Pitavastatin

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Identification

Summary

Pitavastatin is an HMG-CoA reductase inhibitor used to lower lipid levels and reduce the risk of cardiovascular disease including myocardial infarction and stroke.

Brand Names

Livalo, Nikita, Zypitamag

Generic Name

Pitavastatin

DrugBank Accession Number

DB08860

Background

Pitavastatin, also known as the brand name product Livalo, is a lipid-lowering drug belonging to the statin class of medications. By inhibiting the endogenous production of cholesterol within the liver, statins lower abnormal cholesterol and lipid levels and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase,³ which catalyzes the conversion of HMG-CoA to mevalonic acid. This is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as "bad cholesterol"), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America.^4,5

Pitavastatin and other drugs from the statin class of medications including atorvastatin, pravastatin, rosuvastatin, fluvastatin, and lovastatin are considered first-line options for the treatment of dyslipidemia.^4,5 Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world.⁶ Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.^4,29 Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.^{8,9,10,11,12,13} Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.^4,5 Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.^15,14

While all statin medications are considered equally effective from a clinical standpoint, rosuvastatin is considered the most potent; doses of 10 to 40mg rosuvastatin per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels.^16,17,13,18 Study data has confirmed that pitavastatin's potency in lowering LDL-C is comparable to that of other statins but also has increased efficacy in increasing HDL-C (also known as "good cholesterol").^21,22,23 Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.^13,11

Type

Small Molecule

Groups

Approved

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Pitavastatin (DB08860)

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Weight

Average: 421.4608
Monoisotopic: 421.168936466

Chemical Formula

C₂₅H₂₄FNO₄

Synonyms

• Pitavastatia
• Pitavastatin
• Pitavastatina
• Pitavastatine
• Pitavastatinum

External IDs

• NK 104
• NK-104
• NKS-104
• NKS104

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Pharmacology

Indication

Pitavastatin is indicated for the treatment of adult patients with primary hyperlipidemia or mixed dyslipidemia to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C). It is also indicated for the treatment of pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated TC, LDL-C, and Apo B.³²

Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD. Statin-indicated conditions include diabetes mellitus, clinical atherosclerosis (including myocardial infarction, acute coronary syndromes, stable angina, documented coronary artery disease, stroke, trans ischemic attack (TIA), documented carotid disease, peripheral artery disease, and claudication), abdominal aortic aneurysm, chronic kidney disease, and severely elevated LDL-C levels.^4,5

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Adjunct therapy in management of	Apolipoprotein b increased		••••••••••••	•••••••••		••••••
Adjunct therapy in management of	Apolipoprotein b increased		••••••••••••	•••••		••••••
Adjunct therapy in management of	Apolipoprotein b increased		••••••••••••	•••••		••••••
Adjunct therapy in management of	Elevation of serum triglyceride levels		••••••••••••	•••••		••••••
Adjunct therapy in management of	Elevation of serum triglyceride levels		••••••••••••	•••••		••••••

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Pharmacodynamics

Pitavastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.^4,5

Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.⁴ Use of statins to target and reduce LDL levels has been shown in a number of landmark studies to significantly reduce the risk of development of CVD and all-cause mortality.^8,9,10,11,12 Statins are considered a cost-effective treatment option for CVD due to their evidence of reducing all-cause mortality including fatal and non-fatal CVD as well as the need for surgical revascularization or angioplasty following a heart attack.^4,5 Evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within 5 years) statins cause a 20%-22% relative reduction in major cardiovascular events (heart attack, stroke, coronary revascularization, and coronary death) for every 1 mmol/L reduction in LDL without any significant side effects or risks.^15,14

Skeletal Muscle Effects

Pitavastatin may cause myopathy (muscle pain, tenderness, or weakness with creatine kinase (CK) above ten times the upper limit of normal) and rhabdomyolysis (with or without acute renal failure secondary to myoglobinuria). Rare fatalities have occurred as a result of rhabdomyolysis with statin use, including pitavastatin. Predisposing factors for myopathy include advanced age (≥65 years), female gender, uncontrolled hypothyroidism, and renal impairment. In most cases, muscle symptoms and CK increases resolved when treatment was promptly discontinued. As dosages of pitavastatin greater than 4mg per day were associated with an increased risk of severe myopathy, the product monograph recommends a maximum daily dose of 4mg once daily.³²

