ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 1 مورد

Lovastatin: Pediatric drug information

Lovastatin: Pediatric drug information
2025© UpToDate, Inc. and its affiliates and/or licensors. All Rights Reserved.
For additional information see "Lovastatin: Drug information" and "Lovastatin: Patient drug information"

For abbreviations, symbols, and age group definitions show table
Brand Names: US
  • Altoprev
Brand Names: Canada
  • ACT Lovastatin [DSC];
  • GMD-Lovastatin
Therapeutic Category
  • Antilipemic Agent;
  • HMG-CoA Reductase Inhibitor
Dosing: Pediatric
Dyslipidemia; prevention coronary artery disease

Dyslipidemia; prevention coronary artery disease (CAD): Adolescents ≥18 years: Oral: Immediate release: Initial: 20 mg once daily with evening meal, then adjust at 4-week intervals; maximum daily dose: 80 mg/day. Note: Doses should be individualized according to the baseline LDL-cholesterol levels, the recommended goal of therapy, and patient response.

Heterozygous familial hypercholesterolemia

Heterozygous familial hypercholesterolemia: Note: Begin treatment if after adequate (eg, 6 month) trial of lifestyle/diet modifications the following are present: LDL-C ≥190 mg/dL or LDL-C remains ≥160 mg/dL with either a positive family history of premature cardiovascular disease or at least 1 high-level or 2 moderate-level risk factors. Females must be ≥1 year postmenarche (Ref).

Children ≥10 years and Adolescents ≤17 years: Oral: Immediate release: Initial: 10 mg once daily with evening meal (Ref); if target LDL-C levels are not reached within 3 months, increase dose in 10 mg increments every 3 months until target LDL-C achieved; usual effective range: 10 to 40 mg once daily; maximum daily dose: 80 mg/day (Ref). Lower initial doses or maximum daily doses may be necessary for some concomitant medications (eg, amiodarone, verapamil, danazol, diltiazem). Note: Children 8 to <10 years of age are not typically treated unless severe primary hyperlipidemias and high-risk condition associated with high morbidity; data for the use of lovastatin in these younger patients is lacking (Ref).

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

Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥10 years and Adolescents: Discontinue use until symptoms can be evaluated; check creatine phosphokinase (CPK) level; based on experience in adult patients, also evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism; reduced renal or hepatic function; rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution (symptoms and any associated CPK abnormalities), resume the original or consider a lower dose of lovastatin and retitrate. If muscle symptoms recur, discontinue lovastatin use. After muscle symptom resolution, may then reinitiate a different statin at an initial low dose; gradually increase if tolerated. Based on experience in adult patients, if muscle symptoms or elevated CPK persists for 2 months in the absence of continued statin use, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (Ref).

Dosing: Kidney Impairment: Pediatric

CrCl <30 mL/minute: Immediate release: Children ≥10 years and Adolescents: Doses exceeding 20 mg/day should be carefully considered and implemented cautiously

Dosing: Liver Impairment: Pediatric

There are no dosage adjustment provided in manufacturer's labeling (has not been studied); use is contraindicated in active liver disease or unexplained transaminase elevations.

Dosing: Adult

(For additional information see "Lovastatin: Drug information")

Dosage guidance:

Dosing: Lovastatin 40 to 80 mg/day is considered a moderate-intensity statin (generally reduces low-density lipoprotein-cholesterol [LDL-C] by ~30% to 49%). Lovastatin 20 mg/day is considered a low-intensity statin (reduces LDL-C <30%). If LDL-C must be lowered ≥50%, select a high-intensity statin (atorvastatin or rosuvastatin). Assess response ~1 to 3 months after therapy initiation or dose adjustment and every 3 to 12 months thereafter (Ref).

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

Atherosclerotic cardiovascular disease, primary or secondary prevention

Atherosclerotic cardiovascular disease, primary or secondary prevention:

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

Primary prevention:

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

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

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal to reduce LDL-C by ~30% to 49% (Ref).

Extended release: 40 to 60 mg once daily at bedtime to reduce LDL-C by ~30% to 49% (Ref).

ASCVD 10-year risk ≥7.5% to <20%:

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal to reduce LDL-C by ~30% to 49% (Ref).

Extended release: 40 to 60 mg once daily at bedtime to reduce LDL-C by ~30% to 49% (Ref).

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

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

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal (Ref).

Extended release: 40 to 60 mg once daily at bedtime (Ref).

Patients with diabetes:

40 to 75 years of age without additional ASCVD risk factors:

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal to reduce LDL-C by ~30% to 49% (Ref).

Extended release: 40 to 60 mg once daily at bedtime to reduce LDL-C by ~30% to 49% (Ref).

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

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

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal (Ref).

Extended release: 40 to 60 mg once daily at bedtime (Ref).

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

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

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal (Ref).

Extended release: 40 to 60 mg once daily at bedtime (Ref).

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

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

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

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal (Ref).

Extended release: 40 to 60 mg once daily at bedtime (Ref).

Heterozygous familial hyperlipidemia

Heterozygous familial hyperlipidemia (alternative agent):

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

Patients unable to tolerate high-intensity therapy:

Moderate-intensity therapy: Oral:

Immediate release: 40 to 80 mg once daily with evening meal (Ref).

Extended release: 40 to 60 mg once daily at bedtime (Ref).

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

Dosing: Kidney Impairment: Adult

Mild to moderate impairment: No dosage adjustment necessary.

Severe impairment (CrCl <30 mL/minute): There are no dosage adjustments provided in the manufacturer's labeling; use with caution and carefully consider doses >20 mg/day.

Dosing: Liver Impairment: Adult

No dosage adjustment provided in manufacturer’s labeling (has not been studied); contraindicated in patients with acute liver failure or decompensated cirrhosis.

