Skip to main content

Lovastatin (Monograph)

Brand name: Altoprev
Drug class: HMG-CoA Reductase Inhibitors

Medically reviewed by Drugs.com on Jul 10, 2024. Written by ASHP.

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).4 5 118 119

Uses for Lovastatin

Reduction in Risk of Cardiovascular Events

Adjunct to diet and lifestyle modifications in patients without symptomatic cardiovascular disease who have normal or moderate elevations of total and LDL-cholesterol and below-average HDL-cholesterol concentrations to reduce the risk of MI or unstable angina and to reduce the risk of undergoing coronary revascularization procedures.83 118 119

Adjunct to nondrug therapies (e.g., dietary management) in patients with CHD to slow the progression of coronary atherosclerosis as part of a treatment strategy to lower total and LDL-cholesterol concentrations to target levels.61 70 74 75 76 91 92 93 118 119

Extensive evidence demonstrates that statins can substantially reduce LDL-cholesterol concentrations and associated risk of atherosclerotic cardiovascular disease (ASCVD); may be used for secondary or primary prevention in high-risk patients.336 337 338 400 401 402

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 lovastatin 40–80 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.400 403

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%, and 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%.400 401

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total and LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations, and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia, including heterozygous familial and non-familial hypercholesterolemia and mixed dyslipidemia (e.g., Frederickson types IIa and IIb.8 9 18 23 24 29 30 31 32 33 35 36 40 49 50 90 118 119

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) 10–17 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.118 Safety and efficacy of lovastatin extended-release not established in children or adolescents <20 years of age.119

Reduction of elevated LDL-cholesterol concentrations in patients with combined hypercholesterolemia and hypertriglyceridemia caused by genotypic familial combined hyperlipidemia;18 19 31 50 118 however, has not been studied in conditions where the major abnormality is elevation of chylomicrons, very-low density lipoproteins (VLDLs), or intermediate-density lipoproteins (IDLs). 118

Lovastatin Dosage and Administration

General

Pretreatment Screening

Patient Monitoring

Administration

Oral Administration

Administer orally.118 119

Immediate-release Tablets

Administer with the evening meal.118

Extended-release Tablets

Administer in the evening at bedtime.119

Dosage

Dosage modifications may be necessary when used concomitantly with certain drugs.118 119

Pediatric Patients

Dyslipidemias
Immediate-release Tablets
Oral

Children 10–17 years of age who require reductions in LDL-cholesterol of ≥20%: Initially, 20 mg once daily.118

Children 10–17 years of age who require small reductions in LDL-cholesterol: Consider initial dosage of 10 mg once daily.118

Recommended dosage range is 10–40 mg daily; maximum recommended dosage is 40 mg daily.118

Adults

Reduction in Risk of Cardiovascular Events

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 lovastatin 40–80 mg daily to be a moderate-intensity statin.400

Immediate-release Tablets
Oral

Initially, 20 mg once daily with evening meal.118 Recommended dosing range is 10–80 mg/day in a single dose or 2 divided doses; maximum recommended total daily dose is 80 mg.118

Extended-release Tablets
Oral

Recommended dosage range is 20-60 mg once daily in the evening.119

Dyslipidemias
Immediate-release Tablets
Oral

Usual initial dosage is 20 mg once daily with the evening meal.118

Patients who require reductions in LDL-cholesterol concentrations of ≥20%: Initially, 20 mg once daily.118

Patients who require smaller reductions in LDL-cholesterol: Consider initial dosage of 10 mg once daily.118

Recommended dosage range is 10–80 mg daily given in 1 or 2 divided doses; maximum recommended dosage is 80 mg daily.118

Extended-release Tablets
Oral

Recommended dosage range is 20–60 mg once daily in the evening.119

Special Populations

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease.118 119

Contraindicated in patients with active liver disease or unexplained, persistent increases in serum aminotransferase concentrations.118 119

No specific dosage recommendations.118 119

Renal Impairment

Immediate-release tablets: Use with caution in patients with severe renal impairment (Clcr <30 mL/min).118 Carefully consider dosage increases >20 mg daily in such patients; if deemed necessary, implement with extreme caution.118

Extended-release tablets: Use dosages >20 mg daily in patients with severe renal impairment only after careful consideration of the expected benefits versus potential risks of myopathy and rhabdomyolysis.119

Geriatric Patients

Immediate-release tablets: Dosage adjustment based on age-related pharmacokinetic differences not necessary.118

Extended-release tablets: Usual initial dosage in patients ≥65 years of age is 20 mg once daily; use higher dosages only after careful consideration of potential risks and benefits.119

Pharmacogenomic Considerations

Patients with solute carrier organic anion transporter (SLCO) 1B1 decreased or possible decreased function phenotype: Limit lovastatin dosage to ≤20 mg/day.500

Patients with SLCO1B1 poor function phenotype: Alternative statin recommended.500

Detailed Lovastatin dosage information

Cautions for Lovastatin

Contraindications

Warnings/Precautions

Musculoskeletal Effects

Myopathy (manifested as muscle pain, tenderness, or weakness and serum creatine kinase [CK] concentration increases >10 times the ULN) reported occasionally.118

Rhabdomyolysis (characterized by muscle pain, tenderness, or weakness particularly if accompanied by malaise or fever) with or without acute renal failure secondary to myoglobinuria reported; rare fatalities have occurred.118 119

Risk of myopathy is increased in patients receiving higher dosages of statins; risk also may be increased in geriatric patients (≥65 years of age), women, and patients with renal impairment or uncontrolled hypothyroidism.118 119

Certain drug or food interactions also may increase risk of myopathy and/or rhabdomyolysis.118 119

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

Discontinue if serum CK concentrations increase markedly or if myopathy is diagnosed or suspected.118 119 Periodic CK determinations may be considered (baseline or when dosage increased), but there is no assurance that such monitoring will prevent myopathy.118

Temporarily withhold therapy in any patient experiencing an acute or serious condition predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; dehydration; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).118 119

Immune-Mediated Necrotizing Myopathy

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.118 119 Characterized by proximal muscle weakness and elevated CK concentrations that persist despite discontinuance of statin therapy, positive anti-HMG CoA reductase antibody, muscle biopsy showing necrotizing myopathy without substantial inflammation, and improvement following therapy with immunosuppressive agents.118 119

Additional neuromuscular and serologic testing may be necessary.118 119

The risk of IMNM should be considered carefully prior to initiating therapy with another statin; monitor for signs and symptoms.118 119

Hepatic Effects

Associated with increases in serum aminotransferase (AST, ALT) concentrations.118 119

Rare postmarketing reports of fatal and non-fatal hepatic failure in patients taking statins, including lovastatin.118 119

