Avelumab is a fully humanIgG1anti-PD-L1monoclonal antibody with potential antibody-dependent cell-mediated cytotoxicity.

PD-1/PD-L1^[1]

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 (P=0.01) 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; P=0.001), UM-Chor1 (7.34-fold; P<0.001), U-CH2 (2.6 fold; P=0.008), MUG-Chor1 (8.38-fold; P=0.0016). 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].

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].

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