Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR signaling (RAS–RAF–MEK–ERK and PI3K–AKT) and can trigger antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling and inducing Fc-mediated ADCC.
Cetuximab binds EGFR on target cells and its Fc engages Fcγ receptors on immune effectors (e.g., NK cells), inducing ADCC (and some CDC), leading to killing of EGFR+ cells; signaling blockade itself is mainly cytostatic.
An autologous anti‑CD19 CAR T‑cell therapy that targets CD19 on malignant B cells to trigger T‑cell activation and cytotoxic killing; administered after lymphodepleting chemotherapy to support CAR‑T expansion.
Autologous T cells genetically engineered to express an anti-CD19 chimeric antigen receptor (scFv-CD28-CD3zeta) recognize CD19 on malignant B cells, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing; lymphodepleting chemotherapy is given to enhance in vivo CAR-T expansion.
Anti-CD19 CAR-T cells bind CD19 on target cells, activate, and kill via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL).
Autologous T cells genetically modified to express a chimeric antigen receptor that targets BAFFR (TNFRSF13C) on malignant B cells, leading to T-cell activation and cytotoxic killing.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds BAFFR (TNFRSF13C) on malignant B cells; CAR engagement triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BAFFR-expressing B cells.
BAFFR-specific CAR T cells bind BAFFR on target B cells and, upon engagement, activate cytotoxic pathways (perforin/granzyme-mediated killing and death receptor signaling) to induce apoptosis.
Off-the-shelf allogeneic CD19-directed chimeric antigen receptor natural killer (CAR-NK) cell therapy designed to deplete CD19+ B-lineage cells to reduce pathogenic autoantibodies.
Off-the-shelf allogeneic NK cells engineered with a CD19-targeted CAR containing OX40 and CD3ζ signaling domains and membrane-bound IL-15. Upon binding CD19 on B-lineage cells, the CAR-NK cells are activated to release cytotoxic mediators and pro-inflammatory cytokines, leading to depletion of CD19+ B cells and reduction of pathogenic autoantibodies.
CAR-NK cells bind CD19 on target cells, become activated, and kill via degranulation with perforin/granzymes leading to lysis/apoptosis of CD19+ cells.
Human IgG1κ anti-CD38 monoclonal antibody (DARZALEX) given IV weekly for 8 doses (4, 8, or 16 mg/kg); depletes CD38+ cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis; inhibits CD38 ectoenzyme (NADase) activity affecting adenosine signaling.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis to deplete target cells; also inhibits CD38 ectoenzyme (NADase) activity, modulating NAD/adenosine signaling.
Anti-CD38 IgG1 mAb binds CD38 on target cells and induces complement-mediated lysis (CDC), Fc-mediated ADCC/ADCP by immune effectors, and apoptosis, depleting CD38+ cells.