ArticleJournal of medicinal chemistry2026
A Subcellular Keap1-Nrf2 Disruption Strategy for Atopic Dermatitis Therapy.
Article in Journal of medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a promising target for atopic dermatitis due to its role in skin barrier repair, yet effective modulators of Nrf2 are lacking. Here, we report an itaconate-iridium(III) complex conjugation strategy for the disruption of the Keap1-Nrf2 protein-protein interaction (PPI) for treating atopic dermatitis. The conjugate (1) specifically engages cytoplasmic Keap1 to restore Nrf2 activity, thus upregulating anti-inflammatory genes HO-1 and NQO1 while suppressing reactive oxygen species (ROS) in keratinocytes. It also reduces IL-13 production and boosts skin barrier proteins filaggrin and involucrin in a reconstructed human epidermis (RHE) model. In vivo studies revealed that compound 1 ameliorated DNFB-induced atopic dermatitis-like lesions and hypersensitivity. Its optical characteristics further enabled the flow cytometric discrimination of HaCaT cells based on Keap1 levels. This work provides a promising strategy for developing bioactive molecules to efficiently disrupt subcellular PPIs, laying the basis to progress theranostic candidates for atopic dermatitis.
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