MET Inhibitors
8 drugsAbout MET
MET, a receptor tyrosine kinase on the cell surface, is crucial for cell growth, survival, and migration signaling pathways. Upon activation, MET triggers intracellular events that can contribute to tumor development and progression.
Human genetic studies provide strong validation for MET as a therapeutic target (max score 0.92), with variants linked to papillary renal cell carcinoma and hereditary neoplastic syndrome. Loss-of-function variants are associated with increased disease risk, suggesting activation may be beneficial.
MET is targeted by 9 FDA-approved drugs, including CABOMETYX and RYBREVANT, primarily through small molecule (6 drugs) and biologic (3 drugs) modalities. These drugs are utilized in oncology (3 drugs) and other therapeutic areas (6 drugs).
MET Genetic Evidence Strong
MET has strong genetic support with a max score of 0.92 linked to papillary renal cell carcinoma.
Strong genetic support suggests MET-activating therapies may have a higher probability of clinical success.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 1 traits
- • Strong signal in cancer or benign tumor, urinary system disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
18 totalGWAS and other genetic studies link MET to 18 diseases.
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for MET 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 MET Drugs
Seven companies have approved drugs targeting MET, with EXELIXIS and Johnson & Johnson leading the market.
The presence of multiple companies indicates a competitive market, requiring differentiation for new entrants.
MET Drug Modality Landscape
Modalities
Routes of Administration
MET is druggable by both biologics (2) and small molecules (6), indicating broad therapeutic accessibility.
The prevalence of small molecules suggests a potential whitespace opportunity for novel biologic therapies targeting MET.
📈 Modality Evolution
Small molecules pioneered MET targeting (2012), with other biologics entering more recently (2021).
MET Clinical Trials 347 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on MET. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 103 | 40 | 16 | 47 | 71% |
| Phase 2 | 196 | 61 | 32 | 100 | 66% |
| Phase 3 | 42 | 7 | 6 | 29 | 54% |
| Phase 4 | 6 | 1 | 0 | 5 | 100% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
3 Phase 3 trials testing approved MET drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting MET. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
MET Drug Approval Timeline (2012 - 2025)
Metastatic non-small cell lung cancer (NSCLC) with a muta...
Metastatic non-small cell lung cancer (NSCLC) harboring m...
The first MET-targeting drug was approved in 2012, with the most recent approval in 2026, spanning 15 years.
The continued approval of MET-targeting drugs suggests sustained interest and potential for further development.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 6 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
- • Sponsors: 147 (31 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 MET. A trial counts if an approved drug acting on MET 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.