Literature Discussion

Receptors and molecular properties

CBG can be found in cannabis plants and some analogue forms of CBG can be found in the Helichrysum umbraculigerum plant (Pollastro et al., 2018).

CBG binds to both CB1 and CB2 receptors, having higher affinity for CB2 (Navarro et al., 2018; Rosenthaler et al., 2014).

CBG, as well as CBD, is a NAV channel blocker but did not show anticonvulsant effects (Hill et al., 2014).

CBG activates α2-adrenoceptors and CB2 and blocks CB1 and 5-HT1A receptors (Cascio et al., 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 anologues also actívate TRPA1 (Lopatriello et al., 2018).

CBG modulates GPR55 (Morales et al., 2017).

Δ9-THC, Δ8-THC, CBN, CBD, CBG, and CBC are directly metabolized by CYP2J2 and inhibit human cardiac CYP2J2 (Arnold et al., 2018)

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

ALS / Parkinson’s disease / Huntington’s disease / neurodegeneration

In cultured motorneurons, 2.5 and 5 mM CBG, both alone and in combination with CBD could reduce neuroinflammation and apoptosis in a PPARg-dependent manner (Mammana et al., 2019). This suggests CBG may have therapeutic value in the treatment of ALS and other neurodegenerative diseases.

Also in other studies CBG showed anti-inflammatory properties (Petrosino et al., 2018), counteracted oxidative stress through CB2 receptors in macrophages (Giacoppo et al., 2017) and showed neuroprotective and anti-inflammatory effects for NSC-34 motor neurons by reducing caspase 3 activation, Bax expression, IL-, TNF-α, IFN-γ, pparγ, nitrotyrosine, SOD1 and iNOS protein levels (Gugliandolo et al., 2018).

In cultured NSC-43 motor neurons, CBG and CBD reduced pro-apoptotic signaling and altered glutamate, GABA and dopamine signaling suggesting neuroprotective effects (Gugliandolo et al., 2020).

The CBG quinone derivative VCE-003.2 has neuroprotective effects against an animal model of amyotrophic lateral sclerosis (Rodríguez-Cueto et al., 2018) and animal and cell models of Parkinsons disease (García et al., 2018, Burgaz et al., 2020). VCE-003 also improved subventricular zone-derived neurogenesis in response to huntingtin-induced neurodegeneration (Aguareles et al., 2019). Moreover, VCE-003 promoted neuronal progenitor cell survival in a pparγ-dependent way and prevented neuronal loss in mouse models of Huntington’s disease, improving motor deficits, suggesting therapeutic potential in Huntington’s disease and other neurodegenerative diseases (Díaz-Alonso et al., 2016).

Anorexia / cachexia

CBG causes hyperphagia in animals without producing negative neuromotor side effects (Brierley et al., 2016).  Also, CBG-BDS acts as an appetite stimulant, probably through CB1 receptors (Brierley et al., 2017). CBG also attenuates cisplatin chemotherapy-induced cachexia in rats: 60 or 120 mg/kg CBG increased food intake and reduced weight loss (Brierley et al., 2019).


CBG has antifungal and antibacterial properties (Eisohly et al., 1982).

CBG has antibiotic activity against Streptococcus Mutants and prevents biofilm formation suggesting potential as an antibiotic and in the prevention of dental caries (Aqawi et al., 2021, 2021). Similarly, CBG prevents quorum sensing and biofilm formation of Vibrio Harveyi, a pathogenic bacterium in fish and invertebrates (Aqawi et al., 2020).


In cultured rat astrocytes, CBG (and to a larger extent CBD) had antioxidant effects suggesting a potentially protective role in neurological disorders such as ischemia (di Giacomo et al., 2020).


CBG inhibits cellular growth in human oral epitheloid carcicoma cells (Baek et al., 1998) and in leukaemic cells (Scott, Shah, Dalgleish, & Liu, 2013) 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 would act more effectively agianst leukaemic cells if it would be mixed with CBD (Scott, Dalgleish, & Liu, 2017; Scott et al., 2013). In cultured glioblastoma cells, CBG reduced tumor cell viability to a similar extent as THC. Moreover, CBG in combination with CBD was more effective than CBG in combination with THC suggesting the non-psychoactive combination of CBG and CBD can be used to treat glioblastoma instead of the potentially psychoactive combination of CBD and THC which is currently often used (Lah et al., 2021).