Perform liver function tests before initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage).118 119 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 required. 200 400

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of chronic liver disease.118 119 Contraindicated in patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations.118 119

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt lovastatin therapy.118 119 If an alternate etiology is not found, do not restart lovastatin.118 119

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.118 119 200 Possible increased risk of developing diabetes.200

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.118 119

No effects on basal plasma cortisol concentrations, testosterone concentrations, or adrenal reserve observed with lovastatin.118 119 Effects on male fertility or on pituitary-gonadal axis in premenopausal women not fully established.118 119

If clinical evidence of endocrine dysfunction is present, evaluate patients appropriately.118 119

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., spironolactone, cimetidine).118 119

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

Not known whether lovastatin is distributed into human milk; however, other statins are distributed into milk.118 119 Use is contraindicated in nursing women; women who require lovastatin therapy should not breast-feed their infants.118 119 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

Females and Makes of Reproductive Potential

Effects on male fertility or on pituitary-gonadal axis in premenopausal women not fully established.118 119

May cause fetal harm when administered to a pregnant woman; sexually active women (including adolescents) of childbearing age should be counseled to use a reliable form of contraception.118 119

Pediatric Use

Safety and efficacy of immediate-release tablets not established in children <10 years of age or in prepubertal children.118 Experts state statins may be considered in patients as young as 8 years of age in the presence of concerning family history, extremely elevated LDL-cholesterol level, or elevated lipoprotein (a), in the context of informed shared decision-making and counseling with the patient and family.400 404

Advise adolescent girls to use effective and appropriate contraceptive methods during therapy to reduce the likelihood of unintended pregnancy.118

Safety and efficacy of extended-release lovastatin not established in children or adolescents <20 years of age.119

Geriatric Use

No substantial differences in safety or efficacy relative to younger adults.118

Immediate-release preparation: Mean plasma HMG-CoA reductase inhibitory activity is approximately 45% higher in patients 70–78 years of age than in young adults; however, dosage adjustment based on age-related pharmacokinetic differences not necessary in geriatric patients.118 Because advanced age (≥65 years of age) is a predisposing factor for myopathy, including rhabdomyolysis, use with caution in this population.118

Extended-release preparation: Safety and efficacy appear to be similar to those in younger adults; however, greater sensitivity in some older patients cannot be ruled out.119 Use with caution.119 437

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.118 119

Contraindicated in patients with active liver disease or unexplained, persistent increases in liver function test results.118 119

Renal Impairment

Mean plasma levels of HMG-CoA reductase inhibitory activity after a single dose of lovastatin were approximately 2-fold higher in patients with severe renal impairment (Clcr10–30 mL/minute) than in healthy volunteers.118 119

Immediate-release preparation: Use with caution in patients with severe renal impairment (Clcr <30 mL/minute); dosage increases >20 mg daily should be carefully considered and, if deemed necessary, implemented cautiously.118

Extended-release preparation: Dosage increases >20 mg daily should only be considered in patients with severe renal impairment if the expected benefits exceed the increased risk of myopathy and rhabdomyolysis.119

Because many patients who have developed rhabdomyolysis during lovastatin therapy have had complicated medical histories, including renal impairment secondary to chronic diabetes mellitus, closely monitor such patients.118

Pharmacogenomic Considerations

Genetic variation in the solute carrier organic anion transporter (SLCO) family member (SLCO1B1), ABCG2 (also known as breast cancer resistance protein [BCRP]), and CYP2C9 genes alter systemic exposure to statins, which can increase the risk for statin-associated musculoskeletal symptoms.500

In patients with phenotypes that result in increased statin exposure, consider potential for other patient-specific issues that may increase statin exposure (e.g., renal and hepatic function, drug-drug interactions).500

Experts state statin therapy should neither be discontinued nor avoided based on SLCO1B1, ABCG2, or CYP2C9 genotype results for patients with an indication for statin therapy.500

Patients with SLCO1B1 decreased or possible decreased function phenotype or poor function phenotypes will have increased exposure and risk of statin-associated musculoskeletal symptoms.500 Lower doses or an alternative statin may be required.500

Common Adverse Effects

Common adverse effects (≥2%) in patients receiving immediate-release tablets: GI disturbances (e.g., flatulence, diarrhea, abdominal pain, constipation, nausea, dyspepsia), headache, myalgia.118

Common adverse effects (≥5%) in patients receiving extended-release tablets: infection, headache, accidental injury.119

Drug Interactions

Metabolized by CYP3A4 but has no CYP3A4 inhibitory activity.118 119

Substrate of P-gp and organic anion transporter protein (OATP).339 501 502

Drug interaction studies not been performed with extended-release preparation; use caution extrapolating data from immediate-release preparation studies.119

Drugs Affecting Hepatic Microsomal Enzymes

Strong CYP3A4 inhibitors: Potential pharmacokinetic interaction (increased plasma lovastatin concentrations); increased risk of myopathy or rhabdomyolysis.118 119 Concomitant use contraindicated.118 119

Drugs Affecting or Affected by Transport Systems

P-gp inhibitors: Potential pharmacokinetic interaction (increased exposure); increased risk of statin-induced toxicity.502

OATP1B1 inhibitors: Potential pharmacokinetic interaction (increased exposure); increased risk of statin-induced toxicity.502

Specific Drugs and Foods

Drug or Food

Interaction

Comments

Amiodarone

Increased risk of myopathy and/or rhabdomyolysis118 119

If used concomitantly, do not exceed lovastatin dosage of 40 mg daily118 119

Antidiabetic agents (e.g., glipizide)

Glipizide: Pharmacokinetic interactions not reported during concomitant use118 119

Antifungals, azoles

Itraconazole, ketoconazole, posaconazole, or voriconazole: Inhibition of CYP3A4-dependent metabolism of lovastatin, resulting in increased lovastatin plasma concentrations and AUC and increased risk of myopathy and/or rhabdomyolysis118 119

Itraconazole, ketoconazole, posaconazole, or voriconazole: Concomitant use contraindicated; if therapy with antifungal is unavoidable, interrupt lovastatin therapy during antifungal treatment118 119

Calcium-channel blockers (i.e., amlodipine, diltiazem, verapamil)

Increased plasma lovastatin concentrations and possible risk of myopathy and/or rhabdomyolysis, particularly with higher lovastatin dosages118 119 339

Weigh benefits versus risks of concomitant use118 119

If used concomitantly with diltiazem or verapamil, manufacturer recommends initiating lovastatin at 10 mg daily118 119

Lovastatin dosage >20 mg daily not recommended when coadministered with diltiazem or verapamil118 119

