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].
To evaluate the effect of Ripasudil on FECD cell migration and wound healing, results showed that Ripasudil significantly enhanced FECD cell migration speed and wound healing ability.
Cells. 2024 Jul 19;13(14):1218.
Normal corneal endothelial cells (SVN1-67F)
1 µM
24 h
To evaluate the effect of Ripasudil on cell migration and wound healing, results showed that Ripasudil significantly enhanced cell migration speed and wound healing ability.
Cells. 2024 Jul 19;13(14):1218.
A10 VSMCs
0.1 μM
30 min
Ripasudil partially blocked the effect of MYDGF on maintaining the differentiated phenotype of A10 VSMCs, indicating that Ripasudil affected MYDGF's role by inhibiting the ROCK signaling pathway.
Acta Pharmacol Sin. 2024 Jan;45(1):98-111.
Hepatocytes
4 µM
1 hour
Ripasudil protects hepatocytes by inhibiting complement activation and blocking the formation of the membrane attack complex, thereby enhancing hepatocyte survival and engraftment.
Mol Ther. 2023 Jun 7;31(6):1846-1856.
Primary human corneal epithelial cells (pHCEpCs)
10 µM and 30 µM
7 days
To investigate the effects of Ripasudil on the barrier function of human corneal epithelial cells, the results showed that Ripasudil upregulated the expression of tight and adherens junction-related genes, improving epithelial barrier function.
Cells. 2025 Feb 11;14(4):258.
Primary human corneal endothelial cells (pHCEnCs)
10 µM and 30 µM
72 h
To investigate the effects of Ripasudil on the proliferation and migration of human corneal endothelial cells, the results showed that Ripasudil significantly increased cell proliferation and migration.
Cells. 2025 Feb 11;14(4):258.
Ripasudil 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
C57BL/6 mice
Intraperitoneal injection
17.3 mg/kg
Once daily for 3 days
Ripasudil significantly enhanced hepatocyte engraftment and accelerated liver repopulation by inhibiting complement activation and Kupffer cell phagocytosis.
Mol Ther. 2023 Jun 7;31(6):1846-1856.
Mice
Acute liver injury model
Intraperitoneal injection
50 mg/kg
Single dose, 5 hours duration
Ripasudil enhanced NEMO expression by inhibiting ROCK1 and ameliorated APAP-induced liver injury.
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