CLINICAL TRIALS PROFILE FOR ADALAT

All Clinical Trials for ADALAT

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00137501 ↗	Two Dose Regimens of Nifedipine for the Management of Preterm Labor	Terminated	American University of Beirut Medical Center	Phase 3	2003-05-01	Preterm birth is one of the most important causes of perinatal morbidity and mortality worldwide. Prevention and treatment of preterm labor is important, not as an end in itself, but as a means of reducing adverse events for the neonate. A wide range of tocolytics, drugs used to suppress uterine contractions, have been tried. Magnesium sulfate (MgSO4) is the most widely used tocolytic at the American University of Beirut Medical Center despite the fact that an effective tocolytic role of MgSO4 has never been established. Moreover, the currently available data are suggestive of deleterious fetal effects of MgSO4 in the setting of preterm labor to the extent that some authorities are recommending abandoning it for routine use as a tocolytic therapy. Calcium channel blockers have the ability to inhibit contractility in smooth muscle cells. Consequently, nifedipine has emerged as an effective and rather safe alternative tocolytic agent for the management of preterm labor after several studies have shown that the use of nifedipine in comparison with other tocolytics is associated with a more frequent successful prolongation of pregnancy, resulting in significantly fewer admissions of newborns to the neonatal intensive care unit, and is associated with a lower incidence of respiratory distress syndrome. The unequivocal impact of this method of tocolysis on short term postponement of delivery and the opportunity that this provides for affecting in-utero transfer and steroid administration has prompted many investigators to recommend focusing future trials on testing different dose regimens of nifedipine. To the best of the investigators' knowledge, no study comparing two different dose regimens of nifedipine has been previously published in the literature. The objective of their study is to compare the effectiveness of a high versus a low dose regimen in a total of 200 patients admitted with the diagnosis of preterm labor between 24 and 34 weeks of gestation. In addition, the investigators' study will try to assess the safety profile of the 2 dose regimens on the mother and the neonate by assessing a selected number of outcome variables. The data generated will be used to change their protocol for managing patients presenting with threatened preterm delivery and will fill the existing gap regarding the most effective and safest dose regimen of nifedipine in such patients.
NCT00173667 ↗	A Study of Nifecardia SRFC and Adalat OROS in the Treatment of Patients With Essential Hypertension	Unknown status	National Taiwan University Hospital	Phase 4	1969-12-31	Objective: - To evaluate the antihypertensive efficacy of two brands of nifedipine 30mg in patients with hypertension. - To assess the safety of 8 weeks of therapy with two brands of nifedipine 30mg in patients with hypertension. - To study flow-mediated dilatation and oxidative stress in nonsmoker with essential hypertension but without diabetes mellitus or dyslipidemia. Study Design: - Head-to-head, randomized and parallel design. - A total of 60 patients with a clinically confirmed diagnosis of hypertension will provide 30 available patients in each treatment group. - The drugs and dosage will be as follows: Group A: nifedipine 30-60mg once daily (Nifecardia, CCPC) Group B: nifedipine 30-60 mg once daily (Adalat OROS, Bayer) Method: After washout period, the eligible patients will randomly be allocated to receive two brands of nifedipine 30 mg once daily. Each patient will receive two times of ambulatory blood pressure measurement (ABPM) at both entrance and final stages of the study. The patients will also undergo complete clinical evaluation. Therapy dosage will be started at a dose of nifedipine 30 mg once daily. Dosage will be adjusted if systolic blood pressure greater than 140 mmHg or diastolic blood pressure greater than 90 mmHg by office measurement after 4 weeks of treatment. Nifedipine will be increased to 60 mg once daily. The Ambulatory blood pressure measurement will be set to take reading at 1-hour intervals during the 24 hours assessment. Physical examination included the measurement of heart rate and blood pressure. The value will be read on Visit 1 and 3-12 hours after the last dose of nifedipine. Routine laboratory test includes hematology, blood chemistry and urinalysis. Hematology test and fasting blood chemistry test will be measured immediately before the start of treatment and after 8 weeks' treatment or at time of discontinuation. Thiobarbituric acid-reactive substances (TBARS) in patient plasma were measured for oxidative stress and endothelium-dependent flow-mediated vasodilation will also be evaluated. Possible concomitant medication will remain constant throughout the study. The physician will question the patients as to their compliance at each visit. If compliance dose not reach 80%, the subject will be dropped out.
NCT00175682 ↗	Prazosin Vibrostimulation Autonomic Dysreflexia and Spinal Cord Injury Study	Completed	University of British Columbia	N/A	2004-12-01	Sexuality is a high rehabilitative priority for persons following a spinal cord injury (SCI). Sexual acts can lead to autonomic dysreflexia (AD), dangerous consequences such as a sudden increase in blood pressure, severe headache, sweating above the level of the lesion and low heart rate to name a few. Ejaculation in men can provoke these significant symptoms and therefore men and women may refrain from a sexual life and biological parenthood. Adalat is the most common antihypertensive used in fertility clinics to reduce the incidence of AD. It dramatically reduces blood pressure and, therefore, results in side effects such as dizziness, fatigue and weakness. The investigators hypothesize that Minipress® (prazosin HCL), a blood pressure medication, which has a slower and less abrupt suppressive effect on blood pressure, would be a safe, effective and more appropriate medication for use in the outpatient sperm retrieval clinic and potentially for private use.
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.
NCT00593463 ↗	Drug Discrimination in Methadone-Maintained Humans Study 1	Completed	University of Arkansas	Phase 1	2006-09-01	This study involves giving psychoactive drugs intramuscularly (injected into the muscle of the upper arm or the hip) and/or orally, and measuring the subject's ability to tell the difference between one drug and another, as well as measuring the effects of the drugs on mood, physiology (e.g., heart rate, blood pressure, respiration rate) and behavior. Each subject will receive 2-4 of the listed interventions.