The risk of myopathy during treatment with pitavstatin may be increased with concurrent administration of interacting drugs such as fenofibrate, niacin, gemfibrozil, and cyclosporine. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors coadministered with colchicine, and caution should therefore be exercised when prescribing these two medications together.³²

Real-world data from observational studies has suggested that 10-15% of people taking statins may experience muscle aches at some point during treatment.²⁸

Hepatic Dysfunction

Increases in serum transaminases have been reported with pitavastatin. In most cases, the elevations were transient and either resolved or improved on continued therapy or after a brief interruption in therapy. There have been rare postmarketing reports of fatal and non-fatal hepatic failure in patients taking statins, including pitavastatin.³²

Patients who consume substantial quantities of alcohol and/or have a history of liver disease may be at increased risk for hepatic injury.³²

Increases in HbA1c and Fasting Serum Glucose Levels

Increases in HbA1c and fasting serum glucose levels have been reported with statins, including pitavastatin. Optimize lifestyle measures, including regular exercise, maintaining a healthy body weight, and making healthy food choices.³²

An in vitro study found that atorvastatin, pravastatin, rosuvastatin, and pitavastatin exhibited a dose-dependent cytotoxic effect on human pancreas islet β cells, with reductions in cell viability of 32, 41, 34 and 29%, respectively, versus control. Moreover, insulin secretion rates were decreased by 34, 30, 27 and 19%, respectively, relative to control.²⁴

Mechanism of action

Pitavastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.³ Pitavastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increase hepatic uptake of LDL, thereby reducing circulating LDL-C levels.

In vitro and in vivo animal studies also demonstrate that statins exert vasculoprotective effects independent of their lipid-lowering properties, also known as the pleiotropic effects of statins.¹⁹ This includes improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response.

Statins have also been found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an important role in leukocyte trafficking and in T cell activation.²⁶

Target	Actions	Organism
A3-hydroxy-3-methylglutaryl-coenzyme A reductase	inhibitor	Humans
UIntegrin alpha-L	Not Available	Humans

Absorption

Pitavastatin peak plasma concentrations are achieved about 1 hour after oral administration. Both C_max and AUC_0-inf increased in an approximately dose-proportional manner for single pitavastatin doses from 1 mg to 24 mg once daily. The absolute bioavailability of pitavastatin oral solution is 51%. The C_max and AUC of pitavastatin did not differ following evening or morning drug administration. In healthy volunteers receiving 4 mg pitavastatin, the percent change from baseline for LDL-C following evening dosing was slightly greater than that following morning dosing. Pitavastatin was absorbed in the small intestine but very little in the colon.³²

Administration of pitavastatin with a high fat meal (50% fat content) decreases pitavastatin C_max by 43% but does not significantly reduce pitavastatin AUC.³²

Compared to other statins, pitavastatin has a relatively high bioavailability, which has been suggested to occur due to enterohepatic reabsorption in the intestine following intestinal absorption.²⁵

Genetic differences in the OATP1B1 (organic-anion-transporting polypeptide 1B1) hepatic transporter encoded by the SCLCO1B1 gene (Solute Carrier Organic Anion Transporter family member 1B1) have been shown to impact pitavastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C single nucleotide polymorphism (SNP) in the gene encoding OATP1B1 (SLCO1B1) demonstrated that pitavastatin AUC was increased 3.08-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals.²⁷ Other statin drugs impacted by this polymorphism include simvastatin, pitavastatin, atorvastatin, and rosuvastatin.²⁰ Individuals with the 521CC genotype may be at increased risk of dose-related adverse effects including myopathy and rhabdomyolysis due to increased exposure to the drug.

