Nav-i-gating antibodies for pain
Nav1.7 entered the limelight in the last decade as a pain target that could provide wide-ranging analgesia, but it has been difficult to target selectively over other voltage-gated sodium channels. Now, a team at the Duke University has found a unique epitope on Nav1.7 and used it to create a highly selective antibody that blocks the channel by locking it in a closed state.1
In mice, the antibody reduced pain and inflammation and suppressed acute and chronic itch. The Duke researchers are in discussions with companies to create a humanized form of the antibody.
Nav1.7 (SCN9A) emerged as a pain target in 2006 when a University of Cambridge team found loss-of-function mutations in the channel in patients with a rare congenital inability to feel pain.2 Because the mutations caused no other overt pathology, drug developers jumped on the possibility that channel inhibitors could provide analgesia without causing major side effects.
At least six companies have Nav1.7-targeted compounds in clinical or preclinical development for