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Last Updated: March 28, 2024

CLINICAL TRIALS PROFILE FOR TEKTURNA


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505(b)(2) Clinical Trials for TEKTURNA

This table shows clinical trials for potential 505(b)(2) applications. See the next table for all clinical trials
Trial Type Trial ID Title Status Sponsor Phase Start Date Summary
New Indication NCT01417104 ↗ Aliskiren Effect on Aortic Plaque Progression Terminated Novartis Phase 2/Phase 3 2009-10-01 This study is being done to assess the effectiveness of short term (~9 months) Aliskiren/Placebo therapy to slow down the progression of atherosclerotic disease in thoracic and abdominal aorta. This will be checked by comparing before and after therapy magnetic resonance imaging (MRI) pictures of the aortic wall. Aliskiren is an FDA approved drug for hypertension but in this study is used for a new indication. Recent studies with animals have shown that Aliskiren therapy reduces the atherosclerotic plaque. Therefore, in this study, the investigators would like to evaluate whether the investigational drug Aliskiren, which is not FDA approved for this indication has the same beneficial effects in people with atherosclerotic disease.
New Indication NCT01417104 ↗ Aliskiren Effect on Aortic Plaque Progression Terminated Ohio State University Phase 2/Phase 3 2009-10-01 This study is being done to assess the effectiveness of short term (~9 months) Aliskiren/Placebo therapy to slow down the progression of atherosclerotic disease in thoracic and abdominal aorta. This will be checked by comparing before and after therapy magnetic resonance imaging (MRI) pictures of the aortic wall. Aliskiren is an FDA approved drug for hypertension but in this study is used for a new indication. Recent studies with animals have shown that Aliskiren therapy reduces the atherosclerotic plaque. Therefore, in this study, the investigators would like to evaluate whether the investigational drug Aliskiren, which is not FDA approved for this indication has the same beneficial effects in people with atherosclerotic disease.
New Indication NCT01417104 ↗ Aliskiren Effect on Aortic Plaque Progression Terminated Sanjay Rajagopalan Phase 2/Phase 3 2009-10-01 This study is being done to assess the effectiveness of short term (~9 months) Aliskiren/Placebo therapy to slow down the progression of atherosclerotic disease in thoracic and abdominal aorta. This will be checked by comparing before and after therapy magnetic resonance imaging (MRI) pictures of the aortic wall. Aliskiren is an FDA approved drug for hypertension but in this study is used for a new indication. Recent studies with animals have shown that Aliskiren therapy reduces the atherosclerotic plaque. Therefore, in this study, the investigators would like to evaluate whether the investigational drug Aliskiren, which is not FDA approved for this indication has the same beneficial effects in people with atherosclerotic disease.
>Trial Type >Trial ID >Title >Status >Phase >Start Date >Summary

All Clinical Trials for TEKTURNA

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.
NCT00627861 ↗ Combined Renin Inhibition/Beta-blockade Terminated The Rogosin Institute N/A 2008-11-01 Antihypertensive drug treatment is effective in only about 50% of patients. One mechanism responsible for treatment failure is a drug related stimulation of the renin-angiotension-aldosterone-system (RAAS). Several classes of medications that treat hypertension by blocking the RAAS system have been developed. However, the kidney responds to these drug treatments by producing greater amounts of renin. This high level of renin can reduce the effectiveness of some of these medications, ultimately causing the blood pressure to rise. This is one reason why blood pressure can be difficult to control in a certain percentage of patients. The hypothesis to be tested in the proposed study is that beta-adrenergic blockade (β-blockade), when superimposed upon aliskiren, a drug that competitively inhibits plasma renin activity (PRA) but stimulates the release of renin by the kidneys (plasma renin concentration [PRC]), can suppress the reactive increase in PRC that occurs during aliskiren monotherapy. The primary aim of this study is to measure plasma renin concentration (PRC) and plasma renin activity (PRA) levels during renin inhibition with aliskiren and combined renin inhibition/β-blocker treatment to determine whether the addition of a β-blocker attenuates the rise in plasma renin concentration (PRC). A secondary aim is to determine whether combined treatment further suppresses PRA and blood pressure.
NCT00773084 ↗ Aliskiren and Renin Inhibition in Diastolic Heart Failure Withdrawn Texas Tech University Health Sciences Center N/A 2008-09-01 This study is being conducted to compare the effects that 2 different combinations of heart failure medications have on the levels of certain blood markers which cause and/or worsen heart failure. Additionally, the investigators will investigate any differences that may exist between Hispanics and Non-Hispanics. The investigators hope to find that Hispanic Americans will have a greater response to this new regimen compared to non-Hispanic Americans.
>Trial ID >Title >Status >Phase >Start Date >Summary

Clinical Trial Conditions for TEKTURNA

Condition Name

Condition Name for TEKTURNA
Intervention Trials
Hypertension 6
Diabetes 2
Diabetes Mellitus 2
Kidney Disease 1
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Condition MeSH

Condition MeSH for TEKTURNA
Intervention Trials
Hypertension 6
Diabetes Mellitus 3
Kidney Diseases 3
Glomerulonephritis, Membranous 2
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Clinical Trial Locations for TEKTURNA

Trials by Country

Trials by Country for TEKTURNA
Location Trials
United States 18
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Trials by US State

Trials by US State for TEKTURNA
Location Trials
Massachusetts 2
Minnesota 2
Michigan 2
Texas 2
New York 2
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Clinical Trial Progress for TEKTURNA

Clinical Trial Phase

Clinical Trial Phase for TEKTURNA
Clinical Trial Phase Trials
Phase 4 10
Phase 3 1
Phase 2/Phase 3 1
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Clinical Trial Status

Clinical Trial Status for TEKTURNA
Clinical Trial Phase Trials
Terminated 8
Completed 5
Withdrawn 3
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Clinical Trial Sponsors for TEKTURNA

Sponsor Name

Sponsor Name for TEKTURNA
Sponsor Trials
Novartis 7
Novartis Pharmaceuticals 3
Vanderbilt University 2
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Sponsor Type

Sponsor Type for TEKTURNA
Sponsor Trials
Other 22
Industry 11
NIH 2
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