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Endocrine · Reference monograph

Full-length human parathyroid hormone for hypoparathyroidism

Reference compound — not available from Purity Peptides. Shown for research context.

Overview

Parathyroid hormone (PTH) is an 84-amino-acid peptide secreted by the chief cells of the parathyroid glands. It is the principal minute-to-minute regulator of extracellular calcium, and its secretion is controlled by the calcium-sensing receptor, a G protein-coupled receptor that suppresses PTH release when calcium rises. Recombinant full-length human PTH(1-84) was developed as a hormone replacement for hypoparathyroidism, a condition in which PTH is deficient.

Recombinant PTH(1-84), marketed as Natpara in the US and Natpar in Europe, was approved by the FDA in 2015 as an adjunct to calcium and vitamin D in chronic hypoparathyroidism, following the REPLACE trial. The original product was later discontinued by its manufacturer, and a sustained-release prodrug of PTH(1-34), palopegteriparatide, has since been approved for the same condition. For researchers, PTH(1-84) is the reference ligand for calcium homeostasis studies, PTH1R signalling, hormone replacement models and urinary calcium handling, and it allows investigation of the C-terminal region absent from shorter fragments.

Mechanism studied

  1. PTH (1-84)
  2. PTH1 receptor
  3. Serum calcium ↑
  4. Calciuria ↓

PTH(1-84) acts on the PTH1 receptor in kidney and bone, coupling to Gs-cAMP and Gq-phospholipase C pathways. In the distal nephron it enhances calcium reabsorption, while in the proximal tubule it reduces phosphate reabsorption by internalising the sodium-phosphate cotransporters NPT2a and NPT2c. It also induces renal 1-alpha-hydroxylase (CYP27B1), increasing calcitriol, which raises intestinal calcium absorption. In bone, sustained PTH stimulates osteoblast and osteocyte RANKL expression, promoting osteoclast-mediated calcium release. The N-terminal region drives PTH1R activation, while C-terminal fragments may act through a separate, uncharacterised receptor, an unresolved question in parathyroid biology.

Research highlights

  • 01The calcium-sensing receptor, cloned in 1993, explained how parathyroid cells detect small changes in calcium.
  • 02Recombinant PTH(1-84) was approved by the FDA in 2015 for chronic hypoparathyroidism based on the REPLACE trial.
  • 03The original PTH(1-84) product was discontinued, and palopegteriparatide was later approved as a sustained PTH(1-34) prodrug.
  • 04Hypoparathyroidism research focuses on serum calcium stability, urinary calcium excretion and kidney endpoints.
  • 05Open questions include the biology of C-terminal PTH fragments and whether the full-length hormone has effects distinct from shorter forms.

Latest published research

39,032 papers on PubMed →

  1. Analytically accurate, clinically inaccurate: A diagnostic case of Pseudohyperparathyroidism

    Swartchick CB et al. · Clinica chimica acta; international journal of clinical chemistry · 2027 Feb 15 · PMID 42580610

  2. PTHrP suppresses BMP2-induced osteochondral differentiation and preserves cartilage phenotype in mesenchymal stem cells via inactivating PI3K-AKT signaling

    Gao S et al. · Genes & diseases · 2027 Feb · PMID 42926813

  3. Bone response to intermittent parathyroid hormone (PTH) is both genetic and sex specific in mice

    Adams DJ et al. · Bone · 2027 Jan · PMID 42829196

  4. Discovery and characterization of potent and efficacious small-molecule parathyroid hormone Receptor-1 (PTH1R) antagonists for the treatment of hypercalcemia

    Pontillo J et al. · Bioorganic & medicinal chemistry letters · 2027 Jan · PMID 42822604

  5. A Mg-Al layered double hydroxide-based nanocomposite functionalized with PTHrP-2 and loaded with polyoxometalates for osteoarthritis therapy

    Li L et al. · Biomaterials · 2027 Jan · PMID 42468384

  6. Long-term follow-up revealed hypocalciuric hypercalcemia in a patient initially treated for primary hyperparathyroidism

    Araya AV et al. · JCEM case reports · 2026 Dec · PMID 42948683

  7. Irisin fails to rescue bone loss in a rat model of chronic kidney disease - mineral bone disorder (CKD-MBD) but interacts with parathyroid hormone (PTH) in vivo and in vitro in IDG-SW3 osteocytes

    Wilson HE et al. · Bone reports · 2026 Dec · PMID 42908875

  8. Early parathyroid hormone elevation after denosumab therapy following parathyroidectomy: a diagnostic pitfall

    Yamashita H et al. · JCEM case reports · 2026 Dec · PMID 42890451

Live feed from PubMed (NCBI) for “Parathyroid Hormone (PTH 1-84)”, updated 2026-10-30. Listing a paper is not an endorsement of its findings.

Registered studies

628 on ClinicalTrials.gov →

From the public ClinicalTrials.gov registry for “Parathyroid Hormone (PTH 1-84)”, updated 2026-10-30. Shown for research context only; Purity Peptides products are not for human use.

Key references

  1. [1]Manufacturer's prescribing information — FDA / EMA / ANVISA
  2. [2]Mannstadt et al., 2013 — Lancet Diabetes Endocrinol

FAQ

  • PTH(1-84) is the full-length natural hormone, whereas teriparatide contains only the first 34 amino acids. Both activate the PTH1 receptor, but the full-length molecule retains the C-terminal region, which circulates as fragments and may have separate biological activities.

  • Parathyroid chief cells express the calcium-sensing receptor. When extracellular calcium rises, receptor activation suppresses PTH secretion and synthesis; when calcium falls, secretion increases within minutes. Phosphate, calcitriol and FGF23 also modulate PTH production over longer periods.

  • Recombinant PTH(1-84) was approved in the US and EU for chronic hypoparathyroidism, but the original product has been discontinued. It remains an important research reference ligand for studies of calcium regulation and receptor biology.

FOR RESEARCH USE ONLY.Not for human or veterinary use. Not intended to diagnose, treat, cure, or prevent any disease.

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