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- B2d7b4af77fc34c1b5042d4e165ee04ea NCIT_P378 "NCI" @default.
- B2d7b4af77fc34c1b5042d4e165ee04ea type Axiom @default.
- B2d7b4af77fc34c1b5042d4e165ee04ea annotatedProperty IAO_0000115 @default.
- B2d7b4af77fc34c1b5042d4e165ee04ea annotatedSource NCIT_C158603 @default.
- B2d7b4af77fc34c1b5042d4e165ee04ea annotatedTarget "An orally bioavailable inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. Upon administration, izorlisib selectively binds to and inhibits PIK3CA and its mutated forms in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, izorlisib may be more efficacious and less toxic than pan-PI3K inhibitors. In addition, izorlisib also targets mutated forms of PI3K gamma (PI3Kg). It may also stimulate the immune system to restore CD8+ T-cell activation and cytotoxicity. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K. In most solid tumors, the activation of the PI3K pathway is induced by mutations of PIK3CA." @default.