Calcitriol 1 ug/mL Solution
🆔 Identity & classification
Where does this data come from?
🏷️ RxNorm drug class
This medicine belongs to the Vitamin D3 Analog class.
Where does this data come from?
🏭 Manufacturer & labeler
Where does this data come from?
🩺 Clinical
Calcitriol is used to treat and prevent low levels of calcium and bone disease in patients whose kidneys or parathyroid glands (glands in the neck that release natural substances to control the amount of calcium in the blood) are not working normally. It is also used to treat secondary hyperparathyroidism (a condition in which the body produces too much parathyroid hormone [PTH; a natural substance needed to control the amount of calcium in the blood]) and metabolic bone disease in people with kidney disease. Calcitriol is in a class of medications called vitamin D analogs. It works by helping...
Read the full MedlinePlus article ↗- Calcitriol is actually the active form that vitamin D becomes after your liver and kidneys process it. If your kidneys aren't working well, they can't make enough calcitriol on the...
- What exactly is calcitriol, and why did my doctor prescribe it instead of regular vitamin D?
- The biggest thing to watch for is high calcium — the early signs are things like unusual weakness, headache, nausea, dry mouth, a metallic taste, or constipation. If those get wors...
- What side effects should I actually watch out for while taking this?
Patient education
Supplement & herbal interactions
Where does this data come from?
Ask a licensed pharmacist directly — free, answered by our team.
🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
-
UNII REK4960K2U
Butylated hydroxyanisole is a synthetic preservative that prevents oils and fats in medicines from spoiling or becoming rancid. It keeps the medicine stable and extends its shelf life.
-
UNII 1P9D0Z171K
BHT is a synthetic antioxidant that prevents fats and oils in medicines from breaking down and becoming rancid. It helps keep the product stable and effective during storage.
-
UNII C9H2L21V7U
A fat derived from coconut or palm oil containing shorter fatty acid chains. It serves as a solvent and carrier to help dissolve or suspend active ingredients, improving absorption and stability in liquid formulations.
3 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
Are inactive ingredients the same for every manufacturer?
Why might an inactive ingredient be missing?
Can inactive ingredients matter?
💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per mL | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | $6.793 | $101.90 / 15 ml |
| Medicaid paysCMS SDUD · 12 mo | $6.57 | $98.58 / 15 ml |
| Medicare drug plans payPart D · Q2 2026 | $6.19 | $92.82 / 15 ml |
Where does this data come from?
🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Calcitriol 1 ug/mL 00054-3120-41 | Hikma | 1 bottle | $6.793 | AA | Availability likely | — |
| Calcitriol 1 ug/mLthis 64980-0447-15 | Rising | 1 bottle | $6.793 | AA | Availability likely | — |
| Calcitriol 1 ug/mL 63304-0241-59 | Sun | 15 ml | $7.289 | AA | Discontinued | +7% |
| Calcitriol 1 ug/mL 39328-0042-15 | Patrin | 1 bottle | — | AA | FDA listed | — |
| Calcitriol 1 ug/mL 70954-0831-10 | ANI | 1 bottle | — | AA | FDA listed | — |
Where does this data come from?
⏳ Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
Where does this data come from?
🗺️ Medicaid utilization & spend
📊 Medicare Part D spend CMS · PART D · 2026 (Q1)
📦 Packaging — all sizes for this product
| Package NDC | Description | Marketing start | Status |
|---|---|---|---|
| 64980-0447-15 You're viewing this | 1 BOTTLE, GLASS in 1 CARTON (64980-447-15) / 15 mL in 1 BOTTLE, GLASS | 2019-01-04 | Active |
📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
INDICATIONS AND USAGE Predialysis Patients Calcitriol Oral Solution is indicated in the management of secondary hyperparathyroidism and resultant metabolic bone disease in patients with moderate to severe chronic renal failure (Ccr 15 to 55 mL/min) not yet on dialysis. In children, the creatinine clearance value must be corrected for a surface area of 1.73 square meters. A serum iPTH level of ≥ 100 pg/mL is strongly suggestive of secondary hyperparathyroidism.
Dialysis Patients Calcitriol Oral Solution is indicated in the management of hypocalcemia and the resultant metabolic bone disease in patients undergoing chronic renal dialysis. In these patients, Calcitriol Oral Solution administration enhances calcium absorption, reduces serum alkaline phosphatase levels, and may reduce elevated parathyroid hormone levels and the histological manifestations of osteitis fibrosa cystica and defective mineralization. Hypoparathyroidism Patients Calcitriol Oral Solution is also indicated in the management of hypocalcemia and its clinical manifestations in patients with postsurgical hypoparathyroidism, idiopathic hypoparathyroidism, and pseudohypoparathyroidism.
