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Last Updated: April 4, 2025

CLINICAL TRIALS PROFILE FOR CATAPRES-TTS-3


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All Clinical Trials for CATAPRES-TTS-3

Trial IDTitleStatusSponsorPhaseStart DateSummary
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.
NCT00262470 ↗ Treatment of Orthostatic Intolerance Active, not recruiting National Institutes of Health (NIH) Phase 1/Phase 2 1997-04-01 This trial is designed to study the effects of various mechanistically unique medications in controlling excessive increases in heart rate with standing and in improving the symptoms of orthostatic intolerance in patients with this disorder.
NCT00262470 ↗ Treatment of Orthostatic Intolerance Active, not recruiting Satish R. Raj Phase 1/Phase 2 1997-04-01 This trial is designed to study the effects of various mechanistically unique medications in controlling excessive increases in heart rate with standing and in improving the symptoms of orthostatic intolerance in patients with this disorder.
>Trial ID>Title>Status>Phase>Start Date>Summary
Showing 1 to 4 of 4 entries

Clinical Trial Conditions for CATAPRES-TTS-3

Condition Name

3221000.511.522.53HypertensionDeliriumFecal IncontinencePostoperative Pain[disabled in preview]
Condition Name for CATAPRES-TTS-3
Intervention Trials
Hypertension 3
Delirium 2
Fecal Incontinence 2
Postoperative Pain 1
[disabled in preview] 0
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Condition MeSH

3322000.511.522.53DeliriumHypertensionFecal IncontinencePain, Postoperative[disabled in preview]
Condition MeSH for CATAPRES-TTS-3
Intervention Trials
Delirium 3
Hypertension 3
Fecal Incontinence 2
Pain, Postoperative 2
[disabled in preview] 0
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Clinical Trial Locations for CATAPRES-TTS-3

Trials by Country

+
Trials by Country for CATAPRES-TTS-3
Location Trials
United States 11
United Kingdom 2
Netherlands 1
Brazil 1
Lithuania 1
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Trials by US State

+
Trials by US State for CATAPRES-TTS-3
Location Trials
Minnesota 3
Maryland 2
California 2
Tennessee 2
Pennsylvania 1
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Clinical Trial Progress for CATAPRES-TTS-3

Clinical Trial Phase

45.5%27.3%9.1%18.2%011.522.533.544.55Phase 4Phase 3Phase 2/Phase 3[disabled in preview]
Clinical Trial Phase for CATAPRES-TTS-3
Clinical Trial Phase Trials
Phase 4 5
Phase 3 3
Phase 2/Phase 3 1
[disabled in preview] 2
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Clinical Trial Status

43.8%18.8%18.8%18.7%033.544.555.566.57CompletedWithdrawnRecruiting[disabled in preview]
Clinical Trial Status for CATAPRES-TTS-3
Clinical Trial Phase Trials
Completed 7
Withdrawn 3
Recruiting 3
[disabled in preview] 3
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Clinical Trial Sponsors for CATAPRES-TTS-3

Sponsor Name

trials0112233Mayo ClinicNational Center for Research Resources (NCRR)King's College London[disabled in preview]
Sponsor Name for CATAPRES-TTS-3
Sponsor Trials
Mayo Clinic 3
National Center for Research Resources (NCRR) 2
King's College London 1
[disabled in preview] 1
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Sponsor Type

80.0%11.1%8.9%005101520253035OtherNIHIndustry[disabled in preview]
Sponsor Type for CATAPRES-TTS-3
Sponsor Trials
Other 36
NIH 5
Industry 4
[disabled in preview] 0
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Catapres-TTS-3: Clinical Trials, Market Analysis, and Projections

Introduction

Catapres-TTS-3, a transdermal therapeutic system containing clonidine, is a widely used medication for the management of hypertension. This article delves into the clinical trials, market analysis, and future projections for this drug.

Clinical Trials and Efficacy

Patient Acceptance and Efficacy

Clinical trials have shown that Catapres-TTS-3 is effective in reducing blood pressure in patients with hypertension. A retrospective review of 25 patients indicated that in those with mild to moderate hypertension, Catapres-TTS resulted in significant blood pressure reductions during the initial four weeks of therapy[1].

Blood Pressure Control

In patients where Catapres-TTS was initiated as monotherapy or added to an oral diuretic, significant reductions in both systolic and diastolic blood pressure were observed. However, in patients with more severe hypertension who were already on multiple antihypertensive agents, the reductions were not statistically significant[1].

