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. 2020 Jan 3;59(6):2420–2428. doi: 10.1002/anie.201912392

Figure 5.

Figure 5

Ezutromid behaves as an aryl hydrocarbon receptor antagonist. a) Ezutromid treatment (+; 3 μm for 24 h; dark bars) increases full‐length utrophin (Utrn) and AhR mRNA expression in dystrophin‐deficient mouse (mdx) and human DMD myoblasts (DMD). Concomitantly, AhR‐responsive genes AhRR and Cyp1b1 illustrate downregulation, indicating antagonism of AhR signalling with compound treatment. Bars represent mean fold change relative to DMSO (−; light bars) and normalised to S13 ± SD (n=3). Fold changes were all statistically significant with p<0.0001 (paired two‐tailed Student t‐test). b) Localisation of AhR induced by compound treatment determined by immunofluroscence. AhR is mostly located in the cytoplasm of human DMD myoblasts; ezutromid does not increase nuclear translocation, unlike agonist 2‐(1′H‐indole‐3′‐carbonyl)‐thiazole‐4‐carboxylic acid methyl ester (ITE), and co‐treatment of ITE with ezutromid results in retention of AhR in the cytoplasm.