Arachidoyl Ethanolamide (Synonyms: N-Arachidoylethanolamine)

The endocannabinoids present a rich system of central cannabinoid (CB1), peripheral cannabinoid (CB2), and non-CB receptor-mediated pharmacology that has stimulated research in many fields including memory, weight loss and appetite, neurodegeneration, tumor surveillance, analgesia, and inflammation.[1][2] Arachidoyl ethanolamide is one of the saturated fatty acyl ethanolamides devoid of classical (CB1/CB2) activity. Arachidoyl ethanolamide does not bind to the murine CB1 receptor [3]  and does not compete with anandamide as a substrate for the endocannabinoid hydrolytic enzyme fatty acid amide hydrolase. [4] Non-CB receptor-mediated pharmacology of the saturated ethanolamides is still being elucidated.[5]

Reference:
[1]. Martin, B.R., Mechoulam, R., and Razdan, R.K. Discovery and characterization of endogenous cannabinoids. Life Sciences 65, 573-595 (1999).
[2]. Pertwee, R.G. Pharmacology of cannabinoid receptor ligands. Curr. Med. Chem. 6(8), 635-664 (1999).
[3]. Sheskin, T., Hanus, L., Slager, J., et al. Structural requirements for binding of anandamide-type compounds to the brain cannabinoid receptor. Journal of Medicinal Chemistry 40, 659-667 (1997).
[4]. Desarnaud, F., Cadas, H., and Piomelli, D. Anandamide amidohydrolase activity in rat brain microsomes. Identification and partial characterization. The Journal of Biological Chemisty 270(11), 6030-6035 (1995).
[5]. Smart, D., Jonsson, K.O., Vandevoorde, S., et al. “Entourage” effects of N-acyl ethanolamines at human vanilloid receptors. Comparison of effects upon anandamide-induced vanilloid receptor activation and upon anandamide metabolism. British Journal of Pharmacology 136, 452-458 (2002).