Cannabigerol – CBG

CBG is a precursor of cannabinoid molecules with significant therapeutic activity. It has low affinity for CB1 and CB2 receptors, on which it acts as a partial agonist and also as a competitive antagonist of the CB1 receptor. It is able to bind to receptors other than cannabinoids, such as the α-2 adrenergic receptor (as a potent agonist) and the serotonergic receptor 5-HT1A (as an antagonist).¹

The 5-HT1A serotonergic receptor is a known target in the therapy of depression. The most popular antidepressant drugs are those that interfere with serotonergic transmission (such as SSRIs). This class of drugs is positively affected by presynaptic 5-HT1A receptor inhibitory agents, both in speed and efficiency of action. This reasoning leads to the comprehension that CBG, with its inhibitory action on the 5-HT1A receptor, is capable of optimising serotonin-modulating drugs, and may be an ally in the refinement of antidepressant therapy by increasing serotonergic bioavailability in the synaptic cleft.²

CBG is a potent α-2 adrenergic receptor agonist. Drugs of this class are known for their peripheral actions as anesthetics, analgesics and antihypertensives. At the central level, such CBG activity appears to be useful in the therapy of neuropsychiatric conditions, such as those related to memory, cognition, and learning functions. CBG may be an important adjuvant drug in the therapy of ADHD, both for allowing reaching favourable results with a lower dose of conventional stimulant drugs used in this condition, as for allowing the reduction of the side effects of these drugs (such as hypertension, anxiety, irritability and development of nervous tics).³

Another relevant receptor family related to CBG is that of peroxisome proliferator-activated receptors (PPARs). These are nuclear receptors involved in the regulation of glucose homeostasis, inflammation, and lipid and hepatic metabolism.4 Particularly for the PPARγ isoform, studies have shown that the affinity of CBG for this receptor is higher than the one shown by CBD and THC, the two most well known cannabinoid compounds.

The therapeutic potential of CBG is huge and requires greater comprehension to be better explored. Studies have shown CBG neuroprotective role in severe neurological conditions such as Huntington’s Disease, Parkinson’s Disease and Multiple Sclerosis, which seems to be mediated by its affinity for the PPARγ receptor.5

Metabolic syndrome treatments can be conducted with PPARγ receptor agonists in cases of imbalances such as hyperglycemia, hyperinsulinemia, hyperlipidemia. Through its affinity with this receptor, CBG is a candidate to treat these conditions, showing potential in type 2 Diabetes Mellitus, for example. Its neuroprotective action, associated with its agonist action on α-2 adrenergic receptors, plays an important role on metabolic syndromes, being of value for hypertensive condition common in metabolic syndromes.6

Still considering metabolic syndromes, insulin resistance is held as a serious and increasingly common health disorder. In vitro studies have demonstrated the ability of CBG (associated or not to CBD) to increase the expression of GLUT4, which is intrinsically related to insulin sensitization, something crucial to reverse cases of resistance to this hormone, having also found CBG to promote an increase in rate of glucose uptake and the improvement in the adipogenic process.6

The action of CBG was also studied in vivo in Inflammatory Bowel Disease, in which it proved to be beneficial for both prevention and treatment of damage caused by the syndrome, such as tissue inflammation. The involved mechanism seems to be related to CBF action in modulating inflammatory cytokines , in inhibiting nitric oxide production by macrophages and in reducing the overall oxidative stress.7


  1. ALOWAY, A. et al. Chapter 77 – Cannabinoid Regulation of Intraocular Pressure: Human and Animal Studies, Cellular and Molecular Targets. Disponível em: <>.
  2. ARTIGAS, F. et al. Acceleration of the effect of selected antidepressant drugs in major depression by 5-HT1A antagonists. Trends in Neurosciences, v. 19, n. 9, p. 378–383, jan. 1996.
  3. ARNSTEN, A. F. The use of α-2A adrenergic agonists for the treatment of attention-deficit/hyperactivity disorder. Expert Review of Neurotherapeutics, v. 10, n. 10, p. 1595–1605, out. 2010.
  4. TAVARES, V.; HIRATA, M. H.; HIRATA, R. D. C. Receptor ativado por proliferadores de peroxissoma gama (Ppargama): estudo molecular na homeostase da glicose, metabolismo de lipídeos e abordagem terapêutica. Arquivos Brasileiros de Endocrinologia & Metabologia, v. 51, n. 4, p. 526–533, jun. 2007.
  5. NACHNANI, R.; RAUP-KONSAVAGE, W. M.; VRANA, K. E. The Pharmacological Case for Cannabigerol. The Journal of Pharmacology and Experimental Therapeutics, v. 376, n. 2, p. 204–212, 1 fev. 2021.
  6. FELLOUS, T. et al. Phytocannabinoids promote viability and functional adipogenesis of bone marrow-derived mesenchymal stem cells through different molecular targets. Biochemical Pharmacology, v. 175, p. 113859, maio 2020.
  7. BORRELLI, F. et al. Beneficial effect of the non-psychotropic plant cannabinoid cannabigerol on experimental inflammatory bowel disease. Biochemical Pharmacology, v. 85, n. 9, p. 1306–1316, 1 maio 2013.