Investigational antibody–drug conjugate administered IV; a tumor-targeting monoclonal antibody is internalized and releases the topoisomerase I inhibitor payload brengitecan, causing DNA damage and tumor cell death.
Tumor-targeting monoclonal antibody binds a surface antigen, is internalized, and releases the camptothecin-derived topoisomerase I inhibitor brengitecan, inducing DNA damage (replication-associated strand breaks) and tumor cell death.
NO
INDIRECT
The ADC binds a different cell-surface antigen, is internalized, and releases the topoisomerase I inhibitor brengitecan; payload causes replication-associated DNA damage and death after delivery via the unrelated surface antigen, not due to Topoisomerase I expression itself.
Autologous T cells genetically engineered to express a chimeric antigen receptor with two nanobody binding domains that recognize distinct BCMA epitopes, aiming to increase avidity, prevent antigen escape, and mediate cytotoxic killing of multiple myeloma cells.
Autologous T cells are engineered to express a chimeric antigen receptor with two nanobody binding domains recognizing distinct BCMA epitopes. Dual-epitope binding increases avidity and reduces antigen escape. Upon BCMA engagement, CAR signaling activates T-cell cytotoxicity (perforin/granzyme and cytokine release), leading to killing of BCMA-expressing multiple myeloma cells and depletion of normal BCMA+ plasma cells.
YES
DIRECT
CAR-T cells bind BCMA on target cells, triggering T-cell activation and killing via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis), eliminating BCMA-expressing cells.
A BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect cytotoxic T‑cell killing in relapsed/refractory multiple myeloma.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to kill BCMA-expressing myeloma cells.
YES
DIRECT
Teclistamab bridges CD3+ T cells to BCMA+ cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme and Fas/FasL) to kill the BCMA-expressing cells.
A BCMA×CD3 bispecific T‑cell–engaging monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect cytotoxic T‑cell killing in relapsed/refractory multiple myeloma.
Humanized bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T-cell cytotoxicity to kill BCMA-expressing myeloma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to engage and activate them while simultaneously binding BCMA on myeloma cells; activated T cells kill BCMA+ tumor cells via perforin/granzyme, not the CD3+ T cells.
A T-cell-engaging bispecific IgG antibody (CD20xCD3) that binds CD20 on B cells and CD3 on T cells to form an immune synapse, activating T cells to kill malignant B cells via cytotoxic granule release and cytokines.
Bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, forming an immune synapse that activates T cells to release cytotoxic granules and cytokines, resulting in targeted lysis of CD20+ malignant B cells.
YES
DIRECT
Bispecific CD20xCD3 antibody crosslinks T cells to CD20+ cells, activating T cells to release perforin/granzymes and cytokines, causing targeted lysis/apoptosis of CD20-expressing cells.