Experimental Drug for Wet Macular Degeneration

An experimental drug has shown promise as a treatment for wet macular degeneration.  Endostatin, a naturally occurring protein in all blood vessels, has shown promise as a macular degeneration treatment when injected into the eyes of mice.

Originally discovered by Dr. Juda Folkman as a major advance to fight cancer, researchers have turned to this drug as a treatment for wet macular degeneration.

Is endostatin all that it is reported to be?  There has been much debate on the effectiveness of this drug and whether it shows any promise in doing what it has been claimed to do, especially as a treatment for macular degeneration.

Dr. Judah Folkman discovered endostatin in 1997 and found that it was effective in treating cancer without toxicity associated with cancer treatments.  Dr. Folkman found that endostatin was effective at inhibiting angiogenesis (blood vessel formation associated with the growth of abnormal cell tissues) and demonstrated how endostatin could shrink tumors in mice by cutting off blood supply.

The discovery of endostatin has been met with much criticism largely because other researchers have been unable to reproduce the results.  Endostatin has been used in ground-breaking research in treating wet macular degeneration, the eye disease characterized by abnormal blood vessel growth in the eye.

Researchers have published their findings in the Journal of American Societies for Experimental Biology (2007, November 30), describing how giving endostatin to mice significally reduced or eliminated the abnormal blood vessel growth within the eye in those patients with wet macular degeneration.
“Our study provides intriguing findings that may lead to a better treatment of age-related macular degeneration,” said Alexander Marneros, the first author of the report, “but clinical studies in patients with age-related macular degeneration are still necessary.”

In this study, researchers describe testing the effects of endostatin on mice lacking this naturally occurring substance. The mice without endostatin were about three times more likely to develop advanced age-related macular degeneration (AMD) than normal mice. Then the researchers administered endostatin to both sets of mice. In the mice lacking endostatin, the number of abnormal blood vessels that cause macular degeneration were reduced to normal levels. In control mice with normal levels of endostatin, the number of abnormal blood vessels were practically undetectable.

While clinical trials are still necessary, this is promising news for those people suffering from the eye disease. Macular degeneration is a progressive disease that affects the part of the eye that allows people to see fine details. The disease gradually destroys sharp, central vision, and in advanced stages ultimately leads to total blindness. Abnormal blood vessel growth, also known as angiogenesis, is a hallmark of advanced wet macular degeneration. These faulty blood vessels leak fluids and blood, causing catastrophic vision loss.

Source: Federation of American Societies for Experimental Biology (2007, November 30)