Polyclonal anti–T-cell antibody that depletes recipient lymphocytes to facilitate donor cell engraftment.
Polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, leading to profound T-cell immunosuppression to facilitate donor cell engraftment.
Polyclonal rATG antibodies can bind HLA‑DR on leukocytes and trigger complement-dependent cytotoxicity and Fc-mediated ADCC/apoptosis, depleting HLA‑DR–expressing cells.
Polyclonal anti–T-cell antibody that depletes recipient lymphocytes to facilitate donor cell engraftment.
Polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, leading to profound T-cell immunosuppression to facilitate donor cell engraftment.
rATG contains polyclonal antibodies that can bind HLA class I (e.g., HLA-A) on lymphocytes; bound cells are eliminated via complement-dependent cytotoxicity and Fc-mediated ADCC, with apoptosis contributing to depletion.
Anti‑CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and recruits immune effectors via its Fc to mediate ADCC; it also activates complement (CDC/MAC) and can trigger apoptosis upon cross-linking, killing CD20+ cells.
An antibody–drug conjugate (HER3-DXd; U3-1402) consisting of a fully human anti-HER3 (ERBB3) IgG1 monoclonal antibody linked via a cleavable linker to DXd, a membrane-permeable topoisomerase I inhibitor. It binds HER3 on tumor cells, is internalized, and releases DXd intracellularly to inhibit topoisomerase I, causing DNA damage and cell death with a potential bystander effect.
Patritumab deruxtecan is a HER3-targeted antibody–drug conjugate. The patritumab antibody binds HER3 (ERBB3) on tumor cells, is internalized, and a cleavable linker releases the DXd payload intracellularly. DXd inhibits topoisomerase I by stabilizing the Topo I–DNA complex and preventing religation of DNA breaks, leading to DNA damage and apoptotic cell death. The membrane-permeable payload can exert a bystander effect on neighboring tumor cells.
An anti-HER3 antibody–drug conjugate binds HER3, is internalized, and releases the DXd payload that inhibits topoisomerase I, causing DNA damage and apoptotic death of HER3+ cells (with potential bystander effect).
Chimeric IgG1 anti-CD20 monoclonal antibody (brands: MabThera, Truxima, Ruxience, Rixathon) that binds CD20 on pre-B and mature B lymphocytes, depleting these cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis; spares CD20− plasma cells and hematopoietic stem cells.
Chimeric IgG1 monoclonal antibody targeting CD20 on pre-B and mature B lymphocytes; depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, while sparing CD20− plasma cells and hematopoietic stem cells.
Binding to CD20 triggers Fc-mediated ADCC and complement-dependent cytotoxicity, and can induce apoptosis of CD20+ B cells.