Adverse Effects

The most common adverse effects associated with Catapres-TTS-3 include localized skin reactions such as erythema, pruritus, and contact dermatitis. These reactions led to treatment discontinuation in about 19% of patients after a mean duration of treatment of 37 weeks[4].

Therapeutic Plasma Levels

Catapres-TTS-3 achieves therapeutic plasma clonidine levels within 2-3 days of application, and these levels remain constant throughout the 7-day patch duration. The system delivers 0.3 mg of clonidine per day, with steady-state plasma concentrations reaching approximately 1.1 ng/mL[4].

Error-Prone Features and Administration Challenges

Labeling and Identification Issues

One of the significant challenges with Catapres-TTS-3 is the lack of clear labeling on the patches, which can lead to medication errors, particularly in long-term care settings. Caregivers may confuse the patch with adhesive bandages or other drug patches, leading to incorrect administration or removal[2].

Patch Application and Removal

The packaging of Catapres-TTS-3 includes an optional white adhesive cover, which can sometimes be mistaken for the actual drug patch. This has resulted in instances where only the cover was applied without the patch containing clonidine[2].

Market Analysis

Global Transdermal Patch Market

The global transdermal patch market, which includes Catapres-TTS-3, is projected to surpass $15 billion by 2026. This growth is driven by the advantages of transdermal drug delivery, such as painless and non-invasive administration, ease of use, and prolonged drug activation[3].

Market Trends and Insights

The market is seeing a continuous rise due to the increasing acceptance and integration of transdermal patches into existing drug delivery methodologies. The report highlights that there are over 100 transdermal patches in clinical trials and 66 commercially available patches, indicating a robust pipeline and market activity[3].

Regional Market Insights

The transdermal patch market is strong in regions such as the US, Europe, and Asia-Pacific. These regions are driving the market growth due to their large patient populations and the increasing demand for convenient and effective drug delivery systems[3].

Projections and Future Outlook

Market Growth

Given the current trends and the ongoing development of new transdermal patches, the market is expected to continue growing. The integration of advanced technologies and the expansion of indications for transdermal patches will further boost the market[3].

Clinical Pipeline

With over 100 transdermal patches in clinical trials, the future looks promising for Catapres-TTS-3 and other similar medications. These trials are expected to introduce new formulations, improve existing ones, and expand the therapeutic applications of transdermal drug delivery[3].

Patient Compliance and Safety

Efforts to improve the labeling and packaging of Catapres-TTS-3 to reduce medication errors are crucial for its future success. Enhancing patient compliance and safety will be key factors in maintaining and growing the market share of this medication[2].

Key Takeaways

  • Efficacy: Catapres-TTS-3 is effective in reducing blood pressure in patients with mild to moderate hypertension.
  • Adverse Effects: Common adverse effects include localized skin reactions and contact dermatitis.
  • Market Growth: The global transdermal patch market is projected to surpass $15 billion by 2026.
  • Challenges: Labeling and packaging issues need to be addressed to reduce medication errors.
  • Future Outlook: The market is expected to grow with ongoing clinical trials and technological advancements.

FAQs

What is Catapres-TTS-3 used for?

Catapres-TTS-3 is a transdermal therapeutic system used for the management of hypertension.

How does Catapres-TTS-3 work?

Catapres-TTS-3 delivers clonidine through the skin, achieving therapeutic plasma levels within 2-3 days and maintaining them for 7 days.

What are the common adverse effects of Catapres-TTS-3?

Common adverse effects include localized skin reactions such as erythema, pruritus, and contact dermatitis.

Why is labeling important for Catapres-TTS-3?

Clear labeling is crucial to avoid medication errors, especially in long-term care settings, as the current patches do not have the name or strength of the drug printed on them.

What is the projected market size for transdermal patches by 2026?

The global transdermal patch market is projected to surpass $15 billion by 2026.

Sources

  1. Patient acceptance of transdermal clonidine - Cleveland Clinic Journal of Medicine[1].
  2. Error-Prone Features of Catapres-TTS - Pharmacy Times[2].
  3. Transdermal Patch Market Study 2020-2026 - Business Insider[3].
  4. Catapres-TTS - FDA Label[4].
  5. Clonidine Patches Drug Quantity Management Policy - Cigna[5].

More… ↓

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