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Potent IKs blocker (IC50 = 64 nM). Displays no effects on other cardiac channels; IC50 values are 3.3, >10, 11.1 and 12.6 μM for INa, ICa, Ito and IKr currents respectively. Prolongs QT and causes unprovoked torsades de pointes (TdP).
Sold with the permission of Janssen Pharmaceutica NV
|Storage||Store at +4°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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 440.98. 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|
|0.25 mM||9.07 mL||45.35 mL||90.71 mL|
|1.25 mM||1.81 mL||9.07 mL||18.14 mL|
|2.5 mM||0.91 mL||4.54 mL||9.07 mL|
|12.5 mM||0.18 mL||0.91 mL||1.81 mL|
References are publications that support the biological activity of the product.
Towart et al (2009) Blockade of the IKs potassium channel: an overlooked cardiovascular liability in drug safety screening? J.Pharm.Toxicol.Meth 60 1
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Keywords: JNJ 303, JNJ 303 supplier, potent, Iks, blockers, JNJ303, potassium, K+, channels, selective, slow, delayed, rectifier, current, KCNQ1, Kv7.1, voltage-gated, voltage-dependent, Voltage-Gated, Potassium, Channels, 3899, Tocris Bioscience
1 Citation for JNJ 303
Citations are publications that use Tocris products. Selected citations for JNJ 303 include:
Björk et al (2017) Evaluation of Optogenetic Electrophysiology Tools in Human Stem Cell-Derived Cardiomyocytes. Front Physiol 8 884 PMID: 29163220
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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.