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.
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.
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.
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.
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.
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.