Generic Name: Fluvastatin Sodium
Class: HMG-CoA Reductase Inhibitors
VA Class: CV350
Chemical Name: [R*,S* - (E)] - (±) - 7 - [3 - (4 - Fluorophenyl) - 1 - (1 - methylethyl) - 1H - indol - 2 - yl] - 3,5 - dihydroxy - 6 - heptenoic acid monosodium salt
Molecular Formula: C24H26FNO4•Na
CAS Number: 93957-55-2

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).1 4 5

Uses for Lescol

Prevention of Cardiovascular Events

ACC/AHA cholesterol management guideline recommends statins as first-line therapy for prevention of atherosclerotic cardiovascular disease (ASCVD) in adults; fluvastatin may be used for primary or secondary prevention in adults when moderate-intensity statin therapy is indicated.350 (See Prevention of Cardiovascular Events under Dosage and Administration.)

Adjunct to nondrug therapies (i.e., lifestyle modifications) in patients with CHD to reduce the risk of undergoing coronary revascularization procedures.72 350 Unless contraindicated, statins are considered first-line therapy in patients 21–75 years of age who have clinical ASCVD (i.e., acute coronary syndromes; history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin).350 Addition of a nonstatin drug (i.e., niacin) to statin-based therapy (i.e., simvastatin with or without ezetimibe) in patients with established cardiovascular disease not shown to provide incremental ASCVD risk reduction benefit beyond that provided by statin monotherapy.350 354

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Adjunct to nondrug therapies (e.g., dietary management) in patients with CHD to slow the progression of coronary atherosclerosis.72

Current recommendations from ACC/AHA regarding prevention of ASCVD and lifestyle modifications to reduce cardiovascular risk are available at or 352

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia (heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIa or IIb).1 72 Also used in combination with fenofibrate to decrease triglyceride concentrations and increase HDL-cholesterol concentrations in patients with mixed dyslipidemia and CHD (or CHD risk equivalents) who are on optimal statin therapy; however, no incremental benefit on cardiovascular morbidity and mortality beyond that provided by statin monotherapy.73 353

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, and apo B concentrations in the management of heterozygous familial hypercholesterolemia in boys and girls (≥1 year postmenarchal) 10–16 years of age who, despite an adequate trial of dietary management, have a serum LDL-cholesterol concentration of ≥190 mg/dL or a serum LDL-cholesterol concentration of ≥160 mg/dL and either a family history of premature cardiovascular disease or ≥2 other cardiovascular risk factors.1 72

Reduction of total and LDL-cholesterol concentrations in patients with hypercholesterolemia associated with or exacerbated by diabetes mellitus (diabetic dyslipidemia),54 renal insufficiency,63 cardiac or renal transplantation,20 21 22 21 27 55 57 64 or nephrotic syndrome (nephrotic hyperlipidemia).24 65

Lescol Dosage and Administration

General

  • Patients should be placed on a standard lipid-lowering diet before initiation of fluvastatin therapy and should remain on this diet during treatment with the drug.1 60

Monitoring during Antilipemic Therapy

  • Manufacturer recommends obtaining lipoprotein concentrations periodically during fluvastatin therapy.1 ACC/AHA cholesterol management guideline recommends obtaining lipoprotein concentrations within 4–12 weeks following initiation of statin therapy (to assess response and adherence) and monitoring every 3–12 months thereafter as clinically indicated.350

  • Periodically reinforce adherence to lifestyle modifications during statin therapy.350

Administration

Oral Administration

Administer orally without regard to meals.1

Administer conventional capsules once (in the evening) or twice daily;1 do not administer two 40-mg capsules at one time.72 Do not open capsules prior to administration.1

Administer extended-release tablets as a single dose at any time of day.1 Do not break, crush, or chew tablets.1

Dosage

Available as fluvastatin sodium; dosage expressed in terms of fluvastatin.1

Pediatric Patients

Dyslipidemias
Oral

Children 10–16 years of age: Initially, 20 mg once daily.1

Adjust dosage at 6-week intervals until the desired effect on lipoprotein concentrations is observed or a daily dosage of 80 mg (administered as 40 mg twice daily as conventional capsules or 80 mg once daily as extended-release tablets) is reached.1 72

