Ripasudil hydrochloride dihydrate

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

Ripasudil (K-115) 盐酸盐二水合物是一种特异性 ROCK 抑制剂（IC50s：ROCK1/ROCK2 为 51/19 nM）。 Ripasudil 对 CaMKIIα、PKACα 和 PKC 表现出较弱的抑制活性（IC50s：370 nM、2.1 μM 和 27 μM） ）。

Ripasudil (K-115) hydrochloride dihydrate is a specific ROCK inhibitor (IC50s: 51/19 nM for ROCK1/ROCK2).Ripasudil shows less potent inhibitory activities against CaMKIIα, PKACα, and PKC (IC50s: 370 nM, 2.1 μM and 27 μM) [1]. Ripasudil (1, 10 μM) induces cytoskeletal changes, including retraction and cell rounding and reduced actin bundles of cultured trabecular meshwork (TM) cells. Ripasudil (5 μM) significantly reduces transendothelial electrical resistance (TEER) and increases FITC-dextran permeability in Schlemm’s canal endothelial (SCE) cell monolayers [2].Ripasudil reduces intraocular pressure 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. Ripasudil (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.(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 CaMKIIα, PKACα and PKC, with IC50s of 370 nM, 2.1 μM and 27 μM, respectively. Ripasudil (K-115; 1, 10 μM) induces cytoskeletal changes, including retraction and cell rounding and reduced actin bundles of cultured trabecular meshwork (TM) cells. Ripasudil (5 μM) sifnificantly reduces transendothelial electrical resistance (TEER), and increases FITC-dextran permeability in Schlemm’s canal endothelial (SCE) cell monolayers.(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. 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.

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 CaMKIIα, PKACα and PKC, with IC50s of 370 nM, 2.1 μM and 27 μM, respectively. Ripasudil (K-115; 1, 10 μM) induces cytoskeletal changes, including retraction and cell rounding and reduced actin bundles of cultured trabecular meshwork (TM) cells. Ripasudil (5 μM) sifnificantly reduces transendothelial electrical resistance (TEER), and increases FITC-dextran permeability in Schlemm’s canal endothelial (SCE) cell monolayers.

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. 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.

K-115

Cell Cycle/DNA Damage

ROCK

ROCK1| ROCK2

Others

Diabetic retinopathy; Fuchs' endothelial dystrophy

887375-67-9

395.88

C15H23ClFN3O4S

>98% (HPLC)

Water:45 mg/mL (113.67 mM)

O.O.Cl.C[C@H]1CNCCCN1S(=O)(=O)c1cccc2cncc(F)c12

——

(-20℃)

With Ice Pack

≥ 2 years