CLINICAL TRIALS PROFILE FOR COZAAR

All Clinical Trials for COZAAR

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00168857 ↗	A Prospective, Randomised, Double-blind, Double-dummy, Forced-titration, Multicentre, Parallel Group, One Year Treatment Trial to Compare Telmisartan (MICARDIS) 80 mg Versus Losartan (COZAAR) 100 mg, in Hypertensive Type 2 Diabetic Patients With Ove	Completed	Boehringer Ingelheim	Phase 4	2003-07-01	A number of blood pressure lowering drugs in the class known as angiotensin receptor blockers (ARB) have been shown to slow the decline in kidney function of patients with type 2 diabetes, high blood pressure, and kidney disease. Losartan (COZAAR), is one such drug. The purpose of this research study is to determine if after one year of treatment telmisartan (MICARDIS, GLIOSARTAN, KINZAL, KINZALMONO, PREDXAL, PRITOR, SAMERTAN, TELMISARTAN) 80 mg, another blood pressure lowering drug from the ARB class, is as effective as losartan (COZAAR) 100 mg in reducing the level of urinary protein (indicative of improved kidney function).
NCT00223717 ↗	Treatment of Supine Hypertension in Autonomic Failure	Completed	Vanderbilt University	Phase 1	2001-01-01	Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general.
NCT00223717 ↗	Treatment of Supine Hypertension in Autonomic Failure	Completed	Vanderbilt University Medical Center	Phase 1	2001-01-01	Supine hypertension is a common problem that affects at least 50% of patients with primary autonomic failure. Supine hypertension can be severe, and complicates the treatment of orthostatic hypotension. Drugs used for the treatment of orthostatic hypotension (eg, fludrocortisone and pressor agents), worsen supine hypertension. High blood pressure may also cause target organ damage in this group of patients. The pathophysiologic mechanisms causing supine hypertension in patients with autonomic failure have not been defined. In a study, we, the investigators at Vanderbilt University, examined 64 patients with AF, 29 with pure autonomic failure (PAF) and 35 with multiple system atrophy (MSA). 66% of patients had supine systolic (systolic blood pressure [SBP] > 150 mmHg) or diastolic (diastolic blood pressure [DBP] > 90 mmHg) hypertension (average blood pressure [BP]: 179 ± 5/89 ± 3 mmHg in 21 PAF and 175 ± 5/92 ± 3 mmHg in 21 MSA patients). Plasma norepinephrine (92 ± 15 pg/mL) and plasma renin activity (0.3 ± 0.05 ng/mL per hour) were very low in a subset of patients with AF and supine hypertension. (Shannon et al., 1997). Our group has showed that a residual sympathetic function contributes to supine hypertension in patients with severe autonomic failure and that this effect is more prominent in patients with MSA than in those with PAF (Shannon et al., 2000). MSA patients had a marked depressor response to low infusion rates of trimethaphan, a ganglionic blocker; the response in PAF patients was more variable. At 1 mg/min, trimethaphan decreased supine SBP by 67 +/- 8 and 12 +/- 6 mmHg in MSA and PAF patients, respectively (P < 0.0001). MSA patients with supine hypertension also had greater SBP response to oral yohimbine, a central alpha2 receptor blocker, than PAF patients. Plasma norepinephrine decreased in both groups, but heart rate did not change in either group. This result suggests that residual sympathetic activity drives supine hypertension in MSA; in contrast, supine hypertension in PAF. It is hoped that from this study will emerge a complete picture of the supine hypertension of autonomic failure. Understanding the mechanism of this paradoxical hypertension in the setting of profound loss of sympathetic function will improve our approach to the treatment of hypertension in autonomic failure, and it could also contribute to our understanding of hypertension in general.
NCT00275639 ↗	The Effects of Angiotensin II Receptor Blockade on Kidney Function and Scarring After Liver Transplant	Completed	Mayo Clinic	Phase 4	2004-12-01	This research study is being done to study the effects, both good and bad, of calcineurin inhibitors and the drug Cozaar (losartan), on kidney function and kidney scarring following a liver transplant.
NCT00340678 ↗	Renoprotection in Early Diabetic Nephropathy in Pima Indians	Completed	National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)	Phase 3	1995-08-01	This investigation is a randomized, double-blinded, placebo-controlled clinical trial in adult diabetic Pima Indians with normal urinary albumin excretion (albumin-to-creatinine ration less than 30 mg/g) or microalbuminuria (albumin-to-creatinine ration = 30-299 mg/g) to test the hypothesis that blockade of the renin-angiotensin system with the angiotensin receptor blocker (ARB) losartan can prevent or further attenuate the development and progression of early diabetic nephropathy in subjects with type 2 diabetes mellitus who are receiving standard diabetes care. One hundred seventy subjects were recruited for the study, all of whom had type 2 diabetes for at least 5 years, serum creatinine concentrations less than 1.4 mg/dl, and no evidence of non-diabetic renal diseases. Ninety-two of the subjects had normal urinary albumin excretion at baseline and other 78 had microalbuminuria. Subjects in each albumin excretion group were randomized to treatment with either the angiotensin II receptor antagonist, losartan, or placebo. Measurements of glomerular filtration rate (GFR), renal plasma flow (RPF) and fractional clearances of albumin and IgG will be made initially, at one month, and at 12-month intervals from baseline thereafter. A kidney biopsy was performed after six years in 111 subjects. Morphometric analysis of renal biopsies was used to determine differences in glomerular structure between treatment groups.
NCT00449111 ↗	An Open Label Study to Assess the Efficacy, Safety and Tolerability of COZAAR Plus (Losartan Potassium 50mg/Hydrochlorothiazide 12.5mg) Possibly Titrated up to COZAAR Plus-F (Losartan Potassium 100mg/Hydrochlorothiazide 25mg) in Patients With Essent	Terminated	Merck Sharp & Dohme Corp.	Phase 3	2006-03-13	Evaluate blood pressure after 6 weeks of treatment with COZAAR plus.

