Figure 2.
Teclistamab-induced cytotoxicity and activation of MM BM MNC cells ex vivo. Each row represents a different patient sample. Frozen BM MNCs were incubated with various concentrations of teclistamab (0-532 nM) with or without exogenous healthy T cells to measure target binding and killing. BCMA protein density was 2451 receptors per plasma cell in one of the patient samples (ID BM 240 MM). (A) Dose-dependent binding of teclistamab to target cells. (B) Dose-dependent plasma cell depletion. BM MNCs were incubated for 48 hours with exogenous healthy T cells at a 1:1 E:T ratio in the presence of teclistamab and depletion measured as remaining CD138+ cells. (C) Teclistamab-mediated T-cell activation was measured via flow cytometry by gating T cells using CD3 surface marker and CD25 activation marker. Percent CD25+ T cell values were plotted on the y-axis. Teclistamab was able to activate T cells efficiently when incubated with BM MNCs, whereas the control antibodies had no effect.

Teclistamab-induced cytotoxicity and activation of MM BM MNC cells ex vivo. Each row represents a different patient sample. Frozen BM MNCs were incubated with various concentrations of teclistamab (0-532 nM) with or without exogenous healthy T cells to measure target binding and killing. BCMA protein density was 2451 receptors per plasma cell in one of the patient samples (ID BM 240 MM). (A) Dose-dependent binding of teclistamab to target cells. (B) Dose-dependent plasma cell depletion. BM MNCs were incubated for 48 hours with exogenous healthy T cells at a 1:1 E:T ratio in the presence of teclistamab and depletion measured as remaining CD138+ cells. (C) Teclistamab-mediated T-cell activation was measured via flow cytometry by gating T cells using CD3 surface marker and CD25 activation marker. Percent CD25+ T cell values were plotted on the y-axis. Teclistamab was able to activate T cells efficiently when incubated with BM MNCs, whereas the control antibodies had no effect.

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