Anti-HER2 antibody–drug conjugate (ADC) that binds HER2 (ERBB2), is internalized, and releases a cytotoxic payload to kill tumor cells; intended for HER2-high and HER2-low cohorts.
HER2-directed ADC (trastuzumab rezetecan). The antibody binds HER2 (ERBB2) on tumor cells and is internalized; a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that stabilizes TOP1–DNA complexes, causing DNA breaks, replication arrest, apoptosis, and tumor cell death in HER2-expressing tumors (including HER2-low).
YES
INDIRECT
HER2-directed ADC binds HER2, is internalized, and releases a camptothecin-derived TOP1 inhibitor that traps TOP1–DNA complexes, causing DNA damage, replication arrest, and apoptosis in the targeted cells.
Anti-TROP2 antibody–drug conjugate (ADC) that delivers a cytotoxic payload to TROP2-expressing tumor cells.
Anti-TROP2 IgG1 antibody–drug conjugate linked via a cleavable linker to an exatecan-derived topoisomerase I inhibitor (SHR9265). After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in TROP2-expressing cells.
YES
DIRECT
ADC binds TROP2, is internalized, linker is cleaved, and an exatecan-derived topoisomerase I inhibitor is released inside the cell, blocking DNA replication and inducing cell-cycle arrest and apoptosis.
Anti-TROP2 antibody–drug conjugate (ADC) that delivers a cytotoxic payload to TROP2-expressing tumor cells.
Anti-TROP2 IgG1 antibody–drug conjugate linked via a cleavable linker to an exatecan-derived topoisomerase I inhibitor (SHR9265). After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in TROP2-expressing cells.
NO
INDIRECT
The ADC binds TROP2 on tumor cells and is internalized; a cleavable linker releases an exatecan-derived topoisomerase I inhibitor that blocks Topo I, causing DNA damage, cell-cycle arrest, and apoptosis. DNA topoisomerase I is the intracellular payload target, not the directly targeted antigen for cell killing.
Type II, glycoengineered, humanized anti-CD20 monoclonal antibody that binds CD20 on B cells to induce direct cell death and enhance antibody-dependent cellular cytotoxicity and phagocytosis, depleting malignant CD20+ B cells.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes malignant CD20+ cells by inducing direct cell death and enhancing FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis; Fc glycoengineering (reduced fucosylation) increases effector function.
YES
DIRECT
Anti-CD20 mAb that induces type II CD20-mediated direct cell death and, via its afucosylated Fc, engages FcγRIIIa on effector cells to drive ADCC (NK cells) and antibody-dependent phagocytosis, depleting CD20+ cells.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
YES
DIRECT
Antigen-specific CTLs recognize the tumor peptide–HLA-C complex via their TCR and directly kill target cells through perforin/granzyme release and death-receptor (FasL/TRAIL) pathways.