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KEAP1 acts as an OS sensor to regulate NRF2 turnover within the cell/body, while NRF2 activation leads to the production of antioxidant and detoxifying substances that decrease OS [66,67,68]

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The development of more potent GlyT1 inhibitors was initially inspired by structural modifications of sarcosine, particularly through the introduction of bulky hydrophobic substituents at the nitrogen atom, an approach guided by emerging structural and pharmacological insights into GlyT1 and its relationship to other members of the SLC6 transporter family