Adverse Reactions

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

>10%:

Infection: Infection (11% to 16%)

Neuromuscular & skeletal: Increased creatine phosphokinase in blood specimen (≥2 × ULN: 11%)

1% to 10%:

Dermatologic: Skin rash (1%)

Gastrointestinal: Abdominal pain (3%), constipation (3% to 4%), diarrhea (3%), flatulence (5%)

Hepatic: Increased serum transaminases (≥3 × ULN: 2%; including increased serum alanine aminotransferase, increased serum alkaline phosphatase, increased serum aspartate aminotransferase, increased serum bilirubin)

Nervous system: Asthenia (2%), dizziness (1%), headache (7% to 8%), pain (3% to 5%)

Neuromuscular & skeletal: Back pain (5%), muscle cramps (1%), myalgia (3%)

Ophthalmic: Blurred vision (1%)

Respiratory: Flu-like symptoms (5%), sinusitis (4% to 6%)

<1%:

Cardiovascular: Chest pain

Dermatologic: Alopecia, pruritus

Gastrointestinal: Acid regurgitation, vomiting, xerostomia

Nervous system: Insomnia, paresthesia

Neuromuscular & skeletal: Arthralgia, lower extremity pain, myopathy, shoulder pain

Ophthalmic: Eye irritation

Postmarketing:

Cardiovascular: Flushing, vasculitis

Dermatologic: Changes in nails, changes of hair, cutaneous nodule, erythema multiforme, lichen planus, skin discoloration, skin photosensitivity, Stevens-Johnson syndrome, toxic epidermal necrolysis, urticaria, xeroderma

Endocrine & metabolic: Elevated glycosylated hemoglobin, gynecomastia, increase in fasting plasma glucose, loss of libido, thyroid dysfunction

Gastrointestinal: Anorexia, dry mucous membranes, pancreatitis

Genitourinary: Cystitis (interstitial; Huang 2015), erectile dysfunction

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

Hepatic: Cholestatic jaundice, chronic active hepatitis, hepatic cirrhosis, hepatic failure, hepatic neoplasm, hepatitis, increased gamma-glutamyl transferase

Hypersensitivity: Hypersensitivity reaction (including anaphylaxis, angioedema)

Immunologic: Dermatomyositis (Rodriguez-Garcia 1996)

Nervous system: Anxiety, chills, cognitive dysfunction (including amnesia, confusion, memory impairment), cranial nerve disorder (including dysgeusia, facial paresis, impairment of extraocular movement), depression, malaise, myasthenia gravis (including exacerbation of myasthenia gravis, ocular myasthenia), peripheral nerve palsy, peripheral neuropathy, psychic disorder, tremor, vertigo

Neuromuscular & skeletal: Arthritis, lupus-like syndrome, polymyalgia rheumatica, rhabdomyolysis

Ophthalmic: Ophthalmoplegia, progression of cataract

Respiratory: Dyspnea, interstitial lung disease

Miscellaneous: Fever

Contraindications

Hypersensitivity (eg, anaphylaxis, angioedema, Stevens-Johnson syndrome) to lovastatin or any component of the formulation; active liver failure or decompensated cirrhosis; concomitant use of strong CYP3A4 inhibitors and erythromycin.

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

Canadian labeling: Additional contraindications (not in US labeling): Concomitant use of cyclosporine; unexplained persistent elevated transaminases; pregnancy; breastfeeding.

Warnings/Precautions

Concerns related to adverse effects:

• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported with HMG-CoA reductase inhibitors; however, the benefits of statin therapy far outweigh the risk of dysglycemia. If a patient develops diabetes mellitus during therapy, continue use of lovastatin and encourage patient to adhere to healthy lifestyle regimens (eg, heart healthy dietary pattern, engage in physical activity, achieve and maintain a healthy body weight) (ACC/AHA [Grudy 2019]).

• Endocrine effects: Reduced cholesterol synthesis as a result of therapy could theoretically lead to reduced adrenal or gonadal steroid hormone production; clinical trial data are inconsistent in regard to the effect on basal steroid hormone levels. Patients with signs/symptoms of endocrine dysfunction should be evaluated as clinically indicated; use caution with concomitant medications (eg, spironolactone, cimetidine, ketoconazole) that may reduce steroid hormone levels/activity.

• Hepatotoxicity: Persistent elevations in serum transaminases have been reported; upon dose reduction, drug interruption, or discontinuation, transaminase levels returned to or near pretreatment levels. Postmarketing reports of fatal and nonfatal hepatic failure are rare. If serious hepatotoxicity with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, interrupt therapy promptly. If an alternate etiology is not identified, do not restart lovastatin. Liver enzyme tests should be obtained at baseline and as clinically indicated; routine periodic monitoring of liver enzymes is not necessary. Ethanol may enhance the potential of adverse hepatic effects; instruct patients to avoid excessive ethanol consumption.

• Myopathy/rhabdomyolysis: Rhabdomyolysis with acute renal failure secondary to myoglobinuria and/or myopathy has been reported; patients should be monitored closely. This risk is dose-related and is increased with concurrent use of strong CYP3A4 inhibitors (eg, clarithromycin, itraconazole, protease inhibitors), cyclosporine, fibric acid derivatives (eg, gemfibrozil), or niacin (doses ≥1 g/day); if concurrent use is warranted, consider lower starting and maintenance doses of lovastatin. Use caution in patients with inadequately treated hypothyroidism and those taking other drugs associated with myopathy (eg, colchicine), ≥65 years of age, and women; these patients are predisposed to myopathy. Immune-mediated necrotizing myopathy associated with HMG-CoA reductase inhibitor use has also been reported. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine, particularly if accompanied by malaise or fever. Discontinue therapy if markedly elevated CPK levels occur or if myopathy is diagnosed/suspected; consider treatment with immunosuppressants and additional neuromuscular and serologic testing. Prior to initiating a different HMG-CoA reductase inhibitor, consider risk of immune-mediated necrotizing myopathy; monitor closely.

Disease-related concerns:

• Hepatic impairment and/or ethanol use: Use with caution in patients who consume large amounts of ethanol or have a history of liver disease. Use is contraindicated in patients with active liver disease or unexplained transaminase elevations.

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

• Renal impairment: Use with caution in patients with renal impairment; risk of myopathy is increased.

