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. 2022 Mar 28;11(7):1142. doi: 10.3390/cells11071142

Figure 1.

Figure 1

Cannabinoids and their affinities to the classical cannabinoid CB1 and CB2 receptors and to other receptors sensitive to cannabinoids, as well as to inhibitors of enzymes involved in the synthesis and/or degradation of AEA and 2-AG. Note that the numbers in the superscript indicate the appropriate reference [15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38]. The figure presents only phytocannabinoids (green font), synthetic cannabinoids and other compounds discussed in this article (black font), endogenous cannabinoids (pink font) and inhibitors of the endocannabinoid synthesis and degradation (blue font) that have been considered in this review. ECS, endocannabinoid system; the “plus sign” indicates agonism and the “minus sign” antagonism, inverse agonism or inhibition versus the respective receptors/enzymes. The intensity of blue color next to the compound is higher the lower the values of Ki, IC50 or EC50 are (expressed in nM). Based on Pertwee et al. [39] unless stated otherwise (superscript). WIN55212-3, inactive S(–)enantiomer of WIN55212-2 [40]; AM404, an inhibitor of anandamide transport [41]. Abbreviations: Δ9-THC, Δ9-tetrahydrocannabinol; 2-AG, 2-arachidonoylglycerol; abn-CBD, abnormal cannabidiol; ACEA, arachidonoyl-2’-chlorethylamide; ACPA, arachidonylcyclopropylamide; AEA, anandamide; CB1, cannabinoid CB1 receptor; CB2, cannabinoid CB2 receptor; CBD, cannabidiol; DAGL, diacylglycerol lipase; ECS, endocannabinoid system; FAAH, fatty-acid amide hydrolase; GPR18, G protein-coupled receptor 18; GPR55, G protein-coupled receptor 55; LPI, L-alpha-lysophosphatidylinositol; MethAEA, methanandamide; n.d., not determined; OEA, oleoylethanolamide; PEA, palmitoylethanolamide; TRPV1 transient receptor-potential cation-channel subfamily V member 1; URB597, inhibitor of fatty-acid amide hydrolase.