Background:

IC50: 1.8, 1.4 and 2.4 μM for mouse, rat and human FAAH, respectively

Biochanin A is a natural inhibitor of fatty acid amide hydrolase. Inhibitors of fatty acid amide hydrolase (FAAH), which responsible for the metabolism of the endogenous cannabinoid (CB) receptor ligand anandamide (AEA), are effective in a number of animal models of pain.

In vitro: Biochanin A was found to be the most promising candidate. Biochanin A inhibited the hydrolysis of 0.5 mM AEA by mouse, rat and human FAAH with IC50 values of 1.8, 1.4 and 2.4 μM respectively. Biochanin A was found to not interact to any extent with CB1 or CB2 receptors, nor with FAAH-2 [1].

In vivo: In anaesthetized mice, both URB597 and biochanin A inhibited the spinal phosphorylation of extracellular signal-regulated kinase caused by the intraplantar injection of formalin. The effects of both URB597 and biochanin A were found to be significantly reduced by the CB1 receptor antagonist/inverse agonist AM251. In addition, in the tetrad test, biochanin A did not increase brain AEA concentrations, but produced a modest potentiation of the effects of 10 mg·kg-1 i.v. AEA [1].

Clinical trial: N/A

Reference:
[1] Thors L,Burston JJ,Alter BJ,McKinney MK,Cravatt BF,Ross RA,Pertwee RG,Gereau RW 4th,Wiley JL,Fowler CJ.  Biochanin A, a naturally occurring inhibitor of fatty acid amide hydrolase. Br J Pharmacol.2010 Jun;160(3):549-60.