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KN-93 hydrochloride CaMK II inhibitor

Catalog No.B1306
Size Price Stock Qty
10mM (in 1mL DMSO)
$340.00
In stock
1mg
$57.00
In stock
5mg
$150.00
In stock
10mg
$280.00
In stock
25mg
$520.00
In stock

Tel: +1-832-696-8203

Email: [email protected]

Worldwide Distributors

Sample solution is provided at 25 µL, 10mM.

Quality Control

Quality Control & MSDS

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Chemical structure

KN-93 hydrochloride

Protocol

Cell experiment[1]:

Cell lines

NIH 3T3 fibroblasts

Preparation method

The solubility of this compound in DMSO is > 10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.

Reacting condition

24-72 h, 24 μM

Applications

KN-93 is an inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMK-II). It inhibits fibroblast CaMK-II activity and cell growth in a dose-dependent manner, reversibly arrests cells in G1 and induces apoptosis.

Animal experiment [2]:

Animal models

8-24-week-old CaMKIV TG mice

Dosage form

10 to 30 μmol/kg IP

Application

KN-93 significantly suppressed isoproterenol-induced arrhythmias in CaMKIV TG mice compared with isoproterenol-treated WT mice, indicating CaMKII is a proarrhythmic molecule in the mouse model of cardiac hypertrophy.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1]. Tombes R M, Grant S, Westin E H, et al. G1 cell cycle arrest and apoptosis are induced in NIH 3T3 cells by KN-93, an inhibitor of CaMK-II (the multifunctional Ca2+/CaM kinase)[J]. Cell growth & differentiation: the molecular biology journal of the American Association for Cancer Research, 1995, 6(9): 1063.

[2]. Wu Y, Temple J, Zhang R, et al. Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophy[J]. Circulation, 2002, 106(10): 1288-1293.

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Chemical Properties

Cas No. 1956426-56-4 SDF Download SDF
Chemical Name (E)-N-(2-(((3-(4-chlorophenyl)allyl)(methyl)amino)methyl)phenyl)-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamide hydrochloride
Canonical SMILES CN(CC1=CC=CC=C1N(S(C2=CC=C(OC)C=C2)(=O)=O)CCO)C/C([H])=C([H])/C3=CC=C(Cl)C=C3.Cl
Formula C26H30Cl2N2O4S M.Wt 537.5
Solubility >26.9mg/mL in DMSO Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

Background

KN-93 hydrochloride is a potent inhibitor of Ca2+/calmodulin-dependent protein kinase II (CaMK II) with Ki value of 0.37μM [1].

KN-93 is an inhibitor of CaMK II. It exerts its effect by competing for the calmodulin binding site of CaMK II with IC50 value of 370nM. In isolated gastric parietal cells, KN-93 shows a potent inhibition of acid secretion induced by carbachol and histamine with IC50 values of 0.15μM and 0.3μM, respectively. It also inhibits forskolin induced aminopyrine uptake with IC50 value of 0.6μM. KN-93 is also found to have effects on the H+, K+-ATPase. 10μM KN-93 and 20μM KN-93 can inhibit 26% and 35% activity of the enzyme, respectively. Moreover, KN-93 is reported to act as an extracellular blocker of Kv channels through enhancing C-type inactivation [1, 2].

References:
[1] Mamiya N, Goldenring J R, Tsunoda Y, et al. Inhibition of Acid Secretion in Gastric Parietal Cells by the Ca2+/Calmodulin-Dependent Protein Kinase II Inhibitor KN-93. Biochemical and biophysical research communications, 1993, 195(2): 608-615.
[2] Rezazadeh S, Claydon T W, Fedida D. 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 potassium channels. Journal of Pharmacology and Experimental Therapeutics, 2006, 317(1): 292-299.