nav1.4 channel

µ-Conotoxin-CnIIIC acetate is a potent NaV1.4 sodium channel antagonist, a conotoxin peptide consisting of 22 amino acids, used for muscle relaxation and pain relief.

μ-Conotoxin-CnIIIC, a 22-residue conopeptide derived from Conus consors, acts as a potent and persistent NaV1.4 channel blocker, exhibiting analgesic, anaesthetic, and myorelaxant properties [1] [2].

μ-Conotoxin GIIIB, a 22-residue polypeptide derived from the venom of the piscivorous cone snail Conus geographus, serves as an inhibitor of the Na V 1.4 channel, effectively blocking muscle cell contraction [1] [2] [3].

GrTx1, a peptide toxin derived from Grammostola rosea spider venom, selectively inhibits sodium channels Nav1.1, Nav1.2, Nav1.3, Nav1.4, Nav1.6, and Nav1.7, with IC50 values of 0.63 µM, 0.23 µM, 0.77 µM, 1.29 µM, 0.63 µM, and 0.37 µM, respectively [2]. This compound has applications in neurological disease research [1].

Ceratotoxin-1 (CcoTx1) is a peptide toxin that functions as an inhibitor of various voltage-gated sodium channel subtypes. It selectively inhibits Nav1.1 β1, Nav1.2 β1, Nav1.4 β1, and Nav1.5 β1 with IC50 values of 523 nM, 3 nM, 888 nM, and 323 nM, respectively. Additionally, Ceratotoxin-1 is known to inhibit Nav1.8 β1 [1].

μ-Conotoxin BuIIIC (Mu-Conotoxin BuIIIC) effectively inhibits the NaV1.4 sodium channel [1].

Potent rat Nav1.7, human Nav1.4 and rat Nav1.6 channel activator (EC50 values are 7, 10 and 47 nM, respectively). Exhibits minimal activation at mammalian Nav1.2, Nav1.3 and Nav1.5 (EC50 values >3 μM). Inhibits fast inactivation on all channels. Increases

Selective NaV1.7 channel blocker. Preferentially inhibits neuronal NaV1.7, 1.2 and 1.3 (IC50 values are 26, 150 and 338 nM respectively), compared to muscle subtypes NaV1.4 and 1.5 (IC50 = >10 μM). Inhibits the channel by binding at the neurotoxin recepto