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Pravastatin: Drug information

Pravastatin: Drug information
2024© UpToDate, Inc. and its affiliates and/or licensors. All Rights Reserved.
For additional information see "Pravastatin: Patient drug information" and "Pravastatin: Pediatric drug information"

For abbreviations, symbols, and age group definitions show table
Brand Names: US
  • Pravachol [DSC]
Brand Names: Canada
  • ACH-Pravastatin;
  • AG-Pravastatin;
  • APO-Pravastatin;
  • AURO-Pravastatin;
  • BIO-Pravastatin;
  • DOM-Pravastatin [DSC];
  • JAMP-Pravastatin;
  • M-Pravastatin;
  • MAR-Pravastatin;
  • MINT-Pravastatin;
  • PMS-Pravastatin;
  • Pravachol [DSC];
  • Priva-Pravastatin [DSC];
  • SANDOZ Pravastatin;
  • TARO-Pravastatin;
  • TEVA-Pravastatin
Pharmacologic Category
  • Antilipemic Agent, HMG-CoA Reductase Inhibitor
Dosing: Adult

Dosage guidance:

Dosing: Pravastatin 40 to 80 mg/day is considered a moderate-intensity statin (generally reduces low-density lipoprotein cholesterol [LDL-C] by ~30% to 49%). If LDL-C must be lowered ≥50%, select an alternative a high-intensity statin (atorvastatin or rosuvastatin). Assess response ~1 to 3 months after therapy initiation or dose adjustment and every 3 to 12 months thereafter (Ref).

Clinical considerations: Use in conjunction with lifestyle modification (eg, diet, exercise). When initiating therapy and selecting dose intensity, consider age, baseline LDL-C, 10-year atherosclerotic cardiovascular disease (ASCVD) risk, risk-enhancing factors, potential adverse effects, and drug interactions (Ref).

Heterozygous familial hypercholesterolemia

Heterozygous familial hypercholesterolemia (alternative agent):

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin. Multiple lipid-lowering therapies may be needed if statin monotherapy is not effective. Referral to a lipid specialist should be considered if treatment goals are not met (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Homozygous familial hypercholesterolemia

Homozygous familial hypercholesterolemia (alternative agent):

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin. Multiple lipid-lowering therapies may be needed if statin monotherapy is not effective. Referral to a lipid specialist should be considered if treatment goals are not met (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Prevention of atherosclerotic cardiovascular disease

Prevention of atherosclerotic cardiovascular disease:

Note: If LDL-C goal (eg, percent reduction or absolute goal) is not met with the initial dose, may consider up-titration based on estimated 10-year ASCVD risk (see ACC/AHA ASCVD Risk Estimator Plus online), LDL-C response, and tolerability. If LDL-C goal is not met with maximally tolerated dose, consider switching to a high-intensity statin (atorvastatin or rosuvastatin); additional lipid-lowering therapy may be warranted (Ref).

Primary prevention:

Patients without diabetes, 40 to 75 years of age, and LDL-C 70 to 189 mg/dL:

ASCVD 10-year risk 5% to <7.5%:

Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest shared decision-making if ASCVD 10-year risk is 5% to 10%; however, in patients with a baseline LDL-C ≥160 mg/dL, statin therapy is usually recommended (Ref).

Moderate-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by 30% to 49% (Ref).

ASCVD 10-year risk ≥7.5% to <20%:

Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest initiating moderate-intensity statin therapy in most patients if ASCVD 10-year risk is >10% to <20% and LDL-C is >100 mg/dL (Ref).

Moderate-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by 30% to 49%; higher-risk patients with multiple risk-enhancing factors may benefit from high-intensity statin therapy (ie, with atorvastatin or rosuvastatin) to reduce LDL-C by ≥50% (Ref).

ASCVD 10-year risk ≥20% (alternative agent):

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Patients with diabetes:

Age 40 to 75 years without additional ASCVD risk factors :

Moderate-intensity therapy: Oral: 40 to 80 mg once daily to reduce LDL-C by 30% to 49% (Ref).

ASCVD 10-year risk ≥7.5% or multiple ASCVD risk factors (alternative agent) :

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Patients with LDL-C ≥190 mg/dL and 20 to 75 years of age (regardless of ASCVD risk estimate or coexisting diabetes mellitus) (alternative agent):

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Secondary prevention in patients with established atherosclerotic cardiovascular disease (eg, coronary heart disease, cerebrovascular disease [ischemic stroke or transient ischemic attack], peripheral arterial disease) (alternative agent):

Note: Use of pravastatin should be limited to patients unable to tolerate a high-intensity statin (Ref). Patients with high-risk ASCVD may require additional therapies to achieve LDL-C goal (eg, <70 mg/dL or <50 mg/dL if very high risk) (Ref).

Patients unable to tolerate high-intensity therapy (eg, appropriate dose of atorvastatin or rosuvastatin):

Moderate-intensity therapy: Oral: 40 to 80 mg once daily (Ref).

Transplantation

Transplantation:

Note: Certain immunosuppressive drugs can induce or exacerbate hypercholesterolemia. Significant drug interactions between statins and immunosuppressant drugs are frequent; some interactions can increase statin serum concentrations and risk of toxicity (eg, myopathy) (Ref). Consult drug interactions database for more detailed information.

Transplantation, post heart (off-label use): Oral: Initial: 20 mg once daily starting 1 to 2 weeks after transplant, regardless of baseline cholesterol levels; increase to the maximum tolerated dose within 4 to 8 weeks of transplantation based on response and concomitant drugs up to 40 mg once daily (Ref).

Transplantation, post kidney (off-label use):

Note: The decision to initiate therapy for primary or secondary prevention is similar to the nontransplant population (see "Use: Prevention of atherosclerotic cardiovascular disease"). However, in patients who are 30 to 39 years of age, some experts suggest statin therapy post-kidney transplantation for primary prevention of ASCVD. For primary prevention of ASCVD in patients 18 to 29 years of age, use shared decision making while considering risks and benefits (Ref).

Oral: Initial: 20 mg once daily; increase dose based on response, tolerability, and concomitant drugs up to 40 mg once daily (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

The renal dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Bruce Mueller, PharmD, FCCP, FASN, FNKF; Jason A. Roberts, PhD, BPharm (Hons), B App Sc, FSHP, FISAC; Michael Heung, MD, MS

Altered kidney function: Oral:

CrCl >30 mL/minute: No dosage adjustment necessary (Ref).

