Normal bone marrow B-cells, activated B cells and plasma cells have been shown to undergo apoptosis in a concentration dependent manner with rATG. The rATG has been shown to bind to B cells and this binding competitively inhibits several B cell specific monoclonal antibodies. The apoptosis can be inhibited by specific pathway inhibitors to caspases, cathepsin B and lysosomal cysteine proteases, indicating that each of these pathways is stimulated by thymoglobulin exposure. 18