This 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 this. Metabolism of AEA by cyclooxygenase-2, leading to formation of prostaglandin ethanolamides, and by lipoxygenases has also been documented as well. This is a potential cytochrome P450 (CYP450) metabolite of AEA, which may be particularly relevant under conditions of FAAH inhibition. Evidence for the formation of 20-HETE ethanolamide in vivo has not been documented.
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