[{"from": "human", "value": "Provide a description of this molecule. [C][C][C][=C][Branch2][Ring2][O][C][=C][Branch2][Ring1][S][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][C][N][C][C][N][Branch1][Branch1][C][C][Ring1][=Branch1][C][=N][C][=C][Branch1][Branch1][C][=C][Ring1][=Branch1][C][#N][N][C][Ring2][Ring1][=Branch2][=O][N][C][Ring2][Ring1][=C]"}, {"from": "gpt", "value": "The molecule is an orally bioavailable second-generation inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) type 1 (PARP1) and 2 (PARP2) and tankyrase (TNK; TNKS; TANK) 1 and 2, with potential chemo/radiosensitizing and antineoplastic activities. Upon oral administration, nesuparib selectively and simultaneously targets and binds to PARP1/2 and TNK1/2. Inhibiting PARP activity prevents PARP-mediated DNA repair of single-strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. This may enhance the cytotoxicity of DNA-damaging agents. Inhibiting TNK activity blocks the tankyrase-mediated poly(ADP-ribosyl)ation of multiple target proteins including various tumor suppressors. This may include the blockage of the poly(ADP-ribosyl)ation and destabilization of AXIN, a negative regulator of beta-catenin, thereby stabilizing AXIN. This prevents Wnt/beta-catenin signaling and may inhibit the activation of transcription of a wide range of Wnt/beta-catenin target genes. This may suppress proliferation of cancer cells in which Wnt/beta-catenin signaling is overactivated. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks. The PARP-mediated repair pathway is dysregulated in a variety of cancer cell types. TNK, a member of the PARP family, plays an important role in the regulation of the Wnt/beta-catenin signaling pathway."}]