Termination of the anandamide (arachidonoylethanolamide, an endocannabinoid) signaling in the central nervous system and in peripheral tissues is mediated by the fatty acid amide hydrolase (FAAH; EC 188.8.131.52), an integral membrane serine hydrolase that degrades the fatty acid amide family of signaling lipids. Genetic or pharmacological inactivation of FAAH leads to analgesic and anti-inflammatory phenotypes in rodents without showing the undesirable side effects observed with direct cannabinoid receptor agonists, indicating that FAAH may represent an attractive therapeutic target for the treatment of inflammatory pain and other nervous system disorders.
 D.G. Deutsch, N. Ueda, S. Yamamoto. The fatty acid amide hydrolase (FAAH). Prost. Leuk. Ess. Fat. Ac. 2002, 66, 201-210.
 D.S.Johnson et al. Discovery of PF-04457845: A Highly Potent, Orally Bioavailable, and Selective Urea FAAH Inhibitor.ACS Med. Chem. Lett. 2011, 2, 91-96.