CLINICAL TRIALS PROFILE FOR FLOMAX

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.

Clinical Trial Conditions for FLOMAX

Condition Name

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

Condition MeSH

Condition MeSH for FLOMAX
Intervention	Trials
Prostatic Hyperplasia	13
Hyperplasia	13
Urinary Retention	10
Kidney Calculi	6

Clinical Trial Locations for FLOMAX

Trials by Country

Trials by Country for FLOMAX
Location	Trials
United States	53
Canada	7
Korea, Republic of	7
Germany	3
Australia	3

Trials by US State

Trials by US State for FLOMAX
Location	Trials
California	5
Georgia	4
Alabama	3
New York	3
Texas	3

Clinical Trial Progress for FLOMAX

Clinical Trial Phase

Clinical Trial Phase for FLOMAX
Clinical Trial Phase	Trials
PHASE3	1
Phase 4	16
Phase 3	6

Clinical Trial Status

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

Clinical Trial Sponsors for FLOMAX

Sponsor Name

Sponsor Name for FLOMAX
Sponsor	Trials
GlaxoSmithKline	6
Boehringer Ingelheim	6
University of Alabama at Birmingham	2

Sponsor Type

Sponsor Type for FLOMAX
Sponsor	Trials
Other	36
Industry	21
U.S. Fed	2

Flomax (tamsulosin) Clinical Trials Update, Market Analysis, and Projection

Last updated: April 28, 2026

What is Flomax in the market and in clinical use?

Flomax is tamsulosin (alpha-1 adrenergic receptor blocker), approved for lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH). The product is marketed in multiple strengths and formulations globally under the tamsulosin hydrochloride brand ecosystem.

Key clinical use pattern:

• Indication focus: symptomatic relief of LUTS/BPH
• Therapeutic class: alpha-1 selective antagonist (tamsulosin has functional selectivity for alpha-1A receptors)

What is the current clinical-trials landscape for tamsulosin/Flomax?

A “Flomax”-labeled pipeline is not the same as “tamsulosin in general.” Most late-stage activity is typically formulation, comparative effectiveness, combination regimens, or post-marketing work because the active ingredient is mature.

Given the constraint to provide complete, accurate information, a full, date-specific “clinical trials update” for “Flomax” requires up-to-date registry pulls and line-item extraction by brand and sponsor. No source set was provided in the prompt, and without registry access or a cited dataset, a complete trials table cannot be produced to the standard expected for investment-grade analysis.

What does the market look like for tamsulosin (Flomax) today?

Market structure

The tamsulosin market behaves like a mature, off-patent small-molecule segment:

• Originator brand exposure declines as generic tamsulosin expands in major markets.
• Brand differentiation tends to persist via formulation, bioavailability claims, and payer contracting, not via new mechanisms.

Competitive set

Competitive pressure comes from:

• Generic tamsulosin hydrochloride and equivalent extended-release formulations
• Competitors in LUTS/BPH include other alpha-blockers and combination regimens, but tamsulosin retains a large share due to long-standing prescribing patterns and class comfort.

Pricing and access dynamics (typical for mature generics)

Commercial drivers commonly include:

• Wholesale and reimbursement compression post-generic entry
• Formulary tiering based on lowest net cost plus patient persistence and safety profile

How do you project Flomax/tamsulosin demand going forward?

Demand projection logic (mature alpha-blocker segment)

A forecast for tamsulosin is usually shaped by:

• BPH prevalence and aging demographics
• Treatment penetration (share of eligible men treated)
• Generic share vs brand retention
• Switching dynamics to other classes (5-alpha-reductase inhibitors, PDE5 inhibitors, combination therapy)
• Safety-driven persistence (orthostatic hypotension and tolerability)

Scenario framework (directional)

For investment decisions, projection is typically reported across:

• Base case: steady growth in total LUTS/BPH-treated population offset by net price erosion
• Upside: sustained persistence in alpha-blocker monotherapy and durable brand pull-through in markets where brand contracting holds
• Downside: accelerated switching to other regimens or further payer tightening that accelerates generic substitution

A numerically precise market forecast (CAGR, TAM/SAM assumptions, or unit and dollar splits by region) requires current market sizing data and trend history by geography. No figures or sourced datasets were provided in the prompt, so a quantified projection cannot be produced without risking inaccuracies.

What patent and exclusivity realities matter for the Flomax economic outlook?

The economic trajectory of Flomax in most jurisdictions is governed by:

• Expired composition-of-matter protection for tamsulosin
• Dependence on any remaining exclusivity only for specific formulation variants (if any)
• Generic competition as the dominant pricing factor

A proper patent/exclusivity mapping requires:

• Specific jurisdiction filings (US, EP, JP, etc.)
• Patent family list and status per member
• Any formulation-specific exclusivities No such patent dataset was provided in the prompt, so a complete, citation-backed patent status report cannot be generated.

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Key Takeaways

• Flomax is tamsulosin, a mature alpha-1 blocker for LUTS/BPH.
• The clinical and commercial story is dominated by generics and lifecycle management, so value drivers skew toward formulation, contracting, and persistence, not new mechanism breakthroughs.
• A complete, date-specific clinical-trials update, plus numerical market projections, needs registry-level and market-size datasets to produce investment-grade figures; they are not present in the prompt.

FAQs

1. Is Flomax the only tamsulosin product that matters for clinical activity?
   No. Most late-stage research and evidence updates are published under sponsors and formulations without always using the Flomax brand label.

2. Why does market growth for tamsulosin often look modest?
   Because generic competition compresses net price and limits brand expansion even as BPH prevalence rises.

3. What drives patient persistence on tamsulosin?
   Symptom relief durability and tolerability, particularly cardiovascular tolerability related to alpha-blockade effects.

4. How do payers usually influence tamsulosin outcomes?
   Through formulary placement, step edits, and net price contracting that favors lowest-cost equivalents.

5. What would change the outlook for Flomax materially?
   A new clinically differentiated formulation with meaningful adherence or safety advantages, or new label expansion that shifts treatment pathways.

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References

1. (No sources were provided in the prompt.)