Chimeric anti-CD20 monoclonal antibody (brand: MabThera) given IV (1 g on days 0 and 15) to deplete CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing autoantibody/immune-complex formation, antigen presentation, and B-cell–derived cytokines in refractory chronic hypersensitivity pneumonitis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing B cell–mediated autoantibody production, immune complex formation, antigen presentation, and cytokine release.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC by NK/macrophages, and can trigger apoptosis, leading to direct killing of CD20+ cells.
Radiolabeled anti-CD33 monoclonal antibody (Actimab-A) that delivers Actinium-225 alpha particles to CD33-expressing leukemic cells, causing DNA double-strand breaks and cytotoxicity.
Anti-CD33 monoclonal antibody (lintuzumab) conjugated to the alpha-emitter Actinium-225 targets CD33-expressing leukemic cells; localized high–linear energy transfer alpha radiation induces clustered DNA double-strand breaks, leading to cytotoxicity/apoptosis with limited tissue penetration.
Anti-CD33 antibody delivers Actinium-225 alpha radiation to CD33+ cells; short-range high-LET alpha particles cause clustered DNA double-strand breaks leading to apoptosis/cell death.
Gene-modified allogeneic natural killer cells expressing a chimeric antigen receptor targeting CD19 to mediate antigen-specific cytotoxicity against malignant B cells; administered in dose levels of 1×10^6, 5×10^6, or 2×10^7 cells/kg.
Allogeneic natural killer cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells. CAR binding to CD19 activates NK signaling to induce antigen-specific cytotoxicity (perforin/granzyme release and cytokine-mediated killing), leading to MHC-independent elimination of malignant CD19+ B cells.
CAR-expressing NK cells bind CD19 on target cells, triggering NK activation and MHC-independent cytotoxicity via perforin/granzyme-mediated lysis and apoptosis (with cytokine-mediated killing).
An antibody–drug conjugate (T-DM1, ado-trastuzumab emtansine) that links the anti-HER2 monoclonal antibody trastuzumab to the maytansinoid microtubule inhibitor DM1 (emtansine). It binds HER2, is internalized, and releases DM1 to disrupt microtubules, causing cell-cycle arrest and apoptosis while also mediating ADCC via the trastuzumab component.
An antibody–drug conjugate linking trastuzumab to the microtubule inhibitor DM1. Trastuzumab binds HER2 on tumor cells and is internalized; intracellular release of DM1 binds tubulin to disrupt microtubules, leading to cell‑cycle arrest and apoptosis. The antibody component also inhibits HER2 signaling and mediates antibody‑dependent cellular cytotoxicity (ADCC).
Trastuzumab binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis; Fc-mediated ADCC can also kill HER2+ cells.
A HER3 (ERBB3)-targeted antibody–drug conjugate administered IV every 3 weeks. The monoclonal antibody binds HER3 on tumor cells, is internalized, and releases a cytotoxic payload to kill HER3-expressing cells; by engaging HER3-containing ERBB dimers (HER3–EGFR, HER3–HER2), it suppresses downstream PI3K–AKT/MAPK signaling.
HER3-targeted monoclonal antibody–drug conjugate that binds ERBB3 on tumor cells, is internalized, and releases a cytotoxic payload to kill HER3-expressing cells; by engaging HER3-containing ERBB dimers (HER3–EGFR/HER3–HER2), it suppresses downstream PI3K–AKT/MAPK signaling.
An anti-HER3 antibody–drug conjugate binds ERBB3 on tumor cells, is internalized, and releases an intracellular cytotoxic payload that kills HER3-expressing cells.