Special populations:

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

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

Other warnings/precautions:

• Hyperlipidemia: Secondary causes of hyperlipidemia should be ruled out prior to therapy.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Generic: 10 mg, 20 mg, 40 mg

Tablet Extended Release 24 Hour, Oral:

Altoprev: 20 mg, 40 mg, 60 mg [contains corn starch, fd&c yellow #6 (sunset yellow)]

Generic Equivalent Available: US

May be product dependent

Pricing: US

Tablet, 24-hour (Altoprev Oral)

20 mg (per each): $47.22

40 mg (per each): $47.22

60 mg (per each): $47.22

Tablets (Lovastatin Oral)

10 mg (per each): $1.35 - $1.61

20 mg (per each): $2.25 - $2.71

40 mg (per each): $4.06 - $4.87

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

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Generic: 20 mg, 40 mg

Administration: Pediatric

Oral:

Immediate release tablets: Take with the evening meal.

Extended release tablets: Take at bedtime; do not crush or chew.

Administration: Adult

Oral: Administer IR tablet with the evening meal. Administer ER tablet in the evening; swallow whole and do not cut, crush, or chew.

Bariatric surgery: Tablet, extended release: Some institutions may have specific protocols that conflict with these recommendations; refer to institutional protocols as appropriate. Switch to IR formulation.

Storage/Stability

Tablet, immediate release: Store at 20°C to 25°C (68°F to 77°F). Protect from light

Tablet, extended release: Store at 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C to 30°C (59°F to 86°F). Avoid excessive heat and humidity.

Use

Treatment of heterozygous familial hypercholesterolemia as adjunct to dietary therapy to decrease elevated serum total and low density lipoprotein and apolipoprotein B levels (immediate release tablets: FDA approved in males and postmenarcheal [≥1 year] females ages 10 to 17 years)

Treatment of primary hypercholesterolemia as adjunct to dietary therapy to decrease elevated serum total and low density lipoprotein cholesterol (LDL-C) (immediate and extended release tablets: FDA approved in adults); to reduce the risk of myocardial infarction, unstable angina, and coronary revascularization procedures in patients without symptomatic disease with average to moderately elevated total and LDL-C and below average HDL-cholesterol (primary prevention) and slow progression of coronary atherosclerosis in patients with coronary heart disease (immediate and extended release tablets: FDA approved in adults)

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

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

Lovastatin may be confused with atorvastatin, Leustatin, Livostin, Lotensin, nystatin, pitavastatin.

International issues:

Lovacol [Chile and Finland] may be confused with Levatol brand name for penbutolol [U.S.]

Lovastin [Malaysia, Poland, and Singapore] may be confused with Livostin brand name for levocabastine [multiple international markets]

Mevacor [US, Canada, and multiple international markets] may be confused with Mivacron brand name for mivacurium [multiple international markets]

Metabolism/Transport Effects

Substrate of CYP3A4 (Major with inhibitors), CYP3A4 (Minor with inducers), OATP1B1/1B3; Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;

Drug Interactions

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

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

Abiraterone Acetate: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Acipimox: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Amiodarone: May increase serum concentration of Lovastatin. Management: Consider using a non-interacting statin (pravastatin, pitavastatin) in patients on amiodarone. If combined, limit the lovastatin dose to 40 mg daily and monitor for lovastatin toxicities (eg, myalgia, liver function test elevations, rhabdomyolysis). Risk D: Consider Therapy Modification

AmLODIPine: May increase serum concentration of Lovastatin. Risk C: Monitor

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

Azithromycin (Systemic): May increase myopathic (rhabdomyolysis) effects of Lovastatin. Risk C: Monitor

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

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

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

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

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

Clofazimine: May increase serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor

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

CycloSPORINE (Systemic): May increase serum concentration of Lovastatin. Risk X: Avoid

CYP3A4 Inducers (Moderate): May decrease serum concentration of Lovastatin. Risk C: Monitor

CYP3A4 Inducers (Strong): May decrease serum concentration of Lovastatin. Risk C: Monitor

CYP3A4 Inhibitors (Moderate): May increase serum concentration of Lovastatin. Risk C: Monitor

CYP3A4 Inhibitors (Strong): May increase active metabolite exposure of Lovastatin. CYP3A4 Inhibitors (Strong) may increase serum concentration of Lovastatin. Risk X: Avoid

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

Dabigatran Etexilate: Lovastatin may increase anticoagulant effects of Dabigatran Etexilate. Risk C: Monitor

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

Danazol: May increase serum concentration of Lovastatin. Management: Initiate immediate release lovastatin at a dose of 10 mg/day, and do not exceed 20 mg/day for immediate or extended release lovastatin, in patients receiving danazol. Monitor closely for signs of lovastatin toxicity (eg, myositis, rhabdomyolysis). Risk D: Consider Therapy Modification

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

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

DilTIAZem: May increase serum concentration of Lovastatin. Management: Initiate immediate release lovastatin at a dose of 10 mg/day, and do not exceed 20 mg/day for immediate or extended release lovastatin, in patients receiving diltiazem. Monitor closely for signs of lovastatin toxicity (eg, myositis, rhabdomyolysis). Risk D: Consider Therapy Modification

Dronedarone: May increase serum concentration of Lovastatin. Management: Initiate immediate release lovastatin at a dose of 10 mg/day, and do not exceed 20 mg/day for immediate or extended release lovastatin, in patients receiving dronedarone. Monitor closely for signs of lovastatin toxicity (eg, myositis, rhabdomyolysis). Risk D: Consider Therapy Modification

Elafibranor: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk of muscle toxicity may be increased. Risk C: Monitor

Elbasvir and Grazoprevir: May increase serum concentration of Lovastatin. Risk C: Monitor

Elexacaftor, Tezacaftor, and Ivacaftor: May increase serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

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

Encorafenib: May decrease serum concentration of Lovastatin. Encorafenib may increase serum concentration of Lovastatin. Risk C: Monitor

Erythromycin (Systemic): May increase serum concentration of Lovastatin. Risk X: Avoid

