Anti-mouse VEGF (B20-4.1.1) In Vivo Antibody - Low Endotoxin (ICH1278-1mg)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

This antibody is clone B20-4.1.1, a mouse IgG2a directed against mouse VEGF-A (UniProt Q00731). B20-4.1.1 is a widely used, function-blocking anti-VEGF-A reagent that, unlike bevacizumab, cross-reacts with and neutralizes both human and mouse VEGF-A, which makes it valuable in immunocompetent mouse models where a mouse-reactive neutralizing tool is required. It is well suited to in vivo and functional research: it blocks ligand binding to VEGFR1 and VEGFR2, and is applied in tumour angiogenesis, ocular neovascularization, vascular permeability, and combination immuno-oncology studies. The mouse IgG2a format supports in vivo dosing and is compatible with syngeneic settings. The preparation is offered low endotoxin (research grade less than 1 EU/mg; ultra-low grade less than 0.5 EU/mg) and in bulk milligram-to-gram quantities to support repeat-dose in vivo regimens, and is provided as a research-use-only reagent. Listed applications include ELISA, neutralization, and functional assays such as bioanalytical PK and ADA assays, as well as assays studying pathways affected by mouse VEGF-A. VEGF-A (vascular endothelial growth factor A) is the prototypic member of the VEGF family and the master regulator of physiological and pathological angiogenesis. Produced as several splice isoforms (e.g. VEGF120, VEGF164, VEGF188 in mouse), it is a secreted, disulfide-linked homodimer that signals mainly through the receptor tyrosine kinases VEGFR1 (FLT1) and VEGFR2 (KDR/FLK1), with co-receptor input from neuropilins. VEGFR2 engagement drives endothelial cell proliferation, migration, survival, and vascular permeability, while VEGFR1 acts partly as a decoy and modulator. VEGF-A expression is strongly induced by hypoxia via HIF signalling. It is central to tumour neovascularization, wound healing, and developmental vasculogenesis, and its dysregulation underlies pathological angiogenesis in cancer and in ocular diseases such as neovascular age-related macular degeneration, making it a validated therapeutic and experimental target.