Last updated 9 August 2026 · Originally published 29 February 2020
Cannabigerol turns up in an increasing number of products, usually described as the next big cannabinoid. For years the honest answer to “does it work?” was that nobody had tested it in people.
That began to change in 2024. Since then two more controlled human studies have added to the picture: one found no clear benefit for sleep, another found single doses as high as 200 mg generally well tolerated. The human evidence is still small, but CBG is no longer resting entirely on cell and animal research.
What CBG is
CBGA is the starting material that plant enzymes convert into THCA, CBDA and CBCA — the acidic precursors of THC, CBD and CBC. That’s why it’s often called the mother cannabinoid.
The catch is that the plant converts nearly all of it. Most conventional cultivars contain well under 1% CBG by maturity, which has historically made it expensive to produce and expensive to study — though breeders have now developed CBG-dominant varieties.
Like CBD, it’s non-intoxicating.
The first anxiety trial
In 2024, researchers published the first controlled human trial examining CBG’s acute effects on anxiety, stress and mood.[1]
Thirty-four healthy adults took 20 mg of hemp-derived CBG and a placebo in separate sessions a week apart, with neither participants nor the researchers running the sessions knowing which was which.
Across three measurements, participants reported a greater reduction in anxiety after CBG than after placebo. The difference was modest: anxiety fell by an average of 0.95 points on a ten-point scale with CBG, against 0.66 points with placebo. Stress was lower at the first measurement, but not after the stress test or at the final one. A longer, well-established anxiety questionnaire found no significant benefit.
CBG produced no noticeable intoxication and no measurable motor impairment. Participants also recalled slightly more words during part of a verbal-learning test — an unexpected result that needs replication before anyone calls it a memory benefit.
Worth keeping in proportion: 34 healthy cannabis users, one dose, assessed remotely over Zoom. The researchers made many comparisons without correcting for them, so some positive findings could have arisen by chance. The study was funded by CReDO Science, which works with CBG, and its founder was a co-author — though the funder reportedly had no role in analysing or interpreting the results.
What the later trials added
Two newer studies broaden the human evidence beyond anxiety.
In a trial of 63 US veterans with sleep problems, participants took 25 mg of CBG daily for two weeks, then 50 mg for a further two. Sleep improved — but it improved on placebo too, leaving no significant difference between the groups. Quality of life and PTSD symptoms followed the same pattern. Dropout was substantial and the study was too small for a firm conclusion, but CBG was well tolerated.[2] It was funded by Metta Medical, which trades as the cannabinoid company LEVEL, and several authors were employees or paid consultants — worth noting, though the trial was negative.
A 2026 laboratory study gave 12 healthy adults single doses from 25 to 200 mg of purified CBG. Researchers reported no drug-related adverse events, no robust psychoactive effects, and no liver-test results above the normal range after the two highest doses. Higher doses produced higher blood concentrations, though exposure varied considerably between individuals.[3]
That doesn’t establish long-term safety — both studies were small, and the laboratory experiment tested single doses only. But it’s reassuring that controlled human research has so far found CBG well tolerated.
What the preclinical work suggests
Most CBG research is still in cells and animals. Two areas come up most consistently.
Inflammatory bowel conditions. CBG reduced inflammation in a mouse model of colitis, and the gut is one of the more promising directions for it.[6]
Neuroprotection. Native CBG produced protective effects in mouse models of Huntington’s disease.[7] Chemically modified CBG derivatives have also been investigated in models of other neurodegenerative diseases, though those aren’t equivalent to the CBG in retail products.
Both are a long way from a person taking a tincture, and neither has been tested in humans.
How it works, roughly
CBG acts on several signalling systems, and its pharmacology is considerably more complicated than the familiar picture of THC acting at cannabinoid receptors.
Laboratory studies suggest CBG binds to CB1 and CB2, though generally less strongly than THC. One study found it behaved as a partial agonist at CB2, while its action at CB1 was measurable but less certain.[4]
It also acts on targets outside the classical endocannabinoid system, with particularly strong activity at α2-adrenergic receptors and some blocking of 5-HT1A serotonin signalling.[5] It affects several TRP channels involved in sensation, pain and inflammation too.
That gives CBG several plausible routes by which it might work. What it doesn’t yet tell us is which mechanism, if any, explains the effects reported in people.
So is CBG the new CBD?
Not really, and that framing misses what’s interesting about it.
They’re different compounds with different receptor profiles and, on the evidence so far, different therapeutic possibilities. CBG isn’t a replacement for CBD any more than CBD is a replacement for THC.
What can be said is that CBG now has something most minor cannabinoids don’t: controlled human trials. Three of them, with one modest positive result, one null result and one safety study. That’s a thin evidence base by any standard — but it’s a real one, and it’s why the research interest isn’t purely commercial.
If you’re thinking of trying it
The anxiety trial used 20 mg. Useful to know, because it’s a dose retail products actually deliver — but it isn’t an established treatment dose, and taking more hasn’t been shown to work better.
Check what you’re buying. CBG is expensive to produce, which creates an incentive to under-dose. A batch-specific lab report showing CBG content is the only way to know.
Expect less than the marketing promises. One anxiety trial in healthy adults is not evidence for the longer list of conditions CBG products tend to claim.
Medication interactions remain uncertain. CBG has been studied far less than CBD, so if you take prescription medication, ask a pharmacist before using it regularly.
None of this is medical advice.
For more, see our guides to CBGA and CBD vs CBN, our guide to CBD and what the research actually shows, or browse Cannabinoid Science.
References
- Cuttler C, Stueber A, Cooper ZD, Russo E. Acute effects of cannabigerol on anxiety, stress, and mood: a double-blind, placebo-controlled, crossover, field trial. Scientific Reports. 2024;14:16575. doi:10.1038/s41598-024-66879-0
- Emerson CR, Webster CE, Daza EJ, Klamer BG, Tummalacherla M. Effect of cannabigerol on sleep and quality of life in Veterans: a decentralized, randomized, placebo-controlled trial. Medical Cannabis and Cannabinoids. 2026;9(1):1–14. doi:10.1159/000549902
- Wolinsky D, Srungaram D, Zhang A, et al. Safety, pharmacodynamics, and pharmacokinetics of oral cannabigerol (CBG) in healthy adults. The Journal of Pharmacology and Experimental Therapeutics. 2026:104984. doi:10.1016/j.jpet.2026.104984
- Navarro G, Varani K, Reyes-Resina I, et al. Cannabigerol action at cannabinoid CB1 and CB2 receptors and at CB1–CB2 heteroreceptor complexes. Frontiers in Pharmacology. 2018;9:632. doi:10.3389/fphar.2018.00632
- Cascio MG, Gauson LA, Stevenson LA, Ross RA, Pertwee RG. Evidence that the plant cannabinoid cannabigerol is a highly potent α2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist. British Journal of Pharmacology. 2010;159(1):129–141.
- Borrelli F, Fasolino I, Romano B, et al. Beneficial effect of the non-psychotropic plant cannabinoid cannabigerol on experimental inflammatory bowel disease. Biochemical Pharmacology. 2013;85(9):1306–1316.
- Valdeolivas S, Navarrete C, Cantarero I, et al. Neuroprotective properties of cannabigerol in Huntington’s disease: studies in R6/2 mice and 3-nitropropionate-lesioned mice. Neurotherapeutics. 2015;12(1):185–199.
About this article
Substantially rewritten in August 2026, consolidating our earlier reporting on CBG. This update adds the three controlled human studies published from 2024 to 2026, and sets out how CBG’s receptor profile differs from CBD’s. With earlier reporting by Lydia Kariuki.
