TRKC Inhibitors
6 drugsAbout TRKC
TRKC (tropomyosin receptor kinase C) is a receptor tyrosine kinase crucial for nervous system development and function. It plays a key role in cell signaling pathways, influencing neuronal survival, differentiation, and synaptic plasticity.
Human genetics provide moderate support for TRKC as a therapeutic target, with variants linked to ovarian neoplasm (score 0.60) and smoking initiation (score 0.58). Inhibition is likely beneficial based on genetic evidence.
Six FDA-approved drugs target TRKC, including VITRAKVI, ROZLYTREK, GAVRETO, AUGTYRO, and IBTROZI, all of which are small molecules. Three drugs are for oncology, and three address other therapeutic areas.
TRKC Genetic Evidence Moderate
Genetic evidence offers moderate support for TRKC, with a max score of 0.60.
Moderate genetic support suggests potential for clinical success, warranting further investigation.
💡 Why inhibition?
- • Gain-of-function variants increase disease risk — blocking overactivity may help
- • 100% directional consistency across 1 traits
- • Strong signal in endocrine system disease, reproductive system or breast disease, cancer or benign tumor pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
10 totalGWAS and other genetic studies link NTRK3 to 10 diseases.
Gain-of-function causes disease; inhibition may help
🔗 Colocalization Evidence 20 strong
max H4: 1.00eQTL/pQTL signals for NTRK3 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 TRKC Drugs
Six companies have approved TRKC-targeting drugs, including Roche and Bayer.
The competitive landscape is moderately concentrated, indicating potential entry barriers for new players.
TRKC Drug Modality Landscape
Modalities
Routes of Administration
TRKC is amenable to small molecule drugs, with oral options available for convenient dosing.
The modality landscape is saturated with small molecules, suggesting an opportunity for novel modalities.
TRKC Clinical Trials 99 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on TRKC. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 34 | 17 | 5 | 12 | 77% |
| Phase 2 | 46 | 6 | 5 | 34 | 55% |
| Phase 3 | 11 | 0 | 2 | 9 | 0% |
| Phase 4 | 8 | 2 | 0 | 6 | 100% |
Top Sponsors
By Modality
Top Conditions
Phase 3 Readout Calendar Pro
2 Phase 3 trials testing approved TRKC drugs across all sponsors.
Coverage: trials whose intervention is an approved drug targeting TRKC. Pre-approval candidates with development codes (e.g. AZD0901, MK-7240) are not yet linked. Anchored on CT.gov primary completion date.
TRKC Drug Approval Timeline (2018 - 2025)
The first TRKC-targeting drug was approved in 2018, with the most recent in 2025.
The approval timeline shows continued interest in TRKC, but approaching saturation.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 6 companies competing
- • Market share by company
Full Drug Portfolio
- • All 6 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 6-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 47 (12 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 TRKC. A trial counts if an approved drug acting on TRKC 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.