This is an unconjugated, non-therapeutic recombinant analog of the anti-LAG-3 antibody relatlimab, engineered as a human IgG4 (S228P) kappa molecule directed against human LAG3 (Lymphocyte-activation gene 3, UniProt P18627). It is supplied for research use only and is not the clinical drug, nor is it intended for human or veterinary use. Built around the LAG3 target, it is useful as a well-characterized binding and blocking reagent for immuno-oncology and checkpoint-biology workflows: as a positive control or reference antibody in target-engagement and epitope-competition assays, for probing LAG3 expression and downregulation on activated T cells, in receptor-blockade and functional T-cell restoration experiments in vitro, and as a benchmark tool alongside anti-PD-1 reagents for combination studies. The S228P hinge stabilization reduces Fab-arm exchange, giving consistent bivalent behavior. Material is offered at research grade with low endotoxin (<1 EU/mg; ultra-low <0.5 EU/mg options) and in bulk milligram-to-gram quantities to support assay development, screening, and preclinical modeling where lot-to-lot consistency and scale matter.
LAG3 (CD223) is an inhibitory immune checkpoint receptor expressed on activated CD4+ and CD8+ T cells, regulatory T cells, NK cells, B cells, and plasmacytoid dendritic cells. Structurally related to CD4, it contains four extracellular immunoglobulin-like domains and binds MHC class II with higher affinity than CD4. Additional reported ligands include fibrinogen-like protein 1 (FGL1), galectin-3, and LSECtin. Engagement transmits inhibitory signals via its cytoplasmic domain, notably a conserved KIEELE motif, dampening T-cell proliferation, cytokine production, and effector function while contributing to regulatory T-cell suppressive activity. LAG3 is upregulated on chronically stimulated, exhausted T cells within tumors and chronic infection, often co-expressed with PD-1, making it a prominent target for checkpoint blockade. Blocking LAG3 can restore antitumor T-cell responses, and dual LAG3/PD-1 inhibition shows cooperative reinvigoration of exhausted T cells.