Mapping Cardiac Sodium Channel Isoform Composition to Improve Ion Channel Selectivity & Reduce Arrhythmia Risk During Drug Development

  • Revealing how neuronal and skeletal muscle sodium channel isoforms are differentially expressed across cardiac tissues beyond the canonical NaV1.5 paradigm
  • Demonstrating how disease remodeling and pharmacological perturbation alter sodium channel composition to influence cardiac arrhythmia risk
  • Applying protein engineering and ion channel pharmacology approaches to improve safety assessment for next-generation voltage-gated sodium channel therapeutics