Anti-Human CTLA4 (IB8) Antibody (ICH4025A-0.1mg)

Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.

Anti-Human CTLA-4 clone IB8 is a humanized recombinant monoclonal antibody of the human IgG1 kappa isotype that recognises human CTLA-4 (CD152). As a humanized IgG1 reagent directed against a human target, it is well suited to in-vitro functional assays, receptor-blockade and ligand-competition studies, and characterization work in humanized or human-cell systems rather than conventional wild-type mouse in-vivo models. It is supplied research-grade with low endotoxin (<1 EU/mg; ultra-low <0.5 EU/mg options), which supports sensitive primary-cell and T-cell functional assays where endotoxin can confound activation readouts. The antibody is available in bulk milligram-to-gram quantities to support screening cascades, assay development, reproducibility across batches, and scale-up. It is intended for research use only (RUO) and is not for diagnostic or therapeutic use. The recombinant format offers lot-to-lot consistency and a defined sequence, making it appropriate for reproducible mechanistic studies of the CTLA-4/CD80/CD86 costimulatory axis. CTLA-4 (CD152) is a co-inhibitory immune checkpoint receptor expressed by activated conventional T cells and constitutively by regulatory T cells (Tregs). It shares the ligands CD80 (B7-1) and CD86 (B7-2) with the costimulatory receptor CD28 but binds them with substantially higher avidity, allowing CTLA-4 to outcompete CD28 and dampen T-cell activation. It acts largely during the priming phase in lymphoid tissue, raising the threshold for T-cell activation and contributing to peripheral tolerance. CTLA-4 can also physically remove CD80/CD86 from antigen-presenting cells by trans-endocytosis, reducing costimulatory ligand availability. Its central role in restraining T-cell responses makes CTLA-4 a validated immuno-oncology target: blocking the receptor can enhance T-cell activation and, in tumour settings, deplete or modulate intratumoural Tregs. Germline loss-of-function underlies immune-dysregulation syndromes, underscoring its non-redundant regulatory function.