembrolizumab||Study of Pembrolizumab Combined With Decitabine and Pralatrexate in PTCL and CTCL||Recruiting||USA||0|