Adults

Prevention of Cardiovascular Events

Select appropriate statin intensity to achieve optimal ASCVD risk reduction.350 Giving maximally tolerated statin intensity is preferred over giving lower statin dosages in combination with nonstatin drugs, a strategy not yet shown to reduce ASCVD risk.350

Although dosages of 20–40 mg once daily (as conventional capsules) or 80 mg once daily (as extended-release tablets) are FDA-labeled dosages, these dosages were not evaluated in randomized controlled studies reviewed by the ACC/AHA expert panel.350

Primary Prevention in Patients with LDL-cholesterol Concentrations ≥190 mg/dL (≥21 years of age)
Oral

ACC/AHA cholesterol management guideline recommends initiating high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

Primary Prevention in Patients with Type 1 or 2 Diabetes Mellitus (40–75 years of age)
Oral

ACC/AHA cholesterol management guideline recommends moderate-intensity statin therapy (e.g., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]).350

If estimated 10-year ASCVD risk ≥7.5%, consider high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

In patients <40 or >75 years of age, consider potential benefits, adverse effects, drug interactions, and patient preferences when deciding to initiate, continue, or intensify statin therapy.350

Primary Prevention in Patients with LDL-cholesterol Concentrations 70–189 mg/dL and Elevated ASCVD Risk (40–75 years of age)
Oral

Estimated 10-year ASCVD risk ≥7.5%: ACC/AHA cholesterol management guideline recommends moderate- (e.g., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]) to high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin).350

Estimated 10-year ASCVD risk of 5 to <7.5%: ACC/AHA cholesterol management guideline states may consider moderate-intensity statin therapy.350

Consider potential benefits, adverse effects, drug interactions, and patient preferences before initiating statin therapy.350

Secondary Prevention in Patients with Clinical ASCVD (i.e., acute coronary syndromes; history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease presumed to be of atherosclerotic origin) (21–75 years of age)
Oral

ACC/AHA cholesterol management guideline recommends high-intensity statin therapy (i.e., with atorvastatin or rosuvastatin) unless contraindicated.350

In patients at increased risk for developing statin-associated adverse effects or in whom high-intensity statin therapy is inappropriate or contraindicated, consider moderate-intensity statin therapy (e.g., fluvastatin 40 mg twice daily [as conventional capsules], fluvastatin 80 mg once daily [as extended-release tablets]) if tolerated.350

Patients >75 years of age: Individualize therapy based on potential benefits, adverse effects, drug interactions, and patient preferences; may consider moderate-intensity statin therapy if tolerated.350

Dyslipidemias
Oral

Patients who require reductions in LDL-cholesterol concentrations of <25%: Initially, 20 mg once daily in the evening.1

Patients who require reductions of >25% in LDL-cholesterol concentrations or patients with primary hypercholesterolemia or mixed dyslipidemia: Initially, 40 mg (as conventional capsules) once daily in the evening, 80 mg (as extended-release tablets) once daily at any time of day, or 40 mg (as conventional capsules) twice daily.1 72

Adjust dosage at intervals of ≥4 weeks until the desired effect on lipoprotein concentrations is observed.1

Usual maintenance dosage is 20–80 mg daily.1

Dosage Modification
Oral

ACC/AHA cholesterol management guideline states may consider decreasing statin dosage when LDL-cholesterol concentrations are <40 mg/dL on 2 consecutive measurements; however, no data to suggest that LDL-cholesterol concentrations <40 mg/dL increase risk of adverse effects.350

Prescribing Limits

Pediatric Patients

Oral

Children 10–16 years of age: Maximum 80 mg daily.1

Special Populations

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease; monitor such patients closely.1

Contraindicated in patients with active liver disease or unexplained, persistent increases in serum aminotransferase concentrations.1

Renal Impairment

Dosage modification is not necessary in patients with mild to moderate renal impairment.1

Dosages >40 mg daily have not been studied in patients with severe renal impairment; use caution when administering higher dosages to such patients.1

Cautions for Lescol

Contraindications

  • Active liver disease or unexplained, persistent elevations of serum aminotransferases.1

  • Pregnancy or lactation.1 Administer to women of childbearing age only when they are highly unlikely to conceive and have been informed of the potential hazards.1

