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Teriparatide

Also known as Forteo, Forsteo, rhPTH(1-34), Bonsity, Terrosa, Movymia

Recombinant parathyroid hormone fragment (1-34), a daily injection that builds new bone in osteoporosis.

clinically proven Hormonal & sexual approved drug

At a glance

Category
Hormonal & sexual
Status
approved drug
Made from
recombinant The 1-34 fragment of human parathyroid hormone, produced in Escherichia coli by recombinant DNA technology.
Route
subcutaneous injection into the thigh or abdominal wall
Half-life
about 1 hour after subcutaneous injection, with peak concentration around 30 minutes and serum concentrations undetectable within about 3 hours; subcutaneous bioavailability is roughly 95% 4
Onset
bone formation markers rise within 1-3 months; measurable bone mineral density gains by 3-6 months; fracture risk reduction demonstrated over roughly 18 months
Molecular weight
4117.8 daltons 4
Sequence
SVSEIQLMHNLGKHLNSMERVEWLRKKLQDVHNF — the first 34 amino acids of human parathyroid hormone, produced recombinantly in E. coli

Approved by the FDA in 2002 (Forteo) and by the EMA on 10 June 2003 (Forsteo) for osteoporosis at high fracture risk 3. Biosimilars (Terrosa, Movymia, Livogiva) have been authorised in the EU since 2017. Prescription only. The osteosarcoma boxed warning that accompanied the original US label was removed when the label was updated in 2020 2.

Doping status: Not listed by WADA

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

Teriparatide is the biologically active N-terminal fragment of parathyroid hormone and binds the PTH1 receptor, a class B G-protein-coupled receptor expressed on osteoblasts, osteocytes and renal tubular cells. Receptor activation signals through both Gs/cAMP/protein kinase A and Gq/phospholipase C pathways.

The decisive variable is not the drug but the exposure pattern. Continuously elevated parathyroid hormone, as in hyperparathyroidism, is catabolic: it drives osteoblast expression of RANKL, recruits and activates osteoclasts, and dissolves bone to defend serum calcium. A brief daily spike, which is what a once-daily subcutaneous injection produces, is anabolic instead: it increases osteoblast number by recruiting bone lining cells, promoting preosteoblast differentiation and suppressing osteoblast apoptosis, while the RANKL-driven resorptive response has largely subsided before the next dose. Downstream this involves Wnt signalling (partly through suppression of the osteocyte-derived inhibitor sclerostin), RUNX2 and IGF-1.

The result is an 'anabolic window' in the first 6-12 months, when formation markers such as P1NP rise steeply while resorption markers lag. As treatment continues, resorption catches up and the net gain per month falls, which is one reason treatment courses are finite. Teriparatide also increases renal tubular calcium reabsorption, decreases phosphate reabsorption, and raises 1,25-dihydroxyvitamin D synthesis, which in turn increases intestinal calcium absorption. This produces the characteristic transient hypercalcaemia peaking 4-6 hours after each dose.

Because the effect depends on adding new bone rather than slowing its removal, the gains are not self-sustaining. Stopping teriparatide without following it with an antiresorptive agent leads to rapid loss of the acquired bone mineral density; sequential therapy is therefore considered part of the treatment plan rather than an optional extra.

What the research shows

The evidence is strong and derives from large, randomised, placebo- and active-controlled fracture-endpoint trials. Teriparatide is one of the few osteoporosis drugs with demonstrated superiority over an oral bisphosphonate for fracture prevention in high-risk patients. The osteosarcoma question, which dominated the drug's first two decades, has been settled reassuringly by long-term registry data 2.

Research in humans

The pivotal Fracture Prevention Trial (Neer et al., New England Journal of Medicine, 2001; n=1637 postmenopausal women, median 21 months of observation) found that teriparatide 20 mcg daily reduced new vertebral fractures by 65% and new non-vertebral fragility fractures by 53% relative to placebo, with lumbar spine bone mineral density gains of roughly 9-13%. The VERO trial subsequently showed fewer new vertebral and clinical fractures with teriparatide than with risedronate in women with severe osteoporosis. Teriparatide is also effective in men with osteoporosis and in glucocorticoid-induced osteoporosis, where it outperformed alendronate on bone density and vertebral fracture endpoints.

Animal and lab research

The osteosarcoma concern originated in a lifetime rat carcinogenicity study in Fischer 344 rats given high doses of teriparatide from a young age throughout life, in which osteosarcoma occurred in a dose-dependent manner. That finding halted the phase 3 programme early and produced the original boxed warning. It was subsequently recognised that the rat model is poorly predictive here: rats have continuously growing bone with open growth plates and no basic multicellular unit remodelling, and the exposure (near-lifetime, high dose, growing skeleton) does not correspond to a two-year course in an adult human.

Caveats. Follow-up in the pivotal trial was cut short by the rat findings, so long-term fracture data on continuous therapy are thinner than for bisphosphonates. Almost all major trials were manufacturer-sponsored. Benefit is contingent on daily adherence to an injection, and on being followed by an antiresorptive; without that sequencing, bone density gains are lost within one to two years. Comparative data against other anabolic agents such as abaloparatide and romosozumab are limited.

