Reviewed on July 17, 2025
calcitonin,salmon,synthetic
(KAL-si-TOE-nin)
This medication is used to treat brittle bone disease (osteoporosis) in women who are at least 5 years past "the change of life" (menopause). Calcitonin works by slowing bone loss to help maintain strong bones and reduce your risk of fractures. This product has been withdrawn from the Canadian market due to safety problems.
Read the patient and product information sheets if available from your pharmacist before you start using calcitonin and each time you get a refill. If you have any questions, ask your doctor or pharmacist. This medication is for use in the nose as directed, usually one spray in one nostril each day, alternating nostrils daily. It is recommended to use this medication at the lowest effective dosage and for the shortest possible duration to treat your condition. Patients treated long-term with this medication have shown a rare risk of developing cancer. Discuss the benefits and risks of long term treatment with this medication. Remove a new bottle from the refrigerator and allow it to reach room temperature. Follow the instructions on how to prime the pump the first time you use a new bottle. Once the pump is primed, it does not have to be reprimed if the bottle is properly stored in an upright position. Consult your pharmacist if you have any questions. To use the nasal spray, remove the protective cap, keep your head upright and insert the tip into a nostril. Press down firmly on the pump to deliver the medication. Replace the protective cap. Use the other nostril the next day. Use this medication regularly in order to get the most benefit from it. Remember to use it at the same time each day.
If you miss a dose, use it as soon as you remember. If it is near the time of the next dose, skip the missed dose. Use your next dose at the regular time. Do not double the dose to catch up.
For the nose. It is very important that you take or use this exactly as directed. Do not skip doses or discontinue unless directed by your doctor. Refrigerate unopened product. May store at room temperature after opening for use. Do not refrigerate this product after opening for use. Store at room temperature. See instructions for priming this product. Store container in an upright position after opening. Do not freeze Discard unused portion after the expiration date of _______________. Discard after using the number of doses or number of days after opening as described on the label.
Calcitonin salmon has been shown to decrease fetal birthweight in rabbits when given in dosages 14-56 times the recommended human parenteral dose. Because calcitonin does not cross the placenta, this adverse fetal effect may result from metabolic effects of calcitonin in the pregnant animal. Parenteral calcitonin salmon should be used during pregnancy only when the potential benefits justify the possible risks to the fetus. Calcitonin salmon nasal spray should not be used in pregnant women.
Drug interactions may change how your medications work or increase your risk for serious side effects. This document does not contain all possible drug interactions. Keep a list of all the products you use (including prescription/nonprescription drugs and herbal products) and share it with your doctor and pharmacist. Do not start, stop, or change the dosage of any medicines without your doctor's approval. A product that may interact with this drug is: lithium.
An increased incidence of pituitary adenomas has been observed in rats given calcitonin salmon subcutaneously in dosages of 80 units/kg daily (16-19 times the recommended human parenteral dose and 130-160 times the human intranasal dose based on body surface area). Calcitonin salmon has not exhibited mutagenic activity to date in microbial and mammalian test systems.
Calcitonin is a polypeptide hormone secreted by the parafollicular cells (C cells) of the thyroid gland in mammals and by the ultimobranchial gland in birds and fish. Calcitonin, from any source, is a 32-amino acid polypeptide chain with a disulfide bridge and a molecular weight of about 3600. Prolinamide at the carboxyl terminus, glycine at position 28, and 7 of the first 9 amino acids are common to all calcitonins, but the remaining amino acid sequence may differ considerably from that of human calcitonin, depending on the species. Structural relationships to potency and duration of effect are complex and may depend more on spatial relationships than on the amino acid sequence. Calcitonin is commercially available as calcitonin salmon. Calcitonin salmon and calcitonin human differ structurally at amino acids 2, 8, 11-13, 15-17, 19, 20, 22, 24, 26, 27, 29, and 31 in the sequence. The pharmacologic activity of these calcitonins is the same, but calcitonin salmon is substantially more potent on a weight basis (approximately 50 times that of calcitonin human) and has a longer duration of action. Calcitonin salmon is prepared synthetically and contains the 32 amino acids in the same linear sequence as occurs in natural calcitonin of salmon origin. Calcitonin salmon also is prepared using recombinant DNA technology; calcitonin salmon prepared by recombinant DNA technology is structurally identical to calcitonin salmon produced by chemical synthesis. Calcitonin salmon occurs as a white, fluffy powder and is very soluble in water and very slightly soluble in alcohol. The potency of calcitonin salmon is expressed in International Units (units) based on bioassay in comparison with the International Reference Preparation of Salmon Calcitonin for Bioassay, distributed by the National Institute for Biological Standards and Control, Holly Hill, London. The commercially available calcitonin salmon injection contains sodium chloride, sodium acetate, and acetic acid; the injections also contain phenol as a preservative. Miacalcin(R) nasal solution contains sodium chloride, hydrochloric acid, benzalkonium chloride, and purified water. Fortical(R) nasal solution contains sodium chloride, citric acid, phenylethyl alcohol, benzyl alcohol, polysorbate 80, hydrochloric acid or sodium hydroxide (to adjust pH), and purified water.
