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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.