An antibody–drug conjugate targeting HER2, consisting of trastuzumab linked to deruxtecan (a topoisomerase I inhibitor). It binds HER2 on tumor cells, is internalized, and releases a DNA-damaging payload with a bystander effect; it also inhibits HER2 signaling and can mediate ADCC.
Anti-HER2 monoclonal antibody (trastuzumab) linked to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After HER2 binding and internalization, lysosomal cleavage releases DXd to cause DNA damage (topoisomerase I inhibition) with a bystander effect in neighboring cells. The antibody component also inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
The anti-HER2 antibody binds HER2 and is internalized; lysosomal cleavage releases deruxtecan, a topoisomerase I inhibitor, causing DNA damage and death of HER2+ cells. The Fc domain can also trigger ADCC; the payload may exert a bystander effect on neighboring cells.
An antibody–drug conjugate targeting HER2, consisting of trastuzumab linked to deruxtecan (a topoisomerase I inhibitor). It binds HER2 on tumor cells, is internalized, and releases a DNA-damaging payload with a bystander effect; it also inhibits HER2 signaling and can mediate ADCC.
Anti-HER2 monoclonal antibody (trastuzumab) linked to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. After HER2 binding and internalization, lysosomal cleavage releases DXd to cause DNA damage (topoisomerase I inhibition) with a bystander effect in neighboring cells. The antibody component also inhibits HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
INDIRECT
T-DXd binds HER2, is internalized, and releases deruxtecan, which inhibits DNA topoisomerase I to cause DNA damage and apoptosis (with a bystander effect). Topoisomerase I is not the antigen recognized by the drug.
Autologous tumor-infiltrating lymphocytes (TILs) expanded/activated ex vivo and reinfused as cellular immunotherapy targeting patient-specific tumor antigens.
Autologous tumor-infiltrating lymphocytes are expanded and activated ex vivo and reinfused; they recognize patient-specific tumor antigens via endogenous TCRs and mediate cytotoxicity through perforin/granzyme release and proinflammatory cytokines (e.g., IFN-gamma), leading to targeted tumor cell killing.
YES
DIRECT
Adoptively transferred TILs recognize the mutant neoantigen peptide–HLA complex via their endogenous TCR and kill target cells by perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis, aided by proinflammatory cytokines (e.g., IFN-γ).
Autologous tumor-infiltrating lymphocytes (TILs) expanded/activated ex vivo and reinfused as cellular immunotherapy targeting patient-specific tumor antigens.
Autologous tumor-infiltrating lymphocytes are expanded and activated ex vivo and reinfused; they recognize patient-specific tumor antigens via endogenous TCRs and mediate cytotoxicity through perforin/granzyme release and proinflammatory cytokines (e.g., IFN-gamma), leading to targeted tumor cell killing.
YES
DIRECT
Infused TILs use their endogenous TCRs to recognize the tumor-associated peptide–MHC on target cells and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL), with cytokines (e.g., IFN-γ) supporting the response.
Subcutaneous anti-CD38 IgG1 monoclonal antibody that targets CD38 on myeloma cells, mediating ADCC, CDC, and ADCP, and depleting CD38+ immunosuppressive cells.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells and mediates Fc-dependent cytotoxicity (ADCC, CDC, ADCP) and apoptosis, resulting in lysis of CD38-expressing tumor cells; also depletes CD38+ immunosuppressive cells and can inhibit CD38 ectoenzyme activity, reducing adenosine-mediated immunosuppression.
YES
DIRECT
Isatuximab binds CD38 on target cells and engages effector functions via its Fc to induce NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and macrophage ADCP; it can also trigger apoptosis upon receptor crosslinking.