⏱️ Dosage and Administration ▾
DOSAGE AND ADMINISTRATION The optimal daily dose of Calcitriol Oral Solution must be carefully determined for each patient. Calcitriol Oral Solution can be administered as an oral solution (1 mcg/mL). Calcitriol Oral Solution therapy should always be started at the lowest possible dose and should not be increased without careful monitoring of serum calcium.
The effectiveness of Calcitriol Oral Solution therapy is predicated on the assumption that each patient is receiving an adequate but not excessive daily intake of calcium. Patients are advised to have a dietary intake of calcium at a minimum of 600 mg daily. The U.S.
RDA for calcium in adults is 800 mg to 1200 mg. To ensure that each patient receives an adequate daily intake of calcium, the physician should either prescribe a calcium supplement or instruct the patient in proper dietary measures. Because of improved calcium absorption from the gastrointestinal tract, some patients on Calcitriol Oral Solution may be maintained on a lower calcium intake.
Patients who tend to develop hypercalcemia may require only low doses of calcium or no supplementation at all. During the titration period of treatment with Calcitriol Oral Solution, serum calcium levels should be checked at least twice weekly. When the optimal dosage of Calcitriol Oral Solution has been determined, serum calcium levels should be checked every month (or as given below for individual indications).
Samples for serum calcium estimation should be taken without a tourniquet. Dialysis Patients The recommended initial dose of Calcitriol Oral Solution is 0.25 mcg/day. If a satisfactory response in the biochemical parameters and clinical manifestations of the disease state is not observed, dosage may be increased by 0.25 mcg/day at 4- to 8-week intervals.
During this titration period, serum calcium levels should be obtained at least twice weekly, and if hypercalcemia is noted, the drug should be immediately discontinued until normocalcemia ensues (see PRECAUTIONS: GENERAL ). Phosphorus, magnesium, and alkaline phosphatase should be determined periodically. Patients with normal or only slightly reduced serum calcium levels may respond to Calcitriol Oral Solution doses of 0.25 mcg every other day.
Most patients undergoing hemodialysis respond to doses between 0.5 and 1 mcg/day. Calcitriol Oral Solution may normalize plasma-ionized calcium in some uremic patients, yet fail to suppress parathyroid hyperfunction. In these individuals with autonomous parathyroid hyper-function, Calcitriol Oral Solution may be useful to maintain normocalcemia, but has not been shown to be adequate treatment for hyperparathyroidism.
Hypoparathyroidism The recommended initial dosage of Calcitriol Oral Solution is 0.25 mcg/day given in the morning. If a satisfactory response in the biochemical parameters and clinical manifestations of the disease is not observed, the dose may be increased at 2- to 4-week intervals. During the dosage titration period, serum calcium levels should be obtained at least twice weekly and, if hypercalcemia is noted, Calcitriol Oral Solution should be immediately discontinued until normocalcemia ensues (see PRECAUTIONS: GENERAL ).
Careful consideration should also be given to lowering the dietary calcium intake. Serum calcium, phosphorus, and 24-hour urinary calcium should be determined periodically. Most adult patients and pediatric patients age 6 years and older have responded to dosages in the range of 0.5 mcg to 2 mcg daily.
Pediatric patients in the 1- to 5-year age group with hypoparathyroidism have usually been given 0.25 mcg to 0.75 mcg daily. The number of treated patients with pseudohypoparathyroidism less than 6 years of age is too small to make dosage recommendations. Malabsorption is occasionally noted in patients with hypoparathyroidism; hence, larger doses of Calcitriol Oral Solution may be needed.
Predialysis Patients The recommended initial dosage of Calcitriol Oral Solution is 0.25 mcg/day in adults an…
⛔ Contraindications ▾
CONTRAINDICATIONS Calcitriol Oral Solution should not be given to patients with hypercalcemia or evidence of vitamin D toxicity. Use of Calcitriol Oral Solution in patients with known hypersensitivity to Calcitriol Oral Solution (or drugs of the same class) or any of the inactive ingredients is contraindicated.
⚠️ Warnings ▾
WARNINGS Overdosage of any form of vitamin D is dangerous (see OVERDOSAGE ). Progressive hypercalcemia due to overdosage of vitamin D and its metabolites may be so severe as to require emergency attention. Chronic hypercalcemia can lead to generalized vascular calcification, nephrocalcinosis and other soft-tissue calcification.
