As shown in Figure 6B, the addition of catalase partially protected compound 2-treated cells, enhancing cell survival in the presence of the compound. The addition of SOD did not protect cells against compound 2 and the combination of catalase and SOD did not protect the cells against compound 2 Topiroxostat beyond that provided by catalase alone. The addition of catalase, SOD, or a combination of the two also did not protect cells treated with the highly cytotoxic compound 5. In parallel experiments, the cells to be treated with the MI-773 compounds were first pre-loaded for 4 h with ascorbic acid. Ascorbic acid is a small molecule which sacrificially reacts with and eliminates oxidative radicals, and was used as a non-protein control for protection against ROS. As shown in Figure 6B, the cells treated with either compound 2 or 5 were partially protected from cell death when pre-treated with ascorbic acid. Thus, the data demonstrates that the cytotoxic naphthoquinone compounds induce oxidative radicals however, this is unlikely the only mechanism by which the compounds induce cell death. Twelve 2, 3-1, 4-naphthoquinone compounds produced by a novel organic synthetic scheme were screened for cytotoxicity against a murine fibroblast cell line. Two of the compounds, which occur naturally in plants as chemicals for defense, were used as internal controls for synthesis of biologically relevant 1, 4naphthoquinone derivatives. The scheme utilized was unique in that it was the first report to demonstrate the use of the Do��tz benzannulation of Fischer carbene complexes with alkynes to form substituted phenols and was the first report to apply these reactions to solid-phase organic synthesis. The goal of the current study was to determine if the products generated by this process possessed the biological activity commonly associated with naphthoquinones. The small library of twelve compounds presented with three categories of cytotoxicity: no cytotoxicity, low/intermediate cytotoxicity, and high cytotoxicity. Through further analysis, the low/intermediate, and highly cytotoxic compounds were determined to promote cell death as demonstrated by membrane PS externalization and by the activation of caspase 3.