Progesterone Receptor Modulators
5 drugsAbout Progesterone Receptor
The Progesterone Receptor (PR), a member of the nuclear receptor superfamily, is a ligand-activated transcription factor that regulates gene expression in response to progesterone, influencing various physiological processes.
Genetic evidence offers moderate support for targeting PGR, with variants linked to uterine fibroid (score 0.61), abnormal blistering of the skin (0.55), and congestive heart failure (0.53); inhibition is likely beneficial. There are also 17 strong eQTL/pQTL signals (max H4: 1.00).
Five FDA-approved small molecule drugs target the progesterone receptor, including MIFEPRISTONE, MIFEPREX, KORLYM, MYFEMBREE and NUBEQA, spanning metabolic, oncology and other indications.
Progesterone Receptor Genetic Evidence Moderate
Genetic evidence provides moderate support for PGR as a drug target, with a max score of 0.61.
Moderate genetic support suggests further investigation into the causal link between PGR and disease is warranted to increase confidence.
💡 Why inhibition?
- • Loss-of-function variants reduce disease risk (OR < 1)
- • 100% directional consistency across 1 traits
- • Strong signal in musculoskeletal or connective tissue disease, genetic, familial or congenital disease, cancer or benign tumor pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
17 totalGWAS and other genetic studies link PGR to 17 diseases.
Inhibiting this target may be therapeutic
🔗 Colocalization Evidence 17 strong
max H4: 1.00eQTL/pQTL signals for PGR 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 Progesterone Receptor Drugs
Five companies have approved drugs targeting the progesterone receptor, including Bayer, EVITA SOLUTIONS, and CORCEPT THERAP.
The presence of multiple players suggests a moderately competitive landscape, requiring a differentiated approach for new entrants.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| MIFEPRISTONE | Teva | 2019 | 5 |
| KORLYM | CORCEPT THERAP | 2012 | 5 |
Progesterone Receptor Drug Modality Landscape
Modalities
Routes of Administration
Progesterone Receptor is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or PROTACs could provide a competitive advantage and expand therapeutic options.
Progesterone Receptor Clinical Trials 446 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on Progesterone Receptor. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 116 | 81 | 12 | 22 | 87% |
| Phase 2 | 121 | 50 | 23 | 48 | 68% |
| Phase 3 | 88 | 52 | 11 | 25 | 83% |
| Phase 4 | 121 | 73 | 22 | 26 | 77% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
1 Phase 3 trial testing approved Progesterone Receptor drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting Progesterone Receptor. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
Progesterone Receptor Drug Approval Timeline (2000 - 2021)
The first drug was approved in 2000 (MIFEPREX), and the most recent in 2021 (MYFEMBREE), spanning 22 years.
The recent approval suggests continued interest in the target, but a slowing approval rate may indicate market saturation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 5 companies competing
- • Market share by company
Full Drug Portfolio
- • All 5 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 5-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 255 (66 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 Progesterone Receptor. A trial counts if an approved drug acting on Progesterone 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.