O-1918
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| Formula | C19H26O2 |
| Molar mass | 286.415 g·mol−1 |
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O-1918 is a synthetic compound related to cannabidiol, which is an antagonist at two former orphan receptors GPR18 and GPR55, that appear to be related to the cannabinoid receptors. O-1918 is used in the study of these receptors, which have been found to be targets for a number of endogenous and synthetic cannabinoid compounds, and are thought to be responsible for most of the non-CB1, non-CB2 mediated effects that have become evident in the course of cannabinoid research.[1][2][3][4][5]
Subsequent research by using electrophysiological approach has shown that O-1918 is a potent BKCa channel inhibitor.[6][7][8]
See also
[edit]- Abnormal cannabidiol
- Cannabidiol dimethyl ether
- CID-16020046
- CID-85469571
- O-1602
- O-1821
- Tetrahydrocannabiorcol
References
[edit]- ^ Offertáler L, Mo FM, Bátkai S, Liu J, Begg M, Razdan RK, et al. (March 2003). "Selective ligands and cellular effectors of a G protein-coupled endothelial cannabinoid receptor". Molecular Pharmacology. 63 (3): 699–705. doi:10.1124/mol.63.3.699. PMID 12606780.
- ^ Zakrzeska A, Schlicker E, Baranowska M, Kozłowska H, Kwolek G, Malinowska B (June 2010). "A cannabinoid receptor, sensitive to O-1918, is involved in the delayed hypotension induced by anandamide in anaesthetized rats". British Journal of Pharmacology. 160 (3): 574–84. doi:10.1111/j.1476-5381.2009.00579.x. PMC 2931558. PMID 20105178.
- ^ Schuelert N, McDougall JJ (August 2011). "The abnormal cannabidiol analogue O-1602 reduces nociception in a rat model of acute arthritis via the putative cannabinoid receptor GPR55". Neuroscience Letters. 500 (1): 72–6. doi:10.1016/j.neulet.2011.06.004. PMID 21683763. S2CID 3410391.
- ^ Szczesniak AM, Maor Y, Robertson H, Hung O, Kelly ME (October 2011). "Nonpsychotropic cannabinoids, abnormal cannabidiol and canabigerol-dimethyl heptyl, act at novel cannabinoid receptors to reduce intraocular pressure". Journal of Ocular Pharmacology and Therapeutics. 27 (5): 427–35. doi:10.1089/jop.2011.0041. PMID 21770780.
- ^ Caldwell MD, Hu SS, Viswanathan S, Bradshaw H, Kelly ME, Straiker A (June 2013). "A GPR18-based signalling system regulates IOP in murine eye". British Journal of Pharmacology. 169 (4): 834–43. doi:10.1111/bph.12136. PMC 3687663. PMID 23461720.
- ^ Godlewski G, Offertáler L, Osei-Hyiaman D, Mo FM, Harvey-White J, Liu J, et al. (January 2009). "The endogenous brain constituent N-arachidonoyl L-serine is an activator of large conductance Ca2+-activated K+ channels". The Journal of Pharmacology and Experimental Therapeutics. 328 (1): 351–361. doi:10.1124/jpet.108.144717. PMC 2605781. PMID 18923087.
- ^ Bondarenko AI, Panasiuk O, Drachuk K, Montecucco F, Brandt KJ, Mach F (March 2018). "The quest for endothelial atypical cannabinoid receptor: BKCa channels act as cellular sensors for cannabinoids in in vitro and in situ endothelial cells". Vascular Pharmacology. 102: 44–55. doi:10.1016/j.vph.2018.01.004. PMC 6481560. PMID 29355732.
- ^ Bondarenko AI, Panasiuk O, Okhai I, Montecucco F, Brandt KJ, Mach F (June 2017). "Direct activation of Ca2+ and voltage-gated potassium channels of large conductance by anandamide in endothelial cells does not support the presence of endothelial atypical cannabinoid receptor". European Journal of Pharmacology. 805: 14–24. doi:10.1016/j.ejphar.2017.03.038. PMC 6520242. PMID 28327344.