Chemical Name |
KN-93 |
CAS Number |
139298-40-1 |
MDL Number |
MFCD00236424 |
Molecular Formula |
C26H29ClN2O4S |
Molecular Weight |
501.04 |
Introduction of 139298-40-1 :
KN-93 is a cell-permeable, reversible and competitive inhibitor calmodulin-dependent kinase type II (CaMKII) with a Ki of 370 nM. IC50 & Target: Ki: 370 nM (CaMK) In Vitro: 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-93 also blocks cell growth stimulated by basic fibroblast growth factor, platelet-derived growth factor-BB, and epidermal growth factor in NIH 3T3 fibroblasts[1]. KN-93 inhibits the H+, K+-ATPase activity but strongly dissipates the proton gradient formed in the gastric membrane vesicles and reduces the volume of luminal space[2]. KN-93 (0.5 μM) prevents increased LV developed pressure during action potential prolongation and early afterdepolarizations. Ca2+-independent CaM kinase activity is increased during early afterdepolarizations and this increase is prevented by KN-93[3]. KN-93 (10 μM )significantly inhibits the activation of CaMKII/NF-κB signaling induced by elevated glucose, and subsequently decreases the expression of VEGF, iNOS and ICAM-1 in Müller cells[4]. In Vivo: KN-93 (1 mg/kg/day, i.p.) inhibits retinal vascular leakage induced by diabetes, and suppresses phosphorylation of CaMKII and NF-κB in diabetic retina[4].
Purity |
NLT 98% |
Storage |
at 20ºC 2 years |
*The above information is for reference only.