Calcitonin

Miacalcin, Miacalcic, Calcimar, Fortical (nasal), salcatonin, sCT, thyrocalcitonin (the human hormone)

Metabolic & weight
Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates
Note on this profile. Salmon calcitonin is an approved prescription medicine with a long history and a shrinking set of indications after a 2012–2014 safety review. This page explains the published science. Community/self-directed use is essentially none documented.

1What it is

Calcitonin is a hormone made by the C cells of the thyroid gland. It was discovered in 1962 and named for its ability to lower blood calcium. In adult humans its physiological importance is minor — people without a thyroid, or with excess calcitonin from a C-cell tumour, have essentially normal calcium and bone — but pharmacological doses have a strong anti-resorptive effect on bone. Salmon calcitonin was chosen for the drug because it binds the human receptor more tightly and lasts longer than the human hormone.

Injectable salmon calcitonin was approved in the US in 1975 and the nasal spray in 1995. For two decades it was a mainstay for osteoporosis and Paget's disease. It was then overtaken by bisphosphonates, and in 2012–2013 a pooled analysis of trials found a small excess of cancers in calcitonin-treated patients. The EMA withdrew the nasal spray and the osteoporosis indication; an FDA advisory committee voted in 2013 that benefit no longer outweighed risk for osteoporosis, and the US label was narrowed and given a cancer-risk warning in 2014, although the products remain available.

Serum calcitonin is also a laboratory marker (for medullary thyroid cancer, and in the context of the GLP-1 drug class warning — see the Semaglutide profile), which is the main reason the word appears in peptide discussions.


2How it's thought to work

Osteoclasts carry abundant calcitonin receptors. Binding rapidly causes them to retract, stop resorbing bone and detach from the bone surface. The effect is powerful but short, and prolonged exposure leads to receptor down-regulation ("escape").
In the kidney it increases excretion of calcium, phosphate and sodium.
Calcitonin receptors are also found in the brain; the analgesic (pain-relieving) effect in acute vertebral fracture appears to involve central serotonergic and endorphin pathways rather than the bone effect.
It is a member of the calcitonin/CGRP/amylin peptide family; the same receptor family is the target of CGRP migraine drugs and of amylin analogues (pramlintide, cagrilintide).
Calcitonin at its receptor on the osteoclast, the multinucleated cell that resorbs bone. The ruffled border it dissolves bone with withdraws, resorption slows, and calcium stays in the skeleton rather than entering the blood.Schematic — not to scale

3What the research shows

Graded A (modest and inconsistent)

Vertebral fracture reduction in postmenopausal osteoporosis

PROOF (n=1,255; 5 years) found 200 IU/day nasal reduced new vertebral fractures by 33% vs placebo, but neither 100 IU nor 400 IU did, and BMD gains were small (1–1.5%); drop-out was ~60% (Chesnut 2000, Am J Med). The absent dose-response is a long-standing concern. No non-vertebral or hip fracture benefit has been shown. [1]
Graded B/A

Paget's disease of bone

Older studies show calcitonin lowers alkaline phosphatase and bone pain in Paget's disease; bisphosphonates are more effective and have largely replaced it. The EU restricts calcitonin for Paget's to patients who cannot take bisphosphonates, for up to 3 months.

Hypercalcaemia of malignancy

Rapid but short-lived (24–48 h) calcium lowering, useful as a bridge while bisphosphonates or denosumab take effect; "escape" occurs within days.
Graded A (meta-analysis of small trials)

Pain from acute osteoporotic vertebral fracture

A systematic review of 13 trials found calcitonin reduced pain at rest and with movement over the first 4 weeks after acute vertebral fracture, with no benefit for chronic pain (Knopp-Sihota 2012, Osteoporos Int). This remains a common off-label use. [2]
Graded A (negative)

Oral calcitonin for osteoporosis and osteoarthritis

An oral formulation (SMC021) failed to reduce fractures in a 3-year phase 3 trial (Binkley 2012, J Bone Miner Res) and did not succeed in knee osteoarthritis trials; it was never approved. [3]

Prevention of bone loss during immobilisation

Small studies support short courses (2–4 weeks) to limit acute bone loss during immobilisation; this is a retained EU indication.

4Reported side effects and interactions

Literature-reported

nausea (most common with injection, ~10%), facial flushing, injection-site reactions, metallic taste, polyuria; with nasal spray, rhinitis, nasal dryness, irritation and nosebleeds. Mild, transient hypocalcaemia is possible. Neutralising antibodies develop in a substantial fraction of long-term users and can reduce effect. Allergic reactions including rare anaphylaxis (skin testing is suggested before injection in patients with suspected sensitivity). The cancer signal: a meta-analysis of randomised trials found malignancy in about 4.1% of calcitonin-treated versus 2.9% of placebo patients, with no single tumour type and no mechanism identified; regulators treat this as unexplained but real enough to restrict long-term use.