CrCl ≤30 mL/minute: Initial: 10 mg once daily. May increase based on efficacy and tolerability up to the indication-specific usual recommended dose (Ref).

Hemodialysis, intermittent (thrice weekly): Not significantly dialyzed (Ref):

Note: Kidney Disease Improving Global Outcomes (KDIGO) guidelines recommend not initiating a statin in dialysis patients due to lack of benefits shown in this population; however, patients initiated on a statin before progressing to dialysis may continue to receive therapy (Ref).

Oral: Dose as for CrCl ≤30 mL/minute (Ref).

Peritoneal dialysis: Unlikely to be significantly dialyzed (Ref):

Note: KDIGO guidelines recommend not initiating a statin in dialysis patients due to lack of benefits shown in this population; however, patients initiated on a statin before progressing to dialysis may continue to receive therapy (Ref).

Oral: Dose as for CrCl ≤30 mL/minute (Ref).

CRRT: Dose as for CrCl ≤30 mL/minute (Ref).

PIRRT (eg, sustained, low-efficiency diafiltration): Oral: Dose as for CrCl ≤30 mL/minute (Ref).

Dosing: Hepatic Impairment: Adult

The hepatic dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Matt Harris, PharmD, MHS, BCPS, FAST, Jeong Park, PharmD, MS, BCTXP, FCCP, FAST, Arun Jesudian, MD, Sasan Sakiani, MD.

Note: Although use is contraindicated in patients with active liver failure or decompensated cirrhosis according to the manufacturer's labeling, baseline elevation in AST/ALT should not preclude use of statins for compelling indications in patients with chronic stable liver disease including compensated cirrhosis (Ref).

Hepatic impairment prior to treatment initiation:

Child-Turcotte-Pugh class A: No dosage adjustment necessary (Ref).

Child-Turcotte-Pugh class B: Oral: 40 mg once daily; maximum: 40 mg/day (Ref).

Child-Turcotte-Pugh class C: Use generally not recommended.

Acute hepatotoxicity or worsening of hepatic function (eg, progression from Child-Turcotte-Pugh class A to B) during treatment:

Progression from baseline to Child-Turcotte-Pugh class A through C: Although use is contraindicated in patients with active liver failure or decompensated cirrhosis according to the manufacturer's labeling, if pravastatin-induced hepatotoxicity (eg, liver injury, rhabdomyolysis) has been ruled out, may continue current dose for hypercholesterolemia and atherosclerotic cardiovascular disease risk management, not to exceed 80 mg once daily (Ref); however, in patients with decompensated cirrhosis, consider not exceeding 40 mg once daily (Ref). Continued use of statin therapy may be hepatoprotective in patients with decompensated cirrhosis (Ref).

Dosing: Adjustment for Toxicity: Adult

Severe muscle symptoms or fatigue: Promptly discontinue use; evaluate CPK, creatinine, and urinalysis for myoglobinuria (Ref).

Mild to moderate muscle symptoms: Discontinue use until symptoms can be evaluated; evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, primary muscle diseases). Upon resolution, resume the original or lower dose of pravastatin. If muscle symptoms recur, discontinue pravastatin use. After muscle symptom resolution, may then use a low dose of a different statin; gradually increase if tolerated. In the absence of continued statin use, if muscle symptoms or elevated CPK continues after 2 months, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (Ref).

Dosing: Older Adult

Refer to adult dosing.

Dosing: Pediatric

(For additional information see "Pravastatin: Pediatric drug information")

Dosage guidance:

Dosing: Dosage should be individualized according to the baseline low-density lipoprotein cholesterol (LDL-C) level, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks.

Hyperlipidemia or heterozygous familial and nonfamilial hypercholesterolemia

Hyperlipidemia or heterozygous familial and nonfamilial hypercholesterolemia:

Note: Begin treatment if, after adequate trial (6 to 12 months) of intensive lifestyle modification emphasizing body weight normalization and diet, the following are present (Ref):

LDL-C ≥190 mg/dL or

LDL-C remains ≥160 mg/dL and two or more cardiovascular risk factors: Family history of premature atherosclerotic cardiovascular disease (<55 years of age), overweight, obesity, or other elements of insulin resistance syndrome or

LDL-C ≥130 mg/dL and diabetes mellitus (Ref).

Therapy may also be considered for children 8 to 9 years of age meeting the above criteria or for children with diabetes mellitus and LDL-C ≥130 mg/dL (Ref).

Children and Adolescents 8 to 13 years: Oral: 20 mg once daily; lower doses (5 and 10 mg/day) have been evaluated and less efficacy observed compared to 20 mg doses (Ref); doses >20 mg have not been studied (Vuorio 2017).

Adolescents 14 to 18 years: Oral: 40 mg once daily; lower doses have been evaluated and less efficacy observed; doses >40 mg have not been studied (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥8 years and Adolescents: Discontinue use until symptoms can be evaluated; check CPK level; based on experience in adult patients, also evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution (symptoms and any associated CPK abnormalities), resume the original or consider a lower dose of pravastatin and retitrate. If muscle symptoms recur, discontinue pravastatin use. After muscle symptom resolution, may then reinitiate a different statin at an initial low dose; gradually increase if tolerated. Based on experience in adult patients, if muscle symptoms or elevated CPK persists for 2 months in the absence of continued statin use, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (Ref).

Dosing: Kidney Impairment: Pediatric

There are no pediatric specific recommendations; based on experience in adult patients, dosing adjustment suggested

Dosing: Hepatic Impairment: Pediatric

There are no dosage adjustments provided in the manufacturer labeling; contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.

Adverse Reactions (Significant): Considerations
Hepatic effects

Statins are associated with increased serum transaminases and hepatotoxicity (Ref). Asymptomatic transient or persistent increases both <3 or >3 times the ULN in serum transaminases may occur with all statins; the increased serum alanine aminotransferase (ALT) is typically greater than the increased serum aspartate aminotransferase (AST) (Ref). Acute hepatotoxicity has been documented (Ref).

Upon dose reduction or discontinuation, transaminase levels return to or near pretreatment levels; although, mild elevations resolve with continued use in some cases (Ref). Chronic liver injury (defined as liver biochemical or histological abnormalities that persisted for 6 months or more after onset) has been reported (Ref).

