Class: HMG-CoA Reductase Inhibitors
VA Class: CV350
Molecular Formula: C50H46CaF2N2O8
Brands: Livalo
Introduction
Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).1
Uses for Pitavastatin Calcium
Dyslipidemias
Adjunct to dietary therapy to decrease elevated serum total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations, and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia.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
Safety and efficacy not established in patients with Fredrickson Type I, III, or V dyslipidemia.1 Effect on cardiovascular morbidity and mortality not established.1
Pitavastatin Calcium Dosage and Administration
General
Patients should be placed on a standard lipid-lowering diet before initiation of pitavastatin therapy and should remain on this diet during treatment with the drug.1
Monitoring during Antilipemic Therapy
Monitor lipoprotein concentrations periodically to ensure that target LDL-cholesterol goals are achieved and maintained at <100 mg/dL (optional goal: <70 mg/dL) for patients with CHD or CHD risk equivalents; <130 mg/dL (optional goal: <100 mg/dL) for patients with ≥2 risk factors and 10-year risk of 10–20%; <130 mg/dL for patients with ≥2 risk factors and 10-year risk <10%; or <160 mg/dL for patients with 0–1 risk factor.32
Administration
Oral Administration
Administer orally once daily at any time of day, without regard to food.1
Dosage
Available as pitavastatin calcium; dosage expressed in terms of pitavastatin.1
Adults
Dyslipidemias
Primary Hypercholesterolemia or Mixed Dyslipidemia
Oral
Initially, 2 mg once daily.1 Determine serum lipoprotein concentrations 4 weeks after initiating or titrating therapy and adjust dosage accordingly.1 Usual maintenance dosage is 1–4 mg once daily.1
Prescribing Limits
Adults
Dyslipidemias
Primary Hypercholesterolemia or Mixed Dyslipidemia
Oral
Maximum 4 mg once daily.1
Special Populations
Hepatic Impairment
No specific dosage recommendations at this time.1 (See Contraindications under Cautions, and also see Absorption: Special Populations and Elimination: Special Populations under Pharmacokinetics.)
Renal Impairment
Patients with moderate renal impairment (GFR 30–59 mL/minute per 1.73 m2) or patients with end-stage renal disease (ESRD) undergoing hemodialysis: Initially, 1 mg once daily.1 Maximum 2 mg once daily.1
Patients with severe renal impairment (GFR <30 mL/minute per 1.73 m2) not undergoing hemodialysis: Not evaluated systematically in this population; use not recommended.1
Geriatric Patients
No specific dosage recommendations at this time.1 (See Geriatric Use under Cautions.)
Cautions for Pitavastatin Calcium
Contraindications
Active liver disease, including unexplained, persistent elevations of serum aminotransferase concentrations.1
Pregnancy or lactation.1 (See Lactation and also see Fetal/Neonatal Morbidity and Mortality under Cautions.)
Concomitant use with cyclosporine.1 (See Specific Drugs and Foods under Interactions.)
Known hypersensitivity to pitavastatin or any ingredient in the formulation.1
Warnings/Precautions
Sensitivity Reactions
Hypersensitivity
Rash, pruritus, and urticaria reported.1
Fetal/Neonatal Morbidity and Mortality
Suppression of cholesterol biosynthesis could cause fetal harm.1 Congenital anomalies following intrauterine exposure to statins reported rarely.1
Advise women of childbearing potential to use effective contraceptive methods during pitavastatin therapy.1 If the patient becomes pregnant while taking the drug, discontinue therapy and apprise patient of potential fetal hazard.1
Hepatic Effects
Associated with increases in serum aminotransferase (i.e., AST, ALT) concentrations.1 Increases usually transient and resolve or improve with continued therapy or after temporary interruption of therapy.1 Increases in alkaline phosphatase and bilirubin concentrations also reported.1
Perform liver function tests prior to initiation of therapy, at 12 weeks after initiation of therapy or any increase in dosage, and periodically (e.g., semiannually) thereafter.1
Patients who develop increased aminotransferase concentrations should be monitored until abnormalities return to normal.1 If increases in AST or ALT concentrations >3 times the ULN persist, reduce dosage or discontinue therapy.1
Use with caution in patients who consume substantial amounts of alcohol.1 Contraindicated in patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations.1
Musculoskeletal Effects
Myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria 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
Use with caution in patients with predisposing factors for myopathy (e.g., advanced age [>65 years of age], renal impairment, inadequately treated hypothyroidism) and in patients receiving concomitant therapy with certain antilipemic agents (i.e., fibric acid derivatives, antilipemic dosages of niacin).1
Discontinue if serum CK concentrations become markedly elevated or if myopathy is diagnosed or suspected.1 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; hypotension; dehydration; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures). (See Advice to Patients.)1
Specific Populations
Pregnancy
Category X.1 (See Contraindications and also see Fetal/Neonatal Morbidity and Mortality under Cautions.)
