CLINICAL TRIALS PROFILE FOR TRACLEER

All Clinical Trials for Tracleer

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00071461 ↗	Efficacy and Safety of Oral Bosentan in Patients With Idiopathic Pulmonary Fibrosis	Completed	Actelion	Phase 2/Phase 3	2003-08-01	Endothelin-1 (ET-1) is expressed in a variety of pulmonary pathological conditions including pulmonary vascular disease and pulmonary fibrosis. Bosentan (an oral dual ET-1 receptor antagonist) could delay the progression of idiopathic pulmonary fibrosis (IPF), a condition for which no established treatment is available. The present trial investigates a possible use of bosentan, which is currently approved for the treatment of symptoms of pulmonary arterial hypertension (PAH) WHO class III and IV, to a new category of patients suffering from IPF. It was decided to offer Open Label treatment (bosentan) for patients willing to continue in the BUILD 1 study.
NCT00080457 ↗	Safety and Efficacy Study of Sitaxentan Sodium (Thelin™) in Patients With Pulmonary Arterial Hypertension	Completed	Encysive Pharmaceuticals	Phase 3	2003-05-01	The purpose of this study is to evaluate the safety and efficacy of Thelin™ (sitaxsentan sodium) compared to placebo (sugar pill) in the treatment of patients with pulmonary arterial hypertension (PAH).
NCT00082186 ↗	The Effect of Tracleer® on Male Fertility	Completed	Actelion	Phase 4	2003-07-01	The objective of the study is to evaluate the effects of chronic TRACLEER® treatment on testicular function via semen analysis in male patients with primary pulmonary arterial hypertension (PAH).
NCT00086463 ↗	Trial of Iloprost Inhaled Solution as Add-On Therapy With Bosentan in Subjects With Pulmonary Arterial Hypertension (PAH)	Completed	Actelion	Phase 2	2004-06-01	The purpose of this study is to determine the safety and efficacy of Iloprost in subjects that have Pulmonary Arterial Hypertension who are concurrently taking bosentan (Tracleer TM).
NCT00091715 ↗	Efficacy and Safety of Oral Bosentan in Pulmonary Arterial Hypertension Class II	Completed	Actelion	Phase 3	2004-04-01	The present trial investigates a possible use of oral bosentan, which is currently approved for the treatment of symptoms of pulmonary arterial hypertension (PAH) Class III and IV, to patients suffering from PAH Class II.
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 Tracleer

Condition Name

Condition Name for Tracleer
Intervention	Trials
Pulmonary Arterial Hypertension	13
Pulmonary Hypertension	5
Hypertension	4
Idiopathic Pulmonary Fibrosis	4

Condition MeSH

Condition MeSH for Tracleer
Intervention	Trials
Hypertension	26
Pulmonary Arterial Hypertension	20
Familial Primary Pulmonary Hypertension	17
Hypertension, Pulmonary	12

Clinical Trial Locations for Tracleer

Trials by Country

Trials by Country for Tracleer
Location	Trials
United States	82
Germany	18
Canada	16
France	11
United Kingdom	10

Trials by US State

Trials by US State for Tracleer
Location	Trials
California	10
Texas	9
Colorado	6
Alabama	6
New York	5

Clinical Trial Progress for Tracleer

Clinical Trial Phase

Clinical Trial Phase for Tracleer
Clinical Trial Phase	Trials
PHASE1	1
Phase 4	13
Phase 3	7

Clinical Trial Status

Clinical Trial Status for Tracleer
Clinical Trial Phase	Trials
Completed	31
Unknown status	5
Terminated	4

Clinical Trial Sponsors for Tracleer

Sponsor Name

Sponsor Name for Tracleer
Sponsor	Trials
Actelion	22
Encysive Pharmaceuticals	2
Radboud University	2

Sponsor Type

Sponsor Type for Tracleer
Sponsor	Trials
Other	36
Industry	28
NIH	2

TRACLEER (bosentan) — Clinical Trials Update, Market Analysis, and Projection

Last updated: April 27, 2026

What is TRACLEER and how is it positioned today?

TRACLEER is bosentan, an oral endothelin receptor antagonist (ERA) used in pulmonary arterial hypertension (PAH) and to reduce the risk of clinical worsening events in adult patients with PAH. The current commercial thesis is mature, with primary demand tied to PAH treated populations, persistence/line-of-therapy dynamics, and geographic reimbursement.

Core indications (label basis):

• PAH (adults):
  • WHO Group 1 pulmonary arterial hypertension
  • Used to reduce morbidity and delay clinical worsening
• Functional class focus: label-based use across symptomatic PAH, typically informed by risk stratification and combination therapy practice.

What clinical-trial activity matters now for TRACLEER?

TRACLEER’s major pivots occurred earlier in PAH clinical development. In the modern cycle, “updates” are less about new phase starts and more about:

• post-authorization evidence (registry-like datasets, long-term extensions, real-world persistence and safety)
• comparison/combination optimization against newer PAH standards (prostacyclin pathway agents, sGC stimulators, and other ERAs)

Clinical development profile (high-level)

Bosentan development historically built the PAH foundation via:

• randomized evidence establishing efficacy in PAH outcomes
• long-term studies supporting durability and safety monitoring requirements (notably liver enzyme monitoring and hematologic surveillance practices)

Regulatory and safety monitoring remains a key “trial-like” operational constraint

Even without new late-stage pivotal trials, TRACLEER’s safety program drives clinical workflows:

• liver monitoring is standard-of-care for bosentan use
• hematology and drug interaction management affects tolerability and adherence

This monitoring burden influences patient retention and prescriber preference versus newer agents with different monitoring profiles.

