Anti-Human PD-1 (Tislelizumab)

PD-1 is expressed on activated T cells, B cells, a subset of thymocytes, macrophages, dendritic cells, and some tumor cells and is also retained in the intracellular compartments of regulatory T cells (Tregs).

? 5.0 mg/ml

Purified No Carrier Protein

This biosimilar antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.

This biosimilar antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.

Human PD-1

Programmed cell death 1 (PD-1) is a transmembrane protein in the Ig superfamily1,2 that acts as an immune checkpoint receptor3, a T cell inhibitory receptor, plays critical roles in peripheral tolerance induction, autoimmune disease prevention, macrophage phagocytosis, tumor cell glycolysis, and dendritic cell survival2. PD-1 prevents uncontrolled T cell activity, leading to attenuation of T cell proliferation, cytokine production, and cytolytic activities. Additionally, the PD-1 pathway is a major mechanism of tumor immune evasion, and, as such, PD-1 is a target of cancer immunotherapy2. Programmed cell death 1 ligand 1 (PD-L1; CD274; B7H1) and programmed cell death 1 ligand 2 (PD-L2; CD273; B7DC) are ligands1. Tislelizumab was developed by BeiGene as an immunotherapeutic for hematological cancers and advanced solid tumors4. Tislelizumab is a humanized mouse monoclonal antibody designed as a synthetic protein fusion of the 317-4B6 heavy chain VH fragment with human γ4 chain clone mut10 effector/constant domain fragment (disulfide with anti-human PD-1) and synthetic clone 317-4B6 light chain VL fragment with human κ chain constant region fragment, dimer4,5. Tislelizumab binds to PD-1 with high specificity and affinity using the critical epitopes Gln75, Thr76, Asp77 and Arg86, blocking PD-1 and preventing ligand binding4. The epitope is located on the CC? loop of the front β sheet face of PD-1 and causes stereospecific hindrance to PD-L1 binding6. Unlike other IgG4 anti-PD-1 blocking antibodies, the S228P mutation known to bind to Fc-γ receptor 1 (FcγRI) and induce antibody-dependent cellular phagocytosis of T cells is not present4 and several mutations in the Fc-hinge region render tislelizumab unable to bind to FcγRs generally6. Consequently, tislelizumab has low affinity for FcγRI and baseline antibody-dependent cellular phagocytosis relative to control antibodies4. Additionally, FcR-mediated effects such as antibody-dependent cell-mediated cytotoxicity or compliment-dependent cytotoxicity are not observed4,6.

5133

?95% by SDS Page, ?95% monomer by analytical SEC

PD-1