Etravirine: May decrease serum concentration of HMG-CoA Reductase Inhibitors (Statins). This applies to atorvastatin, lovastatin and simvastatin. Risk C: Monitor

Fenofibrate and Derivatives: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Fosamprenavir: May increase serum concentration of Lovastatin. Risk X: Avoid

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

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

Gemfibrozil: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid

Glecaprevir and Pibrentasvir: May increase serum concentration of Lovastatin. Risk X: Avoid

Grapefruit Juice: May increase serum concentration of Lovastatin. Grapefruit Juice may increase active metabolite exposure of Lovastatin. Risk X: Avoid

Interleukin-6 (IL-6) Inhibiting Therapies: May decrease serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Itraconazole: May increase serum concentration of Lovastatin. Risk X: Avoid

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

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

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

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

Levamlodipine: May increase serum concentration of Lovastatin. Risk C: Monitor

Lomitapide: May increase serum concentration of Lovastatin. Management: Consider reducing lovastatin doses during concomitant treatment with lomitapide, and monitor for signs and symptoms of muscle toxicity. Specific dosing recommendations are not presently available. Risk D: Consider Therapy Modification

Niacin: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Nirmatrelvir and Ritonavir: May increase serum concentration of Lovastatin. Risk X: Avoid

Pectin: May decrease therapeutic effects of Lovastatin. Risk C: Monitor

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

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

Raltegravir: May increase myopathic (rhabdomyolysis) effects of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor

Ranolazine: May increase serum concentration of Lovastatin. Ranolazine may also enhance the distribution of lovastatin to specific cells/tissues/organs where P-glycoprotein is present in large amounts (eg, brain, T-lymphocytes, testes, etc.). Management: Consider a lovastatin dose reduction if combined with ranolazine. An American Heart Association scientific statement recommends limiting lovastatin doses to 20 mg daily when used with ranolazine. Monitor closely for lovastatin toxicity. Risk D: Consider Therapy Modification

Red Yeast Rice: May increase adverse/toxic effects of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid

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

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

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

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

St John's Wort: May decrease active metabolite exposure of HMG-CoA Reductase Inhibitors (Statins). Management: Consider avoiding the concomitant administration of St John's Wort with atorvastatin, lovastatin and simvastatin in order to avoid the potential for decreased effects statins. If coadministered, monitor for decreased statin efficacy. Risk D: Consider Therapy Modification

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

Ticagrelor: May increase serum concentration of Lovastatin. Management: Limit lovastatin doses to 40 mg/day if coadministered with ticagrelor. Risk D: Consider Therapy Modification

Tipranavir: May increase serum concentration of Lovastatin. Risk X: Avoid

Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may increase myopathic (rhabdomyolysis) effects of Trabectedin. Risk C: Monitor

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

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

Verapamil: May increase serum concentration of Lovastatin. Management: Initiate immediate release lovastatin at a dose of 10 mg/day, and do not exceed 20 mg/day for immediate or extended release lovastatin, in patients receiving verapamil. Monitor closely for signs of lovastatin toxicity (eg, myositis, rhabdomyolysis). Risk D: Consider Therapy Modification

Vitamin K Antagonists: HMG-CoA Reductase Inhibitors (Statins) may increase anticoagulant effects of Vitamin K Antagonists. Risk C: Monitor

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

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

Food Interactions

Food decreases the bioavailability of lovastatin extended release tablets and increases the bioavailability of lovastatin immediate release tablets. Lovastatin serum concentrations may be increased if taken with grapefruit juice. Management: Avoid combination.

Dietary Considerations

Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 6 weeks and the diet should be continued during drug therapy. Avoid intake of grapefruit juice; may increase toxicity. Immediate release tablet should be taken with the evening meal.

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

Reproductive Considerations

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

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

Pregnancy Considerations

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

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

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

Monitoring Parameters

Pediatric patients: Baseline: ALT, AST, and creatine phosphokinase levels (CPK); fasting lipid panel (FLP) and repeat ALT and AST should be checked after 4 weeks of therapy; if no myopathy symptoms or laboratory abnormalities, then monitor FLP, ALT, and AST every 3 to 4 months during the first year and then every 6 months thereafter (NHLBI 2011).

Adults:

2013 ACC/AHA Blood Cholesterol Guideline recommendations (Stone 2013):

Lipid panel (total cholesterol, HDL, LDL, triglycerides): Baseline lipid panel; fasting lipid profile within 4 to 12 weeks after initiation or dose adjustment and every 3 to 12 months (as clinically indicated) thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.

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

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

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

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

Manufacturer recommendations: Liver enzyme tests at baseline and repeated when clinically indicated. Upon initiation or titration, lipid panel should be analyzed within 2 to 4 weeks.

Mechanism of Action

Lovastatin acts by competitively inhibiting 3-hydroxyl-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis. In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), they also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects (de Denus 2002; Ray 2005).

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: LDL-cholesterol reductions: 3 days

Absorption: 30% absorbed but less than 5% reaches the systemic circulation due to an extensive first-pass effect; increased with extended release tablets when taken in the fasting state

Protein binding: >95%

Metabolism: Hepatic; extensive first-pass effect; hydrolyzed to β-hydroxyacid (active)

Bioavailability: Increased with extended release tablets

Half-life elimination: 1.1-1.7 hours

Time to peak, serum: Immediate release: 2-4 hours; extended release: 12-14 hours

Excretion: Feces (~80% to 85%); urine (10%)

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Altered kidney function: Plasma concentrations of total inhibitors are increased 2-fold in severe renal insufficiency (CrCl <30 mL/minute).

Older adult: The mean plasma level of HMG-CoA reductase inhibitory activity was increased approximately 45% in elderly patients 70 to 78 years of age compared with patients 18 to 30 years of age.

