MAGL (Monoacylglycerol Lipase)
The primary enzyme responsible for degrading 2-arachidonoylglycerol (2-AG) in the brain. A therapeutic target for increasing endocannabinoid tone.
In Depth
MAGL accounts for approximately 85% of 2-AG hydrolysis in the brain. MAGL inhibitors (e.g., JZL184, MJN110) increase 2-AG levels and have shown analgesic, anti-inflammatory, and neuroprotective effects in preclinical models. Unlike FAAH inhibitors, MAGL inhibitors also reduce arachidonic acid levels, which may contribute to anti-inflammatory effects through reduced prostaglandin synthesis. MAGL inhibition is being explored for pain, neurodegeneration, and cancer.
Related Terms
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.