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 receptor site 4 in the S3-S4 linker of domain II, trapping the voltage sensor in the inward, closed configuration.
(Modifications: Disulfide bridge: 2-17,9-24,16-31)
(Modifications: Ile-35 = C-terminal amide)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 1 mg/ml in water|
References are publications that support the biological activity of the product.
Xiao et al (2008) Tarantula huwentoxin-IV inhibits neuronal sodium channels by binding to receptor site 4 and trapping the domain II voltage sensor in the closed configuration. J.Biol.Chem. 283 27300 PMID: 18628201
Xiao et al (2011) Common molecular determinants of tarantula huwentoxin-IV inhibition of Na+ channel voltage sensors in domains II and IV. J.Biol.Chem. 286 27301 PMID: 21659528
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Keywords: Huwentoxin IV, Huwentoxin IV supplier, Huwentoxin, 4, sodium, channels, NaV1.7, blockers, antagonists, toxins, voltage, gated, Na+, selective, venoms, Voltage-gated, Sodium, Channels, 4718, Tocris Bioscience
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.