Diabetic Macular Edema

What is Diabetic Macular Edema?

Myopia, also known as nearsightedness, usually continues to worsen year after year before the age of 17. It is caused by an increase in eye ball length or corneal curvature and this condition causes light from distant objects to focus in front of the retina, which leads to blurred long-distance vision, generally characterized by a refractive error of −0.5 or −1 diopters. It has been estimated that currently 1.4 billion people in the world are myopic (22.9% of the population), and crude estimates suggest that, by 2050, there will be 4.7 billion people affected (nearly 50% of world population). If left uncorrected, myopia has been shown to have major consequences on children’s level of education, quality of life, and personal and psychological well-being, and its economic impact on society has been estimated at US$244 billion from global potential productivity loss.

Current Treatment

Because of the role of VEGF and inflammation, two of the most common treatments for DME are therapies that inhibit these pathways (anti-VEGF-A biologics and steroids). Both therapies are delivered by an injection to the back of the eye, a route termed as intravitreal injection.

Anti-VEGF agents are considered the gold standard for the treatment of DME. However, many patients are non-responsive to anti-VEGF therapy, some from the beginning of treatment but mostly those that become non-responsive after an initial good response. The non-responder rate in DME can be as high as 50%. In the cases of non-response, a switch to another anti-VEGF agent or a switch to steroids is attempted to regain a therapeutic effect. 

Cloudbreak Solution

Cloudbreak developed a novel way to improve DME treatment: antibody-drug synergism (ADS). The idea is to connect an antiangiogenesis antibody to another small molecule drug via a linker that can be enzymatically cleaved in the vitreous humor to separate the two agents. The small drug targets additional pathological pathways to enhance the effectiveness of the antibody. By targeting multiple pathways, the approach maybe help DME patients as a first-line treatment and also help those that develop non-response to anti-VEGF agents.