Gene-modified natural killer cells engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on myeloma cells, activating NK cytotoxic pathways to kill malignant plasma cells.
Ex vivo–engineered natural killer cells expressing a chimeric antigen receptor specific for BCMA (TNFRSF17) recognize and bind BCMA on malignant plasma cells, triggering NK activation and targeted cytotoxicity via perforin/granzyme release and cytokine-mediated killing, independent of MHC.
CAR-expressing NK cells bind BCMA on target cells, triggering NK activation and degranulation (perforin/granzyme) and cytokine-mediated killing, leading to direct lysis/apoptosis of BCMA+ cells.
Recombinant humanized IgG1 monoclonal antibody targeting HER2/ERBB2 (subdomain II). It blocks ligand-induced heterodimerization with EGFR/HER3/HER4, inhibiting downstream PI3K/AKT and MAPK/ERK signaling and reducing tumor cell proliferation/survival; also engages Fcγ receptors to mediate ADCC. In this trial, a biosimilar pertuzumab is compared with the reference product Perjeta (pertuzumab), both given intravenously.
Humanized IgG1 monoclonal antibody that binds the HER2/ERBB2 extracellular dimerization domain (subdomain II), preventing HER2 heterodimerization with EGFR/HER3/HER4, thereby inhibiting downstream PI3K/AKT and MAPK/ERK signaling and reducing tumor cell proliferation and survival; additionally engages Fc gamma receptors to mediate ADCC.
Binds HER2 on target cells and engages Fcγ receptors on NK cells/macrophages to trigger ADCC (and phagocytosis); also blocks HER2 dimerization/signaling, leading to growth arrest and apoptosis.
HER2-directed antibody-drug conjugate that binds HER2, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to induce DNA damage; Fc region may trigger ADCC.
HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor payload to cause DNA damage and cell death; the antibody Fc may also mediate ADCC.
The ADC binds HER2 on target cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that induces DNA damage leading to cell death; its Fc can also trigger ADCC against HER2+ cells.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
ATG antibodies bind CD8 on T cells and induce complement-dependent lysis and Fc receptor–mediated ADCC, with additional apoptosis of the bound cells.
Humanized anti-HER2 monoclonal antibody that binds HER2 domain II to block ligand-dependent dimerization (HER2/HER3, HER2/EGFR), suppressing PI3K/AKT and MAPK signaling; can mediate ADCC.
Humanized anti-HER2 monoclonal antibody that binds HER2 domain II to block ligand-dependent dimerization (e.g., HER2/HER3, HER2/EGFR), thereby inhibiting downstream PI3K/AKT and MAPK signaling and reducing tumor growth; may also mediate ADCC via its Fc region.
Pertuzumab (IgG1) binds HER2 on target cells and engages FcγR-expressing immune effectors (e.g., NK cells) to mediate ADCC, killing HER2+ cells; HER2 signaling blockade can also promote apoptosis.