Cinnabarinic acid 

Cinnabarinic acid is a specific orthosteric agonist of mGlu₄ by interacting with residues of the glutamate binding pocket of mGlu4, has no activity at other mGlu receptors. Cinnabarinic acid is an endogenous metabolite of the kynurenine pathway of tryptophan. Cinnabarinic acid induces cell apoptosis^[1].

Cinnabarinic acid (0-100 μM) does not activate mGlu1, mGlu2, mGlu5, mGlu6, mGlu7, and mGlu8 receptors as shown by measurements of [³H]InsP formation. In contrast, cinnabarinic acid acts as a partial agonist of mGlu4 receptors by increasing [³H]InsP formation by approximately 35% at 100 μM, which is 5-fold less efficacious than ACPT-I in activating mGlu4 receptors in HEK293 cells transiently transfected with rat mGlu1, -2, -4, -5, -6, -7, or -8 receptors^[1].
Cinnabarinic acid (0-100 μM) reduces cAMP formation in a concentration-dependent manner with an excellent potency and efficacy. At 30 μM, cinnabarinic acid is effective at 30 μM, and substantially inhibits cAMP formation in cultured cerebellar granule cells^[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

300.22

C₁₄H₈N₂O₆

606-59-7

O=C(C1=C(N)C(C=C2OC3=C(N=C21)C(C(O)=O)=CC=C3)=O)O

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. F Fazio, et al. Cinnabarinic acid, an endogenous metabolite of the kynurenine pathway, activates type 4 metabotropic glutamate receptors.Mol Pharmacol. 2012 May;81(5):643-56.  [Content Brief]

  [2]. Martina Ulivieri, et al. The Trace Kynurenine, Cinnabarinic Acid, Displays Potent Antipsychotic-Like Activity in Mice and Its Levels Are Reduced in the Prefrontal Cortex of Individuals Affected by Schizophrenia. Schizophr Bull. 2020 Jun 7;sbaa074.  [Content Brief]

  [3]. Francesco Fazio, et al. Cinnabarinic acid and xanthurenic acid: Two kynurenine metabolites that interact with metabotropic glutamate receptors. Neuropharmacology. 2017 Jan;112(Pt B):365-372.  [Content Brief]