in addition, bds-1 enhances the current flowing through several voltage-gated sodium channels. the toxin binds to the s3-s4 linker of domain iv and slows the inactivation of the channel, resulting in increased current upon depolarization. bds-1 has a very strong potency for the human nav1.7 channel. in mice, bds-1 slows the inactivation of nav1.3 channels but has smaller effects on the inactivation of nav1.1 and nav1.6 channels. this is probably due to a different channel sensitivity for the toxin.