It has been shown that the actions of abnormal cannabidiol are mediated through a site separate from the
CB1 and
CB2 receptors,[2][3] which responds to abnormal cannabidiol,
O-1602, and the
endogenous ligands:
anandamide (AEA),
N-arachidonoyl glycine (NAGly) and
N-arachidonoyl L-serine.[2][4][5][6] Multiple lines of evidence support the proposed identification of this novel target in
microglia as the previously "orphan" receptor
GPR18.[2] Another possible target of abnormal cannabidiol is
GPR55, which has also received much attention as a putative cannabinoid receptor,[7][8] although a growing body of evidence points to
lysophosphatidylinositol (LPI) as the
endogenous ligand for GPR55.[9][10] Further research suggests there are yet more additional cannabinoid receptors.[11][12][13][14]
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.[15]
^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.
PMID12606780.
^McHugh D, Tanner C, Mechoulam R, Pertwee RG, Ross RA (February 2008). "Inhibition of human neutrophil chemotaxis by endogenous cannabinoids and phytocannabinoids: evidence for a site distinct from CB1 and CB2". Molecular Pharmacology. 73 (2): 441–450.
doi:
10.1124/mol.107.041863.
PMID17965195.
S2CID15182303.
^Kreutz S, Koch M, Böttger C, Ghadban C, Korf HW, Dehghani F (February 2009). "2-Arachidonoylglycerol elicits neuroprotective effects on excitotoxically lesioned dentate gyrus granule cells via abnormal-cannabidiol-sensitive receptors on microglial cells". Glia. 57 (3): 286–294.
doi:
10.1002/glia.20756.
PMID18837048.
S2CID37531270.