产品
编 号：F148590
分子式：C26H29ClN2O4S
分子量：501.04
分子式：C26H29ClN2O4S
分子量：501.04
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
970
In-stock
1mg
395
In-stock
5mg
880
In-stock
10mg
1216
In-stock
25mg
2010
In-stock
50mg
询价
In-stock
100mg
询价
In-stock
结构图
CAS No: 139298-40-1
产品详情
生物活性：
KN-93 is a cell-permeable, reversible and competitive inhibitor calmodulin-dependent kinase type II (CaMKII) with a Ki of 370 nM.
体内研究：
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.
体外研究：
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. 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. 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. 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.
KN-93 is a cell-permeable, reversible and competitive inhibitor calmodulin-dependent kinase type II (CaMKII) with a Ki of 370 nM.
体内研究：
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.
体外研究：
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. 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. 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. 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.
产品资料
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