PTH receptor Inhibitors
3 drugsAbout PTH receptor
The parathyroid hormone receptor (PTH1R) is a G protein-coupled receptor crucial for maintaining calcium homeostasis and bone metabolism. Activation of PTH1R by parathyroid hormone regulates calcium levels in the blood and influences bone remodeling.
Human genetics strongly support PTH1R as a therapeutic target, with a maximum genetic score of 0.88 linking it to skeletal abnormalities. Loss-of-function variants are associated with increased risk of metaphyseal chondrodysplasia and primary failure of tooth eruption, suggesting activation may be beneficial.
PTH1R is targeted by 3 FDA-approved peptide drugs: TERIPARATIDE, BONSITY, and FORTEO, all indicated for other therapeutic areas. These drugs modulate PTH1R activity to influence bone metabolism and calcium regulation.
PTH receptor Genetic Evidence Strong
Strong genetic evidence supports PTH1R's role in skeletal disorders, with a max score of 0.88.
High genetic support suggests drug development for skeletal abnormalities has increased probability of success.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 2 traits
- • Strong signal in genetic, familial or congenital disease, musculoskeletal or connective tissue disease, phenotype pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link PTH1R to 21 diseases.
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for PTH1R colocalize with these GWAS traits, providing causal evidence that gene expression changes drive disease risk.
Understanding these scores
Association Score (0-1): Combines all evidence types (genetic, literature, drugs, animal models). Higher = more evidence linking target to disease. This is a ranking heuristic, not a confidence score.
L2G Score: Open Targets uses a machine learning model (Locus-to-Gene) to predict which gene is causal at each GWAS locus. L2G=0.5 means ~50% probability of being the causal gene. Only associations with L2G > 0.05 are included.
Odds Ratio (OR): From gene burden studies (UK Biobank, AstraZeneca PheWAS). Measures how loss-of-function variants affect disease risk. OR<1 = protective (inhibiting target may help), OR>1 = risk (losing function causes disease).
Beta (β): Effect size for continuous traits. β<0 = protective, β>0 = risk.
Clinical Translation (~1.8x): Based on Nelson et al. 2015: drug targets with genetic evidence have ~2x higher success rates in clinical trials. We estimate: Strong support (score ≥0.7) → ~1.8x, Moderate (0.3-0.7) → ~1.3x, Weak → baseline.
Colocalization (H4): Tests whether a GWAS signal and an eQTL/pQTL signal share the same causal variant. H4 is the posterior probability that both traits are associated AND share a causal variant. H4 > 0.8 = strong evidence that gene expression/protein levels drive disease risk. This links genetic variation → gene expression → disease, supporting the target-disease connection.
Top PTH receptor Drugs
Apotex, ALVOGEN, and Eli Lilly are the companies with approved PTH1R-targeting drugs.
The PTH1R market is concentrated among three players, potentially creating high barriers to entry.
PTH receptor Drug Modality Landscape
Modalities
Routes of Administration
PTH receptor is primarily targeted by peptide modalities (100% of approved drugs).
Exploring non-peptide modalities could provide a competitive advantage in the PTH1R space.
PTH receptor Clinical Trials 67 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on PTH receptor. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 8 | 7 | 0 | 1 | 100% |
| Phase 2 | 20 | 15 | 5 | 0 | 75% |
| Phase 3 | 12 | 10 | 1 | 1 | 91% |
| Phase 4 | 27 | 21 | 0 | 5 | 100% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
PTH receptor Drug Approval Timeline (2002 - 2023)
The first PTH1R-targeting drug was approved in 2002, with the most recent in 2023.
The approval timeline indicates continued interest in PTH1R, but potential saturation warrants careful indication selection.
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Deep insights for drug target analysis
Competitive Landscape
- • 3 companies competing
- • Market share by company
Full Drug Portfolio
- • All 3 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 3-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 45 (12 companies)
- • Completion rates by condition
Full summary • All drugs • Genetic evidence • Trials • Timeline
How We Count Trials
- Trials: phase 1-4 interventional trials on ClinicalTrials.gov that started in 2008 or later and test an FDA-approved drug acting on PTH receptor. A trial counts if an approved drug acting on PTH receptor is in any arm, including as a comparator, and a trial that tests two such drugs counts once. Trials that test only unapproved drugs are not counted. A trial listed as phase 1/2 counts as phase 1, and phase 2/3 as phase 2.
- Active: recruiting, not yet recruiting, enrolling by invitation, or active and no longer recruiting.
- Completion rate: of the trials that have ended, the share marked Completed rather than Terminated or Withdrawn. Completed means the trial ended as planned; it does not mean the drug worked. Suspended trials are not counted as ended.
- Stopped: terminated or withdrawn. Trials stop for many reasons, including slow enrolment and business decisions, not only safety or efficacy.
- Sponsors: the lead sponsor of each trial. Companies are the sponsors ClinicalTrials.gov classes as industry; the rest are universities, hospitals, cooperative groups, government bodies and individuals.