TORONTO, Ontario (PRWEB) May 07, 2020
Voltage-gated sodium channels (Nav) are integral in almost all aspects of human physiology, including cardiac and muscle function and pain perception. In this webinar, peptide inhibitors derived from venomous toxins will be explored.
The sodium channel subtype Nav1.7 has been genetically validated to be involved in nociception. Peptide toxins isolated from venomous creatures are potent inhibitors of human voltage-gated sodium channels, with venom peptides selective against Nav1.7 showing great potential as therapeutic pain relief agents. They function to inhibit Nav activity by blocking the pore domain (pore blockers) or by binding to the membrane-embedded voltage sensor domain of the sodium channel (gating-modifier toxins).
However, despite intensive research efforts into Nav1.7 inhibitors, there has been little in the way of translation, likely due to our lack of understanding on how to achieve subtype selectivity, completely inhibit Nav1.7 and how to move from effective in vitro to in vivo inhibitors.
In this webinar, delineating the mechanism of action behind venom peptide inhibition of voltage-gated sodium channels will be presented. This will include discussion on engineering peptides to achieve subtype specificity and complete inhibition of specific sodium channels to unlock the potential of potent venom peptides as therapeutic leads for the treatment of pain.
Join Christina I. Schroeder, Stadtman Investigator, National Cancer Institute, National Institutes of Health in a live webinar on Friday, May 22, 2020 at 10am EDT (3pm BST/UK).
For more information or to register for this event, visit Venom Peptides: Rethinking Voltage-Gated Sodium Channel Inhibition.
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