Researchers at the Institute for Molecular Bioscience (IMB) at The University of Queensland (UQ) have developed a novel peptide-based inhibitor of the voltage-gated sodium channel 1.7 (Nav1.7). Loss-of-function mutations of SCN9A, the gene encoding Nav1.7, have been identified as the cause of congenital insensitivity to pain, a rare condition characterized by the inability to sense pain in otherwise normal individuals.  Gain-of-function mutations of SCN9A are the cause of two hereditary pain disorders, inherited erythromelalgia and paroxysmal extreme pain disorder. Both disorders are associated with redness, swelling and burning pain and thus, pharmacological inhibition of Nav1.7 is a promising therapeutic strategy for the treatment pain.

Key features

  • A peptide-based inhibitor targeting the resting state of voltage-gated sodium channel 1.7 (Nav7)
  • Potent (nanomolar activity) and selective for Nav7 over other Nav isoforms
  • Proof of concept data in post-surgical and other rodent models of pain
  • Potential for use in other indications.


Therapeutic applications of the Nav1.7 inhibitor include:

  • Post-operative pain;
  • Acute pain;
  • Chronic cough;
  • Cancer, and
  • Itch.

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