[{"from": "human", "value": "Provide a brief overview of this molecule. [C][C][Branch1][C][C][Branch1][C][C][C][C@H1][C@@][Branch2][Ring2][=Branch2][C@H1][Branch2][Ring1][#Branch1][C@@H1][Branch1][Ring2][N][Ring1][Branch1][C][=Branch1][C][=O][N][C][C][C][C][Branch1][Branch1][C][C][Ring1][=Branch1][O][C][=C][Branch1][#Branch2][C][=Branch1][=Branch1][=C][C][=C][Ring1][=Branch1][Cl][F][C][=C][Branch1][#Branch2][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][Cl][N][C][Ring2][Ring1][#C][=O]"}, {"from": "gpt", "value": "The molecule is an orally available spiro-oxindole HDM2 (human double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, the p53-HDM2 protein-protein interaction inhibitor MI-773 binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteasome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored, which may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival."}]