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

  • (AE) United Arab Emirates: Mevacor;
  • (AR) Argentina: Hipovastin | Loriter | Lovastatin ilab | Mevlor | Sivlor;
  • (AT) Austria: Lovastatin hexal | Lovastatin stada artzneimittel | Mevacor;
  • (BD) Bangladesh: Aztatin | Lovatin;
  • (BG) Bulgaria: Holetar | Lipopres | Mevacor;
  • (BR) Brazil: Lipoclin | Lovastatina | Lovasterol | Lovaton | Mevacor | Mevalip | Neolipid | Reducol;
  • (CL) Chile: Colevix | Hiposterol | Lispor | Lovacol | Lovalip | Lovastatina | Mevacor | Sanelor;
  • (CN) China: Ai le ting | Hai li | Le fu xin | Luo hua ning | Mei xin jie | Xin lu | Xue qing;
  • (CO) Colombia: Closterol | Colevix | Corastan | Dislipin | Lincil | Lovastan | Lovastatina | Lovasterol | Mevacor;
  • (CR) Costa Rica: Lovastina;
  • (CZ) Czech Republic: Apo lovastatin | Holetar | Lovacard | Medostatin | Mevacor;
  • (DE) Germany: Lova | Lovabeta | Lovadura | Lovagamma | Lovahexal | Lovastatin Actavis | Lovastatin al | Lovastatin CT | Lovastatin Isis | Lovastatin ratiopharm | Lovastatin saar | Lovastatin Stada | Lovastatin Teva | Mevacor | Mevinacor;
  • (DK) Denmark: Lovastatin ratiopharm;
  • (DO) Dominican Republic: Hexaltina | Lipostatin | Lovastatina | Mevinacor;
  • (EC) Ecuador: Lipivas | Lovasin | Lovastatina | Lovastatina mk | Lovastin | Rovacor;
  • (EE) Estonia: Mevacor;
  • (EG) Egypt: Cholilysis | Lipdip | Lovastan | Lovastmed | Lowchol | Sabastatin;
  • (ES) Spain: Aterkey | Colesvir | Liposcler | Lovastatina aphar | Lovastatina bexal | Lovastatina centrum | Lovastatina cinfa | Lovastatina combinopharm | Lovastatina cuve | Lovastatina Davur | Lovastatina grapa | Lovastatina juventus | Lovastatina kern | Lovastatina lareq | Lovastatina lasa | Lovastatina mabo | Lovastatina merck | Lovastatina normon | Lovastatina Pensa | Lovastatina Sandoz | Lovastatina vir | Mevacor | Mevasterol | Nergadan | Taucor;
  • (ET) Ethiopia: Medostatin;
  • (FI) Finland: Lovacol | Lovastatiini ennapharma | Lovastatin alternova | Lovastatin hexal | Lovastatin ratiopharm | Lovastatin sandoz | Lovastatin Stada | Mevacor;
  • (GR) Greece: Liferzit | Lipidless | Lostin | Lovadrug | Lovapen | Lovasten | Lovatex | Lovatop | Lowlipid | Medovascin | Mevacor | Mevastin | Mevinol | Misodomin | Nabicortin | Terveson | Viking;
  • (HK) Hong Kong: Apo lovastatin | Cysin | Lofacol | Lomar | Lovatin | Lozutin | Medostatin | Mevacor;
  • (HU) Hungary: Mevacor | Stoplip;
  • (ID) Indonesia: Belvas | Cholestra | Cholvastin | Justin | Lipovas | Lofacol | Lotyn | Lovatrol | Paschol;
  • (IL) Israel: Lovalip;
  • (IN) India: Aztatin | Elstatin | Elstin | Favolip | Lestric | Lipdip | Lipistat | Lochol | Lostatin | Lotin | Lova | Lovacard | Lovadac | Lovalip | Lovameg | Lovastat | Lovastrol | Lovatin | Lovex | Pro-hdl | Recol | Rovacor | Satin;
  • (IT) Italy: Lovastatina doc | Lovastatina eg | Lovastatina mylan pharma | Lovastatina provvisoria | Lovastatina teva | Lovinacor | Rextat | Tavacor;
  • (JO) Jordan: Lostin;
  • (KR) Korea, Republic of: Arbatin | Birotin | Cholvatin | Dovastin | Loctin | Lostatin | Lostin | Lovaclin | Lovacol | Lovaitin | Lovalord | Lovarex | Lovast | Lovastatin dongsung | Lovastin | Lovatadin | Lovatone | Lowtin | Mevacor | Meverstin | Ovasta | Rostatin | Vaslotin | Vasterol | Vastin;
  • (KW) Kuwait: Mevacor;
  • (LB) Lebanon: Aterkey;
  • (LT) Lithuania: Holetar | Mevacor;
  • (LU) Luxembourg: Lovahexal | Mevacor;
  • (LV) Latvia: Lovahexal | Lovasterol | Mevacor;
  • (MX) Mexico: Casbame | Dilucid | Liperol | Mevacor | Sidevar;
  • (MY) Malaysia: Apo lovastatin | Ellanco | Lestric | Loactin | Lostatin | Lovacard | Lovarem | Lovastin | Lovatin | Medostatin | Mevacor | Rovacor | Sunocor;
  • (NL) Netherlands: Lucovitaal rode gist rijst;
  • (NO) Norway: Liprox | Lovabeta | Lovastatin ratiopharm | Mevacor;
  • (PE) Peru: Colevastina | Liporedux | Lostatin | Lovacol | Lovastatina | Lowcol | Mevacor | Rovacor;
  • (PK) Pakistan: Cholescor | Clolip | Colostin | Cutcol | Hypolip | Lestin | Lo-lipid | Lovacor | Lovastat | Lovax | Lovestan | Mevacor;
  • (PL) Poland: Anlostin | Apo-lova | Liprox | Lovastatinum | Lovasterol | Lovastin | Lowastatyna | Mevacor;
  • (PR) Puerto Rico: Altoprev | Mevacor;
  • (PT) Portugal: Flozul | Lipdaune | Lipus | Lovastatina | Lovastatina azevedos | Lovastatina germed | Lovastatina mepha | Lovastatina Sandoz | Mevinacor | Mevlor | Tecnolip;
  • (PY) Paraguay: Lovacol | Lovastatina genfar;
  • (QA) Qatar: Medostatin;
  • (RO) Romania: Lovastatina arena;
  • (RU) Russian Federation: Apextatin | Cardiostatin | Choletar | Holetar | Lovastatin vero | Medostatin | Mevacor | Rovacor | Vero lovastatin;
  • (SG) Singapore: Apo lovastatin | Elstatin | Lochol | Lostatin | Lovastin | Lovatin | Medostatin | Rovacor;
  • (SI) Slovenia: Artein | Holetar;
  • (SK) Slovakia: Medostatin;
  • (TN) Tunisia: Lovastatine Cinfa;
  • (TR) Turkey: Lovakor;
  • (TW) Taiwan: Apo lovastatin | Asacor | Celeton | Clatin | Cysin | Delipic | Leslipid | Lova | Lovacor | Lovast | Lovasta | Lovastin | Lovatin | Lozutin | Medostatin | Melova | Mevacor | Rodatin | Sancos | Trunshay | Ulova;
  • (UA) Ukraine: Lovameg | Mevacor;
