CLINICAL TRIALS PROFILE FOR CARDIZEM

All Clinical Trials for CARDIZEM

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.
NCT00313157 ↗	RATe Control in Atrial Fibrillation	Completed	Asker & Baerum Hospital	Phase 3	2006-04-01	The purpose of this study is to compare the effect of metoprolol, verapamil, diltiazem and carvedilol on ventricular rate, working capacity and quality of life in patients with chronic atrial fibrillation.
NCT00578617 ↗	Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial	Completed	Abbott Medical Devices	N/A	2006-09-01	The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.
NCT00578617 ↗	Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial	Completed	Duke Clinical Research Institute	N/A	2006-09-01	The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.
NCT00578617 ↗	Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial	Completed	St. Jude Medical	N/A	2006-09-01	The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.
NCT00578617 ↗	Ablation vs Drug Therapy for Atrial Fibrillation - Pilot Trial	Completed	Mayo Clinic	N/A	2006-09-01	The CABANA pilot study is designed to test the hypothesis that the treatment strategy of percutaneous left atrial catheter ablation for the purpose of the elimination of atrial fibrillation (AF) is superior to current state-of-the-art therapy with either rate control or anti-arrhythmic drugs for reducing AF recurrences at 1 year follow-up.

Clinical Trial Conditions for CARDIZEM

Condition Name

Condition Name for CARDIZEM
Intervention	Trials
Atrial Fibrillation	4
Atrial Flutter	1
Pulmonary Arterial Hypertension	1
Diltiazim	1

Condition MeSH

Condition MeSH for CARDIZEM
Intervention	Trials
Atrial Fibrillation	4
Hypertension	2
Familial Primary Pulmonary Hypertension	1
Substance-Related Disorders	1

Clinical Trial Locations for CARDIZEM

Trials by Country

Trials by Country for CARDIZEM
Location	Trials
United States	21
Canada	1
Norway	1

Trials by US State

Trials by US State for CARDIZEM
Location	Trials
Minnesota	2
Tennessee	2
West Virginia	1
Florida	1
Texas	1

Clinical Trial Progress for CARDIZEM

Clinical Trial Phase

Clinical Trial Phase for CARDIZEM
Clinical Trial Phase	Trials
Phase 4	2
Phase 3	2
Phase 1	3

Clinical Trial Status

Clinical Trial Status for CARDIZEM
Clinical Trial Phase	Trials
Completed	6
Not yet recruiting	1
Terminated	1

Clinical Trial Sponsors for CARDIZEM

Sponsor Name

Sponsor Name for CARDIZEM
Sponsor	Trials
Mayo Clinic	2
Asker & Baerum Hospital	1
Assiut University	1

Sponsor Type

Sponsor Type for CARDIZEM
Sponsor	Trials
Other	10
Industry	5

CARDIZEM Market Analysis and Financial Projection

Last updated: April 28, 2026

Cardizem (diltiazem): Clinical-Trial Update, Market Analysis, and Projection

What is the current clinical-trial status for Cardizem (diltiazem)?

Cardizem is the brand name for diltiazem, a calcium-channel blocker used for hypertension and certain cardiac indications. In practice, branded “Cardizem” trials track through multiple program filings and legacy sponsor activity, with ongoing registries and limited active interventional studies in the US under the “Cardizem” brand name.

Publicly visible trial activity for diltiazem overall (not brand-restricted):

• Active interventional studies are limited, and most observable activity clusters around:
  • Comparative or observational studies (real-world effectiveness, adherence, switching between formulations).
  • Pharmacokinetic (PK) studies tied to formulation changes (e.g., extended-release vs immediate-release) and drug-product equivalence rather than new clinical entities.
  • Safety surveillance and database-driven analyses.
• Cardiovascular outcomes trials tied to new molecular entities are not typical for diltiazem because the compound is established, off-patent, and widely generic.

Practical implication for investors and R&D planners: the “clinical trial update” for Cardizem is mostly about formulation-level studies and registry work, not new labeled-efficacy expansion.

What do the US label and treatment positioning imply for market dynamics?

Cardizem’s market is shaped by the standard-of-care role of diltiazem in:

• Hypertension (often as part of multi-drug regimens)
• Rate control in certain supraventricular arrhythmias (brand usage overlaps with guideline-driven practice for rate management)
• Chronic stable angina (depending on formulation and physician preference)

Market reality for diltiazem brands:

• Brand versions compete against a large generic supply and physician familiarity with generics.
• Demand is driven by:
  • Formulary positioning in large pharmacy benefit managers (PBMs)
  • Acquisition cost and rebate dynamics
  • Patient-level switching among AB-rated alternatives (other calcium-channel blockers, including verapamil and amlodipine)

How big is the diltiazem market and what is the brand-level outlook for Cardizem?

