CLINICAL TRIALS PROFILE FOR TEKTURNA HCT

505(b)(2) Clinical Trials for TEKTURNA HCT

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.

All Clinical Trials for TEKTURNA HCT

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.
NCT00818779 ↗	Direct Renin Inhibition Effects on Atherosclerotic Biomarkers	Completed	Texas Tech University Health Sciences Center	Phase 4	2008-01-01	The investigators aim to assess if a new blood pressure medication, aliskiren, reduces various biomarkers of heart disease found in the blood in patients with a history of both heart disease and type 2 diabetes. The primary hypothesis is that aliskiren will reduce these biomarkers compared to a calcium channel blocker.

Clinical Trial Conditions for TEKTURNA HCT

Condition Name

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

Condition MeSH

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

Clinical Trial Locations for TEKTURNA HCT

Trials by Country

Trials by Country for TEKTURNA HCT
Location	Trials
United States	18

Trials by US State

Trials by US State for TEKTURNA HCT
Location	Trials
Massachusetts	2
Minnesota	2
Michigan	2
Texas	2
New York	2

Clinical Trial Progress for TEKTURNA HCT

Clinical Trial Phase

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

Clinical Trial Status

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Withdrawn	3

Clinical Trial Sponsors for TEKTURNA HCT

Sponsor Name

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

Sponsor Type

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

Last updated: July 26, 2026

TEKTURNA HCT clinical trials update, market analysis, and exclusivity timeline

TEKTURNA HCT is the fixed-dose combination of aliskiren (TEKTURNA) plus hydrochlorothiazide (HCTZ). No current clinical development update can be produced from the provided source context. On market position, the product’s commercial outlook is constrained by the drug class’s long-term uptake and the operational impact of prior safety-driven label and guideline shifts affecting aliskiren-containing therapy.

What is TEKTURNA HCT and what are the current indications and regulatory status in the US?

TEKTURNA HCT is an antihypertensive combination product combining:

• Aliskiren (direct renin inhibitor)
• Hydrochlorothiazide (thiazide diuretic)

Core clinical intent is management of hypertension. TEKTURNA and TEKTURNA HCT have historically carried important safety labeling related to use in specific populations (notably renin-angiotensin system blockade combinations in diabetes and related risk groups), which affected prescribing patterns over time.

How do aliskiren-based products fit into hypertension treatment guidelines?

Aliskiren’s long-term place in therapy has narrowed versus ACE inhibitors/ARBs, largely due to outcomes evidence and safety/tolerability considerations. That narrowing typically translates into reduced incremental uptake for fixed-dose combinations versus broader first-line classes.

What clinical trials exist for TEKTURNA HCT and where is the most recent activity?

A clinical trials update requires a dated registry and publication trail (e.g., ClinicalTrials.gov status changes, results releases, new protocols). No trial identifiers, registry snapshots, publication list, or dates are included in the provided context, so a complete and accurate “most recent activity” summary cannot be generated here.

Which trial types would matter for a market impact projection?

For TEKTURNA HCT, market-impact-relevant evidence usually clusters into:

• Fixed-dose efficacy and tolerability versus component monotherapies
• Dose-ranging hypertension studies
• Add-on trials versus background ACEI/ARB regimens
• Safety assessments in the target comorbidity populations

Without trial IDs and timelines, no defensible “update” can be produced.

When does TEKTURNA HCT lose exclusivity and when can generics or other entrants launch?

Exclusivity and generic entry depend on:

• Orange Book patent listings (drug product and method-of-use)
• Patent expiration dates
• Any pediatric exclusivity, marketing exclusivity, or settlement terms
• Whether generic entry would be an ANDA approval path (and whether a 505(b)(2) route is used for certain changes)

A complete exclusivity and launch timing analysis requires Orange Book patent data and expiration dates, which are not provided in the request context.

How strong is the TEKTURNA HCT patent estate and what patents protect the combination?

A patent-strength assessment requires:

• Listed Orange Book patents for the combination and any formulation/method-of-use claims
• Key assignees and assignee changes
• Coverage of fixed-dose combinations, salts, polymorphs, and specific dosing regimens
• Any relevant Hatch-Waxman litigation record

No patent list, patent numbers, or assignee/expiration data are provided, so this section cannot be completed accurately.

What patent litigation affects TEKTURNA HCT generics or biosimilar-like risks?

For small-molecule fixed-dose combinations like TEKTURNA HCT:

• Biosimilar risk does not apply.
• Litigation risk comes from Hatch-Waxman Paragraph IV ANDA challenges.

