Nectin-4–directed antibody–drug conjugate targeting PVRL4; binds to Nectin-4 on tumor cells, is internalized, and releases a cytotoxic payload.
Nectin-4 (PVRL4)–targeted IgG1 antibody–drug conjugate. After binding Nectin-4 on tumor cells, the ADC is internalized and a cleavable linker releases a topoisomerase I inhibitor payload, blocking DNA replication and inducing cell cycle arrest and apoptosis in Nectin-4–expressing cells.
YES
DIRECT
The ADC binds Nectin-4 on target cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload that inhibits DNA replication, leading to cell-cycle arrest and apoptosis.
HER2-targeted bispecific monoclonal antibody that binds two distinct HER2 epitopes to inhibit HER2 signaling and potentially enhance antibody-dependent cellular cytotoxicity (ADCC).
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes, inhibits HER2 heterodimerization and downstream signaling, and induces Fc-mediated ADCC to kill HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 on tumor cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity (ADCC), leading to target-cell lysis; also blocks HER2 signaling.
HER2-targeted bispecific monoclonal antibody that binds two distinct HER2 epitopes to inhibit HER2 signaling and potentially enhance antibody-dependent cellular cytotoxicity (ADCC).
Bispecific anti-HER2 monoclonal antibody that binds two non-overlapping HER2 epitopes, inhibits HER2 heterodimerization and downstream signaling, and induces Fc-mediated ADCC to kill HER2-overexpressing tumor cells.
YES
DIRECT
Antibody binds HER2 and recruits FcγR-expressing effector cells to mediate ADCC, killing HER2+ cells; HER2 signaling blockade can also promote apoptosis.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding and downstream MAPK/ERK and PI3K/AKT signaling and can induce ADCC against EGFR-expressing tumor cells.
Cetuximab is a chimeric IgG1 monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and receptor dimerization, thereby inhibiting downstream MAPK/ERK and PI3K/AKT signaling; its Fc can also engage immune effector cells to mediate ADCC against EGFR-expressing tumor cells.
YES
DIRECT
IgG1 Fc engages FcγR-bearing effector cells to mediate ADCC (and some CDC/ADCP), leading to lysis/phagocytosis of EGFR-expressing cells; signaling blockade is antiproliferative rather than cytotoxic.
Autologous BCMA-targeted chimeric antigen receptor T-cell (CAR-T) therapy; patient T cells are gene-modified to express a CAR recognizing BCMA (TNFRSF17) to eliminate BCMA+ plasmablasts/plasma cells and some memory B cells, reducing pathogenic autoantibody production.
Autologous T cells are engineered to express a CAR targeting BCMA (TNFRSF17). Upon binding BCMA on plasmablasts/plasma cells (and some memory B cells), the CAR T cells activate and kill these cells, depleting antibody-secreting populations and reducing pathogenic autoantibody production.
YES
DIRECT
BCMA-targeted CAR T cells bind BCMA on plasmablasts/plasma cells, become activated, and induce cytotoxicity via perforin/granzyme-mediated apoptosis (and Fas/FasL signaling).