What does TRACLEER’s market look like by geography and channel?

Bosentan is widely genericized in many markets, which compresses pricing and shifts strategy toward:

• portfolio management in PAH (brand survival where protected or where fewer generics penetrate)
• channel contracting and payor-specific formularies
• tender outcomes and hospital buying dynamics where PAH care is institutionalized

Market structure

• Brand economics: TRACLEER brand value is constrained by generic entry.
• Generic dominance: In most mature PAH markets, bosentan is priced as a commoditized chronic therapy.
• Competitive set: current PAH standards compete across multiple mechanisms:
  • prostacyclin pathway agents
  • soluble guanylate cyclase (sGC) stimulators
  • other endothelin pathway options (including ambrisentan and macitentan)
  • combination regimens that target risk reduction

Demand drivers

• PAH prevalence and diagnosis rates
• payer coverage and formularies
• patient switching behavior driven by:
  • tolerability and monitoring burden
  • perceived efficacy in risk-stratified subgroups
  • drug interaction management

Primary constraints

• pricing erosion post-generic entry
• treatment guideline evolution that favors newer ERAs or combination approaches in many settings
• monitoring and real-world adherence friction tied to liver enzyme requirements

How does TRACLEER compete versus modern PAH therapies?

TRACLEER’s competitive position is mainly about ERAs in established PAH treatment algorithms, but with two practical disadvantages versus several newer options:

1. Monitoring and clinical workflow burden can reduce initiation and persistence.
2. Evolving standard-of-care increasingly uses newer agents as first-line or backbone therapy in many markets.

Relative mechanism positioning

• TRACLEER (bosentan): broad endothelin receptor blockade (both ETA and ETB).
• Competitors:
  • other ERAs with different receptor selectivity profiles
  • pathway-specific agents for prostacyclin and NO-sGC axes, frequently preferred for risk reduction strategies.

What is the market outlook and projection path?

TRACLEER’s projection follows a predictable mature-drug curve:

• near-term: stable-to-declining volumes depending on PAH diagnosis and generic penetration intensity
• medium-term: continued erosion of brand share where generic substitution is complete, with modest stability in geographies where channel contracting sustains basket share
• long-term: growth in treated population may be offset by mechanism shifts toward newer PAH agents and combination standards

Projection framework (directional, decision-grade)

Use three variables to model TRACLEER-like assets in mature PAH:

1. PAH treated population growth (diagnosis and survival improvements)
2. Mechanism preference shift (erosion from newer PAH agents)
3. Pricing pressure (generic and tender compression)

For TRACLEER, the net effect is typically:

• Volume: slight growth or flat-to-decline depending on local substitution dynamics
• Net revenue: decline-driven by pricing, with potential stability in markets where reimbursement holds

Business implications for R&D and investment decisions

1) TRACLEER is a “monitoring-constrained” chronic therapy

The safety program and drug interaction handling materially affect:

• time-to-initiation
• adherence
• switching rates

This matters for any attempt to expand IP or develop lifecycle strategy because real-world usability drives retention.

2) The commercial upside is limited by generic pricing

Late-cycle brand value in bosentan is structurally capped where generic substitution is widespread.

3) Best ROI is comparative positioning, not mechanism novelty

If a sponsor is considering downstream assets or line extensions, the highest-value angle usually comes from:

• improved dosing convenience
• reduced monitoring burden
• better interaction management
• targeted subgroup evidence for PAH risk phenotypes

Key metrics to track for TRACLEER (operational dashboard)

For quarterly decisioning, track:

• market share by mechanism class (ERA vs other PAH backbones)
• net price vs tender index in institutional procurement markets
• persistence (time on therapy) as liver-monitoring adherence changes
• switching drivers (side effects, interactions, formulary changes)
• formulary status across top payers in each geography

Key Takeaways

• TRACLEER (bosentan) remains an ERA backbone in PAH algorithms, but its market is mature and heavily shaped by generic pricing and real-world monitoring friction.
• Clinical “updates” in the current era are mainly post-authorization evidence and practice-based outcomes rather than new pivotal programs.
• Market projection trends toward stable-to-declining brand value, with volume limited by substitution and mechanism preference drift toward newer PAH agents.
• The operational determinant of performance is payer and channel positioning plus persistence, not late-stage efficacy innovation.

FAQs

1) Is TRACLEER still used as monotherapy in PAH?
It is used within label-based PAH frameworks, but real-world use commonly aligns with risk stratification and combination therapy practices driven by current guideline patterns.

2) What is the biggest driver of TRACLEER discontinuation risk?
The bosentan liver-monitoring workflow and drug interaction management can increase friction, affecting persistence.

3) How does generic entry typically change TRACLEER pricing?
It compresses branded net price through substitution and tender-based procurement, shifting performance toward remaining differentiated channels and contracts.

4) What PAH drug classes most strongly compete with TRACLEER?
Other ERAs and agents targeting the prostacyclin and NO-sGC pathways, which are often favored in combination regimens for risk reduction.

5) Does PAH incidence growth guarantee TRACLEER revenue growth?
No. Treated-population growth can be offset by mechanism preference shift and pricing erosion from generic and competitive substitution.

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References

[1] FDA. Tracleer (bosentan) prescribing information. U.S. Food and Drug Administration.
[2] EMA. Tracleer (bosentan) summary of product characteristics (SmPC). European Medicines Agency.
[3] ClinicalTrials.gov. Bosentan (TRACLEER) interventional studies and related records. U.S. National Library of Medicine.