Terpenes Reduce Pain Hypersensitivity by Indirectly Activating CB1 Receptors via Endocannabinoids скачать в хорошем качестве

Terpenes Reduce Pain Hypersensitivity by Indirectly Activating CB1 Receptors via Endocannabinoids

At the May CMCR Investigators’ Meeting, Catherine Cahill, Ph.D., a neuropharmacologist at UCLA supported by NIH funding including HEAL drug development initiatives, presented her research on the potential of cannabis-derived compounds for the treatment of chronic pain. Chronic pain affects approximately 20% of the U.S. population, and current therapies often fail to provide adequate relief, underscoring a critical unmet medical need. Dr. Cahill highlighted the high prevalence of cannabis use among individuals with chronic pain, referencing clinical data in which patients reported a 64% reduction in opioid use following cannabis substitution. Her presentation focused specifically on myrcene, a dominant terpene found in cannabis. Preclinical findings demonstrated that myrcene produced significant analgesic effects in rodent models of neuropathic pain, with anti-allodynic efficacy observed at doses of 100–200 mg/kg in males and as low as 10 mg/kg in females. Further mechanistic studies suggested that myrcene’s effects were mediated via CB1 receptor signaling, despite lacking direct receptor binding affinity. Notably, myrcene elicited sex-specific responses, producing aversive effects in females but not in males, pointing to the complexity of cannabinoid–terpene interactions in pain modulation. Ongoing investigations aim to further elucidate the pharmacodynamics of myrcene and β-caryophyllene and assess their translational potential as a non-opioid analgesic.