Mu-conotoxins block voltage-gated sodium channels (Nav). This synthetic toxin potently blocks rNav1.4/SCN4A (IC(50)= 7 nM). It also moderately blocks rNav1.1/SCN1A (IC(50)=370 nM), rNav1.2/SCN2A (IC(50)=1 uM), and mNav1.6/SCN6A (IC(50)=570 nM) (PubMed:18831583, PubMed:21652775). It is noteworthy that coexpression of subunits beta-2 or beta-4 (but not beta-1 or beta-3) decrease by about 16-fold the binding potency of the toxin to rNav1.6, since these subunits (thanks to their extracellular domain) covalently bind to the key cysteine of the channel, thus preventing the covalent binding of the toxin (PubMed:25632083). It is also noteworthy that the toxin is 50-fold more potent on mouse Nav1.6 than on rat Nav1.6 (PubMed:25632083). In vivo, when injected intraperitoneally or subcutaneously in mice, causes motor impairment, paralysis and death (PubMed:18831583). Expressed by the venom duct. The cysteine framework is III (CC-C-C-CC). Classified in the M-4 branch, since 4 residues stand between the fourth and the fifth cysteine residues. When injected intraperitoneally or subcutaneously in mice, this toxin causes motor impairment/paralysis and is lethal at doses as low as 0.6 nmol per mouse. Does not inhibit rNav1.3/SCN3A, rNav1.5/SCN5A, rNav1.7/SCN9A and rNav1.8/SCN10A (PubMed:21652775, PubMed:25632083). Belongs to the conotoxin M superfamily.