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Voltage-gated sodium(NaV)channels generate and propagate action potentials in excitable cells,and several NaV subtypes have become important targets for pain management.The μ-conotoxins inhibit subtypes of the NaV with varied specificity,but often lack of specificity to interested subtypes.Engineering the selectivity of the μ-conotoxins presents considerable complexity and challenge,as it involves the optimization of their binding affinities to multiple highly conserved NaV subtypes [1-3].