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Fluvastatin (Monograph)

Brand name: Lescol
Drug class: HMG-CoA Reductase Inhibitors
- Statins
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

Medically reviewed by Drugs.com on Dec 4, 2023. Written by ASHP.

Introduction

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

Uses for Fluvastatin

Reduction in Risk of Cardiovascular Events

Adjunct to nondrug therapies (i.e., lifestyle modifications) in patients with CHD to reduce the risk of undergoing coronary revascularization procedures.72

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

Also has been used for primary prevention† [off-label] of atherosclerotic cardiovascular disease (ASCVD).400

Extensive evidence demonstrates that statins can substantially reduce LDL-cholesterol concentrations and associated risk of ASCVD; may be used for secondary prevention or primary prevention in high-risk patients.336 337 338 350 400

AHA/ACC cholesterol management guideline states that lifestyle modification is the foundation of ASCVD risk reduction.400 Patients with established ASCVD or high risk of ASCVD should also be treated with a statin.400

Because relative ASCVD risk reduction is correlated with degree of LDL-cholesterol lowering, use maximum tolerated intensity of a statin to achieve greatest benefit.400 High-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by ≥50%) is recommended; if high-intensity statin therapy not possible (e.g., because of a contraindication or intolerable adverse effect), may consider moderate-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by 30–49%).400 AHA/ACC considers fluvastatin 40 mg twice daily (or extended-release fluvastatin 80 mg daily) to be a moderate-intensity statin.400

The addition of a nonstatin drug (e.g., ezetimibe, PCSK9 inhibitor) to statin therapy may be considered in certain high-risk patients who require further reduction in LDL-cholesterol concentrations, particularly if there is evidence from randomized controlled studies suggesting that the addition of the nonstatin drug further reduces ASCVD events.400

When considering whether to initiate statin therapy for primary prevention, AHA/ACC recommends an individualized approach and shared decision making between patient and clinician.400 According to the guidelines, statin therapy may be considered in certain high-risk groups such as adults 20–75 years of age with LDL cholesterol ≥190 mg/dL, adults 40–75 years of age with diabetes mellitus, adults 40–75 years of age without diabetes mellitus but with LDL-cholesterol levels ≥70 mg/dL and an estimated 10-year ASCVD risk ≥7.5%, adults 40–75 years of age with chronic kidney disease (not treated with dialysis or transplantation) and LDL-cholesterol concentrations of 70–189 mg/dL who have a 10-year ASCVD risk ≥7.5%.400

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† [off-label] (diabetic dyslipidemia),54 renal insufficiency† [off-label],63 cardiac† [off-label] or renal transplantation† [off-label],20 21 22 21 27 55 57 64 or nephrotic syndrome† (nephrotic hyperlipidemia).24 65

Fluvastatin Dosage and Administration

General

Patient Monitoring

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

Dosage modifications may be necessary when used concomitantly with certain drugs (see Specific Drugs under Interactions).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

Reduction in Risk of Cardiovascular Events
Oral

Use maximally tolerated statin intensity to achieve optimal ASCVD risk reduction.400 High-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by ≥50%) is preferred; if high-intensity statin therapy not possible (e.g., because of a contraindication or intolerable adverse effect), may consider moderate-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by 30–49%).400

The AHA/ACC guideline panel considers fluvastatin 40 mg twice daily (or extended-release fluvastatin 80 mg daily) to be a moderate-intensity statin.400

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

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

Detailed Fluvastatin dosage information

Cautions for Fluvastatin

Contraindications

Warnings/Precautions

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])138 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.72 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.72

Risk of myopathy is increased in geriatric patients (≥65 years of age) and patients with renal impairment or inadequately treated hypothyroidism.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

AHA/ACC recommends measurement of CK levels in patients with severe statin-associated muscle symptoms; however, routine monitoring is not useful.400

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

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.202

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 Serious statin-related liver injury is rare and unpredictable, and routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.200 AHA/ACC cholesterol management guideline states that it is reasonable to obtain liver function tests in patients with symptoms of hepatotoxicity (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark colored urine, yellowing of skin or sclera); however, routine monitoring not recommended.350 400

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

AHA/ACC cholesterol management guideline states that in patients with increased risk of diabetes mellitus or new-onset diabetes mellitus, statin therapy and lifestyle modifications should be continued to reduce risk of ASCVD.400

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

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

All statins were previously contraindicated in pregnant women because fetal risk was thought to outweigh any possible benefit.405 However, the totality of evidence to date indicates limited potential for statins to cause malformations and other adverse embryofetal effects; FDA has therefore requested removal of the contraindication.405 Most pregnant patients should still discontinue statins because of the possibility of fetal harm; however, some patients (e.g., those with homozygous familial hypercholesterolemia or established cardiovascular disease) may benefit from continued therapy.400 405 Consider patient's individual risks and benefits.405

Patients who become pregnant or suspect that they are pregnant while receiving a statin should notify their clinician; clinician should advise patient on the appropriate course of action.405

Increased risk of miscarriage reported in pregnant women exposed to statins; however, not clear whether drug-related or due to other confounding factors.400 405

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 Many patients can stop statin therapy temporarily until breast-feeding is complete; patients who require ongoing statin treatment should not breast-feed and should use alternatives such as infant formula.400 405

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

Patients >75 years of age may have a higher risk of adverse effects and lower adherence to therapy; consider expected benefits versus adverse effects before initiating statin therapy in this population.400

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

Drug Interactions

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;1 339 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 339

Closely monitor PT until stabilized if fluvastatin is initiated or dosage is adjusted in patients receiving warfarin1 339
Fluvastatin drug interactions (more detail)

Fluvastatin 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

Advice to Patients

Preparations

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

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* 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)*

Fluvastatin Sodium Extended-Release Tablets

Lescol XL

Novartis

AHFS DI Essentials™. © Copyright 2024, Selected Revisions December 13, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

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

1. Novartis. Lescol (fluvastatin sodium) capsules and Lescol XL (fluvastatin sodium) extended-release tablets prescribing information. East Hanover, NJ: 2006 Apr.

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