Anti-TROP2 antibody–drug conjugate delivering a topoisomerase I inhibitor payload (deruxtecan).
Datopotamab deruxtecan is an anti‑TROP2 antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the membrane‑permeable topoisomerase I inhibitor payload deruxtecan via a cleavable linker in lysosomes. The released payload inhibits Topo I, causing DNA damage and tumor cell death, with potential bystander killing of adjacent cells.
YES
DIRECT
ADC binds TROP2 on target cells, is internalized, and releases the deruxtecan topoisomerase I inhibitor via lysosomal linker cleavage, causing DNA damage and apoptosis; membrane-permeable payload can also produce bystander killing.
Autologous T-cell receptor–engineered T-cell therapy in which patient T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted TCR that recognizes mutant NPM1 (dNPM1) peptides; the cells are expanded and reinfused to mediate antigen-specific cytotoxicity against NPM1-mutant AML.
Autologous T cells are lentivirally transduced ex vivo to express an HLA-A*02:01–restricted T-cell receptor specific for mutant NPM1 (dNPM1) peptides; after expansion and reinfusion, these engineered T cells recognize the HLA-A*02:01/dNPM1 peptide complex on NPM1-mutant AML cells and mediate antigen-specific cytotoxic killing.
NO
INDIRECT
Engineered TCR T cells kill AML cells only when HLA-A*02:01 presents the mutant NPM1 peptide; recognition triggers perforin/granzyme-mediated cytotoxicity. HLA-A*02:01 alone is not sufficient for killing.
Anti-TROP2 antibody–drug conjugate delivering a topoisomerase I inhibitor payload (deruxtecan).
Datopotamab deruxtecan is an anti‑TROP2 antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the membrane‑permeable topoisomerase I inhibitor payload deruxtecan via a cleavable linker in lysosomes. The released payload inhibits Topo I, causing DNA damage and tumor cell death, with potential bystander killing of adjacent cells.
NO
INDIRECT
Dato-DXd binds TROP2 (not topoisomerase I), is internalized, and releases deruxtecan that inhibits Topo I to cause DNA damage and cell death; any effect on Topo I–expressing cells is incidental (bystander) rather than due to targeting Topo I.
Type II glycoengineered anti-CD20 monoclonal antibody that induces potent ADCC and direct B-cell death with reduced reliance on complement.
Glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes them via enhanced FcγRIIIa-mediated ADCC and potent type II, caspase‑independent direct B‑cell death, with reduced reliance on complement.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and induces killing via enhanced Fc-gamma RIIIa–mediated ADCC (NK cells/monocytes), antibody-dependent phagocytosis, and direct type II, caspase-independent B-cell death, with minimal reliance on complement.
Humanized Fc-engineered anti-CD19 monoclonal antibody that enhances ADCC/ADCP and can induce direct apoptosis of B cells.
Humanized Fc-engineered anti-CD19 monoclonal antibody that binds CD19 on B cells and enhances Fc-gamma receptor–mediated ADCC and ADCP, leading to depletion of CD19+ malignant B cells; can also induce direct apoptosis.
YES
DIRECT
Binds CD19 on B cells and recruits FcγR-bearing effector cells to mediate ADCC/ADCP; can also trigger direct apoptosis of CD19+ cells.