Mechanism: Unclear; pravastatin undergoes minimal hepatic metabolism. Changes in the lipid components of the hepatocyte membrane may lead to increased permeability and leakage of liver enzymes (Ref). Pravastatin may induce liver mitochondrial redox imbalance, which may contribute to hepatotoxicity (Ref).

Onset: Varied; most cases occur within the first 3 months of initiation or dose escalation (Ref). Duration of pravastatin prior to hepatotoxicity has been reported from approximately 7 weeks to 1 year (Ref).

Risk factors:

• Higher doses may increase the risk of liver injury (Ref)

• Concurrent medications with statin drug-drug interactions or hepatotoxic properties (Ref)

• Hepatotoxicity is more commonly associated with atorvastatin than pravastatin, rosuvastatin, and simvastatin (Ref). Fluvastatin is associated with the greatest risk of developing hepatotoxicity (Ref).

• Cross-reactivity between different statins and the susceptibility to hepatotoxicity is unknown, as data have shown conflicting results (Ref)

• Chronic hepatitis B and alcohol consumption are independent risk factors for hepatic aminotransferase elevation associated with statins in patients 80 years of age or older (Ref)

Muscle-related effects

Statins are associated with several muscle-related effects, including:

Myalgia (muscle symptoms without significant creatine kinase [CK] elevations; also known as statin-associated muscle symptoms) (Ref)

Myopathy (defined as unexplained muscle pain or weakness accompanied by a CK >10 times the ULN) (Ref)

Rhabdomyolysis (CK >40 times the ULN) (Ref) often with acute renal failure secondary to myoglobinuria (Ref)

Immune-mediated necrotizing myopathy (IMNM) (elevated CK plus the presence of autoantibodies against HMG-CoA reductase) (Ref)

Mechanism: Uncertain; alterations in the mevalonate pathway and changes in the electrical and structural characteristics of the sarcolemma related to calcium ion flux possibly contribute (Ref). Decreased ubiquinone, which is essential for energy production in skeletal muscle, may also contribute (Ref). Myopathy/rhabdomyolysis risk is related to circulating active drug concentrations (Ref). IMNM is considered an immune-mediated process; autoantibodies against HMG-CoA reductase (anti-HMG-CoA) have been identified (Ref).

Onset: Delayed; often presents within a few months after starting therapy (highest risk within first year of use), when the dose of the statin is increased, or when introducing an interacting drug (Ref). Muscle symptoms often appear more promptly when patients are reexposed to the same statin (Ref). Duration of statin use prior to development of IMNM is ~2 to 3.5 years (Ref).

Risk factors:

• First year of therapy (Ref)

• Dose increase (for myopathy and rhabdomyolysis, but not IMNM) (Ref)

• Addition of an interacting drug (eg, concurrent use of medications associated with myopathy [eg, gemfibrozil]) (Ref). Since there is minimal metabolism of pravastatin by CYP3A4, low risk for clinically significant drug interactions with CYP3A4 inhibitors; however, concomitant use of inhibitors of OATP1B1 (eg, cyclosporine) or OATP1B3 may result in increased pravastatin plasma levels (Ref)

• Older patients (Ref)

• Hypothyroidism (Ref)

• Preexisting muscle disease (Ref)

• Kidney impairment (Ref)

• Females (Ref)

• Low body mass index (Ref)

• Heavy exercise (Ref)

• Surgery (Ref)

• Higher HMG-COA reductase inhibitory activity (Ref), rosuvastatin > atorvastatin > simvastatin > pravastatin ≈ lovastatin (Ref)

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported adverse reactions are for adults.

>10%:

Neuromuscular & skeletal: Musculoskeletal pain (25%) (table 1)

Pravastatin: Adverse Reaction: Musculoskeletal Pain

Drug (Pravastatin)

Placebo

Dose

Number of Patients (Pravastatin)

Number of Patients (Placebo)

25%

24%

40 mg once daily

10,764

10,719

Respiratory: Upper respiratory tract infection (21%)

1% to 10%: Respiratory: Cough (8%)

<1%: Neuromuscular & skeletal: Myopathy

Frequency not defined: Cardiovascular: Increased serum creatine kinase

Postmarketing:

Cardiovascular: Vasculitis

Dermatologic: Erythema multiforme, lichen planus, skin changes (including changes to hair/nails, discoloration, dryness of mucous membranes, nodules), skin photosensitivity, Stevens-Johnson syndrome, toxic epidermal necrolysis

Endocrine & metabolic: Decreased libido (de Graaf 2004), diabetes mellitus (including exacerbation of diabetes mellitus) (Ohmura 2005), elevated glycosylated hemoglobin (Ohmura 2005), gynecomastia, increased in fasting plasma glucose, thyroid dysfunction

Gastrointestinal: Abdominal pain, constipation, pancreatitis (Tarar 2021; Tsigrelis 2006)

Genitourinary: Cystitis (interstitial) (Huang 2015), dysuria, nocturia, urinary frequency

Hematologic & oncologic: Eosinophilia, hemolytic anemia, increased erythrocyte sedimentation rate, positive ANA titer, purpuric disease

Hepatic: Acute hepatotoxicity (Hartleb 1999), cholestatic jaundice, fulminant hepatic necrosis, hepatic cirrhosis, hepatic failure, hepatic neoplasm, hepatitis, increased serum transaminases, liver steatosis

Hypersensitivity: Anaphylaxis, angioedema

Immunologic: Dermatomyositis (Visconti 2020)

Nervous system: Asthenia, chills, cranial nerve disorder (including dysgeusia, facial paresis, impairment of extraocular movement), malaise, myasthenia (Purvin 2006), nightmares, peripheral nerve palsy

Neuromuscular & skeletal: Arthralgia, arthritis, immune-mediated necrotizing myopathy (Essers 2019), lupus-like syndrome, myalgia (Selva-O’Callaghan 2018, Stroes 2015), polymyalgia rheumatica, polymyositis, rhabdomyolysis (Takei 1999), tendinopathy

Respiratory: Dyspnea, interstitial lung disease, pleural effusion (Kalomenidis 2007)

Contraindications

Hypersensitivity to pravastatin or any component of the formulation; active liver disease or decompensated cirrhosis.

Warnings/Precautions

Concerns related to adverse effects:

• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported with HMG-CoA reductase inhibitors; however, the benefits of statin therapy far outweigh the risk of dysglycemia.

