NK1R Inhibitors
7 drugsAbout NK1R
The neurokinin-1 receptor (NK1R), encoded by the TACR1 gene, is a G protein-coupled receptor involved in various physiological processes. Its activation is linked to nausea, vomiting, and other conditions, making it a target for therapeutic intervention.
Genetic studies provide moderate support for NK1R as a drug target, with a maximum genetic score of 0.55 linking it to ovarian dysfunction and asthma. Colocalization analysis reveals 3 strong eQTL/pQTL signals, suggesting potential regulatory mechanisms.
NK1R is targeted by 7 FDA-approved small molecule drugs, including APREPITANT, FOCINVEZ, VARUBI, LYNKUET, and EMEND. These drugs are approved for other therapeutic areas, with six companies developing approved NK1R-targeting therapies.
Strategic Insights
ℹ️ How we calculate- White space opportunity in Prevention with only 1 trials.
NK1R Genetic Evidence Moderate
Genetic evidence offers moderate support for NK1R's role in diseases like ovarian dysfunction (score 0.55) and asthma (score 0.52).
Further investigation into the genes driving eQTL/pQTL signals (H4: 0.99) may reveal novel therapeutic opportunities.
Evidence Across Diseases
9 totalGWAS and other genetic studies link TACR1 to 9 diseases.
🔗 Colocalization Evidence 3 strong
max H4: 0.99eQTL/pQTL signals for TACR1 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 NK1R Drugs
Six companies have approved drugs targeting NK1R, including GLENMARK SPECLT, STERISCIENCE, and TERSERA.
The presence of multiple players suggests a competitive market, requiring differentiated strategies for new entrants.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| VARUBI | TERSERA | 2015 | 2 |
| FOCINVEZ | STERISCIENCE | 2023 | 2 |
| LYNKUET | Bayer | 2025 | 2 |
| CINVANTI | HERON THERAPS INC | 2017 | 2 |
NK1R Drug Modality Landscape
Modalities
Routes of Administration
NK1R is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or peptides could provide a competitive advantage in the NK1R space.
NK1R Clinical Trials 131 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 31 | 27 | 3 | 1 | 90% |
| Phase 2 | 38 | 26 | 9 | 3 | 74% |
| Phase 3 | 41 | 34 | 3 | 4 | 92% |
| Phase 4 | 21 | 15 | 3 | 3 | 83% |
Top Sponsors
By Modality
Top Conditions
NK1R Drug Approval Timeline (2003 - 2025)
The first NK1R drug was approved in 2003 (EMEND), with the most recent approval in 2025 (LYNKUET).
The continued approval of NK1R drugs indicates sustained interest, but market saturation may increase competition.
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
- • Competition: High (15 sponsors)
- • White space: 10 underexplored indications
- • Success rates by condition
Full summary • All drugs • Genetic evidence • Trials • Timeline
How We Calculate These Metrics
Target Attractiveness Score
A 0-100 score based on trial activity, sponsor diversity, and completion rates. Calculated from 94 clinical trials targeting NK1R.
Completion rate: Percentage of trials that reached their planned endpoint. Trials terminated early, withdrawn, or suspended are not counted—these often indicate safety issues, lack of efficacy, or strategic pivots.
- Highly Attractive (80+): High trial activity, many sponsors, strong completion rates
- Attractive (60-79): Good trial activity and validation
- Moderate (40-59): Moderate interest from sponsors
- Low (under 40): Limited trial activity or validation concerns
Strategic Insights
Auto-generated insights based on trial analytics including competition intensity, white space opportunities, modality shifts, and failure patterns. We analyze trial sponsors, phases, indications, and outcomes.
Risk Signals
- High Competition: Many sponsors competing for this target (may reduce market opportunity)
- High Failure Risk: Low trial completion rates suggest development challenges
- Low Validation: Limited trial activity or poor outcomes indicate uncertain viability
- White Space Available: Underexplored indications present opportunities