CLINICAL TRIALS PROFILE FOR CARDIZEM SR

All Clinical Trials for CARDIZEM SR

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.

Clinical Trial Conditions for CARDIZEM SR

Condition Name

Condition Name for CARDIZEM SR
Intervention	Trials
Atrial Fibrillation	4
Idiopathic Pulmonary Arterial Hypertension	1
Arrhythmia	1
Pharmacokinetics	1

Condition MeSH

Condition MeSH for CARDIZEM SR
Intervention	Trials
Atrial Fibrillation	4
Hypertension	2
Pulmonary Arterial Hypertension	1
Hypertension, Pulmonary	1

Clinical Trial Locations for CARDIZEM SR

Trials by Country

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

Trials by US State

Trials by US State for CARDIZEM SR
Location	Trials
Tennessee	2
Minnesota	2
Illinois	1
California	1
Alabama	1

Clinical Trial Progress for CARDIZEM SR

Clinical Trial Phase

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

Clinical Trial Status

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Withdrawn	1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

Clinical Trial Sponsors for CARDIZEM SR

Sponsor Name

Sponsor Name for CARDIZEM SR
Sponsor	Trials
Mayo Clinic	2
Kowa Research Institute, Inc.	1
Vanderbilt University	1

Sponsor Type

Sponsor Type for CARDIZEM SR
Sponsor	Trials
Other	10
Industry	5

CARDIZEM SR Market Analysis and Financial Projection

Last updated: April 30, 2026

Cardizem SR (diltiazem hydrochloride) — Clinical Trials Update, Market Analysis, and Projection

What is Cardizem SR and what is the current clinical-development posture?

Cardizem SR is an oral sustained-release formulation of diltiazem hydrochloride, a calcium-channel blocker used for cardiovascular indications such as hypertension and angina (and, depending on jurisdiction and labeling history, other rhythm/heart-rate-related indications).

Because Cardizem SR is an established, long-marketed small-molecule product, clinical-trials activity is dominated by:

• Bioequivalence (BE) studies supporting generic and follow-on formulations
• Occasional formulation/performance studies (release profile, food effects) rather than new phase programs
• Post-marketing observational evidence consolidated in reviews and guideline updates rather than new registrational RCTs

No credible, actionable “live registrational” phase program for Cardizem SR itself is typically the center of market-moving activity at this stage; market shifts usually come from generic entry, label updates, and payer contracting rather than new clinical efficacy milestones.

Which trials exist that can move market perception?

For a mature molecule/formulation like Cardizem SR, the trials with direct commercial relevance are usually:

• BE trials for generic versions of the SR tablet
• Bridging studies for strength changes, manufacturing changes, or alternative release behavior
• Safety/real-world evidence that affects formulary positioning

Actionable marker to track is the cadence of BE/generic filings rather than phase progression. In practice, that means the clinical “update” for Cardizem SR is less about new RCT endpoints and more about whether new entrants are filing and clearing approval thresholds on time.

What is the market context for oral sustained-release diltiazem?

Cardizem SR competes in a therapeutic class with multiple brands and generics across:

• Non-dihydropyridine calcium-channel blockers (diltiazem, verapamil)
• Alternative mechanisms (beta-blockers, dihydropyridine CCBs such as amlodipine)
• Symptom- and comorbidity-based prescribing patterns

Key market realities for an older, high-availability molecule:

• Generic dominance reduces brand economics
• Wholesale acquisition cost compression and payer preference drive substitution
• Formulary tier placement is influenced more by contracting than by new clinical evidence

Where does Cardizem SR sit in the payer-and-prescriber decision tree?

In cardiovascular care, sustained-release formulations are chosen for:

• Dosing convenience relative to immediate-release forms
• Tolerability profile consistent with class experience
• Continuity of therapy for stable patients when switching is operationally burdensome

However, substitution pressure is strong once multiple multisource products exist for the same dosing frequency.

Market Analysis and Projection

How big is the market and what forces shape growth or shrinkage?

A quantitative market size and forecast for “Cardizem SR specifically” is rarely reported cleanly because commercial datasets often consolidate:

• Diltiazem total (all formulations, IR and ER)
• Or CCB class totals
• Or the branded subset without isolating “SR” versus “ER” versus generic equivalents

For forecasting decisions, the correct modeling driver for mature products is typically:

1. Generic penetration and number of labeled multisource SKUs
2. Net price erosion from contracting and PBM formularies
3. Volume stability driven by patient persistence and ongoing incident use
4. Switching dynamics between IR and ER forms and across CCBs

Net: the trajectory for Cardizem SR is generally flat-to-declining in branded units, with modest stabilization possible if dosing persistence remains high and competitors are constrained.

What matters most for 2025-2030 projections?

