CLINICAL TRIALS PROFILE FOR METOPROLOL TARTRATE

All Clinical Trials for METOPROLOL TARTRATE

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.
NCT00226096 ↗	Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage	Completed	National Health and Medical Research Council, Australia	N/A	2005-11-01	The purpose of the study is to determine whether lowering high blood pressure levels after the start of a stroke caused by bleeding in the brain (intracerebral haemorrhage) will reduce the chances of a person dying or surviving with a long term disability. The study will be undertaken in two phases: a vanguard phase in 400 patients, to plan for a main phase in 2000 patients.
NCT00226096 ↗	Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage	Completed	The George Institute	N/A	2005-11-01	The purpose of the study is to determine whether lowering high blood pressure levels after the start of a stroke caused by bleeding in the brain (intracerebral haemorrhage) will reduce the chances of a person dying or surviving with a long term disability. The study will be undertaken in two phases: a vanguard phase in 400 patients, to plan for a main phase in 2000 patients.
NCT00648271 ↗	Fed Study of Metoprolol Tartrate Tablets 25 mg and Lopressor® 50 mg	Completed	Mylan Pharmaceuticals	Phase 1	2002-12-01	The objective of this study was to investigate the bioequivalence of Mylan's metoprolol tartrate tablets to Novartis' Lopressor® tablets following a single, oral 50 mg (2 x 25 mg tablets for Mylan's formulation and 1 x 50 mg for Lopressor®) dose administered under fed conditions.

Clinical Trial Conditions for METOPROLOL TARTRATE

Condition Name

Condition Name for METOPROLOL TARTRATE
Intervention	Trials
Healthy	6
Hypertension	4
Cardiac Failure	2
Heart Failure	2

Condition MeSH

Condition MeSH for METOPROLOL TARTRATE
Intervention	Trials
Hypertension	4
Heart Diseases	3
Ventricular Premature Complexes	2
Stroke	2

Clinical Trial Locations for METOPROLOL TARTRATE

Trials by Country

Trials by Country for METOPROLOL TARTRATE
Location	Trials
United States	13
Australia	5
Spain	4
China	3
Denmark	2

Trials by US State

Trials by US State for METOPROLOL TARTRATE
Location	Trials
Nebraska	2
North Dakota	2
West Virginia	2
Tennessee	2
New York	2

Clinical Trial Progress for METOPROLOL TARTRATE

Clinical Trial Phase

Clinical Trial Phase for METOPROLOL TARTRATE
Clinical Trial Phase	Trials
PHASE4	1
PHASE3	1
PHASE2	2

Clinical Trial Status

Clinical Trial Status for METOPROLOL TARTRATE
Clinical Trial Phase	Trials
COMPLETED	15
Not yet recruiting	3
Enrolling by invitation	2

Clinical Trial Sponsors for METOPROLOL TARTRATE

Sponsor Name

Sponsor Name for METOPROLOL TARTRATE
Sponsor	Trials
Mylan Pharmaceuticals	4
National Health and Medical Research Council, Australia	2
The George Institute	2

Sponsor Type

Sponsor Type for METOPROLOL TARTRATE
Sponsor	Trials
Other	35
Industry	9
NIH	2

Metoprolol Tartrate clinical trials update, market analysis, and 2026–2036 sales projection

Last updated: July 26, 2026

Metoprolol tartrate is an established, off-patent small-molecule beta-blocker with broad generic availability in the US and major EU markets. Clinical-trials activity is dominated by new formulations, bioequivalence, and mechanistic studies rather than first-in-class development. Market growth is driven by chronic cardiovascular incidence, pipeline-dependent take-up of fixed-dose combinations, and health-system prescribing patterns; unit pricing remains structurally pressured by competition and interchangeability. A base-case market model projects modest global value growth through 2036, with volume growth offset by generics-driven price compression.

What is the current clinical trials landscape for metoprolol tartrate?

Featured snippet: Current activity is largely incremental: bioequivalence, formulation work, dose-titration or switching studies, and mechanistic comparisons in hypertension, angina, and heart-rate control.

Which trial types are most common

1. Bioequivalence (BE) and formulation equivalence
   • Immediate-release tablet BE studies in healthy volunteers and sometimes in cardiovascular populations.
   • Changes typically involve strength, excipients, manufacturing site, or packaging.
2. Comparative effectiveness and switching
   • Studies comparing metoprolol tartrate against other beta-blockers or titration strategies.
   • Common endpoints: heart rate control, blood pressure response, tolerability, adherence.
3. Peri-procedural and physiologic studies
   • Short-duration studies in settings such as perioperative tachycardia control or stress testing.
   • Endpoints focus on hemodynamics rather than long-term outcomes.

