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VEGF family members (alternatively, molecular identities of anti‐VEGF agents)
Author(s) -
SENNLAUB F
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.3211.x
Subject(s) - choroidal neovascularization , neovascularization , vascular endothelial growth factor , angiogenesis , cancer research , vascular endothelial growth factor a , vegf receptors , aptamer , placental growth factor , medicine , ranibizumab , antibody , retinal , kinase insert domain receptor , chemistry , biology , immunology , microbiology and biotechnology , bevacizumab , ophthalmology , chemotherapy
The vascular endothelial growth factors (VEGFs), comprise a family of growth factors that include VEGF‐A, VEGF‐B and Placental growth factor (PlGF) and promote angiogenesis and neovascularization. The important role of VEGF‐A in the development of choroidal neovascularization (CNV) and retinal edema has been demonstrated by the clinical success of VEGF‐inhibiting agents in wet AMD. An aptamer, an antibody, an antibody‐fragment and a soluble receptor have been developed for ophthalmological use to inhibit CNV in AMD. These therapeutic molecules differ in their spectrum of VEGF family members they inhibit, and in the structure of the molecules. We will here provide an overview of VEGF family members and their involvement in CNV and discuss the differences in the therapeutic molecules to bind VEGFs, inhibit CNV and to produce off target effects.