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Sodium channels are central mediators of action potentials and, therefore, critical to neural and cardiac function. The NAV1.7 sodium channel is important in nociceptive neurons that sense pain — humans missing function of this channel are insensitive to pain and have anosmia; those with hyperactive mutant channels suffer from erythromelalgia or paroxysmal pain disorders. However, targeted treatment of sodium channels has been difficult because current drugs are poorly selective.
Here, Lee and colleagues take immunotherapy to a different place by using an antibody to target the voltage sensor of the sodium channel. They showed that this voltage-sensor-paddle–targeting antibody inhibited the ability of NAV1.7 sodium channels to conduct. Given…