Lactation
Distributed into milk in rats.1 Not known whether distributed into human milk; however, a small amount of another statin is distributed into human milk.1 Use is contraindicated; discontinue nursing or pitavastatin.1
Pediatric Use
Safety and efficacy not established in pediatric patients <18 years of age.1 29
Geriatric Use
No substantial differences in safety or efficacy relative to younger adults, but increased sensitivity cannot be ruled out.1
Hepatic Impairment
Contraindicated in patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations.1 (See Absorption: Special Populations and also Elimination: Special Populations, under Pharmacokinetics.)
Renal Impairment
Dosage adjustments necessary in patients with moderate renal impairment (GFR 30–59 mL/minute per 1.73 m2) and in patients with ESRD undergoing hemodialysis.1 (See Renal Impairment under Dosage and Administration.)
Do not use in patients with severe renal impairment (GFR <30 mL/minute per 1.73 m2) who are not undergoing hemodialysis (inadequate data/experience).1
Common Adverse Effects
Myalgia, back pain, diarrhea, constipation, pain in extremity.1
Interactions for Pitavastatin Calcium
Minimally metabolized by CYP isoenzymes 2C9 and 2C8.1 7 8
Substrate of organic anionic transport polypeptide (OATP) 1B1 (OATP2) (see Extent under Pharmacokinetics);7 8 30 pharmacokinetic interactions observed with drugs that inhibit OATP1B1.1 7 9 30
Specific Drugs and Foods
Drug or Food | Interaction | Comments |
|---|---|---|
Cyclosporine | Substantially increased peak plasma concentrations and AUC of pitavastatin1 | Concomitant use contraindicated1 |
Digoxin | Slight decrease in peak plasma concentrations and increase in AUC of pitavastatin1 Slight decrease in peak plasma concentrations and AUC of digoxin1 | Not considered clinically important29 |
Enalapril | Decreased peak plasma concentrations and increased AUC of pitavastatin1 Increased peak plasma concentrations and AUC of enalapril1 | Not considered clinically important29 |
Erythromycin | Substantially increased peak plasma concentrations and AUC of pitavastatin1 | Do not exceed pitavastatin dosage of 1 mg once daily 1 |
Ezetimibe | Negligible decreases in peak plasma concentrations and AUC of pitavastatin1 Increased peak plasma concentrations and AUC of ezetimibe1 | Not considered clinically important29 |
Fibric acid derivatives (e.g., gemfibrozil) | Possible pharmacodynamic interaction (increased risk of adverse musculoskeletal effects [e.g., myopathy, rhabdomyolysis])1 Increased peak plasma concentrations and AUC of pitavastatin; increases more pronounced when used concomitantly with gemfibrozil than with fenofibrate1 | Use concomitantly with caution1 |
Grapefruit juice | Decreased peak plasma concentrations and increased AUC of pitavastatin1 | Not considered clinically important29 |
HIV protease inhibitors | Atazanavir: Increased peak plasma concentrations and AUC of pitavastatin and atazanavir1 31 Ritonavir-boosted protease inhibitors: Possible increased pitavastatin concentrations and rhabdomyolysis1 31 | Atazanavir: Not considered clinically important;29 dosage adjustment not necessary31 Ritonavir-boosted protease inhibitors: Manufacturer recommends avoiding concomitant use with lopinavir/ritonavir;1 however, some clinicians recommend avoiding concomitant use with any ritonavir-boosted protease inhibitor31 |
Itraconazole | Decreased peak plasma concentrations and AUC of pitavastatin1 | Not considered clinically important29 |
Niacin (at antilipemic dosages29 ) | Possible increased risk of adverse musculoskeletal effects (e.g., myopathy, rhabdomyolysis)1 | Consider reducing pitavastatin dosage1 |
Rifampin | Substantially increased peak plasma concentrations and AUC of pitavastatin1 Decreased peak plasma concentrations and AUC of rifampin1 | Do not exceed pitavastatin dosage of 2 mg once daily1 |
Warfarin | Pharmacokinetic and pharmacodynamic (i.e., effects on PT and INR) interaction unlikely1 Increased peak plasma concentrations and AUC of R-warfarin and S-warfarin1 | Monitor PT and INR when pitavastatin is initiated in patients receiving warfarin1 |
Pitavastatin Calcium Pharmacokinetics
Absorption
Bioavailability
Absorbed from GI tract, principally from small intestine, with very small amounts absorbed from colon.1
Absolute bioavailability of oral solution (not commercially available in the US) is 51%.1
Peak plasma concentrations attained approximately 1 hour after administration of tablets29 .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
Onset
Therapeutic response observed within one week; maximal response occurs within 2–4 weeks.29
Food
High-fat meal (50% fat content) reduces peak plasma concentrations by 43% but does not substantially reduce extent of absorption (i.e., AUC).1
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; however, no difference in safety or efficacy observed in clinical trials.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 (See Geriatric Use under Cautions.)
