[6] It acts to reduce blood calcium (Ca2+), opposing the effects of parathyroid hormone (PTH).

The reason provided is that prolactin induces the release of PTH related peptide which enhances bone resorption, but is still under investigation.

Also, calcitonin inhibits food intake in rats and monkeys, and may have CNS action involving the regulation of feeding and appetite.

It is coupled to a Gsα subunit, thus stimulating cAMP production by adenylate cyclase in target cells.

[citation needed] Calcitonin was first purified in 1962 by Douglas Harold Copp and B. Cheney at the University of British Columbia, Canada.

A malignancy of the parafollicular cells, i.e. medullary thyroid cancer (MTC), typically produces an elevated serum calcitonin level.

[31] The following information is from the UK Electronic Medicines Compendium[32] Salmon calcitonin is rapidly absorbed and eliminated.

Animal studies have shown that calcitonin is primarily metabolised via proteolysis in the kidney following parenteral administration.

Salmon calcitonin is primarily and almost exclusively degraded in the kidneys, forming pharmacologically inactive fragments of the molecule.

Conventional long-term toxicity, reproduction, mutagenicity, and carcinogenicity studies have been performed in laboratory animals.

An increased incidence of pituitary adenomas has been reported in rats given synthetic salmon calcitonin for 1 year.

The pharmacological properties of the synthetic and recombinant peptides have been demonstrated to be qualitatively and quantitatively equivalent.

It may even be used on biopsy samples from suspicious lesions (e.g., lymph nodes that are swollen) to establish whether they are metastases of the original cancer.

[38] Overall, the value of routine testing of calcitonin for diagnosis and prognosis of Medullary Thyroid Cancer remains uncertain and questionable.

In addition to the injectable and nasal spray dosage forms of the salmon calcitonin, noninvasive oral formulations of the peptide are currently under clinical development.

This novel oral platform in a number of clinical trials at different phases has demonstrated promising enhanced pharmacokinetic profile, high bioavailability, well-established safety and comparable efficacy to that of nasal calcitonin especially for treatment of postmenopausal bone loss.