Source: Medicines & Healthcare Products Regulatory Agency (GB) Revision Year: 2016 Publisher: Essential Pharma Ltd., 7 Egham Business Village, Crabtree Road, Egham, Surrey, TW20 8RB, United Kingdom
Pharmacotherapeutic group: antiparathyroid hormone
ATC code: H05BA01 (calcitonin, salmon)
The pharmacological properties of the synthetic and recombinant peptides have been demonstrated to be qualitatively and quantitatively equivalent.
Calcitonin is a calciotropic hormone, which inhibits bone resorption by a direct action on osteoclasts. By inhibiting osteoclast activity via its specific receptors, salmon calcitonin decreases bone resorption. In pharmacological studies, calcitonin has been shown to have analgesic activity in animal models.
Calcitonin markedly reduces bone turnover in conditions with an increased rate of bone resorption such as Paget’s disease and acute bone loss due to sudden immobilisation. The absence of mineralisation defect with calcitonin has been demonstrated by bone histomorphometric studies both in man and in animals.
Decreases in bone resorption as judged by a reduction in urinary hydroxyproline and deoxypyridinoline are observed following calcitonin treatment in both normal volunteers and patients with bone-related disorders, including Paget’s disease and osteoporosis.
The calcium-lowering effect of calcitonin is caused both by a decrease in the efflux of calcium from the bone to the ECF and inhibition of renal tubular reabsorption of calcium.
Salmon calcitonin is rapidly absorbed and eliminated.
Peak plasma concentrations are attained within the first hour of administration. After subcutaneous administration, peak plasma levels are reached in about 23 minutes.
Animal studies have shown that calcitonin is primarily metabolised via proteolysis in the kidney following parenteral administration. The metabolites lack the specific biological activity of calcitonin.
Bioavailability following subcutaneous and intramuscular injection in humans is high and similar for the two routes of administration (71% and 66%, respectively).
Calcitonin has a short absorption half-life of 10-15 minutes. The elimination half-life is about 1 hour for intramuscular administration and 1 to 1.5 hours for subcutaneous administration. Salmon calcitonin is primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule. Therefore, the metabolic clearance is much lower in patients with end-stage renal failure than in healthy subjects. However, the clinical relevance of this finding is not known.
Plasma protein binding is 30 to 40%.
There is a relationship between the subcutaneous dose of calcitonin and peak plasma concentrations. Following parenteral administration of 100 IU calcitonin, peak plasma concentration lies between about 200 and 400pg/ml. Higher blood levels may be associated with increased incidence of nausea and vomiting.
Conventional long-term toxicity, reproduction, mutagenicity and carcinogenicity studies have been performed in laboratory animals. Salmon calcitonin is devoid of embryotoxic, teratogenic and mutagenic potential.
An increased incidence of pituitary adenomas has been reported in rats given synthetic salmon calcitonin for 1 year. This is considered a species-specific effect and of no clinical relevance. It is not known whether salmon calcitonin crosses the placental barrier.
In lactating animals given calcitonin, suppression of milk production has been observed. Calcitonin is secreted into the milk.
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