VEGFR-1 Inhibitors
10 drugsAbout VEGFR-1
VEGFR-1 (Vascular Endothelial Growth Factor Receptor 1) is a receptor tyrosine kinase that regulates angiogenesis by binding VEGF and modulating endothelial cell behavior. Its signaling plays a crucial role in blood vessel formation and vascular homeostasis.
Human genetic studies provide strong support for VEGFR-1 as a therapeutic target (max score 0.85), with variants linked to skeletal abnormalities (0.85), and coronary artery disease (0.84). These findings support therapeutic interventions modulating VEGFR-1 activity.
VEGFR-1 is targeted by 10 approved small molecule drugs including CABOMETYX, SORAFENIB TOSYLATE and INLYTA, spanning oncology (4 drugs) and other therapeutic areas (6 drugs). The first drug was approved in 2005 (NEXAVAR) and the most recent in 2023 (FRUZAQLA).
Human Genetic Evidence Strong
VEGFR-1 has strong genetic support with a max score of 0.85 linked to skeletal abnormalities.
Strong genetic support suggests a higher likelihood of clinical success, potentially justifying increased investment in VEGFR-1 targeted therapies.
Evidence Across Diseases
19 totalGWAS and other genetic studies link FLT1 to 19 diseases.
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for FLT1 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 Drugs
Ten companies have approved VEGFR-1 targeting drugs, including Viatris, NOVUGEN and EXELIXIS.
A fragmented competitive landscape suggests relatively low barriers to entry for new VEGFR-1 inhibitors.
Drug Modality Landscape
Modalities
Routes of Administration
VEGFR-1 is amenable to small molecule drugs, with oral options available for convenient dosing.
The absence of antibody or protein modalities represents a whitespace opportunity for novel VEGFR-1 targeting strategies.
Clinical Trials 1,053 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 348 | 218 | 67 | 61 | 76% |
| Phase 2 | 560 | 263 | 113 | 182 | 70% |
| Phase 3 | 118 | 56 | 17 | 45 | 77% |
| Phase 4 | 27 | 16 | 2 | 9 | 89% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
7 Phase 3 trials testing approved VEGFR-1 drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting VEGFR-1. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
Drug Approval Timeline (2005 - 2023)
The approval timeline spans 19 years, from 2005 to 2023.
Continued approvals indicate sustained interest, but recent approvals may signal increasing market saturation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 10 companies competing
- • Market share by company
Full Drug Portfolio
- • All 10 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 10-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Competition: High (15 sponsors)
- • 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 523 clinical trials targeting VEGFR-1.
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