AT1 receptor Inhibitors
26 drugsAbout AT1 receptor
The Angiotensin II Type 1 receptor (AT1 receptor) is a key component of the renin-angiotensin-aldosterone system (RAAS), regulating blood pressure and fluid balance. As a result, it is a significant drug target, particularly in the cardiovascular therapeutic area.
Human genetic studies provide strong validation for AT1 receptor as a therapeutic target (max score 0.82), with variants linked to renal tubular dysgenesis and essential hypertension. Loss-of-function variants are associated with increased disease risk, suggesting activation may be beneficial.
AT1 receptor is targeted by 26 FDA-approved small molecule drugs, including COZAAR, DIOVAN and ARBLI, primarily for cardiovascular indications. Seventeen companies have approved drugs, including Lupin, COSETTE, ALEMBIC, Teva, and GLENMARK PHARMS LTD.
AT1 receptor Genetic Evidence Strong
Genetic evidence strongly supports the AT1 receptor as a drug target, with a maximum score of 0.82.
Strong genetic support increases the likelihood of clinical trial success, making AT1 receptor a promising target for drug development.
💡 Why activation?
- • Loss-of-function variants increase disease risk (OR > 1) — restoring function may help
- • 100% directional consistency across 3 traits
- • Strong signal in genetic, familial or congenital disease, urinary system disease pathways
Cross-Disease Effects
Trade-off: LowDirection of Effect
100% alignedEvidence Across Diseases
16 totalGWAS and other genetic studies link AGTR1 to 16 diseases.
Loss-of-function causes disease; activation may help
Loss-of-function causes disease; activation may help
🔗 Colocalization Evidence 1 strong
max H4: 0.95eQTL/pQTL signals for AGTR1 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 AT1 receptor Drugs
Seventeen companies have approved drugs targeting the AT1 receptor, indicating a moderately competitive landscape.
The presence of multiple players suggests moderate entry barriers, requiring differentiated strategies for new entrants.
| Drug | Company | Approved | Indications |
|---|---|---|---|
| OLMESARTAN MEDOXOMIL, AMLODIPINE AND HYDROCHLOROTHIAZIDE | MICRO LABS | 2016 | 3 |
| HYZAAR | Merck | 1995 | 3 |
| ARBLI | SCIENTURE | 2025 | 3 |
| DIOVAN HCT | Novartis | 1998 | 3 |
| VALSARTAN AND HYDROCHLOROTHIAZIDE | Lupin | 2012 | 2 |
| EDARBYCLOR | AZURITY | 2011 | 2 |
| SACUBITRIL AND VALSARTAN | CRYSTAL | 2024 | 2 |
| CANDESARTAN CILEXETIL | ALEMBIC | 2013 | 2 |
| AZILSARTAN MEDOXOMIL AND CHLORTHALIDONE | ALKEM LABS LTD | 2025 | 2 |
| ATACAND | ANI PHARMS | 1998 | 2 |
| ENTRESTO | Novartis | 2015 | 2 |
| ENTRESTO SPRINKLE | Novartis | 2024 | 2 |
| AVAPRO | Sanofi | 1997 | 2 |
| CANDESARTAN CILEXETIL AND HYDROCHLOROTHIAZIDE | PHARMOBEDIENT | 2012 | 1 |
| TELMISARTAN | ZYDUS PHARMS | 2014 | 1 |
| OLMESARTAN MEDOXOMIL AND HYDROCHLOROTHIAZIDE | Aurobindo Pharma | 2016 | 1 |
| FILSPARI | TRAVERE | 2023 | 1 |
| ATACAND HCT | ANI PHARMS | 2000 | 1 |
| EDARBI | AZURITY | 2011 | 1 |
| BENICAR | COSETTE | 2002 | 1 |
| TRIBENZOR | COSETTE | 2010 | 1 |
| BENICAR HCT | COSETTE | 2003 | 1 |
| MICARDIS HCT | Boehringer Ingelheim | 2000 | 1 |
AT1 receptor Drug Modality Landscape
Modalities
Routes of Administration
AT1 receptor is amenable to small molecule drugs, with oral options available for convenient dosing.
The absence of other modalities like antibodies or biologics represents a whitespace opportunity for innovation.
AT1 receptor Clinical Trials 705 trials
Phase 1-4 trials started in 2008 or later that test an FDA-approved drug acting on AT1 receptor. Source: ClinicalTrials.gov. How we count
Completion by Phase
| Phase | Total | Completed | Stopped | Active | Completion |
|---|---|---|---|---|---|
| Phase 1 | 156 | 131 | 8 | 16 | 94% |
| Phase 2 | 140 | 89 | 27 | 24 | 77% |
| Phase 3 | 177 | 130 | 28 | 18 | 82% |
| Phase 4 | 232 | 162 | 38 | 32 | 81% |
Top Sponsors
By Modality
Top Conditions
Top Drugs
AT1 receptor Drug Approval Timeline (1995 - 2025)
The first AT1 receptor drug was approved in 1995 (COZAAR), with the most recent in 2025 (AZILSARTAN MEDOXOMIL AND CHLORTHALIDONE).
The continued approvals over 31 years suggest sustained interest and potential for further development in this target area.
Pro Intelligence Preview
Deep insights for drug target analysis
Competitive Landscape
- • 17 companies competing
- • Market share by company
Full Drug Portfolio
- • All 26 approved drugs
- • Approval dates & indications
Genetic Validation
- • Full genetic evidence table
- • Effect sizes & directions
Approval Timeline
- • Full 26-drug timeline
- • First-of-modality markers
Clinical Trials Analysis
- • Sponsors: 345 (86 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 AT1 receptor. A trial counts if an approved drug acting on AT1 receptor 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.