Pitavastatin Calcium, Pitavastatin Magnesium (Monograph)

Brand names: Livalo, Zypitamag
Drug class: HMG-CoA Reductase Inhibitors

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

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).^{1 36}

Uses for Pitavastatin Calcium, Pitavastatin Magnesium

Available as pitavastatin calcium (e.g., Livalo and generic equivalents) and pitavastatin magnesium (i.e., Zypitamag).^{1 36} FDA considers pitavastatin magnesium tablets to be a pharmaceutical alternative (as described in section 505[b][2] of the Federal Food, Drug, and Cosmetic Act) and not a pharmaceutical (generic) equivalent to pitavastatin calcium tablets, since both contain the same active moiety (pitavastatin) but have different salts.^{1 36 38 39 40 41} Clinical efficacy and safety expected to be similar between the 2 salt forms of the drug.^{1 36 38 41 42}

Dyslipidemias

Pitavastatin calcium (Livalo and generic equivalents) and pitavastatin magnesium (i.e., Zypitamag) are used as adjuncts to diet to decrease LDL-cholesterol in adults with primary hyperlipidemia.^{1 3 4 5 6 36}

Pitavastatin calcium (Livalo and generic equivalents) is also used as an adjunct to diet to reduce LDL-cholesterol in pediatric patients ≥8 years of age with heterozygous familial hypercholesterolemia (HeFH).¹ Safety and efficacy not established in pediatric patients <8 years of age with HeFH or in pediatric patients with other types of hyperlipidemia.¹

Reductions in LDL-cholesterol concentrations achieved with usual dosages (1–4 mg daily) of pitavastatin are similar to or greater than those achieved with low to medium dosages of certain other statins (i.e., atorvastatin, pravastatin, simvastatin).^{1 3 4 5 9} Greater reductions in LDL-cholesterol were observed with concomitant administration of ezetimibe.^{48 49}

Reduction in Risk of Cardiovascular Events

Also has been used for reduction in the risk of atherosclerotic cardiovascular disease (ASCVD)^{† [off-label]} in patients with established ASCVD or at high risk of ASCVD.^{49 50 400}

Extensive evidence demonstrates that statins can substantially reduce LDL-cholesterol concentrations and associated risk of ASCVD; may be used for secondary or primary prevention.^{336 337 338 400 401 402 403}

AHA/ACC cholesterol management guideline states that lifestyle modification is the foundation of ASCVD risk reduction.⁴⁰⁰ Patients with established ASCVD or at 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 pitavastatin 1–4 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 additional 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}

Pitavastatin Calcium, Pitavastatin Magnesium Dosage and Administration

General

Pretreatment Screening

• Obtain baseline liver enzyme tests (e.g., AST, ALT).^{1 36}

• Obtain baseline hepatic panel in appropriate patients with chronic stable liver disease (including non-alcoholic fatty liver disease).⁴⁰⁰

• Obtain baseline fasting lipid panel.⁴⁰⁰

Patient Monitoring

• Perform fasting lipid panel periodically 4–12 weeks after statin initiation or dose adjustment; monitoring should continue every 3–12 months thereafter as clinically indicated.^{1 400}

• Periodically reinforce adherence to lifestyle modifications.⁴⁰⁰ Antilipemic therapy is an adjunct to, not a substitute for, lifestyle modification therapies that reduce the risk of ASCVD.⁴⁰⁰

• Perform repeat liver function tests (e.g., AST, ALT, total bilirubin, alkaline phosphatase) when clinically indicated (i.e., symptoms suggesting hepatotoxicity); routine monitoring in the absence of symptoms is not recommended.^{1 36 400}

• Monitor hepatic panel in appropriate patients with chronic stable liver disease (including non-alcoholic fatty liver disease).⁴⁰⁰

• Obtain creatine kinase (CK) levels in patients with severe statin-associated muscle weakness; routine monitoring in the absence of symptoms is not recommended.⁴⁰⁰

• Monitor for signs and symptoms of immune-mediated necrotizing myopathy (i.e., proximal muscle weakness, elevated serum CK) which persist despite discontinuation of statin treatment.^{1 36}

Administration

Oral Administration

Administer orally once daily at any time of day, without regard to food.^{1 36}

Dosage

Available as pitavastatin calcium (e.g., Livaloand generic equivalents) and pitavastatin magnesium (i.e., Zypitamag); dosages expressed in terms of pitavastatin.^{1 36} Commercially available tablets of Livalo and Zypitamag are considered bioequivalent.^{37 42}

Dosage modifications may be necessary when used concomitantly with certain drugs .^{1 36}

Pediatric Patients

Heterozygous Familial Hypercholesterolemia

Oral

Pediatric patients ≥8 years of age: Usual dosage range is 2–4 mg once daily.¹ Maximum dosage is 4 mg once daily.¹