Volume of distribution

The mean volume of distribution is approximately 148 L.³²

Protein binding

Pitavstatin is more than 99% protein bound in human plasma, mainly to albumin and alpha 1-acid glycoprotein.³²

Metabolism

The principal route of pitavastatin metabolism is glucuronidation via liver uridine 5'-diphosphate glucuronosyltransferase (UGT) with subsequent formation of pitavastatin lactone. There is only minimal metabolism by the cytochrome P450 system. Pitavastatin is marginally metabolized by CYP2C9 and to a lesser extent by CYP2C8. The major metabolite in human plasma is the lactone, which is formed via an ester-type pitavastatin glucuronide conjugate by UGTs (UGT1A3 and UGT2B7).^32,25

Hover over products below to view reaction partners

• Pitavastatin
  • Pitavastatin glucuronide
    • Pitavastatin lactone
      • M3 pitavastatin
  • M13 pitavastatin

Route of elimination

A mean of 15% of radioactivity of orally administered, single 32 mg ¹⁴C-labeled pitavastatin dose was excreted in urine, whereas a mean of 79% of the dose was excreted in feces within 7 days.L48616]

Half-life

The mean plasma elimination half-life is approximately 12 hours.L48616]

Clearance

Following a single dose, the apparent mean oral clearance of pitavastatin is 43.4 L/h.²⁵

Adverse Effects

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Toxicity

Pitavastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, pitavastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action. In addition, treatment of hyperlipidemia is not generally necessary during pregnancy. Atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients.³²

A Medicaid cohort linkage study of 1152 statin-exposed pregnant women compared to 886,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential confounders – including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use – using propensity score-based methods. The relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus. There were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for confounders. In the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. Study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births.³²

No specific treatment for pitavastatin overdose is known. Contact Poison Control (1-800-222-1222) for latest recommendations. Hemodialysis is unlikely to be of benefit due to high protein binding ratio of pitavastatin.³²

In a 92-week carcinogenicity study in mice given pitavastatin, at the maximum tolerated dose of 75 mg/kg/day with systemic maximum exposures (AUC) 26 times the clinical maximum exposure at 4 mg daily, there was an absence of drug-related tumors.³²

In a 92-week carcinogenicity study in rats given pitavastatin at 1, 5, 25 mg/kg/day by oral gavage there was a significant increase in the incidence of thyroid follicular cell tumors at 25 mg/kg/day, which represents 295 times human systemic exposures based on AUC at the 4 mg daily maximum human dose. In a 26-week transgenic mouse (Tg rasH2) carcinogenicity study where animals were given pitavastatin at 30, 75, and 150 mg/kg/day by oral gavage, no clinically significant tumors were observed.³²

Pitavastatin was not mutagenic in the Ames test with Salmonella typhimurium and Escherichia coli with and without metabolic activation, the micronucleus test following a single administration in mice and multiple administrations in rats, the unscheduled DNA synthesis test in rats, and a Comet assay in mice. In the chromosomal aberration test, clastogenicity was observed at the highest doses tested, which also elicited high levels of cytotoxicity.³²

Pitavastatin had no adverse effects on male and female rat fertility at oral doses of 10 and 30 mg/kg/day, respectively, at systemic exposures 56- and 354-times clinical exposure at 4 mg daily based on AUC.³²

Pitavastatin treatment in rabbits resulted in mortality in males and females given 1 mg/kg/day (30-times clinical systemic exposure at 4 mg daily based on AUC) and higher during a fertility study. Although the cause of death was not determined, rabbits had gross signs of renal toxicity (kidneys whitened) indicative of possible ischemia. Lower doses (15-times human systemic exposure) did not show significant toxicity in adult males and females. However, decreased implantations, increased resorptions, and decreased viability of fetuses were observed.³²

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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Acenocoumarol	The risk or severity of bleeding can be increased when Pitavastatin is combined with Acenocoumarol.
Acipimox	Acipimox may increase the myopathic rhabdomyolysis activities of Pitavastatin.
Alendronic acid	The risk or severity of myopathy, rhabdomyolysis, and myoglobinuria can be increased when Alendronic acid is combined with Pitavastatin.
Amiodarone	The metabolism of Pitavastatin can be increased when combined with Amiodarone.
Amphotericin B	The risk or severity of myopathy, rhabdomyolysis, and myoglobinuria can be increased when Amphotericin B is combined with Pitavastatin.

