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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
Chimeric IgG1 anti-EGFR monoclonal antibody that inhibits EGFR signaling (MAPK and PI3K/AKT pathways) and induces antibody-dependent cellular cytotoxicity.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream MAPK and PI3K/AKT signaling, and engages Fc receptors to induce antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on immune effectors (e.g., NK cells) to trigger ADCC, leading to lysis of EGFR-expressing cells; EGFR signaling blockade is mainly cytostatic.