What it is used for

  • Osteoporosis in postmenopausal women at high or very high risk of fracture, particularly after a fragility fracture or failure of antiresorptive therapy 4
  • Osteoporosis in men at increased fracture risk, including hypogonadal osteoporosis 4
  • Glucocorticoid-induced osteoporosis in men and women on sustained systemic corticosteroid therapy 4
  • Off-label and investigational: promoting healing of atypical femoral fractures, fracture non-union, and management of hypoparathyroidism (for which the full-length analogue PTH(1-84) is the more appropriate agent)

Dosing

Dose
20 mcg once daily
Frequency
Once daily, at approximately the same time each day
Route
Subcutaneous injection into the thigh or abdominal wall, rotating sites
Duration
Up to 24 months in the EU, which the Forsteo SmPC still specifies as a once-in-a-lifetime maximum. In the US, the 2-year lifetime limitation was removed alongside the boxed warning in November 2020; the current US label allows continued use beyond 2 years in patients who remain at or return to high fracture risk.
  • The first few doses should be taken where the patient can sit or lie down promptly: transient orthostatic hypotension typically began within four hours of dosing and resolved within minutes to hours 4.
  • Adequate calcium and vitamin D supplementation is assumed alongside the daily dose 4; serum calcium and vitamin D status should be normal before starting.
  • Teriparatide must be followed by an antiresorptive agent (bisphosphonate or denosumab) when the course ends, otherwise the bone gained is largely lost. This is standard practice in every major osteoporosis guideline.
  • The 20 mcg daily dose is the licensed regimen from the official product information, and use beyond two years is advised only if the patient remains at high fracture risk 4. This is reference material, not treatment advice.
  • Combining teriparatide with denosumab has produced larger density gains than either alone in trials, but this is not a licensed regimen.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Forsteo / Forteo (osteoporosis)

approved product information

Source: Forsteo (teriparatide) EPAR product information, EMA

Every day of treatment20 mcg once daily, subcutaneously into the thigh or abdominal wall
Total courseup to 24 months

There is no titration - the licensed dose is a single fixed one. The EU SmPC treats the 24 months as a once-in-a-lifetime maximum; the US label dropped its 2-year lifetime limitation in November 2020 and permits continued use in people who remain at high fracture risk. The first few doses should be taken somewhere the patient can sit or lie down, because transient orthostatic hypotension occurs in a minority within four hours. An antiresorptive is started when the course ends, otherwise most of the bone gained is lost again.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
2.4 ml prefilled pen delivering 20 mcg per dose for 28 days (Forteo/Forsteo), 2.4 ml cartridge for a reusable pen (Terrosa, Movymia)
Storage
Refrigerated at 2-8 °C at all times, including while in use — this is unusual and important, since many injectable pens tolerate room temperature once opened. Teriparatide does not. Do not freeze; discard if frozen. Recap the pen after each use to protect from light. Discard 28 days after first use even if solution remains.

Worked example

Not applicable. Teriparatide is supplied as a ready-to-use sterile solution in a prefilled multidose pen or cartridge, delivering a fixed 20 mcg dose. Nothing is reconstituted, diluted or mixed. Each pen contains 28 daily doses.

Because the pen must stay refrigerated in use, travel and power interruptions are a practical adherence problem worth planning for. Do not use if the solution is cloudy, coloured or contains particles.

Safety

Side effects

  • Nausea, most often in the first weeks
  • Headache and dizziness
  • Orthostatic hypotension, typically transient and within four hours of a dose, most likely after the first few injections 4
  • Pain in the limbs, arthralgia and leg cramps
  • Transient hypercalcaemia peaking 4-6 hours after injection and returning to baseline by 16-24 hours 4; persistent hypercalcaemia is uncommon at the 20 mcg dose
  • Hypercalciuria and a modest increase in the risk of kidney stones; the label advises considering the risk in people with active or recent urolithiasis 4
  • Increased serum uric acid, occasionally provoking gout
  • Injection site erythema, pain and bruising
  • Antibodies to teriparatide develop in a minority of users and have not been linked to loss of efficacy or to hypersensitivity in trials
  • Osteosarcoma: no longer carried as a boxed warning. Following the 2020 US label change 2 it appears under Warnings and Precautions, reflecting that claims-data studies found no increase in osteosarcoma among teriparatide users compared with unexposed groups or with the expected population background incidence 2

Do not use if

  • Pre-existing hypercalcaemia 3; the US label advises avoiding teriparatide in anyone with an underlying hypercalcaemic disorder 4
  • Severe renal impairment 3
  • Metabolic bone diseases other than primary osteoporosis or glucocorticoid-induced osteoporosis, including Paget disease of bone and hyperparathyroidism 34
  • Unexplained elevation of alkaline phosphatase 3
  • Prior external beam or implant radiation therapy involving the skeleton 34
  • Skeletal malignancy or bone metastases, and a history of skeletal malignancy 34
  • Pregnancy and breastfeeding 3
  • Hypersensitivity to teriparatide or any excipient, including reported anaphylaxis and angioedema 4
  • Caution in people with active urolithiasis, and in those with a history of hypercalciuria
  • Note that a personal history of osteosarcoma or another risk factor for osteosarcoma (such as Paget disease, open epiphyses or hereditary predisposition to osteosarcoma) remains a reason to avoid the drug under the current label 4, even though the boxed warning was removed

Interactions

Few clinically significant interactions. Teriparatide-induced transient hypercalcaemia may predispose patients on digoxin to digitalis toxicity, so caution is advised 4. Thiazide diuretics and calcium supplements can add to the hypercalcaemic effect. Sequential and combination use with bisphosphonates and denosumab is a therapeutic strategy rather than an interaction concern, though prior long-term bisphosphonate exposure blunts the early anabolic response to teriparatide. No relevant cytochrome P450 interactions, since teriparatide is cleared by peptide hydrolysis rather than hepatic metabolism.

Sources