Patient-derived T cells engineered to express a chimeric antigen receptor targeting CD19 to trigger T-cell activation and cytotoxic killing of malignant B cells.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 on B cells; CD19 binding activates CAR signaling to trigger T-cell cytotoxicity and cytokine release, eliminating CD19-positive malignant B cells.
Anti‑CD19 CAR T cells bind CD19 on target B cells, triggering T‑cell activation and immune synapse formation with perforin/granzyme release (and Fas/FasL signaling), causing lysis/apoptosis of CD19+ cells.
Fully human IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C) on B cells, blocks BAFF (BLyS) survival signaling, and depletes B cells predominantly via antibody-dependent cellular cytotoxicity (ADCC); studied in SLE and Sjogren's.
Fully human IgG1 monoclonal antibody that binds the BAFF receptor (BAFF-R/TNFRSF13C) on B cells, blocks BAFF (BLyS) binding and survival signaling (e.g., NF-kB), and depletes B cells predominantly via antibody-dependent cellular cytotoxicity (ADCC).
Ianalumab binds BAFF-R on B cells and engages Fcγ receptor–bearing effector cells to mediate ADCC (with possible ADCP/CDC), depleting BAFF-R–expressing cells; BAFF signaling blockade may further promote apoptosis.
Intravenous anti-CD20 chimeric monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric monoclonal antibody against CD20 on B cells that induces cell depletion via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Anti-CD20 antibody binds CD20 on B cells, engages FcγR-bearing effector cells to mediate ADCC, activates complement for CDC, and can directly trigger apoptosis upon CD20 ligation.
Anti-EGFR IgG1 monoclonal antibody that blocks EGFR signaling and mediates ADCC.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding and receptor dimerization/activation, inhibiting downstream MAPK and PI3K signaling and tumor-cell proliferation, and engages Fcγ receptors to mediate ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fc gamma receptor–bearing effector cells (e.g., NK cells) to trigger ADCC (and some CDC), causing lysis of EGFR+ cells; EGFR blockade is mainly antiproliferative.
CD123-targeted immunotoxin (IL-3 fused to truncated diphtheria toxin) that binds IL-3Rα (CD123), is internalized, ADP-ribosylates EF-2 to block protein synthesis and induce apoptosis.
Recombinant IL-3–diphtheria toxin immunotoxin that binds CD123 (IL-3Rα) on target cells, is internalized, and the diphtheria toxin catalytic domain ADP-ribosylates elongation factor-2 (EF-2), blocking protein synthesis and inducing apoptotic cell death.
IL-3 binds CD123, the fusion is internalized, and the diphtheria toxin domain ADP-ribosylates EF-2, inhibiting protein synthesis and inducing apoptosis.