Biochemistry Focus webinar series: Neurobiology of chronic pain: mechanisms, management & in-between

Chronic pain is defined as pain experienced for a period of six months or longer and there are currently 28 million people in the UK that live with pain. NaV1.7 is a key ion channel in pain signaling. Gain-of-function mutations in the human NaV1.7 gene produce sensory neurons hyperexcitability associated with severe pain; whereas loss-of-function mutations generate congenital insensibility to pain syndromes. Efforts to develop NaV1.7 inhibitors for pain therapeutics have consistently failed.

Speakers at this webinar present an innovative approach of focusing on a unique mechanism of action of compounds that involve an indirect targeting to control surface expression and activity of the NaV1.7 channel. At this event, you will hear how researchers are capitalizing on this unique pathway for NaV1.7 regulation and have identified compounds designed to inhibit enzyme interactions to block relevant proteins. Over 266 compounds have been identified in this manner and these presentations will explore some of the results where there has been inhibition of interactions, anti-allodynic activities without loss of motoric performance or sympathetic side effects. Animal pharmacological studies have also indicated where some of the compounds displayed extended duration of action compared with morphine upon intrathecal administration to rats. Additional studies demonstrated inhibition of NaV1.7 currents in human and porcine sensory neurons, thus increasing likelihood of translational success and ‘de-risking’ compound selection.

Our invited speakers at this webinar are Professor Rajesh Khanna who discusses channeling chronic pain, and Professor David Finn who speaks on pain and negative affect.

This webinar was chaired by Dr Eilís Dowd, Lecturer in Pharmacology at National University of Ireland, Galway, and Neuronal Signaling journal Associate Editor.

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