  • (UY) Uruguay: Hipovastin | Lovestol | Mevlor | Normosterol;
  • (VE) Venezuela, Bolivarian Republic of: Dislipin | Levistan | Lostatin | Lovanil | Lovastatina | Mevacor;
  • (VN) Viet Nam: Vastanic;
  • (ZA) South Africa: Lovachol;
  • (ZM) Zambia: Lovacard | Lovalip
  1. Altoprev (lovastatin) [prescribing information]. Zug, Switzerland: Covis Pharma; March 2024.
  2. American Academy of Pediatrics Committee on Nutrition, “Cholesterol in Childhood,” Pediatrics, 1998, 101(1 Pt 1):141-7. [PubMed 11345978]
  3. American Academy of Pediatrics, “National Cholesterol Education Program: Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents,” Pediatrics, 1992, 89(3 Pt 2):525-84. [PubMed 1538956]
  4. Bateman BT, Hernandez-Diaz S, Fischer MA, et al. Statins and congenital malformations: cohort study. BMJ. 2015;350:h1035. doi:10.1136/bmj.h1035 [PubMed 25784688]
  5. Berglund L, Brunzell JD, Goldberg AC, et al; Endocrine society. Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline [published correction appears in: J Clin Endocrinol Metab. 2015;100(12):4685]. J Clin Endocrinol Metab. 2012;97(9):2969-2989. doi: 10.1210/jc.2011-3213. [PubMed 22962670]
  6. Bibbins-Domingo K, Grossman DC, Curry, SJ, et al; US Preventive Services Task Force. Statin use for the primary prevention of cardiovascular disease in adults: US Preventive Services Task Force recommendation statement. JAMA. 2016;316(19):1997-2007. doi: 10.1001/jama.2016.15450. [PubMed 27838723]
  7. Brunham LR, Ruel I, Aljenedil S, et al. Canadian Cardiovascular Society position statement on familial hypercholesterolemia: update 2018. Can J Cardiol. 2018;34(12):1553-1563. doi:10.1016/j.cjca.2018.09.005 [PubMed 30527143]
  8. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2013 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diabetes. 2013;35(suppl 1):1-212.
  9. Castro C, Gourley M. Diagnosis and treatment of inflammatory myopathy: issues and management. Ther Adv Musculoskelet Dis. 2012;4(2):111-120. doi: 10.1177/1759720X11425092. [PubMed 22870499]
  10. Chang JC, Chen YJ, Chen IC, Lin WS, Chen YM, Lin CH. Perinatal outcomes after statin exposure during pregnancy. JAMA Netw Open. 2021;4(12):e2141321. doi:10.1001/jamanetworkopen.2021.41321 [PubMed 34967881]
  11. Clauss SB, Holmes KW, Hopkins P, et al. Efficacy and safety of lovastatin therapy in adolescent girls with heterozygous familial hypercholesterolemia. Pediatrics. 2005;116(3):682-688. [PubMed 16140708]
  12. Daniels SR, Greer FR, and Committee on Nutrition, "Lipid Screening and Cardiovascular Health in Childhood," Pediatrics, 2008, 122(1):198-208. [PubMed 18596007]
  13. De Denus S, Spinler SA. Early statin therapy for acute coronary syndromes. Ann Pharmacother. 2002;36(11):1749-1758. doi: 10.1345/aph.1A413. [PubMed 12398573]
  14. Duplaga BA, “Treatment of Childhood Hypercholesterolemia With HMG-CoA Reductase Inhibitors,” Ann Pharmacother, 1999, 33(11):1224-7. [PubMed 10573325]
  15. “Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III),” JAMA, 2001, 285(19):2486-97. [PubMed 11368702]
  16. Fernández AB, Karas RH, Alsheikh-Ali AA, Thompson PD. Statins and interstitial lung disease: a systematic review of the literature and of food and drug administration adverse event reports. Chest. 2008;134(4):824-830. doi: 10.1378/chest.08-0943. [PubMed 18689579]
  17. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130(24):e278-e333. doi: 10.1161/CIR.0000000000000106. [PubMed 25085961]
  18. Fonarow GC, French WJ, Parsons LS, Sun H, Malmgren JA. Use of lipid-lowering medications at discharge in patients with acute myocardial infarction: data from the National Registry of Myocardial Infarction 3. Circulation. 2001;103(1):38-44. [PubMed 11136683]
  19. Godfrey LM, Erramouspe J, Cleveland KW. Teratogenic risk of statins in pregnancy. Ann Pharmacother. 2012;46(10):1419-1424. doi: 10.1345/aph.1R202. [PubMed 23032657]
  20. Grundy SM, Cleeman JI, Merz CN, et al, “Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines,” Circulation, 2004, 110(2):227-39. [PubMed 15249516]
  21. Grundy SM, Cleeman JI, Merz CN, et al; Coordinating Committee of the National Cholesterol Education Program. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Arterioscler Thromb Vasc Biol. 2004;24(8):e149-e161. doi: 10.1161/01.ATV.0000133317.49796.0E. [PubMed 15297292]
  22. 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(25):e1082-e1143. doi:10.1161/CIR.0000000000000625 [PubMed 30586774]
  23. Han BH, Sutin D, Williamson JD, et al; ALLHAT Collaborative Research Group. Effect of statin treatment vs usual care on primary cardiovascular prevention among older adults: The ALLHAT-LLT randomized clinical trial. JAMA Intern Med. 2017;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442. [PubMed 28531241]
  24. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360(9326):7-22. doi: 10.1016/S0140-6736(02)09327-3. [PubMed 12114036]
  25. Heeschen C, Hamm CW, Laufs U, Snapinn S, Böhm M, White HD; Platelet Receptor Inhibition in Ischemic Syndrome Management (PRISM) Investigators. Withdrawal of statins increases event rates in patients with acute coronary syndromes. Circulation. 2002;105(12):1446-1452. [PubMed 11914253]