• Myopathy/rhabdomyolysis: Discontinue therapy in any patient in which CPK levels are markedly elevated (>10 times ULN) or if myopathy is suspected/diagnosed.

Disease-related concerns:

• Hepatic impairment: Use with caution in patients who consume large amounts of ethanol and/or have a history of liver disease. May require dosage adjustment in some patients with hepatic impairment.

• Myasthenia gravis: May rarely worsen or precipitate myasthenia gravis (MG); monitor for worsening MG if treatment is initiated (AAN [Narayanaswami 2021]).

Special Populations:

• Older adult: Use with caution in patients with advanced age, these patients are predisposed to myopathy.

• Surgical patients: Based on current research and clinical guidelines, HMG-CoA reductase inhibitors should be continued in the perioperative period for noncardiac and cardiac surgery (ACC/AHA [Fleisher 2014]; ACC/AHA [Hillis 2011]). Perioperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Tablet, Oral, as sodium:

Pravachol: 20 mg [DSC]

Pravachol: 40 mg [DSC] [contains fd&c blue #1 (brill blue) aluminum lake, quinoline (d&c yellow #10) aluminum lake]

Generic: 10 mg, 20 mg, 40 mg, 80 mg

Generic Equivalent Available: US

Yes

Pricing: US

Tablets (Pravastatin Sodium Oral)

10 mg (per each): $2.61 - $3.22

20 mg (per each): $2.83 - $3.27

40 mg (per each): $4.17 - $4.79

80 mg (per each): $4.79

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product

Tablet, Oral, as sodium:

Pravachol: 20 mg [DSC]

Pravachol: 40 mg [DSC] [contains fd&c blue #1 (brilliant blue), quinoline yellow (d&c yellow #10)]

Generic: 10 mg, 20 mg, 40 mg

Administration: Adult

Oral: Administer without regard to meals.

Administration: Pediatric

Oral: May be taken without regard to meals or time of day; administer at least 1 hour before or 4 hours after bile acid resins.

Use: Labeled Indications

Heterozygous familial hypercholesterolemia: To reduce elevated total cholesterol (total-C), LDL-C, apoB, and triglyceride levels, and to increase HDL-C in patients with primary hypercholesterolemia.

Heterozygous familial hypercholesterolemia (pediatrics): Adjunct to diet in children and adolescents ≥8 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C ≥190 mg/dL, LDL ≥160 mg/dL with positive family history of premature cardiovascular disease (CVD), or LDL ≥160 mg/dL with 2 or more other CVD risk factors.

Homozygous familial hypercholesterolemia: To reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (eg, LDL apheresis) or if such treatments are unavailable.

Prevention of atherosclerotic cardiovascular disease:

Primary prevention of atherosclerotic cardiovascular disease: To reduce the risk of myocardial infarction (MI), stroke, revascularization procedures, and angina in adults without a history of coronary heart disease (CHD) but who have multiple CHD risk factors.

Secondary prevention in patients with established atherosclerotic cardiovascular disease: To reduce the risk of MI, stroke, revascularization procedures, and angina in patients with a history of CHD.

Use: Off-Label: Adult

Transplantation, post heart; Transplantation, post kidney

Medication Safety Issues
Sound-alike/look-alike issues:

HMG-CoA reductase inhibitors (when referred to as "statins") may be confused with nystatin.

Pravachol may be confused with Prevacid, Prinivil, propranolol

Pravastatin may be confused with atorvastatin, nystatin, pitavastatin, prasugrel

Metabolism/Transport Effects

Substrate of CYP3A4 (minor), OAT1/3, OATP1B1/1B3 (SLCO1B1/1B3), P-glycoprotein/ABCB1 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

Abiraterone Acetate: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Acipimox: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Antihepaciviral Combination Products: May increase the serum concentration of Pravastatin. Management: Limit the pravastatin dose to a maximum of 40 mg per day when used with antihepaciviral combination products and monitor patients for evidence of pravastatin toxicities (eg, myopathy). Risk D: Consider therapy modification

Asciminib: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Atazanavir: May increase the serum concentration of Pravastatin. Risk C: Monitor therapy

Belumosudil: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Management: Avoid coadministration of belumosudil with these substrates of OATP1B1/1B3 for which minimal concentration increases can cause serious adverse effects. If coadministration is required, dose reductions of the OATP1B1/1B3 substrate may be required. Risk D: Consider therapy modification

Bempedoic Acid: May increase the serum concentration of Pravastatin. Management: Avoid coadministration of bempedoic acid with pravastatin doses greater than 40 mg due to the potential for increased pravastatin concentrations and pravastatin-related myopathy. Risk D: Consider therapy modification

Bezafibrate: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Bezafibrate may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). More specifically, bezafibrate may increase the serum concentration of fluvastatin Management: Avoid use of bezafibrate and HMG-CoA reductase inhibitors (statins) unless strictly indicated due to the increased of muscle toxicity (including rhabdomyolysis). In patients who may be predisposed to myopathy, concomitant use is contraindicated. Risk D: Consider therapy modification

Bile Acid Sequestrants: May decrease the serum concentration of Pravastatin. Management: Administer pravastatin at least 1 hour before or 4 hours after administration of bile-acid resins (eg, cholestyramine, colestipol, colesevelam) to minimize the risk for any significant interaction. Risk D: Consider therapy modification

Bulevirtide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Management: Coadministration of bulevirtide with OATP1B1/1B3 (also known as SLCO1B1/1B3) substrates should be avoided when possible. If used together, close clinical monitoring is recommended. Risk D: Consider therapy modification

Bulevirtide: May increase the serum concentration of NTCP Substrates. Management: Coadministration of bulevirtide with sodium taurocholate co-transporting polypeptide (NTCP) substrate should be avoided when possible. If used together, close clinical monitoring is recommended. Risk D: Consider therapy modification

CarBAMazepine: May decrease the serum concentration of Pravastatin. Risk C: Monitor therapy

Ceftobiprole Medocaril: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid combination

Ciprofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid the use of HMG-CoA reductase inhibitors and ciprofibrate if possible. If concomitant therapy is considered, benefits should be carefully weighed against the risks, and patients should be monitored closely for signs/symptoms of muscle toxicity. Risk D: Consider therapy modification

