Therapeutic Properties of Cannabigerol (CBG)

Rahul Nachnani
Penn State University

Objective: Cannabigerol (CBG), is the precursor molecule to most cannabinoids including delta 9-tetrahydrocannabinol (THC) and cannabidiol (CBD). Non-psychoactive cannabinoids, such as CBD and CBG, show promise for attenuating substance seeking behavior along with anti-inflammatory, analgesic, and anti-epileptic activity. CBG, in particular, displays potency at distinct non-cannabinoid receptors: alpha-2 adrenoceptors, PPARα/ɣ, and serotonin 5-HT1A receptor. We propose CBG as a novel therapeutic in the cannabinoid class of drugs with potential for pain, inflammation, and psychiatric disorders (substance abuse, ADHD, etc.).

Methods: To study the potential effects of CBG, we performed an array of biochemical, molecular, and radiotelemetric studies to better characterize its molecular mechanism and potential hazards. Mouse models were used to assess analgesic applications of CBG and radiotelemetry sensors were used to monitor blood pressure. Receptor binding characteristics have been investigated for CBG, CBD, and THC.

Results: Data suggest that CBG acutely lowers blood pressure in conscious, freely-moving mice as measured by radiotelemetry. Moreover, it shows a non-significant trend for acute pain reduction in mice, and further study is needed. CBG displays a fundamentally different pharmacological profile from CBD and THC.

Conclusion: Novel compounds of the Cannabis sativa plant show promise as new pharmacotherapeutics; however, most still do not yet have thorough characterization of therapeutic uses and adverse effects. CBG provides new opportunities and hazards as its popularity increases among cannabinoid supplement users. Our findings suggest that CBG has unique pharmacological potential for pain and blood pressure regulation, presumably due to its affinity for alpha-2 adrenoceptors. Translational and clinical research must be prioritized to reduce harm from pharmacological interactions and investigate CBG’s ability to modulate diseases as a therapeutic.

Co-authors: Greer McKendrick1, Diana E. Sepulveda1, Nicholas M. Graziane1, Sarah S. Bingaman1, Amy C. Arnold1, Natalia Loktionova1, Richard B. Mailman1, Wesley M. Raup-Konsavage1, Kent E. Vrana1
1Penn State University

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