[2][4] Monoacylglycerol lipase catalyzes a reaction that uses water molecules to break the glycerol monoesters of long-chain fatty acids: It functions together with hormone-sensitive lipase (LIPE) to hydrolyze intracellular triglyceride stores in adipocytes and other cells to fatty acids and glycerol.

The contribution of MAGL to total brain 2-AG hydrolysis activity has been estimated to be ~85% (ABHD6 and ABHD12 are responsible for ~4% and ~9%, respectively, of the remainder),[8][9] and this in vitro estimate has been confirmed in vivo by the selective MAGL inhibitor JZL184.

[10] Chronic inactivation of MAGL results in massive (>10-fold) elevations of brain 2-AG in mice, along with marked compensatory downregulation of CB1 receptors in selective brain areas.

[11] MAGL enzyme inhibitors, for instance URB-602, URB-754, and JZL-184, produce cannabinoid-like behavioral effects in mice.

[10] Further examples include:[12] As well as the following compounds which are under pharmaceutical development: This article incorporates text from the United States National Library of Medicine, which is in the public domain.