Clarithromycin: May increase the serum concentration of Pravastatin. Management: Limit pravastatin to a maximum of 40 mg/day when used in combination with clarithromycin. If this combination is used, monitor patients more closely for evidence of pravastatin toxicity. Risk D: Consider therapy modification

Colchicine: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Colchicine may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). HMG-CoA Reductase Inhibitors (Statins) may increase the serum concentration of Colchicine. Risk C: Monitor therapy

CycloSPORINE (Systemic): May increase the serum concentration of Pravastatin. Pravastatin may increase the serum concentration of CycloSPORINE (Systemic). Management: Initiate pravastatin dose at 10 mg daily and limit the maximum pravastatin dose to 20 mg daily in patients who are also receiving cyclosporine. Monitor for pravastatin toxicities (eg, myalgia, myopathy, rhabdomyolysis) if combined. Risk D: Consider therapy modification

Daclatasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

DAPTOmycin: HMG-CoA Reductase Inhibitors (Statins) may enhance the adverse/toxic effect of DAPTOmycin. Specifically, the risk of skeletal muscle toxicity may be increased. Management: Consider temporarily stopping statin (HMG-CoA reductase inhibitor) therapy prior to daptomycin. If daptomycin is used with a statin, creatine phosphokinase (CPK) monitoring could be considered. Risk D: Consider therapy modification

Darolutamide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Darunavir: May increase the serum concentration of Pravastatin. This effect has been demonstrated with darunavir/ritonavir and may occur with darunavir/cobicistat. The individual contributions of darunavir, ritonavir, and cobicistat are unknown. Risk C: Monitor therapy

Efavirenz: May decrease the serum concentration of Pravastatin. Risk C: Monitor therapy

Eltrombopag: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Encorafenib: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Erythromycin (Systemic): May increase the serum concentration of Pravastatin. Management: Limit pravastatin dose to a maximum of 40 mg/day when used in combination with erythromycin. If this combination is used, monitor patients more closely for evidence of pravastatin toxicity. Risk D: Consider therapy modification

Fenofibrate and Derivatives: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Fostemsavir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest possible starting statin dose and monitor patients closely for statin-related adverse effects (eg, muscle aches and pains) during coadministration with fostemsavir. Risk D: Consider therapy modification

Fusidic Acid (Systemic): May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for muscle toxicities, including rhabdomyolysis may be significantly increased. Management: Avoid concurrent use whenever possible. Use is listed as contraindicated in product characteristic summaries in several countries, although UK labeling suggests that use could be considered under exceptional circumstances and with close supervision. Risk X: Avoid combination

Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid combination

Glecaprevir and Pibrentasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest statin dose possible if combined with glecaprevir/pibrentasvir and monitor for increased statin effects/toxicities. Avoid concomitant use with atorva-, simva-, or lovastatin. Limit rosuvastatin to 10 mg daily and reduce pravastatin dose 50% Risk D: Consider therapy modification

Itraconazole: May increase the serum concentration of Pravastatin. Risk C: Monitor therapy

Lanthanum: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Administer HMG-CoA reductase inhibitors (eg, statins) at least two hours before or after lanthanum. Risk D: Consider therapy modification

Leflunomide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Leniolisib: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk X: Avoid combination

Letermovir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Nelfinavir: May decrease the serum concentration of Pravastatin. Risk C: Monitor therapy

Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

PARoxetine: Pravastatin may enhance the adverse/toxic effect of PARoxetine. Specifically, blood glucose elevations may occur with the combination. Risk C: Monitor therapy

Pretomanid: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Raltegravir: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid combination

Repaglinide: HMG-CoA Reductase Inhibitors (Statins) may increase the serum concentration of Repaglinide. Risk C: Monitor therapy

Resmetirom: May increase the serum concentration of Pravastatin. Management: Limit the pravastatin dose to 40 mg daily during coadministration with resmetirom. Monitor for increased pravastatin adverse effects (eg, myalgias) during coadministration. Risk D: Consider therapy modification

RifAMPin: May decrease the serum concentration of Pravastatin. Risk C: Monitor therapy

Roxadustat: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Rupatadine: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for increased CPK and/or other muscle toxicities may be increased. Risk C: Monitor therapy

Saquinavir: May decrease the serum concentration of Pravastatin. This effect has only been demonstrated with saquinavir/ritonavir. The individual contributions of saquinavir and ritonavir are unknown. Risk C: Monitor therapy

Simeprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Teriflunomide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Risk C: Monitor therapy

Trofinetide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Management: Avoid concurrent use with OATP1B1/1B3 substrates for which small changes in exposure may be associated with serious toxicities. Monitor for evidence of an altered response to any OATP1B1/1B3 substrate if used together with trofinetide. Risk D: Consider therapy modification

Vadadustat: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Vitamin K Antagonists (eg, warfarin): HMG-CoA Reductase Inhibitors (Statins) may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy

Voclosporin: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates (Clinically Relevant with Inhibitors). Risk C: Monitor therapy

Voxilaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest statin dose possible if combined with voxilaprevir and monitor patients for increased statin effects/toxicities. Avoid concomitant use of voxilaprevir with rosuvastatin or pitavastatin, and limit pravastatin doses to 40 mg daily. Risk D: Consider therapy modification

Reproductive Considerations

Adequate contraception is recommended if an HMG-CoA reductase inhibitor (statin) is required in patients who may become pregnant (AHA/ACC [Grundy 2019]; CCS [Pearson 2021]). Patients planning to become pregnant should discuss their lifetime risk of cardiovascular disease, as well as risks and benefits of statin therapy with their health care team (CCS [Pearson 2021]). When appropriate, statins can be discontinued 1 to 2 months prior to conception (AHA/ACC [Grundy 2019]).

When a statin is needed in a patient of reproductive potential, a more hydrophilic option (eg, pravastatin, rosuvastatin) may be preferred to limit placental transfer (CCS [Pearson 2021]).

Pregnancy Considerations

Pravastatin crosses the placenta (Ahmed 2020; Costantine 2016; Costantine 2021; Nanovskaya 2013).

Cord blood concentrations were near or below the limit of quantification (<0.1 ng/mL) in 10 women administered pravastatin 10 mg once daily (Costantine 2016). Following administration of pravastatin 10 mg once daily to 1 patient during pregnancy, the estimated placental transfer was 25.5%; pravastatin was not detected in the infant serum 4 days after delivery. In a second patient administered pravastatin 10 mg once daily during pregnancy, the estimated placental transfer was 23.8% of the maternal dose, and pravastatin was not detected in infant serum when measured 1 day after birth (Saito 2021).

