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Generic Name: Pitavastatin Calcium
Class: HMG-CoA Reductase Inhibitors
VA Class: CV350
Molecular Formula: C50H46CaF2N2O8

Introduction

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

Uses for Livalo

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations, and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia.1

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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

Livalo 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 see Elimination: Special Populations under Pharmacokinetics.)

Renal Impairment

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

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

Geriatric Patients

No specific dosage recommendations at this time.1 (See Geriatric Use under Cautions.)

Cautions for Livalo

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 (See Sensitivity Reactions under Cautions.)

Warnings/Precautions

Fetal/Neonatal Morbidity and Mortality

Suppression of cholesterol biosynthesis by pitavastatin 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 and the lack of known clinical benefit with continued use during pregnancy.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., age >65 years, renal impairment, inadequately treated hypothyroidism) and in patients receiving concomitant therapy with certain antilipemic agents (i.e., fibric acid derivatives, niacin).1 (See Interactions.)

Discontinue if 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

Hepatic Effects

Increases in serum aminotransferase (i.e., AST, ALT) concentrations reported.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

Fatal and nonfatal hepatic failure reported rarely.1

Perform liver function tests prior to initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage201 ).1 Although manufacturer previously recommended more frequent monitoring, FDA concluded that serious statin-related liver injury with statins is rare and unpredictable, and that routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.200

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt pitavastatin therapy.1 If an alternate etiology is not found, do not restart pitavastatin.1

Also see Hepatic Impairment under Cautions.

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.1 200 Possible increased risk of developing diabetes.200 May need to monitor glucose concentrations following initiation of statin therapy.201

FDA states that cardiovascular benefits of statins outweigh these small increased risks.200

Sensitivity Reactions

Hypersensitivity reactions, including rash, pruritus, and urticaria, reported.1

Cognitive Impairment

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.1

Generally nonserious and reversible, with variable times to symptom onset (1 day to years) and resolution (median of 3 weeks following discontinuance of therapy).1 200 Not associated with fixed or progressive dementia (e.g., Alzheimer’s disease) or clinically important cognitive decline.200 Not associated with any specific statin, patient's age, statin dosage, or concomitant drug therapy.200

FDA states that cardiovascular benefits of statins outweigh the small increased risk of cognitive impairment.200

If manifestations consistent with cognitive impairment occur, National Lipid Association (NLA) statin safety assessment task force recommends evaluating and managing patients appropriately.202

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 or severe renal impairment and patients with ESRD undergoing hemodialysis.1 (See Renal Impairment under Dosage and Administration.)

Common Adverse Effects

Myalgia, back pain, diarrhea, constipation, pain in extremity.1

Interactions for Livalo

Minimally metabolized by CYP2C9 and, to a lesser extent, by CYP2C8.1 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

Diltiazem

Slight increases in peak plasma concentration and AUC of pitavastatin; slight decreases in peak plasma concentration and AUC of diltiazem1

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., fenofibrate, gemfibrozil)

Increased risk of myopathy or rhabdomyolysis1

Increased peak plasma concentration and AUC of pitavastatin; increases more pronounced when used concomitantly with gemfibrozil than with fenofibrate1

Gemfibrozil: Avoid concomitant use1

Other fibric acid derivatives (e.g., fenofibrate): 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 concentration and AUC of pitavastatin and atazanavir1 31

Ritonavir-boosted darunavir: Decreased peak plasma concentration and AUC of pitavastatin; increased peak plasma concentration and AUC of darunavir and ritonavir1 31

Lopinavir/ritonavir: Decreased peak plasma concentration and AUC of pitavastatin, lopinavir, and ritonavir1 31

Atazanavir: Not considered clinically important;29 dosage adjustment not necessary31

Ritonavir-boosted darunavir: Dosage adjustment not necessary31

Lopinavir/ritonavir: Dosage adjustment not necessary31

Itraconazole

Decreased peak plasma concentration and AUC of pitavastatin1

Not considered clinically important29

Niacin (antilipemic dosages29 [≥1 g daily])

Possible increased risk of myopathy1

Use concomitantly with caution; consider reducing pitavastatin dosage1

Rifampin

Substantially increased peak plasma concentration and AUC of pitavastatin; decreased peak plasma concentration and AUC of rifampin1

Do not exceed pitavastatin dosage of 2 mg once daily1

Warfarin

No clinically important pharmacokinetic interaction with R- and S-warfarin1

No clinically important effect on PT and INR in patients receiving long-term warfarin therapy1

Monitor PT and INR when pitavastatin is initiated in patients receiving warfarin1

Livalo 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.)

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

Patients with aminotransferase (AST, ALT) concentrations >1.5 times the ULN were excluded from phase 3 clinical studies.3 4 29

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

Moderate renal impairment (GFR 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 (GFR 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

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, to a lesser extent, by 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

  • 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

  • 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

  • Risk of adverse hepatic effects.1 Importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).1

  • Risk of nonserious, reversible cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion).1 200

  • Risk of increased glucose concentrations and development of type 2 diabetes;1 200 may need to monitor glucose concentrations following initiation of statin therapy.201

  • Importance of advising women to avoid pregnancy (i.e., using effective contraceptive methods) during therapy; if the patient becomes pregnant, importance of discontinuing pitavastatin and contacting a clinician.1

  • Importance of avoiding breast-feeding during therapy.1 If the patient has a lipid disorder and is breast-feeding, importance of discontinuing pitavastatin and contacting a clinician.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.

Pitavastatin Calcium

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

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 02/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Livalo 1MG Tablets (LILLY): 30/$125.30 or 90/$356.45

Livalo 2MG Tablets (LILLY): 30/$124.99 or 90/$351.99

Livalo 4MG Tablets (LILLY): 30/$125.30 or 90/$356.45

AHFS DI Essentials. © Copyright, 2004-2014, Selected Revisions February 15, 2013. 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; 2012 Feb.

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.

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, US Department of Health and Human Services (DHHS). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents (July 5, 2012). Updates available at DHHS AIDS Information (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. [PubMed 16595711]

34. Kowa Pharmaceuticals America, Inc. Livalo (pitavastatin calcium) tablets prescribing information. Montgomery, AL; 2010 Jul.

200. Food and Drug Administration. FDA drug safety communication: Important safety label changes to cholesterol-lowering statin drugs. Rockville, MD; 2012 Feb 28. From FDA website.

201. Food and Drug Administration. FDA expands advice on statin risks. Rockville, MD; 2012 Feb 27. From FDA website.

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

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