Cannabinoids for neuropathic pain conditions

Cannabinoids for neuropathic pain conditions

Neuropathic pain is often very difficult to treat with current Food and Drug Administration (FDA)-approved analgesics.  The most commonly prescribed medication to treat these chronic pain conditions is opioids.  Opioids have very limited efficacy in patients with chronic neuropathic pain conditions.  This has sparked research into new targets for the treatment of these patients.  Promising research by investigators at the Cleveland Clinic demonstrated that microglial inflammation is a common pathway for neuropathic pain and other treatment-resistant neuroinflammatory conditions, such as Alzheimer’s disease (AD).

“Microglial inflammation is a mechanism of many CNS disorder – neuropathic pain, Alzheimer’s disease, multiple sclerosis, parkinsonism, you name it,” said lead researcher Mohamad Naguid, MD, of Cleveland Clinic’s Anesthesiology Institute, Department of Pain Management.

Subsequently, this team of researchers has synthesized a molecule called MDA7, which is a cannabinoid type 2 (CB2) receptor-selective agonist.  Preliminary studies with this new drug candidate have shown that it can inhibit microglial activation and recruitment, which is fundamental to microglial inflammation and neuropathic pain.

Thus far, their research is in the preclinical phase.  They have shown efficacy in a rodent model of Chemotherapy-induced neuropathic pain1, CRPS (not yet published), and some promising results in an animal model of Alzheimer’s disease2.  They hope to test MDA7 in humans as a next step.  The team is very hopeful that their preclinical results translate well to the clinic.  Only time will tell.


1. Naguib, M., Xu, J.J., Diaz, P., Brown, D.L., Cogdell, D., Bie, B., Hu, J., Craig, S., Hittelman, W.N., 2012. Prevention of paclitaxel-induced neuropathy through activation of the central cannabinoid type 2 receptor system. Anesthesia and analgesia 114, 1104-1120.

2. Bie, B., Wu, J., Yang, H., Xu, J.J., Brown, D.L., Naguib, M., 2014. Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency. Nature neuroscience 17, 223-231.