CLINICAL TRIALS PROFILE FOR CAPOTEN

All Clinical Trials for CAPOTEN

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
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.
NCT01292694 ↗	Contribution of Angiotensin II to Supine Hypertension in Autonomic Failure	Terminated	Vanderbilt University	Phase 1	2011-03-01	The purpose of this study is to test the hypothesis that angiotensin II plays a role in the supine hypertension of primary autonomic failure. To determine the contribution of angiotensin II to renin and blood pressure regulation in autonomic failure, patients with multiple system atrophy [MSA] or pure autonomic failure [PAF] and supine hypertension will undergo medication testing with the angiotensin II receptor blocker losartan. The investigators will compare the biochemical and hemodynamic effects between MSA and PAF patients. In a subset of patients, the investigators will also give the ACE inhibitor captopril. Our primary endpoint will be changes in plasma renin activity, and subsequent components of the circulating renin-angiotensin system, in response to angiotensin II blockade. Our secondary outcome will be changes in hemodynamic measures during administration of these drugs.
NCT01669434 ↗	Chronic Angiotensin Converting Enzyme Inhibitors in Intermediate Risk Surgery	Completed	University of Nebraska	Phase 4	2015-06-01	Primary research hypothesis: Patients who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #1: Patients who continue their chronic ACEI up to and including the morning of a non-cardiac, non-vascular surgery will experience better postoperative control of hypertension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #2: Patients who continue their chronic ACEI up to and including the morning of a non-cardiac, non-vascular surgery will experience less acute renal failure than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #3: In the subgroup of patients with a preoperative systolic blood pressure less than 110 mmHg, those who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively. Secondary research hypothesis #4: In the subgroup of patients above the age of 64, those who continue their chronic ACEI therapy up to and including the morning of a non-cardiac, non-vascular surgery will experience more intraoperative hypotension than those who transiently hold their chronic ACEI preoperatively.
NCT03389724 ↗	Prevention of Chemotherapy Induced Cardiotoxicity in Children With Bone Tumors and Acute Myeloid Leukemia	Recruiting	Children's Cancer Hospital Egypt 57357	Phase 3	2017-11-14	Prevention and early detection of chemotherapy-induced cardiotoxicity in children with bone tumors and Acute Myeloid Leukemia by giving capoten

Clinical Trial Conditions for CAPOTEN

Condition Name

Condition Name for CAPOTEN
Intervention	Trials
Hypertension	3
Cardiotoxicity	1
Healthy Volunteers	1
Hypotension on Induction	1

Condition MeSH

Condition MeSH for CAPOTEN
Intervention	Trials
Pure Autonomic Failure	2
Hypertension	2
Hypotension	1
Shy-Drager Syndrome	1

Clinical Trial Locations for CAPOTEN

Trials by Country

Trials by Country for CAPOTEN
Location	Trials
United States	3
Egypt	1

Trials by US State

Trials by US State for CAPOTEN
Location	Trials
Tennessee	2
Nebraska	1

Clinical Trial Progress for CAPOTEN

Clinical Trial Phase

Clinical Trial Phase for CAPOTEN
Clinical Trial Phase	Trials
Phase 4	1
Phase 3	1
Phase 1	3

Clinical Trial Status

Clinical Trial Status for CAPOTEN
Clinical Trial Phase	Trials
Completed	2
Not yet recruiting	1
Recruiting	1

Clinical Trial Sponsors for CAPOTEN

Sponsor Name

Sponsor Name for CAPOTEN
Sponsor	Trials
Vanderbilt University	2
University of Nebraska	1
Children's Cancer Hospital Egypt 57357	1

Sponsor Type

Sponsor Type for CAPOTEN
Sponsor	Trials
Other	5
Industry	1

CAPOTEN Market Analysis and Financial Projection

Last updated: May 1, 2026

CAPOTEN (captopril): Clinical Trial Update and Market Outlook

What is CAPOTEN and what is its current clinical positioning?

CAPOTEN is the brand name for captopril, an oral ACE inhibitor used for hypertension and select cardiovascular indications. CAPOTEN is an established, off-patent small molecule (no ongoing late-stage brand-defining CAPOTEN trials in the open clinical-trials record).

Clinical trial activity today is mostly incremental and comparative, typically involving:

• new formulations or bioequivalence work,
• observational studies and real-world evidence,
• mechanistic studies using captopril as a reference ACE inhibitor.

Late-stage, registrational trial updates specifically under the CAPOTEN brand name are not reported as active in the public trial registries, and the commercial trajectory for CAPOTEN is driven primarily by generic penetration rather than new clinical evidence.

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What do current registries show for captopril clinical activity?

Public clinical-trial registries capture captopril across a wide set of study designs. The key business signal is that trial generation continues at low intensity for captopril, but it does not cluster around CAPOTEN-specific registrational milestones.

Practical read-through for R&D and investment:

• The pipeline risk is lower on “new evidence” because captopril’s clinical profile is already established.
• The pipeline upside is low for brand economics because generic competition is the dominant factor.

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What is the CAPOTEN market structure?

CAPOTEN’s market is shaped by three forces:

1. Patent and exclusivity status

• Captopril is an older drug with broad generic availability.
• CAPOTEN brand value is therefore constrained by pricing power and substitution dynamics.

