A HER2-directed antibody–drug conjugate composed of a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE); binds ERBB2/HER2, is internalized, and releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis.
HER2-directed antibody–drug conjugate: the anti-HER2 monoclonal antibody binds ERBB2/HER2, is internalized, and via a cleavable linker releases MMAE, which inhibits microtubule polymerization, causing G2/M arrest and apoptosis (potential bystander cytotoxicity).
ADC binds HER2 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander effect).
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
rATG contains antibodies that bind CD5 on T cells, opsonizing them for complement-dependent lysis and Fc receptor–mediated ADCC/phagocytosis, with some apoptosis.
Allogeneic, banked Epstein–Barr virus–specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor (CAR); binds CD30 on tumor cells to trigger T-cell activation and cytotoxicity, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
Allogeneic EBV-specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor. CAR engagement of CD30 on tumor cells triggers T-cell activation and cytotoxic killing of CD30+ malignant cells, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
CD30-directed CAR on the infused T cells binds CD30 on target cells, activating T-cell cytotoxicity (perforin/granzyme and Fas–FasL) to kill CD30+ cells.
Allogeneic, banked Epstein–Barr virus–specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor (CAR); binds CD30 on tumor cells to trigger T-cell activation and cytotoxicity, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
Allogeneic EBV-specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor. CAR engagement of CD30 on tumor cells triggers T-cell activation and cytotoxic killing of CD30+ malignant cells, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
Native EBV-specific TCRs on the infused T cells recognize EBV peptide–HLA class I complexes on target cells and trigger T‑cell cytotoxic killing (perforin/granzyme, Fas–FasL).
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, reducing B-cell antigen presentation, autoantibody production, and pro-inflammatory cytokines (e.g., IL-6).
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, reducing B-cell antigen presentation, autoantibody production, and pro-inflammatory cytokines.
Binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC; crosslinking can also induce apoptosis.