HER2-directed antibody-drug conjugate that binds HER2, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to induce DNA damage; Fc region may trigger ADCC.
HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to cause DNA damage and cell death; the antibody Fc may also mediate ADCC.
NO
INDIRECT
BL-M07D1 targets HER2 on the cell surface, is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage and death. DNA topoisomerase I is not the binding target, so its expression alone does not trigger killing.
Humanized anti-HER2 monoclonal antibody that binds HER2 domain II to block ligand-dependent dimerization (HER2/HER3, HER2/EGFR), suppressing PI3K/AKT and MAPK signaling; can mediate ADCC.
Humanized anti-HER2 monoclonal antibody that binds HER2 domain II to block ligand-dependent dimerization (e.g., HER2/HER3, HER2/EGFR), thereby inhibiting downstream PI3K/AKT and MAPK signaling and reducing tumor growth; may also mediate ADCC via its Fc region.
YES
DIRECT
Pertuzumab (IgG1) binds HER2 on target cells and engages FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC, killing HER2+ cells; HER2 signaling blockade can also promote apoptosis.
An afucosylated human IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C) on B cells, blocking BAFF/BLyS survival signaling and enhancing ADCC to deplete B cells; administered subcutaneously (e.g., 300 mg monthly).
Afucosylated human IgG1 monoclonal antibody targeting BAFF receptor (BAFF‑R/TNFRSF13C) on B cells; blocks BAFF/BLyS survival signaling and enhances FcγR-mediated ADCC, leading to depletion of BAFF‑R–expressing B cells and reduced autoantibody production.
YES
DIRECT
Afucosylated IgG1 binds BAFF-R on B cells and engages Fcγ receptors on NK cells/macrophages to induce ADCC/ADCP, depleting BAFF-R+ cells; BAFF signaling blockade may also promote apoptosis.
Recombinant bispecific monoclonal antibody targeting CD38 and CD47; blocks the CD47–SIRPα checkpoint to enhance macrophage-mediated phagocytosis and engages CD38 on malignant plasma/B cells to mediate ADCC and CDC; administered intravenously weekly (0.01–6 mg/kg).
Bispecific monoclonal antibody targeting CD47 and CD38. By blocking the CD47-SIRPa checkpoint it promotes macrophage-mediated phagocytosis of tumor cells, and by binding CD38 on malignant plasma/B cells it engages Fc effector functions to induce ADCC and complement-dependent cytotoxicity, leading to depletion of CD38-positive tumor cells and relief of immunosuppression.
YES
DIRECT
By binding CD38 on target cells, the antibody engages Fc effector functions to trigger NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and antibody-dependent phagocytosis; CD47 blockade further enhances macrophage phagocytosis of CD38+ cells.
Recombinant bispecific monoclonal antibody targeting CD38 and CD47; blocks the CD47–SIRPα checkpoint to enhance macrophage-mediated phagocytosis and engages CD38 on malignant plasma/B cells to mediate ADCC and CDC; administered intravenously weekly (0.01–6 mg/kg).
Bispecific monoclonal antibody targeting CD47 and CD38. By blocking the CD47-SIRPa checkpoint it promotes macrophage-mediated phagocytosis of tumor cells, and by binding CD38 on malignant plasma/B cells it engages Fc effector functions to induce ADCC and complement-dependent cytotoxicity, leading to depletion of CD38-positive tumor cells and relief of immunosuppression.
YES
INDIRECT
Blocking CD47-SIRPa removes the dont-eat-me signal, allowing macrophage-mediated phagocytosis (ADCP) of CD47+ cells.