KN-93 hydrochloride is a cell-permeable, reversible, and competitive inhibitor of calmodulin-dependent kinase type II (CaMKII) with a Ki of 370 nM. KN-93 hydrochloride induces G1 cell cycle arrest in 95% of treated cells after two days, with the arrest being reversible; one day after KN-93 withdrawal, a peak of cells progresses into S and G2-M phases, providing a robust tool for cell cycle regulation studies and mechanistic investigation of CaMKII-dependent signaling.

CaMK II:370 nM (Ki)

In primary cultured rat retinal Müller cells, KN-93 hydrochloride (10 μmol/L, 24 hours) significantly inhibited the activation of the CaMKII/NF-κB signaling pathway induced by high Vitis vinifera sugar conditions, thereby reducing the mRNA and protein expression levels of inflammatory factors such as VEGF, iNOS, and ICAM-1 [2].

KN-93 hydrochloride (1 mg/kg, intraperitoneal injection, for 12 consecutive weeks) significantly inhibited the constitutive activation of the CaMKII/NF-κB signaling pathway in the retina of STZ-induced diabetes mellitus rat models. It effectively reduced the expression levels of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM-1), thereby markedly alleviating diabetes mellitus-induced retinal vascular leakage [2].