The serum calcium times phosphate (Ca x P) product should not be allowed to exceed 70 mg 2 /dL 2 . Radiographic evaluation of suspect anatomical regions may be useful in the early detection of this condition. Calcitriol Oral Solution is the most potent metabolite of vitamin D available.
The administration of Calcitriol Oral Solution to patients in excess of their daily requirements can cause hypercalcemia, hypercalciuria, and hyperphosphatemia. Therefore, pharmacologic doses of vitamin D and its derivatives should be withheld during Calcitriol Oral Solution treatment to avoid possible additive effects and hypercalcemia. If treatment is switched from ergocalciferol (vitamin D 2 ) to calcitriol, it may take several months for the ergocalciferol level in the blood to return to the baseline value (see OVERDOSAGE ).
Calcitriol increases inorganic phosphate levels in serum. While this is desirable in patients with hypophosphatemia, caution is called for in patients with renal failure because of the danger of ectopic calcification. A nonaluminum phosphate-binding compound and a low-phosphate diet should be used to control serum phosphorus levels in patients undergoing dialysis.
Magnesium-containing preparations (eg, antacids) and Calcitriol Oral Solution should not be used concomitantly in patients on chronic renal dialysis because such use may lead to the development of hypermagnesemia. Studies in dogs and rats given calcitriol for up to 26 weeks have shown that small increases of calcitriol above endogenous levels can lead to abnormalities of calcium metabolism with the potential for calcification of many tissues in the body.
🤒 Adverse Reactions ▾
ADVERSE REACTIONS Since Calcitriol Oral Solution is believed to be the active hormone which exerts vitamin D activity in the body, adverse effects are, in general, similar to those encountered with excessive vitamin D intake, ie, hypercalcemia syndrome or calcium intoxication (depending on the severity and duration of hypercalcemia) (see WARNINGS ). Because of the short biological half-life of calcitriol, pharmacokinetic investigations have shown normalization of elevated serum calcium within a few days of treatment withdrawal, ie, much faster than in treatment with vitamin D 3 preparations.
The early and late signs and symptoms of vitamin D intoxication associated with hypercalcemia include: Early : weakness, headache, somnolence, nausea, vomiting, dry mouth, constipation, muscle pain, bone pain, metallic taste, and anorexia, abdominal pain or stomach ache. Late : polyuria, polydipsia, anorexia, weight loss, nocturia, conjunctivitis (calcific), pancreatitis, photophobia, rhinorrhea, pruritus, hyperthermia, decreased libido, elevated BUN, albuminuria, hypercholesterolemia, elevated SGOT (AST) and SGPT (ALT), ectopic calcification, nephrocalcinosis, hypertension, cardiac arrhythmias, dystrophy, sensory disturbances, dehydration, apathy, arrested growth, urinary tract infections, and, rarely, overt psychosis.
In clinical studies on hypoparathyroidism and pseudohypoparathyroidism, hypercalcemia was noted on at least one occasion in about 1 in 3 patients and hypercalciuria in about 1 in 7 patients. Elevated serum creatinine levels were observed in about 1 in 6 patients (approximately one half of whom had normal levels at baseline). In concurrent hypercalcemia and hyperphosphatemia, soft-tissue calcification may occur; this can be seen radiographically (see WARNINGS ).
In patients with normal renal function, chronic hypercalcemia may be associated with an increase in serum creatinine (see PRECAUTIONS: GENERAL ). Hypersensitivity reactions (pruritus, rash, urticaria, and very rarely severe erythematous skin disorders) may occur in susceptible individuals. One case of erythema multiforme and one case of allergic reaction (swelling of lips and hives all over the body) were confirmed by rechallenge.
To report SUSPECTED ADVERSE REACTIONS, contact Rising Pharma Holdings, Inc. at 1-844-874-7464 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
🆘 Overdosage ▾
OVERDOSAGE Administration of Calcitriol Oral Solution to patients in excess of their daily requirements can cause hypercalcemia, hypercalciuria, and hyperphosphatemia. Since calcitriol is a derivative of vitamin D, the signs and symptoms of overdose are the same as for an overdose of vitamin D (see ADVERSE REACTIONS ). High intake of calcium and phosphate concomitant with Calcitriol Oral Solution may lead to similar abnormalities.
