CLINICAL TRIALS PROFILE FOR PRAVASTATIN SODIUM

All Clinical Trials for PRAVASTATIN SODIUM

Trial ID	Title	Status	Sponsor	Phase	Start Date	Summary
NCT00000941 ↗	A Study on Possible Interactions Between Protease Inhibitors (Anti-HIV Drugs) and Drugs Which Lower the Level of Fat in Your Blood	Completed	National Institute of Allergy and Infectious Diseases (NIAID)	Phase 1	1969-12-31	The purpose of this study is to find out whether taking protease inhibitors (anti-HIV drugs) together with lipid-lowering drugs (drugs which lower the amount of fat in the blood) has an effect on the level of drugs found in the blood compared to when these drugs are taken separately. The three protease inhibitors given in this study are ritonavir, saquinavir, and nelfinavir. The lipid-lowering drugs given are pravastatin, simvastatin, and atorvastatin. Anti-HIV drug therapy using protease inhibitors has become very common treatment for HIV-positive patients. Recently, however, serious side effects involving how the body uses fat have been reported in people taking protease inhibitors. Examples of these side effects are redistribution of body fat and development of diabetes. People taking protease inhibitors have been found to have higher levels of fat in their blood than is normal, which can cause heart problems. It is hoped that giving lipid-lowering drugs can help prevent serious heart problems. First, however, it is important to see what happens when protease inhibitors and lipid-lowering drugs are given together.
NCT00006412 ↗	Safety and Effectiveness of Fenofibrate and Pravastatin in HIV-Positive Patients With Abnormal Blood Lipids	Completed	National Institute of Allergy and Infectious Diseases (NIAID)	Phase 3	1969-12-31	The purpose of this study is to compare the safety and effectiveness of fenofibrate and pravastatin in treating HIV-positive patients who have abnormal levels of fat (lipids) in the blood. Increased lipids in the blood associated with HIV infection and anti-HIV drugs is a growing problem. The drugs used in this study are known to reduce certain lipids, but little is known about their safety and effectiveness. This study will see if one of the drugs is safer and more effective than the other, or if combining the drugs is the safest and most effective way to lower lipids. This study has been changed. On June 26, 2001, this study was reviewed by the Data and Safety Monitoring Board (DSMB). The DSMB is an independent board monitoring the progress of the study. The review showed that neither pravastatin nor fenofibrate alone were effective in reaching all the cholesterol and triglyceride goals. There were no safety concerns. It is not known if the combination of fenofibrate and pravastatin is effective and safe. Therefore, it is important to continue this study.
NCT00017758 ↗	The Effect of Efavirenz and Nelfinavir on the Blood Levels of Certain Lipid-Lowering Drugs	Completed	National Institute of Allergy and Infectious Diseases (NIAID)	Phase 1	1969-12-31	The purpose of this study is to find out whether certain anti-HIV drugs (efavirenz [EFV] and nelfinavir [NFV]) affect the amount of certain fat-lowering drugs (atorvastatin, pravastatin, and simvastatin) in the blood. Protease inhibitors (PIs), a type of anti-HIV drug, are known to cause increased lipids (fats) in the blood of HIV-infected patients. EFV also is known to increase blood fats. HIV-infected patients who take PIs and/or EFV may need to take fat-lowering drugs to correct this problem. So it is important to look at possible drug interactions when these drugs are taken together. This study will see if taking EFV or NFV, a protease inhibitor, affects the blood level of simvastatin, atorvastatin, or pravastatin (all fat-lowering drugs). To obtain results more quickly, the study population will be healthy HIV-negative volunteers.
NCT00039663 ↗	Endothelial Dysfunction as a Risk Factor in HIV Study	Completed	National Institutes of Health Clinical Center (CC)	Phase 1	2002-05-01	Highly active antiretroviral therapy (HAART) has proven effective in altering the natural history of HIV infection in many patients. However, this therapy may not be sustainable because of the toxicities of the medications. Evidence suggests that HIV-infected patients on HAART may be at risk for premature coronary artery disease. The exact cause is unknown. It is possible that the medications directly affect the endothelium (the lining of the arteries that supply blood to the heart) and lead to premature heart disease. Or because the medications cause lipid abnormalities (high cholesterol) and a condition of relative insulin resistance, in which the body has a difficult time processing sugars; known risk factors for endothelial dysfunction and heart disease. Therapeutic intervention that reverses these lipid abnormalities and/or insulin resistance may lower these risk factors, normalize endothelial function, and decrease the risk of heart disease. This protocol aims to assess endothelial function among a group of HIV-infected patients with varying degrees of viral activity and levels of immune function on a variety of HAART regimens. It also aims to evaluate the effect of three different medications on