CBG is a non-psychoactive cannabinoid with therapeutic potential in cancer, Huntington's Disease, eating disorders, gastrointestinal inflammation, glaucoma and Psoriasis.

Chemical Name: 
Wikipedia entry: 
Synthetic Pathways: 

CBG is synthesized through decarboxylation of CBGA.

Literature Discussion: 


CBG activates α2-adrenoceptors and CB2 and blocks CB1 and 5-HT1A receptors (Cascio, Gauson, Stevenson, Ross, & Pertwee, 2010).

Also, CBG activates TRPA1, TRPV1 and TRPV2, antagonizes TRPM8 and inhibits ACU. Botanical drug substance (BDS) containing CBD also inhibits MAGL and NAAA. These receptor interactions suggest that CBG could have analgesic, anti-inflammatory and anti-cancer properties (De Petrocellis et al., 2008, 2011).

CBG modulates GPR55 (Morales, Hurst, & Reggio, 2017)

CBG has antifungal and antibacterial properties (Eisohly, Turner, Clark, & Eisohly, 1982).

CBG counteracts oxidative stress through CB2 receptors (Giacoppo et al., 2017).

CBG inhibits platelet aggregation, which increases bleeding time and reduces thromboembolism (Formukong, Evans, & Evans, 1989).


CBG causes hyperphagia in animals without producing negative neuromotor side effects (Brierley, Samuels, Duncan, Whalley, & Williams, 2016).  Also, CBG-BDS acts as an appetite stimulant, probably through CB1 receptors (Brierley, Samuels, Duncan, Whalley, & Williams, 2017).


CBG inhibits cellular growth in human oral epitheloid carcicoma cells (Baek et al., 1998) and showed chemopreventive, curative and pro-apoptotic effects against colorectal cancer cells in vitro and in vivo models through TRPM8 and CB2 receptors (Borrelli et al., 2014).


CBG and related cannabinoids may have therapeutic potential for the treatment of glaucoma.(Colasanti, 1990). Chronic administration of CBG causes ocular hypotensive effects without any toxic effects (Colasanti, Craig, & Allara, 1984). Also, its analog CBG-DMH reduces intraocular pressure (Szczesniak, Maor, Robertson, Hung, & Kelly, 2011).


CBG reduces acetylcholine-induced contractions in the bladder, suggesting a potential effect to treat bladder disorders (Pagano et al., 2015).


CBG can activate α2 receptors and block CB1 and 5-HT1A receptors (Cascio et al., 2010), suggesting CBG does have therapeutic potential in the treatment of depression.

Functional Gastro-Intestinal Disorders

Apart from THC, (relatively) non-psychotropic cannabinoids such as THCVCBD and CBG were found to have anti-inflammatory effects in experimental intestinal inflammation (Alhouayek and Muccioli, 2012). CBG attenuates colitis in animal models, reduces nitric oxide production in macrophages and reduces ROS formation in intestinal epithelial cells, showing therapeutic potential to treat gastrointestinal inflammation (Borrelli et al., 2013).


CBG counteracts the anti-nausea effects produced by THC or CBD, probably due to the activation of 5-HT1A receptor (Rock et al., 2011). This is important to avoid CBG when looking for anti-nausea and anti-vomiting effects of cannabinoids.


CBG improved motor deficits and had neuroprotective effects in animal models of Huntington´s Disease through the modulation of pro-inflammatory markers, reactive microgliosis and improved antioxidant defenses. CBG also normalized gene expression altered in those animal models (Valdeolivas et al., 2015).


The interaction between CBG and the α2 receptor (alpha 2 adrenalin receptor) may prove effective in pain control (Giovannoni et al., 2009).


CBG could be used to treat Psoriasis (Wilkinson & Williamson, 2007) and it shows potential to treat dry-skin syndrome by increasing sebaceous lipid synthesis (Oláh et al., 2016).


Alhouayek, M., and Muccioli, G.G. (2012). The endocannabinoid system in inflammatory bowel diseases: from pathophysiology to therapeutic opportunity. Trends Mol. Med. 18, 615–625.

Baek, S. H., Kim, Y. O., Kwag, J. S., Choi, K. E., Jung, W. Y., & Han, D. S. (1998). Boron trifluoridetherate on silica-A modified Lewis acid reagent (VII). Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research, 21(3), 353-356.

Borrelli, F., Fasolino, I., Romano, B., Capasso, R., Maiello, F., Coppola, D., … Izzo, A. A. (2013). Beneficial effect of the non-psychotropic plant cannabinoid cannabigerol on experimental inflammatory bowel disease. Biochemical Pharmacology, 85(9), 1306-1316. https://doi.org/10.1016/j.bcp.2013.01.017

Borrelli, F., Pagano, E., Romano, B., Panzera, S., Maiello, F., Coppola, D., … Izzo, A. A. (2014). Colon carcinogenesis is inhibited by the TRPM8 antagonist cannabigerol, a Cannabis-derived non-psychotropic cannabinoid. Carcinogenesis, 35(12), 2787-2797. https://doi.org/10.1093/carcin/bgu205

Brierley, D. I., Samuels, J., Duncan, M., Whalley, B. J., & Williams, C. M. (2016). Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats. Psychopharmacology, 233(19-20), 3603-3613. https://doi.org/10.1007/s00213-016-4397-4

