[{"from": "human", "value": "Could you give me a brief overview of this molecule? [C][O][C][=Branch1][C][=O][N][C][=N][C][=C][Branch1][#C][C][=Branch1][Ring2][=C][Ring1][=Branch1][C][Branch1][C][F][Branch1][C][F][F][C][=N][N][C][=C][Branch2][Ring1][Ring1][C][=C][Ring1][Branch1][C][=Branch1][Ring2][=N][Ring1][=Branch2][N][C][C][O][C][C][Ring1][=Branch1][C][N][C][C][N][Branch1][Branch1][C][C][Ring1][=Branch1][S][=Branch1][C][=O][=Branch1][C][=O][C]"}, {"from": "gpt", "value": "The molecule is an orally bioavailable selective inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. Upon administration, PI3Kalpha inhibitor CYH33 selectively targets, binds to and inhibits wild-type 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, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. 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."}]