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Invited Commentary
July 2017

Tyrosine Kinase Inhibitors in Age-Related Macular Degeneration

Author Affiliations
  • 1Departments of Ophthalmology and Visual Sciences, Developmental Biology and Medicine, Washington University School of Medicine, St Louis, Missouri
JAMA Ophthalmol. 2017;135(7):767-768. doi:10.1001/jamaophthalmol.2017.1600

Advanced age-related macular degeneration (AMD) is the leading cause of blindness in individuals older than 50 years in the industrialized world.1 It presents in 2 forms: a dry (nonneovascular) form characterized by atrophy of retinal pigment epithelial cells and subsequent death of the overlying photoreceptor neurons, and a wet (neovascular) form characterized by the development of abnormal blood vessels called choroidal neovascularization.2,3 Neovascular AMD is responsible for 90% of severe vision loss in AMD and is caused by release of vascular endothelial growth factor (VEGF) in response to localized tissue stress. Anti-VEGF therapies have revolutionized treatment of this devastating disease. Despite these advances, a significant proportion of patients are underresponsive to anti-VEGF monotherapy, creating an urgent need for multitarget, synergistic therapeutic approaches.3 In addition, anti-VEGF therapies require frequent, intravitreous injections that create significant patient and caregiver burden and can be associated with the rare but potentially devastating complication of endophthalmitis. As such, novel therapeutic strategies that either complement or improve on current VEGF-directed approaches are highly desirable. Examples of such therapies would be those that do not require intraocular injections, are longer lasting, and have a favorable safety profile. Systemically delivered agents have an added advantage of treating bilateral disease, which must be carefully weighed against adverse reactions.

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