Adoptive cellular immunotherapy using cryopreserved, non–genetically modified natural killer (NK) cells whose surfaces are covalently conjugated to bispecific IgG antibodies to bridge NK cells to malignant B cells and enhance cytotoxicity.
Adoptive infusion of cryopreserved, non‑genetically modified NK cells whose surfaces are covalently decorated with bispecific IgG antibodies (CD19/CD20). The tethered antibodies bridge NK cells to malignant B cells, enable dual‑antigen recognition, promote stable immune‑synapse formation, and enhance NK cytotoxicity via degranulation (perforin/granzyme) and Fc receptor–mediated ADCC, thereby killing CD19+/CD20+ lymphoma cells.
NK cells decorated with CD19/CD20 bispecific IgG are bridged to CD19+ B cells, forming an immune synapse and killing them via NK degranulation (perforin/granzyme) and Fc receptor–mediated ADCC.
Adoptive cellular immunotherapy using cryopreserved, non–genetically modified natural killer (NK) cells whose surfaces are covalently conjugated to bispecific IgG antibodies to bridge NK cells to malignant B cells and enhance cytotoxicity.
Adoptive infusion of cryopreserved, non‑genetically modified NK cells whose surfaces are covalently decorated with bispecific IgG antibodies (CD19/CD20). The tethered antibodies bridge NK cells to malignant B cells, enable dual‑antigen recognition, promote stable immune‑synapse formation, and enhance NK cytotoxicity via degranulation (perforin/granzyme) and Fc receptor–mediated ADCC, thereby killing CD19+/CD20+ lymphoma cells.
NK cells coated with bispecific anti-CD19/CD20 IgG are bridged to CD20+ B cells, inducing immune synapse formation and NK killing via perforin/granzyme release and Fc receptor–mediated ADCC.
Intact bispecific IgG antibody with specificity for CD19 and CD20; covalently linked to NK cell surfaces to enable dual-antigen recognition, stable immune synapse formation, and ADCC against B‑cell lymphomas.
Non–genetically modified NK cells are covalently coated with an intact CD19/CD20 bispecific IgG, enabling dual-antigen recognition on B‑cell lymphomas, stabilizing the immune synapse, and enhancing NK effector functions. The armed NK cells kill target cells via degranulation (perforin/granzyme) and Fc-mediated ADCC against CD19+/CD20+ B-cell tumors.
NK cells armed with a CD19/CD20 bispecific IgG bind CD19 on target B cells, form a stable immune synapse, and kill via perforin/granzyme degranulation and Fc-mediated ADCC.
Intact bispecific IgG antibody with specificity for CD19 and CD20; covalently linked to NK cell surfaces to enable dual-antigen recognition, stable immune synapse formation, and ADCC against B‑cell lymphomas.
Non–genetically modified NK cells are covalently coated with an intact CD19/CD20 bispecific IgG, enabling dual-antigen recognition on B‑cell lymphomas, stabilizing the immune synapse, and enhancing NK effector functions. The armed NK cells kill target cells via degranulation (perforin/granzyme) and Fc-mediated ADCC against CD19+/CD20+ B-cell tumors.
NK cells coated with a CD19/CD20 bispecific IgG bind CD20 on B cells, form an immune synapse, and kill via NK degranulation (perforin/granzyme) and Fc-mediated ADCC.
A subcutaneous, off-the-shelf bispecific T-cell–engaging monoclonal antibody (BCMA×CD3) that binds BCMA on myeloma cells and CD3 on T cells to activate T cells and mediate cytotoxic killing of BCMA-positive plasma cells.
Elranatamab is a bispecific monoclonal antibody that simultaneously binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to activate T cells and trigger cytotoxic killing of BCMA-positive cells.
Elranatamab bridges CD3 on T cells to BCMA on target cells, activating T cells to kill BCMA+ cells via perforin/granzyme-mediated cytotoxic apoptosis.