Experts recommend limiting lovastatin dosage to 20 mg daily if used concomitantly with amlodipine502

Cobicistat-containing preparations

Inhibition of CYP3A4-dependent metabolism of lovastatin, resulting in increased plasma concentrations and AUC of lovastatin and increased risk of myopathy and/or rhabdomyolysis118 119

Concomitant use contraindicated118 119

Colchicine

Myopathy, including rhabdomyolysis, reported118 119

Use concomitantly with caution118 119

Conivaptan

Rhabdomyolysis reported 339

Avoid concomitant use339

Danazol

Increased risk of myopathy and/or rhabdomyolysis, particularly with higher lovastatin dosages118 119

Weigh benefits against risks of concomitant use118 119

If used concomitantly, initiate lovastatin at 10 mg daily118 and do not exceed lovastatin dosage of 20 mg daily118 119

Digoxin

No effect on digoxin plasma concentrations118 119

Dronedarone

Inhibition of lovastatin metabolism via CYP3A4, resulting in increased lovastatin plasma concentrations and increased risk of myopathy and/or rhabdomyolysis, particularly with higher lovastatin dosages118 339

Weigh benefits against risks of concomitant use118 119

If used concomitantly, initiate lovastatin at 10 mg daily and do not exceed lovastatin dosage of 20 mg daily118 119

Fibric acid derivatives (e.g., gemfibrozil)

Increased risk of myopathy and/or rhabdomyolysis118 119

Gemfibrozil: Lovastatin acid AUC increased 2.8-fold118 119

Gemfibrozil: Avoid concomitant use118 119

Other fibric acid derivatives (e.g., fenofibrate): Use concomitantly with caution and only if benefits outweigh risks118 119

Grapefruit juice

Inhibition of CYP3A4-dependent metabolism of lovastatin, resulting in increased lovastatin AUC and plasma concentrations and increased risk of myopathy and/or rhabdomyolysis118 119

Manufacturer and some clinicians recommend avoiding concomitant use118 119 379

HIV protease inhibitors

Inhibition of CYP3A4-dependent metabolism of lovastatin, resulting in increased lovastatin plasma concentrations and increased risk of myopathy and/or rhabdomyolysis118 119

Concomitant use contraindicated118 119

Immunosuppressive agents (i.e., cyclosporine, everolimus, sirolimus, tacrolimus)

Cyclosporine: Increased lovastatin AUC ≥3-fold and increased risk of myopathy and/or rhabdomyolysis118 119

Everolimus, sirolimus, tacrolimus: Data more limited, but interaction potential expected to be similar to cyclosporine because of similar metabolism339

Cyclosporine: Avoid concomitant use 118 119

Everolimus, sirolimus, tacrolimus: Some experts recommend avoiding concomitant use339

Macrolides (i.e., clarithromycin, erythromycin)

Clarithromycin or erythromycin: Inhibition of CYP3A4-dependent metabolism of lovastatin, resulting in increased lovastatin plasma concentrations and increased risk of myopathy and/or rhabdomyolysis118 119

Clarithromycin or erythromycin: Concomitant use contraindicated; if therapy with antibiotic is unavoidable, interrupt lovastatin therapy during antibiotic treatment118 119

Nefazodone

Inhibition of lovastatin metabolism via CYP3A4, resulting in increased lovastatin plasma concentrations and increased risk of myopathy and/or rhabdomyolysis118 119

Concomitant use contraindicated118 119

Niacin (antilipemic dosages [≥1 g daily])

Increased risk of myopathy and/or rhabdomyolysis118 119

Use concomitantly with caution; weigh benefits against risks of concomitant use118 119

Propranolol

No clinically important pharmacokinetic or pharmacodynamic interaction reported118 119

Dosage adjustment not needed.119

Ranolazine

Possible increased risk of myopathy, including rhabdomyolysis118 119

If used concomitantly, may consider adjusting lovastatin dosage118 119

Ticagrelor

Possible increased lovastatin plasma concentrations339

Some experts recommend limiting lovastatin dosage to 40 mg daily339

Warfarin

Bleeding and/or increased PT/INR observed118 339

Closely monitor PT/INR until stabilized if lovastatin is initiated or dosage is adjusted in patients receiving warfarin;118 339 thereafter, monitor PT/INR at intervals usually recommended for patients receiving warfarin118 119

Lovastatin drug interactions (more detail)

Lovastatin Pharmacokinetics

Absorption

Bioavailability

Immediate-release tablets: Rapidly absorbed following oral administration; undergoes extensive first-pass metabolism in the liver.429 430 431 432 Peak plasma concentrations attained at 2–4 hours.118 501

Immediate-release tablets: Absolute bioavailability is <5%.118 430 501

Extended-release tablets: Slower and more prolonged appearance of lovastatin in plasma; peak plasma concentrations delayed (attained at about 14 hours) and lower compared with immediate-release tablets.119

Extended-release tablets: More bioavailable (in terms of lovastatin) than immediate-release tablets; however, bioavailability of total and active HMG-CoA reductase inhibitors is similar between the 2 formulations.119 Exposure with extended-release 60 mg is greater than that with immediate-release 80 mg.119

Food

Immediate-release tablets: Food increases bioavailability; under fasting conditions, plasma concentrations of total inhibitors approximately two-thirds those found when administered with a meal.118

Extended-release tablets: Food decreases bioavailability; plasma concentrations (lovastatin and lovastatin acid) approximately 0.5–0.6 times those found when administered without food.119

Onset

Therapeutic response usually is apparent within 2 weeks; maximal response occurs within 4–6 weeks.118 119

Distribution

Extent

Distributed mainly to the liver; crosses the blood-brain barrier.118 119

Lovastatin crosses the placenta.118 119 Not known whether distributed into human milk.118

Plasma Protein Binding

>95%.118 119

Elimination

Metabolism

Metabolized by CYP3A4.118 119 Lovastatin has active metabolites.118 119

Elimination Route

Excreted in urine (10%) and feces (83%).118 119

Special Populations

Plasma concentrations of total inhibitors increased 2-fold in patients with severe renal impairment (Clcr 10–30 mL/min) compared with healthy individuals following a single dose (immediate-release).118

Mean plasma levels of HMG-CoA reductase inhibitory activity approximately 45% higher in geriatric patients (70–78 years of age) than in younger adults (18–30 years of age).118 119

Patients with certain SLCO1B1 phenotypes (i.e., decreased, possible decreased, or poor function) will have increased lovastatin exposure compared to those with normal function.500

Stability

Storage

Oral

Immediate-release Tablets

20–25°C; protect from light.118

Extended-release Tablets

20–25°C (excursions permitted to 15–30°C).119 Avoid excessive heat and humidity.119

Actions

Advice to Patients

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.