How to interpret “activity” for an off-patent medicine

• For metoprolol tartrate, new NCT registrations and publication cycles often reflect generic launches, reformulation, and optimization, not patent-critical breakthrough efficacy.
• Trial relevance for commercial strategy is highest when it supports:
  • conversion from alternative beta-blockers in hospital formularies,
  • uptake of higher-strength or lower pill burden regimens,
  • or co-administration in combo products.

Trial endpoints that drive payer and formulary decisions

• 24-hour ambulatory BP and heart-rate reduction for hypertension and rate control.
• Tolerability metrics: bradycardia incidence, fatigue, discontinuation rates.
• Adherence: adherence or persistence proxies, pill burden comparisons.
• Switching tolerability: rebound effects or HR overshoot when switching beta-blockers.

Which indications are driving metoprolol tartrate studies today?

Featured snippet: Hypertension, angina, and heart-rate control in cardiovascular disease dominate the trial footprint.

Hypertension

• Trial objectives commonly test:
  • titration schedules and time-to-stable BP control,
  • comparators across beta-blockers,
  • adherence and persistence in real-world-style designs.

Angina and ischemic heart disease

• Studies evaluate:
  • heart rate targets,
  • antianginal tolerability,
  • dosing frequency impact (metoprolol tartrate is typically dosed more than once daily versus succinate).

Rate control in cardiac rhythm settings

• Where studied, endpoints are typically:
  • ventricular rate reduction,
  • acute tolerability and hemodynamic stabilization,
  • hospital workflow outcomes (time to control).

What patents protect metoprolol tartrate and how does exclusivity affect development?

Featured snippet: Metoprolol tartrate’s original composition and many foundational uses are long expired; current competitive protection is mainly related to specific formulations, manufacturing methods, or fixed-dose combinations where applicable.

Why the patent estate matters less for standalone metoprolol tartrate

• The active ingredient is widely generified.
• Market entry often depends on regulatory ANDA pathways, not brand-style exclusivity.

Where patent-like value still shows up

• Fixed-dose combinations (with other antihypertensives or cardiometabolic agents) where combination patents can extend commercial differentiation.
• Formulation and manufacturing
  • controlled release or altered dissolution can be differentiators, though metoprolol tartrate is generally immediate-release.
• Method-of-use for specific titration regimens or subpopulations (less common for the base compound, more plausible for combo products).

What is the FDA and Orange Book status for metoprolol tartrate?

Featured snippet: Orange Book coverage for metoprolol tartrate largely reflects generic listings and legacy brand residuals, with most key patents expired and most approvals on ANDA routes.

What you should expect in FDA documentation

• Multiple ANDAs across strengths, typically immediate-release tablets.
• Orange Book entries concentrate on:
  • listed patents for specific marketed versions,
  • sometimes formulation patents or combination product patents if those exist for a particular NDA/ANDA.

What patent litigation affects metoprolol tartrate generics?

Featured snippet: Patent disputes are generally historical for the active ingredient; current competitive threats are mostly formulation/label differences and regulatory exclusivity rather than ongoing composition litigation.

How litigation risk shows up in practice

• For metoprolol tartrate, the primary commercial risk from litigation typically arises for:
  • new combination products using metoprolol tartrate as one component,
  • rebranded dosage forms tied to specific patents,
  • line extensions when a manufacturer markets a protected formulation.

What generic entry risks exist for metoprolol tartrate in 2026–2031?

Featured snippet: For the standalone active ingredient, generic entry risk is low because supply is already broad; near-term risk is more about price competition, pharmacy channel behavior, and manufacturing quality/regulatory outcomes.

Commercial entry dynamics

• Primary headwinds:
  • aggressive wholesale and pharmacy pricing,
  • substitution rules and payer step edits favoring lowest acquisition cost.
• Primary tailwinds:
  • formulary retention where supply reliability is proven,
  • switch management where metoprolol tartrate remains preferred for dosing flexibility.

How does metoprolol tartrate compare with metoprolol succinate for commercial and clinical use?

Featured snippet: Metoprolol tartrate is immediate-release and often dosed more than once daily; metoprolol succinate is extended-release and frequently preferred for simpler dosing, which can affect adherence and formulary positioning.

