Glycoengineered type II anti-CD20 monoclonal antibody that targets CD20+ B cells, inducing direct cell death with enhanced ADCC/ADCP and complement-mediated cytotoxicity.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and induces direct cell death and enhanced Fc-mediated effector functions (increased affinity for Fc-gamma RIIIa leading to stronger ADCC/ADCP), with some complement-mediated cytotoxicity.
YES
DIRECT
Obinutuzumab binds CD20 on B cells, inducing direct cell death and recruiting immune effectors via FcγRIIIa for enhanced ADCC/ADCP, with some complement-mediated cytotoxicity (CDC).
Glycoengineered type II anti-CD20 monoclonal antibody that targets CD20+ B cells, inducing direct cell death with enhanced ADCC/ADCP and complement-mediated cytotoxicity.
Glycoengineered type II anti-CD20 humanized IgG1 that binds CD20 on B cells and induces direct cell death and enhanced Fc-mediated effector functions (increased affinity for Fc-gamma RIIIa leading to stronger ADCC/ADCP), with some complement-mediated cytotoxicity.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa (CD16A) on NK cells/macrophages to drive ADCC/ADCP that kills CD20+ B cells. CD16A+ cells act as effectors and are not targeted for killing.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK signaling, thereby reducing tumor cell proliferation and survival; IgG1 Fc may also trigger ADCC.
YES
DIRECT
Cetuximab opsonizes EGFR+ cells and engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (with some CDC possible); EGFR signaling blockade is mainly cytostatic.
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK signaling, thereby reducing tumor cell proliferation and survival; IgG1 Fc may also trigger ADCC.
NO
INDIRECT
Cetuximab binds EGFR on target cells; its IgG1 Fc engages CD16a on NK cells to trigger ADCC, killing EGFR+ cells. CD16a-expressing cells are effectors, not targets.
Anti-BCMA monoclonal antibody–drug conjugate that binds BCMA on malignant plasma cells, internalizes, and delivers the microtubule inhibitor MMAF to induce cytotoxicity (with potential Fc-mediated effector functions).
Afucosylated anti-BCMA monoclonal antibody conjugated to the microtubule inhibitor MMAF. Binds BCMA on malignant plasma cells, is internalized, and delivers MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc engineering also enhances ADCC.
YES
DIRECT
ADC binds BCMA, is internalized, and delivers MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; afucosylated Fc can also trigger ADCC.