Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding to EGFR, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; also mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells), triggering ADCC (and possibly complement activation) to kill EGFR-expressing cells.
Anti-CD38 IgG1κ human monoclonal antibody (Darzalex) administered subcutaneously every 28 days; binds CD38 on clonal plasma cells to induce ADCC, CDC, ADCP, and apoptosis, and inhibits CD38 ectoenzyme (NADase) activity to reduce immunosuppressive adenosine.
Human IgG1κ monoclonal antibody targeting CD38; induces tumor cell killing via ADCC, CDC, ADCP, and apoptosis, and inhibits CD38 ectoenzyme (NADase) activity to reduce immunosuppressive adenosine and deplete CD38+ immunosuppressive cells, enhancing anti-tumor immunity.
Daratumumab binds CD38 on target cells and triggers Fc-mediated killing: ADCC by NK cells, CDC via complement, ADCP by macrophages, and can directly induce apoptosis of CD38+ cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy (brand: Kymriah). Patient T cells are engineered to express a CAR recognizing CD19 with CD3ζ signaling and 4-1BB costimulation, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ leukemic blasts, resulting in B-cell aplasia.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with CD3zeta signaling and 4-1BB costimulation. Upon binding CD19 on B-lineage cells, the CAR T cells activate, proliferate, secrete cytokines, and mediate perforin/granzyme-dependent cytotoxicity, eliminating CD19+ malignant cells and causing B-cell aplasia.
Anti-CD19 CAR T cells bind CD19 and directly kill target cells via T-cell cytotoxicity, primarily perforin/granzyme-mediated apoptosis (and Fas/FasL).
FRα-targeting antibody–drug conjugate composed of anti-FRα mAb (M9346A) linked to the maytansinoid DM4, delivering a microtubule inhibitor to FRα-positive ovarian cancer cells.
An FRα-targeting monoclonal antibody delivers the maytansinoid payload DM4 to FRα-positive tumor cells. Upon binding and internalization, a cleavable disulfide linker is reduced to release DM4, which inhibits microtubule assembly, leading to mitotic arrest and apoptosis (with potential bystander killing).
An FRα-targeting antibody–drug conjugate binds FRα, is internalized, and releases the DM4 payload via cleavable linker reduction; DM4 inhibits microtubule assembly, causing mitotic arrest and apoptosis (with possible bystander effect).
Glycoengineered anti-CD20 IgG1 monoclonal antibody that depletes malignant B cells via ADCC and complement.
Glycoengineered anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity, leading to B-cell depletion; low-fucose Fc enhances ADCC.
Binds CD20 on B cells and triggers Fc-mediated ADCC (enhanced by low-fucose Fc) and complement-dependent cytotoxicity, leading to lysis/apoptosis of CD20+ cells.