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. Author manuscript; available in PMC: 2016 Nov 9.
Published in final edited form as: Nat Chem Biol. 2016 May 9;12(7):497–503. doi: 10.1038/nchembio.2079

Figure 2. Optimization of CIL56 revealed a potent and selective ferroptosis inducer.

Figure 2

a, e. HRASG12V selectivity. Viability of four engineered BJ cell lines treated with (a) CIL56 or (e) FIN56 for 48 hrs. mut: cells tumor-transformed due to HRASG12V overexpression, wt: isogenic cells without HRASG12V. b. Lipid ROS generation. Flow cytometry analysis with BODIPY-581/591 C11 staining in HT-1080 cells incubated with test compounds for six hours. DFOM: 152 μM deferoxamine. c, f. Effects of ferroptosis inhibitors on viability of HT-1080 cells co-treated with (c) CIL56 or (f) FIN56 for 48 hrs. αToc: 100 μM α-tocopherol, U0126: 3.8 μM. d. Chemical structures of CIL56 and FIN56. See Supplementary Fig. 5 for structure activity relationship around the CIL56 scaffold. Experiments in a-f were performed in biological triplicates, and single representative results were shown; error-bars indicate s.e.m. of technical triplicates.