CD20×CD3 bispecific antibody that redirects T cells to kill CD20-positive B cells; administered subcutaneously.
Humanized CD20×CD3 bispecific antibody that binds CD20 on malignant B cells and CD3 on T cells, cross-linking them to redirect and activate T cells, inducing cytotoxic killing of CD20-positive B cells; administered subcutaneously.
CD20×CD3 bispecific antibody crosslinks T cells to CD20+ cells, activating T-cell cytotoxicity (perforin/granzyme) to lyse CD20-expressing B cells.
Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1); activates NK cells via SLAMF7 and engages Fc gamma receptors to mediate ADCC against SLAMF7-positive myeloma cells.
Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1). It activates NK cells via SLAMF7 signaling and engages Fc gamma receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against SLAMF7-positive myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages Fcγ receptors on NK cells to trigger antibody‑dependent cellular cytotoxicity (ADCC); it also activates NK cells via SLAMF7, enhancing killing.
A HER2-targeted antibody–drug conjugate composed of a monoclonal antibody linked to the microtubule inhibitor MMAE (vedotin). It binds HER2 (including HER2-low), is internalized, and releases MMAE to disrupt microtubules causing mitotic arrest and apoptosis; Fc-mediated ADCC may also contribute.
HER2-directed antibody–drug conjugate that binds HER2 (including HER2-low), is internalized, and releases the microtubule inhibitor MMAE (vedotin) to disrupt tubulin polymerization, causing microtubule disruption, mitotic arrest, and apoptosis; Fc effector function may also mediate ADCC.
The ADC binds HER2 on target cells, is internalized, and releases MMAE, which disrupts microtubules to cause mitotic arrest and apoptosis; Fc effector function can also trigger ADCC.
Chimeric anti-CD20 monoclonal antibody administered intravenously (375 mg/m² ×2, 14 days apart) to deplete CD20+ B cells via complement-dependent cytotoxicity, ADCC, and apoptosis, aiming to reduce autoantibody production and immune-complex–mediated inflammation in rheumatic carditis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing autoantibody production and immune-complex–mediated inflammation.
Binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC lysis), antibody-dependent cellular cytotoxicity via FcγR-bearing effector cells (e.g., NK cells/macrophages), and apoptosis upon CD20 cross-linking.
A chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Rituximab is a chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells through antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Anti‑CD20 antibody binds CD20 on B cells and triggers Fc‑mediated ADCC (NK cells/macrophages) and complement‑dependent cytotoxicity; CD20 ligation can also induce apoptosis.