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|Therapy Name||Gemcitabine + JQ1|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|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).|
|JQ1||BET Inhibitor (Pan) 27||JQ1 is a BET bromodomain inhibitor with greatest specificity towards BRD4, resulting in decreased Myc expression, increased cell death, reduced macrophage immunosuppression, and inhibition of tumor growth (PMID: 24231268, PMID: 31018997, PMID: 30906568).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|Unknown unknown||pancreatic ductal adenocarcinoma||not applicable||Gemcitabine + JQ1||Preclinical - Pdx||Actionable||In a preclinical study, combination treatment with JQ1 and Gemzar (gemcitabine) resulted in tumor microenvironment alterations and greater reductions of tumor growth and weight when compared to Gemzar (gemcitabine) alone in patient derived xenograft (PDX) models of pancreatic ductal adenocarcinoma (PMID: 27528027).||27528027|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status|