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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.
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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 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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Related Experiment Video

Updated: Jan 6, 2026

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
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A Small-Molecule Pan-Id Antagonist Inhibits Pathologic Ocular Neovascularization.

Paulina M Wojnarowicz1, Raquel Lima E Silva2, Masayuki Ohnaka2

  • 1Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.

Cell Reports
|October 3, 2019
PubMed
Summary
This summary is machine-generated.

A new drug, AGX51, successfully inhibits Id proteins, which drive diseases like wet age-related macular degeneration (AMD) and retinopathy of prematurity (ROP). This first-in-class compound offers a potential new treatment for these conditions.

Keywords:
Id proteinsangiogenesismacular degenerationprotein-protein interactionsretinopathy of prematurity

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Pharmacology

Background:

  • Id helix-loop-helix (HLH) proteins (Id1-4) inhibit E protein transcription factors, preventing cell differentiation.
  • Id proteins are crucial during development but re-emerge in vascular diseases and cancer.

Purpose of the Study:

  • To investigate the role of Id proteins in ocular neovascularization.
  • To identify and characterize a small-molecule inhibitor of Id proteins.

Main Methods:

  • Genetic loss of Id1/Id3 in mouse models of wet age-related macular degeneration (AMD) and retinopathy of prematurity (ROP).
  • In silico screening to identify Id antagonists.
  • Biochemical assays to assess AGX51's inhibition of the Id1-E47 interaction and subsequent protein degradation.
  • Evaluation of AGX51's efficacy in mouse models of ocular neovascularization.

Main Results:

  • Genetic loss of Id1/Id3 significantly reduced ocular neovascularization in AMD and ROP models.
  • AGX51, a small-molecule Id antagonist, was identified.
  • AGX51 inhibits the Id1-E47 interaction, inducing ubiquitin-mediated degradation of Id proteins, cell growth arrest, and reduced viability.
  • AGX51 treatment inhibited retinal neovascularization in AMD and ROP models and was well-tolerated in mice.

Conclusions:

  • AGX51 is a first-in-class Id antagonist targeting a previously undruggable interaction.
  • AGX51 effectively inhibits ocular neovascularization in preclinical models.
  • AGX51 shows potential therapeutic utility for vascular diseases, including wet AMD and ROP.