vision loss
Age-related macular degeneration (AMD) is the leading cause of vision loss in adults over the age of 50. Afflicted individuals find it difficult, if not impossible, to read or recognize faces. Although such individuals usually retain enough peripheral vision to carry on daily self-maintenance, the loss of the central vision has an obvious effect on the quality of life. Nearly 1.6 million Americans suffer from the wet form of the disease called Wet AMD with 500,000 new cases being added each year. The remaining 90% of the market is occupied by the Dry AMD variety. Collectively, the market for AMD in total is expected to exceed $25 billion dollars within in the next several years.
Dry AMD is characterized by the presence of drusen (yellow crystalline deposits) that develop within the macula) and causes thinning of the macula. Dry AMD reduces the central vision and affects color perception. The "dry" form is followed by "wet" form. Although Wet AMD affects only 10 percent of the total AMD condition, it accounts for 90% of the severe vision loss caused by macular degeneration.
In Wet AMD, the Bruch’s membrane underlying the retina thickens and breaks. New, abnormal blood vessels form and grow through the breaks of the membrane. These abnormal blood vessels are leaky and bleed causing scarring of the macula resulting in rapid vision loss. The destroyed vision cannot be restored. Currently the most effective treatment for Wet AMD are anti-VEGF therapies from Genentech. There are no effective treatments available for Dry AMD.
Current treatments for Wet AMD are inadequate and are able to control only neovascularization without any effect on inflammation. Lucentis® neutralizes VEGF and dampens the progression of Wet AMD but does not control underlying inflammation. NovelMed is developing targeted therapies for both forms of AMD. NovelMed scientists have demonstrated that our portfolio of neutralizing monoclonal antibodies prevent the formation of VEGF and TNF, the two most potent molecules involved in pathogenesis of Wet AMD. By inhibiting the formation of both cytokines, progression of disease and underlying inflammation can be treated simultaneously.
It is expected that our neutralizing monoclonal antibodies are capable of controlling inflammation and neovascularization and therefore could provide benefit in both the Dry and the Wet AMD. Our preclinical studies provide strong evidence that these therapeutic monoclonal antibodies could provide the following key benefits to AMD patients: