Humanized IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, mediates ADCC, CDC, and ADCP, directly induces apoptosis, and inhibits CD38 ectoenzyme (NADase) activity, leading to lysis and depletion of CD38-expressing tumor cells.
YES
DIRECT
Binds CD38 on target cells and elicits Fc-mediated immune effector killing (ADCC by NK cells, CDC, ADCP) and can directly induce apoptosis, leading to lysis of CD38+ cells.
Subcutaneous bispecific T‑cell–redirecting antibody that binds BCMA on myeloma cells and CD3 on T cells to induce cytotoxic killing.
Bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to activate T cells and drive perforin/granzyme-mediated cytotoxic killing of BCMA-expressing myeloma cells.
YES
DIRECT
Bispecific T-cell engager binds BCMA on target cells and CD3 on T cells, forming an immune synapse and triggering perforin/granzyme-mediated cytotoxic killing of BCMA-expressing cells.
Subcutaneous bispecific T‑cell–redirecting antibody that binds BCMA on myeloma cells and CD3 on T cells to induce cytotoxic killing.
Bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to activate T cells and drive perforin/granzyme-mediated cytotoxic killing of BCMA-expressing myeloma cells.
NO
INDIRECT
Binds CD3 on T cells to redirect them to BCMA+ myeloma cells; the activated T cells kill BCMA-expressing tumor cells via perforin/granzyme, not the CD3+ T cells.
Anti-HER2 antibody–drug conjugate that binds HER2, is internalized, and releases MMAE to inhibit microtubules, causing cell-cycle arrest/apoptosis and potential ADCC.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to G2/M cell-cycle arrest and apoptosis; may also mediate Fc-dependent ADCC.
NO
INDIRECT
Disitamab vedotin targets HER2 on tumor cells, is internalized, and releases MMAE that binds beta‑tubulin to disrupt microtubules, causing G2/M arrest and apoptosis; killing is determined by HER2 binding, not beta‑tubulin expression.
Autologous ROR1-directed CAR T-cell therapy; patient T cells are engineered to express a chimeric antigen receptor targeting ROR1 on malignant B cells, triggering T-cell activation, proliferation, cytokine release, and cytolytic killing of ROR1-positive tumor cells.
Autologous T cells are engineered to express a chimeric antigen receptor targeting ROR1 on malignant B cells; antigen engagement activates the T cells, driving proliferation, cytokine release, and perforin/granzyme-mediated cytolytic killing of ROR1-positive tumor cells.
YES
DIRECT
Anti-ROR1 CAR T cells bind ROR1 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolytic killing.