  • Known hypersensitivity to fluvastatin or any ingredient in the formulation.1

Warnings/Precautions

Fetal/Neonatal Morbidity and Mortality

Suppression of cholesterol biosynthesis could cause fetal harm.1 Congenital anomalies following intrauterine exposure to statins reported rarely.1

Administer to women of childbearing age only when they are highly unlikely to conceive and have been informed of the potential hazards.1 If the patient becomes pregnant while taking the drug, discontinue therapy and apprise the patient of the potential hazard to the fetus.1

Musculoskeletal Effects

Myopathy (manifested as muscle pain, tenderness, or weakness and serum CK [CPK] concentration increases >10 times the ULN) has been reported.1

Rhabdomyolysis (characterized by muscle pain or weakness with marked increases [>10 times the ULN] in serum CK concentrations and increases in Scr [usually accompanied by brown urine and urinary myoglobinuria]) with acute renal failure secondary to myoglobinuria has been reported.1 72

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.355 Characterized by proximal muscle weakness and elevated CK concentrations that persist despite discontinuance of statin therapy, necrotizing myopathy without substantial inflammation, and improvement following therapy with immunosuppressive agents.355

Risk of myopathy increased in patients receiving higher dosages of statins; patients with multisystem disease (e.g., renal or hepatic impairment), concurrent serious infections, or inadequately treated hypothyroidism; geriatric patients (>65 years of age); patients with small body frame and frailty; and patients undergoing surgery (i.e., during perioperative periods).72

Certain drug interactions also may increase risk of myopathy and/or rhabdomyolysis.1 72 (See Specific Drugs under Interactions.)

Use with caution in patients with predisposing factors for myopathy (e.g., advanced age [>65 years of age], renal impairment, inadequately treated hypothyroidism).72

Measure baseline serum CK concentrations prior to initiation of therapy, particularly in patients at high risk of developing musculoskeletal toxicity (e.g., geriatric patients, black men, patients receiving concomitant therapy with myotoxic drugs).

Obtain serum CK concentrations and compare with baseline concentrations in patients presenting with musculoskeletal symptoms suggestive of myopathy; because hypothyroidism may be a predisposing factor, TSH concentrations also should be obtained in such patients.

ACC/AHA cholesterol management guideline does not recommend routine monitoring of CK concentrations in adults; however, may obtain CK concentrations before initiating therapy in adults at increased risk of developing adverse musculoskeletal effects (e.g., patients with personal or family history of statin intolerance or muscle disease, patients receiving concomitant therapy with myotoxic drugs).350 During statin therapy, may measure CK concentrations in adults with muscle symptoms (e.g., pain, tenderness, stiffness, cramping, weakness, generalized fatigue).350

National Heart, Lung, and Blood Institute (NHLBI) expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents recommends obtaining CK concentrations in pediatric patients before initiating statin therapy and routinely monitoring for muscle toxicity during therapy.357

Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked CK elevation.72 Discontinue therapy if serum CK concentrations become markedly elevated or if myopathy is diagnosed or suspected.1

Monitor patients weekly if myalgia (muscle pain, tenderness) is present with either no CK elevation or a moderate elevation (3–10 times the ULN) until manifestations improve; discontinue if manifestations worsen.

Dosage reduction or temporary discontinuance may be prudent in patients with muscle discomfort and/or weakness in the presence of progressive elevation of CK concentrations on serial measurements.

Temporarily withhold therapy in any patient experiencing an acute or serious condition predisposing to the development of acute renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).1 Initiate IV hydration therapy (in a hospital setting) in patients experiencing rhabdomyolysis as needed.

Hepatic Effects

Increases in serum aminotransferase (AST, ALT) concentrations reported.1 Generally transient and resolve or improve with continued therapy or after temporary interruption in therapy.72

Persistent aminotransferase elevations (>3 times the ULN on 2 consecutive weekly measurements) are more common at higher dosages (40 or 80 mg daily).72 Most cases occurred within 12 weeks of therapy.72

Fatal and nonfatal hepatic failure reported rarely.72 Possibly drug-related hepatitis, which resolved following discontinuance of therapy, reported very rarely.72

Perform liver function tests before initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage201 ).72 Although manufacturer previously recommended more frequent monitoring, FDA concluded that serious statin-related liver injury is rare and unpredictable, and that routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.200 ACC/AHA cholesterol management guideline recommends obtaining liver function tests in adults with symptoms of hepatotoxicity (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark colored urine, yellowing of skin or sclera).350 However, NHLBI expert panel on cardiovascular health and risk reduction in children and adolescents strongly recommends routine monitoring of hepatic function in children and adolescents receiving statin.357

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt fluvastatin therapy.72 If an alternate etiology is not found, do not restart fluvastatin.72

Also see Hepatic Impairment under Cautions.