The main projection levers for Cardizem SR are:

• Additional generic entries (more SKUs, more price pressure)
• Payer preferred drug lists (diltiazem generics vs class alternatives)
• Safety signaling and label positioning (less common at this stage, but any class-wide restrictions can change mix)
• Formulary management that favors lower-cost equivalents

Given typical class and molecule lifecycle patterns, a practical projection expectation is:

• Branded share erosion continues while branded net sales are supported only by residual remaining patients and market access arrangements
• Total diltiazem ER volume can remain steady if incidence and persistence remain steady, even as branded share shrinks

Base-case forecast logic (directional, decision-useful)

Below is a decision-ready directional framework for Cardizem SR rather than a speculative numeric TAM that cannot be reliably separated from diltiazem ER generics using public, consistently reported market datasets.

Driver	2025-2030 Expected Direction	Commercial Impact on Cardizem SR
Generic penetration	Up or stable-high	Down on brand unit share and net price
PBM formularies	Favor lowest-cost multisource	Further brand pressure
Patient persistence	Stable (class familiarity)	Limits volume collapse, but not share erosion
Class competition (other CCBs, beta-blockers)	Substitution continues	Mix shift away from diltiazem in some cohorts
Regimen simplification	ER advantage persists	Maintains baseline ER category use

Projection headline: Cardizem SR is likely to show declining branded net sales with volume stability at best, while total category may remain stable. Any upside scenario depends on label expansion or sustained payer preference, which is atypical for a mature, well-substituted molecule.

Clinical Trials Update: What to monitor next

BE and manufacturing change watchlist

For a mature SR formulation, the “clinical update” that matters for competitive pressure is:

• New generic ANDAs/approvals referencing diltiazem ER/SR strengths
• BE study results clearing interchangeability
• Manufacturing site changes that require bridging studies

In business terms, if BE approvals accelerate, the market impact typically shows up first in price erosion and then in brand volume contraction.

Safety and label updates

For decision-makers, track:

• Any FDA label changes impacting class usage restrictions
• Any new boxed warnings or strengthened warnings would be rare but market-moving if they occur
• Any new guidance from major cardiology groups that changes first-line preferences across CCB subclasses

Investment and R&D Implications

What does this mean for downstream development?

If Cardizem SR itself is not the basis of new R&D, then the competitive strategy is usually one of these:

• Next-generation diltiazem formulations with better release profiles, reduced GI effects, or improved adherence
• Combination products (less common for diltiazem, more common for other cardiovascular agents)
• Digital adherence or persistence programs to reduce discontinuation and switching (execution-heavy, not patent-blocking)

Where can patent value still exist in the ecosystem?

For established molecules, patent value usually migrates to:

• Formulation patents (polymorphs, release-control matrices)
• Method-of-use under narrower patient subsets (if supported by credible data)
• Regulatory exclusivities tied to specific changes (rare for old products)

Cardizem SR, as a legacy brand, typically does not offer a near-term “patent catalyst” similar to a new chemical entity.

Key Takeaways

• Cardizem SR is a mature diltiazem hydrochloride sustained-release product; commercial dynamics are driven primarily by generic substitution and payer contracting, not new phase clinical breakthroughs.
• The clinical “update” that matters is mainly bioequivalence and follow-on formulation activity, plus any label or safety changes with class-wide impact.
• The market outlook for Cardizem SR is generally brand-declining with possible volume stability due to persistence in treated cohorts.
• Near-term market movement is most likely to come from continued generic entry and net price compression rather than new clinical efficacy data.

FAQs

1. Is Cardizem SR still undergoing phase 3 or registrational trials?
   Not typically as a market-moving driver for the original branded product; activity is usually BE and formulation-related in a mature therapeutic category.

2. What is the main competitive threat to Cardizem SR?
   Multisource generic diltiazem SR/ER products and payer selection of lower-cost equivalents.

3. Does sustained-release diltiazem protect Cardizem SR from substitution?
   It supports persistence but does not stop substitution once equivalent multisource products exist on formularies.

4. What clinical events would be most market-moving?
   Any FDA label change that restricts use, or any new high-impact guidance shifting first-line preferences across CCB classes.

5. How should projections be modeled for Cardizem SR?
   Use generic penetration, net price erosion, PBM formulary dynamics, and persistence/continuation rates rather than expecting RCT-driven demand shocks.

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References

[1] FDA. Drugs@FDA: Cardizem SR (diltiazem hydrochloride) product information and approvals. https://www.accessdata.fda.gov/scripts/cder/daf/
[2] FDA. Drugs@FDA: Search results for diltiazem hydrochloride extended-release and sustained-release products (for ANDA and approval history context). https://www.accessdata.fda.gov/scripts/cder/daf/
[3] DailyMed. Cardizem SR (diltiazem hydrochloride) prescribing information (label data, indications, and safety text). https://dailymed.nlm.nih.gov/
[4] National Library of Medicine. ClinicalTrials.gov: diltiazem sustained release studies (for BE/formulation and any ongoing observational trial context). https://clinicaltrials.gov/