Fig. 1: Binding of VIS832 was significantly more intense than BB4 to CD138 on MM cell membrane, potentiating FcR-mediated MM cell cytotoxicity.

a Indicated MM cell lines (n = 8) were incubated with a serial dilution of VIS832 or BB4 (0–10 μg/ml) followed by flow cytometry (FC) analysis using an APC-conjugated secondary anti-human IgG1 antibody for detection. Binding intensity was reported as geometric mean fluorescence intensity (MFI) normalized to isotype control. Isotype control for VIS832 and BB4 (10 μg/ml) were used as background controls. Three experiments were done in triplicates for each concentration. Data were presented as means (MFIs) ± standard errors of means (SEMs, error bars). **P < 0.01, ***P < 0.005, ****P < 0.001. b Bone marrow mononuclear cells (BMMCs) from five patients (MM1-5) were incubated with VIS832 (0–10 µg/ml). Cells were subsequently co-stained with PE-BCMA antibody (to identify patient myeloma cells) and APC-anti-human IgG1 followed by FC analysis on PE + APC + cells. All data is presented as means (MFIs) ± SEMs (error bars) of triplicates at each VIS832 concentration. c Relative antibody-dependent cellular cytotoxicity (ADCC) of VIS832 vs. BB4 possessing an isotype matched human IgG1 were measured using an ADCC reporter cell assay where Jurkat cells stably transfected with human FcRIIIa as surrogate for effector cells were co-cultured with target U266 MM cells. ADCC is reported as a fold induction over no antibody background control (effector + target cells only).