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KN-93 目录号 GC10629

CaMKII inhibitor,selective and cometitive

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10mM (in 1mL DMSO)

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Sample solution is provided at 25 µL, 10mM.


Quality Control & SDS

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Kinase experiment [1]:

Measurement of activities of autophosphorylated/non-autophosphorylate CaMKII

CaMKII activity was measured utilizing syntideII as a substrate. Purified CaMKII was pre-incubated in the assay mixture (35 mM Hepes-Na ( pH 8.0), 10 mM MgC12, 0.5 μM CaM, 5 μM ATP, 1 mM CaCl2 or 1 mM EGTA, total 25 μL) at 30°C for 2 mins. After this pre-incubation, the protein substrate/radioactive ATP mixture was added to the same test tube and the preparation was further incubated at 30°C, for 5 mins (final assay condition: 35 mM Hepes-Na (pH 8.0), 10 mM MgCl2, 0.125 μM CaCl2, 20 μM syntideII, 11.25 μM [γ-32P] ATP, 10 % DMSO and indicated concentrations of KN-93, supplemented with 0.25 mM CaCl2 and 2 mM EGTA (for autophosphorylated samples) or 0.25 mM EGTA and 2 mM CaCl2 (for nonautophosphorylated samples ), total 100 μL). The reaction was terminated by adding of 25 μL of 100 % (w/v) ice-cold TCA. After centrifugation, 80 μL of the supernatant was applied to phosphocellulose paper. The filters were then washed with 75 mM H3PO4 for 15 mins with continuous agitation. After 4-cycles of washing, the radioactivity retains on the filter paper was quantified in a liquid scintillation counter.

Cell experiment [2]:

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.

Reaction Conditions

~ 24 μM; 70 hrs


KN-93 inhibited serum-induced fibroblast cell growth with an IC50 value of 8 μM, and induced apoptosis after prolonged G1 arrest at the concentration of 24 μM.

Animal experiment [3]:

Animal models

Parkinson’s disease (PD) rats

Dosage form

1, 2 or 5 μg; intrastriatal administration; b.i.d., for 21 days


In PD rats, KN-93 (5 μg) ameliorated levodopa-induced dyskinesia through lowering the expression of pGluR1S845.

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.


[1]. Sumi M, Kiuchi K, Ishikawa T, Ishii A, Hagiwara M, Nagatsu T, Hidaka H. The newly synthesized selective Ca2+/calmodulin dependent protein kinase II inhibitor KN-93 reduces dopamine contents in PC12h cells. Biochem Biophys Res Commun. 1991 Dec 31;181(3):968-75.

[2]. Tombes RM, Grant S, Westin EH, Krystal G: 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). Cell Growth Differ 1995, 6(9):1063-1070.

[3]. Yang X, Wu N, Song L, Liu Z. Intrastriatal injections of KN-93 ameliorates levodopa-induced dyskinesia in a rat model of Parkinson's disease. Neuropsychiatr Dis Treat. 2013;9:1213-20.

Chemical Properties

Cas No. 139298-40-1 SDF
别名 KN 93;KN93
化学名 N-[2-[[[(E)-3-(4-chlorophenyl)prop-2-enyl]-methylamino]methyl]phenyl]-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamide
Canonical SMILES CN(CC=CC1=CC=C(C=C1)Cl)CC2=CC=CC=C2N(CCO)S(=O)(=O)C3=CC=C(C=C3)OC
分子式 C26H29ClN2O4S 分子量 501.04
溶解度 ≥ 19.15mg/mL in DMSO 储存条件 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.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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KN-93 is a potent and selective inhibitor of CaM kinase II with IC50 value of 0.37μM.[1]
CaM kinase II means Ca2+/calmodulin-dependent protein kinase II which is a serine/threonine-specific protein kinase. It is regulated by the Ca2+/calmodulin complex. CaMKII has 28 different isoforms. The structure governs an autoinhibition which is the Threonine 286 residue. When this site is phosphorylated, it will permanently activate the CaMKII enzyme. The variable and self-associative domains of CaMKII enzyme govern the sensitivity to calcium and calmodulin. CaMKII is related to many signaling pathways. CaMKII is considered to play an important role in learning and memory. CaMKII is also important for reuptake in cardiomyocytes and Ca2+ homeostasis, and CD8 T-cell activation. Misregulation of CaMKII is considered to be related to Alzheimer’s disease, heart arrhythmia , and Angelman syndrome.[2]
KN-93 significantly inhibited CaM kinase activity at 0.5μM in vitro CaM kinase assay. KN-93 potent inhibited CaM kinase II activity In vitro CaM kinase activity with rabbit myocardium with Ki value of 2.58μM. [1] KN-93 inhibited cell growth at 12μM in NIH 3T3 cells and arrested cells in G1 cycle. KN-93 induced cell apoptosis at 24μM in NIH 3T3 cells. [3] KN-93 inhibits expression of Mcl-1which is an anti-apoptotic protein, It also induces p53-independent cell death in PCa cells. KN-93 also induces  the  generation  of ROS and inhibits AR activity then induces cell death.
[1].    Anderson ME, Braun AP, Wu Y, Lu T, Schulman H, Sung RJ: KN-93, an inhibitor of multifunctional Ca++/calmodulin-dependent protein kinase, decreases early afterdepolarizations in rabbit heart. J Pharmacol Exp Ther 1998, 287(3):996-1006.
[2].    Yamauchi T: Neuronal Ca2+/calmodulin-dependent protein kinase II--discovery, progress in a quarter of a century, and perspective: implication for learning and memory. Biol Pharm Bull 2005, 28(8):1342-1354.
[3].    Tombes RM, Grant S, Westin EH, Krystal G: 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). Cell Growth Differ 1995, 6(9):1063-1070.