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. 2023 May 10;13:7604. doi: 10.1038/s41598-023-34440-0

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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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Stabilization of CFTR fragments by CFTR correctors. Each panel shows immunoblot analysis of cells transfected with MSD1 (A), MSD1-NBD1(∆F) (B), MSD1-NBD1(∆F)-R (C), and MSD1-NBD1(∆F)-R-MSD2 (D). Cells were incubated for 24 h with: vehicle, 1 µM VX-809, 10 µM PP028, or 5 µM VX-445, as single agents or as combinations. Scatter dot plots show densitometric analysis of CFTR fragments. For panel A, the upper band (37 kDa) was considered for analysis. Data report the ratio of CFTR fragment intensity to GAPDH or beta-actin (ACTB) band intensity. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ns, not significant vs. vehicle. #, p < 0.05; ###, p < 0.001 vs. VX-809 (ANOVA with Tukey’s post-hoc test).