CLINICAL TRIALS PROFILE FOR ADALAT CC

All Clinical Trials for ADALAT CC

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 CC

Condition Name

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

Condition MeSH

Condition MeSH for ADALAT CC
Intervention	Trials
Hypertension	17
Essential Hypertension	3
Renal Insufficiency, Chronic	2
Kidney Diseases	2

Clinical Trial Locations for ADALAT CC

Trials by Country

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

Trials by US State

Trials by US State for ADALAT CC
Location	Trials
North Dakota	2
Arkansas	2
Tennessee	2
South Carolina	1
Rhode Island	1

Clinical Trial Progress for ADALAT CC

Clinical Trial Phase

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

Clinical Trial Status

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

Clinical Trial Sponsors for ADALAT CC

Sponsor Name

Sponsor Name for ADALAT CC
Sponsor	Trials
Bayer	8
Vanderbilt University	2
University of Arkansas	2

Sponsor Type

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

Adalat CC (nifedipine extended-release) clinical trials update, market analysis, and near-term projections (US-focused)

Last updated: May 21, 2026

Adalat CC is an extended-release nifedipine brand with limited visibility of new late-stage trials in the public domain. Commercially, the product competes primarily with generic extended-release nifedipine and alternative antihypertensive regimens; market outlook is driven by generic penetration, payer formulary positioning, and patient persistence rather than new clinical differentiation.

What is Adalat CC and what is its current clinical evidence base?

Adalat CC is an extended-release formulation of nifedipine (a dihydropyridine calcium-channel blocker) used in hypertension and chronic stable angina. The clinical evidence for nifedipine extended-release is largely historical, anchored in comparative efficacy/safety findings and long-established clinical use patterns rather than ongoing phase 3 programs.

Is there evidence of new late-stage (Phase 2/3) trials for Adalat CC specifically?

No current, clearly attributable public late-stage trial pipeline updates for “Adalat CC” as a branded product are available in the public trial registries record set used for routine market monitoring. Observed clinical activity in this therapeutic area is mostly generic development, comparative effectiveness studies, or investigations of other CCB classes or combination strategies rather than new branded Adalat CC phase development.

How do ongoing studies in nifedipine extended-release typically differ from Adalat CC?

When new studies appear for nifedipine ER, they commonly include:

• Comparative pharmacokinetic or bioequivalence work for generic ER products
• Real-world adherence, persistence, and adverse event monitoring
• Safety studies in broader hypertension populations
• Investigations of drug-drug interactions or subgroup risk

These do not typically create incremental branded exclusivity value for Adalat CC.

What clinical trial endpoints and safety issues matter most for nifedipine ER?

For nifedipine ER and closely related CCBs, the clinical monitoring emphasis typically includes:

• Blood pressure lowering efficacy (mean change from baseline; responder rates)
• Angina control endpoints (frequency of angina attacks; use of rescue nitrates)
• Safety: peripheral edema, headache, flushing, dizziness, and reflex tachycardia signals
• Drug discontinuation rates due to tolerability
• Electrolyte and hemodynamic impacts are usually tracked as supportive endpoints in hypertension studies

What safety signals affect switching and persistence in real-world use?

The main real-world drivers of discontinuation and formulary switching are:

• Peripheral edema incidence and severity
• Dosing-timing tolerability (ER profiles reduce peak-related effects versus immediate-release)
• Dose-dependent hypotension or dizziness in older cohorts
• Co-morbidity management (polypharmacy risk)

These factors influence commercial outcomes as much as efficacy.

How does Adalat CC compare with other extended-release nifedipine products clinically?

Clinical differentiation between Adalat CC and generic nifedipine ER is generally not framed as a new efficacy class, because therapeutic effect is tied to nifedipine exposure. If regulatory bioequivalence standards are met, branded and generic ER products are expected to show comparable clinical performance in practice.

Where can meaningful differences still exist?

Commercial and patient-experience differences can still arise from:

• Tablet technology and release profile within ER specifications
• Excipients affecting tolerability
• Patient adherence and pill burden depending on strengths available and dosing instructions
• Payer copay structures and substitution rules

What is the market size for Adalat CC and what drives demand?

Adalat CC is a mature, off-patent branded product in a category dominated by generics. Market demand is primarily a function of:

• Residual brand share vs generic substitution
• Payer coverage for branded products and utilization management
• Geographic formularies and pharmacy substitution practices
• Patient persistence in stable hypertension regimens

What are the main competitors to Adalat CC?

The competitive set is dominated by:

• Generic extended-release nifedipine products (multiple manufacturers)
• Alternative antihypertensives and angina regimens (other CCBs such as amlodipine ER; ACE inhibitors/ARBs; beta blockers; nitrates and antianginals depending on indication)

What does this imply for brand economics?

Brand economics typically decline as generics capture majority share. Unless Adalat CC has special access programs or pricing power in specific payer segments, revenue is usually pressured by:

• Wholesale channel inventory shifts to generics
• Increased substitution at point-of-sale
• Formulary tiering that disadvantages branded nifedipine ER

What is the competitive landscape for nifedipine ER in the US?

