HER2-targeted antibody-drug conjugate composed of an anti-HER2 monoclonal antibody linked to a topoisomerase I/camptothecin-class cytotoxic payload; binds HER2 on tumor cells, is internalized, and releases the payload to cause DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
Anti-HER2 monoclonal antibody linked to a topoisomerase I (camptothecin-class) cytotoxic payload. Binds HER2 on tumor cells, is internalized, and releases the payload to induce DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
NO
INDIRECT
BL-M07D1 binds HER2 (not topoisomerase I), is internalized, and releases a camptothecin-class payload that inhibits topoisomerase I to cause DNA damage and cell death; killing is restricted to HER2-targeted cells, not cells merely expressing topoisomerase I.
Autologous anti-CD19 CAR T-cell therapy; patient T cells engineered to express a CD19-directed CAR (with CD3ζ and costimulatory signaling) to proliferate and kill CD19+ malignant B cells.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor containing CD3zeta and costimulatory signaling domains. Binding to CD19 on malignant B cells activates T-cell effector functions, driving proliferation, cytokine release, and cytolytic killing of CD19-positive cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, activate, form an immunologic synapse, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
YES
DIRECT
ATG binds CD2 on T cells and depletes them via complement-dependent lysis and Fc-mediated ADCC, with additional apoptosis induction upon crosslinking.
ImmTAC bispecific (IMC‑F106C): affinity‑enhanced PRAME‑specific TCR fused to anti‑CD3 scFv that binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and recruits/activates T cells via CD3 to kill PRAME+ cells.
ImmTAC bispecific composed of an affinity‑enhanced PRAME‑specific TCR fused to an anti‑CD3 scFv; binds PRAME peptide presented by HLA‑A*02:01 on tumor cells and simultaneously engages CD3 on T cells, activating and redirecting polyclonal T cells to kill PRAME‑positive cells.
NO
INDIRECT
The drug engages CD3ε on T cells to activate and recruit them to PRAME/HLA-A*02:01–positive tumor cells; the T cells then kill the PRAME+ tumor cells (perforin/granzyme), not the CD3+ T cells.
Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
YES
DIRECT
ATG binds CD3ε on T cells and induces complement-dependent lysis and Fc-mediated ADCC; antibody cross-linking can also trigger apoptosis, leading to T-cell depletion.