Arachidonoyl ethanolamide (AEA) is an endogenous lipid neurotransmitter with cannabinergic activity, binding both the central cannabinoid (CB1) and peripheral cannabinoid (CB2) receptors. Fatty acid amide hydrolase (FAAH) is the enzyme responsible for the hydrolysis and inactivation of AEA. Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented. 20-HETE ethanolamide is a potential cytochrome P450 metabolite of arachidonoyl ethanolamide, which may be particularly relevant under conditions of fatty acid amide hydrolase inhibition. Evidence for the formation of 20-HETE ethanolamide in vivo has not been documented.