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Discontinued ProductBatrachotoxin (Cat. No. 2914) has been withdrawn from sale for commercial reasons.
Potent neurotoxin that activates voltage-gated sodium channels. Shifts voltage-dependent activation to more negative potentials, inactivation is disabled and pore conductance and selectivity are altered (displays increased permeability for NH4+, K+ and Cs+ ions).
|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.
References are publications that support the biological activity of the product.
Li et al (2002) The batrachotoxin receptor on the voltage-gated sodium channel is guarded by the channel activation gate. Mol.Pharmacol. 61 905 PMID: 11901230
Bosmans et al (2004) The poison dart frog's batrachotoxin modulates NaV1.8. FEBS Lett. 577 245 PMID: 15527793
Wang et al (2006) How batrachotocin modifies the sodium channel permeation pathway: computer modeling and site-directed mutagenesis. Mol.Pharmacol. 69 788 PMID: 16354762
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Keywords: Batrachotoxin, Batrachotoxin supplier, voltage-gated, voltage-dependent, Na+, channel, activators, Sodium, NaV, Channels, neurotoxins, BTX, Voltage-gated, 2914, 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.