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parathyroid hormone (Natpara / NPSP558 / SHP634)

✓ Approved

AstraZeneca UK Limited · PTH1R · Recombinant Proteins

What is parathyroid hormone?

parathyroid hormone is a recombinant proteins developed by AstraZeneca UK Limited. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesNatpara, NPSP558, SHP634
CompanyAstraZeneca UK Limited
Drug ClassRecombinant Proteins
Molecular TargetPTH1R
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, AstraZeneca UK Limited

Mechanism of Action

Molecular Targets

parathyroid hormone acts on 1 molecular target:

PTH1Rparathyroid hormone 1 receptor (PTHR, EKNS)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

parathyroid hormone is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Endocrine disordersHypoparathyroidism✓ Approved
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

Related Research Articles

PubMedExperimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation2026-10-16

Robot-Assisted Radical Prostatectomy in Kidney Transplant Recipients: an Updated Systematic Review and Surgical Perspective>.

Navratil Pavel P, Princlova Hanka H, Izmaylov Olec O, Tranova Minh Nguyet MN

Persistent hyperparathyroidism and calcitriol deficiency coexist in most long -term kidney transplant recipients, yet the combined skeletal effects of these presentations have not been formally quantified. In this cross -sectional analytical study at People's Hospital 115 (Ho Chi Minh City, Vietnam ), we studied 135 kidney transplant recipients (mean age 51.0 ± 11.3 years; 66.7 % male; mean time posttransplant 71.4 ± 28.1 months ) who underwent simultaneous measurement of serum intact parathyroid hormone, 1,25 -dihydroxyvitamin D, and dual -energy x -ray absorptiometry at 3 skeletal sites. A prespecified piecewise ordinary least -squares model characterized the relationship between parathyroid hormone and bone mineral density; a confirmatory sensitivity analysis used KDIGO -motivated breakpoint of 65 pg /mL for parathyroid hormone. We evaluated parathyroid hormone -to -vitamin D ratio as a prespecified secondary exposure measure. Bone loss (worst -site T score of < -1.0 ) was present in 103 participants (76.3 % ) and osteoporosis in 27 (20.0 % ). The confirmatory piecewise model at 65 pg /mL demonstrated that above -threshold parathyroid hormone was inversely associated with T -score composite ( β = -0.00367 per pg /mL; bootstrap 95 % CI, -0.0066 to -0.0013; P < .001 ), a 100 pg /mL increment above the threshold corresponded to a -0.37 T -score decrement. Body mass index was the strongest predictor (β = +0.129 per kg /m ²; P < .001 ). The ratio of parathyroid hormone to vitamin D (ρ = -0.262; P = .002 ) provided modestly better model fit than parathyroid hormone alone (R ² = 0.247 vs 0.229; change in Akaike Information Criterion = 3.2 ). Parathyroid hormone exerted a threshold -dependent inverse effect on bone mineral density in long -term kidney transplant recipients, confirmed at the KDIGO lower boundary of 65 pg /mL. The ratio of parathyroid hormone to vitamin D captured the combined mineral burden more efficiently than parathyroid hormone level alone, warranting further prospective evaluation as a monitoring target in posttransplant mineral disease.

PMID 42885700
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PubMedDiagnostics (Basel, Switzerland)2026-10-16

Effects of Dialysate Calcium Concentration on Bone, Mineral Metabolism, and Vascular Outcomes in Maintenance Hemodialysis: A Systematic Review and Meta-Analysis.

Alabid Ibrahim I, Alghoul Wasim Iyad Ibrahim WII, Abedi Malak M, El-Tanani Mohamed M et al.

