This is an unconjugated, non-therapeutic recombinant research-grade analog of brolucizumab, a humanized single-chain antibody fragment (scFv) directed against human vascular endothelial growth factor A (VEGF-A). It reproduces the antigen-binding specificity of the originator molecule and is supplied for research use only; it is not the clinical product and is not intended for human or veterinary use. Because it is delivered as a small scFv format built around the VEGF-A target, it is a convenient reagent for anti-VEGF binding and neutralisation experiments, as a positive control or benchmark alongside other anti-VEGF-A binders, and for antibody-format and assay development work. The molecule is offered at low endotoxin levels (research grade <1 EU/mg; ultra-low <0.5 EU/mg options) and in bulk milligram-to-gram quantities to support in-vitro assays, comparability panels, and preclinical model work. Use it where a well-characterised, cost-effective VEGF-A-binding analog is needed rather than a formulated therapeutic. Guidance provided here is for ichorbio internal review.
VEGF-A (gene VEGFA; UniProt P15692) is the prototypical member of the VEGF/PDGF growth-factor family and the master regulator of angiogenesis and vascular permeability. It is produced as multiple isoforms by alternative splicing (e.g. VEGF121, VEGF165, VEGF189), which differ in heparin- and neuropilin-binding and in diffusibility. VEGF-A signals as a disulfide-linked homodimer chiefly through the receptor tyrosine kinases VEGFR-1 (FLT1) and VEGFR-2 (KDR), with VEGFR-2 driving endothelial proliferation, migration, survival and permeability. Its expression is strongly induced by hypoxia via HIF-1alpha. Pathological VEGF-A activity underlies tumour neovascularisation and ocular neovascular disease, making VEGF-A neutralisation a central therapeutic and research strategy. Anti-VEGF-A binders act by sequestering the ligand and preventing receptor engagement.