Community-reported

none documented.

Theoretical. the salmon sequence is a foreign protein, so immunogenicity is expected; long-term use carries the unresolved cancer question.

Interactions. may reduce lithium levels (via increased renal clearance); additive calcium-lowering with bisphosphonates; otherwise few.

Markers researchers commonly monitor

MarkerWhy it's watched
Serum calcium and phosphatethe direct pharmacological effect; hypocalcaemia is uncommon but possible with higher doses.
Alkaline phosphatase (bone-specific if available)the standard marker of Paget's disease activity and of response.
Urinary NTX or CTXbone resorption markers that fall within weeks if the drug is working and rise again with "escape".
Lithium levelonly for people on lithium.
Serum calcitonin as a markernote that measuring endogenous calcitonin is meaningless while taking the drug; assays cross-react.
Pain score (0–10) and mobilitythe practical outcome for acute vertebral fracture use.

Free for everyone. Safety information is never behind a paywall.


5Reconstitution and handling

Supplied as a ready-to-use injection solution (200 IU/mL ampoules or vials) or a metered nasal spray — no . Doses are in international units (IU), not milligrams; 1 IU of salmon calcitonin is approximately 0.2 µg. The calculator is not relevant for this compound.


6Commonly studied alongside

Teriparatide (profile 121) and abaloparatide (profile 122) as the newer bone peptides; bisphosphonates and denosumab (the agents that replaced it); pramlintide and cagrilintide (same peptide family, acting at amylin receptors); CGRP antagonists (same receptor family). The serum marker is monitored in the GLP-1 class — see the Semaglutide profile.

Informational cross-links. Not stack recommendations.


7Regulatory status by region

RegionStatus (checked —)
United StatesFDA-approved injection (Miacalcin, 1975) for Paget's disease, hypercalcaemia and postmenopausal osteoporosis in women >5 years post-menopause who cannot use alternatives; nasal spray (Miacalcin, Fortical and generics) for osteoporosis only. Label carries a malignancy warning since 2014
European UnionOsteoporosis indication and all nasal formulations withdrawn in 2012 (EMA review). Injection remains for Paget's disease (max 3 months), hypercalcaemia of malignancy, and prevention of acute bone loss due to sudden immobilisation (2–4 weeks)
United KingdomFollows the EU 2012 decision; injection only (Miacalcic) for the restricted indications
AustraliaTGA review 2013 removed osteoporosis indication; injection remains for Paget's disease and hypercalcaemia †
South AfricaRegistered injection; indications follow the manufacturer label †
SportNot on the WADA Prohibited List

8Open questions

  • Is the malignancy signal real, and if so by what mechanism? Trials were not designed to detect it and the signal lacks tumour-type specificity.
  • Does the analgesic effect justify short courses for acute fractures given newer options?
  • Why the lack of dose-response in PROOF, and whether any fracture benefit is genuine.

9References

  1. 1Chesnut CH 3rd et al. (2000). A randomized trial of nasal spray salmon calcitonin in postmenopausal women with established osteoporosis: the Prevent Recurrence of Osteoporotic Fractures study (PROOF). Am J Med. PubMed · DOI
  2. 2Knopp-Sihota JA et al. (2012). Calcitonin for treating acute and chronic pain of recent and remote osteoporotic vertebral compression fractures: a systematic review and meta-analysis. Osteoporos Int. PubMed · DOI
  3. 3Binkley N et al. (2012). A phase 3 trial of the efficacy and safety of oral recombinant calcitonin: the Oral Calcitonin in Postmenopausal Osteoporosis (ORACAL) trial. J Bone Miner Res. PubMed · DOI
  4. 4Overman RA et al. (2013). Salmon calcitonin use and associated cancer risk. Ann Pharmacother. PubMed · DOI
  5. 5European Medicines Agency (2012). European Medicines Agency recommends limiting long-term use of calcitonin medicines (press release and referral assessment report). PubMed
  6. 6US FDA (2013). Reproductive Health Drugs Advisory Committee briefing document: calcitonin salmon and malignancy. PubMed
  7. 7Chambers TJ, Magnus CJ (1982). Calcitonin alters behaviour of isolated osteoclasts. J Pathol. PubMed · DOI
  8. 8Novartis / Mylan. Miacalcin (calcitonin salmon) injection and nasal spray prescribing information (current label). PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.


10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

30 Oct 2026Profile published — awaiting medical review

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