Arachidonoyl cyclopropylamide (ACPA) is a potent and selective cannabinoid (CB) receptor 1 agonist with Ki values of 2.2 and 715 nM for CB1 and CB2 receptors, respectively. In whole animal experiments, ACPA induces hypothermia in mice with the same efficacy as arachidonoyl ethanolamide (AEA; ), in spite of its higher affinity for the CB1 receptor. These data have been interpreted to indicate that ACEA may be a substrate for fatty acid amide hydrolase (FAAH), and thus only transiently available in whole animal experiments.
A synthetic agonist of the cannabinoid receptor 1 (CB1R). ACPA is considered to be a selective cannabinoid agonist as it binds primarily to the CB1R and has low affinity to the cannabinoid receptor 2
(CB2R).
Potent and selective CB 1 agonist (K i = 2.2 nM). Displays 325-fold selectivity over CB 2 receptors. Active in vivo . Also available in water soluble emulsion (N-(Cyclopropyl)-5Z,8Z,11Z,14Z-eicosatetraenamide ).
This highly selective, synthetic CB1 receptor agonist (FW = 343.55 g/mol; CAS 229021-64-1), also known as arachidonylcyclopropylamide and N(cyclopropyl)-5Z,8Z,11Z,14Z-eicosatetraenamide, targets CB1 cannabinoid receptor agonist (Ki = 2.2 nM) with >325-fold selectivity over CB2 receptors. Two subtypes of the cannabinoid receptor (CB1 and CB2) are expressed in mammalian tissues. Although selective antagonists are available for each of the subtypes, most of the available cannabinoid agonists bind to both CB1 and CB2 with similar affinities. ACPA possesses the characteristics of CB1 receptor agonists, inhibiting forskolininduced cAMP accumulation in Chinese hamster ovary cells expressing the human CB1 receptor. It also increases the binding of [35S]GTPgS to cerebellar membranes and inhibits electrically evoked contractions of the mouse vas deferens. See also ACEA
