Choroidal neovascularization (CNV) due to
age-related macular degeneration (AMD) is an important cause of visual morbidity globally. Modern treatment strategies for neovascular AMD achieve regression of CNV by suppressing the activity of key
growth factors that mediate angiogenesis.
Vascular endothelial growth factor (
VEGF) has been the major target of neovascular AMD
therapy for almost two decades, and there have been several intravitreally-administered agents that have enabled anatomical restitution and improvement in visual function with continual dosing.
Aflibercept (
EYLEA(®)), initially named
VEGF Trap-eye, is the most recent anti-
VEGF agent to be granted US Food and Drug Administration approval for the treatment of neovascular AMD.
Biologic advantages of
aflibercept include its greater binding affinity for
VEGF, a longer intravitreal half-life relative to other anti-
VEGF agents, and the capacity to antagonize
growth factors other than
VEGF. This paper provides an up-to-date summary of the molecular mechanisms mediating CNV. The structural, pharmacodynamic, and pharmacokinetic advantages of
aflibercept are also reviewed to rationalize the utility of this agent for treating CNV. Results of landmark clinical investigations, including VIEW 1 and 2 trials, and other important studies are then summarized and used to illustrate the efficacy of
aflibercept for managing treatment-naïve CNV, recalcitrant CNV, and CNV due to
polypoidal choroidal vasculopathy. Safety profile, patient tolerability, and quality of life measures related to
aflibercept are also provided. The evidence provided in this paper suggests
aflibercept to be a promising agent that can be used to reduce the treatment burden of neovascular AMD.