  26. Hillis LD, Smith PK, Anderson JL, et al, “2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,” Circulation, 2011, 124(23):2610-42. [PubMed 22064600]
  27. Holmsen ST, Bakkebø T, Seferowicz M, Retterstøl K. Statins and breastfeeding in familial hypercholesterolaemia. Tidsskr Nor Laegeforen. 2017;137(10):686-687. doi:10.4045/tidsskr.16.0838 [PubMed 28551957]
  28. Huang CY, Chung SD, Kao LT, Lin HC, Wang LH. Statin use is associated with bladder pain syndrome/interstitial cystitis: a population-based case-control study. Urol Int. 2015;95(2):227-232. doi: 10.1159/000431185. [PubMed 26184102]
  29. Jacobson TA, Ito MK, Maki KC, et al. National lipid association recommendations for patient-centered management of dyslipidemia: part 1--full report. J Clin Lipidol. 2015;9(2):129-169. doi: 10.1016/j.jacl.2015.02.003. [PubMed 25911072]
  30. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2014;130(23):e199-e267. doi: 10.1161/CIR.0000000000000041. [PubMed 24682347]
  31. Jellinger PS, Handelsman Y, Rosenblit PD, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(suppl 2):1-87. doi: 10.4158/EP171764.APPGL. [PubMed 28437620]
  32. Kernan WN, Ovbiagele B, Black HR, et al; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; Council on Peripheral Vascular Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association [published correction appears in Stroke. 2015;46(2):e54]. Stroke. 2014;45(7):2160-2236. doi: 10.1161/STR.0000000000000024. [PubMed 24788967]
  33. Kulik A, Ruel M, Jneid H, et al; American Heart Association Council on Cardiovascular Surgery and Anesthesia. Secondary prevention after coronary artery bypass graft surgery: a scientific statement from the American Heart Association. Circulation. 2015;131(10):927-964. doi: 10.1161/CIR.0000000000000182. [PubMed 25679302]
  34. Lambert M, Lupien PJ, Gagne C, et al, “Treatment of Familial Hypercholesterolemia in Children and Adolescents: Effect of Lovastatin. Canadian Lovastatin in Children Study Group,” Pediatrics, 1996, 97(5):619-28. [PubMed 8628597]
  35. Lapi F, Gallo E, Bernasconi S, et al. Myopathies associated with red yeast rice and liquorice: spontaneous reports from the Italian Surveillance System of Natural Health Products. Br J Clin Pharmacol. 2008;66(4):572-574. doi: 10.1111/j.1365-2125.2008.03224.x. [PubMed 18637891]
  36. LaRosa JC, Grundy SM, Waters DD, et al; Treating to New Targets (TNT) Investigators. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-1435. doi: 10.1056/NEJMoa050461. [PubMed 15755765]
  37. Lecarpentier E, Morel O, Fournier T, Elefant E, Chavatte-Palmer P, Tsatsaris V. Statins and pregnancy: between supposed risks and theoretical benefits. Drugs. 2012;72(6):773-788. doi:10.2165/11632010-000000000-00000 [PubMed 22480340]
  38. Le Manach Y, Godet G, Coriat P, et al. The impact of postoperative discontinuation or continuation of chronic statin therapy on cardiac outcome after major vascular surgery. Anesth Analg. 2007;104(6):1326-1333. [PubMed 17513620]
  39. Lovastatin [prescribing information]. Baltimore, MD: Lupin Pharmaceuticals Inc; April 2017.
  40. Lovastatin tablet [prescribing information]. Princeton, NJ; BluePoint Laboratories; July 2020.
  41. Lovastatin tablets [product monograph]. Vaughan, Ontario, Canada: AA Pharma Inc; February 2021.
  42. 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(14):1366-1418. doi:10.1016/j.jacc.2022.07.006 [PubMed 36031461]
  43. McCrindle BW, Urbina EM, Dennison BA, et al, "Drug Therapy of High-Risk Lipid Abnormalities in Children and Adolescents: A Scientific Statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee, Council of Cardiovascular Disease in the Young, With the Council on Cardiovascular Nursing," Circulation, 2007, 115(14):1948-67. [PubMed 17377073]
  44. McPherson R, Frohlich J, Fodor G, et al. Canadian Cardiovascular Society Position Statement--Recommendations for the Diagnosis and Treatment of Dyslipidemia and Prevention of Cardiovascular Disease [published correction appears in Can J Cardiol. 2006;22(12):1077]. Can J Cardiol. 2006;22(11):913-927. [PubMed 16971976]
  45. Mevacor (lovastatin) [prescribing information]. Whitehouse Station, NJ: Merck & Co Inc; February 2014.
  46. Mortensen MB, Falk E. Primary prevention with statins in the elderly. J Am Coll Cardiol. 2018;71(1):85-94. doi: 10.1016/j.jacc.2017.10.080. [PubMed 29301631]
  47. Narayanaswami P, Sanders DB, Wolfe G, et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology. 2021;96(3):114-122. doi:10.1212/WNL.0000000000011124 [PubMed 33144515]
  48. National Heart, Lung, and Blood Institute, "Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents," Clinical Practice Guidelines, 2011, National Institutes of Health. Available at http://www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf
  49. Newson RS, Felix JF, Heeringa J, Hofman A, Witteman JC, Tiemeier H. Association between serum cholesterol and noncardiovascular mortality in older age. J Am Geriatr Soc. 2011;59(10):1779-1785. doi: 10.1111/j.1532-5415.2011.03593.x. [PubMed 22091490]
