What is CBG (cannabigerol)?

CBG (cannabigerol) is referred to as the “stem cell of cannabinoids” – and rightly so: CBGA (cannabigerolic acid) is the biosynthetic precursor of all other cannabinoids in the plant. Enzymes convert CBGA into THCA, CBDA or CBCA; in mature plants, therefore, only little CBG remains (usually <1 % of the total weight). Modern CBG-rich varieties (with up to 20 % CBG) have been specially bred by harvesting before full maturity.

CBG was first isolated in 1964 by Gaoni and Mechoulam, but was long considered an inactive by-product. Since around 2015, interest has grown considerably: CBG has its own pharmacological activity via CB1, CB2, TRPV1, α2-adrenoceptors and 5-HT1A.

Pharmacological mechanisms

CB1 agonism: CBG binds to CB1 – weaker than THC, without a significant intoxicating effect. Via CB1 in the basal ganglia system, CBG shows influence on motor function and pain processing in animal models.

CB2 agonism: CBG acts on CB2 as a full agonist, which explains anti-inflammatory and immunomodulatory effects – similar to CBD, but with a more direct CB2 profile.

TRPV1 antagonism: In contrast to CBD (TRPV1 agonist), CBG blocks TRPV1 – which can counteract an “overstimulation” of pain receptors.

α2-adrenoceptor: CBG is a partial agonist at α2-adrenoceptors. This explains potential blood pressure lowering and anxiolytic effects (analogous mechanism to clonidine).

5-HT1A antagonism: CBG blocks 5-HT1A – in contrast to CBD (agonist). This difference is pharmacologically important and explains why CBG and CBD can have opposite effects in certain indications.

State of research: What the studies show

Possible areas of application

Inflammatory bowel disease (IBD): Crohn’s disease, ulcerative colitis – CB2 in intestinal mucosa and immune cells. CBG showed stronger anticolitis effects than CBD in animal models with the same mechanism. Clinical human studies are still lacking.

Glaucoma: CBG reduces intraocular pressure in animal models – more than THC in some studies. Mechanism: CB1-mediated reduction of aqueous humor production + α2-adrenoceptor activation (similar to timolol eye drops).

Antibiotic of the future: MRSA-resistant germs are a global health problem. CBG acts against gram-positive bacteria through membrane depolarization – a completely different mechanism than classic antibiotics. Particularly interesting: synergism with existing antibiotics.

Neuroprotection in Huntington’s disease/ALS: Valdeolivas 2015 shows CBG neuroprotection in the striatum. Early research on ALS (Loría 2010) shows slowing of motor neuron degeneration by CBG.

Appetite stimulation: In animal models, CBG stimulates food intake more strongly than CBD – without any psychoactive effect (relevant for cachexia in cancer or AIDS).

CBG vs CBD: The most important differences

Buying CBG: What to look out for

CBG oils are available in Germany as food supplements (similar to the former CBD legal situation). Quality criteria:
– COA (Certificate of Analysis) from independent ISO 17025 laboratory
– Full spectrum or broad spectrum (entourage effect with other cannabinoids)
– CBG content and residual THC content (<0.2 %) indicated
– EU-certified hemp cultivation (no pesticides)

Dosage (empirical): 10-50 mg CBG daily. No established clinical dosage guidelines available.

FAQ: CBG – the cannabinoid strain

Summary

CBG is the biosynthetic precursor of all cannabinoids and shows remarkable properties in preclinical studies: strongest antibiotic effect of all cannabinoids against MRSA, CB2-mediated inhibition of inflammation in intestinal diseases, neuroprotection in Huntington’s disease. Compared to CBD, CBG has more direct CB2 binding, but opposite TRPV1/5-HT1A effect. Human studies are largely lacking – CBG remains a high-potential research candidate that is most effective in the entourage effect with other cannabinoids.