N-methyl-D-aspartate receptor Inhibitors
4 drugsAbout N-methyl-D-aspartate receptor
The N-methyl-D-aspartate receptor (NMDAR) is a glutamate-gated ion channel in nerve cells, crucial for excitatory neurotransmission, synaptic plasticity, learning, and memory. Dysregulation of NMDAR activity is implicated in neurological and psychiatric disorders.
Human genetic studies provide strong validation for NMDAR (GRIN1) as a therapeutic target (max score 0.97), with variants linked to neurodevelopmental disorders. Loss-of-function variants are associated with increased disease risk, suggesting activation may be beneficial.
NMDAR is targeted by 4 FDA-approved small molecule drugs including Ketalar and Spravato, spanning pain management and CNS disorders. Top companies in the space include Hikma, Johnson & Johnson, and PH HEALTH.
N-methyl-D-aspartate receptor Genetic Evidence Strong
Strong genetic evidence supports NMDAR as a target, with a max score of 0.97 linking it to neurodevelopmental disorders.
The strong genetic support suggests a higher probability of clinical trial success for NMDAR-targeting drugs.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 3 traits
- • Strong signal in nervous system disease, genetic, familial or congenital disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
20 totalGWAS and other genetic studies link GRIN1 to 23 diseases.
Loss-of-function causes disease; activation may help
Loss-of-function causes disease; activation may help
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 N-methyl-D-aspartate receptor Drugs
The competitive landscape includes 3 companies with approved drugs, with Hikma and Johnson & Johnson leading.
The relatively low number of players suggests moderate barriers to entry, making it attractive for new entrants.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| METHADONE HYDROCHLORIDE INTENSOL | Hikma | 1988 | 2 |
N-methyl-D-aspartate receptor Drug Modality Landscape
Modalities
Routes of Administration
N-methyl-D-aspartate receptor is amenable to small molecule drugs, with oral options available for convenient dosing.
Exploring alternative modalities like antibodies or gene therapies could provide a competitive advantage.
N-methyl-D-aspartate receptor Clinical Trials 617 trials
Completion by Phase
| Phase | Total | Completed | Failed | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 124 | 79 | 21 | 20 | 79% |
| Phase 2 | 163 | 89 | 35 | 37 | 72% |
| Phase 3 | 90 | 41 | 19 | 30 | 68% |
| Phase 4 | 240 | 148 | 37 | 54 | 80% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
N-methyl-D-aspartate receptor Drug Approval Timeline (1947 - 2019)
The first drug was approved in 1947, with the most recent approval in 2019, spanning 73 years.
The long approval span indicates sustained interest, but recent approvals suggest renewed opportunities.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 4 companies competing
- • Market share by company
Full Drug Portfolio
- • All 4 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 4-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Competition: High (15 sponsors)
- • 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 463 clinical trials targeting N-methyl-D-aspartate receptor.
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