  50. Parikh NI, Gonzalez JM, Anderson CAM, et al; American Heart Association Council on Epidemiology and Prevention; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Cardiovascular and Stroke Nursing; and the Stroke Council. Adverse pregnancy outcomes and cardiovascular disease risk: unique opportunities for cardiovascular disease prevention in women: a scientific statement from the American Heart Association. Circulation. 2021;143(18):e902-e916. doi:10.1161/CIR.0000000000000961 [PubMed 33779213]
  51. Pasternak RC, Smith SC Jr, Bairey-Merz CN, Grundy SM, Cleeman JI, Lenfant C; American College of Cardiology; American Heart Association; National Heart, Lung and Blood Institute. ACC/AHA/NHLBI clinical advisory on the use and safety of statins. Stroke. 2002;33(9):2337-2341. http://stroke.ahajournals.org/cgi/content/short/33/9/2337 [PubMed 12215610]
  52. Pearson GJ, Thanassoulis G, Anderson TJ, et al. 2021 Canadian Cardiovascular Society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in adults. Can J Cardiol. 2021;37(8):1129-1150. doi:10.1016/j.cjca.2021.03.016 [PubMed 33781847]
  53. Pearson TA, Mensah GA, Alexander RW, et al; Centers for Disease Control and Prevention; American Heart Association. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107(3):499-511. [PubMed 12551878]
  54. Phillips BG, Yim JM, Brown EJ Jr, et al. Pharmacologic profile of survivors of acute myocardial infarction at United States academic hospitals. Am Heart J. 1996;131(5):872-878. [PubMed 8615304]
  55. Pignone M. Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed December 20, 2022.
  56. Poldermans D, Bax JJ, Kertai MD, et al. Statins are associated with a reduced incidence of perioperative mortality in patients undergoing major noncardiac vascular surgery. Circulation. 2003;107(14):1848-1851. doi: 10.1161/01.CIR.0000066286.15621.98. [PubMed 12695283]
  57. Ray KK and Cannon CP. The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes. J Am Coll Cardiol. 2005;46(8):1425-1433. doi: 10.1016/j.jacc.2005.05.086. [PubMed 16226165]
  58. Refer to manufacturer's labeling.
  59. Ridker PM, Danielson E, Fonseca FA, et al; JUPITER Study Group. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359(21):2195-2207. doi: 10.1056/NEJMoa0807646. [PubMed 18997196]
  60. Rodriguez-Garcia JL, Serrano Commino M. Lovastatin-associated dermatomyositis. Postgrad Med J. 1996;72(853):694. doi:10.1136/pgmj.72.853.694 [PubMed 8944218]
  61. Rosenson RS, Durrington P. Familial hypercholesterolemia in adults: Treatment. Connor RF, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed December 10, 2021a.
  62. Rosenson RS, Hayward RA, Lopez-Sendon J. Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed December 10, 2021b.
  63. Sever PS, Dahlöf B, Poulter NR, et al; ASCOT investigators. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet. 2003;361(9364):1149-1158. doi: 10.1016/S0140-6736(03)12948-0. [PubMed 12686036]
  64. Shepherd J, Blauw GJ, Murphy MB, et al; PROSPER study group. PROspective Study of Pravastatin in the Elderly at Risk. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet. 2002;360(9346):1623-1630. [PubMed 12457784]
  65. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med. 1995;333(20):1301-1307. doi: 10.1056/NEJM199511163332001. [PubMed 7566020]
  66. Smith DJ, Olive KE. Chinese red rice-induced myopathy. South Med J. 2003;96(12):1265-1267. doi: 10.1097/01.SMJ.0000100117.79718.DC. [PubMed 14696880]
  67. Stein EA, Illingworth DR, Kwiterovich PO Jr, et al, “Efficacy and Safety of Lovastatin in Adolescent Males With Heterozygous Familial Hypercholesterolemia: A Randomized Controlled Trial,” JAMA, 1999, 281(2):137-44. [PubMed 9917116]
  68. Stone NJ, Robinson JG, Lichtenstein AH, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 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. 2014;129(25 Suppl 2):S1-45. doi:10.1161/01.cir.0000437738.63853.7a [PubMed 24222016]
  69. Sun JX, Niecestro R, Phillips G, Shen J, Lukacsko P, Friedhoff L. Comparative pharmacokinetics of lovastatin extended-release tablets and lovastatin immediate-release tablets in humans. J Clin Pharmacol. 2002;42(2):198-204. [PubMed 11831543]
  70. “Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III),” May 2001, www.nhlbi.nih.gov/guidelines/cholesterol.
  71. Tonelli M, Wanner C; Kidney Disease: Improving Global Outcomes Lipid Guideline Development Work Group Members. Lipid management in chronic kidney disease: synopsis of the Kidney Disease: Improving Global Outcomes 2013 clinical practice guideline. Ann Intern Med. 2014;160(3):182. doi: 10.7326/M13-2453. [PubMed 24323134]
  72. Vahedian-Azimi A, Bianconi V, Makvandi S, et al. A systematic review and meta-analysis on the effects of statins on pregnancy outcomes. Atherosclerosis. 2021b;336:1-11. doi:10.1016/j.atherosclerosis.2021.09.010 [PubMed 34601188]
  73. Vahedian-Azimi A, Makvandi S, Banach M, Reiner Ž, Sahebkar A. Fetal toxicity associated with statins: a systematic review and meta-analysis. Atherosclerosis. 2021a;327:59-67. doi:10.1016/j.atherosclerosis.2021.05.006 [PubMed 34044205]
  74. Vuorio A, Kuoppala J, Kovanen PT, et al. Statins for children with familial hypercholesterolemia. Cochrane Database Syst Rev. 2017;7:CD006401. [PubMed 28685504]
Topic 12566 Version 573.0