SRC Inhibitors
4 drugsAbout SRC
SRC Proto-Oncogene Tyrosine Kinase regulates cell growth, differentiation, survival, and motility via tyrosine phosphorylation. As a tyrosine kinase, SRC activates or deactivates other proteins, influencing downstream cellular processes.
Human genetic studies provide moderate support for SRC as a therapeutic target, with variants linked to skeletal abnormalities (score 0.66) and rare hemorrhagic disorders (score 0.59). Strong eQTL/pQTL signals further support its role in disease.
SRC is targeted by 4 FDA-approved small molecule drugs, including DASATINIB (SPRYCEL), BOSULIF, and PHYRAGO. Three drugs are used in oncology, while one targets a different therapeutic area.
Strategic Insights
ℹ️ How we calculate- White space opportunity in Advanced Lymphoma with only 2 trials.
- phase1 represents biological uncertainty with 57% completion.
SRC Genetic Evidence Moderate
Genetic evidence provides moderate support for SRC's role in various diseases.
Further research into the genetic links could reveal novel therapeutic opportunities.
Evidence Across Diseases
7 totalGWAS and other genetic studies link SRC to 7 diseases.
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for SRC 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 SRC Drugs
Four companies, including Apotex and Bristol-Myers Squibb, have approved drugs targeting SRC.
The presence of multiple players indicates a competitive market with potential for differentiation.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| BOSULIF | PF PRISM CV | 2012 | 1 |
SRC Drug Modality Landscape
Modalities
Routes of Administration
SRC is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or PROTACs could expand therapeutic options.
SRC Clinical Trials 246 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 104 | 56 | 34 | 14 | 62% |
| Phase 2 | 121 | 54 | 29 | 37 | 65% |
| Phase 3 | 14 | 9 | 1 | 4 | 90% |
| Phase 4 | 7 | 2 | 1 | 4 | 67% |
Top Sponsors
By Modality
Top Conditions
SRC Drug Approval Timeline (2006 - 2023)
The first SRC-targeting drug was approved in 2006, with the most recent in 2023.
The continued approval of new drugs suggests ongoing interest and potential for innovation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 4 companies competing
- • Market share by company
Full Drug Portfolio
- • All 4 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 4-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 136 clinical trials targeting SRC.
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