ArticleDrug design, development and therapy2026
Effect of Rho Kinase Inhibitor RKI-1447 on Dexamethasone-Induced Ocular Hypertension and Its Molecular Mechanisms in Sprague-Dawley Rats.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To evaluate the ocular hypotensive effect of the Rho-associated kinase (ROCK) inhibitor RKI-1447 in normotensive and dexamethasone (DEX)-induced ocular hypertension rats, while elucidating its molecular mechanisms involving cytoskeletal remodeling and extracellular matrix (ECM) metabolism via the RhoA/ROCK pathway in trabecular meshwork (TM) cells. Methods: In vivo: Intraocular pressure (IOP) dynamics were monitored in normotensive and DEX-induced ocular hypertension rats following topical RKI-1447 administration. Conjunctival hyperemia, systemic safety (body weight), and IOP recovery post-withdrawal were assessed. In vitro: Primary human trabecular meshwork (HTM) cells were used to observe the effects of RKI-1447 on morphology and migration. Immunofluorescence assessed cross-linked actin networks (CLANs), ECM proteins, and alpha smooth muscle actin (α-SMA) expression. RhoA activity and the phosphorylation of myosin light chain (MLC) and myosin phosphatase target subunit-1 (MYPT-1) were detected via Pull-down assays and Western blot. Results: Topical RKI-1447 was associated with a dose-dependent trend in IOP reduction in both normotensive and DEX-induced ocular hypertension rats, with a peak effect observed at approximately 2 hours and only mild, transient hyperemia. In HTM cells, RKI-1447 treatment was observed to induce reversible morphological changes and mitigate cell migration. Furthermore, descriptive assessments suggested that RKI-1447 appeared to disassemble DEX-induced cytoskeletal assemblies and attenuate the upregulation of collage type IV (COL IV), fibronectin (FN), laminin (LN), and α-SMA. Additionally, RKI-1447 appeared to modulate DEX-associated RhoA activation and demonstrated a trend toward downregulating MLC and MYPT-1 phosphorylation. Conclusion: Our data suggest that RKI-1447 is associated with reduced aqueous outflow resistance, potentially through its inhibitory effect on the RhoA/ROCK pathway and the subsequent mitigation of steroid-induced cytoskeletal and fibrotic alterations. These preliminary observations suggest that RKI-1447 may serve as a viable pharmacological approach for treating steroid-induced glaucoma, although further long-term safety and efficacy evaluations are warranted.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.