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|Therapy Name||Dactolisib + Sorafenib|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Dactolisib||NVP-BEZ235|BEZ235||ATR Inhibitor 12 mTOR Inhibitor 51 PI3K Inhibitor (Pan) 38||Dactolisib (BEZ235) inhibits PI3K kinase, mTOR kinase, and ATR, which may result in tumor cell apoptosis and growth inhibition of tumor cells (PMID: 18606717, PMID: 21552262, PMID: 32088816).|
|Sorafenib||Nexavar||BAY 43-9006||CSF1R Inhibitor 24 FLT3 Inhibitor 55 KIT Inhibitor 51 PDGFR-beta Inhibitor 13 RAF Inhibitor (Pan) 16 RET Inhibitor 39 VEGFR2 Inhibitor 35||Nexavar (sorafenib) is a multikinase inhibitor with activity against several kinases, including RAF kinases, VEGFR2, VEGFR3, PDGFR-beta, KIT, FLT3, RET, and CSF1R, potentially resulting in decreased tumor growth (PMID: 18445656, PMID: 15466206, PMID: 21517818). Nexavar (sorafenib) is approved for metastatic differentiated thyroid carcinoma, hepatocellular carcinoma, and renal cell carcinoma (FDA.gov).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|FGFR3 over exp||urinary bladder cancer||sensitive||Dactolisib + Sorafenib||Preclinical - Pdx||Actionable||In a preclinical study, the combination of BEZ235 and Nexavar (sorafenib) resulted in improved progression-free survival in an FGFR3-over expressing patient-derived xenograft (PDX) model of bladder cancer with secondary resistance to BGJ398 due to reactivation of downstream signaling, as evidenced by increased activation of Akt and Erk (PMID: 26270481).||26270481|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status|