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Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
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Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
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Ophthalmic Drug Delivery Systems

Ophthalmic drug delivery faces major limitations due to poor absorption across the corneal membrane. This process is primarily driven by diffusion and is influenced by two main factors: the physicochemical properties of the drug and tear drainage. Most ophthalmic drugs, such as pilocarpine, epinephrine, atropine, and local anesthetics, are weak bases. They are typically formulated at an acidic pH to enhance chemical stability. However, this leads to high ionization, reducing their ability to...
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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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Related Experiment Video

Updated: May 8, 2026

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
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Published on: February 15, 2022

Topical CAY-10746, a Novel ROCK Inhibitor, Reduces Intraocular Pressure and Modulates the Trabecular Meshwork in

Menglong Hao1,2, Yalong Dang1,2,3,4, Fang Lei4

  • 1Henan International Joint Laboratory of Outflow Engineering, Sanmenxia Central Hospital, School of Medicine, Henan University of Science and TechnologyLuoyang, China.

Current Eye Research
|May 7, 2026
PubMed
Summary

A novel Rho-associated kinase (ROCK) inhibitor, CAY-10746, effectively lowers intraocular pressure (IOP) in rats. This glaucoma drug candidate also alters trabecular meshwork (TM) structure and gene expression, showing therapeutic promise.

Keywords:
Rho-associated kinasegene expressionglaucomaintraocular pressuretrabecular meshwork

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10:10

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Published on: February 15, 2022

Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres
06:35

Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres

Published on: February 2, 2015

Area of Science:

  • Ophthalmology
  • Pharmacology
  • Molecular Biology

Background:

  • Elevated intraocular pressure (IOP) is a primary risk factor for glaucoma.
  • Rho-associated kinase (ROCK) inhibitors reduce IOP by enhancing aqueous humor outflow through the trabecular meshwork (TM).

Purpose of the Study:

  • To evaluate the IOP-lowering efficacy of CAY-10746, a novel ROCK inhibitor.
  • To investigate CAY-10746's effects on TM structure and gene expression in normotensive rats.

Main Methods:

  • Normotensive rats received topical CAY-10746 (10µM or 25µM) or vehicle daily for 5 days.
  • IOP was measured via rebound tonometry; TM morphology was assessed histologically.
  • Gene expression changes were analyzed using RNA sequencing (RNA-Seq); in vitro cytotoxicity was tested on human TM cells.

Main Results:

  • CAY-10746 was non-toxic to human TM cells and significantly lowered IOP in rats dose-dependently.
  • The 25µM dose reduced IOP for over 8 hours (p < 0.001).
  • Histology showed increased TM porosity (p < 0.05); RNA-Seq identified 762 differentially expressed genes, including those in ECM and focal adhesion pathways.

Conclusions:

  • The novel ROCK inhibitor CAY-10746 effectively lowers IOP in normotensive rats.
  • Its mechanism involves structural TM changes and modulation of key gene expression pathways.
  • CAY-10746 shows promise as a potential glaucoma therapeutic.