Background/Objectives: The optimal dialysate calcium concentration in maintenance hemodialysis remains uncertain because reducing calcium exposure may limit calcium loading but can also stimulate parathyroid hormone secretion and impair intradialytic cardiovascular stability. We evaluated randomized evidence across bone, mineral metabolism, vascular, and acute safety outcomes. Methods: PubMed, the Cochrane Central Register of Controlled Trials (CENTRAL), and Scopus were searched from database inception through 10 July 2026, with targeted citation and publication-status updating through 1 August 2026. Randomized parallel, crossover, factorial, and multi-period trials comparing dialysate calcium concentrations in adults receiving hemodialysis or hemodiafiltration were eligible. Acute and chronic outcomes were analyzed separately. Pooled estimates used inverse-variance random-effects models with DerSimonian-Laird estimation and modified Hartung-Knapp confidence intervals. Results: Twenty-four randomized parent trials were included. Lower dialysate calcium reduced end-of-dialysis ionized calcium (paired mean difference, -0.193 mmol/L; 95% CI, -0.258 to -0.128), with substantial heterogeneity. Point estimates for chronic parathyroid hormone and total alkaline phosphatase were higher and serum calcium lower, but all confidence intervals crossed the null. No clear effects were demonstrated for phosphate, calcium-phosphate product, lumbar bone mineral density, coronary artery calcification, or carotid intima-media thickness. Acute parathyroid hormone, blood pressure, calcium-balance, and QTc estimates suggested greater parathyroid stimulation, lower hemodynamic measures, less calcium gain, and longer QTc with lower calcium, but were imprecise. Adverse events were unsuitable for pooling. Conclusions: Lower dialysate calcium consistently lowers postdialysis ionized calcium, but its long-term skeletal and vascular effects remain uncertain. No single concentration appears universally optimal; prescription should be individualized according to mineral metabolism phenotype, cardiovascular tolerance, dialysis modality, and concomitant therapy.

PMID 42882336
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PubMedJournal of clinical medicine2026-10-16

Contemporary and Emerging Therapeutic Strategies in Hypoparathyroidism: From Conventional Treatment to Restoration of Parathyroid Function.

Kochan-Olszewska Dominika D, Kowalska Aldona A

Hypoparathyroidism (HypoPT) is a relatively rare condition characterised by inadequately low levels of calcium and low levels of parathyroid hormone (PTH), or a complete absence of PTH. In consequence, the body loses its ability to correctly regulate the calcium and phosphate metabolism. Low calcium levels (hypocalcemia) and high phosphorus levels (hyperphosphataemia) are observed in the blood serum of patients. Conventional therapy remains the treatment of choice, involving calcium supplementation (most often calcium carbonate) and active forms of vitamin D, such as alfacalcidol or calcitriol. However, this treatment does not always provide optimal control of the disease or a satisfying quality of life for patients. In recent years, development of therapies using PTH analogues has been observed, as well as intensive research into new pharmacological strategies modulating the PTH/PTH1R signalling pathway. The aim of this paper is to present the current state of knowledge on methods of treatment of hypoparathyroidism and to discuss the prospects for the development of new therapeutic strategies.

PMID 42881908
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PubMedJournal of clinical medicine2026-10-16

Gingival Crevicular Fluid Levels of Parathyroid Hormone-Related Protein, RANK Ligand, and Osteoprotegerin in Periodontal Health, Gingivitis, and Periodontitis: A Cross-Sectional Study.

Meracı Yıldıran Bilge B, Ercan Nuray N, Ateş Yıldırım Esra E, Akgül Zeynep Z et al.

Background/Objectives: Parathyroid hormone-related protein (PTHrP) modulates the receptor activator of nuclear factor kappa B ligand (RANKL)/osteoprotegerin (OPG) system in periodontal cells in vitro but has not been measured in gingival crevicular fluid (GCF). This study compared GCF PTHrP, RANKL, and OPG across periodontal health, gingivitis, and periodontitis. Methods: This cross-sectional study included 81 participants with periodontal health, gingivitis, or stage III grade B periodontitis (n = 27 each). GCF was collected from two interproximal sites per participant. PTHrP, RANKL, and OPG were quantified by ELISA and expressed as total amount per site and concentration. Group comparisons were repeated with adjustment for age and sex. Results: PTHrP total amount differed between all three groups, with values of 4.26 ± 2.96, 12.45 ± 5.77, and 19.67 ± 4.59 pg/site in periodontal health, gingivitis, and periodontitis, respectively (p < 0.001). RANKL total amount did not differ among groups (median: 51.40, 51.40, and 51.78 pg/site; p = 0.977). OPG total amount was lower (median: 53.36, 46.70, and 46.70 pg/site; p < 0.001) and the RANKL/OPG ratio higher (median: 0.98, 1.10, and 1.14; p < 0.001) in both disease groups than in periodontal health. After adjustment, PTHrP and OPG differences persisted, whereas no pairwise difference in the RANKL/OPG ratio remained significant. PTHrP correlated negatively with OPG (r = -0.530) and positively with the RANKL/OPG ratio (r = 0.481; both adjusted p < 0.001). Conclusions: GCF PTHrP total amount differed between periodontal health, gingivitis, and periodontitis, with the highest values in periodontitis. These cross-sectional findings identify an association between GCF PTHrP and periodontal status but do not establish a causal role for PTHrP in periodontal tissue breakdown.

