Anti-Human PD-1 (IB12) Antibody (ICH4029A-0.1mg)

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

Clone IB12 is a humanized monoclonal antibody directed against human PD-1 (PDCD1, UniProt Q15116), supplied as a human IgG4 kappa. The IgG4 backbone is deliberate for functional checkpoint work: it minimizes Fc-gamma-receptor engagement and complement activation relative to IgG1, so the antibody blocks the PD-1 axis without driving depletion of the PD-1-expressing T cells it binds. This makes IB12 well suited to in-vitro functional assays and mechanistic checkpoint studies where receptor blockade, not effector killing, is the intended action. As an ichor.bio research reagent it is offered low-endotoxin and in bulk milligram-to-gram quantities, supporting reproducible, larger-scale experiments and repeat dosing designs. It is provided for research use only (RUO) and is not for therapeutic or diagnostic use. Because reactivity is restricted to human PD-1, IB12 is intended for human-cell systems (primary T cells, PBMC, mixed lymphocyte reactions, humanized-mouse models) rather than conventional wild-type mouse studies. Researchers typically identify and order this reagent by its clone designation, IB12. PD-1 (Programmed cell death protein 1; PDCD1, CD279) is an inhibitory immune-checkpoint receptor of the CD28/CTLA-4 immunoglobulin superfamily, expressed on activated T cells and also on B cells, NK cells, and some myeloid subsets. Its ligands PD-L1 (CD274) and PD-L2 (CD273) are broadly upregulated on tumor cells, antigen-presenting cells, and inflamed tissue. Ligand engagement recruits the phosphatase SHP-2 to the receptor's ITIM and ITSM motifs, dephosphorylating proximal TCR and CD28 signaling components and thereby dampening T-cell activation, proliferation, and cytokine production. This pathway maintains peripheral tolerance and limits immunopathology, but is co-opted within the tumor microenvironment and in chronic infection to enforce T-cell exhaustion. Blocking PD-1, or its interaction with PD-L1/PD-L2, restores effector T-cell function and underlies the clinical success of checkpoint-inhibitor immunotherapy, making PD-1 a central target in immuno-oncology research.