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.
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 |
|---|---|---|---|
| PHYRAGO | HANDA THERAP | 2023 | 2 |
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 248 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on SRC. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 104 | 56 | 34 | 14 | 62% |
| Phase 2 | 122 | 56 | 29 | 36 | 66% |
| Phase 3 | 15 | 9 | 1 | 5 | 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
- • Sponsors: 120 (15 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 SRC. A trial counts if an approved drug acting on SRC 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.