Background: Vascular endothelial growth factor (VEGF) is a key angiogenic factors. It plays an important role in\r\nboth physiologic and pathologic angiogenesis and increases permeability across the vessels. Using antibody phage\r\ndisplay technology, we obtained a novel anti-VEGFA IgG, named as FD006. In this study, the pharmacological\r\ncharacteristics and efficacy of FD006 in corneal neovascularization (CoNV) were evaluated.\r\nResults: FD006 was predicted to have similar binding mode to bevacizumab. Experimental analysis showed that\r\nthe binding ability of FD006 seemed a little stronger than bevacizumab, for the EC50 of FD006 to bind VEGF\r\nanalyzed by ELISA was about 0.037 �µg/mL while that of bevacizumab was 0.18 �µg/mL. Binding kinetics assays\r\nshowed similar results that FD006 possessed 2-fold higher affinity to bind VEGF than bevacizumab due to slower\r\ndissociation rate of FD006; meanwhile, FD006 inhibited the VEGF-induced proliferation of HUVEC with an IC50 value\r\nof 0.031 �± 0.0064 �µg/ml, which seemed similar or a litter better than bevacizumab (0.047 �± 0.0081 �µg/ml). The\r\nsubconjunctival administration of FD006, bevacizumab or dexamethasone could significantly inhibit the growth of\r\nCoNV contrasting to N.S (p < 0.01). At the early stage, FD006 showed better inhibitory effect on the growth of CoNV\r\ncompared with bevacizumab (p < 0.05). Western blot analysis showed that FD006 could inhibit the expression of\r\nVEGF, VEGFR-1, VEGFR-2, MMP-9 and ICAM-1, which could explain its favorable anti-angiogenic activity.\r\nConclusions: The pharmacological characteristics of FD006 were similar or even a little better than bevacizumab in\r\ninhibiting corneal neovascularization
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