Ripasudil

887375-67-9

C15H23ClFN3O4S

H2O : >= 50 mg/mL (126.30 mM)

TGF-beta/Smad; Stem Cell/Wnt; Cell Cycle/DNA Damage

Ripasudil (K-115) is a specific inhibitor of ROCK, with IC₅₀s of 19 and 51 nM for ROCK2 and ROCK1, respectively. IC50 & Target: IC50: 19 nM (ROCK2), 51 nM (ROCK1)^[1] In Vitro: Ripasudil (K-115) is a potent inhibitor of ROCK, with IC₅₀s of 19 and 51 nM for ROCK2 and ROCK1, respectively. Ripasudil also shows less potent inhibitory activities against CaMKIIalpha, PKACalpha and PKC, with IC₅₀s of 370 nM, 2.1 uM and 27 uM, respectively^[1]. Ripasudil (K-115; 1, 10 uM) induces cytoskeletal changes, including retraction and cell rounding and reduced actin bundles of cultured trabecular meshwork (TM) cells. Ripasudil (5 uM) sifnificantly reduces transendothelial electrical resistance (TEER), and increases FITC-dextran permeability in Schlemm�s canal endothelial (SCE) cell monolayers^[2]. In Vivo: Ripasudil (K-115) reduces intraocular pressure (IOP) in a concentration-dependent manner at concentrations between 0.1% and 0.4% in monkey eyes and 0.0625% to 0.5% in rabbit eyes, respectively^[1]. Ripasudil (K-115; 1 mg/kg, p.o. daily) shows a neuroprotective effect on retinal ganglion cells (RGCs) after nerve crush (NC). Ripasudil also inhibits the oxidative stress induced by axonal injury in mice. Ripasudil suppresses the time-dependent production of ROS in RGCs after NC injury^[3].