Food Interactions

• Take with or without food. Food does not affect oral absorption or bioavailability.

Products

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Pitavastatin calcium	IYD54XEG3W	147526-32-7	RHGYHLPFVJEAOC-WUVPNHNWSA-L
Pitavastatin magnesium	BDS8LUQ384	956116-90-8	MPAZKXHCZWDZDY-FFNUKLMVSA-L
Pitavastatin sodium	29556RBN9P	574705-92-3	Not applicable

Product Images

PreviousNext

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Livalo	Tablet, film coated	2 mg/1	Oral	Eli Lilly & Co. Ltd.	2010-05-15	2016-01-31
Livalo	Tablet, film coated	1.045 mg/1	Oral	Kowa Pharmaceuticals America, Inc.	2019-05-16	Not applicable
Livalo	Tablet, film coated	1 mg/1	Oral	Eli Lilly & Co. Ltd.	2010-05-15	2016-01-31
Livalo	Tablet, film coated	4.18 mg/1	Oral	Kowa Pharmaceuticals America, Inc.	2019-05-16	Not applicable
Livalo	Tablet, film coated	4 mg/1	Oral	Eli Lilly & Co. Ltd.	2010-05-15	2016-01-31

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Pitavastatin	Tablet, film coated	2 mg/1	Oral	Quinn Pharmaceuticals, Llc	2022-12-25	Not applicable
Pitavastatin	Tablet, film coated	1.045 mg/1	Oral	AvKARE	2024-01-16	Not applicable
Pitavastatin	Tablet, film coated	1.045 mg/1	Oral	Teva Pharmaceuticals, Inc.	2023-11-02	Not applicable
Pitavastatin	Tablet, film coated	1 mg/1	Oral	Aurobindo Pharma Limited	2023-11-02	Not applicable
Pitavastatin	Tablet	4 mg/1	Oral	Upsher-Smith Laboratories, LLC	2023-11-02	Not applicable

Categories

ATC Codes

C10AA08 — Pitavastatin

• C10AA — HMG CoA reductase inhibitors
• C10A — LIPID MODIFYING AGENTS, PLAIN
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

Drug Categories

• Agents Causing Muscle Toxicity
• Anticholesteremic Agents
• BCRP/ABCG2 Substrates
• BSEP/ABCB11 Substrates
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP2C9 Substrates
• Cytochrome P-450 Substrates
• Enzyme Inhibitors
• Heterocyclic Compounds, Fused-Ring
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Hypolipidemic Agents
• Hypolipidemic Agents Indicated for Hyperlipidemia
• Lipid Modifying Agents
• Lipid Modifying Agents, Plain
• Lipid Regulating Agents
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B1/SLCO1B1 Substrates
• OATP1B3 substrates
• OATP2B1/SLCO2B1 substrates
• P-glycoprotein substrates
• Toxic Actions
• UGT1A3 substrates
• UGT2B7 substrates

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as phenylquinolines. These are heterocyclic compounds containing a quinoline moiety substituted with a phenyl group.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Quinolines and derivatives

Sub Class

Phenylquinolines

Direct Parent

Phenylquinolines

Alternative Parents

Phenylpyridines / Medium-chain hydroxy acids and derivatives / Medium-chain fatty acids / Beta hydroxy acids and derivatives / Fluorobenzenes / Halogenated fatty acids / Heterocyclic fatty acids / Hydroxy fatty acids / Unsaturated fatty acids / Aryl fluorides / Heteroaromatic compounds / Secondary alcohols / Carboxylic acids / Azacyclic compounds / Monocarboxylic acids and derivatives / Hydrocarbon derivatives / Carbonyl compounds / Organic oxides / Organofluorides / Organonitrogen compounds / Organopnictogen compounds

show 11 more

Substituents

4-phenylpyridine / Alcohol / Aromatic heteropolycyclic compound / Aryl fluoride / Aryl halide / Azacycle / Benzenoid / Beta-hydroxy acid / Carbonyl group / Carboxylic acid / Carboxylic acid derivative / Fatty acid / Fatty acyl / Fluorobenzene / Halobenzene / Halogenated fatty acid / Heteroaromatic compound / Heterocyclic fatty acid / Hydrocarbon derivative / Hydroxy acid / Hydroxy fatty acid / Medium-chain fatty acid / Medium-chain hydroxy acid / Monocarboxylic acid or derivatives / Monocyclic benzene moiety / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organofluoride / Organohalogen compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Phenylquinoline / Pyridine / Secondary alcohol / Unsaturated fatty acid

show 27 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

quinolines, statin (synthetic), cyclopropanes, dihydroxy monocarboxylic acid, monofluorobenzenes (CHEBI:32020)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

