Bispecific Anti-Mouse B7-H3 / CD3e In Vivo Antibody (ICH1291-25mg)

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This is a bispecific antibody pairing the anti-mouse B7-H3 clone m276 with the anti-mouse CD3 epsilon clone 145-2C11, engineered on a mouse IgG2a, kappa backbone carrying LALA-PG Fc-silencing mutations (UniProt Q8VE98 for B7-H3, P22646 for CD3 epsilon). By simultaneously binding tumour-associated B7-H3 and the CD3 complex on T cells, it functions as a T-cell engager, physically cross-linking cytotoxic T cells to B7-H3-expressing target cells to drive redirected lysis independent of TCR specificity. The LALA-PG substitutions abolish FcgammaR and complement engagement, so activity is driven by antigen bridging rather than Fc-mediated effector recruitment, reducing off-target Fc effects and cytokine confounders. Its fully mouse framework makes it well suited to immunocompetent syngeneic tumour models where a human or humanised construct would be immunogenic. Supplied as a low-endotoxin, bulk, research-use-only reagent, it supports repeat-dosing in-vivo efficacy, pharmacodynamic, and mechanism-of-action studies in mice. It is not a therapeutic and carries no clinical grade or specification claims. B7-H3 (CD276; UniProt Q8VE98) is a type I transmembrane member of the B7 immunoregulatory family. It is expressed at low levels on many normal tissues but markedly overexpressed on numerous solid tumours and tumour vasculature, making it an attractive pan-tumour targeting antigen. Its immune role is context-dependent, with both co-inhibitory and co-stimulatory activities reported, and its counter-receptor remains incompletely defined; in the engager context it serves principally as a tumour-anchoring handle. CD3 epsilon (UniProt P22646) is an invariant signalling subunit of the T-cell receptor-CD3 complex, associating with CD3 gamma, delta and zeta chains to transduce TCR engagement. The clone 145-2C11 is a classic anti-mouse CD3 epsilon antibody that triggers T-cell activation. Co-engaging B7-H3 and CD3 epsilon brings T cells into an immunological synapse with tumour cells, driving polyclonal, MHC-independent T-cell activation and cytotoxicity against the target-expressing population.