2. Class-level competition

• ACE inhibitors are a mature category.
• Therapeutic alternatives include ARBs and, in some geographies, other ACE inhibitors with strong supply chains.

3. Formulary and procurement behavior

• Hospital and payer formularies increasingly favor lowest net cost for therapeutics without brand-level differentiation.

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How big is the captopril/ACE-inhibitor opportunity and where does CAPOTEN fit?

A reliable market model for CAPOTEN requires brand-level sales visibility and geography-specific procurement data. Those data are not available in the materials here, so the actionable approach is to project at the class and molecule level, then map CAPOTEN to its likely share dynamics:

Projection logic used for mature generics (ACE inhibitor class)

• Volume trends track underlying cardiovascular disease prevalence and prescribing inertia.
• Price trends are driven by generic competition, substitution to lower-cost equivalents, and tender cycles.
• Net revenue trends follow a typical mature pattern: stable-to-declining unit pricing with modest volume changes.

Most likely CAPOTEN outcome in a genericized environment

• Stable demand for captopril as an ACE inhibitor reference option.
• Ongoing erosion of brand premium due to generic substitution.
• Limited upside unless CAPOTEN retains differentiated advantages in a subset of markets (supply reliability, local tender positions, or specific payer contracts).

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What are the key competitive drivers for CAPOTEN in 2025-2035?

1) Generic substitution and tender pricing

• ACE inhibitors are routinely substitutable at the molecule level.
• Procurement systems select on net price, then adherence.

2) Patient-level switching and tolerability

• Switching from ACE inhibitors is common for side effects such as cough, hypotension, and renal or potassium effects.
• In practice, many patients remain on ACE inhibitors if tolerated, which supports molecule-level stability.

3) Category risk from evolving guideline preferences

• ACE inhibitors face ongoing competition from ARBs where tolerability or class-specific outcomes favor ARBs.
• Still, ACE inhibitors remain guideline-concordant in hypertension and heart failure depending on patient profile and regional guidance.

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Clinical safety and label impact: what matters for future demand?

For a mature ACE inhibitor, demand is driven by safety management rather than new efficacy.

Key clinical handling points that influence real-world continuation rates:

• Renal function monitoring
• Potassium monitoring
• Blood pressure titration
• Management of ACE-inhibitor cough and angioedema risk

These factors do not typically change over time in ways that create sudden demand expansions for a single brand; they mainly shape adherence and discontinuation rates.

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Market projection: CAPOTEN revenue outlook (scenario framework)

Because CAPOTEN’s commercial outcome is dominated by generic economics, a scenario framework based on mature-drug behavior is the most actionable approach:

Scenario	Assumption	Expected CAPOTEN commercial trajectory
Base	Generic pricing remains competitive; CAPOTEN retains some formulary presence	Modest volume stability with low-to-mid single digit annual revenue pressure from price
Downside	Intensified tendering shifts share to lower-cost equivalents	Continued revenue decline with faster unit price erosion
Upside	Contracted supply or localized premium positioning retains share; volume growth from population and hypertension diagnosis	Flatter revenue trend; limited or no decline in net revenue for multiple years

Time horizon: 2025 to 2035
Primary driver: net pricing and share retention in tenders.

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What do these dynamics mean for R&D decisions?

For CAPOTEN specifically (as a brand), future R&D value is constrained by its established formulation and class status. The value frontier is mostly in:

• formulation work for specific markets,
• manufacturing robustness and supply contracts,
• incremental clinical generation only where regulators require it for localized filings.

From a business perspective, CAPOTEN is more likely to be managed as a core generic franchise than as a novel development program.

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Key Takeaways

• CAPOTEN (captopril) has established clinical positioning as an ACE inhibitor with ongoing but low-intensity captopril research activity, mostly non-registrational in character.
• CAPOTEN market performance is primarily determined by generic substitution and tender pricing, not by new brand-defining clinical evidence.
• A realistic 2025-2035 projection is stable-to-declining net revenue under base assumptions, with outcomes dominated by net price and share retention rather than clinical upside.

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FAQs

1) Is CAPOTEN expected to benefit from new registrational clinical trials?
No. Public registries do not indicate CAPOTEN-specific late-stage registrational momentum that would drive a brand-level reset.

2) What most affects CAPOTEN revenue over the next decade?
Net pricing from generic competition and procurement tender cycles, plus formulary share retention.

3) Does captopril’s established safety profile limit demand volatility?
Yes. Safety management drives adherence, but it does not typically create step-change demand spikes for a single brand.

4) Are ACE inhibitors likely to be displaced by ARBs?
Partially, by tolerability and guideline preferences in some patient groups, but ACE inhibitors remain core therapy in multiple indications.

5) What is the most plausible growth lever for CAPOTEN in practice?
Localized contract positions, supply reliability, and maintaining formulary coverage that prevents share loss to lower-cost equivalents.

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References

[1] World Health Organization (WHO). WHO Model List of Essential Medicines. https://www.who.int/teams/health-product-and-policy-standards/standards-and-specifications/essential-medicines
[2] ClinicalTrials.gov. Captopril (captopril) clinical trials. https://clinicaltrials.gov/
[3] U.S. Food and Drug Administration (FDA). Drugs@FDA: Capoten (captopril). https://www.accessdata.fda.gov/scripts/cder/daf/