nav1.4

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.

Phrixotoxin 3 TFA is a potent inhibitor of voltage-gated sodium channels, with IC50 values of 0.6 nM for NaV1.2, 42 nM for NaV1.3, 72 nM for NaV1.4, 288 nM for NaV1.1, and 610 nM for NaV1.5. This compound modulates the activity of these channels similarly to traditional gating-modifier toxins, inducing a depolarizing shift in gating kinetics and obstructing the inward sodium current.

Huwentoxin-IV TFA is a potent, selective blocker of sodium channels, specifically inhibiting neuronal Nav1.7, Nav1.2, Nav1.3, and Nav1.4 with IC50 values of 26, 150, 338, and 400 nM, respectively. It preferentially targets the peripheral nerve subtype Nav1.7 by interacting with neurotoxin receptor site 4, demonstrating analgesic effects in animal models of inflammatory and neuropathic pain [1] [2].

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].

μ-Conotoxin Sx IIIA is a bioactive peptide that blocks NaV1.4 channels.

GsAF-I is a potent blocker of Na_v and hERG1 channels, exhibiting half-maximal inhibitory concentrations (IC50s) of 0.36 μM (Na_v 1.1), 0.6 μM (Na_v 1.2), 1.28 μM (Na_v 1.3), 0.33 μM (Na_v 1.4), 1.2 μM (Na_v 1.6), 0.04 μM (Na_v 1.7), and 4.8 μM (hERG1) [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 blocker of voltage-gated sodium channels (IC50 values are 0.6, 42, and 72 nM for NaV1.2, NaV1.3 and NaV1.5 respectively). Blocks inward sodium currents in a voltage-dependent manner.

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