Hepatic impairment: Patients with aminotransferase (i.e., AST, ALT) concentrations >1.5 times the ULN were excluded from phase 3 clinical studies.3 4 29 In patients with mild (Child-Pugh class A) hepatic impairment, peak plasma concentrations or AUC are 1.3- or 1.6-fold higher, respectively, compared with healthy individuals.1 In patients with moderate (Child-Pugh class B) hepatic impairment, peak plasma concentrations or AUC are 2.7- or 3.8-fold higher, respectively, compared with healthy individuals.1
Renal impairment: Peak plasma concentrations or AUC are 60 or 79% higher, respectively, in patients with moderate renal impairment (GFR 30–59 mL/min per 1.73 m2) compared with healthy individuals.1 In patients with ESRD undergoing hemodialysis, peak plasma concentrations or AUC are 40 or 86% higher, respectively, compared with healthy individuals.1 Effects of mild or severe renal impairment on pitavastatin exposure are unknown.1
Distribution
Extent
Crosses placenta and is distributed into milk in rats.1 (See Pregnancy and also Lactation under Cautions.)
Undergoes carrier-mediated uptake into hepatocytes, principally via OATP1B1 (OATP2) and, to a lesser extent, by OATP1B3 and OATP2B1;7 8 29 33 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
Minimally metabolized by CYP2C9 and CYP2C8.1 7 8
Elimination Route
Excreted in feces (79%) and in urine (15%) within 7 days following administration of oral solution (not commercially available in the US).1 29
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
15–30°C. 1 Protect from light.1
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 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
Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries,10 11 12 13 14 15 16 17 18 19 20 21 22 23 28 modulate BP in hypercholesterolemic patients with hypertension,24 25 and possess anti-inflammatory activity.26 27
Advice to Patients
Risk of myopathy and/or rhabdomyolysis.1 Importance of promptly informing clinicians of any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever.1
Importance of monitoring liver function prior to initiation of therapy, at 12 weeks after initiation of therapy or any increase in dosage, and periodically (e.g., semiannually) thereafter.1
Importance of adhering to nondrug therapies and measures, including dietary management, weight control, physical activity, and management of potentially contributory disease (e.g., diabetes mellitus).2
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1 Necessity for clinicians to advise women to avoid pregnancy (i.e., using effective contraceptive methods) during therapy and to advise pregnant women of risk to the fetus.1
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.1
Importance of informing patients of other important precautionary information.1 (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 1 mg (of pitavastatin) | Livalo | Kowa |
2 mg (of pitavastatin) | Livalo | Kowa | ||
4 mg (of pitavastatin) | Livalo | Kowa |
Disclaimer
This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.
The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.
AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions July 11, 2011. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.
References
1. Kowa Pharmaceuticals America, Inc. Livalo (pitavastatin calcium) tablets prescribing information. Montgomery, AL; 2010 Jul.
2. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Adult Treatment Panel III Report. From NIH web site.
3. Budinski D, Arneson V, Hounslow N, Grasiansky N. Pitavastatin compared with atorvastatin in primary hypercholesterolemia or combined dyslipidemia. Clin Lipidol. 2009; 4:291-302.
4. Ose L, Budinski D, Hounslow N et al. Comparison of pitavastatin with simvastatin in primary hypercholesterolaemia or combined dyslipidaemia. Curr Med Res Opin. 2009; 25:2755-64. [PubMed 19785568]
5. Stender S, Hounslow N. Robust efficacy of pitavastatin and comparable safety to pravastatin. Atherosclerosis Suppl. 2009; 10:945, abstract P770. [PubMed 20624769]
6. Ose L, Budinski D, Hounslow N et al. Long-term treatment with pitavastatin is effective and well tolerated by patients with primary hypercholesterolemia or combined dyslipidemia. Atherosclerosis. 2010; 210:202-8. [PubMed 20080236]
7. Wensel TM, Waldrop BA, Wensel B. Pitavastatin: a new HMG-CoA reductase inhibitor. Ann Pharmacother. 2010; 44:507-14. [PubMed 20179258]
8. Saito Y. Critical appraisal of the role of pitavastatin in treating dyslipidemias and achieving lipid goals. Vasc Health Risk Manag. 2009; 5:921-36. [PubMed 19997573]
9. Food and Drug Administration. Center for Drug Evaluation and Research: Application number 22-363: Summary Review. From FDA website. 2009 Aug 3.
