Anti-CD20 monoclonal antibody that depletes malignant B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and eliminates CD20-positive malignant and normal B cells primarily via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and direct apoptotic signaling.
HER2-targeted monoclonal antibody that blocks HER2/ErbB2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody against HER2 (ErbB2) that binds the extracellular domain, blocks receptor dimerization and downstream PI3K/AKT and MAPK signaling, promotes HER2 downregulation, and mediates antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Fc-mediated ADCC: trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells/macrophages) to lyse the bound cell; it also blocks HER2 signaling and promotes downregulation/apoptosis.
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.
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.
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.
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.