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. 2022 Jan 7;26(1):117–127. doi: 10.1007/s40291-021-00573-z

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

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Fig. 2 — The design of antisense oligonucleotides (ASOs) in this study. The 14-mer gapmer ASO targeting human glucocorticoid receptor (GR) RNA, named gap-GR14 in this study, was selected as a lead sequence. Three 18-mer gapmer ASOs (gap-GR18-1, gap-GR18-2, and gap-GR18-3) were designed based on gap-GR14 sequence by extending the oligonucleotides on the 5′-sides, 3′-sides, and both sides. Gap DNA and LNA are indicated in lowercase and uppercase bold, respectively. All oligonucleotides were fully modified with phosphorothioate linkages. Lead sequences are shown in light orange, extended sequences in light blue, and phosphorothioate is indicated by a “^” symbol