lipids, insulin resistance, and thus endothelial function. Understanding the factors involved in causing endothelial dysfunction will help better characterize the relative risks and benefits of early versus late and continuous versus intermittent HAART therapy. The research may offer some insights into the causes of premature heart disease among HIV-infected patients on HAART that could be more thoroughly investigated in subsequent clinical trials. A total of 75 patients will be recruited: 25 for each arm of the study. Each arm evaluates the potential benefit of a particular medication and will enroll sequentially. An endothelial function test will be performed on an outpatient basis. The first 25 patients will be assigned at random to receive pravastatin sodium or placebo; the next 25 will receive gemfibrozil or placebo; the final 25 will receive rosiglitazone or placebo. Patients will take the pills for 6 weeks, no pills for the next 4 weeks, and then the opposite treatment for 6 more weeks. Two weeks after the start of the study drug, blood will be taken to check for potential toxic side effects. After each 6-week treatment, blood will be drawn and endothelial function tests will be performed.
NCT00232882 ↗	Pharmacodynamic Influences of Candesartan, Atenolol, Hydrochlorothiazide and Drug Combinations in Hypertensive Patients.	Completed	Ottawa Hospital Research Institute	Phase 4	2003-12-01	Angiotensin receptor antagonists (ARA), beta-blockers and diuretics do not seem to confer equivalent cardiovascular protection in hard outcomes clinical trials (beta blockers inferior). These results may be explained by differences in their effects on sympathetic activity, oxidative stress, inflammation and renin angiotensin system activation. How diuretic addition to first line therapy with ARAs and beta-blockers modulates neurohumoral and hemodynamic parameters is not well understood. The main hypothesis of this study is that an ARA (candesartan) combined or not with a diuretic will not increase sympathetic activity as much as a beta blocker (atenolol). Secondary hypothesis are of similar nature but relate to hemodynamic parameters, oxidative stress markers, inflammatory markers, or the renin angiotensin system. The main objective of this study is to assess and compare the effects of candesartan and atenolol and their combination with low dose diuretic therapy on the autonomic nervous system, hemodynamic parameters,on oxidative stress, on inflammatory markers, and on the renin-angiotensin system. Protocol sponsored by Astra Zeneca canada
NCT00232882 ↗	Pharmacodynamic Influences of Candesartan, Atenolol, Hydrochlorothiazide and Drug Combinations in Hypertensive Patients.	Completed	Institut de Recherches Cliniques de Montreal	Phase 4	2003-12-01	Angiotensin receptor antagonists (ARA), beta-blockers and diuretics do not seem to confer equivalent cardiovascular protection in hard outcomes clinical trials (beta blockers inferior). These results may be explained by differences in their effects on sympathetic activity, oxidative stress, inflammation and renin angiotensin system activation. How diuretic addition to first line therapy with ARAs and beta-blockers modulates neurohumoral and hemodynamic parameters is not well understood. The main hypothesis of this study is that an ARA (candesartan) combined or not with a diuretic will not increase sympathetic activity as much as a beta blocker (atenolol). Secondary hypothesis are of similar nature but relate to hemodynamic parameters, oxidative stress markers, inflammatory markers, or the renin angiotensin system. The main objective of this study is to assess and compare the effects of candesartan and atenolol and their combination with low dose diuretic therapy on the autonomic nervous system, hemodynamic parameters,on oxidative stress, on inflammatory markers, and on the renin-angiotensin system. Protocol sponsored by Astra Zeneca canada
NCT00307307 ↗	Carotid Atherosclerosis Regression at Magnetic Resonance Assessment.	Completed	Kos Pharmaceuticals	Phase 4	2000-01-01	The primary objective of this randomized, double blind, placebo controlled pilot study is to determine if therapies aimed at lowering LDL cholesterol (HMGCoA reductase inhibitor - simvastatin) or increasing HDL cholesterol (Niaspan) will induce regression of carotid atherosclerotic plaque in vivo using MRI imaging techniques. MR plaque morphology at baseline will be compared to that after 6 and 12 months of therapy and changes in MR characteristics will be compared to changes in lipoprotein parameters and urinary isoprostanes. The effect of moderate LDL reduction, aggressive LDL reduction and the combination of aggressive LDL reduction and HDL elevation on MRI plaque characteristics will be compared by randomly assigning subjects (n=69) with carotid disease (>30% stenosis by ultrasound criteria) to one of three treatment arms; 1. Simvastatin 20 mg daily and placebo Niaspan (n=23) 2. Simvastatin 80 mg daily and placebo Niaspan (n=23) 3. Simvastatin 20 mg daily and active Niaspan (n=23) Treatment group 2 and 3 will have roughly equivalent LDL lowering because of the synergistic LDL lowering effect of the combination of simvastatin and Niaspan.

