Cannabigerol (CBG) enhanced adenosine signaling at a human receptor involved in inflammation and immune regulation, with laboratory tests showing an approximately 138-fold increase in adenosine’s apparent potency.
The finding comes from a study published in Pharmacological Research that explored how CBG and cannabidiol (CBD) interact with the adenosine A3 receptor. Adenosine helps regulate neurotransmission, immunity, inflammation and tissue protection.
“These results identify CBG as an effective enhancer of adenosine potency at human A3R,” the researchers wrote.
In practical terms, adding CBG allowed a much lower concentration of adenosine to produce a comparable response in the cellular assay. CBD also enhanced adenosine’s apparent potency, but its effect was smaller. CBG additionally increased the maximum measured response.
To investigate these interactions, the team combined experiments in receptor-expressing cells with molecular docking, binding-energy calculations and molecular dynamics simulations.
Both cannabinoids reduced the accumulation of cyclic adenosine monophosphate, or cAMP, a molecule involved in transmitting signals inside cells. Those effects were absent in cells without the introduced receptor and were blocked by a selective A3 receptor antagonist, supporting the receptor’s role in the response.
Computer modeling suggested a possible explanation for how CBG enhances adenosine’s interaction with the receptor. However, the authors said direct binding studies and additional signaling and structural analyses are needed to validate the mechanism.
The research identifies a potential avenue for further cannabinoid investigation. It did not test treatment outcomes in people, and the 138-fold figure should not be interpreted as a corresponding increase in medical benefit.
