2019-020 – Non-Opioid Suppression of Immune Reactivity to Treat Pain and Opioid Addiction

Background The rate of opioid-related overdoses in the United States has reached an unprecedented high in recent years. According to the Centers for Disease Control and Prevention, overdose deaths involving prescription opioids were five times higher in 2016, than in 1991, with more than 46 people dying each day in 2016. An emergent epidemic has been attributed to this drastic increase of misuse. Currently, opioids are prescribed to alleviate pain. However, with chronic exposure, opioids can also induce pain. Opioids activate the toll-like receptor 4 (TLR4), triggering the ultimate production of pro-nociceptive molecule, interleukin-IL-1β (IL-1β), which is known as a pro-inflammatory cytokine. IL-1β is known for mediating inflammation as well as neuroexcitatory events. Therefore, re-administration of opioids can lead to prolonged pain, with increased exposure to opioids for prolonged periods, increasing the risk for addictive side effects. By inhibiting the production of IL-1β, pain can be suppressed. Consequently, it would be beneficial to identify a novel non-opioid treatment that can inhibit or block the actions of IL-1β, and in doing so, also block pain transmission. Notably, this approach would lack direct effects on neurons and reduce the potential addictive side effects. Considering current opioid-related addiction, overdosing and crisis, there is a dire need for an alternative non-opioid treatment to treat chronic pain. Technology Description Researchers at the University of New Mexico have developed an innovative, non-opioid treatment alternative for treating chronic neuropathic pain. The treatment induces the production of endogenous anti-inflammatory mechanisms to the production of pro-inflammatory cytokines, including IL-1β. By avoiding opioid-based treatment, the likelihood of addictive side effects may be prevented. Furthermore, this drug may be applied as an adjunct treatment to patients on opioid therapy, such as methadone and buprenorphine, which may improve the therapeutic efficacy of these opioid compounds. Gregg Banninger GBanninger@innovations.unm.edu 505-272-7908