The dual activation of these pathways may provide enhanced protection against beta cell dysfunction and death, potentially offering disease-modifying effects beyond symptomatic glucose control
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BRCA1, which regulates cell cycle progression, DNA damage signalling and repair, and maintenance of genomic integrity, interacts with NRF2 either directly, through its ETGE motif, preventing KEAP1-dependent ubiquitination of NRF2 and protecting cells against OS, or indirectly, through the interaction with CBP or with c-Myc [186]
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This broad cytoprotective signature is the property from which the compound takes its name