Figure 1.
Teclistamab-induced cytotoxicity and activation of T cells in vitro. (A) Cytotoxicity of various BCMA+ MM cell lines (H929, MM.1R, and RPMI 8226) or BCMA– cells (MV4-11) in the presence of teclistamab and healthy T cells for 48 hours. (B) Activation of T cells as evidenced by the CD25 cell surface marker. No lysis or T-cell activation was observed in the BCMA– cell line MV4-11 or with the control antibodies BCMAxNull or NullxCD3. The data points closely aligned with the generated fit curve with minimal donor-to-donor (n = 6 donors) variability. (C) BCMA detection on the surface of various BCMA+ cells (H929, MM.1R, and RPMI 8226) and BCMA– cells (MV4-11) by FACS. Solid red line, BCMA; dotted/gray shading, isotype control. (D) Ligand (APRIL and BAFF) mediated P38 phosphorylation and teclistamab failed to induce any phosphorylation signal as measured by western blot.

Teclistamab-induced cytotoxicity and activation of T cells in vitro. (A) Cytotoxicity of various BCMA+ MM cell lines (H929, MM.1R, and RPMI 8226) or BCMA cells (MV4-11) in the presence of teclistamab and healthy T cells for 48 hours. (B) Activation of T cells as evidenced by the CD25 cell surface marker. No lysis or T-cell activation was observed in the BCMA cell line MV4-11 or with the control antibodies BCMAxNull or NullxCD3. The data points closely aligned with the generated fit curve with minimal donor-to-donor (n = 6 donors) variability. (C) BCMA detection on the surface of various BCMA+ cells (H929, MM.1R, and RPMI 8226) and BCMA cells (MV4-11) by FACS. Solid red line, BCMA; dotted/gray shading, isotype control. (D) Ligand (APRIL and BAFF) mediated P38 phosphorylation and teclistamab failed to induce any phosphorylation signal as measured by western blot.

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