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Biological Activity for BDS I
BDS I is a potent and reversible Kv3.4 potassium channel blocker (IC50 = 47 nM); also attenuates inactivation of sodium currents by acting on Nav1.7 and Nav1.3 channels. Enhances TTX-sensitive sodium currents in rat small dorsal root ganglion neurons. Neuroprotective.
Technical Data for BDS I
(Modifications: Disulfide bridge: 4-39,6-32,22-40)
|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 Data for BDS I
|Solubility||Soluble to 1 mg/ml in water|
References for BDS I
References are publications that support the biological activity of the product.
Diochot et al (1998) Sea anemone peptides with a specific blocking activity against the fast inactivating potassium channel Kv3.4. J.Biol.Chem. 273 6744 PMID: 9506974
Liu et al (2012) Modulation of neuronal sodium channels by the sea anemone peptide BDS-I. J.Neurophysiol. 107 3155 PMID: 22442564
Pannaccione et al (2007) Up-regulation and increased activity of KV3.4 channels and their accessory subunit MinK-related peptide 2 induced by amyloid peptide are involved in apoptotic neuronal death. Mol.Pharmacol. 72 665 PMID: 17495071
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Citations for BDS I
Citations are publications that use Tocris products.
Currently there are no citations for BDS I. Do you know of a great paper that uses BDS I from Tocris? Please let us know.
Reviews for BDS I
Average Rating: 5 (Based on 1 Review.)
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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* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.