KN-93-hydrochloride|cas | DC Chem|Supplier|Price|Buy  

KN-93-hydrochloride|cas | DC Chem|Supplier|Price|Buy

DC Chemicals Supply: KN-93-hydrochloride, Cas:  ,Cat No. DC7442, Purity>98%, In stock.

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KN-93-hydrochloride|cas , Synonym name: KN 93 hydrochloride; KN93 hydrochloride, Chemical name:　, Molecule weight: 537.5, Molecule Formula: C26H30Cl2N2O4S

KN-93 Hcl is a selective inhibitor of Ca2+/calmodulin-dependent kinase II (CaMKII), competitively blocking CaM binding to the kinase (Ki = 370 nM).

IC50 Value: 12uM (NIH3T3 Cell) [1]

KN-93 is a novel membrane-permeant synthetic inhibitor of CaMK-II,

in vitro: KN-93 inhibits serum-induced fibroblast cell growth in a comparable dose-dependent fashion to its inhibition of CaMK-II activity. After 2 days of KN-93 treatment, 95% of cells are arrested in G1. G1 arrest is reversible; 1 day after KN-93 release, a peak of cells had progressed into S and G2-M. KN-92, a similar but inactive compound, had no effect on CaMK-II activity or cell growth [1]. In contrast effects of carbachol, histamine and forskolin were significantly inhibited by KN-93 with an IC50 of 0.15, 0.3 and 1 microM, respectively; these effects occurred without any changes in intracellular cyclic AMP and Ca2+ levels [2]. KN-93 inhibits expression of the anti-apoptotic protein Mcl-1 and induces expression of the pro-apoptotic protein PUMA; third, KN-93-mediated cell death is p53-independent; and fourth, KN-93 induces the generation of ROS [4].

in vivo: EADs were significantly suppressed by KN-93 (EADs present in 4/10 hearts) compared to KN-92 (EADs present in 10/11 hearts) (P =.024). There were no significant differences in parameters favoring EADs such as monophasic action potential duration or heart rate in KN-93- or KN-92-treated hearts. CaM kinase activity in situ increased 37% in hearts with EADs compared to hearts without EADs (P =.015) [3].

Toxicity: N/A

Clinical trial: N/A