The US market for nifedipine extended-release is structurally generic-dominant. Competitive intensity is high due to:

• Low differentiation between ER nifedipine generics
• Multiple ANDA entrants over time
• Formulary normalization around cheapest-available effective CCBs

How is uptake influenced by indication mix?

• Hypertension patients in stable regimens are less likely to switch absent tolerability or payer pressure.
• Chronic stable angina patients sometimes show regimen-specific switching patterns depending on adverse effect profile and clinician preference.

When does Adalat CC lose exclusivity and what does that mean for branded sales?

Adalat CC is a mature brand. Exclusivity and patent protection, to the extent they existed historically, has long since fully matured and is not a basis for forward-looking revenue protection.

What is the practical impact of generic availability on near-term sales?

Near-term branded sales typically track:

• Residual brand share and retention among patients and prescribers who are not substituted
• Copay and formulary dynamics
• Defect-free supply availability in the brand and generic channels

What generic entry risks exist for Adalat CC?

For a mature ER nifedipine brand, generic entry risk is not a forward pipeline issue but an ongoing competitive baseline:

• Additional generic entrants are possible but generally do not change the category’s commercial reality once generic coverage is extensive.
• The larger risk is erosion of remaining brand share through incremental tiering changes and pharmacy substitution protocol enforcement.

What is the FDA regulatory status of Adalat CC and how does it affect commercialization?

Adalat CC is marketed as an FDA-approved extended-release nifedipine product. Regulatory status mainly affects:

• Manufacturing site compliance and product supply continuity
• Labeling stability for dosing and indications
• Ability to maintain brand distribution under current GMP and postmarketing commitments

What labeling and product-format factors can constrain switching?

Switching friction can rise when:

• Prescribers prefer a specific ER profile or strength set
• Patients stabilize on a brand due to perceived tolerability
• Payers require prior authorization for branded products

Are there any Orange Book exclusivities or patent listings that materially affect Adalat CC availability?

No materially protective, currently relevant exclusivity or patent listings are expected to drive near-term branded market protection for Adalat CC in the same way it would for a still-protected modern branded drug. The market behavior is dominated by generic substitution rather than patent lifelines.

How strong is the patent estate for Adalat CC?

For a mature nifedipine ER brand, the practical patent estate strength is low for forward barriers to generic competition. In business terms, the category is structurally open, and differentiation is not protected through ongoing patent-driven exclusivity.

What formulation patents and method-of-use claims could still matter?

Where they exist historically, they typically do not block entry for a generically acceptable ER nifedipine formulation. Remaining relevance is usually limited to:

• Specific manufacturing-process variants
• Rare dosage form specifics tied to proprietary release technologies

In a generic-dominant market, such barriers are typically weak relative to bioequivalence-based entry.

What clinical and regulatory events would most likely move Adalat CC demand in the next 12–24 months?

Expected market-moving events are operational rather than breakthrough science:

• Supply disruptions affecting either brand or key generics
• Payer formulary changes that alter brand vs generic tiering
• Public safety communications or new pharmacovigilance insights about CCB-related adverse events (category-wide)
• Local contracting changes by major pharmacy benefit managers (PBMs)

Near-term market projections for Adalat CC (brand share and demand direction)

Given a generic-dominant category structure and lack of identifiable late-stage branded pipeline that would reset demand, the near-term outlook is typically:

• Continued share pressure from generic extended-release nifedipine
• Revenue stabilization only if branded access remains favorable in certain plans or if substitution frictions persist
• Modest unit growth or decline depending on antihypertensive market growth and patient pool size, but brand units usually decline faster than category units due to substitution

What is the most likely projection shape?

A gradual decline in brand share with potential volatility tied to formulary and supply events. Any growth would likely be episodic and contract-specific rather than driven by new clinical differentiation.

Key takeaways

• Adalat CC clinical activity is largely historical; no clear late-stage branded trial acceleration is evident in public records used for pipeline monitoring.
• Demand is driven by payer coverage, substitution behavior, and patient persistence, not new efficacy evidence.
• Competitive pressure is structurally high due to generic extended-release nifedipine dominance.
• Near-term projections point to continued branded share erosion, with outcomes sensitive to formulary contracting and supply continuity.

FAQs

1) What conditions are treated with Adalat CC?
Hypertension and chronic stable angina.

2) Does Adalat CC have clinical differentiation versus generic nifedipine ER?
Typically not in efficacy terms; differences are mainly tolerability perception, excipients, and release-profile implementation within ER regulatory limits.

3) What adverse effects most influence switching away from nifedipine ER?
Peripheral edema, headache, flushing, dizziness, and dose-tolerability issues.

4) What factors determine whether patients stay on Adalat CC?
Copay tiering, prior authorization requirements, prescriber preference, and perceived tolerability.

5) What would most likely increase Adalat CC utilization quickly?
A payer contracting shift that improves branded access or a temporary supply disruption affecting major generic alternatives.

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References

1. FDA. Drug approvals and labeling for nifedipine extended-release products (Adalat CC). U.S. Food and Drug Administration.
2. ClinicalTrials.gov. Search results for nifedipine extended-release and Adalat CC-related entries. National Library of Medicine.
3. American Heart Association (AHA). Hypertension and angina treatment guidance relevant to calcium-channel blockers. AHA publications.