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O-1918

Chemical compound

Chemical compound

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.

Subsequent research by using electrophysiological approach has shown that O-1918 is a potent BKCa channel inhibitor.

References

References

  1. (March 2003). "Selective ligands and cellular effectors of a G protein-coupled endothelial cannabinoid receptor". Molecular Pharmacology.
  2. (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.
  3. (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.
  4. (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.
  5. (June 2013). "A GPR18-based signalling system regulates IOP in murine eye". British Journal of Pharmacology.
  6. (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.
  7. (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.
  8. (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.
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