Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
Anti-thymocyte globulin binds CD2 on T cells and triggers complement-dependent lysis and Fc-mediated ADCC/phagocytosis; crosslinking can also induce apoptosis.
Humanized IgG1 monoclonal antibody against HER2/ERBB2 that binds the receptor on tumor cells, blocks HER2 activation/dimerization and downstream PI3K/AKT/MAPK signaling, promotes receptor internalization, and mediates Fcγ-dependent ADCC against HER2-overexpressing cells.
Trastuzumab coats HER2-expressing cells and engages Fcγ receptors on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (ADCC), killing the target cells; it also blocks HER2 signaling (growth inhibition).
Glycoengineered chimeric IgG1 anti‑CD20 monoclonal antibody (brand: BRIUMVI) that depletes CD20+ B cells primarily via enhanced antibody‑dependent cellular cytotoxicity, and also through complement‑dependent cytotoxicity and apoptosis; used in relapsing multiple sclerosis.
Glycoengineered chimeric IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ B cells primarily via enhanced antibody‑dependent cellular cytotoxicity, and additionally through complement‑dependent cytotoxicity and apoptosis.
Anti-CD20 IgG1 binds CD20 on B cells and eliminates them via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and induction of apoptosis.
Investigational adoptive cellular immunotherapy given as a single IV infusion (2.0×10^8 to 6.0×10^9 cells); BGT007H cells are intended to recognize a predefined tumor-associated antigen and mediate antigen-directed cytotoxicity against target-expressing tumor cells via cytotoxic lymphocyte mechanisms.
Adoptive transfer of genetically engineered cytotoxic lymphocytes that recognize a predefined tumor-associated antigen on tumor cells and induce antigen-directed killing via perforin/granzyme-mediated cytolysis and cytokine-driven immune activation.
Engineered cytotoxic lymphocytes recognize the tumor-associated antigen and kill target cells via immune synapse formation and perforin/granzyme-mediated cytolysis (with cytokine-driven cytotoxicity).
Chimeric type I anti-CD20 monoclonal antibody that depletes CD20+ B cells primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC).
Chimeric type I anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC), leading to elimination of CD20+ B cells.
After binding CD20, rituximab triggers complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (NK cells/macrophages), leading to lysis and clearance of CD20+ B cells.