TROP2-directed antibody–drug conjugate that delivers a topoisomerase I inhibitor payload via a cleavable linker to induce DNA damage and apoptosis (potential bystander effect).
TROP2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the cytotoxic payload, causing DNA damage and apoptosis; membrane-permeable payload may enable a bystander effect on neighboring cells.
YES
DIRECT
An anti-TROP2 ADC binds TROP2, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that induces DNA damage and apoptosis; the membrane-permeable payload can also cause a bystander effect.
TROP2-directed antibody–drug conjugate that delivers a topoisomerase I inhibitor payload via a cleavable linker to induce DNA damage and apoptosis (potential bystander effect).
TROP2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the cytotoxic payload, causing DNA damage and apoptosis; membrane-permeable payload may enable a bystander effect on neighboring cells.
NO
INDIRECT
The ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis; DNA topoisomerase I is the intracellular enzyme inhibited by the payload, not the antigen used for targeting, so cells are not killed specifically for expressing topoisomerase I (though bystander killing may occur).
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy expanded ex vivo and infused IV after lymphodepletion to mediate tumor cell killing via TCR recognition of neoantigens.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepletion to recognize patient-specific tumor neoantigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine-driven immune activation and persistence.
YES
DIRECT
Infused TILs recognize the neoantigen peptide–HLA class I complex via native TCRs and kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Intravenous type II glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances Fc-mediated ADCC/ADCP.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and, via enhanced Fc gamma RIIIa interaction, induces potent ADCC/ADCP and direct cell death, resulting in depletion of malignant CD20-positive B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and recruits immune effectors via Fc gamma RIIIa to mediate ADCC/ADCP, and as a type II anti-CD20 it also induces direct, caspase-independent cell death of CD20-positive cells.
Chimeric anti-CD20 monoclonal antibody that mediates complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, leading to B-cell depletion.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and induces B-cell depletion via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (and phagocytosis), with additional direct apoptotic signaling.
YES
DIRECT
Rituximab binds CD20 on B cells and kills them via complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP by NK cells and macrophages; it can also trigger direct apoptotic signaling.