Tissue factor (TF) overexpression may play a role in several retinal diseases, including wet age-related macular degeneration (AMD) and diabetic retinopathy. These retinal diseases are characterized by abnormal blood vessel growth, which can cause patients to lose their vision and eventually go blind.

Wet AMD: A Leading Cause of Blindness
Wet AMD is a devastating progressive retinal disease that affects the macula, the part of the eye responsible for central vision. A leading cause of blindness in the United States and other industrialized countries, wet AMD is most common in people older than 55. Globally, an estimated 22 million people are affected. In the United States, 2 million people are affected by wet AMD, and there are approximately 200,000 new cases each year. The incidence in the United States is expected to increase about 2 percent per year as the population ages.1

Recent evidence suggests that TF plays an important role in the formation of choroidal neovasculature (CNV), the pathologic blood vessels that represent the major feature of wet AMD. These blood vessels (lesions) leak blood and fluid, which causes inflammation and edema (swelling). Typically, a patient’s central vision deteriorates and they experience permanent blind spots.

A class of U.S. Food and Drug Administration (FDA) approved drugs known as anti-VEGF therapies are considered the standard of care. However, the effectiveness of these therapies remains limited and there are unresolved concerns regarding the safety of long-term use. Additionally, while anti-VEGF agents can alleviate symptoms in the near term, they do not stop disease progression. As a result, the disease remains active and the lesions continue to grow. Patients treated with these agents may experience initial vision gains, but those deteriorate over time and many continue to lose vision. In fact, 20-37 percent of patients ultimately become legally blind (20/200 or worse vision) despite anti-VEGF therapy.2, 3

New treatment options are needed for patients with wet AMD that can interfere with the root cause of the disease to halt disease progression and delay or prevent long-term loss of vision.

Wong WL et al. The Lancet Global Health. 2014;2(2):106-16. National Eye Institute – AMD. Friedman DS et al. Arch Ophthalmol. 2004;122. American Macular Degeneration Foundation.

Maguire, M.G. et al. Ophthalmology 2016, 123(8), 1751 – 61.

Rofagha, S. et al. Ophthalmology 2013, 120(11):2292-9.