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Most patients tolerate the medication well, but those with existing heart conditions should be monitored closely

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Since previous studies have linked the activation of NRF2 with the repression of lipogenic gene expression 64 , we reasoned that GSH depletion causes oxidation and consequent inactivation of KEAP1 (a repressor of NRF2), thus leading to increased antioxidant and decreased lipogenic gene expression

Lower overall bioavailability compared to injections, leading to inconsistent outcomes

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Metabolomic studies have revealed CKD patients show dysregulation in various biochemical pathways like amino acids, lipids, nucleotides, and glycoses [8]