Ant-Human LAG-3 (IB18) Antibody (ICH5117A-0.1mg)

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Anti-Human LAG-3 (IB18) is a recombinant monoclonal antibody targeting human Lymphocyte-Activation Gene 3 (LAG-3/CD223, UniProt P18627), engineered on a human IgG4 backbone bearing the S228P hinge-stabilising mutation with a kappa light chain. The S228P substitution prevents Fab-arm exchange and locks the IgG4 hinge, yielding a stable, effector-function-attenuated format well suited to receptor-blocking rather than cell-depleting applications. Its fully human framework and defined recombinant sequence give lot-to-lot consistency, making it appropriate for functional immunology studies of the LAG-3 checkpoint axis, in-vitro T-cell assays, and target-engagement work. Supplied as a low-endotoxin, bulk, research-use-only reagent, it is intended for functional and mechanistic research where minimising endotoxin-driven artefacts matters. Because reactivity is human-specific, it is best applied to human primary cells, humanised systems, or human antigen preparations. As a human-target clone, standard mouse in-vivo depletion or checkpoint dosing regimens do not directly translate; it is primarily a tool for human immune-checkpoint and mechanism-of-action research rather than immunocompetent mouse tumour models. LAG-3 (Lymphocyte-Activation Gene 3, CD223) is an inhibitory immune-checkpoint receptor structurally related to CD4, expressed on activated CD4+ and CD8+ T cells, regulatory T cells, natural killer cells, B cells, and plasmacytoid dendritic cells. It binds MHC class II with higher affinity than CD4, and additional ligands including fibrinogen-like protein 1 (FGL1), galectin-3, and LSECtin have been described. Engagement transmits negative signals that dampen T-cell proliferation, cytokine production, and effector function, and LAG-3 contributes to regulatory T-cell suppressive activity. Sustained LAG-3 expression marks exhausted T cells in chronic infection and tumours, where it frequently co-occurs with PD-1. Because LAG-3 and PD-1 act through partly non-redundant pathways, LAG-3 blockade is of major interest for restoring anti-tumour T-cell responses, and combined LAG-3/PD-1 inhibition is an established clinical strategy. LAG-3 is therefore a central node in T-cell exhaustion and checkpoint biology.