10. Merck & Co., Inc. Mevacor (lovastatin) tablets prescribing information. White House Station, NJ; 2005 Nov.
11. Bristol-Myers Squibb Company. Pravachol (pravastatin sodium) tablets prescribing information. Princeton, NJ; 2005 Aug.
12. Merck & Co., Inc. Zocor (simvastatin) tablets prescribing information. Whitehouse Station, NJ; 2008 Jun.
13. Herd JA, Ballantyne CM, Farmer JA et al. Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]). Am J Cardiol. 1997; 80:278-86. [IDIS 391970] [PubMed 9264419]
14. MAAS Investigators. Effect of simvastatin on coronary atheroma: the multicentre anti-atheroma study (MAAS). Lancet. 1994; 344:633-8. [IDIS 335179] [PubMed 7864934]
15. Pitt B, Mancini GBJ, Ellis SG et al. Pravastatin limitation of atherosclerosis in the coronary arteries (PLAC I): reduction in atherosclerosis progression and clinical events. J Am Coll Cardiol. 1995; 26:1133-9. [IDIS 355698] [PubMed 7594023]
16. Crouse JR III, Byington RP, Bond MG et al. Pravastatin, lipids, and atherosclerosis in the carotid arteries (PLAC-II). Am J Cardiol. 1995; 75:455-9. [IDIS 343080] [PubMed 7863988]
17. Jukema JW, Bruschke AVG, van Boven AJ et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation. 1995; 91:2528-40. [IDIS 347552] [PubMed 7743614]
18. Salonen R, Nyyssonen K, Porkkala-Sarataho E et al. The Kuopio Atherosclerosis Prevention Study (KAPS): Effect of pravastatin treatment on lipids, oxidation resistance of lipoproteins, and atherosclerotic progression. Am J Cardiol. 1995; 76:34-9C.
19. Blankenhorn DH, Azen SP, Kramsch DM et al. Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS). The MARS Research Group. Ann Intern Med. 1993; 119:969-76.
20. Waters D, Higginson L, Gladstone P et al. Effects of cholesterol lowering on the progression of coronary atherosclerosis in women. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation. 1995; 92:2404-10.
21. Brown G, Albers JJ, Fisher LD et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. 1990; 323:1289-98. [IDIS 273270] [PubMed 2215615]
22. Furberg CD, Adams HP, Applegate WB et al for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation. 1994; 90:1679-87. [IDIS 336970] [PubMed 7734010]
23. DeGroot E, Jukema JW, Montauban AD et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J Am Coll Cardiol. 1998; 31:1561-7. [IDIS 407953] [PubMed 9626835]
24. Glorioso N, Troffa C, Filigheddu F et al. Effect of the HMG-CoA reductase inhibitors on blood pressure in patients with essential hypertension and primary hypercholesterolemia. Hypertension. 1999; 34:1281-6. [PubMed 10601131]
25. Borghi C, Prandin MG, Costa FV et al. Use of statins and blood pressure control in treated hypertensive patients with hypercholesterolemia. J Cardiovasc Pharmacol. 2000; 35:549-55. [IDIS 445493] [PubMed 10774784]
26. Ridker PM, Rifai N, Pfeffer MA et al. Long-term effects of pravastatin on plasma concentration of C-reactive protein. Circulation. 1999; 100:230-5. [IDIS 433588] [PubMed 10411845]
27. Kluft C, de Maat MPM, Leuven JAG et al. Statins and C-reactive protein. Lancet. 1999; 353:1274-5.
28. Novartis Pharmaceuticals Corporation. Lescol (fluvastatin sodium) capsules and Lescol XL (fluvastatin sodium) extended-release tablets prescribing information. East Hanover, NJ; 2006 Apr.
29. Kowa Pharmaceuticals America, Inc., Montgomery, AL: Personal communication.
30. Kalliokoski A, Niemi M. Impact of OATP transporters on pharmacokinetics. Br J Pharmacol. 2009; 158:693-705. [PubMed 19785645]
31. Panel on Antiretroviral Guidelines for Adults and Adolescents of the Department of Health and Human Services (DHHS). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents (January 10, 2011). From the US Department of Health and Human Services HIV/AIDS Information Services (AIDSinfo) website.
32. Grundy SM, Cleeman JI, Bairey Merz CN et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation. 2004; 110: 227-39.
33. Hirano M, Maeda K, Shitara Y et al. Drug-drug interaction between pitavastatin and various drugs via OATP1B1. Drug Metab Dispos. 2006; 34:1229-36.
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