Discontinued ProductKaliotoxin (Cat. No. 3564) has been withdrawn from sale for commercial reasons.
Potent blocker of voltage-sensitive K+ channels (IC50 values are 0.1, 1.1 and 25 nM for KV1.3, KV1.1 and KV1.2 channels) respectively). Also inhibits Ca2+-activated K+ channels.
(Modifications: Disulfide bridge between 8 - 28, 14 - 33, 18 - 35)
|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.
Romi et al (1993) Synthesis and characterization of kaliotoxin: is the 26-32 sequence essential for potassium channel recognition? J.Biol.Chem. 268 26302 PMID: 8253752
Mourre et al (1999) Distribution in rat brain of binding sites of kaliotoxin, a blocker of Kv1.1and Kv1.3 α-subunits. J.Pharmacol.Exp.Ther. 291 943 PMID: 10565809
Korukottu et al (2008) High-resolution 3D structure determination of kaliotoxin by solid-state NMR spectroscopy. PLoS ONE 3 e2359 PMID: 18523586
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Keywords: Kaliotoxin, Kaliotoxin supplier, potassium, channels, blockers, ca2+-activated, voltage, sensitive, gated, K+, venoms, Voltage-Gated, Potassium, Channels, Ca2+-Activated, 3564, Tocris Bioscience
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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.
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.