Abl Inhibitors
3 drugsAbout Abl
Abl (Abelson tyrosine kinase) is a protein kinase involved in cell growth, differentiation, and survival. It plays a role in cellular signaling pathways, making it a relevant target for drug development.
Human genetic studies provide strong validation for ABL1 as a therapeutic target (max score 0.85). Loss-of-function variants are protective against chronic myelogenous leukemia, suggesting inhibition is a viable therapeutic strategy.
Abl is targeted by 2 FDA-approved small molecule drugs: STIVARGA (Bayer) and ICLUSIG (Takeda). These drugs are used in therapeutic areas beyond cancer, highlighting Abl's diverse roles.
Abl Genetic Evidence Strong
Genetic evidence strongly supports ABL1 as a drug target, with a max score of 0.85.
Strong genetic support suggests a higher probability of clinical success for Abl-targeting drugs.
💡 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 Abl Drugs
The competitive landscape includes Bayer and Takeda, each with an approved Abl-targeting drug.
The limited number of companies indicates a concentrated market with potential entry barriers.
Abl Drug Modality Landscape
Modalities
Routes of Administration
Abl is amenable to small molecule drugs, with oral options available for convenient dosing.
The exclusive use of small molecules suggests a whitespace opportunity for alternative modalities like antibodies.
Abl Clinical Trials 286 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on Abl. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 78 | 43 | 13 | 21 | 77% |
| Phase 2 | 168 | 62 | 35 | 71 | 64% |
| Phase 3 | 35 | 14 | 8 | 13 | 64% |
| Phase 4 | 5 | 4 | 1 | 0 | 80% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
3 Phase 3 trials testing approved Abl drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting Abl. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
Abl Drug Approval Timeline (2012 - 2021)
The first Abl-targeting drug was approved in 2012, with the most recent approval also in 2012.
The lack of recent approvals suggests a potentially saturated market or challenges in developing new Abl inhibitors.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 3 companies competing
- • Market share by company
Full Drug Portfolio
- • All 3 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 3-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 152 (32 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 Abl. A trial counts if an approved drug acting on 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.