CBG (cannabigerol): effect, studies & application
- CBG is the biosynthetic precursor of all cannabinoids – CBGA produces THC, CBD and CBC
- Farha 2020: CBG destroyed MRSA more effectively than many standard antibiotics (in vitro + mouse)
- Three independent mechanisms: CB2 + α2-adrenoceptors (glaucoma) + directly antibacterial
CBG: The mother cell of all cannabinoids
Cannabigerol (CBG) is often referred to as the “mother cell of all cannabinoids” because CBGA (the acid form) is the precursor from which THC, CBD and CBC are biosynthesized. In mature cannabis plants, CBG is therefore only present in small amounts (usually <1%) – most CBGA has already been converted into THCA and CBDA.
Young cannabis (before flowering) contains more CBG. Specially bred CBG strains today reach 10-15 % CBG content.
CBG pharmacology: How it works
| Receptor/target | Effect | Clinical relevance |
|---|---|---|
| CB1 (weak partial agonist) | Minimal psychoactive effect | No high at normal doses |
| CB2 (partial agonist) | Anti-inflammatory | Inflammatory diseases |
| α2-adrenoceptor (agonist) | Blood pressure lowering | Glaucoma: IOP reduction |
| 5-HT1A (antagonist) | Antidepressant different from CBD | Depression, anxiety (different mechanism than CBD) |
| TRPV1 (agonist) | Pain modulation | Neuropathic pain |
| TRP channels in general | Antibacterial | MRSA activity in vitro |
CBG in glaucoma: a historical finding
Glaucoma is caused by increased intraocular pressure (IOP). CBG shows a strong IOP-lowering effect in animal models – stronger than THC:
Colasanti et al. 1984 (J Ocul Pharmacol): CBG lowered IOP in cats more than THC. Mechanism: α2-adrenoceptor agonism (same mechanism as timolol eye drops in glaucoma therapy).
Clinical human studies are still lacking for CBG specifically, but the mechanism is pharmacologically sound.
CBG for inflammatory bowel disease
Borrelli et al. 2013 (Biochem Pharmacol): CBG in mouse colitis model. CBG reduced significantly:
– Inflammation parameters (TNF-α, IL-1β)
– Intestinal damage histologically
– iNOS expression (inflammatory nitric oxide)
Mechanism: CB2 activation on intestinal immune cells + PPAR-γ agonism. Conclusion: CBG is an interesting experimental target for Crohn’s disease and ulcerative colitis.
CBG and neurodegeneration
Valdeolivas et al. 2015 (Neurotherapeutics): CBG in Huntington’s disease mouse model. CBG showed:
– Neuroprotective effect (less striatum neuron loss)
– Reduction of neuroinflammation
– Antioxidant effect
CBG in ALS animal model: similar neuroprotective data (Moreno-Martet 2014).
Antibacterial: CBG against MRSA
Farha et al. 2020 (ACS Infect Dis): CBG showed strong antibiotic activity against methicillin-resistant Staphylococcus aureus (MRSA) in vitro and in a mouse model. CBG effectively disrupted the membrane function of MRSA bacteria.
No human clinical studies on CBG as an antibiotic, but preclinical evidence is remarkable.
FAQ: CBG Cannabigerol
Summary
CBG is the biosynthesis precursor of all cannabinoids. Pharmacological: weak CB1/CB2 agonist, α2-adrenoceptor (glaucoma), 5-HT1A antagonist, antibacterial (MRSA). Study evidence: glaucoma IOP reduction (animal model), colitis improvement (Borrelli 2013), neuroprotection (Huntington’s disease model). No high, legally available in Germany. Entourage effect for CBG in full-spectrum context; CBD vs. THC for main cannabinoid comparison.
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