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. Author manuscript; available in PMC: 2015 Sep 11.
Published in final edited form as: Cell. 2014 Sep 11;158(6):1324–1334. doi: 10.1016/j.cell.2014.07.040

Figure 5. Active variants of P7C3 compensate NAD exhaustion induced by doxorubicin.

Figure 5

(A) U2OS cells were treated with the indicated concentration of P7C3-A20. Cells were harvested and NAD metabolites were measured by LC-MS/MS. Abundance of NAD was normalized relative to total metabolites (Experimental Procedures). The data are represented as the mean ± SD of experimental duplicates. (B) Active derivatives P7C3-A20 and P7C3-S243, but not inactive derivatives P7C3-S6, or P7C3-S117, facilitate replenishment of NAD levels in doxorubicin-treated cells. Cells were grown in 96-well plates and treated with the indicated concentrations of P7C3-A20, P7C3-S243, P7C3-S6 or P7C3-S117 together with 0.5μM doxorubicin for 45h. Cellular NAD abundance was determined by NAD/NADH Glo assay kit. See also Figure S5 and Table S2. (C) Scatter plots revealed a strong correlation between dox:tox protective activities of 159 compounds and their relative abilities to replenish NAD levels. The activities in both assays are represented by (Sinf-S0)/AC50 in dose response curves of test compounds. See also Table S1.