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One compound, CB-27, exhibited antiplasmodial activity with an EC 50 of 0.5 M toward P
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compounded under Section 503A for individual prescriptions Hepatic impairment data / no controlled pharmacokinetic studies in liver disease populations Copper clearance / 85-95% of circulating copper is bound to ceruloplasmin, which is synthesized exclusively in the liver [1] Wilson disease parallel / hepatic copper accumulation can reach 250+ mcg/g dry weight in impaired biliary excretion [2] Child-Pugh A / may proceed with standard dosing and baseline copper labs Child-Pugh B / dose reduction recommended with monthly copper monitoring Child-Pugh C / use generally not recommended due to impaired biliary copper excretion Standard compounded dose / 1-2 mg subcutaneously daily or 3 times weekly Key monitoring labs / serum copper, ceruloplasmin, 24-hour urine copper, liver function tests What Is GHK-Cu and How Does It Work
US department of Health and Human Services
Considering that PSC activation is a key factor in pancreatic fibrosis, we speculated that excess ROS production induced by high glucose may induce PSC activation in vivo
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