[{"from": "human", "value": "Provide a description of this molecule. [C][C][O][C][=C][Branch1][Ring2][O][Ring1][=Branch1][C][=C][Branch1][Branch1][C][=N][Ring1][#Branch1][S][=Branch1][C][=O][=Branch1][C][=O][N][C][C][=C][Branch1][Ring2][C][Ring1][Branch1][C][N][Branch1][Ring2][C][Ring1][=Branch1][C][=Branch1][C][=O][C@H1][Branch1][Ring1][C][O][C][=C][C][=C][C][=C][Ring1][=Branch1]"}, {"from": "gpt", "value": "The molecule is an orally available, small-molecule allosteric activator of the selective red blood cell (RBC) isoform of pyruvate kinase (PK-R), with potential to improve symptoms in sickly cell disease (SCD) patients. Upon oral administration, etavopivat allosterically binds to and activates PK-R, thereby enhancing the glycolytic pathway activity in RBCs. This improves adenosine triphosphate (ATP) levels and reduces 2,3-diphosphoglycerate (2,3-DPG) levels in RBCs. This results in increased oxygen affinity, improved RBC deformability, decreased sickle RBC hemolysis, increased hemoglobin (Hb) levels and improved RBC membrane function. Mutations in PK-R cause deficiency in PK-R which prevents adequate RBC glycolysis, leading to a buildup of the upstream glycolytic intermediate 2,3-DPG and deficiency in the PK-R product ATP."}]