Nav1.7 channels are mainly distributed in the peripheral nervous system.Blockade of Nav1.7 channels with small-molecule inhibitors in humans might provide pain relief without affecting the central nervous system.Based on the facts that many reported Nav1.7-selective inhibitors contain aryl sulfonamide fragments,as well as a tricyclic antidepressant,maprotiline,has been found to inhibit Nav1.7 channels,we designed and synthesized a series of compounds with ethanoanthracene and aryl sulfonamide moieties.Their inhibitory activity on sodium channels were detected with electrophysiological techniques.We found that compound 10o potently inhibited Nav1.7 channels stably expressed in HEK293 cells (ICso =0.64 + 0.30 nmol/L) and displayed a high Nav1.7/Nav1.5 selectivity.In mouse small-sized dorsal root ganglion neurons,compound 10o (10,100 nmol/L) dosedependently decreased the sodium currents and dramatically suppressed depolarizing current-elicited neuronal discharge.Preliminary in vivo experiments showed that compound 10o possessed good analgesic activity:in a mouse visceral pain model,administration of compound 10o (30-100 mg/kg,i.p.) effectively and dose-dependently suppressed acetic acid-induced writhing.