[{"from": "human", "value": "Could you provide a description of this molecule? [C][C][=C][N][Branch2][Ring1][Ring2][C][=C][C][=C][C][=Branch1][=Branch1][=C][Ring1][=Branch2][Ring1][=Branch1][/C][=C][/C][=Branch1][C][=O][O][C][=Branch1][C][=O][C][=C][Branch2][Ring1][Branch1][O][N][=C][Ring1][Branch1][C][=C][Branch1][O][C][=C][Branch1][=Branch1][C][=C][Ring1][=Branch1][Cl][Cl][Cl][C][Branch1][C][C][Branch1][C][C][F]"}, {"from": "gpt", "value": "The molecule is an orally available inhibitor of isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble) mutant forms, including substitution mutations at the arginine in position 132, IDH1(R132) (IDH1-R132), with potential antineoplastic activity. Upon oral administration, safusidenib specifically binds to and inhibits certain mutant forms of IDH1, thereby inhibiting the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH1 mutations. IDH1(R132) mutations are highly expressed in certain malignancies, including gliomas; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG. Safusidenib minimally targets and affects wild-type IDH1, which is expressed in normal, healthy cells."}]