Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a 4-1BB costimulatory domain that targets CD19+ B cells to induce cytotoxic killing; may cause on-target B-cell aplasia.
Autologous T cells are genetically engineered to express an anti-CD19 chimeric antigen receptor with a CD3-zeta signaling domain and 4-1BB costimulatory domain. After infusion, the CAR T cells recognize CD19 on malignant and normal B cells in an HLA-independent manner, activate and proliferate, and induce cytotoxic killing, often leading to on-target B-cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target cells, become activated via CD3-zeta and 4-1BB costimulation, and kill through T-cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling).
Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a CD28 costimulatory domain that targets CD19+ B cells to induce cytotoxic killing.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with a CD28 costimulatory and CD3 zeta signaling domain; after infusion they recognize CD19 on B cells and induce HLA-independent T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant and normal B cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and, upon activation via CD28/CD3ζ signaling, kill CD19+ cells through T cell cytotoxic mechanisms (perforin/granzyme and Fas–FasL), with cytokine release.
Autologous, genetically engineered anti-CD19 CAR T-cell therapy (CD28 costimulation) directed against CD19+ B-cell malignancies.
Autologous T lymphocytes genetically engineered to express an anti-CD19 chimeric antigen receptor with CD28 costimulatory and CD3 zeta signaling domains; after infusion, the CAR enables HLA-independent recognition of CD19 on B-cell malignancies, triggering T-cell activation, proliferation, and cytotoxic killing of CD19+ cells, resulting in antitumor activity and on-target B-cell aplasia.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells and induce T-cell cytotoxic killing via perforin/granzyme-mediated lysis and apoptosis (HLA-independent).
Autologous, genetically engineered anti-CD19 CAR T-cell therapy with a 4-1BB costimulatory domain and defined CD4/CD8 composition, targeting CD19+ B cells.
Autologous T cells are lentivirally engineered to express an anti‑CD19 CAR with a 4‑1BB costimulatory and CD3ζ signaling domain. Upon binding CD19 on B‑cell malignancies, the CAR triggers HLA‑independent T‑cell activation, proliferation, and cytotoxic killing of CD19+ cells; an EGFRt tag enables in vivo tracking and potential cetuximab-mediated ablation.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and, via CD3ζ/4-1BB signaling, are activated to kill CD19+ cells through perforin/granzyme release and death-receptor pathways (HLA-independent).
HER2‑directed antibody–drug conjugate that binds HER2 via trastuzumab, mediates ADCC, is internalized, and releases a topoisomerase I inhibitor payload (deruxtecan) causing DNA damage and cell death, including a bystander effect.
HER2-directed antibody–drug conjugate: trastuzumab binds HER2 and mediates ADCC, is internalized, and releases the deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and tumor cell death with a bystander killing effect.
NO
INDIRECT
Cells are not targeted for killing based on topoisomerase I. The ADC binds HER2, is internalized, then releases deruxtecan that inhibits topoisomerase I to cause DNA damage and apoptosis (with ADCC and bystander effects).