Abnormal cannabidiol

Receptor activity

It has been shown that the actions of abnormal cannabidiol are mediated through a site separate from the CB1 and CB2 receptors, which responds to abnormal cannabidiol, O-1602, and the endogenous ligands: anandamide (AEA), N-arachidonoylglycine (NAGly) and N-arachidonoyl-L-serine. Multiple lines of evidence support the proposed identification of this novel target in microglia as the previously orphan receptor GPR18. Another possible target of abnormal cannabidiol is GPR55, which has also received much attention as a putative cannabinoid receptor, although a growing body of evidence points to lysophosphatidylinositol (LPI) as the endogenous ligand for GPR55. Further research suggests there are yet more additional cannabinoid receptors.

Pharmacodynamics

Research of the effects on abnormal cannabidiol in mice has indicated that atypical cannabinoids have therapeutic potential in a variety of inflammatory conditions, including those of the gastrointestinal tract. After inducing colitis by means of trinitrobenzene sulfonic acid, wound healing of both human umbilical vein endothelial and epithelial cells was enhanced by the Abn-CBD.

References

References

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11. (January 2009). "The GPR55 ligand L-alpha-lysophosphatidylinositol promotes RhoA-dependent Ca2+ signaling and NFAT activation". FASEB Journal.
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15. (February 2009). "2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal-cannabidiol-sensitive receptors on microglial cells". Glia.
16. (2016). "Abnormal cannabidiol attenuates experimental colitis in mice, promotes wound healing and inhibits neutrophil recruitment". Journal of Inflammation.