Bispecific Anti-Mouse PD-L1 / CD28 In Vivo Antibody (ICH1292-5mg)

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This is a bispecific in vivo antibody targeting mouse PD-L1 and CD28, built on the well-characterized 10F.9G2 (anti-PD-L1) and PV-1 (anti-CD28) binding specificities. It is a mouse IgG2a, kappa antibody engineered with LALA-PG Fc mutations, which silence FcgammaR engagement and complement fixation so that biological activity derives from dual antigen binding rather than Fc-mediated effector function. The format is designed to co-engage a checkpoint ligand and a costimulatory receptor, conditionally focusing CD28 costimulation in a PD-L1-rich context such as the tumour microenvironment. Supplied at low endotoxin (research-grade <1 EU/mg; ultra-low <0.5 EU/mg), in bulk milligram-to-gram quantities, it is intended for in vivo dosing in immuno-oncology and tolerance/costimulation studies in mice. As a mouse-host reagent it minimizes anti-isotype responses in mouse models over repeat dosing. For research use only; not for diagnostic or therapeutic use. All content is provided as guidance for ichorbio to review before publishing. PD-L1 (CD274; UniProt Q9EP73) is a B7-family ligand expressed on tumour cells, antigen-presenting cells, and many stromal and inflamed tissues. By engaging PD-1 on activated T cells it delivers an inhibitory signal that dampens TCR signalling, promoting T-cell exhaustion and peripheral tolerance; PD-L1 also binds CD80. CD28 (UniProt P31041) is the principal costimulatory receptor on T cells, binding B7-1 (CD80) and B7-2 (CD86) on antigen-presenting cells. Signal 2 through CD28 is required alongside TCR engagement (signal 1) for full T-cell activation, IL-2 production, proliferation, and survival; without it T cells become anergic. A bispecific that simultaneously blocks PD-L1 inhibition and provides CD28 costimulation is designed to lower the activation threshold selectively where PD-L1 is abundant, coupling checkpoint relief with a costimulatory boost. Note that systemic CD28 superagonism carries known cytokine-release liabilities, so spatial restriction of costimulation is a central design rationale.