S1PR3 Inhibitors
3 drugsAbout S1PR3
S1PR3 is a G protein-coupled receptor that binds sphingosine-1-phosphate (S1P), mediating various physiological processes. It plays a crucial role in signaling pathways related to cell migration and inflammation. S1PR3 activation influences cardiovascular and immune functions.
Human genetics provide moderate support for S1PR3 as a therapeutic target, with a maximum genetic score of 0.52 linked to gastrointestinal disease. Additional associations include lymphadenitis (0.43) and thrombocytopenia (0.41), suggesting potential therapeutic applications.
S1PR3 is targeted by three FDA-approved small molecule drugs, including GILENYA and TASCENSO ODT. These drugs, developed by companies like Novartis and CYCLE, are primarily used in CNS indications, with one drug targeting an indication outside the CNS.
Strategic Insights
ℹ️ How we calculate- White space opportunity in Multiple Sclerosis (MS) with only 1 trials.
- phase3 represents biological uncertainty with 0% completion.
S1PR3 Genetic Evidence Moderate
Genetic evidence offers moderate support, with a top score of 0.52.
Further research is needed to validate the causal link between S1PR3 and gastrointestinal disease.
Evidence Across Diseases
9 totalGWAS and other genetic studies link S1PR3 to 9 diseases.
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for S1PR3 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 S1PR3 Drugs
Three companies have approved S1PR3-targeting drugs.
The limited number of players suggests potential for new entrants with differentiated therapies.
S1PR3 Drug Modality Landscape
Modalities
Routes of Administration
S1PR3 is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or peptides could diversify the therapeutic landscape.
S1PR3 Clinical Trials 55 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 6 | 6 | 0 | 0 | 100% |
| Phase 2 | 12 | 5 | 4 | 2 | 56% |
| Phase 3 | 13 | 5 | 3 | 5 | 63% |
| Phase 4 | 24 | 16 | 6 | 2 | 73% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
S1PR3 Drug Approval Timeline (2010 - 2021)
The first drug was approved in 2010, and the most recent in 2021.
The approval timeline indicates continued interest, but potential saturation warrants novel approaches.
Pro Intelligence Preview
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
- • Competition: High (15 sponsors)
- • White space: 10 underexplored indications
- • Success rates by condition
Full summary • All drugs • Genetic evidence • Trials • Timeline
How We Calculate These Metrics
Target Attractiveness Score
A 0-100 score based on trial activity, sponsor diversity, and completion rates. Calculated from 24 clinical trials targeting S1PR3.
Completion rate: Percentage of trials that reached their planned endpoint. Trials terminated early, withdrawn, or suspended are not counted—these often indicate safety issues, lack of efficacy, or strategic pivots.
- Highly Attractive (80+): High trial activity, many sponsors, strong completion rates
- Attractive (60-79): Good trial activity and validation
- Moderate (40-59): Moderate interest from sponsors
- Low (under 40): Limited trial activity or validation concerns
Strategic Insights
Auto-generated insights based on trial analytics including competition intensity, white space opportunities, modality shifts, and failure patterns. We analyze trial sponsors, phases, indications, and outcomes.
Risk Signals
- High Competition: Many sponsors competing for this target (may reduce market opportunity)
- High Failure Risk: Low trial completion rates suggest development challenges
- Low Validation: Limited trial activity or poor outcomes indicate uncertain viability
- White Space Available: Underexplored indications present opportunities