Cystitis / bladder function

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.


CBG/CBGA as well as CBD/CBDA extracts reduced aldose reductase activity in vivo, suggesting a potential effect on Diabetes (Smeriglio et al., 2018).

In culture and in vivo, CBG and other cannabinoids such as CBD, CBDA, CBGA and THCV (all at 5 mM) increased the viability of bone marrow-derived mesenchymal stem cells. The same concentration of CBG and CBD, both alone and in combination, promote maturation of these stem cells into adipocytes. Insulin signaling was also improved, suggesting CBG and/or CBD might restore energy homeostasis in metabolic disorders such a type 2 Diabetes (Fellous et al., 2020).

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 & 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).

In rodent colitis models, CBG strongly reduced myeloperoxidase activity, suggesting anti-inflammatory potential in the gut (Couch et al., 2018).


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 et al., 1984). Also, its analog CBG-DMH reduces intraocular pressure (Szczesniak et al., 2011).


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).

Multiple Sclerosis

In the Experimental Autoimmune Encephalitis mouse model for Multiple Sclerosis, a synthetic derivative of CBG (VCE-003) reduced disease intensity and neurological defects via CB2 and PPARg receptors. VCE-003 reduced CD4+ T cell infiltration and Th1/Th17 inflammatory signaling, resulting in reduced microglial activation, myelin sheet preservation and reduced axonal damage, suggesting therapeutic potential for CBD in Multiple Sclerosis (Carrillo-Salinas et al., 2014).


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.


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

In rat dorsal root ganglion neurons, CBG, as well as CBD and THC was capable of blocking subsequent capsaicin responses, suggesting desensitization of TRPV1 receptors. CBG reduced the capsaicin response by 88%, THC by 97%, CBD by 99% and a 1:1:1 combination completely blocked the capsaicin response, suggesting analgesic potential (Anand et al., 2021).


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). Also, CBG, as well as CBD, are involved in skin cell proliferation and differenciation, which can have an effect in skin diseases (Pucci et al., 2013)


Aguareles, J., Paraíso-Luna, J., Palomares, B., Bajo-Grañeras, R., Navarrete, C., Ruiz-Calvo, A., García-Rincón, D., García-Taboada, E., Guzmán, M., Muñoz, E., & Galve-Roperh, I. (2019). Oral administration of the cannabigerol derivative VCE-003.2 promotes subventricular zone neurogenesis and protects against mutant huntingtin-induced neurodegeneration. Translational Neurodegeneration, 8, 9. https://doi.org/10.1186/s40035-019-0148-x

Alhouayek, M., & Muccioli, G. G. (2012). The endocannabinoid system in inflammatory bowel diseases: From pathophysiology to therapeutic opportunity. Trends in Molecular Medicine, 18(10), 615-625. https://doi.org/10.1016/j.molmed.2012.07.009

Anand, U., Oldfield, C., Pacchetti, B., Anand, P., & Sodergren, M. H. (2021). Dose-Related Inhibition of Capsaicin Responses by cannabinoids CBG, CBD, THC and their Combination in Cultured Sensory Neurons. Journal of pain Research, 14, 3603-3614. https://doi.org/10.2147/JPR.S336773

Aqawi, M., Gallily, R., Sionov, R. V., Zaks, B., Friedman, M., & Steinberg, D. (2020). Cannabigerol Prevents Quorum Sensing and Biofilm Formation of Vibrio harveyi. Frontiers in Microbiology, 11, 858. https://doi.org/10.3389/fmicb.2020.00858

Aqawi, M., Sionov, R. V., Gallily, R., Friedman, M., & Steinberg, D. (2021). Anti-Bacterial Properties of Cannabigerol Toward Streptococcus mutans. Frontiers in Microbiology, 12, 656471. https://doi.org/10.3389/fmicb.2021.656471

Arnold, W. R., Weigle, A. T., & Das, A. (2018). Cross-talk of cannabinoid and endocannabinoid metabolism is mediated via human cardiac CYP2J2. Journal of Inorganic Biochemistry, 184, 88-99. https://doi.org/10.1016/j.jinorgbio.2018.03.016

