Anti-HER2 antibody–drug conjugate that binds HER2 (effective in HER2-low), is internalized, and releases the MMAE payload to disrupt microtubules causing mitotic arrest and apoptosis; can also mediate ADCC and bystander killing.
Anti-HER2 antibody–drug conjugate that binds HER2 (effective in HER2-low), is internalized, and releases the MMAE payload to disrupt microtubules, causing mitotic arrest and apoptosis; can also mediate ADCC and bystander killing.
The ADC binds HER2 on target cells, is internalized, and releases the MMAE payload, which disrupts microtubules causing mitotic arrest and apoptosis; Fc engagement can also trigger ADCC.
A FAP-targeted radiopharmaceutical: a 177Lu-labeled small-molecule FAPI ligand that selectively binds fibroblast activation protein on cancer-associated fibroblasts in the tumor stroma and delivers beta-emitting lutetium-177 to induce localized DNA double-strand breaks and cell death, with crossfire irradiation of adjacent tumor cells.
A 177Lu-labeled FAP inhibitor ligand that binds fibroblast activation protein on cancer-associated fibroblasts and delivers beta-emitting lutetium-177 to induce DNA double-strand breaks and cell death, with crossfire irradiation of adjacent tumor cells in the tumor microenvironment.
The 177Lu-labeled FAP inhibitor binds FAP on cancer-associated fibroblasts; beta emissions from 177Lu induce DNA double-strand breaks in the FAP-expressing cells, killing them, with crossfire irradiation of nearby tumor cells.
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.
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).
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.
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.
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.
CD19-directed CAR NK cells recognize CD19 on target cells and directly kill them via NK degranulation (perforin/granzyme-mediated lysis) and apoptotic pathways.