Bone & calcium
Calcitonin (salmon)
A salmon-derived hormone peptide once common in bone disease, now used more narrowly after regulators weighed modest benefit against a debated malignancy signal.
Also known as: salmon calcitonin, Miacalcin, Fortical
Evidence passport
Last reviewed 2026-08-23
- Evidence level
- L4Strong human
- Confidence
- Moderate confidence
- Human efficacy
- 65/100
- Human safety
- 60/100
- Regulatory status
- Approved medicine
- Development
- Approved
- Routes
- NasalSC injectionIM
- Evidence base
- Includes human data
- Furthest stage
- Approved
- Source curation
- Source curation pending
- Clinical maturity
- Established medicine with a narrowed modern role
Overview
Clinical maturity: Established medicine with a narrowed modern role
Routes & formulations
Studied / approved routes
Injectable and nasal products carry different approved indications; evidence for one does not generalise to the other.
Route availability is not evidence of efficacy, and evidence from one route does not transfer to another. The Registry never provides dosing or sourcing information.
Peptide lifecycle
Discovery
Preclinical
Phase I
Phase II
Phase III
Approved
What it is
A synthetic version of salmon calcitonin, a hormone peptide that slows bone breakdown by acting on osteoclasts; more potent milligram-for-milligram than human calcitonin.
What people claim
- Slows bone loss in postmenopausal osteoporosis
- Treats Paget's disease and high blood calcium
What the evidence actually says
Older controlled trials support its labelled bone indications, but its fracture-prevention effect is weaker than newer osteoporosis medicines, and regulators in Europe and the US have weighed a small numerical imbalance in malignancy rates seen across long-term trials. Its modern role is deliberately narrow.
Human evidence
- Randomised trials in postmenopausal osteoporosis and Paget's disease.
- Regulatory safety reviews (EU 2012; US advisory discussion in 2013) of a malignancy imbalance.
Preclinical evidence
- Osteoclast pharmacology and bone-turnover models.
Animal and cell findings are Level 1–2 evidence.
Mechanism and pathways
- Calcitonin-receptor activation inhibits osteoclast-mediated bone resorption.
Safety and unknowns
- Regulators reviewed a small numerical imbalance in malignancy rates across long-term trials; causality was not established, but EU indications were narrowed.
- Hypocalcaemia and hypersensitivity reactions are labelled.
Cancer relevance
Monitored in trials; not demonstrated in humans
Regulatory status
Approved formulations have included injectable products (e.g. for Paget's disease and hypercalcaemia) and nasal spray products (for postmenopausal osteoporosis in women at least five years past menopause when alternatives are unsuitable). Availability and indications vary by product and market; European regulators restricted uses after a 2012 safety review.
Evidence grade
Solid controlled human trials, though not yet definitive or fully replicated.
What would change our rating?
- Definitive resolution of the long-standing malignancy-imbalance question.
References and sources
- To be curatedSources to be curated
Source hierarchy: regulatory documents and trial registries first, peer-reviewed work next, sponsor material flagged as non-independent. We never use supplier or clinic marketing as evidence, and where a verified source has not yet been curated we say so rather than inventing one.
Evidence change history
No recorded changes yet. Baseline position set on 2026-08-23.