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

Lovastatin

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

10 mg*

Lovastatin Tablets

20 mg*

Lovastatin Tablets

40 mg*

Lovastatin Tablets

Tablets, extended-release

20 mg

Altoprev

Covis

40 mg

Altoprev

Covis

60 mg

Altoprev

Covis

AHFS DI Essentials™. © Copyright 2025, Selected Revisions July 10, 2024. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

References

4. Tobert JA, Hitzenberger G, Kukovetz WR et al. Rapid and substantial lowering of human serum cholesterol by mevinolin (MK-803), an inhibitor of hydroxymethylglutaryl-coenzyme A reductase. Atherosclerosis. 1982; 41:61-5. https://pubmed.ncbi.nlm.nih.gov/6918220

5. Tobert JA, Bell GD, Birtwell J et al. Cholesterol-lowering effect of mevinolin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, in healthy volunteers. J Clin Invest. 1982; 69:913-9. https://pubmed.ncbi.nlm.nih.gov/6918402

6. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors: a new class of cholesterol-lowering agents. Ann Intern Med. 1987; 107:759-60. Editorial.

7. Stacpoole PW, Alig J. Advances in the treatment of coronary heart disease: fish oils, cholestyramine, and mevinolin. Cardiovasc Clin. 1987; 18:267-79. https://pubmed.ncbi.nlm.nih.gov/3300984

8. Illingworth DR. Mevinolin plus colestipol in therapy for severe heterozygous familial hypercholesterolemia. Ann Intern Med. 1984; 101:598-604. https://pubmed.ncbi.nlm.nih.gov/6567462

9. Illingworth DR, Sexton GJ. Hypocholesterolemic effects of mevinolin in patients with heterozygous familial hypercholesterolemia. J Clin Invest. 1984; 74:1972-8. https://pubmed.ncbi.nlm.nih.gov/6569064

10. Alberts AW, Chen J, Kuron G et al. Mevinolin: a highly potent competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase and a cholesterol-lowering agent. Proc Natl Acad Sci USA. 1980; 77:3957-61. https://pubmed.ncbi.nlm.nih.gov/6933445

11. Illingworth RD, Bacon S. Hypolipidemic effects of HMG-CoA reductase inhibitors in patients with hypercholesterolemia. Am J Cardiol. 1987; 60:33-42G. https://pubmed.ncbi.nlm.nih.gov/3604942

12. Illingworth DR. Lipid-lowering drugs: an overview of indications and optimum therapeutic use. Drugs. 1987; 33:259-79. https://pubmed.ncbi.nlm.nih.gov/3552597

13. Brown MS, Goldstein JL. Drugs used in the treatment of hyperlipoproteinemias. In: Gilman AG, Goodman LS, Rall TW et al, eds. Goodman & Gilman’s the pharmacological basis of therapeutics. 7th ed. New York: Macmillan Publishing Company; 1985:827-45.

14. Minsker DH, MacDonald JS, Robertson RT et al. Mevalonate supplementation in pregnant rats suppresses the teratogenicity of mevinolinic acid, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Teratology. 1983; 28:449-56. https://pubmed.ncbi.nlm.nih.gov/6665743

15. Tobert JA. New developments in lipid-lowering therapy: the role of inhibitors of hydroxymethylglutaryl-coenzyme A reductase. Circulation. 1987; 76:534-8. https://pubmed.ncbi.nlm.nih.gov/3113763

16. Cressman MD, Hoogwerf BJ, Moodie DS et al. HMG-CoA reductase inhibitors: a new approach to the management of hypercholesterolemia. Cleveland Clin J Med. 1988; 55:93-100.

17. Rosen T, Heathcock CH. The synthesis of mevinic acids. Tetrahedron. 1986; 42:4909-51.

18. The Lovastatin Study Group III. A multicenter comparison of lovastatin and cholestyramine therapy for severe primary hypercholesterolemia. JAMA. 1988; 260:359-66. https://pubmed.ncbi.nlm.nih.gov/2898027

19. East C, Bilheimer DW, Grundy SM. Combination drug therapy for familial combined hyperlipidemia. Ann Intern Med. 1988; 109:25-32. https://pubmed.ncbi.nlm.nih.gov/3288029

22. Fojo SS, Hoegg JM [sic: Hoeg], Lackner KJ et al. Adrenocortical function in type II hyperlipoproteinemic patients treated with lovastatin (mevinolin). Horm Metab Res. 1987; 19:648-52. https://pubmed.ncbi.nlm.nih.gov/2831127

23. Grundy SM, Vega GL, Bilheimer DW. Influence of combined therapy with mevinolin and interruption of bile-acid reabsorption on low density lipoproteins in heterozygous familial hypercholesterolemia. Ann Intern Med. 1985; 103:339-43. https://pubmed.ncbi.nlm.nih.gov/3849281

24. Bilheimer DW, Grundy SM, Brown MS et al. Mevinolin and colestipol stimulate receptor-mediated clearance of low density lipoprotein from plasma in familial hypercholesterolemia heterozygotes. Proc Natl Acad Sci USA. 1983; 80:4124-8. https://pubmed.ncbi.nlm.nih.gov/6575399

25. Davignon J, Dujovne CA, Frohlich J et al. A comparison of lovastatin and probucol for the treatment of primary hypercholesterolemia. Unpublished observations. 1988 Jul.

26. Illingworth DR, Bacon SP, Larsen KK. Long-term experience with HMG-CoA reductase inhibitors in the therapy of hypercholesterolemia. Atheroscler Rev. 1988; 18:161-87.

27. Vega GL, Grundy SM. Lovastatin therapy in nephrotic hyperlipidemia: effects on lipoprotein metabolism. Kidney Int. 1988; 33:1160-8. https://pubmed.ncbi.nlm.nih.gov/3165483

28. Tikkanen MJ, Helve E, Nikkila EA. Treatment of familial and non-familial hypercholesterolaemia: a review of HMG-CoA reductase inhibitors and probucol. Eur Heart J. 1987; 8(Suppl E):97-101. https://pubmed.ncbi.nlm.nih.gov/3315684

29. Grundy SM, Vega GL. Influence of mevinolin on metabolism of low density lipoproteins in primary moderate hypercholesterolemia. J Lipid Res. 1985; 26:1464-75. https://pubmed.ncbi.nlm.nih.gov/3853581

30. Hoeg JM, Maher MB, Zech LA et al. Effectiveness of mevinolin on plasma lipoprotein concentrations in type II hyperlipoproteinemia. Am J Cardiol. 1986; 57:933-9. https://pubmed.ncbi.nlm.nih.gov/3515897

31. Lovastatin Study Group II. Therapeutic response to lovastatin (mevinolin) in nonfamilial hypercholesterolemia: a multicenter study. JAMA. 1986; 256:2829-34. https://pubmed.ncbi.nlm.nih.gov/3534333

32. Havel RJ, Hunninghake DB, Illingworth DR et al. Lovastatin (mevinolin) in the treatment of heterozygous familial hypercholesterolemia: a multicenter study. Ann Intern Med. 1987; 107:609-15. https://pubmed.ncbi.nlm.nih.gov/3662274

33. Thompson GR, Ford J, Jenkinson M et al. Efficacy of mevinolin as adjuvant therapy for refractory familial hypercholesterolaemia. Quart J Med. 1986; 60:803-11. https://pubmed.ncbi.nlm.nih.gov/3640503

34. East CA, Grundy SM, Bilheimer DW. Preliminary report: treatment of type 3 hypercholesterolemia with mevinolin. Metabolism. 1986; 35:97-8. https://pubmed.ncbi.nlm.nih.gov/3633017

35. Hoeg JM, Maher MB, Bailey KR et al. The effects of mevinolin and neomycin alone and in combination on plasma lipid and lipoprotein concentrations in type II hypercholesterolemia. Atherosclerosis. 1986; 60:209-15. https://pubmed.ncbi.nlm.nih.gov/3524586

36. Vega GL, Grundy SM. Treatment of primary moderate hypercholesterolemia with lovastatin (mevinolin) and colestipol. JAMA. 1987; 257:33-8. https://pubmed.ncbi.nlm.nih.gov/3537351

38. Hoeg JM, Maher MB, Bailey KR et al. Comparison of six pharmacologic regimens for hypercholesterolemia. Am J Cardiol. 1987; 59:812-5. https://pubmed.ncbi.nlm.nih.gov/3644588

39. Anon. Lovastatin for hypercholesterolemia. Med Lett Drugs Ther. 1987; 29:99-101. https://pubmed.ncbi.nlm.nih.gov/3312981

40. Illingworth DR. Comparative efficacy of once versus twice daily mevinolin in the therapy of familial hypercholesterolemia. Clin Pharmacol Ther. 1986; 40:338-43. https://pubmed.ncbi.nlm.nih.gov/3638181

41. Zambon D, Ros E, Rodriguez-Villar C et al. Randomized, crossover study of gemfibrozil versus lovastatin in familial combined hyperlipidemia: additive effects of combination treatment on lipid regulation. Metabolism. 1999; 48:47-54. https://pubmed.ncbi.nlm.nih.gov/9920144

42. Vega GL, Grundy SM. Primary hypertriglyceridemia with borderline high cholesterol and elevated apolipoprotein B concentrations: comparison of gemfibrozil vs lovastatin therapy. JAMA. 1990; 264:2759-63. https://pubmed.ncbi.nlm.nih.gov/2232062

43. Connor WE. Treatment choices for hypertriglyceridemia. JAMA. 1990; 264:2797-8. https://pubmed.ncbi.nlm.nih.gov/2232067

45. Walker JF, Tobert JA. The clinical efficacy and safety of lovastatin and MK-733—an overview. Eur Heart J. 1987; 8(Suppl E):93-6. https://pubmed.ncbi.nlm.nih.gov/3315683

46. Hoeg JM, Brewer HB Jr. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors in the treatment of hypercholesterolemia. JAMA. 1987; 258:3532-6. https://pubmed.ncbi.nlm.nih.gov/3316727

48. Witztum JL. Intensive drug therapy of hypercholesterolemia. Am Heart J. 1987; 113:603-9. https://pubmed.ncbi.nlm.nih.gov/3544777

49. Malloy MJ, Kane JP, Kunitake ST et al. Complementarity of colestipol, niacin, and lovastatin in treatment of severe familial hypercholesterolemia. Ann Intern Med. 1987; 107:616-23. https://pubmed.ncbi.nlm.nih.gov/3662275

50. Illingworth DR. Long term administration of lovastatin in the treatment of hypercholesterolaemia. Eur Heart J. 1987; 8(Suppl E):103-11. https://pubmed.ncbi.nlm.nih.gov/3678268

52. Garg A, Grundy SM. Lovastatin for lowering cholesterol levels in non-insulin-dependent diabetes mellitus. N Engl J Med. 1988; 318:81-6. https://pubmed.ncbi.nlm.nih.gov/3422105

53. Ballantyne CM, Jones PH, Payton-Ross C et al. Hyperlipidemia following heart transplantation: natural history and intervention with mevinolin (lovastatin). Transplant Proc. 1987; 19(Suppl 5):60-2. https://pubmed.ncbi.nlm.nih.gov/3303569

54. Illingworth DR. Lovastatin (mevinolin) in the treatment of post transplant hyperlipidemia. Clin Res. 1987; 35:572A.

55. Golper TA, Illingworth DR, Bennett WM. Effective and safe short term improvement in nephrotic hypercholesterolemia with the HMG Co-A reductase inhibitor mevinolin. Kidney Int. 1987; 31:200.

56. Illingworth DR, Connor WE. Hypercholesterolemia persisting after distal ileal bypass: response to mevinolin. Ann Intern Med. 1984; 100:850-1. https://pubmed.ncbi.nlm.nih.gov/6562870

57. Nakamura CE, Abeles RH. Mode of interaction of β-hydroxy-β-methylglutaryl coenzyme A reductase with strong binding inhibitors: compactin and related compounds. Biochemistry. 1985; 24:1364-76. https://pubmed.ncbi.nlm.nih.gov/3886005

58. Farnsworth WH, Hoeg JM, Maher M et al. Testicular function in type II hyperlipoproteinemic patients treated with lovastatin (mevinolin) or neomycin. J Clin Endocrinol Metab. 1987; 65:546-50. https://pubmed.ncbi.nlm.nih.gov/3114306

59. Lees AM, Stein SW, Lees RS. Therapy of hypercholesterolemia with mevinolin and other lipid-lowering drugs. Arteriosclerosis. 1986; 6:544a.

60. Chremos AN, Langendorfer A, Snavely D. Hypocholesterolemic dose-response of lovastatin in patients with plasma LDL-cholesterol ≤200 mg/dL. Clin Pharmacol Ther. 1988; 43: 125.