Clinical Trial Conditions for COZAAR

Condition Name

Condition Name for COZAAR
Intervention	Trials
Hypertension	27
Healthy	6
Chronic Bronchitis	2
Diabetic Nephropathies	2

Condition MeSH

Condition MeSH for COZAAR
Intervention	Trials
Hypertension	27
Kidney Diseases	10
Fibrosis	5
Renal Insufficiency, Chronic	4

Clinical Trial Locations for COZAAR

Trials by Country

Trials by Country for COZAAR
Location	Trials
United States	114
China	29
Canada	11
Korea, Republic of	6
Argentina	4

Trials by US State

Trials by US State for COZAAR
Location	Trials
Florida	9
California	9
New York	7
Massachusetts	7
Georgia	7

Clinical Trial Progress for COZAAR

Clinical Trial Phase

Clinical Trial Phase for COZAAR
Clinical Trial Phase	Trials
Phase 4	24
Phase 3	11
Phase 2/Phase 3	2

Clinical Trial Status

Clinical Trial Status for COZAAR
Clinical Trial Phase	Trials
Completed	54
Terminated	8
Recruiting	7

Clinical Trial Sponsors for COZAAR

Sponsor Name

Sponsor Name for COZAAR
Sponsor	Trials
Merck Sharp & Dohme Corp.	10
University of Kansas Medical Center	3
University of Miami	3

Sponsor Type

Sponsor Type for COZAAR
Sponsor	Trials
Other	90
Industry	38
NIH	11

Last updated: May 1, 2026

Cozaar (losartan): Clinical-trials update, market analysis, and projection

What is Cozaar and how is it used commercially?

Cozaar is the brand name for losartan potassium, an angiotensin II receptor blocker (ARB). It is marketed for indications that include hypertension and selected cardiovascular and renal disease settings (label specifics vary by territory). Cozaar is an off-patent product in major markets; competitive dynamics therefore center on generic penetration, formulation and access, and class share versus other ARBs and antihypertensives.

Where is Cozaar’s clinical-development pipeline today?

No active, brand-sponsored late-stage (Phase 3) development for Cozaar is expected given the molecule’s long product lifecycle and widespread generic availability. Clinical activity in the losartan space in practice is dominated by:

• Bioequivalence studies for generic versions
• Comparative studies within antihypertensive classes
• Real-world evidence and guideline-adjacent outcomes research using existing losartan formulations

Market implication: a brand-level clinical “update” for Cozaar usually does not translate into a near-term product-claim upgrade for investors unless a new formulation or combination changes regulatory status in a specific jurisdiction.

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What do recent clinical-trials signals show for losartan?

How active is clinical research mentioning losartan?

Across public clinical-trials registries, losartan appears consistently, but the majority of new records are not “Cozaar-only” branded programs. They are typically:

• Trials of generic losartan
• Studies of combination regimens using losartan as an ARB comparator
• Studies addressing adherence, dosing schedules, or special populations

What is the highest-value interpretive point for decision-makers?

The practical decision signal is whether any trial is trying to create a new label or new clinical endpoint for losartan (rather than a reformulation or equivalence question). For Cozaar specifically, that signal is typically low relative to patent-stage assets.

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What does the market look like for losartan/Cozaar today?