Clinical Trial Conditions for ADALAT

Condition Name

Condition Name for ADALAT
Intervention	Trials
Hypertension	14
Essential Hypertension	2
Healthy	2
Bioequivalence	2

Condition MeSH

Condition MeSH for ADALAT
Intervention	Trials
Hypertension	17
Essential Hypertension	3
Proteinuria	2
Obstetric Labor, Premature	2

Clinical Trial Locations for ADALAT

Trials by Country

Trials by Country for ADALAT
Location	Trials
United States	34
China	14
Japan	4
Korea, Republic of	4
United Kingdom	2

Trials by US State

Trials by US State for ADALAT
Location	Trials
North Dakota	2
Arkansas	2
Tennessee	2
Georgia	1
Florida	1

Clinical Trial Progress for ADALAT

Clinical Trial Phase

Clinical Trial Phase for ADALAT
Clinical Trial Phase	Trials
Phase 4	15
Phase 3	2
Phase 2	1

Clinical Trial Status

Clinical Trial Status for ADALAT
Clinical Trial Phase	Trials
Completed	19
Unknown status	5
Recruiting	2

Clinical Trial Sponsors for ADALAT

Sponsor Name

Sponsor Name for ADALAT
Sponsor	Trials
Bayer	8
Shanghai Shyndec Pharmaceutical Co., Ltd.	2
Actavis Inc.	2

Sponsor Type

Sponsor Type for ADALAT
Sponsor	Trials
Other	86
Industry	18
NIH	1

Last updated: April 27, 2026

Adalat (nifedipine): Clinical Trials Update, Market Analysis, and Forward Projection

What is Adalat and what products drive it today?

Adalat is the brand name for nifedipine, a calcium-channel blocker (CCB) used primarily for hypertension and chronic stable angina. In most regulated markets, “Adalat” is associated with oral nifedipine formulations rather than injectable therapies.

Market relevance depends on which nifedipine salt/formulation and release type is approved locally (e.g., immediate-release versus extended-release). Across global markets, nifedipine remains a long-established generic category with limited branded differentiation outside originator lineages.

Key implication for market modeling: “Adalat” pricing and volume are constrained by (1) generic competition, (2) formulation-level substitution, and (3) guideline positioning relative to other first-line or second-line antihypertensive classes.

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What does the clinical-trials picture look like for Adalat (nifedipine)?

For an established generic chemical entity like nifedipine under a long-running brand, the modern clinical-trials footprint is typically dominated by:

• Bioequivalence studies for reformulated or locally approved generics/line extensions
• Comparative effectiveness or safety studies at the class level (CCBs) rather than brand-specific efficacy
• Population or tolerability studies tied to specific release profiles and co-medications
• Special population studies (renal/hepatic impairment, elderly) and protocol updates required for labeling maintenance

A brand-level “Adalat” trials cadence is usually low in absolute terms compared with originator-era investigations because the active ingredient is off-patent in most jurisdictions and development activity shifts to:

• Regulatory compliance,
• Product lifecycle management (release mechanism, excipient systems),
• Patent landscape navigation via reformulation or controlled-release variants.

Practical read for R&D and investment: new clinical claims that change market access for nifedipine brands typically do not require large Phase 3 programs; they more often rely on pharmaceutical development, bridging studies, and label updates.

Clinical-trials update (status): No current, widely reported Phase 3 brand-defining Adalat-specific program is typically evident for nifedipine at brand level; clinical activity is mostly regulatory and formulation-level rather than novel therapeutic development.

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How big is the Adalat market and what is the demand profile?

Nifedipine demand is best modeled as part of the oral CCBs and antihypertensive class market, then apportioned to nifedipine by:

• guideline usage patterns,
• availability of extended-release formulations,
• clinician prescribing habits in key markets (hospital versus outpatient),
• payer formularies and copay bands, and
• local generic penetration.

Category drivers

• Chronic therapy with repeat scripts.
• Periodic utilization spikes due to seasonal cardiovascular admissions and policy-driven prescribing campaigns in some regions.
• Switching between CCBs is common when tolerability or co-morbidity influences choice (edema, headache, hypotension, drug-drug interactions).

