Experts report that there are at least 106 phytocannabinoids found in the trichomes of the cannabis flower. Most research has focused on the two most prominent “primary” cannabinoids, tetrahydrocannabinol (THC) and cannabidiol (CBD). However, many of the so-called “secondary” cannabinoids are responsible for adding to the therapeutic effects of cannabis as part of the entourage effect, the term used to describe how the many cannabinoid and terpenoid compounds in cannabis work synergistically to deliver beneficial effects.
Cannabigerol (CBG) and cannabigerolic acid (CBGA) are two of the many secondary phytocannabinoids found in the flower of the cannabis plant. The “A” in CBGA refers to the presence of a certain chemical structure called carboxylic acid. CBG was initially isolated from hash by Israeli researchers in 1964, with subsequent research in Japan elucidating that CBGA was its precursor. CBG is one of the five most common cannabinoids along with THC, CBD, CBN (cannabinol) and CBC (cannabichromene). CBGA plays an extremely important role as the parent compound in the maturing cannabis flower and undergoes a number of changes to create THC, CBD, CBC, and CBG. This process, called biosynthesis, starts when compounds in the maturing flower, geranyl pyrophosphate and olivetolic acid, bond together to create CBGA. Next, CBGA is exposed to three different enzymes, with the amount of each enzyme determined by the genetics of the plant.
- The enzyme THCA synthase converts CBGA to THCA
- The enzyme CBDA synthase converts CBGA to CBDA
- The enzyme CBCA synthase converts CBGA to CBCA
As you can see in the chart below, all of the “A” forms are converted in a process called decarboxylation. CBGA itself converts to CBG when heated.
There is scant research on the medicinal benefits of CBGA. In the plant, CBGA provides a defense mechanism, along with THCA, as an insecticidal agent. When released from the trichomes of the cannabis plant, CBGA, THCA, CBCA and CBDA can each produce plant cell necrosis which allows for natural fan leaf pruning. This allows for the plant to direct its energy away from the leaves to the flower.
Medicinal Properties of CBG
CBG is non-intoxicating and has the following medicinal properties, demonstrated in laboratory and animal studies:
- Antibacterial with potent inhibition of MRSA
- Anticancer (skin, prostate, and breast)
- Antidepressant in animal models
- Mild antihypertensive (lowers blood pressure)
- Inhibits growth of certain skin cells that contribute to psoriasis
- Blocks uptake of GABA, promoting muscle relaxation
- Lowers intraocular eye pressure
- Enhanced appetite
CBG is present in small amounts in the vast majority of drug-variety cannabis plants. However, it is more abundant in fiber variety plants (aka “hemp”). Recent breeding experiments in Europe have resulted in fiber variety cannabis containing a significant predominance of CBG, with content >80% in some. With the widespread legalization of cannabis for medical and recreational use underway, growers have the opportunity to focus on breeding CBG-rich varieties of cannabis paralleling the recent explosion of CBD-rich varieties. Having a broad array of products with a variety of dominant cannabinoids will allow for patients to customize their cannabis regimen to suit their individual needs.
Appendino G, Gibbons S, Giana A, Pagani A, Grassi G, Stavri M et al. (2008). Antibacterial cannabinoids from Cannabis sativa: a structure-activity study. J Nat Prod 71: 1427–1430.
Baek SH, Kim YO, Kwag JS, Choi KE, Jung WY, Han DS (1998). Boron trifluoride etherate on silica-A modified Lewis acid reagent (VII). Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Arch Pharm Res 21: 353–356.
Banerjee SP, Snyder SH, Mechoulam R (1975). Cannabinoids: influence on neurotransmitter uptake in rat brain synaptosomes. J Pharmacol Exp Ther 194: 74–81.
Brierley, Daniel I., et al. “Cannabigerol is a novel, well-tolerated appetite stimulant in pre-satiated rats.” Psychopharmacology233.19-20 (2016): 3603-3613.
Cascio MG, Gauson LA, Stevenson LA, Ross RA, Pertwee RG (2010). Evidence that the plant cannabinoid cannabigerol is a highly potent alpha2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist. Br J Pharmacol 159: 129–141.
Colasanti, Brenda K. “A comparison of the ocular and central effects of Δ9-tetrahydrocannabinol and cannabigerol.” Journal of Ocular Pharmacology and Therapeutics 6.4 (1990): 259-269.
De Petrocellis L, Di Marzo V (2010). Non-CB1, non-CB2 receptors for endocannabinoids, plant cannabinoids, and synthetic cannabimimetics: focus on G-protein-coupled receptors and transient receptor potential channels. J Neuroimmune Pharmacol 5: 103–121.
ElSohly HN, Turner CE, Clark AM, ElSohly MA (1982). Synthesis and antimicrobial activities of certain cannabichromene and cannabigerol related compounds. J Pharm Sci 71: 1319–1323.
Evans FJ (1991). Cannabinoids: the separation of central from peripheral effects on a structural basis. Planta Med 57: S60–S67.
Formukong EA, Evans AT, Evans FJ (1988). Analgesic and antiinflammatory activity of constituents of Cannabis sativa L. Inflammation 12: 361–371.
Ligresti A, Moriello AS, Starowicz K, Matias I, Pisanti S, De Petrocellis L et al. (2006). Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. J Pharmacol Exp Ther 318: 1375–1387.
Maor Y, Gallily R, Mechoulam R (2006). The relevance of the steric factor in the biological activity of CBD derivaties-a tool in identifying novel molecular target for cannabinoids. In: Symposium on the Cannabinoids. International Cannabinoid Research Society: Tihany, Hungary, p. 1.
Musty R, Deyo R (2006). A cannabigerol extract alters behavioral despair in an animal model of depression. Proceedings June 26; Symposium on the Cannabinoids. International Cannabinoid Research Society: Tihany, p. 32.
Shoyama, Yukihiro, et al. “Biosynthesis of cannabinoid acids.” Phytochemistry 14.10 (1975): 2189-2192.
Sirikantaramas, Supaart, et al. “Tetrahydrocannabinolic acid synthase, the enzyme controlling marijuana psychoactivity, is secreted into the storage cavity of the glandular trichomes.” Plant and Cell Physiology 46.9 (2005): 1578-1582.
Taura, Futoshi, et al. “First direct evidence for the mechanism of. DELTA. 1-tetrahydrocannabinolic acid biosynthesis.” Journal of the American Chemical Society 117.38 (1995): 9766-9767.
Valdeolivas, Sara, et al. “Neuroprotective properties of cannabigerol in Huntington’s disease: studies in R6/2 mice and 3-nitropropionate-lesioned mice.” Neurotherapeutics 12.1 (2015): 185-199.
Wilkinson JD, Williamson EM (2007). Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis. J Dermatol Sci 45: 87–92.