Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
IgG1 monoclonal antibody targeting nectin‑4 binds tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload that blocks DNA topoisomerase I, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis in nectin‑4–expressing cancers.
NO
INDIRECT
SHR-A2102 binds nectin-4 on tumor cells, is internalized, and releases a topoisomerase I–inhibitor payload that poisons DNA topoisomerase I, blocking replication and inducing apoptosis. DNA topoisomerase I expression alone does not make cells targets; nectin-4 is the targeting determinant.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC and modulates immune responses, used to attenuate humoral autoimmunity.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them primarily via antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing pathogenic humoral immune responses.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers antibody-dependent cellular cytotoxicity via FcγR-bearing effector cells and complement-dependent cytotoxicity, with possible direct apoptosis upon crosslinking.
An autologous EBV-targeted chimeric antigen receptor T-cell (CAR-T) therapy for EBV-positive nasopharyngeal carcinoma. Patient T cells are engineered to express a CAR that binds an EBV-specific antigen on tumor cells, triggering CAR signaling, T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity. Administered intravenously at 3.0×10^6, 9.0×10^6, or 1.5×10^7 CAR-T cells/kg in this study.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes an EBV-specific antigen on EBV-positive tumor cells. Antigen engagement triggers CAR signaling, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of the cancer cells.
YES
DIRECT
CAR-T cells bind the EBV-associated surface antigen and directly lyse antigen-positive tumor cells via T-cell effector functions, primarily perforin/granzyme-mediated cytotoxicity.
Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and reinfused after lymphodepletion to mediate tumor-specific cytotoxicity in advanced/metastatic NSCLC.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These native T cells recognize tumor-specific antigens via their endogenous TCRs (MHC-restricted) and mediate tumor killing through perforin/granzyme release and cytokine secretion; lymphodepletion (and adjunct PD-1 blockade in the regimen) enhances engraftment, proliferation, and effector function.
YES
DIRECT
Autologous TILs recognize the neoantigen–HLA class I complex via their endogenous TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis, with proinflammatory cytokines aiding.
Patient-derived tumor-infiltrating lymphocytes expanded ex vivo and reinfused after lymphodepletion to mediate tumor-specific cytotoxicity in advanced/metastatic NSCLC.
Autologous tumor-infiltrating T cells are isolated from the patient’s tumor, expanded ex vivo, and reinfused after lymphodepletion. These native T cells recognize tumor-specific antigens via their endogenous TCRs (MHC-restricted) and mediate tumor killing through perforin/granzyme release and cytokine secretion; lymphodepletion (and adjunct PD-1 blockade in the regimen) enhances engraftment, proliferation, and effector function.
YES
DIRECT
Endogenous TCRs on reinfused TILs recognize the tumor-associated peptide–HLA class I complex and directly kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).