nav1.4 channel

hERG-IN-3 is an orally active hERG inhibitor with an IC50 of 44.5 nM. It has a Ki value of 14 nM for the β2-adrenergic receptor. hERG-IN-3 exhibits skeletal muscle Nav1.4 sodium channel blocking activity with an IC50 of 4.4 μM, which is three times higher than that for hNav1.5. In animal models, hERG-IN-3 demonstrates potent antimyotonic activity and can be utilized in the study of congenital myotonia.

Lu AE98134, an activator of voltage-gated sodium channels, acts as a partly selective positive modulator of Nav1.1 channels and also increases the activity of Nav1.2 and Nav1.5 channels while not affecting Nav1.4, Nav1.6, and Nav1.7 channels. Lu AE98134 can be used to analyze pathophysiological functions of the Nav1.1 channel in various central nervous system diseases, including cognitive restoring in schizophrenia, et al[1].

ICA-121431 (2,2-Diphenyl-N-[4-(thiazol-2-ylsulfamoyl) is a nanomolar potent small molecule Nav1.7 channel inhibitor with IC50 of 19 nM for rat Nav1.7, with little or no activity against human Nav1.5 or Nav1.7 channels.

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

GpTx-1 TFA is a polypeptide NaV1.7 sodium channel antagonist isolated from the venom of the Chilean spider Grammostola porter. It exhibits potent inhibitory activity on the NaV1.7 channel with an IC50 value of 10 nM, demonstrating excellent selectivity over NaV1.4 (IC50 = 0.301 μM) and NaV1.5 (IC50 = 4.20 μM) with >20-fold and >950-fold selectivity, respectively.