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|Therapy Name||Adavosertib + Carboplatin + Paclitaxel|
|Drug Name||Trade Name||Synonyms||Drug Classes||Drug Description|
|Adavosertib||MK-1775|AZD1775|AZ1775||WEE1 Inhibitor 6||Adavosertib (MK-1775) is a small molecule inhibitor of the tyrosine kinase WEE1 with potential antineoplastic sensitizing activity (PMID: 22084170, PMID: 32611648).|
|Carboplatin||Paraplatin||CBDCA||Chemotherapy - Platinum 7||Paraplatin (carboplatin) is a second-generation platinum compound and is activated intracellularly to form reactive platinum complexes that cross link DNA with DNA and with proteins. This induces apoptosis and inhibits cell growth (NCI Drug Dictionary).|
|Paclitaxel||Taxol||7-Epipaclitaxel||Antimicrotubule Agent 14 BCL2 Family Inhibitor 6||Taxol (paclitaxel) binds to tubulin to inhibit microtubule disassembly, which results in decreased cell division, and also binds to the anti-apoptotic factor Bcl-2, promoting apoptosis (NCI Drug Dictionary).|
|Molecular Profile||Indication/Tumor Type||Response Type||Therapy Name||Approval Status||Evidence Type||Efficacy Evidence||References|
|TP53 inact mut||ovarian cancer||sensitive||Adavosertib + Carboplatin + Paclitaxel||Phase I||Actionable||In a Phase I trial, treatment with Adavosertib (MK-1775) plus Paraplatin (carboplatin) and Taxol (paclitaxel) resulted in an improved progression-free survival by enhanced RECIST of 7.9 mo vs. 7.3 mo with placebo plus chemotherapy, and complete response in 11/9% (7/59) vs. 8.9% (5/62), partial response in 62.7% (37/59) vs. 61.3% (38/62), and stable disease in 5.1% (3/59) vs. 4.8% (3/62) of patients with platinum-sensitive ovarian cancer harboring an inactivating TP53 mutation (PMID: 32611648; NCT01357161)||32611648|
|Clinical Trial||Phase||Therapies||Title||Recruitment Status||Covered Countries||Other Countries|