Bispecific T‑cell–engaging monoclonal antibody (ELREXFIO) that binds BCMA on myeloma cells and CD3 on T cells to redirect and activate cytotoxic T cells against BCMA-positive malignant plasma cells; immunotherapy with CRS/ICANS risk.
Elranatamab is a bispecific monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, physically linking T cells to BCMA+ myeloma cells to form an immune synapse. This activates cytotoxic T cells to release perforin and granzymes and kill target cells, with associated cytokine release that can lead to CRS and ICANS.
NO
INDIRECT
Elranatamab binds CD3ε on T cells and BCMA on myeloma cells to form an immune synapse; the activated T cells release perforin/granzymes to kill BCMA+ tumor cells, not the CD3+ T cells.
An investigational antibody–drug conjugate (ADC) consisting of a monoclonal antibody linked to a camptothecin-derived topoisomerase I inhibitor. It binds a tumor-associated surface antigen on SCLC cells, is internalized, and releases the payload to cause DNA damage and tumor cell death, with potential bystander effect.
Monoclonal antibody targets a tumor-associated surface antigen on SCLC cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload that induces DNA damage and tumor cell death, with potential bystander killing of neighboring tumor cells.
NO
INDIRECT
IBI3009 is an ADC that binds a tumor-surface antigen (not Topoisomerase I), is internalized, and releases a topoisomerase I–inhibiting payload that causes DNA damage in antigen-positive cells. Topoisomerase I expression alone is not directly targeted.
Anti-CD38 monoclonal antibody that induces ADCC/ADCP/CDC and apoptosis of malignant plasma cells.
Anti-CD38 IgG1κ monoclonal antibody that binds CD38 on malignant plasma cells, inducing Fc-mediated ADCC, ADCP, and complement-dependent cytotoxicity, promoting direct apoptosis, and depleting CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs).
YES
DIRECT
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), complement-dependent cytotoxicity, and can induce apoptosis upon binding/crosslinking.
Bispecific T-cell engager (GPRC5D×CD3) that redirects T cells to kill GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking them to activate T cells and drive cytotoxic lysis of GPRC5D-positive tumor cells.
YES
DIRECT
Talquetamab bridges CD3 on T cells to GPRC5D on target cells, activating T cells to form an immune synapse and kill GPRC5D+ cells via perforin/granzyme-mediated cytotoxicity.
Bispecific T-cell engager (GPRC5D×CD3) that redirects T cells to kill GPRC5D-positive myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, cross-linking them to activate T cells and drive cytotoxic lysis of GPRC5D-positive tumor cells.
NO
INDIRECT
Talquetamab engages CD3 on T cells to activate and redirect them to lyse GPRC5D-positive tumor cells (perforin/granzyme). CD3+ T cells are effectors, not killed by the drug.