Kynurenicacid, an active metabolite of tryptophan, is synthesized through a kynurenine intermediate by kynurenine aminotransferases (KATs). It acts as an antagonist of both NMDA and AMPA receptors, as well as α7 nicotinic acetylcholine receptors (nAChRs; EC50s = 235, 101, and 7 µM, respectively), and functions as an agonist for the aryl hydrocarbon receptor (AhR) and G protein-coupled receptor 35 (GPR35; EC50s = 1.4 and 39 µM, respectively). In a neonatal rat model of cerebral hypoxic-ischemia, induced by carotid artery ligation, administration of kynurenicacid at 300 mg kg prevents weight loss in the lesioned hemisphere. Additionally, at concentrations of 1 and 5 mg ml, it protects against neurodegeneration in the rhabdomere of the eye in an Htt93QtransgenicDrosophila model of Huntington's disease. Elevated levels of kynurenicacid in the cerebrospinal fluid have been observed in patients with schizophrenia.
7-Chlorokynurenicacid sodium salt (7-CKA sodium salt) is a potent and selective antagonist of the glycine B coagonist site of the NMDA receptor (IC50: 0.56 μM). It is also a potent inhibitor of the reuptake of glutamate into synaptic vesicles (Ki: 0.59 μ
Kynurenine sulfate monohydrate is a precursor of kynurenicacid which is the only recognized endogenous excitatory amino acid receptor antagonist agent in the central nervous system. L-Kyn is known to be a pigment generating component in animals. In mamma