Intravenous type II anti-CD20 monoclonal antibody that depletes B cells via ADCC, direct cell death, and complement-dependent cytotoxicity.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC, direct caspase-independent cell death, and complement-dependent cytotoxicity (CDC).
Binds CD20 on B cells and induces killing via enhanced Fc gamma RIIIa–mediated ADCC by immune effectors, complement-dependent cytotoxicity (CDC), and direct caspase-independent cell death.
Chimeric anti-CD20 monoclonal antibody (IV; 1000 mg ×2, 2 weeks apart) that depletes CD20+ B cells via complement- and antibody-dependent cytotoxicity and apoptosis to reduce pathogenic autoantibodies and immune-mediated inflammation in SLE-PAH. Brand used: Hanlikang.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and induces complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis, leading to depletion of CD20+ B cells and reduction of autoantibody-driven inflammation.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages, and can directly induce apoptosis of CD20+ cells.
Anti-CD38 monoclonal antibody that depletes clonal plasma cells via ADCC, CDC, apoptosis, and immunomodulation.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on clonal plasma cells, triggering ADCC, CDC, ADCP, and direct apoptosis; also depletes CD38+ immunosuppressive cells, producing antitumor immunomodulation.
Anti-CD38 IgG1 mAb binds CD38 on target cells and kills them via Fc-mediated ADCC, complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can induce direct apoptosis.
BCL-2 inhibitor (BH3 mimetic) that restores apoptosis, particularly effective in t(11;14) BCL-2–dependent clones.
Selective BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocking its anti-apoptotic function and freeing pro-apoptotic proteins to activate BAX/BAK, restoring mitochondrial apoptosis; particularly effective in BCL-2–dependent t(11;14) clones and has minimal BCL-XL inhibition.
Venetoclax binds and inhibits BCL-2 (BH3 mimetic), releasing pro-apoptotic proteins to activate BAX/BAK, causing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.
Autologous BCMA-directed CAR T-cell therapy in which a patient’s T cells are engineered to express an anti-BCMA CAR to recognize and kill myeloma plasma cells.
Autologous T cells are engineered to express an anti-BCMA chimeric antigen receptor (with costimulatory and CD3ζ signaling domains). Upon binding BCMA on myeloma plasma cells, the CAR T cells activate, proliferate, release cytotoxic granules and cytokines, and lyse BCMA-expressing tumor cells.
Anti-BCMA CAR T cells bind BCMA on target cells, activate, and kill via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas/FasL), leading to apoptosis/lysis of BCMA-expressing cells.