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. 2023 Sep 7;14:5497. doi: 10.1038/s41467-023-41190-0

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© The Author(s) 2023

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 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/4.0/.

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Fig. 3 — a TR-FRET assay using recombinant hIL-1α (filled squares) or hIL-1β (filled circles) in the absence (control, 100%) or presence of graded concentrations of compound (S)-2 (IL-1α, N = 2; IL-1β, N = 5). b IL-6 release in fibroblasts stimulated with 30 pg/ml IL-1β for 6 h in the presence of a concentration range of canakinumab (open triangles) or compound (S)-2 (open circles); data are presented as % of maximal inhibition of IL-6 release (N = 3). c IL-6 release by human fibroblasts stimulated with graded concentrations of hIL-1β (left panel) or hIL-1α (right panel), in the absence (filled circles, control) or presence of 50 μM compound (S)-2 (empty circles), 3 nM canakinumab (upward triangles), or 3 nM anakinra (downward triangle) (N = 5). d Reporter gene assay in HEK293 cells stimulated and treated as described in (c); hIL-1β (left panel), hIL-1α (right panel) (N = 3). Representative data are shown as mean ± SD; measurements were taken from distinct samples; full data are recapitulated in Table 1. Source data are provided as a Source Data file.