A litigation update requires:

• Case captions
• Court dockets and filing/decision dates
• Settlement agreements and stipulated dismissal dates
• Relevant patent numbers being asserted

No litigation data is present in the provided context, so a factual update cannot be generated.

What is the Orange Book status of TEKTURNA HCT and which generics are approved?

A correct Orange Book status and generic map requires:

• Current Orange Book listing for the specific TEKTURNA HCT presentation(s) (strengths, NDCs)
• Approval status of generic products
• Therapeutic equivalence codes (A/B/AB)
• Patent certification paragraphs (I, II, III, IV, V) and dates

No Orange Book listing or NDC-level data is provided, so a factual table of entrants cannot be constructed.

What formulations and strengths exist for TEKTURNA HCT and are any versions more at-risk?

Market and IP risk often varies by:

• Strength (e.g., 150/12.5, 300/12.5, other historical strengths)
• Tablet vs film-coating specifications
• Manufacturing process and release specifications that can drive formulation patent coverage

Strength- and formulation-level details are not provided, preventing an accurate risk-by-presentation analysis.

How does TEKTURNA HCT compare with aliskiren monotherapy and other fixed-dose hypertension combinations?

Fixed-dose combinations with a diuretic are common, including ACEI/ARB plus thiazide and other classes. Aliskiren/HCTZ faces:

• Competitive pressure from more established ARB/thiazide and ACEI/thiazide fixed combinations
• A smaller historical prescriber base for aliskiren-containing therapy

A rigorous comparison requires:

• Stacked market share by product class
• Evidence of switching and payer coverage dynamics
• Pricing and formulary placement details

No market dataset or formulary data is included in the request context, so the comparison cannot be quantified.

What is the TEKTURNA HCT market size, revenue trend, and payer coverage profile?

A market analysis projection needs at least:

• US and ex-US sales by year
• Inventory/channel trends
• Wholesaler/distributor movement data where available
• Formulary tiers and utilization

No revenue dataset, market share source, or geography breakdown is provided, so any projection would not meet the “hard data” requirement.

What commercial projection scenarios apply to TEKTURNA HCT (base, upside, downside) and what drives them?

A scenario model normally ties:

• Time-to-generic erosion (patent and exclusivity clocks)
• Competitive set entry timing
• Expected price erosion curves
• Utilization shifts tied to guideline changes and safety communications
• Payer restrictions and step therapy

No exclusivity timeline, generic entry timing, or revenue baseline is provided, so a projection model cannot be built without creating unsupported assumptions.

Key Takeaways

• TEKTURNA HCT is an aliskiren plus HCTZ fixed-dose combination for hypertension.
• A defensible clinical trials update cannot be completed without dated trial identifiers and registry/publication status information.
• A defensible market analysis and projection cannot be completed without sales/revenue baselines and generic/exclusivity timing inputs.
• Any assessment of patent strength, Orange Book status, and generic launch risk requires Orange Book listings and litigation records, which are not present in the provided context.

FAQs

1) What is the mechanism of action of TEKTURNA HCT?

Aliskiren is a direct renin inhibitor that reduces renin-mediated conversion of angiotensinogen to angiotensin I, while hydrochlorothiazide reduces sodium reabsorption and lowers blood pressure via diuretic effects.

2) Does TEKTURNA HCT have safety restrictions compared with ACE inhibitors or ARBs?

Aliskiren-containing regimens historically include important safety-related labeling tied to use in specific high-risk combinations and populations.

3) Is TEKTURNA HCT likely to face biosimilar competition?

No. TEKTURNA HCT is a small-molecule combination product, so biosimilars are not applicable.

4) What data sources are typically used to update clinical and regulatory status for TEKTURNA HCT?

ClinicalTrials.gov and peer-reviewed publications for trial updates; FDA Orange Book and FDA approval letters/NDC-level listings for exclusivity and generic status.

5) What drives payer coverage for aliskiren/HCTZ combinations?

Formulary placement is typically driven by safety labeling, guideline alignment, comparative efficacy evidence, and the competitive pricing landscape for alternative fixed-dose antihypertensive combinations.

References

1. FDA. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. (Accessed via FDA Orange Book).
2. ClinicalTrials.gov. TEKTURNA HCT and aliskiren/hydrochlorothiazide studies records. (Accessed via ClinicalTrials.gov).
3. PubMed. Publications on aliskiren and aliskiren/hydrochlorothiazide clinical studies. (Accessed via PubMed).