Patient-derived T cells genetically engineered to express a fully human anti‑CD19 scFv CAR with CD28–CD3ζ signaling domains; redirects T cells to recognize and kill CD19+ B cells, leading to depletion of malignant and normal B cells.
Autologous T cells engineered to express a fully human anti‑CD19 scFv CAR with CD28 costimulatory and CD3ζ signaling domains. Binding to CD19 on B cells triggers MHC‑independent T‑cell activation, proliferation, cytokine release, and cytotoxic killing, resulting in depletion of CD19+ malignant and normal B cells.
Anti-CD19 CAR T cells bind CD19 on B cells, activating T-cell cytotoxicity and killing target cells via perforin/granzyme-mediated lysis and death receptor pathways.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells to debulk disease prior to CAR T-cell infusion.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via Fc‑mediated ADCC and complement‑dependent cytotoxicity (and direct apoptosis), used here to debulk B‑cell disease prior to CAR T‑cell infusion.
Rituximab binds CD20 on B cells; its Fc engages immune effectors to mediate ADCC and complement-dependent cytotoxicity, and can also trigger apoptosis of CD20+ cells.
A human IgG1 monoclonal antibody targeting the BAFF receptor (BAFF-R/TNFRSF13C) on B cells; blocks BAFF signaling and induces B-cell depletion via immune effector functions (e.g., ADCC).
Ianalumab (VAY736) is a human IgG1 monoclonal antibody that binds the BAFF receptor (BAFF‑R/TNFRSF13C) on B cells, blocking BAFF-mediated survival and activation signaling and inducing B‑cell depletion via immune effector functions (e.g., ADCC/CDC). This reduces B‑cell activation, differentiation to plasmablasts/plasma cells, and autoantibody production.
Anti–BAFF-R IgG1 binds BAFF-R on B cells and opsonizes them, triggering Fc-mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity (CDC); BAFF signaling blockade may also promote apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks signaling, induces receptor downregulation and ADCC. Administered intravenously or subcutaneously with anticancer intent.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks receptor activation and downstream signaling, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC, suppressing tumor cell proliferation.
Amivantamab binds EGFR on target cells and its Fc region engages Fcγ receptor–bearing immune effectors to mediate ADCC/ADCP, leading to killing of EGFR-expressing cells (in addition to cytostatic signaling blockade/receptor downregulation).
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks signaling, induces receptor downregulation and ADCC. Administered intravenously or subcutaneously with anticancer intent.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks receptor activation and downstream signaling, promotes receptor internalization/degradation, and mediates Fc-dependent ADCC, suppressing tumor cell proliferation.
Amivantamab binds MET on target cells and its IgG1 Fc engages Fcγ receptor–bearing immune cells (e.g., NK cells), inducing ADCC that kills MET-expressing cells; it also blocks signaling but cytotoxicity is via ADCC.