Avelumab (anti-PD-L1)

Avelumab (anti-PD-L1) a fully human IgG1 anti-PD-L1 monoclonal antibody (mAb) with potential antibody-dependent cell-mediated cytotoxicity (ADCC). Avelumab (anti-PD-L1) enhances ADCC on several cancer cell lines expressing PD-L1. Avelumab (anti-PD-L1) can be used for the study of chordoma^[1]. In Vitro:Avelumab is a fully human IgG1 anti-PD-L1 monoclonal antibody with potential antibody-dependent cell-mediated cytotoxicity property. Avelumab increases NK-cell lysis 3.1-fold in JHC7 cells relative to isotype control. When the cells are treated with IFN-γ, Avelumab markedly enhances NK-cell lysis relative to isotype control in the following cell lines: JHC7 (7.56-fold), UM-Chor1 (7.34-fold), U-CH2 (2.6 fold), MUG-Chor1 (8.38-fold). Avelumab effectively increases antibody-dependent cell-mediated cytotoxicity (ADCC) of both the non-cancer stem cell (CSC) and CSC subpopulations to the same degree^[1]. Results also demonstrate that the addition of Avelumab increases the frequency of antigen-specific multifunctional CD8⁺ T cells by more than fivefold, relative to the isotype control in CEFT-stimulated peripheral blood mononuclear cells (PBMCs)^[2]. In Vivo:Measurement of individual tumors clearly shows a slowing of tumor growth in the Avelumab-treated mice. By day 36 post-tumor implantation, there is a significant (P<0.01) reduction in the average tumor volume of the Avelumab-treated mice. Reduction in MB49 tumor growth in the mice treated with Avelumab is durable and leads to a significant (P<0.05) improvement in percent survival. Avelumab treatment of 10 mice with bladder tumors results in complete tumor regression in 8 mice, confirmed by histopathology. However, in mice depleted of either CD4 or CD8 cells, Avelumab treatment is much less effective in controlling bladder tumor burden with tumor breakthrough occurring in a higher frequency in mice depleted of CD4 T cells^[3].