Clinical Trial Conditions for PRAVASTATIN SODIUM

Condition Name

Condition Name for PRAVASTATIN SODIUM
Intervention	Trials
Healthy	6
HIV Infections	4
Adult Acute Monoblastic Leukemia (M5a)	2
Adult Pure Erythroid Leukemia (M6b)	2

Condition MeSH

Condition MeSH for PRAVASTATIN SODIUM
Intervention	Trials
HIV Infections	4
Leukemia, Myeloid, Acute	3
Leukemia, Myeloid	3
Leukemia	3

Clinical Trial Locations for PRAVASTATIN SODIUM

Trials by Country

Trials by Country for PRAVASTATIN SODIUM
Location	Trials
United States	83
Canada	7
Greece	5
United Kingdom	3
Korea, Republic of	1

Trials by US State

Trials by US State for PRAVASTATIN SODIUM
Location	Trials
California	6
Washington	6
Maryland	5
Colorado	4
Missouri	4

Clinical Trial Progress for PRAVASTATIN SODIUM

Clinical Trial Phase

Clinical Trial Phase for PRAVASTATIN SODIUM
Clinical Trial Phase	Trials
PHASE4	1
Phase 4	5
Phase 3	4

Clinical Trial Status

Clinical Trial Status for PRAVASTATIN SODIUM
Clinical Trial Phase	Trials
Completed	23
Recruiting	3
Active, not recruiting	2

Clinical Trial Sponsors for PRAVASTATIN SODIUM

Sponsor Name

Sponsor Name for PRAVASTATIN SODIUM
Sponsor	Trials
National Institute of Allergy and Infectious Diseases (NIAID)	4
Teva Pharmaceuticals USA	4
National Cancer Institute (NCI)	3

Sponsor Type

Sponsor Type for PRAVASTATIN SODIUM
Sponsor	Trials
Other	27
Industry	15
NIH	9

Last updated: July 25, 2026

Pravastatin Sodium Clinical Trials Update, Market Analysis and Revenue Projection (2024–2035)

Pravastatin sodium is a long-established, generic statin with no current sponsor-level “pipeline” visibility comparable to newer cardiovascular assets. Clinical activity is dominated by comparative effectiveness, outcomes research using established formulations, and pharmacology or special-population studies rather than late-stage new molecular entity development. From a market standpoint, demand is driven by cholesterol-lowering guidelines, formulary access, and payer preference for low-cost statins, with pricing pressure and volume stability as the core dynamics.

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What is the current clinical trial landscape for pravastatin sodium (2024–2026)?

What types of studies are running now

Clinical activity for pravastatin sodium is concentrated in four buckets:

• Comparative lipid-lowering trials versus other statins (dose-ranging or head-to-head effectiveness endpoints).
• Special populations (elderly, chronic kidney disease, hepatic impairment risk stratification, statin intolerance phenotypes).
• Pharmacokinetic and drug interaction studies (P450 and transporter-related interaction characterization).
• Outcome-adjacent observational or registry-linked interventional designs using pravastatin-containing regimens.

What that means for “late-stage pipeline” expectations

Because pravastatin sodium is off-patent in most jurisdictions, trial design emphasis typically shifts to:

• comparative endpoints (LDL-C change, adherence, safety signals),
• real-world-like endpoints, and
• label-constrained new indications, if any, that do not require a full new-drug registration.

Actionable read-through: near-term clinical trial “updates” do not translate into a credible probability of meaningful market disruption through a new patentable product. The practical value of ongoing trials is payer and guideline support, plus incremental claims that can sustain substitution markets against higher-priced branded statins and combination therapies.

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Are there new late-stage pravastatin sodium trials that could change labeling?

Key question for investors and licensors

For a generic statin, “label change” typically comes only from:

• new dosing regimens (formulation or regimen refinement),
• expanded population claims, or
• new safety or interaction statements that are compatible with existing manufacturing and regulatory history.

Decision-level impact

Even when label expansions occur, the ability to generate incremental revenue is constrained by:

• generic substitution dynamics,
• payer formularies that already cover multiple statins, and
• the dominance of cost and coverage in statin prescribing.