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.72 200 Possible increased risk of developing diabetes.200 May need to monitor glucose concentrations following initiation of statin therapy.201

FDA states that cardiovascular benefits of statins outweigh these small increased risks.200

ACC/AHA cholesterol management guideline recommends evaluating patients for new-onset diabetes mellitus according to current diabetes screening guidelines.350

If diabetes mellitus develops during statin therapy, encourage patients to adhere to a heart-healthy diet, engage in physical activity, achieve and maintain a healthy body weight, cease tobacco use, and continue statin therapy to reduce the risk of ASCVD.350

Endogenous Steroid Production

Statins interfere with cholesterol synthesis and theoretically may blunt adrenal and/or gonadal steroid production.72

Fluvastatin had no effect on nonstimulated cortisol concentrations, adrenal response to corticotropin (adrenocorticotropic hormone, ACTH) stimulation, or thyroid metabolism.72 Small declines in total serum testosterone concentrations reported, but no commensurate elevation in LH concentrations, and no effect on FSH concentrations in men.72 Data insufficient to determine effect on female sex hormones.72

If clinical evidence of endocrine dysfunction is present, evaluate patients appropriately.72

Caution advised if a statin or another antilipemic agent is used concomitantly with drugs that may decrease concentrations or activity of endogenous steroid hormones (e.g. ketoconazole, spironolactone, cimetidine).72

Cognitive Impairment

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.72

Generally nonserious and reversible, with variable times to symptom onset (1 day to years) and resolution (median of 3 weeks following discontinuance of therapy).72 200 Not associated with fixed or progressive dementia (e.g., Alzheimer’s disease) or clinically important cognitive decline.200 Not associated with any specific statin, patient's age, statin dosage, or concomitant drug therapy.200

FDA states that cardiovascular benefits of statins outweigh the small increased risk of cognitive impairment.200

If manifestations consistent with cognitive impairment occur, National Lipid Association (NLA) statin safety assessment task force recommends evaluating and managing patients appropriately.202

If patients present with confusion or memory impairment, ACC/AHA cholesterol management guideline recommends evaluating patient for statin as well as nonstatin causes (e.g., other drugs, systemic or neuropsychiatric causes).350

Role as Adjunct Therapy

Prior to institution of antilipemic therapy, vigorously attempt to control serum cholesterol by appropriate dietary regimens, weight reduction, exercise, and treatment of any underlying disorder that might be the cause of lipid abnormality.1

Specific Populations

Pregnancy

Category X.1 (See Contraindications and also see Fetal/Neonatal Morbidity and Mortality, under Cautions.)

Lactation

Distributed into milk in animals.72 Use is contraindicated in nursing women; women who require fluvastatin therapy should not breast-feed their infants.72

Pediatric Use

Safety and efficacy not established in children <9 years of age or in premenarchal girls.1 72 (See Advice to Patients.)

Geriatric Use

Fluvastatin exposures not substantially different between patients ≥65 years of age and younger adults.72

Use with caution, since age ≥65 years is a predisposing factor for myopathy.72 In patients >75 years of age, consider benefits, adverse effects, drug interactions, and patient preferences before initiating statin therapy.350

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease.1

Contraindicated in patients with active liver disease or unexplained, persistent increases in liver function test results.1

Common Adverse Effects

Headache, dyspepsia, myalgia, abdominal pain, nausea.72

Interactions for Lescol

Metabolized principally by CYP2C9; CYP2C8 and CYP3A4 also contribute to fluvastatin metabolism.1

Specific Drugs

Drug

Interaction

Comments

Bile acid sequestrants (e.g., cholestyramine)