The serum calcium times phosphate (Ca x P) product should not be allowed to exceed 70 mg 2 /dL 2 . High levels of calcium in the dialysate bath may contribute to the hypercalcemia (see WARNINGS ). Treatment of Hypercalcemia and Overdosage in Dialysis Patients and Hypoparathyroidism Patients General treatment of hypercalcemia (greater than 1 mg/dL above the upper limit of the normal range) consists of immediate discontinuation of Calcitriol Oral Solution therapy, institution of a low-calcium diet and withdrawal of calcium supplements.
Serum calcium levels should be determined daily until normocalcemia ensues. Hypercalcemia frequently resolves in 2 to 7 days. When serum calcium levels have returned to within normal limits, Calcitriol Oral Solution therapy may be reinstituted at a dose of 0.25 mcg/day less than prior therapy.
Serum calcium levels should be obtained at least twice weekly after all dosage changes and subsequent dosage titration. In dialysis patients, persistent or markedly elevated serum calcium levels may be corrected by dialysis against a calcium-free dialysate. Treatment of Hypercalcemia and Overdosage in Predialysis Patients If hypercalcemia ensues (greater than 1 mg/dL above the upper limit of the normal range), adjust dosage to achieve normocalcemia by reducing Calcitriol Oral Solution therapy from 0.5 mcg to 0.25 mcg daily.
If the patient is receiving a therapy of 0.25 mcg daily, discontinue Calcitriol Oral Solution until patient becomes normocalcemic. Calcium supplements should also be reduced or discontinued. Serum calcium levels should be determined 1 week after withdrawal of calcium supplements.
If serum calcium levels have returned to normal, Calcitriol Oral Solution therapy may be reinstituted at a dosage of 0.25 mcg/day if previous therapy was at a dosage of 0.5 mcg/day. If Calcitriol Oral Solution therapy was previously administered at a dosage of 0.25 mcg/day, Calcitriol Oral Solution therapy may be reinstituted at a dosage of 0.25 mcg every other day. If hypercalcemia is persistent at the reduced dosage, serum PTH should be measured.
If serum PTH is normal, discontinue Calcitriol Oral Solution therapy and monitor patient in 3 months' time. Treatment of Hyperphosphatemia in Predialysis Patients If serum phosphorus levels exceed 5.0 mg/dL to 5.5 mg/dL, a calcium-containing phosphate-binding agent (ie, calcium carbonate or calcium acetate) should be taken with meals. Serum phosphorus levels should be determined as described earlier (see PRECAUTIONS: LABORATORY TESTS ).
Aluminum-containing gels should be used with caution as phosphate-binding agents because of the risk of slow aluminum accumulation. Treatment of Accidental Overdosage of Rocaltrol The treatment of acute accidental overdosage of Calcitriol Oral Solution should consist of general supportive measures. If drug ingestion is discovered within a relatively short time, induction of emesis or gastric lavage may be of benefit in preventing further absorption.
If the drug has passed through the stomach, the administration of mineral oil may promote its fecal elimination. Serial serum electrolyte determinations (especially calcium), rate of urinary calcium excretion, and assessment of electrocardiographic abnormalities due to hypercalcemia should be obtained. Such monitoring is critical in patients receiving digitalis.
Discontinuation of supplemental calcium and a low-calcium diet are also indicated in accidental overdosage. Due to the relatively short duration of the pharmacological action of calcitriol, further measures…
🧬 Clinical Pharmacology ▾
CLINICAL PHARMACOLOGY Man's natural supply of vitamin D depends mainly on exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol in the skin to vitamin D 3 (cholecalciferol). Vitamin D 3 must be metabolically activated in the liver and the kidney before it is fully active as a regulator of calcium and phosphorus metabolism at target tissues. The initial transformation of vitamin D 3 is catalyzed by a vitamin D 3 -25-hydroxylase enzyme (25-OHase) present in the liver, and the product of this reaction is 25-hydroxyvitamin D 3 [25-(OH)D 3 ].
Hydroxylation of 25-(OH)D 3 occurs in the mitochondria of kidney tissue, activated by the renal 25-hydroxyvitamin D 3 -1 alpha-hydroxylase (alpha-OHase), to produce 1,25-(OH) 2 D 3 (calcitriol), the active form of vitamin D 3 . Endogenous synthesis and catabolism of calcitriol, as well as physiological control mechanisms affecting these processes, play a critical role regulating the serum level of calcitriol. Physiological daily production is normally 0.5 to 1.0 mcg and is somewhat higher during periods of increased bone synthesis (eg, growth or pregnancy).
