An antibody–drug conjugate (ADC) consisting of a humanized anti-HER2 IgG1 (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). It binds HER2, is internalized, and releases DXd in lysosomes to cause topoisomerase I–mediated DNA damage and tumor cell death; also inhibits HER2 signaling and can induce Fc-mediated ADCC with potential bystander killing.
An anti-HER2 monoclonal antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). After HER2 binding and internalization, lysosomal cleavage releases DXd, which inhibits topoisomerase I, causing DNA damage, cell cycle arrest, and apoptosis; the antibody also inhibits HER2 signaling, can trigger Fc-mediated ADCC, and supports bystander killing.
YES
DIRECT
ADC binds HER2, is internalized, and lysosomal cleavage releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; trastuzumab Fc can also induce ADCC, with potential bystander killing from the membrane-permeable payload.
Autologous gamma delta T cells engineered to express a third-generation chimeric antigen receptor targeting mesothelin with co-stimulatory domains to enhance activation and tumor cell lysis.
Autologous γδ T cells are genetically engineered to express a third‑generation chimeric antigen receptor that binds mesothelin. Antigen engagement delivers CD3ζ signaling with co‑stimulation, activating the γδ T cells to proliferate, secrete cytotoxic molecules and cytokines, and lyse mesothelin‑expressing tumor cells in an MHC‑independent manner while leveraging innate γδ T cell tumor‑targeting properties.
YES
DIRECT
Mesothelin engagement by the CAR on engineered γδ T cells activates them to kill target cells via perforin/granzyme release and related cytotoxic pathways (MHC-independent).
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization/degradation, and mediates ADCC.
Human bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, inhibits downstream EGFR/MET signaling (MAPK/PI3K pathways), and mediates ADCC to suppress tumor cell growth.
YES
DIRECT
Amivantamab binds EGFR on tumor cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC/ADCP, causing target-cell lysis; receptor blockade/degradation may further induce apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization/degradation, and mediates ADCC.
Human bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, inhibits downstream EGFR/MET signaling (MAPK/PI3K pathways), and mediates ADCC to suppress tumor cell growth.
YES
DIRECT
Amivantamab binds MET on target cells and engages Fc-gamma receptors on immune effectors (e.g., NK cells, macrophages) to mediate ADCC/ADCP, killing MET-expressing cells.
Chimeric IgG1 anti-EGFR monoclonal antibody that inhibits EGFR signaling and can induce ADCC.
Chimeric IgG1 monoclonal antibody targeting the extracellular domain of EGFR, blocking ligand binding and receptor activation/dimerization to inhibit downstream signaling and tumor cell proliferation; can also mediate Fc-dependent ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages Fcγ receptors on immune effectors (e.g., NK cells) to mediate ADCC (and some CDC), leading to lysis; EGFR signaling blockade is mainly cytostatic.