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.
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.
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.
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.
Humanized IgG1 monoclonal antibody against HER2 (ERBB2) that binds the extracellular domain of HER2 on tumor cells, inhibits HER2-driven signaling and receptor shedding, and engages immune effector cells via Fc-gamma receptors to trigger antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and engages Fc-gamma receptors (e.g., CD16) on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity and phagocytosis, killing HER2-expressing cells.
Humanized monoclonal antibody targeting the HER2 (ERBB2) extracellular dimerization domain (domain II); blocks HER2 heterodimerization (e.g., with HER3), inhibiting downstream signaling (PI3K/AKT, MAPK) and inducing tumor cell death, while also mediating Fc-dependent ADCC.
IgG1 antibody binds HER2 and engages Fcγ receptors on immune effectors (e.g., NK cells) to mediate ADCC/ADCP, killing HER2+ cells; blockade of HER2 dimerization also promotes apoptosis via signaling inhibition.