Brierley, D. I., Samuels, J., Duncan, M., Whalley, B. J., & Williams, C. M. (2017). A cannabigerol-rich Cannabis sativa extract, devoid of [INCREMENT]9-tetrahydrocannabinol, elicits hyperphagia in rats. Behavioural Pharmacology. https://doi.org/10.1097/FBP.0000000000000285

Cascio, M. G., Gauson, L. A., Stevenson, L. A., Ross, R. A., & Pertwee, R. G. (2010). Evidence that the plant cannabinoid cannabigerol is a highly potent alpha2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist. British Journal of Pharmacology, 159(1), 129-141. https://doi.org/10.1111/j.1476-5381.2009.00515.x

Colasanti, B. K. (1990). A comparison of the ocular and central effects of delta 9-tetrahydrocannabinol and cannabigerol. Journal of Ocular Pharmacology, 6(4), 259-269.

Colasanti, B. K., Craig, C. R., & Allara, R. D. (1984). Intraocular pressure, ocular toxicity and neurotoxicity after administration of cannabinol or cannabigerol. Experimental Eye Research, 39(3), 251-259.

De Petrocellis, L., Ligresti, A., Moriello, A. S., Allarà, M., Bisogno, T., Petrosino, S., … Di Marzo, V. (2011). Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes. British Journal of Pharmacology, 163(7), 1479-1494. https://doi.org/10.1111/j.1476-5381.2010.01166.x

De Petrocellis, L., Vellani, V., Schiano-Moriello, A., Marini, P., Magherini, P. C., Orlando, P., & Di Marzo, V. (2008). Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8. The Journal of Pharmacology and Experimental Therapeutics, 325(3), 1007-1015. https://doi.org/10.1124/jpet.107.134809

Eisohly, H. N., Turner, C. E., Clark, A. M., & Eisohly, M. A. (1982). Synthesis and antimicrobial activities of certain cannabichromene and cannabigerol related compounds. Journal of Pharmaceutical Sciences, 71(12), 1319-1323.

Formukong, E. A., Evans, A. T., & Evans, F. J. (1989). The inhibitory effects of cannabinoids, the active constituents of Cannabis sativa L. on human and rabbit platelet aggregation. The Journal of Pharmacy and Pharmacology, 41(10), 705-709.

Giacoppo, S., Gugliandolo, A., Trubiani, O., Pollastro, F., Grassi, G., Bramanti, P., & Mazzon, E. (2017). cannabinoid CB2 receptors are involved in the protection of RAW264.7 macrophages against the oxidative stress: an in vitro study. European Journal of Histochemistry: EJH, 61(1), 2749. https://doi.org/10.4081/ejh.2017.2749

Morales, P., Hurst, D. P., & Reggio, P. H. (2017). Molecular Targets of the Phytocannabinoids-A Complex Picture. Progress in the chemistry of organic natural products, 103, 103-131. https://doi.org/10.1007/978-3-319-45541-9_4

Oláh, A., Markovics, A., Szabó-Papp, J., Szabó, P. T., Stott, C., Zouboulis, C. C., & Bíró, T. (2016). Differential effectiveness of selected non-psychotropic phytocannabinoids on human sebocyte functions implicates their introduction in dry/seborrhoeic skin and acne treatment. Experimental Dermatology, 25(9), 701-707. https://doi.org/10.1111/exd.13042

Pagano, E., Montanaro, V., Di Girolamo, A., Pistone, A., Altieri, V., Zjawiony, J. K., … Capasso, R. (2015). Effect of Non-psychotropic Plant-derived cannabinoids on Bladder Contractility: Focus on Cannabigerol. Natural Product Communications, 10(6), 1009-1012.

Rock, E. M., Goodwin, J. M., Limebeer, C. L., Breuer, A., Pertwee, R. G., Mechoulam, R., & Parker, L. A. (2011). Interaction between non-psychotropic cannabinoids in marihuana: effect of cannabigerol (CBG) on the anti-nausea or anti-emetic effects of cannabidiol (CBD) in rats and shrews. Psychopharmacology, 215(3), 505-512. https://doi.org/10.1007/s00213-010-2157-4

Szczesniak, A.-M., Maor, Y., Robertson, H., Hung, O., & Kelly, M. E. M. (2011). Nonpsychotropic cannabinoids, abnormal cannabidiol and canabigerol-dimethyl heptyl, act at novel cannabinoid receptors to reduce intraocular pressure. Journal of Ocular Pharmacology and Therapeutics: The Official Journal of the Association for Ocular Pharmacology and Therapeutics, 27(5), 427-435. https://doi.org/10.1089/jop.2011.0041

Valdeolivas, S., Navarrete, C., Cantarero, I., Bellido, M. L., Muñoz, E., & Sagredo, O. (2015). Neuroprotective properties of cannabigerol in Huntington’s disease: studies in R6/2 mice and 3-nitropropionate-lesioned mice. Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics, 12(1), 185-199. https://doi.org/10.1007/s13311-014-0304-z

Wilkinson, J. D., & Williamson, E. M. (2007). cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of Psoriasis. Journal of Dermatological Science, 45(2), 87-92. https://doi.org/10.1016/j.jdermsci.2006.10.009