NK1R Inhibitors
8 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.
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 |
|---|---|---|---|
| CINVANTI | HERON THERAPS INC | 2017 | 2 |
| APREPITANT | AZURITY | 2012 | 2 |
| LYNKUET | Bayer | 2025 | 2 |
| FOCINVEZ | STERISCIENCE | 2023 | 2 |
| APONVIE | HERON THERAPS INC | 2022 | 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 150 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on NK1R. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 35 | 28 | 4 | 3 | 88% |
| Phase 2 | 46 | 31 | 10 | 5 | 76% |
| Phase 3 | 46 | 40 | 3 | 3 | 93% |
| Phase 4 | 23 | 16 | 3 | 4 | 84% |
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
- • 7 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: 89 (15 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 NK1R. A trial counts if an approved drug acting on NK1R 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.