DDR1 Inhibitors
4 drugsAbout DDR1
Discoidin Domain Receptor 1 (DDR1) is a receptor tyrosine kinase mediating cell-cell and cell-matrix interactions. As a kinase, DDR1 phosphorylates proteins, influencing signal transduction and cellular processes.
Genetic evidence weakly supports DDR1 as a therapeutic target, with associations to ankylosing spondylitis (score 0.26) and multiple sclerosis (score 0.15). Loss-of-function variants are associated with increased risk, suggesting activation may be beneficial.
Four FDA-approved small molecule drugs target DDR1, including TASIGNA, GAVRETO, DANZITEN, and VIZIMPRO. One drug is approved for oncology, while the remaining three target other therapeutic areas.
DDR1 Genetic Evidence
Genetic evidence provides weak support for DDR1, with a maximum score of 0.26.
Low genetic support suggests prioritizing indications with strong preclinical rationale to improve success.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 2 traits
- • Strong signal in immune system disease, musculoskeletal or connective tissue disease, phenotype pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
2 totalGWAS and other genetic studies link DDR1 to 2 diseases.
Loss-of-function causes disease; activation may help
Effect Sizes
Genetic effect on disease risk. OR<1 or β<0 = loss-of-function is protective (inhibiting target may help).
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for DDR1 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 DDR1 Drugs
Four companies have approved DDR1-targeting drugs, including Novartis and Pfizer.
Relatively low market concentration suggests opportunities for new entrants with differentiated therapies.
DDR1 Drug Modality Landscape
Modalities
Routes of Administration
DDR1 is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or PROTACs may offer differentiation opportunities.
DDR1 Clinical Trials 170 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on DDR1. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 41 | 30 | 8 | 3 | 79% |
| Phase 2 | 81 | 47 | 12 | 22 | 80% |
| Phase 3 | 30 | 17 | 8 | 5 | 68% |
| Phase 4 | 18 | 12 | 2 | 4 | 86% |
Top Sponsors
By Modality
Top Conditions
DDR1 Drug Approval Timeline (2007 - 2024)
The first DDR1-targeting drug was approved in 2007, with the most recent in 2024.
Consistent approval rate suggests sustained interest, but increasing competition warrants strategic positioning.
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: 82 (13 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 DDR1. A trial counts if an approved drug acting on DDR1 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.