CAS NO: | 53847-30-6 |
规格: | 95% |
分子量: | 378.55 |
包装 | 价格(元) |
1mg | 电议 |
5mg | 电议 |
10mg | 电议 |
25mg | 电议 |
C23H38O4
CAS:53847-30-6
分子式:C23H38O4
分子量:378.55
纯度:95%
存储:Store at -20°C
Background:
2-Arachidonoyl glycerol (2-AG) is an endogenous agonist of the cannabinoid (CB) receptors CB1 and CB2 (Kis = 25.3-472 and 145-1,400 nM, respectively).[1],[2],[3] Unlike arachidonoyl ethanolamide, 2-AG is present at relatively high levels in the central nervous system and is the most abundant molecular species of monoacylglycerol (MAG) found in rat brain.[1],[4] Formation of 2-AG is calcium-dependent and is mediated by the activities of phospholipase C (PLC) and diacylglycerol (DAG) lipase.1 2-AG acts as a full agonist at the CB1 receptor. At a concentration of 0.3 nM, 2-AG induces a rapid, transient increase in intracellular free calcium in NG108-15 neuroblastoma X glioma cells through a CB1 receptor-dependent mechanism.2 2-AG is metabolized in vitro by MAG lipase and fatty acid amide hydrolase (FAAH), with MAG lipase likely being the principle metabolizing enzyme in vivo.[5]
Reference:
[1]. Stella, N., Schweitzer, P., and Piomelli, D. A second endogenous cannabinoid that modulates long-term potentiation. Nature 388(6644), 773-778 (1997).
[2]. Sugiura, T., Kodaka, T., Nakane, S., et al. Evidence that the cannabinoid CB1 receptor is a 2-arachidonoylglycerol receptor. Structure-activity relationship of 2-arachidonoylglycerol, ether-linked analogues, and related compounds. J. Biol. Chem. 274(5), 2794-2801 (1999).
[3]. Pertwee, R.G. Pharmacology of cannabinoid receptor ligands. Curr. Med. Chem. 6(8), 635-664 (1999).
[4]. Kondo, S., Kondo, H., Nakane, S., et al. 2-Arachidonoylglycerol, an endogenous cannabinoid receptor agonist: Identification as one of the major species of monoacylglycerols in various rat tissues, and evidence for its generation through Ca2+-dependent and -independent mechanisms. FEBS Letters 429(2), 152-156 (1998).
[5]. Dinh, T.P., Carpenter, D., Leslie, F.M., et al. Brain monoglyceride lipase participating in endocannabinoid inactivation. Proceedings of the National Academy of Sciences of the United States of America 99(16), 10819-10824 (2002).