BRAF Inhibitors
7 drugsAbout BRAF
BRAF, or B-Raf Proto-Oncogene, is a protein kinase in the RAS/MAPK pathway, regulating cell growth and differentiation. Aberrant BRAF activation drives uncontrolled cell growth, implicating it in various diseases.
Human genetics strongly support BRAF as a target, with a max score of 0.96 linking it to rasopathy and cardiofaciocutaneous syndromes. Inhibition is likely beneficial based on genetic evidence.
BRAF is targeted by 7 FDA-approved small molecule drugs, including TAFINLAR, SORAFENIB TOSYLATE and STIVARGA. These drugs are used in oncology and other therapeutic areas.
BRAF Genetic Evidence Strong
BRAF has strong genetic support with a max score of 0.96 across 28 diseases.
Strong genetic support suggests BRAF-targeting therapies have a higher probability of clinical success.
💡 Why inhibition?
- • Gain-of-function variants increase disease risk — blocking overactivity may help
- • 100% directional consistency across 1 traits
- • Strong signal in genetic, familial or congenital disease, integumentary system disease, cardiovascular disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link BRAF to 28 diseases.
Gain-of-function causes disease; inhibition may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for BRAF 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 BRAF Drugs
Six companies have approved BRAF-targeting drugs, including Viatris, Bayer and Novartis.
The presence of multiple players indicates a competitive market with moderate entry barriers.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| SORAFENIB TOSYLATE | YABAO PHARM | 2020 | 3 |
| ZELBORAF | Roche | 2011 | 2 |
| QINLOCK | DECIPHERA PHARMS | 2020 | 1 |
| OJEMDA | DAY ONE BIOPHARMS | 2024 | 1 |
BRAF Drug Modality Landscape
Modalities
Routes of Administration
BRAF is amenable to small molecule drugs, with oral options available for convenient dosing.
The absence of other modalities suggests an opportunity for novel BRAF-targeting approaches.
BRAF Clinical Trials 821 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on BRAF. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 301 | 193 | 70 | 33 | 73% |
| Phase 2 | 402 | 189 | 96 | 116 | 66% |
| Phase 3 | 102 | 59 | 18 | 25 | 77% |
| Phase 4 | 16 | 9 | 3 | 4 | 75% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
6 Phase 3 trials testing approved BRAF drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting BRAF. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
BRAF Drug Approval Timeline (2005 - 2024)
The first BRAF inhibitor was approved in 2005, with the most recent approval in 2024.
The 20-year approval span suggests continued interest and potential for further innovation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 6 companies competing
- • Market share by company
Full Drug Portfolio
- • All 7 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 7-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 347 (91 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 BRAF. A trial counts if an approved drug acting on BRAF 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.