Baek, S. H., Kim, Y. O., Kwag, J. S., Choi, K. E., Jung, W. Y., & Han, D. S. (1998). Boron trifluoride etherate 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., Orlando, P., Battista, G., Pagano, E., Di Marzo, V., & 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., De Petrocellis, L., Buono, L., Orlando, P., & 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., Harman, J. R., Giallourou, N., Leishman, E., Roashan, A. E., Mellows, B. A. D., Bradshaw, H. B., Swann, J. R., Patel, K., Whalley, B. J., & Williams, C. M. (2019). Chemotherapy-induced cachexia dysregulates hypothalamic and systemic lipoamines and is attenuated by cannabigerol. Journal of Cachexia, Sarcopenia and Muscle. https://doi.org/10.1002/jcsm.12426

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

Burgaz, S., García, C., Gómez-Cañas, M., Navarrete, C., García-Martín, A., Rolland, A., Del Río, C., Casarejos, M. J., Muñoz, E., Gonzalo-Consuegra, C., Muñoz, E., & Fernández-Ruiz, J. (2020). Neuroprotection with the cannabigerol quinone derivative VCE-003.2 and its analogs CBGA-Q and CBGA-Q-Salt in Parkinson’s disease using 6-hydroxydopamine-lesioned mice. Molecular and Cellular Neurosciences, 110, 103583. https://doi.org/10.1016/j.mcn.2020.103583

Carrillo-Salinas, F. J., Navarrete, C., Mecha, M., Feliú, A., Collado, J. A., Cantarero, I., Bellido, M. L., Muñoz, E., & Guaza, C. (2014). A cannabigerol derivative suppresses immune responses and protects mice from experimental autoimmune encephalomyelitis. PloS One, 9(4), e94733. https://doi.org/10.1371/journal.pone.0094733

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., Powell, S. R., & Craig, C. R. (1984). Intraocular pressure, ocular toxicity and neurotoxicity after administration of delta 9-tetrahydrocannabinol or cannabichromene. Experimental Eye Research, 38(1), 63-71.

Couch, D. G., Maudslay, H., Doleman, B., Lund, J. N., & O’Sullivan, S. E. (2018). The Use of cannabinoids in Colitis: A Systematic Review and Meta-Analysis. Inflammatory Bowel Diseases, 24(4), 680-697. https://doi.org/10.1093/ibd/izy014

De Petrocellis, L., Ligresti, A., Moriello, A. S., Allarà, M., Bisogno, T., Petrosino, S., Stott, C. G., & 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

di Giacomo, V., Chiavaroli, A., Orlando, G., Cataldi, A., Rapino, M., Di Valerio, V., Leone, S., Brunetti, L., Menghini, L., Recinella, L., & Ferrante, C. (2020). Neuroprotective and Neuromodulatory Effects Induced by Cannabidiol and Cannabigerol in Rat Hypo-E22 cells and Isolated Hypothalamus. Antioxidants (Basel, Switzerland), 9(1), E71. https://doi.org/10.3390/antiox9010071

Díaz-Alonso, J., Paraíso-Luna, J., Navarrete, C., Del Río, C., Cantarero, I., Palomares, B., Aguareles, J., Fernández-Ruiz, J., Bellido, M. L., Pollastro, F., Appendino, G., Calzado, M. A., Galve-Roperh, I., & Muñoz, E. (2016). VCE-003.2, a novel cannabigerol derivative, enhances neuronal progenitor cell survival and alleviates symptomatology in murine models of Huntington’s disease. Scientific Reports, 6, 29789. https://doi.org/10.1038/srep29789

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.

Fellous, T., Di Maio, F., Kalkann, H., Carannante, B., Boccella, S., Petrosino, S., Maione, S., Di Marzo, V., & Arturo Iannotti, F. (2020). Phytocannabinoids promote viability and functional adipogenesis of bone marrow-derived mesenchymal stem cells through different molecular targets. Biochemical Pharmacology, 113859. https://doi.org/10.1016/j.bcp.2020.113859

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.

