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- W2551155385 abstract "Oxidative stress is well recognized to contribute to the cause of a wide range of diseases, such as cancer, diabetes, Alzheimer's disease, arteriosclerosis, and inflammation. The Keap1-Nrf2-ARE pathway plays a critical regulatory role and can protect cells from oxidative stress through activating Nrf2 to induce its downstream phase II enzymes. Nrf2 activation through the covalent inactivation of Keap1 may cause unpredictable side effects. Non-covalent disruption of the Keap1-Nrf2 protein-protein interactions is an alternative strategy for Nrf2 activation, potentially with reduced risk of toxicity. Efforts have been made in recent years to develop peptide- and small molecule-based Keap1-Nrf2 PPI inhibitors via different approaches, including high-throughput screening, target-based virtual screening, structure-based optimization, and fragment-based drug design. This review aims to highlight the recently discovered small-molecule inhibitors as well as their therapeutic potential." @default.
- W2551155385 created "2016-11-30" @default.
- W2551155385 creator A5001631388 @default.
- W2551155385 creator A5005969908 @default.
- W2551155385 creator A5024129015 @default.
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- W2551155385 date "2017-01-01" @default.
- W2551155385 modified "2023-10-17" @default.
- W2551155385 title "Small molecules inhibiting Keap1–Nrf2 protein–protein interactions: a novel approach to activate Nrf2 function" @default.
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- W2551155385 doi "https://doi.org/10.1039/c6md00500d" @default.
- W2551155385 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6072482" @default.
- W2551155385 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30108745" @default.
- W2551155385 hasPublicationYear "2017" @default.
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