Cyclooxygenase Inhibitors
11 drugsAbout Cyclooxygenase
Cyclooxygenase (COX), also known as prostaglandin-endoperoxide synthase (PTGS2), is an enzyme that catalyzes the synthesis of prostaglandins, signaling molecules involved in inflammation, pain, and fever. Inhibition of COX reduces prostaglandin production, alleviating symptoms associated with various conditions.
Human genetic studies provide moderate support for targeting PTGS2, with variants linked to nephrolithiasis (score 0.65) and chronic kidney disease (score 0.22). Loss-of-function variants are protective against these diseases, suggesting inhibition may be beneficial. There are also 20 strong eQTL/pQTL signals.
Cyclooxygenase is targeted by 10 FDA-approved small molecule drugs, including Rowasa, Nevanac, and Aspirin with Dipyridamole. These drugs are primarily used in immunology, cardiovascular health and pain management.
Cyclooxygenase Genetic Evidence Moderate
Genetic evidence shows moderate support for PTGS2 as a drug target, with a max score of 0.65 for nephrolithiasis.
Moderate genetic support suggests further validation studies are needed to increase confidence in clinical trials.
💡 Why inhibition?
- • Loss-of-function variants reduce disease risk (OR < 1)
- • 100% directional consistency across 2 traits
- • Strong signal in urinary system disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
2 totalGWAS and other genetic studies link PTGS2 to 2 diseases.
Inhibiting this target may be therapeutic
🔗 Colocalization Evidence 20 strong
max H4: 0.96eQTL/pQTL signals for PTGS2 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 Cyclooxygenase Drugs
Seven companies have approved drugs targeting cyclooxygenase, with Zydus Pharms and Amneal Pharms among the top players.
The presence of multiple players indicates a competitive market, requiring a differentiated strategy for new entrants.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| MESALAMINE | ZYDUS PHARMS | 2004 | 1 |
| BUTALBITAL, ASPIRIN, CAFFEINE, AND CODEINE PHOSPHATE | NOVITIUM PHARMA | 1995 | 1 |
| BALSALAZIDE DISODIUM | Hikma | 2007 | 1 |
| ASPIRIN AND DIPYRIDAMOLE | ZYDUS PHARMS | 2009 | 1 |
| PENTASA | Takeda | 1993 | 1 |
| SFROWASA | Viatris | 1987 | 1 |
| DIPENTUM | Viatris | 1990 | 1 |
| LIALDA | Takeda | 2007 | 1 |
Cyclooxygenase Drug Modality Landscape
Modalities
Routes of Administration
Cyclooxygenase is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or biologics could provide a competitive advantage.
Cyclooxygenase Clinical Trials 695 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on Cyclooxygenase. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 142 | 119 | 6 | 15 | 95% |
| Phase 2 | 137 | 85 | 21 | 30 | 80% |
| Phase 3 | 157 | 76 | 28 | 53 | 73% |
| Phase 4 | 259 | 154 | 32 | 73 | 83% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
Cyclooxygenase Drug Approval Timeline (1990 - 2009)
The first drug was approved in 1987 (Rowasa), and the most recent in 2009 (Aspirin and Dipyridamole), spanning 23 years.
The lack of recent approvals suggests a saturated market or challenges in developing novel COX inhibitors.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 8 companies competing
- • Market share by company
Full Drug Portfolio
- • All 11 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 11-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 415 (77 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 Cyclooxygenase. A trial counts if an approved drug acting on Cyclooxygenase 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.