VEGFR2 Inhibitors
8 drugsAbout VEGFR2
Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) is a protein kinase crucial for angiogenesis, the formation of new blood vessels. While vital for normal development and wound healing, it also promotes tumor growth, making it a significant oncology target.
Human genetic studies provide strong validation for VEGFR2 as a therapeutic target, with variants linked to endometriosis (score 0.92) and female infertility (score 0.72). Loss-of-function variants are protective, suggesting inhibition is a viable therapeutic strategy.
VEGFR2 is targeted by 8 FDA-approved drugs, including LENVIMA, CYRAMZA and SUTENT. Small molecules dominate (7 drugs), with one antibody also approved. Applications span oncology, respiratory diseases and other conditions.
Strategic Insights
ℹ️ How we calculate- Validated target with strong trial activity and 80% attractiveness score.
- Emerging modalities (Antibody) signal innovation opportunity.
VEGFR2 Genetic Evidence Strong
VEGFR2 has strong genetic support with a max score of 0.92 linked to endometriosis.
Strong genetic support increases clinical success probability and justifies investment in VEGFR2-targeting therapies.
💡 Why inhibition?
- • Loss-of-function variants reduce disease risk (OR < 1)
- • 100% directional consistency across 1 traits
- • Strong signal in reproductive system or breast disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
16 totalGWAS and other genetic studies link KDR to 16 diseases.
Inhibiting this target may be therapeutic
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for KDR 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 VEGFR2 Drugs
Eight companies have approved VEGFR2-targeting drugs, including EISAI INC and Eli Lilly.
The fragmented market indicates relatively low barriers to entry for new VEGFR2 inhibitors.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| OFEV | Boehringer Ingelheim | 2014 | 3 |
| SUNITINIB MALATE | MSN | 2021 | 3 |
| STIVARGA | Bayer | 2012 | 3 |
| GAVRETO | RIGEL PHARMS | 2020 | 2 |
| QINLOCK | DECIPHERA PHARMS | 2020 | 1 |
VEGFR2 Drug Modality Landscape
Modalities
Routes of Administration
VEGFR2 is druggable by both biologics (1) and small molecules (7), indicating broad therapeutic accessibility.
The dominance of small molecules suggests an opportunity for novel modalities like biologics.
📈 Modality Evolution
Small molecules pioneered VEGFR2 targeting (2006), with antibodies entering more recently (2014).
VEGFR2 Clinical Trials 1,020 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 266 | 156 | 38 | 71 | 80% |
| Phase 2 | 588 | 223 | 106 | 254 | 68% |
| Phase 3 | 138 | 67 | 16 | 55 | 81% |
| Phase 4 | 28 | 17 | 3 | 8 | 85% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
6 Phase 3 trials testing approved VEGFR2 drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting VEGFR2. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
VEGFR2 Drug Approval Timeline (2006 - 2021)
The first VEGFR2 drug was approved in 2006, with the most recent in 2021.
The approval timeline indicates continued interest, but potential saturation in the VEGFR2 space.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 8 companies competing
- • Market share by company
Full Drug Portfolio
- • All 8 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 8-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 815 clinical trials targeting VEGFR2.
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