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Therapy Name | Dactolisib + Sorafenib |
Synonyms | |
Therapy Description | |
Drug Name | Trade Name | Synonyms | Drug Classes | Drug Description |
---|---|---|---|---|
Dactolisib | NVP-BEZ235|BEZ235 | ATR Inhibitor 16 mTOR Inhibitor 51 PI3K Inhibitor (Pan) 42 | 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 28 FLT3 Inhibitor 69 KIT Inhibitor 57 PDGFR-beta Inhibitor 14 RAF Inhibitor (Pan) 28 RET Inhibitor 53 VEGFR2 Inhibitor 37 | 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 FDA 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 | Covered Countries | Other Countries |
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