BCR-ABL Inhibitors
5 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.
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.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| DASATINIB | Teva | 2016 | 2 |
| PHYRAGO | HANDA THERAP | 2023 | 2 |
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 331 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on BCR-ABL. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 114 | 64 | 36 | 14 | 64% |
| Phase 2 | 166 | 86 | 36 | 43 | 70% |
| Phase 3 | 32 | 20 | 6 | 6 | 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
- • 5 companies competing
- • Market share by company
Full Drug Portfolio
- • All 5 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 5-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 149 (16 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 BCR-ABL. A trial counts if an approved drug acting on BCR-ABL 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.