Glycoengineered type II anti-CD20 monoclonal antibody with enhanced ADCC and induction of direct cell death.
Glycoengineered humanized IgG1 type II anti‑CD20 monoclonal antibody that binds CD20 on B cells; afucosylated Fc increases affinity for FcγRIIIa to enhance antibody‑dependent cellular cytotoxicity (and phagocytosis), and it induces potent direct, caspase‑independent cell death with relatively limited complement activation, leading to B‑cell depletion.
YES
DIRECT
Anti-CD20 IgG1 binds CD20 on B cells and engages Fc gamma RIIIa (CD16a) on NK cells/macrophages to mediate ADCC/ADCP; as a type II antibody it also induces caspase-independent direct cell death (with limited CDC).
Antibody–drug conjugate targeting CD79b; internalization releases MMAE (a microtubule inhibitor) causing mitotic arrest and apoptosis.
CD79b-directed monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE; binding to CD79b on B cells triggers internalization and release of MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
YES
DIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis of the target-expressing cells.
Antibody–drug conjugate targeting CD79b; internalization releases MMAE (a microtubule inhibitor) causing mitotic arrest and apoptosis.
CD79b-directed monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE; binding to CD79b on B cells triggers internalization and release of MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells and is internalized; the released MMAE then binds the β-tubulin (vinca) domain to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. β‑tubulin expression alone is not the targeted determinant of killing.
A humanized IgG1 kappa monoclonal antibody targeting HER2/ErbB2. It binds the HER2 extracellular domain to block receptor dimerization and downstream signaling (e.g., PI3K/AKT, MAPK) and mediates antibody-dependent cellular cytotoxicity (ADCC). In this trial, both Roche’s Herclon and a proposed Incepta biosimilar administer trastuzumab as a single 6 mg/kg IV dose.
Humanized IgG1 monoclonal antibody that binds the HER2/ErbB2 extracellular domain, preventing receptor dimerization and downstream PI3K/AKT and MAPK signaling; promotes receptor downregulation and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Fc-mediated ADCC: trastuzumab binds HER2 on tumor cells and its Fc engages FcγR-bearing effector cells (e.g., NK cells, macrophages) to lyse the target; may also contribute via CDC, while signaling blockade is mainly antiproliferative.
A humanized IgG1 kappa monoclonal antibody targeting HER2/ErbB2. It binds the HER2 extracellular domain to block receptor dimerization and downstream signaling (e.g., PI3K/AKT, MAPK) and mediates antibody-dependent cellular cytotoxicity (ADCC). In this trial, both Roche’s Herclon and a proposed Incepta biosimilar administer trastuzumab as a single 6 mg/kg IV dose.
Humanized IgG1 monoclonal antibody that binds the HER2/ErbB2 extracellular domain, preventing receptor dimerization and downstream PI3K/AKT and MAPK signaling; promotes receptor downregulation and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
NO
INDIRECT
Trastuzumab binds HER2 on tumor cells; its Fc engages CD16a on NK cells to mediate ADCC against HER2+ cells. CD16a-expressing cells are effectors, not killed by the drug.