M5681Q5F9P

CAS number

147511-69-1

InChI Key

VGYFMXBACGZSIL-MCBHFWOFSA-N

InChI

InChI=1S/C25H24FNO4/c26-17-9-7-15(8-10-17)24-20-3-1-2-4-22(20)27-25(16-5-6-16)21(24)12-11-18(28)13-19(29)14-23(30)31/h1-4,7-12,16,18-19,28-29H,5-6,13-14H2,(H,30,31)/b12-11+/t18-,19-/m1/s1

IUPAC Name

(3R,5S,6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxyhept-6-enoic acid

SMILES

O[C@H](C[C@H](O)\C=C\C1=C(N=C2C=CC=CC2=C1C1=CC=C(F)C=C1)C1CC1)CC(O)=O

References

Synthesis Reference

Shriprakash Dhar DWIVEDI, Dhimant Jasubhai PATEL, Alpesh Pravinchandra SHAH, "METHOD FOR PREPARATION OF PITAVASTATIN AND ITS PHARMACEUTICAL ACCEPTABLE SALTS THEREOF." U.S. Patent US20120022102, issued January 26, 2012.

US20120022102

General References

1. Morgan RE, Campbell SE, Yu CY, Sponseller CA, Muster HA: Comparison of the safety, tolerability, and pharmacokinetic profile of a single oral dose of pitavastatin 4 mg in adult subjects with severe renal impairment not on hemodialysis versus healthy adult subjects. J Cardiovasc Pharmacol. 2012 Jul;60(1):42-8. doi: 10.1097/FJC.0b013e318256cdf0. [Article]
2. Jung JA, Noh YH, Jin S, Kim MJ, Kim YH, Jung JA, Lim HS, Bae KS: Pharmacokinetic interaction between pitavastatin and valsartan: a randomized, open-labeled crossover study in healthy male Korean volunteers. Clin Ther. 2012 Apr;34(4):958-65. doi: 10.1016/j.clinthera.2012.01.026. Epub 2012 Mar 10. [Article]
3. Moghadasian MH: Clinical pharmacology of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Life Sci. 1999;65(13):1329-37. doi: 10.1016/s0024-3205(99)00199-x. [Article]
4. Anderson TJ, Gregoire J, Pearson GJ, Barry AR, Couture P, Dawes M, Francis GA, Genest J Jr, Grover S, Gupta M, Hegele RA, Lau DC, Leiter LA, Lonn E, Mancini GB, McPherson R, Ngui D, Poirier P, Sievenpiper JL, Stone JA, Thanassoulis G, Ward R: 2016 Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult. Can J Cardiol. 2016 Nov;32(11):1263-1282. doi: 10.1016/j.cjca.2016.07.510. Epub 2016 Jul 25. [Article]
5. Grundy SM, Stone NJ: 2018 American Heart Association/American College of Cardiology Multisociety Guideline on the Management of Blood Cholesterol: Primary Prevention. JAMA Cardiol. 2019 Apr 10. pii: 2730287. doi: 10.1001/jamacardio.2019.0777. [Article]
6. Kreatsoulas C, Anand SS: The impact of social determinants on cardiovascular disease. Can J Cardiol. 2010 Aug-Sep;26 Suppl C:8C-13C. doi: 10.1016/s0828-282x(10)71075-8. [Article]
7. Tardy B, Lecompte T, Boelhen F, Tardy-Poncet B, Elalamy I, Morange P, Gruel Y, Wolf M, Francois D, Racadot E, Camarasa P, Blouch MT, Nguyen F, Doubine S, Dutrillaux F, Alhenc-Gelas M, Martin-Toutain I, Bauters A, Ffrench P, de Maistre E, Grunebaum L, Mouton C, Huisse MG, Gouault-Heilmann M, Lucke V: Predictive factors for thrombosis and major bleeding in an observational study in 181 patients with heparin-induced thrombocytopenia treated with lepirudin. Blood. 2006 Sep 1;108(5):1492-6. Epub 2006 May 11. [Article]
8. Authors unspecified: Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998 Nov 5;339(19):1349-57. doi: 10.1056/NEJM199811053391902. [Article]
