Atezolizumab biosimilar, human IgG4 S228P mutant

Recombinant Humanized IgG1 Monoclonal Antibody.
Isotype: Human IgG1 kappa.
Source: The anti-human programmed cell death ligand 1 (PD-L1) monoclonal antibody atezolizumab biosimilar was produced in the atezolizumab biosimilar CHO stable cell line.
Specificity/Sensitivity: The in vivo grade atezolizumab biosimilar specifically binds to the human PDL1 protein.
Applications: ELISA, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by atezolizumab.
Form of Antibody: 0.2 uM filtered solution, pH 6.0, no stabilizers or preservatives.
Endotoxin: < 1 EU per 1 mg of the protein by the LAL method.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

Shipping: The research grade atezolizumab biosimilar is shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70°C as supplied.
1 month from date of receipt, 2 to 8°C as supplied.

Background

Atezolizumab is a humanized monoclonal antibody directed against the human protein ligand PD-L1, with potential immune checkpoint inhibitory and antineoplastic activities. Atezolizumab is an Fc-engineered, humanized, monoclonal antibody (IgG1κ isotype). Atezolizumab biosimilar uses the same protein sequences as the therapeutic antibody atezolizumab. Atezolizumab lacks the N-glycosylation site in its Fc region by changing an aspartic acid into alanine at amino acid position 298 (amino acid position 297 according to EU nomenclature, N297A) in the heavy chain leading to minimized binding to FcγRs.

PD-L1 (B7-H1 or CD274, programmed cell death ligand 1) and PD-L2 (B2-DC or CD273, programmed cell death ligand 2) are the two ligands for the receptor PD-1 (CD279, programmed death 1). PD-L1 is an immune checkpoint molecule expressed on both tumor cells and certain immune cells. The binding of PD-L1 to its receptors PD-1 or B7.1 on activated T cells causes an inhibitory signal to suppress their production in the lymph nodes, thereby preventing immune responses to events such as pregnancy or autoimmune disease. This pathway is also utilized by cancer cells to evade the immune system through evasion of anti-tumor T-cell response. Furthermore, over-expression of PD-L1 and PD-1 has been linked to increased tumor aggressiveness and poorer prognosis. Atezolizumab binds directly and selectively to PD-L1 and blocks interaction with both PD-1 and B7.1 receptors, thus reinvigorates and enhances the body’s adaptive anti-cancer activity. Disrupting the PD-L1/B7.1 interaction may also enhance T-cell priming, which could result in increased duration of response and survival.