Rho-Kinase Inhibitor—A Molecule for Pharmacological Treatment of Decompensated Corneas: Case Series

Objective: Rho-associated protein kinase (ROCK) inhibitors have recently emerged as promising agents for the treatment of corneal endothelial dysfunction. Because corneal transparency critically depends on endothelial cell function, endothelial failure can lead to persistent visual impairment. However, clinical evidence regarding the use of topical ROCK inhibition in various etiologies of endothelial decompensation remains limited. The aim of this study was to evaluate changes in central corneal thickness (CCT), best-corrected visual acuity (BCVA), and treatment-related adverse events in eyes with corneal edema of different etiologies treated with fixed-combination drops of netarsudil 0.02%/latanoprost 0.005%, Roclanda®. Methods: In this prospective, uncontrolled, exploratory case series, we investigated the effects of topical ROCK inhibition on corneal endothelial cell function in 13 eyes of 11 patients with persistent, nonhealing corneal edema following intraocular procedures. Patients were treated with topical Roclanda® once daily for three months. Clinical evaluation included BCVA, CCT, and safety assessment. Changes in CCT and BCVA were assessed before therapy, and after 1 and 3 months of treatment. Results: Mean baseline CCT was 782.8 µm and decreased significantly by 71.0 µm at 1 month and by 120.2 µm at 3 months (p = 0.0074 and 0.0012, respectively). Complete resolution of corneal edema was achieved in 38% of eyes. Mean BCVA improved from 0.744 before treatment to 0.518 logMAR at 3 months (p = 0.0026), with 46.2% of eyes gaining two or more Snellen lines. The analysis including only one eye per patient showed similar results, with statistically significant reductions in CCT at both 1 and 3 months and a significant improvement in BCVA at 3 months after the exclusion of the second eye in bilaterally included patients. Treatment was well tolerated; with mild conjunctival hyperemia as the most common adverse effect, while reticular epithelial corneal edema occurred in one eye and resolved after the completion of the treatment. Conclusions: In this prospective, exploratory case series of patients with nonhealing corneal edema, 3 months of a fixed-dose netarsudil 0.02%/latanoprost 0.005% treatment resulted in significant reduction in CCT, as well as clinically important improvement in BCVA. These exploratory findings cannot explain the mechanism of action, but suggest a potential therapeutic role for ROCK inhibitors in eyes with nonhealing corneal edema and possibly residual endothelial reserve. Larger controlled studies are needed to confirm these observations and further define indications for treatment.