Biparatopic bispecific anti-HER2 IgG1 monoclonal antibody that binds two non-overlapping HER2 epitopes (domains II and IV), blocks dimerization/signaling, promotes receptor internalization/downregulation, and mediates ADCC.
Biparatopic, bispecific IgG1 monoclonal antibody that binds two non-overlapping HER2 epitopes (domains II and IV), blocks HER2 dimerization and signaling, induces receptor clustering, internalization and downregulation, and elicits Fc-mediated ADCC and ADCP against HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 on tumor cells and engages FcγR-bearing immune effectors to mediate ADCC (NK cells) and ADCP (macrophages), leading to killing of HER2-expressing cells; also blocks HER2 signaling but cytotoxicity is via Fc-mediated effector functions.
Biparatopic bispecific anti-HER2 IgG1 monoclonal antibody that binds two non-overlapping HER2 epitopes (domains II and IV), blocks dimerization/signaling, promotes receptor internalization/downregulation, and mediates ADCC.
Biparatopic, bispecific IgG1 monoclonal antibody that binds two non-overlapping HER2 epitopes (domains II and IV), blocks HER2 dimerization and signaling, induces receptor clustering, internalization and downregulation, and elicits Fc-mediated ADCC and ADCP against HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 and recruits immune effectors via its Fc to mediate antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), leading to killing of HER2-expressing cells; also blocks HER2 signaling.
Anti-HER2 IgG1 monoclonal antibody that binds HER2 domain IV, inhibits downstream signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 IgG1 that binds domain IV of HER2/ERBB2 on tumor cells, inhibits downstream signaling and tumor cell proliferation, and engages Fcγ receptors on immune effector cells to mediate ADCC.
YES
DIRECT
Trastuzumab binds HER2 on tumor cells and engages FcγR-expressing immune effectors to mediate ADCC (± complement), and HER2 signaling blockade can induce apoptosis.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
YES
DIRECT
TIL TCRs recognize Survivin (BIRC5)-derived peptides presented on MHC; antigen recognition triggers cytotoxic degranulation (perforin/granzymes) and death-receptor signaling (e.g., FasL), inducing apoptosis of the target cell.
Anti–TROP-2 antibody–drug conjugate delivering SN-38 (topoisomerase I inhibitor) to TROP-2–positive tumor cells.
Humanized anti–TROP-2 monoclonal antibody (hRS7) delivers the topoisomerase I inhibitor payload SN-38 to TROP-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, replication arrest, and apoptosis.
YES
DIRECT
The ADC binds TROP-2, is internalized, and releases SN-38, a topoisomerase I inhibitor that induces DNA damage and apoptosis in the TROP-2–expressing cell.