Market structure

Losartan is a widely used ARB with broad global availability. The brand economics are driven by:

• Patent expiry and generic entry
• National formulary placement and reimbursement rules
• Switching behavior within ARBs (patients and prescribers move by cost and formulary rules)
• U.S. pharmacy benefit design and retail acquisition costs

Competitive set

In ARBs, losartan competes with:

• Valsartan
• Olmesartan
• Irbesartan
• Telmisartan
• Others (class share varies by country)

Generic share effect

When a molecule is fully off-patent, the brand’s market share depends less on medical differentiation and more on:

• Contracting and rebates
• Formulary tiering
• Pack size and strength availability
• Therapeutic interchange policies

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What are the market drivers and constraints for Cozaar?

Key demand drivers

• Hypertension prevalence and chronic treatment adherence
• Ongoing guideline use of ARBs in appropriate patient subsets
• Availability in multiple strengths supporting titration and continuity

Key constraints

• Generic substitution and price compression
• ARB-class switching based on net price and coverage
• Head-to-head prescriber behavior is often ARB-to-ARB, not brand-to-brand

Where growth can still occur

Growth, where it occurs, comes from:

• Population growth and long-term antihypertensive treatment continuity
• Expansion within specific therapeutic segments (where label language supports use)
• Geographic mix where contracting supports branded products temporarily (less common than pure generic dominance)

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What is a realistic market projection for Cozaar (brand-level)?

Projection logic for off-patent brands

A brand projection for an off-patent ARB is usually modeled as:

• Start with current brand units and net sales trajectory
• Apply generic erosion, tiering changes, and rebate pressure
• Assume limited incremental clinical differentiation from Cozaar itself

Directionally expected path (brand-level)

For Cozaar, the expected trajectory is:

• Flat-to-declining brand share in mature markets
• Slow unit retention only when contracting advantages or supply patterns favor branded inventory
• Net sales pressure from ongoing generic discounting

Practical projection ranges (business-use framing)

Without jurisdiction- and payer-specific unit and pricing inputs, a high-confidence numerical forecast for Cozaar brand net sales is not supportable. What is supportable is the projection framework:

• Competitive ARB class price pressure remains the dominant variable
• Generic share continues to cap brand volume
• Any upside requires a non-generic differentiator: new combination, fixed-dose pairing under a distinct label, or specialty access via payer contracts

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What business actions follow from the clinical and market read-through?

If you are underwriting R&D or investment

• Treat Cozaar as a mature, off-patent cash product at most, not as a catalyst for new clinical value creation.
• Prioritize pipeline assets where label expansion or new MOA is plausible; losartan studies are more likely to support class evidence than to create proprietary upside for the brand.

If you are benchmarking a competitor

• Monitor payer contracting: ARBs often shift based on formulary tier design and net price.
• Track generic entry waves by geography and pack size; those changes typically drive near-term share movement more than clinical trial outcomes.

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Key Takeaways

• Cozaar (losartan) is an off-patent ARB with no credible expectation of brand-specific late-stage clinical development driving label change in the near term; clinical activity in registries is largely equivalence/comparator rather than new-label.
• The market is structurally dominated by generic substitution and ongoing ARB class price competition (valsartan, olmesartan, telmisartan).
• A brand-level forecast for Cozaar is primarily a function of payer contracting, tiering, and net pricing, not trial-driven differentiation; directionally, the brand typically faces share pressure and net sales compression.

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FAQs

1) Is Cozaar still being studied in clinical trials?

Losartan continues to appear in clinical-trials registries, but most activity reflects generic use, comparative designs, or evidence generation rather than Cozaar-specific branded development.

2) What most affects Cozaar’s sales: clinical outcomes or pricing?

Pricing and formulary access dominate for an off-patent product, with net price and tier placement determining real-world prescribing more than incremental trial endpoints.

3) Does any new trial data typically create new Cozaar label changes?

For established, off-patent losartan, label-updating trials are less common; most new studies do not lead to proprietary brand expansion.

4) How does Cozaar compete within the ARB class?

Cozaar competes on coverage and net cost against other ARBs, with formulary rules and patient switching behavior usually driving performance.

5) What is the best way to model Cozaar’s market outlook?

Use payer contracting and generic erosion inputs, then apply ARB class share dynamics; a clinical-trials timeline alone rarely explains off-patent brand revenue trajectories.

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References

[1] ClinicalTrials.gov. (n.d.). Losartan studies (search results). https://clinicaltrials.gov/
[2] U.S. Food and Drug Administration. (n.d.). COZAAR (losartan potassium) label / prescribing information (archived access varies by year). https://www.accessdata.fda.gov/