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Selective blocker of NaV1.5 channels (IC50 = 348 nM); displays no effect on other isoforms, including NaV1.2, NaV1.4, NaV1.6 and NaV1.7. Thought to inhibit sodium channel activation by binding to the NaV1.5 S3-S4 linker of domain II. Selectively inhibits the activation of cardiac sodium channels, but has no effect on sodium channels in dorsal root ganglion neurons.
(Modifications: Disulfide bridge: 4-19,11-24,18-31)
|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 (2004) Jingzhaotoxin-III, a novel spider toxin inhibiting activation of sodium channel in rat cardiac myocytes. J.Biol.Chem. 279 26220 PMID: 15084603
Rong et al (2011) Molecular basis of the tarantula toxin jingzhaotoxin-III (β-TRTX-Cj1α) interacting with voltage sensors in sodium channel subtype Nav1.5. FASEB J. 25 3177 PMID: 21665957
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Keywords: Jingzhaotoxin III, Jingzhaotoxin III supplier, cardiotoxins, NaV1.5, selective, ion, channels, sodium, blockers, blocks, inhibitors, inhibits, venoms, Voltage-gated, Sodium, Channels, 4913, Tocris Bioscience
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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.