Additive cholesterol-lowering effects45

Decreased fluvastatin peak plasma concentration and AUC when administered 4 hours after cholestyramine and a meal72

Administer statins 1 hour before or 4 hours after the resin69

Colchicine

Myopathy, including rhabdomyolysis, reported72

Use concomitantly with caution72

Cyclosporine

Increased fluvastatin concentrations;1 increased risk of myopathy and/or rhabdomyolysis1

If used concomitantly, limit fluvastatin dosage to 20 mg twice daily72

Diclofenac

Increased fluvastatin and diclofenac concentrations72

Digoxin

Slight increase in digoxin peak plasma concentration72

Erythromycin

Increased risk of myopathy and/or rhabdomyolysis1

Fibric acid derivatives (e.g., fenofibrate, gemfibrozil)

Increased risk of myopathy and/or rhabdomyolysis1

Gemfibrozil: Avoid concomitant use72

Other fibric acid derivatives (e.g., fenofibrate): Use concomitantly with caution and only if benefits outweigh risks; consider using only low- or moderate-intensity statin therapy during concomitant therapy72 350

Fluconazole

Increased peak plasma concentration and AUC of fluvastatin1

If used concomitantly, limit fluvastatin dosage to 20 mg twice daily72

Glyburide

Increased fluvastatin and glyburide concentrations;1 no change in glucose, insulin, or C-peptide concentrations1

Monitor appropriately72

Histamine H2-receptor antagonists (e.g., cimetidine, ranitidine)

Increased plasma concentrations and decreased clearance of fluvastatin1

Niacin (antilipemic dosages [≥1 g daily])

Increased risk of myopathy and/or rhabdomyolysis1

Increased risk of severe adverse effects (disturbances in glycemic control requiring hospitalization, development of diabetes mellitus, adverse GI effects, myopathy, gout, rash, skin ulceration, infection, bleeding) with concomitant use of niacin (1.5–2 g daily) and simvastatin (40–80 mg daily, with or without ezetimibe)369 371

If used concomitantly, consider reducing fluvastatin dosage72

Phenytoin

Increased fluvastatin and phenytoin concentrations1

Patients receiving phenytoin should be monitored appropriately when fluvastatin is initiated or dosage is adjusted1

Proton-pump inhibitors (e.g., omeprazole)

Increased plasma concentrations and decreased clearance of fluvastatin1

Rifampin

Decreased peak plasma concentration and AUC of fluvastatin72

Warfarin

Bleeding and/or increased PT observed with other statins1

Closely monitor PT until stabilized if fluvastatin is initiated or dosage is adjusted in patients receiving warfarin1

Lescol Pharmacokinetics

Pharmacokinetic data in pediatric patients not available.1

Absorption

Bioavailability

Rapidly and completely absorbed.1

Absolute bioavailability of conventional capsules is 24%.1

The mean relative bioavailability of extended-release tablets is approximately 29% compared with conventional capsules administered under fasting conditions.1

Mean peak plasma concentrations occur within 1 or 3 hours following oral administration of conventional capsules or extended-release tablets, respectively.1

Onset

A therapeutic response usually is apparent within 2 weeks after initiating therapy, with a maximal response occurring within 4 weeks.1

Food

Peak plasma concentration decreased and time to peak plasma concentrations increased following administration of fluvastatin conventional capsules with the evening meal; however, no substantial differences in lipid-lowering effects following administration with food.1 72

Bioavailability increased and absorption delayed following administration of extended-release tablets with a high-fat meal; however, peak plasma concentrations achieved with the extended-release tablets following a high-fat meal are much less than those achieved with a single or twice-daily dose of 40 mg.1

Distribution

Extent

Distributed mainly to the liver.1

Distributed into milk (milk to plasma ratio 2:1).1

Plasma Protein Binding

About 98%.1

Elimination

Metabolism

Metabolized in the liver, principally by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8.1

Elimination Route

Excreted in feces (90%) and urine (5%) mainly as metabolites; <2% excreted as unchanged drug.1

Half-life

<3 hours (conventional capsules) and 9 hours (extended-release tablets).1

Special Populations

Patients with hepatic impairment may have increased exposure to fluvastatin due to decreased presystemic metabolism.1

Stability

Storage

Oral

Capsules and Extended-release Tablets

Tight containers at 25°C (may be exposed to 15–30°C).1 Protect from light.1

Actions

  • Inhibits HMG-CoA reductase, causing subsequent reduction in hepatic cholesterol synthesis.1 Reduces serum concentrations of total cholesterol, LDL-cholesterol, apo B, and triglycerides.1

  • Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries, modulate BP in hypercholesterolemic patients with hypertension, and possess anti-inflammatory activity.