Adults

Primary Hyperlipidemia

Oral

Usual dosage range is 2–4 mg once daily.^{1 36} Maximum dosage is 4 mg once daily.^{1 36} Alternative LDL-cholesterol-lowering therapy recommended for patients unable to achieve their LDL-cholesterol goal with pitavastatin 4 mg daily or for patients who require a high-intensity statin.^{1 36}

Reduction in Risk of Cardiovascular Events† [off-label]

Oral

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

The AHA/ACC guideline panel considers pitavastatin 1–4 mg daily to be a moderate-intensity statin.⁴⁰⁰

Dosage Modification for Concomitant Therapy

Erythromycin: Dosage should not exceed 1 mg daily.^{1 36}

Rifampin: Dosage should not exceed 2 mg daily.^{1 36}

Special Populations

Hepatic Impairment

No specific dosage recommendations at this time.^{1 36}

Renal Impairment

Moderate to severe renal impairment (eGFR 15–59 mL/minute per 1.73 m², not undergoing hemodialysis): Initially, 1 mg once daily.^{1 36} Maximum 2 mg once daily.^{1 36}

End-stage renal disease (ESRD) requiring hemodialysis: Initially, 1 mg once daily.^{1 36} Maximum 2 mg once daily.^{1 36}

Mild renal impairment: No specific dosage recommendations at this time.^{1 36}

Geriatric Patients

No specific dosage recommendations at this time; however use with caution.^{1 36}

Pharmacogenomic Considerations

Solute carrier organic anion transporter (SLCO) 1B1 decreased or possible decreased function phenotype: Initial dosage ≤2 mg daily.⁵⁰⁰

SLCO1B1 poor function phenotype: Initial dosage ≤1 mg daily.⁵⁰⁰

Cautions for Pitavastatin Calcium, Pitavastatin Magnesium

Contraindications

• Active liver failure or decompensated cirrhosis.^{1 36}

• Concomitant use with cyclosporine.^{1 36}

• Known hypersensitivity to pitavastatin or any ingredient in the formulation.^{1 36} Hypersensitivity reactions including angioedema, rash, pruritus, and urticaria have been reported.^{1 36}

Warnings/Precautions

Musculoskeletal Effects

Myopathy (manifested as muscle pain, tenderness or weakness associated with elevated CK) and rhabdomyolysis may occur.¹ Acute kidney injury secondary to myoglobinuria and rare fatalities reported.¹ May occur at any dosage, but risk increases with increasing dosage; in clinical studies, risk of severe myopathy increased with dosages >4 mg daily.¹ Maximum dosage is 4 mg once daily.^{1 36}

Use with caution in patients with predisposing factors for myopathy (e.g., age ≥65 years, renal impairment, inadequately treated hypothyroidism) and in patients receiving concomitant therapy with colchicine or certain antilipemic agents (i.e., fibric acid derivatives, niacin).^{1 36} Contraindicated with concomitant cyclosporine, concomitant gemfibrozil not recommended, and dosage restrictions recommended when used with erythromycin or rifampin.^{1 36}

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

Discontinue if CK concentrations become markedly elevated or if myopathy is diagnosed or suspected.^{1 36} Muscle symptoms and CK elevations may resolve if pitavastatin is discontinued.^{1 36}

Temporarily withhold therapy in patients experiencing an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., sepsis; shock; severe hypovolemia; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).^{1 36}

Immune-mediated Necrotizing Myopathy

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.^{1 36} 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, and improvement following therapy with immunosuppressive agents.^{1 36}

Additional neuromuscular and serologic testing may be necessary; treatment with immunosuppressive agents may be required.^{1 36}

Discontinue pitavastatin if IMNM is suspected.^{1 36}

Hepatic Effects

Increases in serum aminotransferase (i.e., AST, ALT) concentrations reported.¹ Increases usually appear soon after initiation, are transient and asymptomatic, and resolve or improve with continued therapy or after temporary interruption of therapy.¹

Postmarketing reports of fatal and nonfatal hepatic failure reported rarely.^{1 36}

Consider liver enzyme tests prior to initiation of therapy and as clinically indicated.^{1 36} Serious statin-related liver injury is rare and unpredictable, and routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.²⁰⁰ AHA/ACC cholesterol management guideline states that it is reasonable to obtain liver function tests in patients with symptoms of hepatotoxicity (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark colored urine, yellowing of skin or sclera); however, routine monitoring not recommended.⁴⁰⁰

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt pitavastatin therapy.^{1 36}

Use with caution in patients who consume substantial amounts of alcohol.^{1 36} Contraindicated in patients with active liver failure or decompensated cirrhosis.^{1 36}

