[{"from": "human", "value": "Describe this molecule. [C][=C][C][=Branch1][=Branch2][=C][C][=Branch1][Ring2][=C][Ring1][=Branch1][Cl][C][=C][C][=Branch2][Ring1][Ring1][=C][Branch1][Branch1][N][=C][Ring1][=Branch1][C][=Branch1][C][=O][N][C][C][=Branch1][C][=O][O][O]"}, {"from": "gpt", "value": "The molecule is anemia, caused primarily by the inability of the kidney to respond to anemic conditions with a corresponding increase in [erythropoietin] (EPO) production. Treatment of anemia of chronic kidney disease (CKD) has traditionally involved the administration of exogenous erythropoiesis-stimulating agents (ESAs), such as [darbepoetin alfa], to counter the decrease in endogenous EPO production. While efficacious, the overuse of ESAs has been associated with cardiovascular complications, progression of CKD, and increases in overall mortality.  A relatively new and alternative treatment option for patients with anemia of CKD are small molecule inhibitors of hypoxia-inducible factor prolyl-hydroxylase (HIF-PH). These agents inhibit prolyl-hydroxylase domain oxygen sensors, which essentially mimics hypoxic conditions and activates hypoxia-inducible factor, a transcription factor that serves a multitude of roles, including the stimulation erythropoiesis.  Vadadustat is an orally administered inhibitor of hypoxia-inducible factor prolyl-hydroxylase (HIF-PH) which is currently approved in Japan for the treatment for anemia due to CKD in both dialysis-dependent and non-dialysis dependent adult patients, and is currently awaiting a regulatory decision by the FDA for the same indication. The safety and efficacy of vadadustat have been shown to be non-inferior to darbepoetin alfa in patients with anemia of CKD undergoing dialysis, but it did not meet the prespecified noninferiority criterion for cardiovascular safety in a similar study in patients with non-dialysis-dependent CKD."}]