Category constraints

• Generic substitution compresses branded net sales.
• Product differentiation is largely formulation-based.
• Clinical benefit is typically “within-class,” limiting ability to win at formulary committees without payor-specific value arguments.

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Where does Adalat sit versus other antihypertensive options?

In most major markets, nifedipine and other CCBs compete with:

• ACE inhibitors (ACEi),
• ARBs,
• thiazide(-like) diuretics,
• beta blockers (selected patients),
• other CCBs such as amlodipine (often used as a once-daily option in practice).

Market behavior

• If extended-release nifedipine offers adherence advantages in a given local label, it can retain share.
• If dosing convenience and side-effect profiles favor alternatives (notably once-daily options), nifedipine share can erode.

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What is the most likely commercial trajectory for Adalat over the next 3 to 5 years?

Because nifedipine is entrenched and widely generic, the base case is low growth in aggregate for branded lines and flat-to-declining if pricing pressure persists. Forward projections should therefore be framed by unit volume stability and net price compression, not by therapeutic expansion.

Base case projection logic

• Volumes: stable to mildly declining as patients switch among generic CCBs.
• Branded net revenue: declines at the rate of price compression and share dilution.
• Share: stable only in geographies where the specific Adalat formulation remains entrenched or where payor rules limit interchange.

3-scenario projection framework (directional)

Scenario	Volume	Net price	Branded net sales direction
Base case	Flat to -2% CAGR	-2% to -4% CAGR	-2% to -5% CAGR
Upside	+1% to +3% CAGR	-1% to -2% CAGR	Flat to -1% CAGR
Downside	-2% to -4% CAGR	-3% to -5% CAGR	-4% to -9% CAGR

What determines which path is realized

• Extent of generic switching in target formularies
• Adoption of alternative CCBs (especially once-daily regimens)
• Any label changes that improve prescriber confidence for specific subpopulations
• Local manufacturing competition affecting supply and reimbursement

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What does the competitive landscape look like for Adalat (nifedipine)?

Competition is typically dominated by:

• Generic nifedipine immediate-release products,
• Generic nifedipine extended-release products,
• Competing CCBs (e.g., amlodipine) depending on country formulary preferences.

Brand survival pattern

• Branded lines persist where the product has a distinct extended-release profile and a stable prescriber base.
• In highly competitive markets, branded net sales often become small relative to generics and are maintained through contracts, tender outcomes, and payer-specific positioning.

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Does Adalat have IP tail risk that affects the market outlook?

For nifedipine brands, IP is usually not the primary driver of current market dynamics. Instead, economics are dominated by:

• generic entry,
• tender cycles and interchange rules,
• reimbursement, and
• product lifecycle management.

Any meaningful market upside would generally require:

• demonstrable differentiation,
• payer-backed clinical value, or
• regulatory label improvements that move usage across patient segments.

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Actionable implications for R&D and investment

If your goal is R&D prioritization for Adalat-like positioning:

• Target formulation-level differentiation (release kinetics, tolerability, adherence) rather than novel clinical efficacy.
• Use bioequivalence and bridging strategies instead of costly late-stage development unless a differentiated clinical claim can be validated.

If your goal is investment positioning in Adalat-related revenues:

• Model net sales on net price erosion and tender pressure rather than on clinical growth.
• Treat Adalat as a cash-flow durability asset with upside tied to localized reimbursement stickiness.

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Key Takeaways

• Adalat is nifedipine, an established oral CCB where contemporary development is usually formulation and regulatory oriented rather than brand-defining Phase 3 innovation.
• The market outlook is constrained by generic substitution and within-class switching, making branded growth typically modest.
• Forward projections are most sensitive to net price compression and formulary/tender dynamics, not to new clinical efficacy breakthroughs.
• Base case direction for branded net sales is typically flat-to-declining over 3 to 5 years.

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FAQs

1) Is Adalat still a growth drug?

It behaves like a mature branded therapy: growth is usually limited and driven by localized formulary/reimbursement dynamics rather than new clinical demand expansion.

2) What drives prescribing for nifedipine today?

Formulation and dosing convenience, tolerability, local label positioning, and payer rules that influence interchange with other CCBs and generic nifedipine products.

3) What kind of trials are most common for nifedipine brands now?

Bioequivalence, bridging studies for new formulations, and label maintenance studies rather than large efficacy trials that create new standards of care.

4) How should market projections be modeled for Adalat?

Use a framework that separates unit volume (tender and switch behavior) from net price (contracting and generic competition).

5) Where is the biggest commercial risk for Adalat?

Price erosion and formulary substitution by other generics or alternative CCBs, which can outpace any volume retention.

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References

[1] American Heart Association. (n.d.). High Blood Pressure (Hypertension).
[2] FDA. (n.d.). Calcium Channel Blockers: Information for Patients and Clinicians.
[3] EMA. (n.d.). Guideline on the requirements for bioequivalence studies.
[4] World Health Organization. (n.d.). Hypertension fact sheets.
[5] National Institute for Health and Care Excellence (NICE). (n.d.). Hypertension in adults: diagnosis and management.