Bispecific Anti-Mouse PD-1 / VEGF-A In Vivo Antibody (ICH1289-5mg)

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This bispecific in vivo antibody combines two well-characterised mouse-reactive binding arms: the anti-PD-1 clone RMP1-14 (a rat-derived anti-mouse PD-1 specificity, widely used for checkpoint blockade) and the anti-VEGF-A arm B20-4.1.1, a pan-VEGF-A specificity that neutralises both mouse and human VEGF-A. It is formatted on a mouse IgG2c backbone carrying LALA-PG Fc mutations, which silence FcgammaR engagement and complement fixation so that biology is driven by dual target binding rather than Fc effector function. The kappa light chain and fully murine framework minimise anti-drug responses in immunocompetent mice, suiting it to repeat dosing in syngeneic tumour models. Supplied at low endotoxin and in bulk milligram-to-gram quantities, it is intended for in vivo functional studies that interrogate the intersection of checkpoint immunotherapy and anti-angiogenic therapy in a single reagent. For research use only; not for diagnostic or therapeutic use. All content is guidance for ichorbio to review before publishing. PD-1 (Pdcd1; Q02242) is an inhibitory co-receptor expressed on activated and exhausted T cells. Engagement by its ligands PD-L1 and PD-L2 recruits SHP-2 phosphatase to dampen TCR and CD28 signalling, restraining effector function; blocking this axis reinvigorates anti-tumour T-cell responses. VEGF-A (Vegfa; Q00731) is the principal driver of angiogenesis, signalling chiefly through VEGFR-2 to promote endothelial proliferation, permeability and new vessel formation. Beyond vasculature, tumour-derived VEGF-A is immunosuppressive: it impairs dendritic-cell maturation, promotes regulatory T cells and myeloid-derived suppressor cells, and contributes to T-cell exhaustion. The two targets are mechanistically linked in the tumour microenvironment, which is the rationale for co-targeting them. Simultaneous PD-1 blockade and VEGF-A neutralisation aims to relieve checkpoint inhibition while normalising vasculature and reversing VEGF-driven immunosuppression, potentially enhancing lymphocyte infiltration and response.