Bigstock Excitement is growing about cannabigerol (CBG), a molecule found naturally in the cannabis plant. Early research suggests its anti-inflammatory effects may outpace those of CBD, and it also lends itself to topical applications for skin irritation–a much-needed route of administration and an additional option for problems, such as atopic dermatitis. Plus, CBG may aid patients with both inflammatory bowel disease and metabolic syndrome. What accounts for these differences between cannabinoid effects? The clearest picture emerges from studying cannabinoids and other receptors that change their behavior when exposed to one or more circulating cannabinoids.1 That is, some cannabinoids in the same mixture may serve as agonists to a receptor while others act as antagonists. CBD, for example, blunts or modulates the excitatory effects of delta-9 tetrahydrocannabinol (THC), thereby reducing the “high” THC causes. While researchers have identified more than 150 cannabinoids in the cannabis plant, this discussion focuses on the top three: CBD, THC, and CBG. Veterinarians typically avoid THC in all but trace quantities due to its toxicity. However, to understand how CBG works and what the fuss is all about, learning about the pharmacology of THC and CBD first makes sense. This is because CBG resembles both cannabinoids in the way it works. Early on, scientific study on cannabinoids focused on the psychotropic effects of THC.2 In fact, it was the search for endogenous THC receptors that gave rise to the discovery of the endocannabinoid system (ECS). Harvard Health describes the ECS as comprising “…a vast network of chemical signals and cellular receptors that are densely packed throughout our brains and bodies. The ‘cannabinoid’ receptors in the brain—the CB1 receptors—outnumber many of the other receptor types on the brain. They act like traffic cops to control the levels and activity of most of the other neurotransmitters. This is how they regulate things: by immediate feedback, turning up or down the activity of whichever system needs to be adjusted, whether that is hunger, temperature, or alertness.”3 Further, “A second type of cannabinoid receptor, the CB2 receptor, exists mostly in our immune tissues and is critical to helping control our immune functioning, and it plays a role in modulating intestinal inflammation, contraction, and pain in inflammatory bowel conditions. CB2 receptors are particularly exciting targets of drug development because they don’t cause the high associated with cannabis that stimulating the CB1 receptors does (which is often an unwanted side effect).” In contrast to the way in which THC activates CB1 receptors so intensively and extensively, CBD modulates this exuberance through negative allosteric modulation. In other words, CBD alters the shape of the receptor’s binding site in a way that inhibits THC from attaching as strongly. This is how, in low to moderate amounts,4 CBD mitigates some of the most undesirable effects of THC (i.e., tachycardia and paranoia). CBD’s main effects arise from the impact it has on noncannabinoid receptors, such as those involved in day-to-day neurotransmission by a variety of circulating ligands. For example, CBD’s anti-anxiety benefits arise, at least in part, from its activation of the serotonin 1A (5-HT1A) receptor. Also, CBD regulates the signaling of gamma-aminobutyric acid (GABA), which benefits patients with anxiety, seizures, and sleeping disorders.5 CBD also affects a variety of other receptors. By enhancing adenosine signaling, CBD confers an antiarrhythmic effect during ischemia/reperfusion. Its anti-inflammatory effects may be related to reduced serum TNF-alpha, IL-6, and COX-2 expressions. After connecting to and promoting transcriptional activity of the nuclear transcription factor peroxisome proliferator-activated receptor (PPAR-gamma), CBD increases anti-inflammatory cytokines while inhibiting inducible nitric oxide synthase (iNOS) expression. Further, CBD downregulates nuclear factor kappa B (NF-kappa B) and modulates still other pro-inflammatory signaling cascades. CBD also serves to regulate/modulate calcium, sodium, and potassium channels.6 With all CBD can do, is there really a need for another cannabinoid? Yes, and here’s why. As aforementioned, CBG resembles both CBD and THC in several ways. Even so, CBG displays unique mechanisms of action, receptor profiles, and therapeutic value. Practical applications include dermatologic issues, inflammatory bowel disease, antibiotic-resistant staphylococcal infections, and metabolic syndrome. Like CBD, CBG is nonintoxicating, nonhallucinogenic, and noneuphorigenic. In describing its pharmacological profile, Nachnani et al. wrote, “In a variety of different ways, CBG seems to reside, pharmacologically, in between delta-9-THC and CBD…. CBG is more like Δ9-THC at the CB1/CB2 receptors than CBD, but with a lower affinity (by a factor of between 5-fold and 27-fold) …In addition, CBD and CBG are very comparable at six transient receptor potential cation channels (TRPA1, TRPV1, TRPV2. TRPV3, TRPV4, and TRPM8) with relatively minor differences in affinity… Important differences or gaps in our knowledge, however, exist for three key players. First, for GPR55 (the potential nonhomologous CB3 receptor), there is no information on CBG binding (Ryberg et al., 2007). Second, CBG appears to be a very potent (nanomolar to sub-nanomolar affinity) agonist at the α-2 adrenoceptor (Cascio et al., 2010). Physiologically, this is so potentially important that it is the subject of extensive discussion [within this paper]. At the present time, there are no data on this receptor for CBD and Δ9-THC. Finally, there is a clear differentiation of CBG and CBD at the 5-HT1A receptor, in which the former is reported to be an antagonist, whereas the latter is an indirect agonist…”7 Much remains to be tested and verified with CBG, but for now, below are the areas where CBG matches or exceeds other cannabinoids. Dermatologic problems For skin issues, topically applied CBG has exhibited therapeutic benefits in animal models of atopic dermatitis (AD).8 It reduces inflammation and strengthens barrier function. CBG confers antioxidant, anti-acne, anti-aging, and anti-inflammatory activity. A clinical study in humans applying CBG serum topically showed a statistically significant improvement, compared with placebo, in transepidermal water loss and a reduction in erythema. Although CBD does some of this as well, CBG shows superiority in inhibiting pro-inflammatory cytokine release induced by ultraviolet A, ultraviolet B, and chemical agents, among others.9 Inflammatory bowel disease Both CBD and CBG aid patients with inflammatory bowel disease (IBD), but CBG appears to outperform CBD in terms of its direct impact on gut inflammation, especially in cases of Crohn’s disease and ulcerative colitis. It achieves this, at least in part, by engaging directly with intestinal CB1 and CB2 receptors. Introducing CBD along with CBG aids in lessening pain and anxiety. A study in mice using an inflammatory bowel disease model found that a high-cannabigerol hemp extract containing CBG, CBD, and cannabichromene (CBC) reduced colitis and modulated the microbiome.10 The high CBG hemp extract normalized several metabolic pathways, including those involved in inflammation. Combining CBD and CBG helps reduce damage to the colonic epithelium and reduces pain-related responses.11 Infectious disease Both CBD and CBG are garnering research attention in their ability to directly kill drug-resistant bacteria.12,13 CBG works to damage cell walls of gram-positive bacteria, disrupt mature biofilms, combat drug resistance, and increase bacterial membrane permeability.14,15 Again, according to Nachnani et al., “A number of cannabinoids have been reported to have antibacterial activity; however, CBG was found to be among the most potent cannabinoids tested against antibiotic-resistant strains of Staphylococcus aureus (Appendino et al., 2008). In comparison with conventional antibiotics, CBG had a lower minimum inhibitory concentration than norfloxacin in five of the six strains tested and was more potent than erythromycin, tetracycline, and oxacillin in at least one resistant strain (Appendino et al., 2008). Using a systemic S. aureus infection model in mice, Farha et al. (2020) showed that CBG was as effective at reducing colony forming units as vancomycin.”16 Metabolic syndrome Studies showing the therapeutic possibilities of CBG for managing syndrome are growing steadily and are further outlined in “Cannabinoids, GLP-1 receptor agonists – overlapping benefits.” Bigstock What are the downsides of CBG? A survey of human patients using CBG-predominant cannabis for anxiety, chronic pain, depression, and insomnia reported greater efficacy of CBG-predominant cannabis over conventional drug therapy. Adverse events were manageable, and withdrawal symptoms were reported as negligible.17 A double-blind, placebo-controlled, crossover field trial involving 20 mg of hemp-derived CBG reduced subjective ratings of stress and anxiety with no motor or cognitive impairment, intoxication, heart palpitations, or dry mouth.18 Veterinary research on CBG Research on CBG for dogs remains sparse, but there is a need to expand understanding of its pharmacokinetics, tolerability, and physiological effects in this target species.19-21 Overall, CBG and its precursor, cannabigerolic acid (CBGA), appear to be safe and well-tolerated in canine participants, whether administered alone or in combination with other cannabinoids. These results highlight the disparity between the volume of cannabinoid research versus all other plant-based practices in veterinary medicine. In this author’s opinion, the main problem with cannabinoid medicine pertains not