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. 2020 May 5;10:7604. doi: 10.1038/s41598-020-64348-y

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© The Author(s) 2020

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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RU.521 suppresses cGAS activity in human primary cells from healthy donors. PBMCs were isolated from three human donors and and either directly stimulated with HT-DNA (a) or further differentiated into M1 macrophages (b). RU.521 was also added to a subset of the PBMCs at IC₅₀ and IC₉₀ (0.8 µM and 3 µM, respectively), followed by RT-qPCR analysis for IFNB1 expression (a). M1 macrophages were exposed to HT-DNA +/− RU.521, followed by ELISA for secreted IFNB1 protein levels (b). For PBMCs, each donor had (n = 9) technical replicates; for M1 macrophages, each donor had (n = 4) technical replicates. Error bars represent SEM. Asterisks (*) denote P ≤ 0.05 where an unpaired t-test with Welch’s correction was used to compare the results.