Intravenous anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ malignant and normal B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, antibody‑dependent phagocytosis, and induction of apoptosis.
Anti-CD20 binding triggers Fc-mediated ADCC by NK cells/macrophages, complement-dependent lysis (CDC), antibody-dependent phagocytosis, and can induce apoptosis of CD20+ B cells.
An anti-CD79b antibody-drug conjugate that delivers the microtubule-disrupting payload MMAE to CD79b-positive malignant B cells, causing apoptosis.
Anti‑CD79b monoclonal antibody linked via a cleavable linker to MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CD79b‑positive malignant B cells.
The ADC binds CD79b on B cells, is internalized, and releases MMAE via linker cleavage; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-expressing cells.
A chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and direct induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct induction of apoptosis.
Binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (FcγR-mediated), complement-dependent cytotoxicity, and direct induction of apoptosis.
Oral HER2‑selective small‑molecule tyrosine kinase inhibitor that blocks HER2 kinase activity and downstream PI3K/AKT and MAPK signaling, with minimal EGFR inhibition and CNS activity.
Oral, HER2-selective tyrosine kinase inhibitor that binds the HER2 (ERBB2) kinase domain, inhibits autophosphorylation, and suppresses downstream PI3K/AKT and MAPK signaling, leading to growth inhibition and death of HER2-overexpressing tumor cells; minimal EGFR inhibition with CNS activity.
Tucatinib binds the HER2 (ERBB2) kinase domain and blocks autophosphorylation, inhibiting PI3K/AKT and MAPK signaling, which leads to growth arrest and apoptosis of HER2-expressing tumor cells.
Humanized monoclonal antibody that binds the HER2 extracellular domain, inhibits receptor dimerization/signaling, promotes receptor downregulation, and mediates antibody‑dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody that binds the HER2 (ERBB2) extracellular domain, blocks receptor dimerization and downstream signaling (PI3K/AKT, MAPK), promotes receptor downregulation, and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
Binds HER2 on target cells and engages Fc gamma receptor–bearing immune cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC); may also activate complement.