Discovery of Novel Non-Opioid Drug Compounds

Technology #ua16-044

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May Khanna
Assistant Professor, Pharmacology
Rajesh Khanna
Associate Professor, Pharmacology
Vijay Gokhale
Senior Research Scientist, BIO5
Reena Chawla
Postdoctoral Research Associate I, BIO5 Institute
Managed By
Lisa Lin
Licensing Manager (520) 626-6969

Discovery of novel non-opioid drug compounds for pain reduction


Background: Approximately 1.5 billion people worldwide suffer from chronic pain. Opioids are currently the primary treatment option for chronic pain caused by severe trauma. However, opioids are encumbered with various side effects include constipation, nausea, respiratory depression, drowsiness, and addiction. Novel pain drug targets are necessary to provide multiple therapeutic options to patients to avoid addictions and tolerance to the drugs.


Invention: The invention describes compounds inhibiting CRMP2 SUMOylation, a post-translational modification that adds a small ubiquitin-like modifier (SUMO) tag, for indirect regulation of the voltage-gated sodium channel Nav1.7 channel. Nav1.7 is expressed in the peripheral nervous system within ganglia that are related to nociceptive pain. The Nav1.7 channel modulates current thresholds required to trigger action potentials, which are responsible for generating the sensations of pain. The decrease in SUMOylation of CMRP2 decreases Nav1.7 trafficking to the cell surface, resulting in pain reduction. The inventors at the University of Arizona have computationally and experimentally screened a chemical library and found 4 candidate compounds that decrease Nav1.7 current density on the surface and reduce pain in animal models. These compounds have never been used in pain indications before. They are also developing derivatives based on a structure-function analysis of these 4 candidates.



• Use of these four candidate compounds in pain reduction.

• Novel drug compounds for pain medicine.



• No motor impairment or sedation.

• Higher potency and equivalent efficacy to opioids.

• Reduced potential for rewarding effect and reduced potential for abuse compared to opioids.


Related Publications:

Dustrude ET, Wilson SM, Ju W, Xiao Y, Khanna R. CRMP2 protein SUMOylation modulates NaV1.7 channel trafficking. J Biol Chem. 2013 Aug 23;288(34):24316-31.  doi: 10.1074/jbc.M113.474924. Epub 2013 Jul 8. PubMed PMID: 23836888; PubMed Central PMCID: PMC3750134.

Licensing Manager:

Lisa Lin