Cannabigerol (CBG) is a non-psychoactive cannabinoid and minor constituent of cannabis. It is one of more than 120 identified cannabinoids found in the plant genus Cannabis. The compound is the decarboxylated form of cannabigerolic acid (CBGA), the parent molecule from which other cannabinoids are biosynthesized.

During plant growth, most of the CBG is converted into other cannabinoids, primarily tetrahydrocannabinol (THC) or cannabidiol (CBD), leaving about 1% CBG in finished plant material. Some strains, however, produce larger amounts of CBG and CBGA, while having low quantities of other cannabinoids, like THC and CBD.

The pharmacodynamics of CBG are complex. It is a relatively weak ligand of the cannabinoid receptors, where it acts as a weak partial agonist. Conversely, it is a much more potent agonist of the α₂-adrenergic receptor, antagonist of the serotonin 5-HT_1A receptor, and antagonist of the transient receptor potential channel TRPM8. CBG also has a variety of other actions that may additionally contribute to its effects.

CBG is sold as a dietary supplement. Safety concerns have been raised due to the potent activation of α₂-adrenergic receptors by CBG, which may produce sedation and potentially undesirable cardiovascular effects such as decreased heart rate and blood pressure.

In vitro, CBG has identified pharmacodynamic actions and its mechanism of action appears to be from interactions with multiple targets.

CBG is a weak ligand of the cannabinoid CB₁ and CB₂ receptors with affinities (K_i) of 380–2,600 nM and 153–3,460 nM, respectively. It is a weak partial agonist or antagonist of both of these receptors. There is no information on the binding or activity of CBG at the GPR55 (the potential non-homologous CB₃ receptor). CBG has relatively low affinity for the cannabinoid receptors, with approximately 5-fold lower affinity for the CB₁ receptor and 27-fold lower affinity for the CB₂ receptor than THC.^{[citation needed]}

CBG is a highly potent agonist of the α₂-adrenergic receptor (EC₅₀Tooltip half-maximal effective concentration = 0.2–72.8 nM) and a moderately potent antagonist of the serotonin 5-HT_1A receptor (K_B = 51.9 nM). Activation of the α₂-adrenergic receptor by CBG might produce effects including sedation, dry mouth, and decreased heart rate and blood pressure. This has raised safety concerns about CBG. The actions of CBG at the α₂-adrenergic receptor and 5-HT_1A receptor are of far greater potency than its interactions with the cannabinoid receptors and are more likely to be involved in its pharmacodynamic effects.^{[citation needed]}

The compound is a weak agonist of the transient receptor potential channels TRPA1 (EC₅₀ = 700 nM), TRPV1 (EC₅₀ = 1,300 nM), TRPV2 (EC₅₀ = 1,720 nM), TRPV3 (EC₅₀ = 1,000 nM), and TRPV4 (EC₅₀ = 5,100 nM) (efficacy 18–100% at these targets) and a more potent antagonist of the transient receptor potential channel TRPM8 (IC₅₀Tooltip half-maximal inhibitory concentration = 160 nM). It is also a weak agonist of the peroxisome proliferator-activated receptor PPAR-γ (EC₅₀ = 1,270–15,700 nM).