Background
N-Acyl ethanolamines (NAEs) have diverse biological actions that are strongly affected by the associated acyl group. Linoleoyl ethanolamide (LOEA) has potential signaling roles in aging and neurological functioning.1,2 LOEA has a weak affinity for cannabinoid (CB) receptors (Ki = 10, 25 μM for CB1, CB2, respectively) and inhibits voltage-gated K+ channels.3,4 LOEA also inhibits fatty acid amide drolase (FAAH; Ki = 9 μM) and is drolyzed by FAAH.5,6 (R)-(?)-Linoleyl-2’-droxy-1’-propylamide is a homolog of LOEA which is characterized by the addition of an (R)-β-metl group at the terminal ethanolamine carbon. A similar modification of arachidonoyl ethanolamide to produce R-2 methanandamide imparts diminished affinity for the CB receptor as well as reduced metabolic stability.7 The psiological actions of this compound have not been evaluated.
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