In healthy pregnancies, changes in lipid synthesis occur that are required for normal placental and fetal growth. Low-density lipoprotein cholesterol and triglycerides increase as pregnancy progresses and decline postpartum. HMG-CoA reductase inhibitors (statins) decrease the synthesis of cholesterol and substances derived from cholesterol. Therefore, based on the mechanism of action, in utero exposure may cause fetal harm (Lecarpentier 2012); however, data from available studies have not shown an increased risk of major congenital anomalies following first trimester exposure (Bateman 2015; Chang 2021; Vahedian-Azimi 2021a). Additional data are needed to evaluate other pregnancy outcomes, such as miscarriage (Vahedian-Azimi 2021b).

Due to pregnancy-induced physiologic changes, some pharmacokinetic properties of pravastatin may be altered (limited data) (Costantine 2016; Costantine 2021).

Because there is potential for fetal harm, statins should be discontinued once pregnancy is recognized (AHA/ACC [Grundy 2019]; Brunham 2018). If lipid-lowering therapy during pregnancy is required, it should be individualized based on the therapeutic needs of the patient, considering the lifetime risk of untreated disease, use of nonstatin therapies, as well as the known risks and benefits of statins. Based on limited data, when a statin is needed in a pregnant patient, a more hydrophilic option (eg, pravastatin, rosuvastatin) may be preferred. Lipophilic statins (eg, atorvastatin, fluvastatin, lovastatin, simvastatin, pitavastatin) may be more likely to cross the placenta and increase the risk of congenital malformations (AHA/ACC [Grundy 2019]; CCS [Pearson 2021]; Lecarpentier 2012).

Additional data are needed to clarify the role of statins for the prevention of atherosclerotic cardiovascular disease in at-risk pregnant patients (AHA/ACC [Grundy 2019]; AHA [Parikh 2021]; CCS [Pearson 2021]).

Breastfeeding Considerations

Pravastatin is present in breast milk.

Data related to the presence of pravastatin in breast milk are available from 8 lactating women administered pravastatin 20 mg twice daily for 2.5 days. After the fifth dose, maximum maternal serum concentrations were ~40 ng/mL (pravastatin) and ~26 ng/mL (metabolite), and maximum breast milk concentrations were ~3.9 ng/mL (pravastatin) and ~2.1 ng/mL (metabolite). Maximum breast milk concentrations were detected ~3 hours after the dose (Pan 1988). Following administration of pravastatin 10 mg once daily during pregnancy, pravastatin was not detected in breast milk when tested in 1 woman 3 days postpartum or another woman 5 days postpartum. Maternal pravastatin use did not continue after delivery (Saito 2021).

HMG-CoA reductase inhibitors (statins) decrease the synthesis of cholesterol and substances derived from cholesterol. Normal concentrations of cholesterol in breast milk are required for infant development (Holmsen 2017; Lecarpentier 2012). Due to the potential for serious adverse reactions in the breastfed infant, based on the mechanism of action, breastfeeding is not recommended by the manufacturer. Available guidelines recommend resuming statin therapy once breastfeeding is completed (AHA/ACC [Grundy 2019]; CCS [Pearson 2021]).

Dietary Considerations

Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 6 weeks and the diet should be continued during drug therapy.

Red yeast rice contains variable amounts of several compounds that are structurally similar to HMG-CoA reductase inhibitors, primarily monacolin K (or mevinolin) which is structurally identical to lovastatin; concurrent use of red yeast rice with HMG-CoA reductase inhibitors may increase the incidence of adverse and toxic effects (Lapi 2008; Smith 2003).

Monitoring Parameters

ACC/AHA Blood Cholesterol Guideline recommendations ( ACC/AHA [Grundy 2019]):

Lipid panel (total cholesterol, HDL, LDL, triglycerides): Lipid profile (fasting or nonfasting) before initiating treatment. Fasting lipid profile should be rechecked 4 to 12 weeks after starting therapy and every 3 to 12 months thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.

Hepatic transaminase levels: Baseline measurement of hepatic transaminase levels (AST and ALT); measure AST, ALT, total bilirubin, and alkaline phosphatase if symptoms suggest hepatotoxicity (eg, unusual fatigue or weakness, loss of appetite, abdominal pain, dark-colored urine or yellowing of skin or sclera) during therapy.

CPK: CPK should not be routinely measured. Baseline CPK measurement is reasonable for some individuals (eg, family history of statin intolerance or muscle disease, clinical presentation, concomitant drug therapy that may increase risk of myopathy). May measure CPK in any patient with symptoms suggestive of myopathy (pain, tenderness, stiffness, cramping, weakness, or generalized fatigue).

Evaluate for new-onset diabetes mellitus during therapy; if diabetes develops, continue statin therapy and encourage adherence to a heart-healthy diet, physical activity, a healthy body weight, and tobacco cessation.

Monitor for signs and/or symptoms of myopathy and rhabdomyolysis (especially in patients who had immune-mediated necrotizing myopathy on a previous HMG-CoA reductase inhibitor).

If patient develops a confusional state or memory impairment, may evaluate patient for nonstatin causes (eg, exposure to other drugs), systemic and neuropsychiatric causes, and the possibility of adverse effects associated with statin therapy.

Manufacturer's labeling: Consider neuromuscular and serologic testing if immune-mediated necrotizing myopathy is suspected.

Mechanism of Action

Pravastatin is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is the rate-limiting enzyme involved in de novo cholesterol synthesis. In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), they also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects (de Denus 2002; Ray 2005).

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: Several days

Peak effect: 4 weeks

LDL-reduction: 40 mg/day: 34% (for each doubling of this dose, LDL-C is lowered by ~6%)

Absorption: Rapidly absorbed; average absorption 34%

Distribution: Vd: 0.46 L/kg

Protein binding: ~50%

Metabolism: Hepatic multiple metabolites; primary metabolite is 3 alpha-hydroxy-iso-pravastatin (2.5% to 10% activity of parent drug); extensive first-pass metabolism

Bioavailability: 17%

Half-life elimination:

Children and Adolescents (4.9 to 15.6 years): 1.6 hours; range: 0.85 to 4.2 hours (Hedman 2003)

Adults: 77 hours (including all metabolites); Pravastatin: ~2 to 3 hours (Pan 1990); 3 alpha-hydroxy-iso-pravastatin: ~1.5 hours (Gustavson 2005)

Time to peak, serum: 1 to 1.5 hours

Excretion: Feces (70%); urine (~20%, 8% as unchanged drug)

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Older adult: Mean AUC was approximately 27% greater and mean cumulative urinary excretion was approximately 19% lower in elderly men. Mean AUC was approximately 46% higher and mean cumulative urinary excretion was approximately 18% lower in elderly women.

