Eliphos (Page 2 of 3)

8.4 Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

8.5 Geriatric Use

Clinical studies of calcium acetate did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other clinical experience has not identified differences in responses between elderly and younger patients. In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.


Administration of ELIPHOS® in excess of the appropriate daily dosage may result in hypercalcemia [see Warnings and Precautions (5.1)].


ELIPHOS® acts as a phosphate binder. Its chemical name is calcium acetate. Its molecular formula is C4 H6 CaO4 , and its molecular weight is 158.17. Its structural formula is:

Chemical Structure

Each round, white tablet is printed with “CYP 910”. Each tablet contains 667 mg calcium acetate, USP (anhydrous; Ca(CH3COO)2 ; MW=158.17 grams) equal to 169 mg (8.45 mEq) calcium, and the following inactive ingredients: polyethylene glycol 8000, NF; sodium lauryl sulfate, NF; and crospovidone, NF.

ELIPHOS® Tablets (calcium acetate) are administered orally for the control of hyperphosphatemia in end-stage renal failure.


Patients with ESRD retain phosphorus and can develop hyperphosphatemia. High serum phosphorus can precipitate serum calcium resulting in ectopic calcification. Hyperphosphatemia also plays a role in the development of secondary hyperparathyroidism in patients with ESRD.

12.1 Mechanism of Action

Calcium acetate (ELIPHOS®), when taken with meals, combines with dietary phosphate to form an insoluble calcium phosphate complex, which is excreted in the feces, resulting in decreased serum phosphorus concentration.

12.2 Pharmacodynamics

Orally administered calcium acetate from pharmaceutical dosage forms is systemically absorbed up to approximately 40% under fasting conditions and up to approximately 30% under non-fasting conditions. This range represents data from both healthy subjects and renal dialysis patients under various conditions.


13.1 Carcinogenesis, Mutagenesis, Impairment and Fertility

No carcinogenicity, mutagenicity, or fertility studies have been conducted with calcium acetate.


Effectiveness of calcium acetate in decreasing serum phosphorus has been demonstrated in two studies of the calcium acetate solid oral dosage form.

Ninety-one patients with end-stage renal disease who were undergoing hemodialysis and were hyperphosphatemic (serum phosphorus >5.5 mg/dL) following a 1-week phosphate binder washout period contributed efficacy data to an open-label, non-randomized study.

The patients received calcium acetate 667 mg tablets at each meal for a period of 12 weeks. The initial starting dose was 2 tablets per meal for 3 meals a day, and the dose was adjusted as necessary to control serum phosphorus levels. The average final dose after 12 weeks of treatment was 3.4 tablets per meal. Although there was a decrease in serum phosphorus, in the absence of a control group the true magnitude of effect is uncertain.

The data presented in Table 2 demonstrate the efficacy of calcium acetate in the treatment of hyperphosphatemia in end-stage renal disease patients. The effects on serum calcium levels are also presented.

Table 2: Average Serum Phosphorous and Calcium Levels at Pre-Study, Interim, and Study Completion Time points
Parameter Pre-Study Week 4 * Week 8 Week 12 p-value
Ninety-one patients completed at least 6 weeks of the study.
ANOVA of difference in values at pre-study and study completion.
Values expressed as mean ± SE.
Phosphorus (mg/dL) 7.4 ± 0.17 5.9 ± 0.16 5.6 ± 0.17 5.2 ± 0.17 •≤0.01
Calcium (mg/dL) 8.9 ± 0.09 9.5 ± 0.10 9.7 ± 0.10 9.7 ± 0.10 •≤0.01

There was a 30% decrease in serum phosphorus levels during the 12 week study period (p<0.01). Two-thirds of the decline occurred in the first month of the study. Serum calcium increased 9% during the study mostly in the first month of the study.

Treatment with the phosphate binder was discontinued for patients from the open-label study, and those patients whose serum phosphorus exceeded 5.5 mg/dL were eligible for entry into a double-blind, placebo-controlled, cross-over study. Patients were randomized to receive calcium acetate or placebo, and each continued to receive the same number of tablets as had been individually established during the previous study. Following 2 weeks of treatment, patients switched to the alternative therapy for an additional 2 weeks.

The phosphate binding effect of calcium acetate is shown in the Table 3.

Table 3: Serum Phosphorous and Calcium Levels at Study Initiation and After Completion of Each Treatment Arm
Parameter Pre-Study Post-Treatment p-value *
Calcium Acetate Placebo
ANOVA of calcium acetate vs. placebo after 2 weeks of treatment.
Values expressed as mean ± SEM
Phosphorus (mg/dL) 7.3 ± 0.18 5.9 ± 0.24 7.8 ± 0.22 <0.01
Calcium (mg/dL) 8.9 ± 0.11 9.5 ± 0.13 8.8 ± 0.12 <0.01

Overall, 2 weeks of treatment with calcium acetate statistically significantly (p<0.01) decreased serum phosphorus by a mean of 19% and increased serum calcium by a statistically significant (p<0.01) but clinically unimportant mean of 7%.

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