to its chemistry and side effects but to the regulatory bodies and licensing boards that still prohibit its use. Not one veterinarian, to this author’s knowledge, has lost his or her veterinary license after selling a client Chinese remedies that harbor secret amounts of herbal strychnine. Yet, veterinarians in some parts of the U.S. are not permitted to even discuss cannabis with clients. How is this protecting the public? How is this benefiting animal health? If keeping veterinarians from prescribing cannabis is not helping clients or their animals, why do these constraints persist? Cannabinoids, GLP-1 receptor agonists – overlapping benefits A curious connection exists between FDA-approved, predominantly injectable drugs called GLP-1 (glucagon-like peptide-1) receptor agonists (GLP-1RAs) and poorly regulated, questionably legal cannabinoids, such as THC, CBD, and CBG. While GLP-1RAs address metabolic syndrome and its core components: obesity, hyperglycemia, hypertension, and dyslipidemia, cannabinoids offer some of these same effects. How? Both cannabinoids and GLP-1RAs reduce inflammation and oxidative stress. In so doing, they inhibit microglial activation, which can cause neurodegeneration and cognitive decline, if left untreated over time.22 Inflammation induces neurotoxicity through reactive oxygen species (ROS) elevation; ROS damage neurons by oxidizing essential lipids, proteins, and DNA.23 Additional shared benefits include mitochondrial protection, slowed cellular aging, reduced neuronal excitotoxicity, enhanced neuronal repair, and improved metabolic function.24,25 Despite their obvious value on many levels, GLP-1RAs may cause a slew of adverse effects, including disordered gastrointestinal motility, tachycardia, headache, and dizziness. GLP-1RAs are relatively new drugs; thus, their long-term impacts are largely unknown. Rare but severe side effects include, but are not limited to, pancreatitis, gastroparesis, biliary disease, ileus, kidney damage, visual disturbances, and a potentially increased risk of thyroid cancer. Negative side effects from cannabinoids vary between cannabinoids as well as dose and route of administration. However, the medical use of cannabis harkens back thousands of years, in contrast to GLP-1RAs. They typically do not cause organ impairment or many of the concerns listed above for GLP-1RAs. Further, the costs of obtaining cannabinoids are likely to fall in the next few years. “Synthetic biologists” at UC Berkeley have developed a low-cost way to create cannabinoid precursors, such as CBGA, THCA, and CBDA, from brewer’s yeast. As manufacturing ramps up, high-quality cannabinoids will become less expensive, more readily available, and less onerous on the environment.26 Narda G. Robinson, DO, DVM, MS, FAAMA, practices osteopathic medicine and veterinary medicine. Dr. Robinson taught science-based integrative medicine at the Colorado State University College of Veterinary Medicine and Biomedical Sciences for 20 years. In 2016, Robinson established CuraCore VET in Fort Collins, Colo., where she teaches medical acupuncture, integrative rehabilitation, medical massage, and other integrative medical approaches. Dr. Robinson is now offering programs in Sidney, British Columbia, through CuraCore Canada Academy of Veterinary Integrative Medicine and Rehabilitation. The author’s opinions do not necessarily reflect those of Veterinary Practice News. References Blebea NM, Pricopie AI, Vlad RA, Hancu G. Phytocannabinoids: Exploring Pharmacological Profiles and Their Impact on Therapeutical Use. Int J Mol Sci. 2024 Apr 10;25(8):4204. doi: 10.3390/ijms25084204. PMID: 38673788; PMCID: PMC11050509. Pertwee RG. Cannabinoid pharmacology: the first 66 years. Br J Pharmacol. 2006 Jan;147 Suppl 1(Suppl 1):S163-71. doi: 10.1038/sj.bjp.0706406. 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J Pharmacol Exp Ther. 2024 Aug 19;390(3):331-341. doi: 10.1124/jpet.124.002204. PMID: 39009468; PMCID: PMC11338277. Godbole SS, Sun D, Coates MD, Himmelberger VJ, Roopchand DE, Raup-Konsavage WM. Orally Administered CBD/CBG Hemp Extract Reduces Severity of Ulcerative Colitis and Pain in a Murine Model. J Clin Med. 2025 Aug 28;14(17):6095. doi: 10.3390/jcm14176095. PMID: 40943856; PMCID: PMC12429149. Barker HA and Ferraro MJ. Leveraging cannabinoids as antimicrobials. American Society for Microbiology. Accessed on April 15, 2026 at https://asm.org/magazine/2025/spring/leveraging-cannabinoids-as-antimicrobials . Niyangoda D, Aung ML, Qader M, Tesfaye W, Bushell M, Chiong F, Tsai D, Ahmad D, Samarawickrema I, Sinnollareddy M, Thomas J. Cannabinoids as Antibacterial Agents: A Systematic and Critical Review of In Vitro Efficacy Against Streptococcusand Staphylococcus. Antibiotics (Basel). 2024 Oct 30;13(11):1023. doi: 10.3390/antibiotics13111023. PMID: 39596719; PMCID: PMC11591022. 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