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Selective blocker of KV11.1 (hERG) channels; inhibits the rapid delayed-rectifier K+ current (IKr). Reversibly prolongs action potential duration in guinea pig papillary muscle and isolated ventricular myocytes, without affecting Na+ or Ca2+ inward currents. Class III antiarrhythmic agent.
|Storage||Desiccate at RT|
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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|DMSO||9.49||20 with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 474.44. Batch specific molecular weights may vary from batch to batch due to the degree 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||2.11 mL||10.54 mL||21.08 mL|
|5 mM||0.42 mL||2.11 mL||4.22 mL|
|10 mM||0.21 mL||1.05 mL||2.11 mL|
|50 mM||0.04 mL||0.21 mL||0.42 mL|
References are publications that support the biological activity of the product.
Ficker et al (2002) The binding site for channel blockers that rescue misprocessed human long QT syndrome type 2 ether-a-gogo-related gene (HERG) mutations. J.Biol.Chem. 277 4989 PMID: 11741928
Verheijck et al (1995) Effects of the delayed rectifier current blockade by E-4031 on impulse generation in single sinoatrial nodal myocytes of the rabbit. Circ.Res. 76 607 PMID: 7895335
Wettwer et al (1991) Effects of the new class III antiarrhythmic drug E-4031 on myocardial contractility and electrophysiological parameters. J.Cardiovasc.Pharmacol. 17 480 PMID: 1711611
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Keywords: E-4031 dihydrochloride, E-4031 dihydrochloride supplier, HERG, KV11.1, channel, blockers, inhibits, inhibitors, rapid, delayed, rectifier, K+, current, IKr, Potassium, KV, Channels, Human, Ether-A-Go-Go, Gene, voltage-gated, voltage-dependent, Voltage-Gated, 1808, Tocris Bioscience
8 Citations for E-4031 dihydrochloride
Citations are publications that use Tocris products. Selected citations for E-4031 dihydrochloride include:
Veldkamp et al (2018) Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel. Nat Commun 9 4357 PMID: 30341287
Zhang et al (2017) Differentiation and characterization of rhesus monkey atrial and ventricular cardiomyocytes from induced pluripotent stem cells. Stem Cell Res 20 21 PMID: 28249229
Pei et al (2017) Chemical-defined and albumin-free generation of human atrial and ventricular myocytes from human pluripotent stem cells. Stem Cell Res 19 94 PMID: 28110125
Yu et al (2014) Apamin does not inhibit human cardiac Na+ current, L-type Ca2+ current or other major K+ currents. Int J Clin Exp Pathol 9 e96691 PMID: 24798465
Guo et al (2015) Use of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes (hiPSC-CMs) to Monitor Compound Effects on Cardiac Myocyte Signaling Pathways. Curr Protoc Chem Biol 7 141 PMID: 26331525
Zhang et al (2015) Cardiac sodium/calcium exchanger preconditioning promotes anti-arrhythmic and cardioprotective effects through mitochondrial calcium-activated potassium channel. PLoS One 8 10239 PMID: 26617732
Bragança et al (2016) Ion Fluxes through KCa2 (SK) and Cav1 (L-type) Channels Contribute to Chronoselectivity of Adenosine A1 Receptor-Mediated Actions in Spontaneously Beating Rat Atria. Front Pharmacol 7 45 PMID: 27014060
Fiore et al (2013) Characterization of hERG1 channel role in mouse colorectal carcinogenesis. Cancer Med 2 583 PMID: 24403225
Do you know of a great paper that uses E-4031 dihydrochloride from Tocris? Please let us know.
Reviews for E-4031 dihydrochloride
Average Rating: 5 (Based on 1 Review.)
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As an antiarrhythmic drug E-4031 was studied to identify drug effect. Concentration dependent Kv channel blocking and control of release were studied. The compound showed blocking activity which is not dependent on concentration administered and data was reproducible. Great product stability and dissolves nicely.
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.
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.