Hyperglycemic Effects

Increases in HbA_1c and fasting serum glucose concentrations reported.^{1 200} 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

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.^{400 405 402} Consider patient's individual risks and benefits.^{402 405}

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 distributed into human milk; however, another statin has been shown to distribute into human milk.^{1 36} Not recommended in nursing women.^{1 36} 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.^{400 402 405}

Females and Males of Reproductive Potential

AHA/ACC cholesterol management guideline states women (including adolescents) of childbearing age who are sexually active should be counseled to use a reliable form of contraception.⁴⁰⁰

Pediatric Use

Pitavastatin calcium: Safety and efficacy not established in pediatric patients <8 years of age with heterozygous familial hypercholesterolemia or in pediatric patients with other types of hyperlipidemia.^{1 36}

Pitavastatin magnesium: Safety and efficacy not established in pediatric patients.³⁶

Geriatric Use

No substantial differences in safety or efficacy relative to younger adults, but increased sensitivity cannot be ruled out.^{1 36}

Peak plasma concentrations and AUC increased in patients ≥65 years of age.¹

Monitor for an increased risk of myopathy.^{1 36}

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

Peak plasma concentrations or AUC higher in patients with mild (Child-Pugh class A) or moderate (Child-Pugh class B) hepatic impairment.¹ Use with caution in patients with a history of liver disease (e.g., chronic alcoholic liver disease) and/or in patients who consume substantial amounts of alcohol.^{1 36} Contraindicated in patients with active liver failure or decompensated cirrhosis.^{1 36}

Renal Impairment

Peak plasma concentrations or AUC higher in patients with moderate or severe renal impairment and patients with ESRD undergoing hemodialysis.¹ Dosage adjustments necessary in patients with moderate or severe renal impairment (eGFR 15–59 mL/minute per 1.73 m²) and patients with ESRD undergoing hemodialysis.^{1 36} Monitor all patients with renal impairment for development of myopathy.^{1 36}

Pharmacogenomic Consideratons

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 that given the balance of statin-associated musculoskeletal symptoms risk versus known cardiovascular disease benefit, for patients who are candidates for new statin therapy, pharmacogenetic test results may provide additional useful information.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 phenotypes or poor function phenotypes will have increased exposure and risk of statin-associated musculoskeletal symptoms.⁵⁰⁰ Lower doses, and/or combination therapy (i.e., pitavastatin plus a nonstatin guideline directed medical therapy), or alternative statin may be required.⁵⁰⁰

Common Adverse Effects

Incidence (≥2%): Myalgia, back pain, diarrhea, constipation, pain in extremity.¹

Drug Interactions

Minimally metabolized by CYP2C9 and, to a lesser extent, by CYP2C8.^{1 7 8}

Substrate of P-gp, organic anionic transport polypeptide (OATP) 1B1 and OATP1B3;^{7 8 30 339 502} pharmacokinetic interactions observed with drugs that inhibit these transporters.^{1 7 8 9 30 339 502}

Specific Drugs and Foods

Pitavastatin Calcium, Pitavastatin Magnesium Pharmacokinetics

Absorption

Bioavailability

Absorbed from GI tract, principally from small intestine, with very small amounts absorbed from colon.¹

Peak plasma concentrations attained approximately 1 hour after administration.¹

Peak plasma concentrations and AUC increase in an approximately dose-proportional manner for single pitavastatin dosages of 1–24 mg once daily.¹

Peak plasma concentrations and AUC reportedly not different following evening or morning administration; however, reductions in LDL-cholesterol concentrations achieved with 4-mg tablets slightly higher following evening administration compared with morning administration in healthy individuals.¹

Pitavastatin calcium tablets (Livalo) are bioequivalent to pitavastatin magnesium tablets (Zypitamag) under fasting conditions.^{37 42}

Food

High-fat meal (50% fat content) reduces peak plasma concentrations of pitavastatin by 43% when administered as the calcium salt;¹ high-fat meal (50% fat content) reduced peak plasma concentrations of pitavastatin by 39% when administered as the magnesium salt.^{36 37} Extent of absorption (i.e., AUC) not substantially reduced when either formulation was administered with a high-fat meal.^{1 37}

Special Populations

Race: Peak plasma concentrations or AUC are 21 or 5% lower, respectively, in Black individuals compared with white individuals; no substantial differences in peak plasma concentrations and AUC observed among Japanese and white individuals.¹

Gender: Peak plasma concentrations or AUC are 60 or 54% higher, respectively, in healthy women compared with healthy men.¹

Geriatric patients: Peak plasma concentrations or AUC are 10 or 30% higher, respectively, in geriatric individuals (≥65 years of age) compared with younger adults.¹

