[{"from": "human", "value": "Provide a description of this molecule. [C][C][N][Branch1][=Branch1][C][C@@H1][Ring1][Branch1][O][C][=C][Branch2][Ring1][P][C][=C][Branch1][Branch1][C][=N][Ring1][=Branch1][C][=Branch1][C][=O][N][C][=C][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][O][C][Branch1][C][F][Branch1][C][F][Cl][C][=C][C][=N][N][Ring1][Branch1].[Cl]"}, {"from": "gpt", "value": "The molecule is the hydrochloride salt form of asciminib, an orally bioavailable, allosteric Bcr-Abl1 tyrosine kinase inhibitor, with antineoplastic activity. Upon administration, asciminib targets and binds to the myristoyl pocket of the Bcr-Abl1 fusion protein at a location that is distinct from the ATP-binding domain, thereby inhibiting the activity of both wild-type Bcr-Abl and certain mutation forms, including the T315I mutation. This binding results in the inhibition of Bcr-Abl1-mediated proliferation and enhanced apoptosis of Philadelphia chromosome-positive (Ph+) hematological malignancies. The Bcr-Abl1 fusion protein tyrosine kinase is an abnormal enzyme produced by leukemia cells that contain the Philadelphia chromosome."}]