Monoclonal antibody that inhibits HER2 dimerization.
Humanized monoclonal antibody that binds the HER2 extracellular dimerization domain (subdomain II), blocking HER2 hetero-/homodimerization, thereby inhibiting downstream HER signaling (e.g., PI3K/AKT, MAPK), suppressing tumor cell proliferation and promoting apoptosis.
Pertuzumab binds HER2 subdomain II and blocks HER2 dimerization, inhibiting downstream signaling and promoting apoptosis; its IgG1 Fc engages FcγR-bearing effector cells to mediate ADCC against HER2-expressing cells.
Antibody–drug conjugate (T‑DM1) combining trastuzumab with the microtubule inhibitor DM1.
HER2-targeted monoclonal antibody (trastuzumab) linked via a nonreducible thioether (MCC) to the microtubule inhibitor DM1. After binding HER2 and internalization, DM1 is released intracellularly to bind tubulin and disrupt microtubule dynamics, leading to cell-cycle arrest and apoptosis in HER2-overexpressing cells; the antibody also inhibits HER2 signaling and can mediate ADCC.
The ADC binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis; the antibody can also mediate ADCC.
Investigational anti-CD20 monoclonal antibody (HS006) that depletes B cells to reduce autoantibody (e.g., anti-PLA2R) production and downstream immune complex/complement-mediated podocyte injury; administered intravenously.
Anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via immune effector mechanisms (e.g., ADCC/CDC), lowering pathogenic autoantibody (e.g., anti-PLA2R) production and reducing immune complex/complement-mediated podocyte injury.
Anti-CD20 IgG binds CD20 on B cells and triggers Fc-mediated ADCC/ADCP by immune effector cells and complement-dependent cytotoxicity (CDC), leading to B-cell lysis and depletion.
CD20×CD3 bispecific T‑cell–engaging antibody that redirects T cells to kill CD20+ B cells; administered IV with step‑up dosing.
Glofitamab is a CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to form an immune synapse and activate T cells, leading to perforin/granzyme‑mediated killing of CD20‑positive B‑cell malignancies.
Bispecific binding to CD20 on B cells and CD3 on T cells forms an immune synapse and activates T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous gene-modified T cells engineered to express an anti-CD19 chimeric antigen receptor, enabling targeted depletion of CD19+ B cells to reduce autoantibody production and reset dysregulated humoral immunity.
Autologous T cells are engineered to express an anti-CD19 chimeric antigen receptor that recognizes CD19 on B cells and triggers T-cell activation and cytotoxic killing, depleting CD19+ B-cell subsets to reduce autoantibody production and B cell–mediated antigen presentation, thereby resetting dysregulated humoral immunity.
CAR-T cells recognize CD19 via the CAR and directly kill CD19+ cells through T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis).