Location : Home > Products > Inhibitors of Meditech > Others
Name:KN-93
| Chemical structure | Code NO. |
MT0810 |
 |
Name |
KN-93 |
Synonym |
KN93; KN 93 | |
CAS NO. |
139298-40-1 | |
Chemical Formula |
C26H29ClN2O4S | |
MW |
501.04 | |
Purity |
>98% | |
Solubility(R.T.: 25℃) |
DMSO > 25 mg/ml Ethanol > 25 mg/ml | |
Stability |
- 20℃, 2 years |
Availability and price
KN-93 is in stock. Bulk available at low price, welcom to inquire quotation.
We offer big discount for bulk quantities. If you have any other questions or needs, please send email to sales@meditechbs.com. We’ll reply you asap.
Description
KN-93 is a selective inhibitor of Ca2+/calmodulin-dependent kinase II (CaMKII), competitively blocking CaM binding to the kinase (Ki = 370 nM).
IC50 Value: 370 nM (Ki); 12uM (NIH3T3 Cell) [1]
Target: CaMKII
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].
IC50 Value: 370 nM (Ki); 12uM (NIH3T3 Cell) [1]
Target: CaMKII
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].
References
Attention
Sold for research purposes only; not for human use of any kind.
