Humanized IgG1 monoclonal antibody against EGFR that inhibits ligand binding and downstream EGFR signaling (MAPK/ERK, PI3K/AKT), reducing proliferation and potentially promoting ADCC.
Humanized IgG1 monoclonal antibody targeting EGFR; blocks ligand binding and receptor activation to inhibit downstream MAPK/ERK and PI3K/AKT signaling, reducing tumor cell proliferation and survival, with potential Fc-mediated ADCC.
IgG1 anti-EGFR antibody binds EGFR on tumor cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC); EGFR signaling blockade is mainly cytostatic but can contribute to apoptosis.
Chimeric IgG1 monoclonal antibody targeting EGFR to inhibit EGFR signaling and promote Fc-mediated ADCC against tumor cells.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream EGFR signaling and tumor cell proliferation; its Fc region also engages Fcγ receptors to promote ADCC against EGFR-expressing tumor cells.
IgG1 Fc of cetuximab engages Fcγ receptors on NK cells and other effectors to mediate ADCC (and ADCP/CDC), directly killing EGFR-expressing cells; EGFR blockade also inhibits proliferation.
Antibody–drug conjugate targeting nectin‑4; the monoclonal antibody delivers the microtubule-disrupting payload MMAE (vedotin) to tumor cells, causing apoptosis.
Monoclonal antibody targets nectin-4 on tumor cells, is internalized, and releases the cytotoxic payload MMAE via a cleavable linker; MMAE binds tubulin, inhibits microtubule polymerization, causes G2/M arrest, and induces apoptosis in nectin-4–expressing cells.
The ADC binds Nectin-4, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of Nectin-4–expressing cells.
Autologous chimeric antigen receptor (CAR) T-cell therapy engineered to dual-target BCMA and CD19, depleting CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
Autologous CAR T cells engineered to dual-target CD19 and BCMA, inducing cytolytic depletion of CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
CD19-expressing cells are recognized by CD19-directed CAR T cells, triggering T-cell cytotoxicity (perforin/granzyme and Fas-FasL pathways) leading to direct lysis/apoptosis.
Autologous chimeric antigen receptor (CAR) T-cell therapy engineered to dual-target BCMA and CD19, depleting CD19+ B cells and BCMA+ plasmablasts/long-lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
Autologous CAR T cells engineered to dual-target CD19 and BCMA, inducing cytolytic depletion of CD19+ B cells and BCMA+ plasmablasts/long‑lived plasma cells to reduce pathogenic autoantibodies and reset humoral immunity in refractory SLE.
BCMA-targeted CAR T cells recognize BCMA on cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL).