Humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); depletes eosinophils (and basophils) primarily via antibody-dependent cell-mediated cytotoxicity (ADCC) by engaging NK cells, thereby inhibiting IL-5/IL-5R signaling and eosinophil survival.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Ralpha); binds IL-5Ralpha on eosinophils/basophils and induces their depletion via Fc-mediated ADCC through NK cells, thereby blocking IL-5 signaling and reducing eosinophil survival and inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and engages NK cells via its afucosylated Fc (FcγRIIIa), triggering potent ADCC that lyses/induces apoptosis of IL-5Rα+ cells.
Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to Trop-2–expressing tumor cells and nearby cells (bystander effect), causing DNA damage.
Trop-2–targeted antibody–drug conjugate that binds Trop-2 on tumor cells, is internalized, and releases SN-38 (a topoisomerase I inhibitor). SN-38 stabilizes Topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; the membrane-permeable payload also produces a bystander killing effect.
YES
DIRECT
ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38; SN-38 inhibits topoisomerase I, causing DNA strand breaks, replication arrest, and apoptosis (with additional bystander killing due to payload permeability).
Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to Trop-2–expressing tumor cells and nearby cells (bystander effect), causing DNA damage.
Trop-2–targeted antibody–drug conjugate that binds Trop-2 on tumor cells, is internalized, and releases SN-38 (a topoisomerase I inhibitor). SN-38 stabilizes Topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; the membrane-permeable payload also produces a bystander killing effect.
YES
INDIRECT
The ADC binds Trop-2, is internalized, and releases SN-38; the payload inhibits topoisomerase I, stabilizing Topo I–DNA complexes to cause DNA damage and apoptosis, with a membrane-permeable bystander effect.
A subcutaneous, T-cell–redirecting bispecific IgG4 monoclonal antibody (JNJ-64007957) that binds BCMA on myeloma/plasma cells and CD3 on T cells, bridging them to activate TCR/CD3 signaling and induce cytotoxic killing and apoptosis of multiple myeloma cells.
Bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, bridging them to form an immune synapse, activate TCR/CD3 signaling, and drive T cell-mediated cytotoxicity and apoptosis of BCMA-positive multiple myeloma cells.
YES
DIRECT
Teclistamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme-mediated apoptosis) to kill BCMA-expressing cells.
A subcutaneous, T-cell–redirecting bispecific IgG4 monoclonal antibody (JNJ-64007957) that binds BCMA on myeloma/plasma cells and CD3 on T cells, bridging them to activate TCR/CD3 signaling and induce cytotoxic killing and apoptosis of multiple myeloma cells.
Bispecific IgG4 antibody that binds BCMA on malignant plasma cells and CD3 on T cells, bridging them to form an immune synapse, activate TCR/CD3 signaling, and drive T cell-mediated cytotoxicity and apoptosis of BCMA-positive multiple myeloma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells and BCMA on myeloma cells to form an immune synapse, activating TCR signaling and T cell perforin/granzyme killing of BCMA-positive tumor cells; CD3-expressing T cells are effectors, not targets.