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Lipostat;
  • (AR) Argentina: Pravacol;
  • (AT) Austria: Panchol | Pravachol | Pravastatin +pharma | Pravastatin 1a pharma gmbh | Pravastatin genericon pharma | Pravastatin hexal pharma | Pravastatin interpharm | Pravastatin ratiopharm | Pravastatin sandoz | Sanaprav | Selipran;
  • (AU) Australia: Apo pravastatin | Auro pravastatin | Chemmart Pravastatin | Cholstat | Cholvastin | Genrx Pravastatin | Liprachol | Pravachol | Pravastatin | Pravastatin actavis | Pravastatin an | Pravastatin Generic Health | Pravastatin ps | Pravastatin RL | Pravastatin sandoz | Pravastatin Winthrop | Pravastatin-GA | Terry White Chemists Pravastatin | Vastoran;
  • (BE) Belgium: Docpravastatine | Prareduct | Pravasine | Pravastatin ab | Pravastatine Arrow | Pravastatine bexal | Pravastatine eg | Pravastatine ratiopharm | Pravastatine Sandoz | Pravastatine sodium accord | Pravastatine teva;
  • (BG) Bulgaria: Lipostat | Pravastatin;
  • (BR) Brazil: Lenitral | Mevalotin | Pravacol | Pravastat Sodic | Pravastatina sodica;
  • (CH) Switzerland: Mevalotin | Prava-Med | Pravalotin | Pravalotin Mepha | Pravasta eco | Pravastatin actavis | Pravastatin Axapharm | Pravastatin mepha | Pravastatin spirig | Pravastatin teva | Pravastatin zentiva | Pravastatin-1 A Pharma | Pravastax | Selipran;
  • (CI) Côte d'Ivoire: Pravastor;
  • (CL) Chile: Pravacol;
  • (CN) China: Fu li ta zhi | Fu ta ning | Mei bai le zhen | Mevalotin | Pravachol | Pu hui zhi;
  • (CO) Colombia: Pranvalotin | Pravacol | Pravalip | Pravalotin | Pravastatina | Pravax | Pravyl;
  • (CZ) Czech Republic: Lipostat | Vitastat;
  • (DE) Germany: Lipifacil | Liprevil | Mevalotin | Mevalotin protect | Prava | Prava basic | Prava Q | Pravabeta | Pravagamma | Pravagodur | Pravalich | Pravalip | Pravasin | Pravasin protect | Pravastatin | Pravastatin AAA | Pravastatin Accord | Pravastatin actavis | Pravastatin AL | Pravastatin almus | Pravastatin Aurus | Pravastatin Corax | Pravastatin CT | Pravastatin dura | Pravastatin Heumann | Pravastatin hexal | Pravastatin Isis | Pravastatin ratiopharm | Pravastatin sandoz | Pravastatin Stada | Pravastatin TAD | Pravastatin-1 A Pharma | Selipran | Sigaprava;
  • (DO) Dominican Republic: Lipina | Prascolend | Pravacol | Pravastatina Genfar;
  • (EC) Ecuador: Pravacol | Pravator;
  • (EE) Estonia: Lipostat | Pravahexal | Pravastatin Accord | Pravastatin Nycomed | Pravastatin Pliva;
  • (EG) Egypt: Cholestate | Lipizad | Lipostat;
  • (ES) Spain: Bristacol | Lipemol | Liplat | Minuscol | Prareduct | Pravastatina acost | Pravastatina actavis | Pravastatina almus | Pravastatina alter | Pravastatina Angenerico | Pravastatina Apotex | Pravastatina aurobindo | Pravastatina aurovistas | Pravastatina bayvit | Pravastatina bexal | Pravastatina cinfa | Pravastatina combix | Pravastatina Cuve | Pravastatina Davur | Pravastatina dermogeneris | Pravastatina Edigen | Pravastatina kern | Pravastatina Korhispana | Pravastatina merck | Pravastatina mylan pharmaceuticals | Pravastatina Normon | Pravastatina Pharmagenus | Pravastatina Qualigen | Pravastatina ratiopharm | Pravastatina Sandoz | Pravastatina Tarbis | Pravastatina Tecnigen | Pravastatina ur | Pravastatina Vir | Pravastatina Winthrop | Pritadol;
  • (FI) Finland: Pravachol | Pravastatin Alternova | Pravastatin arrow | Pravastatin hexal | Pravastatin Orion | Pravastatin ranbaxy | Pravastatin ratiopharma | Pravastatin sandoz | Pravastatin Winthrop;
  • (FR) France: Elisor | Pravastatine | Pravastatine Accord | Pravastatine actavis | Pravastatine Almus | Pravastatine Alter | Pravastatine Arrow | Pravastatine Biogaran | Pravastatine Bouchara Recordati | Pravastatine cristers | Pravastatine eg | Pravastatine Evolugen | Pravastatine evolugen pharma | Pravastatine gerda | Pravastatine Isomed | Pravastatine Lbr | Pravastatine merck | Pravastatine phr lab | Pravastatine Qualimed | Pravastatine ratiopharm | Pravastatine RPG | Pravastatine Sandoz | Pravastatine teva | Pravastatine Zydus | Vasten;
  • (GB) United Kingdom: Lipostat | Pravastatin | Pravastatin almus | Pravastatin arrow | Pravastatin cox | Pravastatin focus | Pravastatin kent | Pravastatin medreich | Pravastatin ntn | Pravastatin sandoz;
  • (GR) Greece: Asto-chol | Lipoprav | Maxudin | Ositron | Pravachol | Pravadium | Pravafact | Pravalip | Pravalong | Pravanox | Pravostin | Privast | Sosmin | Vastil;
  • (HK) Hong Kong: Apo pravastatin | Pms Pravastatin | Pravachol;
  • (HR) Croatia: Statim;
  • (HU) Hungary: Nikron | Prastin;
  • (ID) Indonesia: Cholespar | Invastin | Koleskol | Mevachol | Mevalotin | Novales | Pravachol | Pravastatin;
