New drug discovered to slow down vision and retina damage in diabetics

According to a press release, scientists at the Wilmer Eye Institute, John Hopkins Medicine have discovered an experimental drug that can prevent or slow down vision loss in patients with diabetes [1].

The National Institutes of Health reports that diabetes-related vision loss affects nearly 8 million Americans, projected to double by 2050 [2].

In their study, the team used both mouse and human retinal organoids and focused on two prevalent diabetic eye conditions: proliferative diabetic retinopathy and diabetic macular edema.

Both conditions impact the retina, which detects light and transmits visual signals to the brain. However, in proliferative diabetic retinopathy, the retina’s surface experiences an overgrowth of new blood vessels, resulting in vision loss, bleeding, or retinal detachments.

When a person has diabetic macular edema, the central retina becomes swollen and the retinal cells get damaged due to fluid leaking from blood vessels in the eye. This can lead to a loss of central vision.

Is this new drug a safer and better alternative?

Currently, these illnesses are managed through eye injections using anti-vascular endothelial growth factor (anti-VEGF) treatments.

While these treatments can prevent the growth of abnormal blood vessels and reduce leakage, they have proven ineffective for some patients and can lead to long-term side effects like higher internal eye pressure and damage to eye tissue.

The team conducted a study on a compound called 32-134D, previously found to reduce mouse tumor growth. They discovered that patients who used the compound had lower protein hypoxia-inducible factor (HIF) levels.

The walls of arteries activate HIF, which produces proteins that help new blood vessels grow. Lower levels of HIF can prevent diabetic retinal vascular diseases. Also, the research found that doses of 32-134D are safer than other treatments targeting HIF.

According to the new study co-authored by Akrit Sodhi, M.D., Ph.D., an associate professor of ophthalmology and the Branna and Irving Sisenwein Professor of Ophthalmology at the Wilmer Eye Institute, 32-134D, a drug examined in the study, was well-tolerated and effectively reduced HIF levels in diseased eyes.

Is this new drug a safer and better alternative?
Photograph: YuriArcursPeopleimages/Envato

In experiments conducted on two adult mouse models of diabetic eye disease, it was discovered that 32-134D reduced HIF levels and prevented the formation of new blood vessels. This effectively slowed down the progression of the disease by five days after the injection.

The effectiveness of 32-134D was tested on different types of human retinal cells that promote the production of blood vessels. It was discovered that the medication reduced HIF levels, preventing the creation of new blood vessels and restoring them to normal levels.

Sodhi asserts that using 32-134D to hinder HIF is a highly promising and secure approach to combat a disease that affects many individuals. The urgent requirement for safer treatment alternatives for this rapidly growing patient population cannot be emphasized enough.

Study abstract

Diabetic eye disease patients may not respond to anti-VEGF therapies due to high levels of angiogenic proteins regulated by HIF-1 and -2, even after treatment.

In diabetic eye disease models, we found that inhibiting HIFs can normalize the expression of multiple vasoactive mediators. Even without hypoxia, hyperglycemic animals accumulate HIFs and HIF-regulated mediators. Targeting HIFs could be an effective early treatment for diabetic retinopathy.

In diabetic mice, Acriflavine has been found to prevent retinal vascular hyperpermeability. However, its potential toxicity due to long-term accumulation in the retina raises concerns about its safety for patient use.

On the other hand, 32-134D is a new type of HIF inhibitor that is not related to acriflavine in its structure. It does not harm the retina but effectively prevents HIF from accumulating and regulates gene expression in mice and human retinal organoids.

The use of 32-134D through intraocular administration was found to prevent the development of new blood vessels in the retina and excessive leakage of blood vessels in mice. These positive findings pave the way for conducting clinical trials to evaluate the effectiveness of 32-134D in treating diabetic eye disease in patients.

[1]https://www.jci.org/articles/view/163290 
[2]https://www.nei.nih.gov/about/news-and-events/news/visual-impairment-blindness-cases-us-expected-double-2050

Photograph: user18526052/Freepik
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