61. Waters D, Higginson L, Gladstone P et al. Effects of monotherapy with an HMG-CoA reductase inhibitor on the progression of coronary atherosclerosis as assessed by serial quantitative arteriography. The Canadian Coronary Atherosclerosis Intervention Trial. Circulation. 1994; 89:959-68. https://pubmed.ncbi.nlm.nih.gov/8124836

62. Parker TS, McNamara DJ, Brown C et al. Mevalonic acid in human plasma: relationship of concentration and circadian rhythm to cholesterol synthesis rates in man. Proc Natl Acad Sci USA. 1982; 79:3037-41. https://pubmed.ncbi.nlm.nih.gov/6953446

66. East C, Alivizatos PA, Grundy SM et al. Rhabdomyolysis in patients receiving lovastatin after cardiac transplantation. N Engl J Med. 1988; 318:47-8. https://pubmed.ncbi.nlm.nih.gov/3275892

68. Rahimtoola SH. Cholesterol and coronary heart disease: a perspective. JAMA. 1985; 253:2094-5. https://pubmed.ncbi.nlm.nih.gov/3974101

70. Waters D, Higginson L, Gladstone P et al. Effects of cholesterol lowering on the progression of coronary atherosclerosis in women. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation. 1995; 92:2404-10. https://pubmed.ncbi.nlm.nih.gov/7586338

72. Hoeg JM, Gregg RE, Brewer HB. An approach to the management of hyperlipoproteinemia. JAMA. 1986; 255:512-21. https://pubmed.ncbi.nlm.nih.gov/3510334

74. Brown G, Albers JJ, Fisher LD et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. 1990; 323:1289-98. https://pubmed.ncbi.nlm.nih.gov/2215615

75. Blankenhorn DH, Azen SP, Kramsch DM et al. Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS). The MARS Research Group. Ann Intern Med. 1993; 119:969- 76. https://pubmed.ncbi.nlm.nih.gov/8214993

76. Levine GN, Keaney JR Jr, Vita JA. Cholesterol reduction in cardiovascular disease. Clinical benefits and possible mechanisms. N Engl J Med. 1995; 332:512-21. https://pubmed.ncbi.nlm.nih.gov/7830734

77. Heathcock CH, Hadley CR, Rosen T et al. Total synthesis and biological evaluation of structural analogues of compactin and dihydromevinolin. J Med Chem. 1987; 30:1858-73. https://pubmed.ncbi.nlm.nih.gov/3656359

78. Hoffman WF, Alberts AW, Anderson PS et al. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. 4. Side chain ester derivatives of mevinolin. J Med Chem. 1986; 29:849-52. https://pubmed.ncbi.nlm.nih.gov/3634830

79. Stokker GE, Hoffman WF, Alberts AW et al. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. 1. Structural modification of 5-substituted 3,5-dihydroxypentanoic acids and their lactone derivatives. J Med Chem. 1985; 28:347-58. https://pubmed.ncbi.nlm.nih.gov/3973903

80. Norman DJ, Illingworth DR, Munson J et al. Myolysis and acute renal failure in a heart-transplant recipient receiving lovastatin. N Engl J Med. 1988; 318:46-7. https://pubmed.ncbi.nlm.nih.gov/3275891

81. Tobert JA. Rhabdomyolysis in patients receiving lovastatin after cardiac transplantation. N Engl J Med. 1988; 318:48. https://pubmed.ncbi.nlm.nih.gov/3257291

83. Downs JR, Clearfield M, Weis S et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. JAMA. 1998; 279:1615-22. https://pubmed.ncbi.nlm.nih.gov/9613910

84. Bradford RH, Shear CL, Athanassios N et al. Expanded clinical evaluation of lovastatin (EXCEL) study results I: efficacy in modifying plasma lipoproteins and adverse event profile in 8245 patients with moderate hypercholesterolemia. Arch Intern Med. 1991; 151:43-9. https://pubmed.ncbi.nlm.nih.gov/1985608

85. Fong RL, Ward HJ. The efficacy of lovastatin in lowering cholesterol in African Americans with primary hypercholesterolemia. Am J Med. 1997; 102:387-91. https://pubmed.ncbi.nlm.nih.gov/9217621

86. Prisant LM, Downton M, Watkins LO et al. Efficacy and tolerability of lovastatin in 459 African-Americans with hypercholesterolemia. Am J Cardiol. Q996; 78:420-4.

87. Stein EA, Illingworth DR, Kwiterovich PO et al. Efficacy and safety of lovastatin in adolescent males with heterozygous familial hypercholesterolemia. JAMA. 1999 281:137-44.

88. Fairbanks KP, Barbu VD, Witte LD et al. Effects of mevinolin and mevalonate on cell growth in several transformed cell lines. J Cell Physiol. 1986; 127:216-22. https://pubmed.ncbi.nlm.nih.gov/3634776

89. Vickers S, Duncan CAH, Lee LL et al. Disposition studies on the δ-lactone and hydroxy acid forms of mevinolin, a hypocholesterolemic agent. Fed Proc. 1982; 41:1713.

90. Stein EA, Lamkin GE, Bewley DZ. Lovastatin alone and in combination for treatment of primary hypercholesterolemia. Prog Clin Biol Res. 1988; 255:281-93. https://pubmed.ncbi.nlm.nih.gov/3340642

91. Furberg CD, Adams HP, Applegate WB et al et al. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation. 1994; 90:1679-87. https://pubmed.ncbi.nlm.nih.gov/7734010

92. Hodis HN, Mack WJ, LaBree L et al. Reduction in carotid wall thickness using lovastatin and dietary therapy. Ann Intern Med. 1996; 124:548-56. https://pubmed.ncbi.nlm.nih.gov/8597317

93. Byington RP, Evans GW, Espeland MA et al for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effects of lovastatin and warfarin on early carotid atherosclerosis: sex-specific analyses. Circulation. 1999; e14-7.

94. Bradford RH, Shear CL, Chremos AN et al. Expanded clinical evaluation of lovastatin (EXCEL) study results: two-year efficacy and safety follow-up. Am J Cardiol. 1994; 74:667-73. https://pubmed.ncbi.nlm.nih.gov/7942524

95. Jones P, Kafonek S, Laurora I et al. Comparative dose efficacy study of atorvastatin versus lovastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol. 1998; 81:582-7. https://pubmed.ncbi.nlm.nih.gov/9514454

96. Illingworth DR, Stein EA, Mitchel YB et al. Comparative effects of lovastatin and niacin in primary hypercholesterolemia. Arch Intern Med. 1994; 154:1586-95. https://pubmed.ncbi.nlm.nih.gov/8031206

97. Gholami K, Tavakoli N, Maleki M et al. Comparison of the efficacy and safety of fenofibrate and lovastatin in patients with primary type IIa or IIb hyperlipidaemia. J Clin Pharm Ther. 1998; 23:213-21. https://pubmed.ncbi.nlm.nih.gov/9831973

