Redirecting NaV1.7 Trafficking to Deliver Selective Pain Relief Without CNS Liabilities
- Targeting the CRMP2–SUMOylation pathway to indirectly regulate NaV1.7 surface expression and DRG excitability
- Demonstrating a differentiated strategy to overcome the clinical limitations of direct NaV1.7 pore blockers
- Advancing small molecules against the CRMP2–SUMO interface toward first-inhuman development through NIH collaboration