PMID 42882213
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PubMedInternational journal of molecular sciences2026-10-16

Association of PTH1R Gene Polymorphisms with Three-Dimensional Mandibular Morphology Across Three Recruitment Cohorts.

Shin Dongsan D, Kimura Ryosuke R, Kim Yong-Il YI, Adel Mohamed M et al.

Parathyroid hormone 1 receptor (PTH1R) regulates chondrocyte differentiation and mandibular condylar cartilage development, but its contribution to adult mandibular morphology remains unclear. We investigated associations of two PTH1R single-nucleotide polymorphisms (SNPs), rs724448 and rs2242116, with three-dimensional mandibular morphology in 448 orthodontic patients recruited in Japan (199), Korea (79), and Egypt (170). Salivary DNA was genotyped, and computed tomography images were analyzed using geometric morphometrics and conventional measurements. Multivariate Procrustes analysis evaluated overall mandibular shape. Cohort-specific regressions examined natural-log-transformed centroid size (ln(centroid size)), principal component scores, and conventional measurements, adjusting for sex and age and additionally for imaging modality in Japan. Estimates were combined using inverse-variance fixed-effect meta-analysis. Neither variant showed a significant whole-shape association after correction for two SNP tests. Secondary analyses yielded negative estimates for ln(centroid size) and nominal associations with selected anteroposterior dimensions and cohort-specific principal component scores. None remained significant after either Bonferroni or Benjamini-Hochberg false-discovery-rate correction across 408 tests. These findings provide no statistically robust evidence linking either variant to adult mandibular morphology. Nominal findings require independent replication.

PMID 42884137
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PubMedJournal of clinical medicine2026-10-16

Independent Predictors of Symptomatic Hypocalcemia Following Thyroidectomy: Distinguishing Biochemical and Symptomatic Hypocalcemia.

Türkoğlu Furkan F, Gürlük Muhammed M, Akay Ömer Ö, Ertürk Candeniz C et al.

Background/Objectives: Postoperative hypocalcemia is the most common complication following thyroidectomy; however, previous studies have largely relied on biochemical definitions without distinguishing symptomatic hypocalcemia from asymptomatic biochemical abnormalities. This study aimed to identify the independent predictors of symptomatic postoperative hypocalcemia. Methods: This retrospective single-center study included 245 adult patients who underwent thyroidectomy between January 2017 and December 2022. Patients were classified as normocalcemic (n = 88), asymptomatic biochemical hypocalcemic (n = 87), or symptomatic hypocalcemic (n = 70) according to calcium status within the first 72 postoperative hours. Demographic, surgical, biochemical, ultrasonographic, cytological, and histopathological variables were analyzed. Independent predictors were identified using multivariable logistic regression. Results: Symptomatic hypocalcemia occurred more frequently after bilateral total thyroidectomy with central neck dissection (p = 0.001). Patients with symptomatic hypocalcemia had lower preoperative serum calcium and lower postoperative albumin and parathyroid hormone levels than the other groups (all p < 0.05). Although high-risk FNAB cytology and malignant histopathology were associated with hypocalcemia in univariate analyses, neither remained independently predictive after adjustment. Bilateral total thyroidectomy with central neck dissection (adjusted OR 6.63, 95% CI 1.68-26.11; p = 0.007) and lower preoperative serum calcium (adjusted OR 0.46, 95% CI 0.22-0.94; p = 0.036) were independent predictors of symptomatic hypocalcemia after thyroidectomy. Conclusions: Symptomatic postoperative hypocalcemia should be considered a distinct clinical outcome rather than merely a biochemical abnormality. Bilateral total thyroidectomy with central neck dissection and lower preoperative serum calcium independently predicted symptomatic hypocalcemia, whereas ultrasonographic findings, FNAB cytology, histopathological diagnosis, and incidental parathyroidectomy did not. Although the absence of perioperative vitamin D and magnesium measurements is an important limitation, the identified predictors may provide clinically useful information for perioperative risk stratification.

PMID 42881984
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