[{"from": "human", "value": "What can you tell me about this molecule? [C][S][=Branch1][C][=O][=Branch1][C][=O][N][C][C][C][=C][Branch2][Ring1][Ring1][N][=C][Branch1][#Branch1][N][=C][Ring1][=Branch1][Ring1][=Branch2][N][C][C][O][C][C][Ring1][=Branch1][C][=C][N][=C][Branch1][Branch1][N][=C][Ring1][=Branch1][N]"}, {"from": "gpt", "value": "The molecule is 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."}]