CLINICAL TRIALS PROFILE FOR CAPOTEN

All Clinical Trials for CAPOTEN

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT04878315 ↗	Bioequivalence Study Between Capoten Versus Captopril Reference Product in Healthy Adult Participants Under Fasting Conditions	Not yet recruiting	GlaxoSmithKline	Phase 1	2021-12-10	This is a bioequivalence study to compare Capoten (test product [T]) versus captopril (reference product [R]) produced by Mylan Pharmaceuticals Spain, in healthy adult participants under fasting condition. Capoten is the registered trademark of SmithKline Beecham Egypt.
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
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.
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.
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.

Clinical Trial Conditions for CAPOTEN

Condition Name

Condition Name for CAPOTEN
Intervention	Trials
Hypertension	3
Pure Autonomic Failure	1
Acute Myeloid Leukemia in Children	1
Bone Tumor	1

Condition MeSH

Condition MeSH for CAPOTEN
Intervention	Trials
Pure Autonomic Failure	2
Hypertension	2
Multiple System Atrophy	1
Leukemia, Myeloid	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
Terminated	1
Not yet recruiting	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 and Efficacy of CAPOTEN

Introduction to CAPOTEN

CAPOTEN, also known as captopril, is an angiotensin-converting enzyme (ACE) inhibitor used in the treatment of various cardiovascular and renal conditions. Here, we will delve into the clinical trials that have established its efficacy and discuss market projections.

Clinical Trials Overview

Hypertension

Clinical trials have shown that CAPOTEN is effective in treating hypertension. It can be used as initial therapy for patients with normal renal function and is often combined with other antihypertensive agents, such as thiazide-type diuretics, to achieve additive blood pressure lowering effects[3][4].

Heart Failure

CAPOTEN has been proven to improve survival and reduce the incidence of overt heart failure in patients with left ventricular dysfunction following myocardial infarction. Studies have demonstrated a 19% reduction in all-cause mortality and a 21% reduction in cardiovascular death compared to placebo. Additionally, CAPOTEN reduced the risk of first hospitalizations for heart failure by 22%[1][4].

Diabetic Nephropathy

In patients with type I insulin-dependent diabetes mellitus, retinopathy, and proteinuria, CAPOTEN significantly delays the progression of renal insufficiency. Clinical trials showed a 51% reduction in the risk of doubling serum creatinine and a 51% reduction in the risk of end-stage renal disease or death. CAPOTEN also reduced urine protein excretion by 30% within the first three months, an effect that was maintained throughout the trial[1][4].

Renal Protection

CAPOTEN has been shown to protect renal function beyond what would be expected from blood pressure reduction alone. In normotensive patients with insulin-dependent diabetes and microalbuminuria, CAPOTEN delayed the progression to overt nephropathy with a risk reduction of 67% to 76%[1][4].

Side Effects and Tolerability

While CAPOTEN is generally well-tolerated, it can cause several side effects. Common side effects include cough (reported in 0.5 to 2% of patients), rash, and renal issues such as proteinuria. More severe but rare side effects include neutropenia/agranulocytosis, anemia, thrombocytopenia, and angioedema, particularly in black patients[1][3][4].

Dosage and Administration

The dosage of CAPOTEN must be adjusted in patients with renal impairment due to its primary excretion through the kidneys. Initial daily dosages should be reduced, and titration should be slow to avoid adverse effects. Concomitant diuretic therapy, preferably with loop diuretics, is recommended in patients with severe renal impairment[3][4].

Market Analysis and Projections

Current Market Context

The pharmaceutical market, particularly for cardiovascular and renal treatments, is highly competitive and influenced by various factors including regulatory approvals, patent expirations, and emerging therapies.

Economic Outlook and Healthcare Spending

The global economic outlook for 2025 suggests continued growth but with potential inflationary pressures and policy risks. In the healthcare sector, this could translate into increased spending on essential medications, including those for chronic conditions like hypertension and diabetes. However, economic uncertainties may impact the affordability and accessibility of these drugs[5].

Competitive Landscape

CAPOTEN, as an established ACE inhibitor, faces competition from newer classes of drugs such as angiotensin receptor blockers (ARBs) and direct renin inhibitors. However, its proven efficacy and long-standing presence in the market maintain its relevance.

Market Projections

Given the ongoing need for effective treatments for hypertension, heart failure, and diabetic nephropathy, CAPOTEN is likely to remain a significant player in the market. Here are some key projections:

• Stable Demand: The demand for CAPOTEN is expected to remain stable due to its established use in managing chronic cardiovascular and renal conditions.
• Generic Competition: As a generic drug, CAPOTEN faces competition from other generic ACE inhibitors, which could impact its market share but not its overall relevance.
• Emerging Markets: In regions with growing healthcare needs and increasing awareness of cardiovascular diseases, CAPOTEN may see increased adoption.
• Combination Therapies: The trend towards combination therapies may further solidify CAPOTEN's position as it is often used in conjunction with other antihypertensive agents.

Key Takeaways

• Efficacy: CAPOTEN has been clinically proven to be effective in treating hypertension, heart failure, and diabetic nephropathy.
• Renal Protection: It offers significant renal protection beyond blood pressure control.
• Side Effects: While generally well-tolerated, it can cause side effects such as cough and renal issues.
• Market Stability: Despite competition, CAPOTEN is expected to maintain a stable market presence due to its established efficacy and long history of use.
• Economic Factors: Economic uncertainties may impact healthcare spending, but essential medications like CAPOTEN are likely to remain in demand.

FAQs

What are the primary indications for CAPOTEN?

CAPOTEN is indicated for the treatment of hypertension, congestive heart failure, left ventricular dysfunction after myocardial infarction, and diabetic nephropathy.

What are the common side effects of CAPOTEN?

Common side effects include cough, rash, and renal issues such as proteinuria. Rare but severe side effects include neutropenia/agranulocytosis and angioedema.

How does CAPOTEN protect renal function?

CAPOTEN delays the progression of renal insufficiency and reduces the risk of end-stage renal disease or death by more than what would be expected from blood pressure reduction alone.

Can CAPOTEN be used in combination with other medications?

Yes, CAPOTEN is often used in combination with other antihypertensive agents, such as thiazide-type diuretics, beta blockers, and digitalis.

What is the expected market outlook for CAPOTEN in 2025?

The market outlook for CAPOTEN in 2025 is stable, with continued demand due to its established efficacy and long-standing presence in the market, despite potential economic uncertainties.

Sources

1. FDA Label for Capoten Tablets - accessdata.fda.gov
2. PitchBook Releases 2025 Outlooks - businesswire.com
3. Capoten (Captopril): Side Effects, Uses, Dosage, Interactions - rxlist.com
4. CAPOTEN® (Captopril Tablets, USP) Label - accessdata.fda.gov
5. Vanguard Economic and Market Outlook 2025: Global Summary - corporate.vanguard.com