Mild hepatic impairment (Child-Pugh class A): Peak plasma concentrations and AUC are 1.3- and 1.6-fold higher, respectively, than values in healthy individuals.¹

Moderate hepatic impairment (Child-Pugh class B): Peak plasma concentrations and AUC are 2.7- and 3.8-fold higher, respectively, than values in healthy individuals.¹

Mild renal impairment: Effects on pitavastatin exposure are unknown.¹

Moderate renal impairment (eGFR 30–59 mL/minute per 1.73 m²): Peak plasma concentrations and AUC are 60 and 102% higher, respectively, than values in healthy individuals.¹

Severe renal impairment (eGFR 15–29 mL/minute per 1.73 m², not requiring hemodialysis): Peak plasma concentrations and AUC are 18 and 36% higher, respectively, than values in healthy individuals.¹

ESRD requiring hemodialysis: Peak plasma concentrations and AUC are 40 and 86% higher, respectively, than values in healthy individuals.¹

Distribution

Extent

Not known whether pitavastatin is distributed into human milk.^{1 36}

Undergoes carrier-mediated uptake into hepatocytes, principally via OATP1B1 (OATP2) and, to a lesser extent, by OATP1B3 and OATP2B1;^{7 8 33 501} hepatic uptake is required for pharmacologic effects.⁷

Plasma Protein Binding

>99% (mainly albumin and alpha 1-acid glycoprotein).¹

Special Populations

Patients undergoing hemodialysis have a 33 or 36% increase in mean unbound fraction of pitavastatin compared with healthy individuals or patients with moderate renal impairment, respectively.¹

Elimination

Metabolism

Principally metabolized by uridine 5′-diphosphate (UDP) glucuronosyltransferase (i.e., UGT1A1, UGT1A3, UGT2B7) to an ester-type pitavastatin glucuronide conjugate, which is further metabolized to the inactive metabolite pitavastatin lactone.^{1 7 8 36}

Minimally metabolized by CYP2C9 and, to a lesser extent, by CYP2C8.^{1 7 8 36}

Elimination Route

Excreted in feces (79%) and in urine (15%) within 7 days following administration.¹

Unlikely to be removed by hemodialysis because of high (>99%) protein binding.¹

Half-life

Approximately 12 hours.¹

Special Populations

Mean elimination half-life is prolonged in patients with mild (10 hours) or moderate (15 hours) hepatic impairment compared with healthy individuals (8 hours).¹

Stability

Storage

Oral

Tablets

Pitavastatin calcium: 15–30°C.¹ Protect from light.¹

Pitavastatin magnesium: 20–25°C.³⁶ Protect from moisture and light.³⁶

Actions

• Inhibits HMG-CoA reductase, causing reduction in hepatic cholesterol biosynthesis; this leads to compensatory increase in expression of LDL receptors on hepatic cell surfaces and, subsequently, increased hepatic clearance of LDL-cholesterol from blood.^{1 7 8 36} Reduces serum concentrations of total cholesterol, LDL-cholesterol, VLDL-cholesterol, apo B, and triglyceride, and increases serum HDL-cholesterol concentrations in patients with primary hypercholesterolemia or mixed dyslipidemia.^{1 3 4 5 6 36}

• Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries.^{13 14 15 16 17 18 19 20 21 22 23}

• Other favorable (pleitropic) effects include an antiproliferative influence on smooth muscle cells, reconstruction of endothelial activity, antioxidant, antithrombotic, anticancer, and anti-inflammatory effects.^{26 27 501}

Advice to Patients

• Advise patients to read the manufacturer's patient information.^{1 36}

• Advise patients of the importance of adhering to nondrug therapies and measures, including adherence to a heart-healthy diet, regular exercise, avoidance of tobacco products, and maintenance of a healthy weight.^{1 36 400}

• Advise patients of the risk of myopathy and/or rhabdomyolysis; risk is increased with higher dosages or when used concomitantly with certain drugs.^{1 36} Advise patients of the importance of promptly informing clinicians of any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever, or if manifestations persist after discontinuance of therapy.^{1 36}

• Advise patients of the risk of adverse hepatic effects.^{1 36} Advise patients of the importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).^{1 36}

• Advise patients of the risk of increased glucose concentrations and development of type 2 diabetes.^{1 36 200}

• Advise patients that pitavastatin tablets may be administered once a day, at any time of day, with or without food.^{1 36}

• Advise females of reproductive potential (including adolescents) of the risk to a fetus.^{1 36} Advise women to notify their clinician to discuss if pitavastatin should be discontinued if they become pregnant or suspect pregnancy during therapy.^{1 36 405}

• Advise women breast-feeding is not recommended during therapy.^{1 36}

• Advise patients to inform their clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.^{1 36}

• Inform patients of other important precautionary information.^{1 36}

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

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

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