A new experimental drug may be able to combat vision loss. The study was conducted on lab-grown human cells and mice by Johns Hopkins researchers.
The study revealed that a compound known as AXT107 helps to stop abnormal blood vessels in the eye from leaking vision-blocking fluids. Previous research on this compound has found that it helped stop the growth of abnormal vessels in animal studies of diabetic macular edema and wet age-related macular degeneration.
Both these conditions are the leading cause of blindness. A key to preserving vision is by blocking abnormal blood vessels. Current treatment for these conditions involves monthly injections, but this can pose challenges to patients.
Professor Aleksander Popel explained, “Our findings give us a better understanding of how this potential treatment stops the disease from progressing and does it more quickly, efficiently, and has a longer duration than current drugs used in people with vision loss of this kind.”
In healthy eyes, blood vessels are bound together by residing surface proteins directed into place by a protein known as Tie2. Tie2 proteins pack together like Velcro, which creates fluid-tight connections between cells in the blood vessels walls. In cases of diabetic macular edema, Tie2 proteins are unable to keep these tight connections so fluid can pass through the gaps.
To determine their recent findings, the researchers conducted several tests to observe the possible effects of AXT107 on Tie2 connections.
Popel explained that in current studies, AXT107 treatment lasted longer than current standard treatments. If proven effective in humans, it could result in only two injections a year as opposed to monthly injections. Popel concluded, “In addition to potentially improving the response for patients, the longer duration of AXT107 may allow for less frequent dosing, thus reducing the treatment burden for patients.”
The researchers are now moving forward with additional testing to determine safety and effectiveness among patients with diabetic macular edema.