TROP2-targeted antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a cytotoxic topoisomerase I inhibitor payload to induce DNA damage and tumor cell death (with possible bystander effect).
TROP2-targeted IgG1 ADC that binds TROP2 on tumor cells, is internalized, and upon linker cleavage releases an exatecan-derivative topoisomerase I inhibitor (SHR9265), causing DNA replication inhibition, DNA damage, cell-cycle arrest, and apoptosis; payload may exert a bystander effect.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases an exatecan-derived topoisomerase I inhibitor (SHR9265) after linker cleavage, causing DNA damage/replication inhibition leading to cell-cycle arrest and apoptosis (with possible bystander effect).
TROP2-targeted antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a cytotoxic topoisomerase I inhibitor payload to induce DNA damage and tumor cell death (with possible bystander effect).
TROP2-targeted IgG1 ADC that binds TROP2 on tumor cells, is internalized, and upon linker cleavage releases an exatecan-derivative topoisomerase I inhibitor (SHR9265), causing DNA replication inhibition, DNA damage, cell-cycle arrest, and apoptosis; payload may exert a bystander effect.
NO
INDIRECT
The ADC targets TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor (SHR9265) that causes DNA damage and apoptosis; any effect on DNA topoisomerase I–expressing cells occurs only after payload delivery (including possible bystander diffusion), not because they express DNA topoisomerase I.
CD20×CD3 bispecific monoclonal antibody (T-cell engager; brand name Columvi) that redirects CD3+ T cells to kill CD20+ B-cell lymphoma cells.
CD20×CD3 bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to activate and redirect T cells to kill CD20-positive B‑cell lymphoma cells via cytotoxic effector mechanisms.
YES
DIRECT
Bispecific antibody binds CD20 on target cells and CD3 on T cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated killing) of CD20+ cells.
CD20×CD3 bispecific monoclonal antibody (T-cell engager; brand name Columvi) that redirects CD3+ T cells to kill CD20+ B-cell lymphoma cells.
CD20×CD3 bispecific monoclonal antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to activate and redirect T cells to kill CD20-positive B‑cell lymphoma cells via cytotoxic effector mechanisms.
NO
INDIRECT
Glofitamab binds CD3 on T cells to activate and redirect them to kill CD20+ B cells; CD3+ cells are engaged, not targeted for killing.
Allogeneic CD19-directed CAR natural killer (NK) cell therapy; engineered NK cells recognize and kill CD19+ B-lineage cells via NK cytotoxicity to deplete autoreactive B cells/plasmablasts in SLE/LN.
Off-the-shelf allogeneic NK cells engineered with a CD19-specific CAR (OX40 costimulatory domain and CD3ζ signaling) and membrane-bound IL-15. The CAR targets CD19 on B-lineage cells, triggering NK cytotoxicity (perforin/granzyme) and cytokine release to lyse CD19+ cells, depleting autoreactive B cells/plasmablasts; mbIL-15 enhances NK survival and persistence.
YES
DIRECT
CD19-directed CAR NK cells recognize CD19 on target cells and directly kill them via NK degranulation (perforin/granzyme-mediated lysis) and apoptotic pathways.