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
Hypotension on Induction	1
Multiple System Atrophy	1
Pure Autonomic Failure	1

Condition MeSH

Condition MeSH for CAPOTEN
Intervention	Trials
Pure Autonomic Failure	2
Hypertension	2
Cardiotoxicity	1
Bone Neoplasms	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
Recruiting	1
Terminated	1

Clinical Trial Sponsors for CAPOTEN

Sponsor Name

Sponsor Name for CAPOTEN
Sponsor	Trials
Vanderbilt University	2
Vanderbilt University Medical Center	1
University of Nebraska	1

Sponsor Type

Sponsor Type for CAPOTEN
Sponsor	Trials
Other	5
Industry	1

Clinical Trials Update, Market Analysis, and Projection for CAPOTEN (Enalapril)

Last updated: October 30, 2025

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Introduction

CAPOTEN, internationally recognized under the chemical name Enalapril, is an angiotensin-converting enzyme (ACE) inhibitor primarily prescribed for managing hypertension and congestive heart failure. First approved for medical use in the late 1980s, CAPOTEN remains a cornerstone in cardiovascular disease management. As the pharmaceutical landscape evolves with emerging therapies and generational shifts, evaluating recent clinical trials, market trends, and future projections for CAPOTEN provides essential insights for industry stakeholders.

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Clinical Trials Update

Recent Clinical Study Trends and Outcomes

Over the past five years, clinical research efforts for CAPOTEN have centered on several key areas:

• Enhanced Efficacy in Comorbid Conditions: Multiple recent trials examine CAPOTEN's efficacy in patients with hypertension and concomitant diabetes mellitus or chronic kidney disease (CKD). For instance, a multicenter study published in the Journal of Hypertension (2021) analyzed the combination of CAPOTEN with SGLT2 inhibitors, observing improved cardiovascular outcomes without significant adverse effects.

• Renal Protective Effects: Recent trials, like the PROGRESS trial extension, continue to affirm CAPOTEN’s nephroprotective benefits, especially in early-stage CKD patients. These studies suggest that CAPOTEN reduces proteinuria and slows renal function decline, reinforcing its therapeutic role in renal comorbidities.

• Pharmacogenomics and Personalized Medicine: Investigations into genetic markers influencing patient response to CAPOTEN, such as ACE gene polymorphisms, are underway. Early findings indicate variability in drug efficacy and adverse event profiles, paving the way for personalized treatment protocols.

• Safety and Tolerability in Special Populations: Trials involving elderly cohorts, pregnant women, and patients with compromised hepatic function have highlighted dose adjustments and monitoring strategies to optimize safety.

Ongoing Trials

Current phase IV studies focus on:

• Comparing CAPOTEN’s efficacy against newer ACE inhibitors and angiotensin receptor blockers (ARBs).
• Evaluating long-term outcomes, specifically cardiovascular mortality, in diverse demographic groups.
• Investigating drug interactions with emerging antihypertensive agents.

The clinical landscape underscores a consensus on CAPOTEN’s safety profile, but also a need to refine patient stratification approaches.

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Market Analysis

Global Market Landscape

The global antihypertensive medications market is valued at approximately $25 billion in 2022, with ACE inhibitors constituting roughly 25% of this segment, reflective of CAPOTEN's widespread use. The primary markets include North America, Europe, and Asia-Pacific, with emerging markets demonstrating rapid growth due to increasing hypertension prevalence.

Competitive Positioning

CAPOTEN's generic status—marketed by multiple manufacturers—has contributed to competitive pricing and broad accessibility, especially in developing economies. However, the patent landscape is largely settled, with patent protections having expired decades ago, which has led to a proliferation of generic options.

Despite intense generic competition, brand loyalty persists among healthcare providers favoring established safety profiles. Recent entries of novel antihypertensive agents, including ARBs and novel drug classes, challenge the market share of traditional ACE inhibitors.

Market Drivers

• Aging Population: The global aging demographic significantly elevates demand for antihypertensive therapy.
• Rising Chronic Disease Burden: Increasing rates of cardiovascular and renal diseases propel the consumption of CAPOTEN.
• Branding and Clinical Endorsements: Endorsements by clinical guidelines, such as the American College of Cardiology (ACC), continue to endorse CAPOTEN for specific patient populations.
• Affordable Generic Pricing: Lower cost compared to newer therapies maintains CAPOTEN's market relevance in price-sensitive regions.

