MER Inhibitors
3 drugsAbout MER
MER, also known as MER tyrosine kinase, is an enzyme that regulates cellular processes by adding phosphate groups to other proteins. Dysregulation of kinase activity is often implicated in disease, making them attractive targets for therapeutic intervention.
Human genetic studies provide strong validation for MERTK as a therapeutic target, with variants linked to retinal dystrophy (score 0.93) and retinitis pigmentosa (score 0.89). Loss-of-function variants are associated with increased disease risk, suggesting activation may be beneficial.
MER is targeted by 3 FDA-approved small molecule drugs: CABOMETYX, COMETRIQ, and RESNIBEN. These drugs are developed by EXELIXIS and AZURITY, and used in various therapeutic areas.
MER Genetic Evidence Strong
Strong genetic evidence supports MERTK's role in retinal dystrophy and retinitis pigmentosa.
Strong genetic support (score 0.93) increases clinical success probability.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 3 traits
- • Strong signal in phenotype, nervous system disease, genetic, familial or congenital disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link MERTK to 26 diseases.
Loss-of-function causes disease; activation may help
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for MERTK 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 MER Drugs
The competitive landscape is concentrated with EXELIXIS and AZURITY holding all approved drugs.
High market concentration suggests significant entry barriers for new competitors.
MER Drug Modality Landscape
Modalities
Routes of Administration
MER is amenable to small molecule drugs, with oral options available for convenient dosing.
Explore alternative modalities to differentiate from existing MER-targeting therapies.
MER Clinical Trials 233 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on MER. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 62 | 26 | 10 | 26 | 72% |
| Phase 2 | 138 | 54 | 21 | 61 | 72% |
| Phase 3 | 28 | 5 | 4 | 19 | 56% |
| Phase 4 | 5 | 1 | 0 | 4 | 100% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
3 Phase 3 trials testing approved MER drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting MER. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
MER Drug Approval Timeline (2012 - 2016)
The first MER-targeting drug was approved in 2012, with the most recent in 2016.
The limited approval span suggests potential for further innovation in MER-targeted therapies.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 2 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: 106 (18 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 MER. A trial counts if an approved drug acting on MER 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.