Ripasudil (K-115) is a potent inhibitor of ROCK, with IC50 values of 19 nM and 51 nM for ROCK2 and ROCK1, respectively. It also demonstrates less potent inhibitory activity against CaMKIIα, PKACα, and PKC, with IC50 values of 370 nM, 2.1 μM, and 27 μM, respectively[1]. At concentrations of 1 and 10 μM, Ripasudil (K-115) induces cytoskeletal changes in cultured trabecular meshwork (TM) cells, including retraction and cell rounding, as well as reduced actin bundles. Additionally, at a concentration of 5 μM, it significantly reduces transendothelial electrical resistance (TEER) and increases FITC-dextran permeability in Schlemm’s canal endothelial (SCE) cell monolayers[2].
体内研究
Ripasudil (K-115) decreases intraocular pressure (IOP) in a concentration-dependent manner, ranging from 0.1% to 0.4% in monkey eyes and from 0.0625% to 0.5% in rabbit eyes, respectively[1].
Administered orally at a dose of 1 mg/kg daily, Ripasudil (K-115) demonstrates a neuroprotective effect on retinal ganglion cells (RGCs) following nerve crush (NC) injury. It also inhibits oxidative stress induced by axonal injury in mice, suppressing the time-dependent production of reactive oxygen species (ROS) in RGCs after NC injury[3].
体外研究
Ripasudil (K-115) is a potent inhibitor of ROCK, with IC50 values of 19 nM and 51 nM for ROCK2 and ROCK1, respectively. It also demonstrates less potent inhibitory activity against CaMKIIα, PKACα, and PKC, with IC50 values of 370 nM, 2.1 μM, and 27 μM, respectively[1].
At concentrations of 1 and 10 μM, Ripasudil (K-115) induces cytoskeletal changes in cultured trabecular meshwork (TM) cells, including retraction and cell rounding, as well as reduced actin bundles. Additionally, at a concentration of 5 μM, it significantly reduces transendothelial electrical resistance (TEER) and increases FITC-dextran permeability in Schlemm’s canal endothelial (SCE) cell monolayers[2].
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