BmK AS attenuated neuronal hyperexcitability and suppressed neuroinflammation by inhibiting the NLRP1 inflammasome pathway and the associated pyroptosis.<h4>Discussion</h4>Our findings establish BmK AS as a promising multimechanistic therapeutic candidate, highlighting the strategic value of dual therapeutic actions, namely, Nav1.6 modulation and neuroinflammation inhibition, for epilepsy treatment. This evidence concerns the gene SCN8A and epilepsy.