Selective NaV1.7 channel blocker. Shifts activation gating positively and decreases current magnitude. Displays 100-fold selectivity over other sodium channel subtypes.
(Modifications: Disulfide bridge: 2-16, 9-21, 15-25)
|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.
Smith et al (2007) Molecular interactions of the gating modifier toxin ProTx-II with NaV 1.5: implied existence of a novel toxin binding site coupled to activation. J.Biol.Chem. 282 12687 PMID: 17339321
Edgerton et al (2008) Evidence for multiple effects of ProTxII on activation gating in NaV 1.5. Toxicon. 52 489 PMID: 18657562
Schmalhofer et al (2008) ProTx-II, a selective inhibitor of NaV 1.7 sodium channels, blocks action potential propagation in nociceptors. Mol.Pharmacol. 74 1476 PMID: 18728100
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Keywords: ProTx II, ProTx II supplier, toxins, voltage, gated, sodium, Na+, channels, NaV1.7, potent, selective, blockers, venoms, Voltage-gated, Sodium, Channels, 4023, Tocris Bioscience
1 Citation for ProTx II
Citations are publications that use Tocris products. Selected citations for ProTx II include:
Li et al (2017) Membrane protein Nav1.7 contributes to the persistent post-surgical pain regulated by p-p65 in dorsal root ganglion (DRG) of SMIR rats model. BMC Anesthesiol 17 150 PMID: 29115943
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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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.