Treatment with KN-93 for two days results in the arrest of 95% of cells in the G1 phase of the cell cycle, with this arrest being reversible. Following the cessation of KN-93 treatment, a significant number of cells advance to the S and G2-M phases. KN-93 effectively inhibits cell growth induced by various growth factors such as basic fibroblast growth factor, platelet-derived growth factor-BB, and epidermal growth factor in NIH 3T3 fibroblasts[1]. KN-93 has been found to inhibit H+, K+-ATPase activity, disrupt the proton gradient across gastric membrane vesicles, and decrease the volume of the luminal space[2]. Furthermore, KN-93 at a concentration of 0.5 μM prevents an increase in left ventricular developed pressure during action potential prolongation and early afterdepolarizations. It also inhibits the rise in Ca2+-independent CaM kinase activity observed during early afterdepolarizations[3].
体外研究
Treatment with KN-93 for two days results in the arrest of 95% of cells in the G1 phase of the cell cycle, with this arrest being reversible. Following the cessation of KN-93 treatment, a significant number of cells advance to the S and G2-M phases. KN-93 effectively inhibits cell growth induced by various growth factors such as basic fibroblast growth factor, platelet-derived growth factor-BB, and epidermal growth factor in NIH 3T3 fibroblasts[1].
KN-93 has been found to inhibit H+, K+-ATPase activity, disrupt the proton gradient across gastric membrane vesicles, and decrease the volume of the luminal space[2].
Furthermore, KN-93 at a concentration of 0.5 μM prevents an increase in left ventricular developed pressure during action potential prolongation and early afterdepolarizations. It also inhibits the rise in Ca2+-independent CaM kinase activity observed during early afterdepolarizations[3].
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