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. 2018 Dec 3;9:5138. doi: 10.1038/s41467-018-07590-3

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© The Author(s) 2018

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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Fig. 7 — A working model of Cmpd 81 in lowering cholesterol synthesis. All clinically used statins dramatically induce compensatory increase of HMGCR, and the increased HMGCR proteins would blunt statins’ efficacy. However, Cmpd 81 remarkably degrades statins-induced HMGCR protein through the ubiquitin-proteasome pathway to lower the cholesterol synthesis, and to improve the efficacy of statins