Absorption: Because of its polypeptide nature, calcitonin is destroyed in the GI tract and, therefore, must be administered parenterally or intranasally. Following parenteral administration, calcitonin is absorbed directly into the circulation. The range of therapeutically effective plasma concentrations has not been established. Plasma concentrations of 0.1-0.4 ng/mL are achieved following subcutaneous administration of 200 units of calcitonin salmon. The onset of action of calcitonin salmon is immediate following IV administration and occurs in about 15 minutes following IM or subcutaneous administration. Calcitonin salmon has its maximum effect in about 4 hours following IM or subcutaneous administration. The duration of action of calcitonin salmon is 8-24 hours following IM or subcutaneous administration and 30 minutes to 12 hours following IV administration. Clinical and/or biochemical effects may not be evident in patients with Paget disease of bone until after several months of calcitonin therapy. Calcitonin is rapidly absorbed from the nasal mucosa. Following intranasal administration of calcitonin salmon, peak plasma concentrations are attained within 31-39 minutes. Bioavailability of calcitonin salmon administered intranasally is approximately 3% (range: 0.3-30.6%) of that attained with IM administration of the drug. Accumulation of calcitonin was not observed in individuals receiving intranasal calcitonin salmon every 10 hours for up to 15 days. Distribution: It has not been determined whether calcitonin salmon enters CSF or is distributed into milk. Immunoreactive endogenous calcitonin, which was heterogeneous and included 2 forms larger than the monomer, has been detected in human milk in concentrations 10-40 times those in serum. Apparently, calcitonin does not cross the placenta. Elimination: Although the metabolism of calcitonin has not been extensively studied, it is believed that the hormone is rapidly metabolized, principally by the kidneys and in the blood and peripheral tissues. A metabolic clearance of 3.1 mL/kg per minute has been reported following IV infusion of calcitonin salmon in healthy individuals. The elimination half-life is about 43 minutes. Inactive metabolites, as yet unidentified, are excreted in urine. Little (0.1%) urinary excretion of unchanged calcitonin occurs.
The pharmacologic activity of calcitonin salmon and calcitonins of mammalian origin is the same, but calcitonin salmon is substantially more potent on a weight basis and has a longer duration of action. Calcitonin acts predominantly on bone to lower serum calcium concentration, but also has direct effects on the kidneys and the GI tract. The physiologic role of calcitonin is not completely known. Calcitonin is secreted in response to the concentration of calcium in the blood perfusing the thyroid gland. Thus, high serum calcium concentrations cause increased secretion of calcitonin which, in turn, inhibits bone resorption. Calcitonin may act as an emergency hormone lowering serum calcium in patients with acute hypercalcemia. It is believed that calcitonin through its action on bone plays a role, along with parathyroid hormone (PTH), in calcium homeostasis. GI hormones, particularly gastrin, can also stimulate calcitonin secretion and calcitonin may have a regulatory function in the release or catabolism of gastrin. Calcitonin directly inhibits osteoclastic bone resorption, altering the function and/or number of osteoclasts. A single therapeutic dose of calcitonin produces a marked transient inhibition of bone resorption; however, prolonged administration of calcitonin usually produces a persistent but smaller decrease in the rate of bone resorption. Presumably, calcitonin interacts with a specific receptor site on the plasma membrane of the osteoclast which results in intracellular accumulation of cyclic adenosine monophosphate (AMP) and alters calcium and/or phosphate transport across the plasma membrane. It also appears that calcitonin inhibits osteocytic osteolysis. Calcitonin's inhibition of bone resorption decreases both mineral release and matrix or collagen breakdown. Calcitonin opposes the effects of osteoclast stimulators such as PTH; however, calcitonin does not act as a competitive inhibitor of PTH. During hypocalcemic responses to exogenous calcitonin, PTH concentrations show a transient rise, but investigators have not been able to demonstrate persistent hypersecretion of PTH in patients treated chronically with calcitonin. There is some evidence that osteoclasts may escape the inhibitory effects of calcitonin, and bone resorption resumes at its original rate despite the continued presence of the hormone. Calcitonin may promote bone accretion by increasing osteoblastic activity; however, calcitonin's effect on osteoblasts has not been conclusively established and there is some evidence that the hormone may have a suppressive effect on the function and number of osteoblasts. In most patients with Paget disease of bone (osteitis deformans), calcitonin causes a decrease in the rate of bone turnover with a resultant decrease in elevated serum alkaline phosphatase concentrations and urinary hydroxyproline excretion. These biochemical changes appear to correspond to changes toward more normal bone formation. There is considerable interindividual variation, but bone turnover generally decreases by about 30-50% after about 6 months of parenteral calcitonin therapy, as determined by reductions in serum alkaline phosphatase and urinary hydroxyproline excretion, and generally remains at this level during continued therapy. The mechanism for this plateau in biochemical parameters is not known, but clinical response generally continues despite the plateau. Following discontinuance of calcitonin, these biochemical parameters return toward pretreatment values, although symptomatic response may persist. The extent to which calcitonin can inhibit bone resorption may depend on the existing rate of bone resorption--the higher the rate of bone resorption, the more evident the inhibition of bone resorption following calcitonin administration. In healthy adults who have a relatively low rate of bone resorption, exogenous calcitonin produces only a slight decrease in serum calcium but, in healthy children and in patients with generalized Paget disease, bone resorption is increased and serum calcium concentrations show a greater decrease in response to calcitonin admin
