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. 2017 Nov 28;7:16475. doi: 10.1038/s41598-017-16593-x

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Tetrac, triac and T1AM induce apoptosis. Cells were treated with the analogs (10 or 25 μM) for 96 hours and assessed by (A) Cell viability (PrestoBlue) (B) annexin-FITC/PI and (C) Cell cycle distribution. Experiments were repeated 3 times in triplicates. Significance (*p < 0.05, **p < 0.005) from vehicle control (KOH) or from normal control cells (indicated by ) is shown.

Inline graphic — Tetrac, triac and T1AM induce apoptosis. Cells were treated with the analogs (10 or 25 μM) for 96 hours and assessed by (A) Cell viability (PrestoBlue) (B) annexin-FITC/PI and (C) Cell cycle distribution. Experiments were repeated 3 times in triplicates. Significance (*p < 0.05, **p < 0.005) from vehicle control (KOH) or from normal control cells (indicated by ) is shown.