| Target Description |
Atezolizumab (anti-PD-L1) is characterized by being an FcγR binding-deficient antibody inhibitor. It cannot bind to Fc receptors on phagocytes and thus does not induce antibody-dependent cellular cytotoxicity (ADCC). Treatment with atezolizumab causes changes in cytokines, including a transient increase in IL-18, IFNγ, and CXCL11, as well as a transient decrease in IL-6. The number of CD8+ T cells in a proliferative state increases after atezolizumab treatment.Atezolizumab (anti-PD-L1) blocks the PD-L1/PD-1 immune checkpoint, thereby reducing immunosuppressive signals in the tumor microenvironment while enhancing T cell-mediated immune responses against tumors. Initial pharmacokinetic studies of atezolizumab were conducted in cynomolgus monkeys and mice, with a volume of distribution approximately equal to the plasma volume. Twenty-four hours after administration, atezolizumab is biodistributed in vivo in the spleen, kidneys, liver, heart, and muscle (in order of magnitude). In tumor-bearing animals, atezolizumab also accumulates in tumors, initially at the pushing border of the tumor and then progressing toward the tumor core, especially when tumor necrosis occurs. The pharmacokinetic curve of atezolizumab is dose-dependent (non-linear). Twenty-four to forty-eight hours after administration, when the plasma concentration exceeds 0.5 μg/mL, PD-L1 receptors on circulating CD4+ and CD8+ T cells are saturated by atezolizumab. The binding affinity of atezolizumab to PD-L1 is similar in monkeys and humans. |
