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KN 92 is an inactive analog of the CaM kinase II inhibitor KN 93 . Potassium channel (Kv1.2, 1.4, 1.5, 2.1, 3.2 and hERG) blocker in vitro.
Active Analog also available.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
The following data is based on the product molecular weight 554.98. 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|
|0.1 mM||18.02 mL||90.09 mL||180.19 mL|
|0.5 mM||3.6 mL||18.02 mL||36.04 mL|
|1 mM||1.8 mL||9.01 mL||18.02 mL|
|5 mM||0.36 mL||1.8 mL||3.6 mL|
References are publications that support the biological activity of the product.
Rezazadeh et al (2005) KN-93 (2-[N-(2-hydroxyethyl)]-N-(4-methoxybenzenesulfonyl)]amino-N-(4-chlorocinnamyl)-N-methylbenzylamine), a calcium/calmodulin-dependent protein kinase II inhibitor, is a direct extracellular blocker of voltage-gated J.Pharmacol.Exp.Ther. 317 292 PMID: 16368898
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Keywords: KN 92, KN 92 supplier, potassium, K+, blockers, Kv, channels, inactive, analog, KN93, KN92, calcium, binding, protein, modulators, voltage-gated, hERG, Human, Ether-A-Go-Go, Gene, voltage-dependent, CaM, Kinase, II, kinases, Calmodulin-Activated, calmodulin-dependent, Ca2+, Binding, Calcium, Protein, Voltage-Gated, Potassium, Channels, 4130, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for KN 92 include:
Seto et al (2013) Acute SimV. inhibits K ATP channels of porcine coronary artery myocytes. Oncotarget 8 e66404 PMID: 23799098
Weng et al (2017) An Intrinsic Epigenetic Barrier for Functional Axon Regeneration. Neuron 94 337 PMID: 28426967
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Average Rating: 5 (Based on 1 Review.)
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Guinea pig ventricular cardiomyocytes were treated (12-16 h) with KN93 (5 µM), KN92 (5 µM) or Ranolazine (10 µM). Cells were patched and stimulated at a 1 Hz frequency to record action potential. Maximum upstroke velocity was significantly was reduced by KN93 while KN92 was ineffective.