Nav1.1 Drug Discovery

Molecular Physiology and Neurophysics Group


Project 3

Nav1.1 Drug Discovery


We have established a critical role for Nav1.1 in regulating the excitability of sensory nerve fibers that underlie mechanical pain. We also discovered a compound (FB-100) that specifically targets Nav1.1 gating without blocking the conserved pore. Subsequently, we established in vivo efficacy of the Nav1.1 compound in three separate mouse epilepsy models where Nav1.1 controls seizure pathways. We are currently further exploring the role of Nav1.1 as a pain target in parallel to developing FB-100 as a possible therapeutic for allodynia.
Irritable Bowel Syndrome (IBS) patients suffer from chronic gut pain due to visceral hypersensitivity to allodynia. As there is only a limited understanding of the basis of chronic visceral hypersensitivity (CVH), drug-based management strategies are ill-defined. We are now investigating whether Nav1.1 underlies the abdominal pain that occurs with CVH. These results will provide insights into the utility of NaV1.1-selective inhibitors to alleviate hypersensitivity and pain associated with IBS.


Frank Bosmans