Article Figures & Data
Figures
- Fig. 1.
Biosynthesis pathway of the primary cannabinoids. Cannabinoid biosynthesis begins with the combination of geranyl pyrophosphate and olivetolic acid to form CBGA. CBGA serves as the substrate for the synthesis of Δ9-THCA and CBDA. Decarboxylation of CBGA, Δ9-THCA, and CBDA by heat results in CBG, Δ9-THC, and CBD, respectively. Because CBGA serves as the substrate for the synthesis of the major cannabinoids, very little is typically found in material from Cannabis sp.
Tables
- TABLE 1
Pharmacodynamic properties of Δ9-THC, CBD, and CBG at cannabinoid receptors
Binding affinities for Δ9-THC, CBD, and CBG at the two canonical cannabinoid receptors (CB1 and CB2), as well as a third receptor, GPR55 (commonly referred to as CB3). Δ9-THC acts as an agonist at all three receptors, whereas CBD acts as an antagonist; CBG acts as a weak or partial agonist at CB1 and CB2, and its function at GPR55 is currently unknown.
Δ9-THC CBD CBG Receptor Affinity Function Affinity Function Affinity Function nM nM nM CB1 5.1–80.3 (Ki)a,b Partial agonist 1458.5–4900 (Ki)a,b Inverse agonist/antagonist 440–1045 (Ki)b,c,d,e Weak agonist CB2 3.1–75.3 (Ki)a,b Agonist 372.4–4200 (Ki)a,b Inverse agonist 153.4–1225 (Ki)b,c,d,e Partial agonist GPR55 8 (EC50)f Agonist 445 (IC50)f Antagonist N.T. Unknown N.T., not tested.
a Pertwee (2008).
b Rosenthaler et al. (2014).
c Cascio et al. (2010).
d Pollastro et al. (2011).
e Navarro et al. (2018).
f Ryberg et al. (2007).
- TABLE 2
Pharmacodynamic properties of Δ9-THC, CBD, and CBG at noncannabinoid receptors
Binding affinities for Δ9-THC, CBD, and CBG at TRP ion channels, α-2 adrenoceptors, the serotonin receptor 5-HT1A, and PPARγ are presented. Values are all EC50 for agonists and IC50 for antagonists.
Δ9-THC CBD CBG Receptor Affinity Function Affinity Function Affinity Function nM nM nM TRPA1 230a,b Agonist 110a,b Agonist 700a,b,c Agonist TRPV1 N.D.a,b Unknown 1000a,b Agonist 1300a,b,c Agonist TRPV2 650a,b Agonist 1250a,b Agonist 1720a,b,c Agonist TRPV3 9500b,d Agonist 3700b,d Agonist 1000b,d Agonist TRPV4 850b,d Agonist 800b,d Agonist 5100b,d Agonist TRPM8 160a,b Antagonist 140a,b Antagonist 160a,b,c Antagonist ɑ-2 adrenoceptor N.T. Unknown N.T. Unknown 0.2–72.8e Agonist 5-HT1A N.T. Unknown N.D.f,g Indirect agonist 51.9d,e Antagonist PPARγ 2120h Agonist 2010h Agonist 1270h Agonist N.D., not detected; N.T., not tested.
a De Petrocellis et al., 2011.
b Muller et al., 2019.
c Pollastro et al., 2011.
d Rock et al., 2011.
e Cascio et al., 2010.
f Russo et al., 2005.
g Rock et al., 2012.
h Granja et al., 2012.
In this issue
Potential Clinical Uses of CBG