Key differentiators that drive market share

• Dosing convenience
  • Succinate often has once-daily regimens.
  • Tartrate often offers dosing granularity (dose titration flexibility).
• Clinical workflow
  • Tartrate may be favored in settings where rapid titration or short-term control is prioritized.
• Switching behavior
  • Patients switched between tartrate and succinate based on tolerability, adherence, and clinician preference.

How many companies sell metoprolol tartrate tablets and where is competition most intense?

Featured snippet: Competition is intense across the US and in most large EU markets, with multiple generic suppliers and frequent price resets.

US market structure

• Multiple ANDA filers across strengths and pack sizes.
• Channel power typically sits with large generic manufacturers and pharmacy group purchasing organizations.
• Substitution and interchangeability reduce differentiation for standalone tartrate.

EU market structure

• National reimbursement and prescribing guidelines shape distribution.
• Tendering can compress prices rapidly for immediate-release antihypertensives.

Metoprolol tartrate market size today and revenue exposure by region

Featured snippet: Global revenue is dominated by generics; value growth is constrained by price compression, while volume expansion tracks cardiovascular disease prevalence and prescribing stability.

Base-case regional view (directional)

• North America: highest revenue visibility due to market access scale; pricing pressure is strong.
• Europe: steady demand; reimbursement cycles and tendering influence value.
• Emerging markets: higher volume potential, but pricing and procurement volatility affect value stability.

2026–2036 sales projection for metoprolol tartrate

Featured snippet: Base-case model assumes continued volume growth with moderate value growth due to declining average selling prices for generics.

Projection framework (what drives the model)

• Volume: driven by prevalence and persistence in hypertension and ischemic heart disease populations.
• Price: driven by generic mix shifts and tender dynamics.
• Share movement: influenced by formulation convenience, combination products, and competitive pricing.
• Regulatory shocks: supply disruptions and manufacturing quality events can temporarily shift share and price.

Base-case outcome (directional ranges)

• Global value CAGR: low single digits through 2036.
• Global volume CAGR: mid single digits through 2036 in markets with growing cardiovascular burden; lower in mature markets with stable prescribing.
• Margin compression: sustained given generic competition, with best performers maintaining share via manufacturing reliability and efficient distribution.

Upside and downside scenarios

• Upside
  • faster uptake in high-burden markets,
  • favorable formulary inclusion for tartrate where clinicians require titration flexibility,
  • growth in combo products where metoprolol tartrate is used with protected partner ingredients.
• Downside
  • accelerated switching to extended-release beta-blockers where payers prefer once-daily regimens,
  • continued price war dynamics in tendered procurement,
  • supply concentration risk reducing availability or forcing costly relaunches.

What product strategies can increase metoprolol tartrate profitability in a commoditized market?

Featured snippet: Differentiation comes from operational execution and channel strategy, not from clinical novelty for the standalone active ingredient.

Commercial levers

• Strength and packaging optimization
  • aligning pack sizes to prescribing patterns to reduce waste and improve acquisition cost efficiency.
• Formulary execution
  • contracting based on lowest net acquisition cost while ensuring consistent supply.
• Compliance and quality
  • leveraging strong GMP performance and low defect rates to win bid renewals.
• Combination pathways
  • pursuing co-formulated or partnered products where combination patents (or at least fixed-dose exclusivity) can provide commercial breathing room.

Key takeaways

• Metoprolol tartrate clinical development is incremental, dominated by bioequivalence, switching, and mechanistic studies rather than new efficacy breakthroughs.
• Patent and exclusivity constraints are minimal for standalone tartrate because the active ingredient is long off-patent; competitive differentiation is mainly operational and channel driven.
• Market value growth is likely to remain modest due to sustained generic price competition, with volume tracking chronic cardiovascular demand.
• 2026–2036 projections support low single-digit global value growth with mid single-digit volume growth in higher-burden markets, tempered by ongoing payer-driven substitution pressures.

FAQs

1. Does metoprolol tartrate have any remaining regulatory exclusivity in the US that could delay generics?
2. Are there ongoing trials comparing metoprolol tartrate dosing schedules for hypertension that could change practice?
3. How does formulary preference for once-daily beta-blockers affect metoprolol tartrate volume in managed care?
4. What risks matter most for generic metoprolol tartrate manufacturing and supply continuity?
5. Which combo beta-blocker products using metoprolol tartrate show the best commercial differentiation versus standalone tablets?

References

1. FDA Orange Book. Drugs@FDA and the Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/ob/
2. ClinicalTrials.gov. Study records for metoprolol tartrate (search results). https://clinicaltrials.gov/