Cinnabarinic acid (0-100 μM) does not activate mGlu1, mGlu2, mGlu5, mGlu6, mGlu7, and mGlu8 receptors as shown by measurements of [H]InsP formation. In contrast, cinnabarinic acid acts as a partial agonist of mGlu4 receptors by increasing [H]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.
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.