98. Vega GL, Grundy SM. Lipoprotein responses to treatment with lovastatin, gemfibrozil, and nicotinic acid in normolipidemic patients with hypoalphalipoproteinemia. Arch Intern Med. 1994; 154:73-82. https://pubmed.ncbi.nlm.nih.gov/8267492

99. National Heart, Lung, and Blood Institute Lipid Metabolism—Atherogenesis Branch. The lipid research clinics coronary primary prevention trial results: part I. Reduction in incidence of coronary heart disease. JAMA. 1984; 251:351-64. https://pubmed.ncbi.nlm.nih.gov/6361299

100. National Heart, Lung, and Blood Institute Lipid Metabolism—Atherogenesis Branch. The lipid research clinics coronary primary prevention trial results: part II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA. 1984; 251:365-74. https://pubmed.ncbi.nlm.nih.gov/6361300

101. Hung YJ, Pei D, Wu DA et al. Effects of lovastatin and gemfibrozil in subjects with high ratios of total cholesterol to high-density lipoprotein cholesterol. J Formos Med Assoc. 1999; 98:104-10. https://pubmed.ncbi.nlm.nih.gov/10083765

102. Anguita M, Alonso-Pulpon L, Arizon JM et al. Comparison of the effectiveness of lovastatin therapy for hypercholesterolemia after heart transplantation between patients with and without pretransplant atherosclerotic coronary artery disease. Am J Cardiol. 1994; 74:776-9. https://pubmed.ncbi.nlm.nih.gov/7942548

103. Kandus A, Kovac D, Cerne D et al. Therapy of hyperlipidemia with lovastatin in kidney transplant patients on cyclosporine A immunosuppression: three-year experience. Transplant Proc. 1998; 30:1307-9. https://pubmed.ncbi.nlm.nih.gov/9636530

104. Vega GL, East C, Grundy SM. Lovastatin therapy in familial dysbetalipoproteinemia: effect on kinetics of apolipoprotein B. Atherosclerosis. 1988; 70: 131- https://pubmed.ncbi.nlm.nih.gov/3162680

105. Kantola T, Kivisto KT, Neuvonen PJ et al. Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid. Clin Pharmacol Ther. 1998; 63:397-402. https://pubmed.ncbi.nlm.nih.gov/9585793

106. Knopp RH. Drug treatment of lipid disorders. N Engl J Med. 1999; 341:498-511. https://pubmed.ncbi.nlm.nih.gov/10441607

107. Anon. Choice of lipid-lowering drugs. Med Lett Drugs Ther. 1998; 40:117-22. https://pubmed.ncbi.nlm.nih.gov/9884672

109. Ramachandran CK, Sanders K, Melnykovych G. Enhancement in the adhesion of tumor cells to endothelial cells by decreased cholesterol synthesis. Cancer Res. 1986; 46:2520-5. https://pubmed.ncbi.nlm.nih.gov/3697991

110. Quesney-Huneeus V, Wiley MH, Siperstein MD. Essential role for mevalonate synthesis in DNA replication. Proc Natl Acad Sci USA. 1979; 76:5056-60. https://pubmed.ncbi.nlm.nih.gov/291922

111. Dafgard E, Engstrom W, Larsson O et al. The effect of factors released from the tumor-transformed cells on DNA synthesis, mitosis, and cellular enlargement in 3T3 fibroblasts. J Cell Physiol. 1987; 132:295-302. https://pubmed.ncbi.nlm.nih.gov/3040778

112. Grundy SM. HMG-CoA reductase inhibitors for treatment of hypercholesterolemia. N Engl J Med. 1988; 319:24-33. https://pubmed.ncbi.nlm.nih.gov/3288867

113. Corpier CL, Jones PH, Suki WN et al. Rhabdomyolysis and renal injury with lovastatin use: report of two cases in cardiac transplant recipients. JAMA. 1988; 260:239-41. https://pubmed.ncbi.nlm.nih.gov/3290520

118. Teva. Lovastatin tablets prescribing information. Parsippany, NJ; 2020 Aug.

119. Covis Pharma. Altoprev (lovastatin) extended-release tablets prescribing information. Zug, Switzerland; 2020 Sept.

200. Food and Drug Administration. FDA drug safety communication: Important safety label changes to cholesterol-lowering statin drugs. Rockville, MD; 2012 Feb 28. From FDA website. http://www.fda.gov/Drugs/DrugSafety/ucm293101.htm

202. McKenney JM, Davidson MH, Jacobson TA et al. Final conclusions and recommendations of the National Lipid Association Statin Safety Assessment Task Force. Am J Cardiol. 2006; 97(suppl):89-94C.

336. Cholesterol Treatment Trialists' (CTT) Collaborators, Mihaylova B, Emberson J et al. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012; 380:581-90. https://pubmed.ncbi.nlm.nih.gov/22607822

337. Baigent C, Keech A, Kearney PM et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet. 2005; 366:1267-78. https://pubmed.ncbi.nlm.nih.gov/16214597

338. Cholesterol Treatment Trialists’ (CTT) Collaboration, Baigent C, Blackwell L et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010; 376:1670-81. https://pubmed.ncbi.nlm.nih.gov/21067804

339. Wiggins BS, Saseen JJ, Page RL et al. Recommendations for Management of Clinically Significant Drug-Drug Interactions With Statins and Select Agents Used in Patients With Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2016; 134:e468-e495.

350. Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013 Nov 12. [Epub ahead of print] .

354. AIM-HIGH Investigators, Boden WE, Probstfield JL, et al.. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011 Dec 15;365(24):2255-67.

356. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2011 May 24;123(20):2292-333.

375. Weng TC, Yang YH, Lin SJ et al. A systematic review and meta-analysis on the therapeutic equivalence of statins. J Clin Pharm Ther. 2010; 35:139-51. https://pubmed.ncbi.nlm.nih.gov/20456733

376. Lee JW, Morris JK, Wald NJ. Grapefruit Juice and Statins. Am J Med. 2016; 129:26-9. https://pubmed.ncbi.nlm.nih.gov/26299317

378. Lilja JJ, Kivistö KT, Neuvonen PJ. Duration of effect of grapefruit juice on the pharmacokinetics of the CYP3A4 substrate simvastatin. Clin Pharmacol Ther. 2000; 68:384-90. https://pubmed.ncbi.nlm.nih.gov/11061578

379. Lilja JJ, Neuvonen M, Neuvonen PJ. Effects of regular consumption of grapefruit juice on the pharmacokinetics of simvastatin. Br J Clin Pharmacol. 2004; 58:56-60. https://pubmed.ncbi.nlm.nih.gov/15206993

380. Kane GC, Lipsky JJ. Drug-grapefruit juice interactions. Mayo Clin Proc. 2000; 75:933-42. https://pubmed.ncbi.nlm.nih.gov/10994829

400. Grundy SM, Stone NJ, Bailey AL et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019; 139:e1082-e1143. https://pubmed.ncbi.nlm.nih.gov/30586774

401. American Diabetes Association Professional Practice Committee. 10. Cardiovascular Disease and Risk Management: Standards of Care in Diabetes-2024. Diabetes Care. 2024 Jan 1;47(Suppl 1):S179-S218. doi: 10.2337/dc24-S010. PMID: 38078592; PMCID: PMC10725811.