Pharmacodynamics The two known sites of action of calcitriol are intestine and bone. A calcitriol receptor-binding protein appears to exist in the mucosa of human intestine. Additional evidence suggests that calcitriol may also act on the kidney and the parathyroid glands.
Calcitriol is the most active known form of vitamin D 3 in stimulating intestinal calcium transport. In acutely uremic rats calcitriol has been shown to stimulate intestinal calcium absorption. The kidneys of uremic patients cannot adequately synthesize calcitriol, the active hormone formed from precursor vitamin D.
Resultant hypocalcemia and secondary hyperparathyroidism are a major cause of the metabolic bone disease of renal failure. However, other bone-toxic substances which accumulate in uremia (eg, aluminum) may also contribute. The beneficial effect of Calcitriol Oral Solution in renal osteodystrophy appears to result from correction of hypocalcemia and secondary hyperparathyroidism.
It is uncertain whether Calcitriol Oral Solution produces other independent beneficial effects. Calcitriol Oral Solution treatment is not associated with an accelerated rate of renal function deterioration. No radiographic evidence of extraskeletal calcification has been found in predialysis patients following treatment.
The duration of pharmacologic activity of a single dose of calcitriol is about 3 to 5 days. Pharmacokinetics Absorption Calcitriol is rapidly absorbed from the intestine. Peak serum concentrations (above basal values) were reached within 3 to 6 hours following oral administration of single doses of 0.25 to 1.0 mcg of Calcitriol Oral Solution.
Following a single oral dose of 0.5 mcg, mean serum concentrations of calcitriol rose from a baseline value of 40.0±4.4 (SD) pg/mL to 60.0±4.4 pg/mL at 2 hours, and declined to 53.0±6.9 at 4 hours, 50±7.0 at 8 hours, 44±4.6 at 12 hours, and 41.5±5.1 at 24 hours. Following multiple-dose administration, serum calcitriol levels reached steady-state within 7 days. Distribution Calcitriol is approximately 99.9% bound in blood.
Calcitriol and other vitamin D metabolites are transported in blood, by an alpha-globulin vitamin D binding protein. There is evidence that maternal calcitriol may enter the fetal circulation. Calcitriol is transferred into human breast milk at low levels (ie, 2.2±0.1 pg/mL).
Metabolism In vivo and in vitro studies indicate the presence of two pathways of metabolism for calcitriol. The first pathway involves the 24-hydroxylase as the first step in catabolism of calcitriol. There is definite evidence of 24-hydroxylase activity in the kidney; this enzyme is also present in many target tissues which possess the vitamin D receptor such as the intestine.
The end product of this pathway is a side chain shortened metabolite, calcitroic acid. The second pathway involves the conversion of calc…
📦 How Supplied / Storage and Handling ▾
HOW SUPPLIED Oral Solution: a clear, colorless oral solution containing 1 mcg/mL of calcitriol; each amber glass bottle of 15 mL of oral solution supplied with 20 single-use, graduated oral dispensers NDC: 64980-447-15 Calcitriol Oral Solution should be protected from light. Store at 59° to 86°F (15° to 30°C). REFERENCE 1.
Jones CL, et al. Comparisons between oral and intraperitoneal 1,25-dihydroxyvitamin D 3 therapy in children treated with peritoneal dialysis. Clin Nephrol.
1994; 42:44-49. Manufactured for: Rising Pharma Holdings, Inc. East Brunswick, NJ 08816 Revised: 02/2025 PIR44715-00
📋 Description ▾
DESCRIPTION Calcitriol Oral Solution is a synthetic vitamin D analog which is active in the regulation of the absorption of calcium from the gastrointestinal tract and its utilization in the body. Calcitriol oral solution contains 1 mcg/mL of calcitriol. Calcitriol Oral Solution contains butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) as antioxidants.
Calcitriol oral solution contains caprylic triglycerides. The oral solution contains no additional adjuvants or coloring principles. Calcitriol is a white, crystalline compound which occurs naturally in humans.
It has a calculated molecular weight of 416.65 and is soluble in organic solvents but relatively insoluble in water. Chemically, calcitriol is 9,10-seco(5Z,7E)-5,7,10(19)-cholestatriene-1α, 3β, 25-triol and has the following structural formula: The other names frequently used for calcitriol are 1α,25-dihydroxycholecalciferol, 1,25-dihydroxyvitamin D 3 , 1,25-DHCC, 1,25(OH) 2 D 3 and 1,25-diOHC. calcitriol-structure.jpg