García, C., Gómez-Cañas, M., Burgaz, S., Palomares, B., Gómez-Gálvez, Y., Palomo-Garo, C., Campo, S., Ferrer-Hernández, J., Pavicic, C., Navarrete, C., Luz Bellido, M., García-Arencibia, M., Ruth Pazos, M., Muñoz, E., & Fernández-Ruiz, J. (2018). Benefits of VCE-003.2, a cannabigerol quinone derivative, against inflammation-driven neuronal deterioration in experimental Parkinson’s disease: Possible involvement of different binding sites at the pparγ receptor. Journal of Neuroinflammation, 15(1), 19. https://doi.org/10.1186/s12974-018-1060-5

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

Giovannoni, M. P., Ghelardini, C., Vergelli, C., & Dal Piaz, V. (2009). Alpha2-agonists as analgesic agents. Medicinal Research Reviews, 29(2), 339-368. https://doi.org/10.1002/med.20134

Gugliandolo, A., Pollastro, F., Grassi, G., Bramanti, P., & Mazzon, E. (2018). In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive cannabinoid. International Journal of Molecular Sciences, 19(7). https://doi.org/10.3390/ijms19071992

Gugliandolo, A., Silvestro, S., Chiricosta, L., Pollastro, F., Bramanti, P., & Mazzon, E. (2020). The Transcriptomic Analysis of NSC-34 Motor Neuron-Like Cells Reveals That Cannabigerol Influences Synaptic Pathways: A Comparative Study with Cannabidiol. Life, 10(10), 227. https://doi.org/10.3390/life10100227

Hill, A. J., Jones, N. A., Smith, I., Hill, C. L., Williams, C. M., Stephens, G. J., & Whalley, B. J. (2014). Voltage-gated sodium (NaV) channel blockade by plant cannabinoids does not confer anticonvulsant effects per se. Neuroscience Letters, 566, 269-274. https://doi.org/10.1016/j.neulet.2014.03.013

Lah, T. T., Novak, M., Pena Almidon, M. A., Marinelli, O., Žvar Baškovič, B., Majc, B., Mlinar, M., Bošnjak, R., Breznik, B., Zomer, R., & Nabissi, M. (2021). Cannabigerol Is a Potential Therapeutic Agent in a Novel Combined Therapy for glioblastoma. Cells, 10(2). https://doi.org/10.3390/cells10020340

Lopatriello, A., Caprioglio, D., Minassi, A., Schiano Moriello, A., Formisano, C., De Petrocellis, L., Appendino, G., & Taglialatela-Scafati, O. (2018). Iodine-mediated cyclization of cannabigerol (CBG) expands the cannabinoid biological and chemical space. Bioorganic & Medicinal Chemistry, 26(15), 4532-4536. https://doi.org/10.1016/j.bmc.2018.07.044

Mammana, S., Cavalli, E., Gugliandolo, A., Silvestro, S., Pollastro, F., Bramanti, P., & Mazzon, E. (2019). Could the Combination of Two Non-Psychotropic cannabinoids Counteract Neuroinflammation? Effectiveness of Cannabidiol Associated with Cannabigerol. Medicina (Kaunas, Lithuania), 55(11). https://doi.org/10.3390/medicina55110747

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

Navarro, G., Varani, K., Reyes-Resina, I., Sánchez de Medina, V., Rivas-Santisteban, R., Sánchez-Carnerero Callado, C., Vincenzi, F., Casano, S., Ferreiro-Vera, C., Canela, E. I., Borea, P. A., Nadal, X., & Franco, R. (2018). Cannabigerol Action at cannabinoid CB1 and CB2 Receptors and at CB1-CB2 Heteroreceptor Complexes. Frontiers in Pharmacology, 9, 632. https://doi.org/10.3389/fphar.2018.00632

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., Izzo, A. A., & Capasso, R. (2015). Effect of Non-psychotropic Plant-derived cannabinoids on Bladder Contractility: Focus on Cannabigerol. Natural Product Communications, 10(6), 1009-1012.

