GALZIN- zinc acetate capsule
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Zinc acetate as the dihydrate is a salt of zinc used to inhibit the absorption of copper in patients with Wilson’s disease. Its structural formula is:

chemical structure
(click image for full-size original)

C4 H6 O4 Zn•2H2 O    M.W. 219.51.

Zinc acetate occurs as white crystals or granules, freely soluble in water and in boiling alcohol, and slightly soluble in alcohol.

GALZIN® (Zinc Acetate) Capsules contain the equivalent of 25 or 50 mg of zinc, in addition to corn starch and magnesium stearate in gelatin capsules. The 25 mg capsule shells contain titanium dioxide and the 50 mg capsule shells contain titanium dioxide, methylparaben and propylparaben. The 25 mg capsule shells contain FD&C Blue #1; the 50 mg capsule shells contain FD&C Red #40, D&C Red #28, and D&C Yellow #10.



Wilson’s disease (hepatolenticular degeneration) is an autosomal recessive metabolic defect in hepatic excretion of copper in the bile, resulting in accumulation of excess copper in the liver, and subsequently in other organs, including the brain, kidneys, eyes, bone, and muscles. In this disease, hepatocytes store excess copper, but when their capacity is exceeded copper is released into the blood and is taken up in extrahepatic sites, such as the brain, resulting in motor disorders (ataxia, tremors, speech difficulties) and psychiatric manifestations (irritability, depression, deterioration of work performance). Redistribution of excess copper in hepatocytes leads to hepatocellular injury, inflammation, necrosis, and eventual cirrhosis. Patients may present clinically with predominantly hepatic, neurologic, or psychiatric symptoms.

The disease has been treated by restricting copper in the diet, and the use of chelating agents to bind free copper to reduce its toxicity and facilitate its excretion. The purpose of initial treatment of symptomatic patients with a chelating agent is to detoxify copper. Once the patient’s symptoms have stabilized clinically, maintenance treatment begins. Clinical measures are used to determine whether the patient remains stable (See PRECAUTIONS: Monitoring Patients).

The active moiety in zinc acetate is zinc cation. Regardless of the ligand, zinc blocks the intestinal absorption of copper from the diet and the reabsorption of endogenously secreted copper such as that from the saliva, gastric juice and bile. Zinc induces the production of metallothionein in the enterocyte, a protein that binds copper thereby preventing its serosal transfer into the blood. The bound copper is then lost in the stool following desquamation of the intestinal cells.


Because the proposed site of action of zinc is an effect on copper uptake at the level of the intestinal cell, pharmacokinetic evaluations based on blood levels of zinc do not provide useful information on zinc bioavailability at the site of action. Determinations of zinc content in the liver and the plasma zinc concentration after the oral administration of zinc acetate have yielded inconsistent results. However, foods and beverages have been shown to decrease the uptake of zinc thereby decreasing the levels of zinc in the plasma of healthy volunteers. For this reason, the oral dose of zinc should be separated from food and beverages, other than water, by at least one hour.


In pharmacodynamic studies, the methods used included net copper balance and radiolabeled copper uptake in Wilson’s disease patients. These studies showed that a regimen of 50 mg t.i.d. of zinc acetate was effective in inducing a negative mean copper balance (-0.44 mg/day) and an adequate mean 64 Cu uptake (0.82% of the administered dose). A regimen of 25 mg t.i.d. of zinc acetate was also pharmacodynamically active but fewer patients have been treated with this regimen than 50 mg t.i.d.


In the single center United States trial, 60 patients with Wilson’s disease (31 male, 29 female) who had adequate detoxification of copper after initial chelation therapy were entered into a copper balance study of various dose regimens of zinc acetate. Patients were hospitalized to carefully control food and liquid intake. Food, urine and feces were analyzed for copper content, and copper balance was defined as the difference between copper intake and copper elimination/excretion over a 10-day period. A patient was considered in adequate copper balance if the result was less than +0.25 mg copper/day. Results for the groups in each dose regimen tested and for adequacy of individual results are provided in the following table.

Dose Regimen
(mg zinc x number of daily doses)
N* Mean Copper Balance
Number of Patients Inadequately Controlled/Total number of patients studied

50 x 3

50 x 2

25 x 4

25 x 3

37.5 x 2

75 x 1

25 x 2

25 x 1

25 x 6

50 x 1

50 x 5





































*N = number of copper balance studies. Some patients had more than one balance study, at different doses or at the same dose at widely separated intervals.

While all zinc acetate regimens appeared better than no therapy, there was little experience with doses other than 50 mg t.i.d. Once daily dosing did not appear to give satisfactory control in many cases, and would be inadequate in patients with poor compliance. Based on the limited data available 25 mg t.i.d. was also thought to be an adequate dose regimen, and not shown to be inferior to 50 mg t.i.d. Dose related toxicity was not found in this study.

Symptomatic Patients Initially Treated With a Chelating Drug

Clinical parameters such as neuropsychiatric status including evaluation of speech, and liver function tests were followed as the patients continued therapy on an adequate zinc acetate dose regimen. One hundred and thirty-three patients were followed for up to 14 years. There was no deterioration of neuropsychiatric function including speech and biochemical liver function tests, including bilirubin, transaminases, alkaline phosphatase and lactic dehydrogenase. The liver function tests remained either within normal range or slightly above the upper limit of normal for up to 9 years of treatment.

Pre-symptomatic Patients

In this study 30 pre-symptomatic patients were followed for up to 10 years. Diagnosis of the pre-symptomatic Wilson’s disease was made on the basis of a liver copper value greater than 200 μg of copper per gram dry weight of tissue.

Non-ceruloplasmin copper levels, 64 Cu balance studies, and clinical parameters were assessed. No patient developed symptoms of Wilson’s disease in this cohort. Since the cloning and sequencing of the abnormal genes in Wilson’s disease patients, many mutations have been identified that may affect the rate of disease progression. No matched historical control has been compared to this experience, nor has another center replicated this experience.

In a study in the Netherlands, using zinc sulfate, 27 patients were followed up to 29 years by mainly clinical parameters such as tremors, dysarthria, dystonia, ataxia and Kayser-Fleischer rings. No deterioration of the clinical status was observed. In some cases, Kayser-Fleischer rings disappeared and clinical signs and symptoms improved.

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