Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand-mediated activation, inhibits MAPK signaling, and can induce ADCC.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, thereby inhibiting EGFR-driven MAPK/ERK signaling and tumor cell proliferation; Fc region can engage immune effector cells to induce ADCC.
YES
DIRECT
Cetuximab’s IgG1 Fc engages Fcγ receptors on immune effector cells (e.g., NK cells, macrophages) to induce ADCC (and potentially CDC), killing EGFR-expressing cells; EGFR blockade itself is primarily antiproliferative.
Anti-CD20 monoclonal antibody causing B-cell depletion via ADCC/CDC and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis/phagocytosis.
YES
DIRECT
Anti‑CD20 mAb binds CD20 and recruits effectors to kill via ADCC (FcγR+ NK/macrophages), complement‑dependent cytotoxicity, and can induce apoptosis and phagocytosis.
An anti-CD38 antibody–drug conjugate administered IV that binds CD38 on malignant cells, is internalized, and releases a cytotoxic payload to kill tumor cells; Fc-mediated effector functions (ADCC/CDC) may also contribute. Targets CD38-expressing tumor cells and modulates the CD38 ectoenzyme/adenosine pathway in the tumor microenvironment.
An anti-CD38 monoclonal antibody conjugated to the microtubule inhibitor MMAF. After binding CD38 on tumor cells, the ADC is internalized and releases MMAF to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; Fc-mediated ADCC/CDC and modulation of the CD38 ectoenzyme/adenosine pathway may also contribute.
YES
DIRECT
Anti-CD38 ADC binds CD38, is internalized, and releases MMAF to inhibit tubulin polymerization causing G2/M arrest and apoptosis; Fc effector functions (ADCC/CDC) may also kill CD38+ cells.
An anti-CD38 antibody–drug conjugate administered IV that binds CD38 on malignant cells, is internalized, and releases a cytotoxic payload to kill tumor cells; Fc-mediated effector functions (ADCC/CDC) may also contribute. Targets CD38-expressing tumor cells and modulates the CD38 ectoenzyme/adenosine pathway in the tumor microenvironment.
An anti-CD38 monoclonal antibody conjugated to the microtubule inhibitor MMAF. After binding CD38 on tumor cells, the ADC is internalized and releases MMAF to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; Fc-mediated ADCC/CDC and modulation of the CD38 ectoenzyme/adenosine pathway may also contribute.
NO
INDIRECT
STI-6129 binds CD38 on target cells, is internalized, and releases MMAF, which binds beta-tubulin (vinca site) to inhibit microtubule polymerization and cause G2/M arrest and apoptosis; beta-tubulin expression alone does not mediate targeting or killing.
Anti-CD20 chimeric monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), recruits FcγR+ effector cells for antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and can trigger apoptosis of the target cells.