Potent and selective Iks channel blocker (IC50 values are 10.5 and 34 nM in canine and guinea pig ventricular myocytes respectively). Selectively inhibits IKs currents over IKr, IKI, Ito and L-type Ca2+ channel currents. Also has little or no effect on Kv11.1 Kv1.5, Kv1.3, Kir2.1 and HCN2 channel currents. Potentiates E-4031-induced arrhythmias in vivo.
|Storage||Store 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|
Preparing Stock Solutions
The following data is based on the product molecular weight 411.44. 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||2.43 mL||12.15 mL||24.3 mL|
|5 mM||0.49 mL||2.43 mL||4.86 mL|
|10 mM||0.24 mL||1.22 mL||2.43 mL|
|50 mM||0.05 mL||0.24 mL||0.49 mL|
References are publications that support the biological activity of the product.
Gerlach et al (2001) Synthesis and activity of novel and selective I(Ks)-channel blockers. J.Med.Chem. 44 3831 PMID: 11689069
Michael et al (2007) Potentiation of E-4031-induced torsade de pointes by HMR1556 or ATX-II is not predicted by action potential short-term variability or triangulation. Br.J.Pharmacol 152 1215 PMID: 17965747
Thomas et al (2003) HMR 1556, a potent and selective blocker of slowly activating delayed rectifier potassium current. J.Cardiovasc.Pharmacol. 41 140 PMID: 12500032
If you know of a relevant reference for HMR 1556, please let us know.
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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.
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.