Autologous, gene-modified T lymphocytes engineered with a CD70-specific chimeric antigen receptor; a single IV infusion that targets CD70-positive tumor cells to trigger T-cell activation and cytotoxicity.
Autologous T cells genetically engineered to express a CD70-specific chimeric antigen receptor; upon binding CD70 on tumor cells, the CAR triggers T-cell activation and expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD70-positive cells.
YES
DIRECT
CAR-T cells bind CD70 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Antibody–drug conjugate: humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (DXd); binds HER2, is internalized, releases DXd to inhibit topo I causing DNA damage/apoptosis; can mediate ADCC and has a bystander effect.
Humanized anti-HER2 IgG1 antibody–drug conjugate (trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and apoptosis; the Fc can mediate ADCC, and the membrane-permeable payload enables a bystander killing effect.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor inside the cell, causing DNA damage and apoptosis; Fc can also trigger ADCC, with a membrane-permeable payload allowing bystander killing.
Antibody–drug conjugate: humanized anti-HER2 IgG1 (trastuzumab) linked to a topoisomerase I inhibitor payload (DXd); binds HER2, is internalized, releases DXd to inhibit topo I causing DNA damage/apoptosis; can mediate ADCC and has a bystander effect.
Humanized anti-HER2 IgG1 antibody–drug conjugate (trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor DXd). Binds HER2 on tumor cells, is internalized, and releases DXd to inhibit topoisomerase I, causing DNA damage and apoptosis; the Fc can mediate ADCC, and the membrane-permeable payload enables a bystander killing effect.
NO
INDIRECT
T-DXd binds HER2 on cells, is internalized, and releases DXd that inhibits topoisomerase I to cause DNA damage and apoptosis (with a bystander effect). Topoisomerase I expression alone does not make cells targeted or directly killed by the drug.
An antibody–drug conjugate (iza-bren; izalontamab brengitecan; BMS-986507) administered IV every 3 weeks. The monoclonal antibody targets a tumor-associated cell-surface antigen on glioblastoma cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload causing DNA damage and apoptosis; Fc-mediated effector functions may also contribute.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload to cause DNA damage and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.
YES
DIRECT
The ADC binds EGFR on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor that induces DNA damage and apoptosis; Fc-mediated ADCC/CDC may also contribute.
An antibody–drug conjugate (iza-bren; izalontamab brengitecan; BMS-986507) administered IV every 3 weeks. The monoclonal antibody targets a tumor-associated cell-surface antigen on glioblastoma cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload causing DNA damage and apoptosis; Fc-mediated effector functions may also contribute.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate that binds EGFR/HER3 on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload to cause DNA damage and apoptosis; Fc-mediated effector functions (e.g., ADCC/CDC) may also contribute.
YES
DIRECT
The ADC binds HER3 on tumor cells, is internalized, and releases a brengitecan topoisomerase I inhibitor payload that causes DNA damage and apoptosis; Fc-mediated ADCC/CDC may also contribute.