  • (IE) Ireland: Bellprav | Beneprav | Bystat | Lipaprav | Lipostat | Lipovas | Pravamel | Pravastatin | Pravastatin teva | Pravat | Pravitin;
  • (IL) Israel: Lipidal | Pravalip | Pravastatin teva;
  • (IN) India: Prastatin | Pravator | Prestatin;
  • (IT) Italy: Adrestat | Aplactin | Prasterol | Pravaselect | Pravastatina | Pravastatina Acco | Pravastatina actavis | Pravastatina almus | Pravastatina Arrow | Pravastatina aurobindo | Pravastatina Doc | Pravastatina EG | Pravastatina Fg | Pravastatina Fidia | Pravastatina Ipso pharma | Pravastatina MG | Pravastatina mylan | Pravastatina Ranbaxy | Rastanit | Sanaprav | Selectin | Setac | Vasticor;
  • (JO) Jordan: Lipostat | Lowchol;
  • (JP) Japan: Alsetin | Cholerit | Maibastan | Mevalation | Mevalect | Mevalilin | Mevalocut | Mevalotin | Mevan | Mevarich | Mevarich kaken | Mevasrolin | Mevastan | Mevatorte | Mindorotin | Pramevan | Pravalon | Pravamate | Pravapeak | Pravastan | Pravastan chemiphar | Pravastatin Na | Pravastatin na kn | Pravastatin na me | Pravastatin Sododium Tsuruhara | Pravatin | Provatin | Tatsuplamin;
  • (KR) Korea, Republic of: Mevalotin | Mevarotin | Mevatin | Pavatin | Prastan | Pratan | Pravastar | Pravastatin | Stapra | Vasopran;
  • (KW) Kuwait: Lipostat;
  • (LB) Lebanon: Apo pravastatin | Lipostat | Pravastatine | Stavacor;
  • (LT) Lithuania: Lipostat | Pravahexal | Pravastatin Pliva | Pravastatin ratiopharm;
  • (LU) Luxembourg: Docpravastatine | Prareduct | Pravasine | Pravasor | Pravastatin hexal;
  • (LV) Latvia: Lipostat | Pravastatin | Pravastatin-1 A Pharma | Pravastatina Pliva;
  • (MA) Morocco: Elisor | Pravastatine Gt | Pravator;
  • (MX) Mexico: Accogard | Apotivaz | Astin-10 | Astin-20 | Brakhor | Brufincol | Celuterol | Colpradin | Daxon t | Emipastin | Fepina | Genoestatina | Glicosar | Kenstatin | Kenvastin | Lemma ld | Lexet | Loretsin | Mavitina | Novina | Paver | Piflaxan | Prascolend | Prasiver | Pravacol | Pravastatin | Pravastatin landsteiner | Pravastatina | Pravastatina brissa | Pravastatina GI | Pravastatina gi ke | Pravastatina nafar | Striacol | Tratinal | Trydanil H | Valprastin | Vapradem | Varlex | Venxicor | Xipral;
  • (MY) Malaysia: Apo pravastatin | Avaco | Pratin | Pravachol | Pravatas | Pravid;
  • (NL) Netherlands: Elisor | Lipostat | Pravachol | Pravastatin Na | Pravastatine | Pravastatine A | Pravastatine na | Pravastatine Na CF | Pravastatine Na Merck | Pravastatine ranbaxy | Pravastatinenatrium Accord | Pravastatinenatrium alpharma | Pravastatinenatrium Gf | Pravastatinenatrium Katwijk | Pravastatinenatrium PCH | Pravastatinenatrium ratiopharm | Pravastatinenatrium Sandoz | Sanaprav | Selektine;
  • (NO) Norway: Pravachol | Pravastatin | Pravastatin Nycomed | Pravastatin sandoz | Pravastatin teva;
  • (NZ) New Zealand: Apo pravastatin | Cholvastin | Lipostat | Pravastatin mylan | Pravastatin viatris;
  • (PE) Peru: Pravacol | Pravastatina | Pravastine | Pravator;
  • (PH) Philippines: Lipostat | Pravaz;
  • (PK) Pakistan: Lipostat | Nupra | Pralip | Pranu | Pravachol;
  • (PL) Poland: Apo prava | Lipostat | Pravator;
  • (PR) Puerto Rico: Pravachol;
  • (PT) Portugal: Pravacol | Pravastatina | Pravastatina alter | Pravastatina aurobindo | Pravastatina bluepharma | Pravastatina bluesar | Pravastatina Ciclum | Pravastatina cinfa | Pravastatina generis | Pravastatina germed | Pravastatina lizatrovarin | Pravastatina mepha | Pravastatina mylan | Pravastatina Sandoz | Pravastatina Sivatca | Pravastatina Stada | Pritanol | Sanaprav;
  • (QA) Qatar: Lipostat;
  • (RO) Romania: Lipostat;
  • (RU) Russian Federation: Lipostat | Pravastatin;
  • (SA) Saudi Arabia: Lipostat;
  • (SE) Sweden: Pravachol | Pravastatin arrow | Pravastatin copyfarm | Pravastatin ranbaxy | Pravastatin sandoz | Pravastatin teva;
  • (SG) Singapore: Pravachol;
  • (SI) Slovenia: Pravastatin teva;
  • (SK) Slovakia: Lipostat;
  • (TH) Thailand: Mevalotin | Pravatas;
  • (TN) Tunisia: Elisor | Pravast | Pravastatin | Pravastatine winthrop | Pravastatine zentiva;
  • (TR) Turkey: Pravachol;
  • (TW) Taiwan: Dehypotin Protect | Joinlo | Maxatin | Mevalotin | Mevalotin protect | Pavadin | Pavatin Protect | Perastin | Pratin | Pravastatin Na | U-prava;
  • (UA) Ukraine: Pravastatin sandoz;
  • (VE) Venezuela, Bolivarian Republic of: Mevalotin | Pravacol | Pravastatina;
  • (VN) Viet Nam: Agivastar | Fasthan | Hypevas | Hypravas;
  • (ZA) South Africa: Arrow pravastatin | Aspen Pravastatin | Colite | Novales | Pixeta | Pranalip | Prava | Pravacor
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