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Last Updated: December 23, 2024

CLINICAL TRIALS PROFILE FOR FLOMAX


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All Clinical Trials for FLOMAX

Trial ID Title Status Sponsor Phase Start Date Summary
NCT00209131 ↗ Efficacy of Flomax to Improve Stone Passage Following Shock Wave Lithotripsy Terminated Emory University N/A 2005-04-01 The majority of kidney stones are treated with shock wave lithotripsy (SWL). We are examining if the medication Flomax will result in improved stone passage rates following SWL.
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.
NCT00244309 ↗ Study of Tamsulosin and/or Dutasteride to Relieve Urinary Symptoms After Brachytherapy for Localized Prostate Cancer Completed GlaxoSmithKline Phase 3 2005-11-01 The purpose of this study is to determine whether a drug named tamsulosin (Flomax), or another drug named dutasteride (Avodart), or a combination of these two drugs is effective in improving urinary symptoms and decreasing the rate of intermittent self-catheterization after prostate brachytherapy.
>Trial ID >Title >Status >Phase >Start Date >Summary

Clinical Trial Conditions for FLOMAX

Condition Name

Condition Name for FLOMAX
Intervention Trials
Benign Prostatic Hyperplasia 6
Prostatic Hyperplasia 6
Urinary Retention 4
Lower Urinary Tract Symptoms 3
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Condition MeSH

Condition MeSH for FLOMAX
Intervention Trials
Hyperplasia 13
Prostatic Hyperplasia 13
Urinary Retention 10
Calculi 6
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Clinical Trial Locations for FLOMAX

Trials by Country

Trials by Country for FLOMAX
Location Trials
United States 52
Korea, Republic of 7
Canada 7
Australia 3
Germany 3
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Trials by US State

Trials by US State for FLOMAX
Location Trials
California 5
New Jersey 3
Alabama 3
New York 3
Texas 3
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Clinical Trial Progress for FLOMAX

Clinical Trial Phase

Clinical Trial Phase for FLOMAX
Clinical Trial Phase Trials
Phase 4 16
Phase 3 6
Phase 2/Phase 3 2
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Clinical Trial Status

Clinical Trial Status for FLOMAX
Clinical Trial Phase Trials
Completed 28
Terminated 5
Unknown status 5
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Clinical Trial Sponsors for FLOMAX

Sponsor Name

Sponsor Name for FLOMAX
Sponsor Trials
GlaxoSmithKline 6
Boehringer Ingelheim 6
Maine Medical Center 2
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Sponsor Type

Sponsor Type for FLOMAX
Sponsor Trials
Other 35
Industry 21
U.S. Fed 2
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