CLINICAL TRIALS PROFILE FOR CARDIZEM LA

All Clinical Trials for CARDIZEM LA

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.

Clinical Trial Conditions for CARDIZEM LA

Condition Name

Condition Name for CARDIZEM LA
Intervention	Trials
Atrial Fibrillation	4
Familial Primary Pulmonary Hypertension	1
FESS	1

Condition MeSH

Condition MeSH for CARDIZEM LA
Intervention	Trials
Atrial Fibrillation	4
Hypertension	2
Heart Failure	1

Clinical Trial Locations for CARDIZEM LA

Trials by Country

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

Trials by US State

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

Clinical Trial Progress for CARDIZEM LA

Clinical Trial Phase

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

Clinical Trial Status

Clinical Trial Status for CARDIZEM LA
Clinical Trial Phase	Trials
Completed	6
Terminated	1
Unknown status	1

Clinical Trial Sponsors for CARDIZEM LA

Sponsor Name

Sponsor Name for CARDIZEM LA
Sponsor	Trials
Mayo Clinic	2
St. Jude Medical	1
Medtronic	1

Sponsor Type

Sponsor Type for CARDIZEM LA
Sponsor	Trials
Other	10
Industry	5

Clinical Trials Update, Market Analysis, and Projection for Cardizem La

Last updated: April 28, 2026

What is Cardizem LA and what is its current clinical context?

Cardizem LA is an extended-release formulation of diltiazem, a non-dihydropyridine calcium channel blocker used for hypertension and angina (and, in some markets/labels, other rate-control indications). Cardizem is marketed by Boehringer Ingelheim for the US brand product line; “LA” denotes the extended-release dosing form.

A “clinical trials update” for Cardizem LA specifically is constrained by the fact that diltiazem as a molecule is long out of patent in major jurisdictions and most contemporary registrational programs focus on:

• new combinations (generic or brand),
• new formulations (including generics),
• new use cases (rarely with brand-specific enrollment), or
• comparative effectiveness studies using older active ingredients.

As a result, trial activity for Cardizem LA as a stand-alone branded extended-release product is typically not the driver of new evidence, while evidence for diltiazem (including extended-release dosing) continues through post-marketing studies, comparative trials, and guideline-based practice updates.

What do recent registrational-style trial signals typically look like for an old, non-protected molecule?

For an off-patent small-molecule cardiovascular drug like diltiazem, “updates” in the clinical pipeline usually come from:

• Generic bioequivalence work for extended-release versions
• Comparative trials versus other antihypertensives or antianginals (often pragmatic designs)
• Real-world evidence from claims/EHR registries
• Safety and tolerability updates, especially in comorbidity cohorts

Under this structure, trial visibility for a branded ER product such as Cardizem LA tends to be indirect: evidence accrues for diltiazem ER in aggregate rather than for the brand itself.

What is the market structure for Cardizem LA (brand vs generic) and why it matters for projections

Competitive reality

Cardizem LA faces a dominant generic substitution environment for diltiazem extended-release. Extended-release oral calcium channel blockers are widely available as generics, which compresses unit economics and market share for the brand unless:

• there is persistent brand preference in specific prescriber channels, or
• payer policies create short windows of brand coverage, or
• a differentiated patient segment remains strongly routed to the brand.

Key demand drivers

The ongoing demand for diltiazem ER is driven by:

• prevalence of hypertension and chronic stable angina
• clinician familiarity with diltiazem for patients needing rate control while avoiding some dihydropyridine-associated effects
• long-term switching dynamics within class (diltiazem vs verapamil vs dihydropyridines)

Key headwinds

• Generic price pressure
• Therapeutic class substitution based on payer formularies
• shifts toward other regimens depending on guideline emphasis and patient comorbidities

How should market forecasts be modeled for Cardizem LA? (Projection framework)

A practical forecast for a brand like Cardizem LA requires modeling at the intersection of:
1) Total class demand for diltiazem ER
2) Brand share versus generics
3) Price erosion and net revenue changes under payer rebates
4) Volume effects from persistence, switching, and adherence

A typical off-patent branded outlook is:

• Class volume growth tracks population and hypertension/angina incidence trends, but
• Brand volume declines with substitution until share stabilizes, and
• Brand net revenue trends track price compression, partially offset by adherence/persistence effects.

Market projection (high-level directional path)

Base case: continued share erosion with stabilization

• Brand share continues to erode versus generics.
• Volume trends modestly down or flat as existing patients continue therapy.
• Net revenue declines with ongoing price pressure and rebate intensity, with a possible deceleration after the most aggressive substitution wave.

Downside case: payer-driven further displacement

• More formulary movement to generics with tier tightening.
• Increased utilization of alternatives (including other calcium channel blockers and fixed-dose strategies).
• Brand volume declines faster than class volume.

Upside case: payer exception channels

• If payer exceptions and prescriber preference keep a stable niche (for tolerability or patient history), brand share stabilizes earlier.
• Revenue decline slows.

What do business users need to decide now? (Actionable implications)

1) Treat Cardizem LA as a cash-flow brand rather than a growth asset. The core expectation is maintenance of a remnant share, not expansion.
2) Scenario-plan net revenue using class stability plus share erosion, then stress price and rebate.
3) Monitor payer formulary dynamics for sustained brand placement. For off-patent oral cardiovascular therapies, formulary changes are often the marginal driver of near-term revenue movement.

What is the clinical relevance for R&D planning?

For pipeline planning, Cardizem LA is a reference point for:

• established dosing in extended-release form
• safety/tolerability expectations in real-world populations
• class-level evidence used by prescribers and formularies

The “clinical update” utility for decision-making usually lies in understanding where diltiazem ER maintains patient utility versus where practice patterns have shifted to alternatives.

Key Takeaways

• Cardizem LA is an extended-release diltiazem brand; clinical activity in registrational sense is usually limited because the molecule is off-patent.
• Evidence growth is mostly class-wide and post-marketing, not brand-specific new pivotal trials.
• Market outlook is structurally dominated by generic substitution, meaning projections should be driven by payer policy, rebate pressure, and brand share erosion, not molecule breakthroughs.
• Forecasts should model class demand stability plus declining brand share and net price pressure, with downside tied to further formulary tier movement.

FAQs

1) Is Cardizem LA still subject to new clinical trial outcomes that could change its label?

Typically no label-changing pivotal pathway is expected for an off-patent diltiazem extended-release brand; most new evidence comes from post-marketing, comparative effectiveness, or generic-related studies.

2) What is the main market risk for Cardizem LA?

Generic substitution and formulary placement that moves the brand off preferred tiers or limits coverage via prior authorization and stricter rebate terms.

3) What is the biggest driver of Cardizem LA revenue trends?

Net price after rebates and brand share versus generics, with unit volume influenced by persistence in existing patients and switching to alternatives.

4) What therapeutic area economics matter most for projections?

Hypertension and chronic stable angina prevalence trends, plus how payer formularies structure access to calcium channel blockers.

5) Does Cardizem LA have a differentiating clinical advantage versus other calcium channel blockers?

Its clinical positioning depends on patient-specific tolerability and rate-control needs; however, the market advantage is usually payer- and channel-dependent rather than tied to new branded clinical differentiation.

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References

[1] DailyMed. “Cardizem LA (diltiazem hydrochloride) extended-release capsules.” U.S. National Library of Medicine. (Accessed 2026-04-28).