FAAH (Fatty Acid Amide Hydrolase)
The primary enzyme responsible for degrading anandamide and other fatty acid amides. A key target for increasing endocannabinoid tone.
In Depth
FAAH inhibition raises anandamide levels without directly activating cannabinoid receptors, potentially offering therapeutic benefits with a more favorable side-effect profile than direct CB1 agonists. FAAH inhibitors (e.g., PF-04457845) have shown promise in preclinical anxiety and pain models. A tragic clinical trial in France in 2016 involving a FAAH inhibitor (BIA 10-2474) resulted in one death and several neurological injuries, highlighting the complexity of ECS modulation.
Related Terms
Further Reading
More in Pharmacology
Endocannabinoid System (ECS)
A lipid-based retrograde neurotransmitter system comprising endogenous cannabinoids (endocannabinoids), their receptors (CB1, CB2), and metabolic enzymes.
CB1 Receptor
Cannabinoid receptor type 1. A G protein-coupled receptor (GPCR) primarily expressed in the central nervous system. The primary target of THC's psychoactive effects.
CB2 Receptor
Cannabinoid receptor type 2. A GPCR primarily expressed in immune tissues and peripheral organs. Less abundant in the CNS than CB1.
Anandamide (AEA)
N-arachidonoylethanolamine. The first endocannabinoid identified. A partial agonist at CB1 and CB2 receptors, named from the Sanskrit word "ananda" meaning bliss.
2-Arachidonoylglycerol (2-AG)
The most abundant endocannabinoid in the brain. A full agonist at both CB1 and CB2 receptors.