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Research ArticleMinireview
Open Access

The Pharmacological Case for Cannabigerol

Rahul Nachnani, Wesley M. Raup-Konsavage and Kent E. Vrana
Journal of Pharmacology and Experimental Therapeutics February 2021, 376 (2) 204-212; DOI: https://doi.org/10.1124/jpet.120.000340
Rahul Nachnani
Department of Pharmacology, Penn State College of Medicine, Hershey, Pennsylvania
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Wesley M. Raup-Konsavage
Department of Pharmacology, Penn State College of Medicine, Hershey, Pennsylvania
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Kent E. Vrana
Department of Pharmacology, Penn State College of Medicine, Hershey, Pennsylvania
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  • ORCID record for Kent E. Vrana
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    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.

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    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-THCCBDCBG
    ReceptorAffinityFunctionAffinityFunctionAffinityFunction
    nMnMnM
    CB15.1–80.3 (Ki)a,bPartial agonist1458.5–4900 (Ki)a,bInverse agonist/antagonist440–1045 (Ki)b,c,d,eWeak agonist
    CB23.1–75.3 (Ki)a,bAgonist372.4–4200 (Ki)a,bInverse agonist153.4–1225 (Ki)b,c,d,ePartial agonist
    GPR558 (EC50)fAgonist445 (IC50)fAntagonistN.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).

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    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-THCCBDCBG
    ReceptorAffinityFunctionAffinityFunctionAffinityFunction
    nMnMnM
    TRPA1230a,bAgonist110a,bAgonist700a,b,cAgonist
    TRPV1N.D.a,bUnknown1000a,bAgonist1300a,b,cAgonist
    TRPV2650a,bAgonist1250a,bAgonist1720a,b,cAgonist
    TRPV39500b,dAgonist3700b,dAgonist1000b,dAgonist
    TRPV4850b,dAgonist800b,dAgonist5100b,dAgonist
    TRPM8160a,bAntagonist140a,bAntagonist160a,b,cAntagonist
    ɑ-2 adrenoceptorN.T.UnknownN.T.Unknown0.2–72.8eAgonist
    5-HT1AN.T.UnknownN.D.f,gIndirect agonist51.9d,eAntagonist
    PPARγ2120hAgonist2010hAgonist1270hAgonist
    • 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.

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Journal of Pharmacology and Experimental Therapeutics: 376 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 376, Issue 2
1 Feb 2021
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Research ArticleMinireview

Potential Clinical Uses of CBG

Rahul Nachnani, Wesley M. Raup-Konsavage and Kent E. Vrana
Journal of Pharmacology and Experimental Therapeutics February 1, 2021, 376 (2) 204-212; DOI: https://doi.org/10.1124/jpet.120.000340

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Research ArticleMinireview

Potential Clinical Uses of CBG

Rahul Nachnani, Wesley M. Raup-Konsavage and Kent E. Vrana
Journal of Pharmacology and Experimental Therapeutics February 1, 2021, 376 (2) 204-212; DOI: https://doi.org/10.1124/jpet.120.000340
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