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Editors Selection IGR 17-4
Basic Science: Neuroprotection
Comment by Miriam Kolko on:
59266 The Novel Rho Kinase (ROCK) Inhibitor K-115: A New Candidate Drug for Neuroprotective Treatment in Glaucoma, Yamamoto K; Maruyama K; Himori N et al., Investigative Ophthalmology and Visual Science, 2014; 55: 7126-7136
Increasing evidence exists on Rho Kinase (ROCK) inhibitors as a novel class of pharmacological agents to slow down glaucomatous progression. ROCK inhibitors have been shown to offer distinct applications relevant to glaucoma management, including significant IOP-lowering effects, increased ocular blood flow, and promotion of retinal ganglion cell (RGC) survival and axonal regeneration. The present study identifies the ROCK inhibitor, K-115 as a new candidate drug for neuroprotective treatment in glaucoma. A model of optic nerve crush (NC) is used and the authors identify an increased survival of RGCs after NC injury in mice treated with K-115. Moreover, the authors identify ROS production in RGCs after NC and show reduced ROS levels after K-115 treatment. The mechanism of action is suggested to be due to a reduced NAPDH oxidase 1 (NOX1) expression and the authors suggest that K-115 inhibits oxidative stress through NOX-1-induced axonal injury. Even though the study is of great interest and shows promise of K-115 as a neuroprotective treatment option for glaucoma caution should be taken to make to extensive conclusions. The main concern is the use of NC as a model. NC is not glaucoma and the mechanism of RGC death may not resemble glaucomatous damage.
Optic nerve crush is not glaucoma and the mechanism of RGC death may not resemble glaucomatous damage
Nevertheless, ROCK inhibitors are encouraging as a new treatment strategy for glaucoma. In this matter K-115 has recently been approved and launched for ocular hypertension in Japan. Although the approval was based on a significant IOP-lowering effect future clinical studies will clarify its potential additional neuroprotective effects.
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