Actionable read-through: absent clear evidence of phase 3 outcomes trials designed for a new indication or meaningful new population claim, the probability of a market narrative shift is low.

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What is the market size for pravastatin sodium today and what drives demand?

Demand drivers

Pravastatin sodium demand is shaped by:

• Guideline compatibility for primary prevention and secondary prevention of atherosclerotic cardiovascular disease (ASCVD).
• Safety and tolerability perceptions relative to some other statins in subsets of patients who report intolerance.
• Payer formulary behavior, which often pushes use toward low-cost statins but maintains multiple agents for patient-specific tolerability.

Supply and pricing drivers

• Generic erosion is structurally persistent for statins with large molecule longevity.
• Pricing variance is driven by:
  • manufacturer competition,
  • tendering and pharmacy benefit manager (PBM) contracting,
  • package size, dosage strength mix, and distribution channel.

Actionable read-through: growth is volume-driven and contract-driven, not price-driven.

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How does pravastatin sodium revenue compare with other statins (atorvastatin, rosuvastatin, simvastatin)?

Competitive positioning

• Atorvastatin and rosuvastatin typically dominate by payer and prescriber preferences for potency and simplified titration.
• Pravastatin competes through:
  • perceived tolerability and established long-term safety,
  • hepatic and drug interaction management narratives (context-specific),
  • continuity of care where patients are stable on existing therapy.

Commercial implication

Pravastatin tends to maintain share through:

• switching frictions (patients stable on existing regimens),
• contraindication management and tolerability pathways, and
• formularies that retain multiple statins for step-therapy exceptions.

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What are the key geographic dynamics for pravastatin sodium uptake?

High-income markets

• Generic availability is broad and often fully mature.
• Demand is influenced by switching cycles, pharmacy stocking, and ongoing guideline updates rather than new product launches.

Emerging markets

• Adoption can lag due to availability, procurement, and formulary standardization.
• As generic distribution matures, pravastatin can benefit from cost competitiveness among oral statins.

Actionable read-through: global growth is more dependent on distribution penetration and contracting than on clinical differentiation.

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What patents protect pravastatin sodium and how does exclusivity end?

Patent and exclusivity reality

Pravastatin sodium is a mature small molecule statin. In the US, EU, and most major markets, the original composition of matter and basic formulations are long expired. Market access is therefore governed mainly by:

• process, salt, crystal form, and formulation patents (where they exist for specific products),
• and regulatory exclusivity only at a product level (not molecule-level).

Practical implication

From a business standpoint, the “IP estate” affects:

• the specific branded or reformulated product shells,
• manufacturing processes for particular NDA/ANDA holders,
• and any product line that uses protective formulation changes.

Actionable read-through: the molecule is not an IP anchor; product-level and manufacturing IP is the realistic protection layer.

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What is the Orange Book status of pravastatin sodium in the US?

Orange Book usefulness in this asset

For pravastatin sodium, Orange Book coverage is expected to be populated by:

• ANDA listings (generic products),
• old patent remnants and periodic maintenance for specific listed formulations,
• and procedural or method-of-manufacture patents tied to particular ANDAs.

Commercial interpretation

Orange Book status primarily matters for:

• identifying which generic applicants have “clean” freedom-to-market,
• and detecting any still-listed patents that could force Paragraph IV challenges or restrict certain generic product launches.

Actionable read-through: because the active ingredient is widely generic, Orange Book risk usually concentrates on product-level listings rather than blocking access at the ingredient level.

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What formulation types exist for pravastatin sodium and which ones affect market share?

Core dosage forms

The dominant commercial formats are:

• oral tablets in multiple strengths.
• branded and generic offerings differ primarily by:
  • strength,
  • tablet excipient set,
  • packaging configuration,
  • and any product-specific manufacturing controls.

How formulations affect uptake

For statins, formulations rarely drive clinical outcomes unless they:

• alter bioavailability materially,
• improve tolerability, or
• support adherence through convenience.

Actionable read-through: in mature generic markets, formulation differentiation impacts contracting and shelf space more than therapeutic performance.

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What generic entry risks exist for pravastatin sodium?

Where launch risk actually sits

With pravastatin sodium, typical “entry risk” for generics comes from:

• product-specific regulatory history,
• process-related IP claims (method of manufacture),
• and product quality and supply chain credibility (regulatory compliance track record).

Likelihood of business disruption

Disruption from IP litigation is less likely at a molecule level and more likely when:

• a manufacturer attempts a novel formulation or manufacturing improvement still under protective claims, or
• a legacy branded product retains late-listed patents.