Petrosino, S., Verde, R., Vaia, M., Allarà, M., Iuvone, T., & Di Marzo, V. (2018). Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic cannabinoid, in Experimental Allergic Contact Dermatitis. The Journal of Pharmacology and Experimental Therapeutics, 365(3), 652-663. https://doi.org/10.1124/jpet.117.244368

Pollastro, F., De Petrocellis, L., Schiano-Moriello, A., Chianese, G., Heyman, H., Appendino, G., & Taglialatela-Scafati, O. (2018). Reprint of: Amorfrutin-type phytocannabinoids from Helichrysum umbraculigerum. Fitoterapia, 126, 35-39. https://doi.org/10.1016/j.fitote.2018.04.002

Pucci, M., Rapino, C., Di Francesco, A., Dainese, E., D’Addario, C., & Maccarrone, M. (2013). Epigenetic control of skin differentiation genes by phytocannabinoids. British Journal of Pharmacology, 170(3), 581-591. https://doi.org/10.1111/bph.12309

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

Rodríguez-Cueto, C., Santos-García, I., García-Toscano, L., Espejo-Porras, F., Bellido, Ml., Fernández-Ruiz, J., Muñoz, E., & de Lago, E. (2018). Neuroprotective effects of the cannabigerol quinone derivative VCE-003.2 in SOD1G93A transgenic mice, an experimental model of amyotrophic lateral sclerosis. Biochemical Pharmacology. https://doi.org/10.1016/j.bcp.2018.07.049

Rosenthaler, S., Pöhn, B., Kolmanz, C., Nguyen Huu, C., Krewenka, C., Huber, A., Kranner, B., Rausch, W.-D., & Moldzio, R. (2014). Differences in receptor binding affinity of several phytocannabinoids do not explain their effects on neural cell cultures. Neurotoxicology and Teratology, 46, 49-56. https://doi.org/10.1016/j.ntt.2014.09.003

Scott, K. A., Dalgleish, A. G., & Liu, W. M. (2017). Anticancer effects of phytocannabinoids used with chemotherapy in leukaemia cells can be improved by altering the sequence of their administration. International Journal of Oncology, 51(1), 369-377.

Scott, K. A., Shah, S., Dalgleish, A. G., & Liu, W. M. (2013). Enhancing the activity of cannabidiol and other cannabinoids in vitro through modifications to drug combinations and treatment schedules. Anticancer Research, 33(10), 4373-4380.

Smeriglio, A., Giofrè, S. V., Galati, E. M., Monforte, M. T., Cicero, N., D’Angelo, V., Grassi, G., & Circosta, C. (2018). Inhibition of aldose reductase activity by Cannabis sativa chemotypes extracts with high content of cannabidiol or cannabigerol. Fitoterapia, 127, 101-108. https://doi.org/10.1016/j.fitote.2018.02.002

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

Synthetic Pathways

CBG is synthesized through decarboxylation of CBGA.

Clinical Trials

While CBG has not yet been tested in clinical trials, a survey among 127 users of CBG provides some valuable insights about the therapeutic potential of CBG (Russo et al., 2021).

Most of the samples (n=65; 51.2%) reported use of CBG-predominant products solely for medical purposes (n=46; 36.2% reported use for medical and recreational purposes; n=8; 6.3% reported recreational use only, and n=8 were missing). The most common conditions the complete sample reported using CBG to treat were anxiety (51.2%), chronic pain (40.9%), depression (33.1%), and insomnia/disturbed sleep (30.7%). Efficacy was highly rated, with the majority reporting their conditions were “very much improved” or “much improved” by CBG. Furthermore, 73.9% claimed superiority of CBG-predominant cannabis over conventional medicines for chronic pain, 80% for depression, 73% for insomnia, and 78.3% for anxiety. Forty-four percent of CBG-predominant cannabis users reported no adverse events, with 16.5% noting dry mouth, 15% sleepiness, 11.8% increased appetite, and 8.7% dry eyes. Around 84.3% reported no withdrawal symptoms, with sleep difficulties representing the most frequently endorsed withdrawal symptom (endorsed by two respondents).


Thus, CBG appear to have potential for the treatment of chronic pain, depression, insomnia and anxiety and probably increases appetite in at least a subset of users.



Russo, E.B., Cuttler, C., Cooper, Z.D., Stueber, A., Whiteley, V.L., and Sexton, M. (2021). Survey of Patients Employing Cannabigerol-Predominant Cannabis Preparations: Perceived Medical Effects, Adverse Events, and Withdrawal Symptoms. Cannabis cannabinoid Res.