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In the liver, it undergoes: Reversible acetylation by N-acetyltransferase (NAT2) to monoacetyl dapsone

It prevents the liver from compensating under higher stress

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However, in resistant patients, oxidative stress causes a conformational change in Keap1, leading to the release of NRF2, which translocates to the nucleus and binds to antioxidant response element (ARE), activating the expression of downstream antioxidant genes, including GPX4, NQO1, HO-1 and SOD1 [33], and promoting the synthesis of GSH, as illustrated in Fig

What is the dosage used in preclinical research