Actionable read-through: most market entries for pravastatin sodium are governed by contracting and manufacturing capacity rather than prolonged exclusivity.

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What patent litigation or Paragraph IV activity has affected pravastatin sodium historically?

Litigation pattern typical for mature statins

For mature statins, litigation typically includes:

• challenges to listed patents tied to specific ANDAs,
• settlement agreements that shift launch dates for particular strengths or product configurations.

Business implication

Even when litigation occurred historically, its practical role today is:

• identifying which manufacturers gained earlier commercial access to particular SKUs,
• and mapping which players built durable market share through settlement and manufacturing scale.

Actionable read-through: for forward-looking planning, the relevant question is which product line still has live listings or active procedural constraints in the Orange Book.

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How strong is the patent estate for pravastatin sodium in 2026: what could still block competitors?

Strength assessment framework

For pravastatin sodium, patent estate strength is assessed at:

• ANDA product level,
• listed patent claim types (composition, method, formulation, process),
• and whether those patents remain enforceable and still list in US Orange Book.

Expected outcome for the molecule

At the molecule level, strength is generally low due to age. Any remaining strength is:

• narrow,
• product- and process-specific,
• and unlikely to create broad exclusivity beyond specific SKUs.

Actionable read-through: competitor blocking is typically limited to targeted product configurations rather than class-wide prevention.

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Market projection for pravastatin sodium (2024–2035): base case, bull case, bear case

Projection logic for a mature generic statin

Revenue for mature generics is modeled from:

• volume (prescriptions, persistence),
• price (contract and competitive erosion),
• share (formulary mix and patient switching),
• mix (strength and package size),
• policy (US and EU tender systems, reference pricing).

Base-case assumptions (directional)

• Pricing continues downward or stabilizes at low levels depending on country tender cycles.
• Volume stays stable to slightly growing due to:
  • aging demographics,
  • ongoing ASCVD prevention,
  • and retention of patients stable on tolerated statins.
• Share shifts to higher-potency statins keep pressure on pravastatin.

Scenario table (revenue directionality)

Because the prompt does not provide a baseline revenue figure by geography or currency, the projection is stated as directional CAGR ranges, not absolute dollars.

Scenario (global)	Volume trend	Net price trend	Net revenue CAGR (2024–2035)
Bear	Flat/slightly declining	Continued erosion	-1% to -0.5%
Base	Low growth	Stabilizing to modest decline	0% to +0.7%
Bull	Meaningful share retention	Stabilizing price	+0.7% to +1.5%

Actionable read-through: the opportunity is not “growth acceleration.” It is defending market share in a contracting/tilted formulary world and extracting margin through supply efficiency and SKU coverage.

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What is the most likely commercial strategy for manufacturers of pravastatin sodium?

SKU and contracting strategy

• Maintain broad strength coverage and package formats preferred in PBM formularies.
• Optimize tender participation and distribution arrangements.
• Reduce manufacturing cost per tablet while preserving consistent compliance performance.

Portfolio strategy

• Use pravastatin as a stabilizing generic anchor alongside higher-revenue generics from less mature assets or combination products, where possible.

Actionable read-through: competitiveness is an execution game: cost, supply continuity, and formulary access.

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Key Takeaways

• Pravastatin sodium clinical activity is mostly comparative effectiveness and special-population or pharmacology work, with limited likelihood of label-driven market disruption.
• The market is mature and generic; revenue is determined primarily by contracting, volume persistence, and pricing stability rather than innovation.
• Competitive pressure from higher-potency statins persists, but patient switching frictions and tolerability-based prescribing support baseline share.
• Patent exclusivity is effectively over at the molecule level; any remaining barriers are product- and process-specific and typically narrow.

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FAQs

1. Does pravastatin sodium have any ongoing phase 3 trials for new indications?
2. Which populations are most likely to be kept on pravastatin instead of switching to rosuvastatin or atorvastatin?
3. How do PBM formulary rules and step therapy typically affect pravastatin prescription volume?
4. What manufacturing and regulatory factors most often determine successful generic launches for pravastatin tablets?
5. How does therapeutic equivalence switching impact long-term persistence for pravastatin users?

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References

1. FDA. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. https://www.accessdata.fda.gov/scripts/cder/daf/ (accessed 2026-07-25).
2. ClinicalTrials.gov. Search results for “pravastatin sodium” (clinical studies). https://clinicaltrials.gov/ (accessed 2026-07-25).