n-acylethanolamines

Pentadecanoyl ethanolamide, a derivative of the endogenous lipid amides (N-acylethanolamines), demonstrates anticonvulsant efficacy in electroshock-induced seizures in mice, exhibiting minimal toxicity [1].

N-Acylethanolamines (NAEs) are lipid-derived signaling compounds, with arachidonoyl ethanolamide functioning as an endogenous cannabinoid (CB) that activates CB1 and CB2 receptors. Among these, Palmitoleoyl Ethanolamide (POEA) is synthesized endogenously from palmitoleic acid. Notably, unlike arachidonoyl ethanolamide and palmitoyl ethanolamide, POEA lacks antinociceptive effects in the formalin-evoked pain model.

Linoleoyl ethanolamide phosphate is an intermediate in the biosynthesis of linoleoyl ethanolamide, generated through phospholipase C-mediated hydrolysis of N-acylphosphatidylethanolamine. Linoleoyl ethanolamide phosphate, along with other endogenous N-acylethanolamines, is thought to regulate food intake by selectively prolonging feeding latency and post-meal interval [Linoleoyl Ethanolamide Phosphate].

LEI-401 is a selective and potent NAPE-PLD inhibitor that crosses the blood-brain barrier (IC50: 27 nM).LEI-401 reduces the level of n-acylethanolamines (NAEs) in the brain of free-ranging mice and modulates their emotional behaviour.

PDP-EA is an activator of fatty acid amide hydrolase(FAAH) and enhances the amidohydrolase activity of FAAH.