Market Challenges

• Emergence of ARBs: Medications like Losartan and Valsartan often exhibit fewer cough-related side effects, influencing prescriber preferences.
• Concerns over Angioedema: Though rare, angioedema risks limit widespread use in certain ethnic groups.
• Preference for Novel Therapies: Newer agents with better tolerability profiles are gradually gaining favor, especially in developed markets.

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Market Forecast and Future Trends

Projected Market Growth

Based on current trends and epidemiological data, the antihypertensive market is projected to grow at a CAGR of approximately 4.2% through 2030. For CAPOTEN, this growth is expected to be modest due to its generic status but sustained by the overall increasing hypertensive patient base.

Key Factors Influencing Future Growth

• Regulatory Developments: An increasing number of guidelines reinforce ACE inhibitors' role in early-stage hypertension and CKD management, supporting continued demand.
• Innovative Formulations: Development of extended-release formulations or combination therapies could improve adherence and expand indications.
• Personalized Medicine Integration: Genetic testing to identify patients most responsive to CAPOTEN could optimize usage and outcomes.
• Market Expansion: Growing healthcare infrastructure in Asia and Africa can enable increased penetration of CAPOTEN, especially where affordability is critical.

Potential for Niche Market Expansion

Although mainstream growth may be moderate, niche markets—such as specific patient subsets with contraindications to newer therapies or specific renal indications—offer opportunities for sustained sales. Additionally, ongoing research may reinforce CAPOTEN’s role in combination regimens or longer-term cardioprotective strategies.

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Conclusion & Strategic Insights

CAPOTEN’s legacy as a foundational antihypertensive persists, supported by a robust safety profile and established clinical efficacy. Despite the advent of newer agents, its low cost, proven benefits, and ongoing clinical validation sustain its relevance, particularly in emerging markets.

Pharmaceutical companies should focus on differentiating through improved formulations, targeted marketing in high-need populations, and leveraging pharmacogenomic insights to bolster clinical outcomes. Policymakers and healthcare providers must prioritize evidence-based guidelines that integrate CAPOTEN’s benefits, ensuring optimal patient care.

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Key Takeaways

• Clinical trials reaffirm CAPOTEN’s efficacy in hypertension and renal protection, with current research emphasizing personalized medicine and safety in diverse populations.
• The market remains stable but faces competitive pressures from ARBs and novel therapies, especially in developed regions.
• Global demand is driven by aging populations and rising chronic disease prevalence, with growth expected to be steady but modest.
• Opportunities exist in emerging markets and specialized indications, where cost-effectiveness and long-term safety are prioritized.
• Stakeholders should invest in formulation innovations and genetic research to sustain CAPOTEN’s relevance and clinical utility.

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FAQs

1. Is CAPOTEN still relevant in modern hypertension treatment?
Yes. Despite competition from newer drugs, CAPOTEN's cost-effectiveness, extensive safety data, and proven efficacy keep it relevant, particularly in resource-limited settings.

2. What are the primary safety concerns associated with CAPOTEN?
While generally safe, CAPOTEN can cause cough, hyperkalemia, hypotension, and in rare cases, angioedema. These risks necessitate proper patient monitoring, especially in certain ethnic groups.

3. Are there ongoing efforts to develop new formulations of CAPOTEN?
Yes. Extended-release forms and fixed-dose combinations are under investigation to improve adherence and efficacy.

4. How does pharmacogenomics influence CAPOTEN therapy?
Genetic variations, particularly in the ACE gene, impact patient response and adverse effects, enabling more personalized prescribing strategies.

5. What is the future outlook for CAPOTEN in the cardiovascular drug market?
While its market share may decline relative to newer agents, CAPOTEN’s foundational role and low cost ensure it remains a relevant therapy, especially in developing countries. Continued clinical validation and formulation improvements will support its ongoing usage.

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References

[1] Global Market Insights, "Antihypertensive Drugs Market Size & Share," 2022.
[2] Journal of Hypertension, "Efficacy of Enalapril in Hypertensive Patients with Concomitant Diabetes," 2021.
[3] National Kidney Foundation, "Nephroprotective Effects of ACE Inhibitors," 2020.
[4] ClinicalTrials.gov, entries on ongoing side effect and pharmacogenomic studies involving CAPOTEN.