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GSH deficiency induced in cultured hepatocytes caused an increase in oxidative stress and alterations in VD regulatory genes

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Similar to cagrilintide, pramlintide is primarily eliminated via the kidneys and, in a pharmacokinetic study in participants with type 1 diabetes, no statistically significant differences were noted in total (AUC 0- ) and peak ( C max ) exposure after administration of a single pramlintide 60 g dose in participants with mild, moderate or severe renal impairment compared with those with normal renal function, although inter-patient variability was high [20]