Fc-engineered humanized IgG1 anti-CD19 monoclonal antibody given IV; binds CD19 on B cells/leukemic blasts to enhance Fcγ receptor–mediated ADCC and ADCP via NK cells and macrophages and can induce direct apoptosis, leading to depletion of CD19+ cells in B-lineage ALL.
Fc‑engineered humanized IgG1 monoclonal antibody against CD19 that binds CD19 on B cells and leukemic blasts and enhances Fcγ receptor–mediated ADCC and ADCP by NK cells and macrophages; can also induce direct apoptosis, resulting in depletion of CD19‑positive cells.
Binds CD19 on B cells and recruits Fcγ receptor–bearing effector cells (NK cells/macrophages) to mediate ADCC and ADCP; binding can also trigger direct apoptosis of CD19+ cells.
An in vivo CAR-T gene therapy vector (IV) that transduces the patient's autologous T cells to express a CD19-targeted chimeric antigen receptor, leading to recognition and killing of CD19+ B-cell malignancies; dose expressed in transduction units/kg.
Intravenous in vivo vector transduces the patient’s autologous T cells to express a CD19-targeted chimeric antigen receptor, creating CAR-T cells in situ that expand and, upon binding CD19 on malignant B cells, activate CAR signaling (CD3zeta/costimulation) to mediate cytotoxic killing independent of the native TCR.
In vivo–generated CD19 CAR-T cells bind CD19 on target cells and kill them via CAR-activated T-cell cytotoxicity (perforin/granzyme-mediated apoptosis).
CD3×BCMA bispecific antibody that redirects T cells to kill BCMA-expressing myeloma cells.
Humanized CD3×BCMA bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, cross-linking them to activate and redirect T cells to lyse BCMA-positive myeloma cells via immunologic synapse formation, perforin/granzyme release, and cytokine-mediated cytotoxicity.
Teclistamab crosslinks CD3 on T cells with BCMA on target cells, forming an immunologic synapse and triggering T cell cytotoxicity via perforin/granzyme release and cytokine-mediated killing of BCMA+ cells.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D-CAR T cells recognize ULBP5 on target cells, activate, and kill them via perforin/granzyme-dependent cytolysis.
CD3×GPRC5D bispecific antibody that redirects T cells to kill GPRC5D-expressing myeloma cells.
Humanized bispecific antibody that binds CD3 on T cells and GPRC5D on myeloma cells, bringing them into proximity to activate cytotoxic T cells and mediate targeted lysis of GPRC5D-expressing tumor cells.
Talquetamab bridges CD3 on T cells to GPRC5D on target cells, activating T cells to form an immune synapse and kill GPRC5D+ cells via perforin/granzyme-mediated cytolysis (and related apoptotic pathways).