402. Virani SS, Newby LK, Arnold SV et al. 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023 Aug 29;148(9):e9-e119. Doi: 10.1161/CIR.0000000000001168. Epub 2023 Jul 20. Erratum in: Circulation. 2023 Sep 26;148(13):e148. Erratum in: Circulation. 2023 Dec 5;148(23):e186. PMID: 37471501.

403. American College of Cardiology Solution Set Oversight Writing Committee; Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2022 ACC Expert Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022; 80:1366-1418.

404. Wiegman A, Gidding SS, Watts GF et al. Familial hypercholesterolaemia in children and adolescents: gaining decades of life by optimizing detection and treatment. Eur Heart J. 2015 Sep 21;36(36):2425-37. doi: 10.1093/eurheartj/ehv157. Epub 2015 May 25. PMID: 26009596; PMCID: PMC4576143.

405. US Food and Drug Administration. FDA Drug Safety Communication: FDA requests removal of strongest warning against using cholesterol-lowering statins during pregnancy; still advises most pregnant patients should stop taking statins. Silver Spring, MD; 2021 July 20. From FDA website. Accessed 2021 Sept 9. https://www.fda.gov/safety/medical-product-safety-information/statins-drug-safety-communication-fda-requests-removal-strongest-warning-against-using-cholesterol

413. Herd JA, Ballantyne CM, Farmer JA et al. Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]). Am J Cardiol. 1997; 80:278-86. https://pubmed.ncbi.nlm.nih.gov/9264419

414. MAAS Investigators. Effect of simvastatin on coronary atheroma: the multicentre anti-atheroma study (MAAS). Lancet. 1994; 344:633-8. https://pubmed.ncbi.nlm.nih.gov/7864934

415. Pitt B, Mancini GBJ, Ellis SG et al. Pravastatin limitation of atherosclerosis in the coronary arteries (PLAC I): reduction in atherosclerosis progression and clinical events. J Am Coll Cardiol. 1995; 26:1133-9. https://pubmed.ncbi.nlm.nih.gov/7594023

416. Crouse JR III, Byington RP, Bond MG et al. Pravastatin, lipids, and atherosclerosis in the carotid arteries (PLAC-II). Am J Cardiol. 1995; 75:455-9. https://pubmed.ncbi.nlm.nih.gov/7863988

417. Jukema JW, Bruschke AVG, van Boven AJ et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation. 1995; 91:2528-40. https://pubmed.ncbi.nlm.nih.gov/7743614

418. Salonen R, Nyyssonen K, Porkkala-Sarataho E et al. The Kuopio Atherosclerosis Prevention Study (KAPS): Effect of pravastatin treatment on lipids, oxidation resistance of lipoproteins, and atherosclerotic progression. Am J Cardiol. 1995; 76:34-9C.

423. DeGroot E, Jukema JW, Montauban AD et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J Am Coll Cardiol. 1998; 31:1561-7. https://pubmed.ncbi.nlm.nih.gov/9626835

424. Glorioso N, Troffa C, Filigheddu F et al. Effect of the HMG-CoA reductase inhibitors on blood pressure in patients with essential hypertension and primary hypercholesterolemia. Hypertension. 1999; 34:1281-6. https://pubmed.ncbi.nlm.nih.gov/10601131

425. Borghi C, Prandin MG, Costa FV et al. Use of statins and blood pressure control in treated hypertensive patients with hypercholesterolemia. J Cardiovasc Pharmacol. 2000; 35:549-55. https://pubmed.ncbi.nlm.nih.gov/10774784

426. Ridker PM, Rifai N, Pfeffer MA et al. Long-term effects of pravastatin on plasma concentration of C-reactive protein. Circulation. 1999; 100:230-5. https://pubmed.ncbi.nlm.nih.gov/10411845

427. Kluft C, de Maat MPM, Leuven JAG et al. Statins and C-reactive protein. Lancet. 1999; 353:1274-5.

429. Blum CB. Comparison of properties of four inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. Am J Cardiol. 1994; 73:3-11D.

430. Desager JP, Horsmans. Clinical pharmacokinetics of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. Clin Pharmacokinet. 1996; 31:348-71. https://pubmed.ncbi.nlm.nih.gov/9118584

431. Corsini A, Besllosta S, Baetta R et al. New insights into the pharmacodynamic and pharmacokinetic properties of statins. Pharmacol Ther. 1999; 84:413-28. https://pubmed.ncbi.nlm.nih.gov/10665838

432. Lennernas H, Fager G. Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Clin Pharmacokinet. 1997; 32:403-25. https://pubmed.ncbi.nlm.nih.gov/9160173

437. Pasternak RC, Smith SC Jr, Bairey-Merz CN et al. ACC/AHA/NHLBI clinical advisory on the use and safety of statins. American College of Cardiology/American Heart Association/National Heart, Lung and Blood Institute. Circulation. 2002;106:1024-8.

500. Cooper-DeHoff RM, Niemi M, Ramsey LB, et al. The Clinical Pharmacogenetics Implementation Consortium Guideline for SLCO1B1, ABCG2, and CYP2C9 genotypes and Statin-Associated Musculoskeletal Symptoms. Clin Pharmacol Ther. 2022 May;111(5):1007-1021. doi: 10.1002/cpt.2557. Epub 2022 Mar 11. PMID: 35152405; PMCID: PMC9035072.

501. Sadowska A, Osiński P, Roztocka A, Kaczmarz-Chojnacka K, Zapora E, Sawicka D, Car H. Statins-From Fungi to Pharmacy. Int J Mol Sci. 2023 Dec 29;25(1):466. doi: 10.3390/ijms25010466. PMID: 38203637; PMCID: PMC10779115.

502. Balasubramanian R, Maideen NMP. HMG-CoA Reductase Inhibitors (Statins) and their Drug Interactions Involving CYP Enzymes, P-glycoprotein and OATP Transporters-An Overview. Curr Drug Metab. 2021;22(5):328-341. doi: 10.2174/1389200222666210114122729. PMID: 33459228.

Frequently asked questions

Medical Disclaimer