Market sizing for Cardizem specifically is not cleanly separable from the broader diltiazem class in public datasets, because most reporting aggregates by molecule (diltiazem) and often by immediate-release vs extended-release, with brand identifiers diluted by generic substitution.

For business planning, the decision is not “is the diltiazem market growing,” but “how much brand share can Cardizem hold under generic pressure.” That is determined by:

• Contracting with PBMs and payers
• Persistence of patient cohorts on a specific product
• Pay-for-performance or formulary tiering
• State-level and plan-level generic substitution behavior

Market projection framework for Cardizem (diltiazem)

Because Cardizem is an established small-molecule with broad generic availability, projections should be built around volume retention and pricing erosion, not new uptake from clinical breakthroughs.

1) Volume trend: modest decline or flat-to-slight growth in late-stage branded share

• Expect class volumes to remain stable given guideline use.
• Expect brand volumes to face share dilution as generics continue to be preferred on formularies.

2) Price trend: continued downward pressure

• Branded diltiazem pricing generally tracks:
  • Generic price benchmarks
  • Rebate aggressiveness to maintain formulary position
  • Indexing effects across payer formularies

3) Revenue outcome: brand revenue tends to lag molecule revenue

• Even when molecule prescriptions hold steady, brand revenue often declines due to persistent generic substitution.

What do competitive dynamics look like for diltiazem brands?

Direct competitive set

• Other calcium-channel blockers for hypertension and angina:
  • Dihydropyridines: amlodipine class
  • Non-dihydropyridines: verapamil class
• Rate control alternatives:
  • Beta-blockers (widely used, payer-favored in many settings)
  • Other rhythm-control strategies driven by cardiology practice patterns

Key substitution vectors

• If a plan prefers a specific CCB, diltiazem brand share can shift quickly to the lowest net cost generic or to alternative molecules on tier designations.
• Patient adherence and tolerability drive persistence, but those are not enough to fully offset payer substitution at scale.

What are the plausible outcomes for Cardizem over the next 5 years?

Cardizem’s outlook should be treated as a “defend and rationalize” business, where upside comes from contracting gains or niche persistence, and downside comes from additional generic penetration or tier displacement.

Projection ranges (business-use):

• Base case: branded revenue declines at a slower rate than the initial post-generic era, as the product stabilizes in some formularies.
• Adverse case: branded revenue accelerates downward if pricing concessions fail to maintain tier status.
• Favorable case: branded revenue flattens if Cardizem secures broader managed-care coverage and retains patient cohorts (often limited to specific plans or regional formularies).

How do clinical-trial signals map to commercial outcomes for an old molecule?

For diltiazem, clinical-trial activity tends to support:

• Safety and tolerability confidence in real-world use
• Formulation confidence (extended-release consistency, interchangeability)
• Compliance and switching policies that influence payer coverage

In a mature market, trial activity is less about label expansion and more about reducing payer friction and supporting formulary continuity.

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Key Takeaways

• Cardizem (diltiazem) remains a mature cardiovascular therapy where clinical activity is largely formulation and real-world oriented, not new labeled-efficacy expansion.
• The branded outlook is constrained by broad generic penetration, so revenue performance depends on formulary positioning, rebates, and patient persistence, not scientific differentiation.
• Near-term strategy and projections should focus on defense of net price and tier placement, with expected continued branded share erosion unless payer contracts stabilize.

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FAQs

1. Is Cardizem still used for hypertension and angina?
   Yes. Diltiazem continues to be used in hypertension and angina management per established clinical practice patterns for calcium-channel blockers.

2. Does Cardizem have ongoing Phase 3 trials that could expand its label?
   Brand-referenced, new Phase 3 expansion trials are not typical for an established off-patent molecule. Public activity is more commonly observational, registry-driven, or formulation-related.

3. How does generic competition affect Cardizem sales?
   It drives persistent brand share dilution and net price pressure through payer preference for lower-cost AB-rated generics.

4. What determines Cardizem’s brand-level revenue trajectory?
   The primary drivers are formulary tier placement, PBM contracting, rebate levels, and patient persistence on a specific product.

5. What competitive products most affect Cardizem?
   Other calcium-channel blockers (amlodipine-class, verapamil-class) and rate control alternatives such as beta-blockers, depending on guideline and payer patterns.

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References

[1] ClinicalTrials.gov. Diltiazem studies and trial listings. National Library of Medicine (NLM). https://clinicaltrials.gov/
[2] U.S. Food and Drug Administration. Drug product labeling and prescribing information resources for diltiazem products (Cardizem brand pages and approved labeling repository). https://www.accessdata.fda.gov/