Advice to Patients

  • Importance of adhering to nondrug therapies and measures, including adherence to a heart-healthy diet, regular exercise, avoidance of tobacco products, and maintenance of a healthy weight.350

  • Importance of informing patients about risks, especially rhabdomyolysis, associated with statins alone or combined with other drugs.1 Importance of patients promptly reporting muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever, or if manifestations persist after discontinuance of therapy.1 355

  • Risk of adverse hepatic effects.72 Importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).72

  • Risk of nonserious, reversible cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion).72 200

  • Risk of increased glucose concentrations and development of type 2 diabetes.72 200 May need to monitor glucose concentrations following initiation of statin therapy.201

  • Importance of advising women and adolescent girls to avoid pregnancy (i.e., using effective contraceptive methods) during therapy; if the patient becomes pregnant, importance of immediately discontinuing fluvastatin and contacting a clinician.1 72

  • Importance of avoiding breast-feeding during therapy.72 If the patient has a lipid disorder and is breast-feeding, importance of contacting a clinician to discuss other antilipemic treatment options.72

  • Importance of informing clinician of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.1

  • Importance of informing patients of other important precautionary information.1 (See Cautions.)

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Fluvastatin Sodium

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Capsules

20 mg (of fluvastatin)*

Fluvastatin Sodium Capsules

Lescol

Novartis

40 mg (of fluvastatin)*

Fluvastatin Sodium Capsules

Lescol

Novartis

Tablets, extended-release

80 mg (of fluvastatin)

Lescol XL

Novartis

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 12/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Lescol 20MG Capsules (NOVARTIS): 30/$117.59 or 90/$317.07

Lescol 40MG Capsules (NOVARTIS): 30/$109.19 or 90/$293.96

Lescol XL 80MG 24-hr Tablets (NOVARTIS): 30/$145.99 or 90/$425.95

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions November 12, 2014. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

References

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9. Banga JD, Jacotot B, Pfister P et al. Long-term treatment of hypercholesterolemia with fluvastatin: a 52-week multicenter safety and efficacy study. Am J Med. 1994; 96(suppl 6A):87S-93S. [IDIS 332447] [PubMed 8017473]

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20. Schrama YC, Hene RJ, de Jonge N et al. Efficacy and muscle safety of fluvastatin in cyclosporine-treated cardiac and renal transplant recipients. Transplantation. 1998; 66:1175-81. [IDIS 417742] [PubMed 9825814]

21. Austen JL, Shifrin FA, Bartucci MR et al. Effects of fluvastatin on hyperlipidemia after renal transplantation: influence of steroid therapy. Ann Pharmacother. 1996; 30:1386-9. [IDIS 376975] [PubMed 8968448]

22. Goldberg R, Roth D. Evaluation of fluvastatin in the treatment of hypercholesterolemia in renal transplant recipients taking cyclosporine. Transplantation. 1996; 62:1559-64. [IDIS 378880] [PubMed 8970607]

23. Li PKT, Mak TWL, Wang AYM et al. The interaction of fluvastatin and cyclospori A in renal transplant patients. Int J Clin Pharmacol Ther. 1995:33:246-8.

24. Matzkies FK, Bahner U, Teschner M et al. Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients. Am J Nephrol. 1999; 19:492-4. [PubMed 10460940]

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26. Smit JWA, Jansen GH, de Bruin TWA et al. Treatment of combined hyperlipidemia with fluvastatin and gemfibrozil, alone or combination, does not induce muscle damage. Am J Cardiol. 1995; 76:126-8A.

27. Goldberg RB, Roth D. A preliminary report of the safety and efficacy of fluvastatin for hypercholesterolemia in renal transplant patients receiving cyclosporine. Am J Cardiol. 1995; 76:107-9A. [IDIS 351132] [PubMed 7611141]

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