Linoleylethanolamide (CAS 68171-52-8)

Linoleylethanolamide is an inactive analog of anandamide. Linoleylethanolamide is an endocannabinoid detected in porcine brain and murine peritoneal macrophages which contains linoleate in place of the arachidonate moiety of arachidonyl ethanolamide (AEA). It has weak affinity for the cannabinoid 1 (CB1) and CB2 receptors. In addition, linoleoyl ethanolamide increases ERK phosphorylation and AP-1-dependent transcription. However, cellular toxicity is readily apparent at concentrations of 10-20 µM. Linoleylethanolamide inhibits human fatty acid amide hydrolase-dependent hydrolysis of AEA but also is hydrolyzed effectively by the enzyme. Linoleylethanolamide is an N-(long-chain-acyl)ethanolamine that is the ethanolamide of linoleic acid. It has a role as an fatty acid amide hydrolase inhibitor. It is a N-(long-chain-acyl)ethanolamine, a N-(polyunsaturated fatty acyl)ethanolamine and a N-acylethanolamine 18:2. It derives from a linoleic acid. Anandamide (18:2, N-6), also known as linoleamide mea or linoleoylethanolamide, belongs to the class of organic compounds known as n-acylethanolamines. N-acylethanolamines are compounds containing an N-acyethanolamine moiety, which is characterized by an acyl group is linked to the nitrogen atom of ethanolamine. Thus, anandamide (18:2, N-6) is considered to be a fatty amide lipid molecule. Anandamide (18:2, N-6) is considered to be a practically insoluble (in water) and relatively neutral molecule. Anandamide (18:2, N-6) has been primarily detected in blood. Within the cell, anandamide (18:2, N-6) is primarily located in the membrane (predicted from logP). Anandamide (18:2, N-6) can be biosynthesized from linoleic acid.