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].
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.
AM-3102 is an OEA analog that stimulates PPARα transcriptional activity and prolongs feeding latency. It is resistant to enzymatic hydrolysis and is as potent as OEA in enhancing transcriptional activity of PPARα and reducing food intake in free-feeding r