Kv11.1 (hERG) channel blocker, blocks rapidly activating and slowly activating components of delayed rectifier K+ currents (IC50 of 0.4 mM and 3 mM, respectively). Also inhibits Na+/Ca2+ exchanger in vitro. Shows inhibition of Na+ currents, L-type Ca2+ currents and other K+ currents at high concentrations.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 530.88. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||1.88 mL||9.42 mL||18.84 mL|
|5 mM||0.38 mL||1.88 mL||3.77 mL|
|10 mM||0.19 mL||0.94 mL||1.88 mL|
|50 mM||0.04 mL||0.19 mL||0.38 mL|
References are publications that support the products' biological activity.
Watanabe and Kimura (2010) Inhibitory Effect of Azimilide on Na+/Ca2+ Exchange Current in Guinae-Pig Cardiac Myocytes. J.Pharmacol.Sci. 114 111 PMID: 20710119
Busch et al (1998) Blockade of HERG channels by the class III antiarrhythmic Azimilide: mode of action. Br.J.Pharmacol. 123 23 PMID: 9484850
Busch et al (1995) Blockade of Human IsK channels expression in Xenopus oocytes by the novel class III antiarrhythmic NE-10064. Eur.J.Pharmacol. 264 33 PMID: 7828640
Fermini et al (1995) Use-dependent effects of the class III antiarrhythmic agent NE-10064 (azimilide) on cardiac repolarisation: block of delayed rectifier potassium and L-type calcium currents. J.Cardiovasc.Pharmacol. 26 259 PMID: 7475051
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Keywords: Azimilide dihydrochloride, supplier, potassium, channel, blockers, Kv11.1, hERG, blocks, Voltage-Gated, Potassium, Channels, Na+/Ca2+, Exchanger, Voltage-Gated, Potassium, Channels, Tocris Bioscience
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Literature in this Area
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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.