BCR-ABL Inhibitors
6 drugsAbout BCR-ABL
BCR-ABL (Breakpoint Cluster Region-Abelson) is a protein tyrosine kinase. It is a crucial target in oncology drug development due to its role in certain cancers.
Human genetics provide strong validation for BCR-ABL as a therapeutic target (max score 0.85). Loss-of-function variants are protective against chronic myelogenous leukemia (score 0.80), supporting inhibition-based therapies.
BCR-ABL is targeted by five FDA-approved small molecule drugs, including DASATINIB (SPRYCEL), TASIGNA, DANZITEN, and PHYRAGO. Three drugs are used in oncology, while two target other therapeutic areas.
Strategic Insights
ℹ️ How we calculate- White space opportunity in Advanced Lymphoma with only 2 trials.
- phase1 represents biological uncertainty with 59% completion.
BCR-ABL Genetic Evidence Strong
BCR-ABL has strong genetic support with a max score of 0.85 across nine diseases.
Strong genetic support may increase the probability of clinical success for BCR-ABL inhibitors.
💡 Why inhibition?
- • Loss-of-function variants reduce disease risk (OR < 1)
- • 100% directional consistency across 1 traits
- • Strong signal in musculoskeletal or connective tissue disease, genetic, familial or congenital disease, hematologic disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
9 totalGWAS and other genetic studies link ABL1 to 9 diseases.
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for ABL1 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 BCR-ABL Drugs
Five companies have approved BCR-ABL drugs, including Apotex, Novartis and Bristol-Myers Squibb.
The BCR-ABL market has moderate fragmentation, suggesting potential for new entrants.
BCR-ABL Drug Modality Landscape
Modalities
Routes of Administration
BCR-ABL is amenable to small molecule drugs, with oral options available for convenient dosing.
The BCR-ABL space may benefit from novel modalities beyond small molecules.
BCR-ABL Clinical Trials 329 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 114 | 64 | 36 | 14 | 64% |
| Phase 2 | 165 | 85 | 35 | 44 | 71% |
| Phase 3 | 31 | 20 | 6 | 5 | 77% |
| Phase 4 | 19 | 13 | 2 | 4 | 87% |
Top Sponsors
By Modality
Top Conditions
BCR-ABL Drug Approval Timeline (2006 - 2024)
The first BCR-ABL drug was approved in 2006, with the most recent in 2024.
The BCR-ABL approval timeline shows continued interest, but may be approaching saturation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 6 companies competing
- • Market share by company
Full Drug Portfolio
- • All 6 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 6-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 161 clinical trials targeting BCR-ABL.
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