9. Cannon CP, Braunwald E, McCabe CH, Rader DJ, Rouleau JL, Belder R, Joyal SV, Hill KA, Pfeffer MA, Skene AM: Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004 Apr 8;350(15):1495-504. doi: 10.1056/NEJMoa040583. Epub 2004 Mar 8. [Article]
10. Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Glynn RJ: Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008 Nov 20;359(21):2195-207. doi: 10.1056/NEJMoa0807646. Epub 2008 Nov 9. [Article]
11. Nicholls SJ, Ballantyne CM, Barter PJ, Chapman MJ, Erbel RM, Libby P, Raichlen JS, Uno K, Borgman M, Wolski K, Nissen SE: Effect of two intensive statin regimens on progression of coronary disease. N Engl J Med. 2011 Dec 1;365(22):2078-87. doi: 10.1056/NEJMoa1110874. Epub 2011 Nov 15. [Article]
12. Authors unspecified: MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002 Jul 6;360(9326):7-22. doi: 10.1016/S0140-6736(02)09327-3. [Article]
13. Authors unspecified: Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet. 1994 Nov 19;344(8934):1383-9. [Article]
14. Taylor F, Huffman MD, Macedo AF, Moore TH, Burke M, Davey Smith G, Ward K, Ebrahim S: Statins for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2013 Jan 31;(1):CD004816. doi: 10.1002/14651858.CD004816.pub5. [Article]
15. Mihaylova B, Emberson J, Blackwell L, Keech A, Simes J, Barnes EH, Voysey M, Gray A, Collins R, Baigent C: The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012 Aug 11;380(9841):581-90. doi: 10.1016/S0140-6736(12)60367-5. Epub 2012 May 17. [Article]
16. Adams SP, Sekhon SS, Wright JM: Lipid-lowering efficacy of rosuvastatin. Cochrane Database Syst Rev. 2014 Nov 21;(11):CD010254. doi: 10.1002/14651858.CD010254.pub2. [Article]
17. Pedersen TR, Faergeman O, Kastelein JJ, Olsson AG, Tikkanen MJ, Holme I, Larsen ML, Bendiksen FS, Lindahl C, Szarek M, Tsai J: High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial. JAMA. 2005 Nov 16;294(19):2437-45. doi: 10.1001/jama.294.19.2437. [Article]
18. Jones PH, Davidson MH, Stein EA, Bays HE, McKenney JM, Miller E, Cain VA, Blasetto JW: Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol. 2003 Jul 15;92(2):152-60. [Article]
19. Liao JK, Laufs U: Pleiotropic effects of statins. Annu Rev Pharmacol Toxicol. 2005;45:89-118. doi: 10.1146/annurev.pharmtox.45.120403.095748. [Article]
20. Elsby R, Hilgendorf C, Fenner K: Understanding the critical disposition pathways of statins to assess drug-drug interaction risk during drug development: it's not just about OATP1B1. Clin Pharmacol Ther. 2012 Nov;92(5):584-98. doi: 10.1038/clpt.2012.163. Epub 2012 Oct 10. [Article]
21. Saku K, Zhang B, Noda K: Randomized head-to-head comparison of pitavastatin, atorvastatin, and rosuvastatin for safety and efficacy (quantity and quality of LDL): the PATROL trial. Circ J. 2011;75(6):1493-505. Epub 2011 Apr 15. [Article]
22. Teramoto T: The clinical impact of pitavastatin: comparative studies with other statins on LDL-C and HDL-C. Expert Opin Pharmacother. 2012 Apr;13(6):859-65. doi: 10.1517/14656566.2012.660525. Epub 2012 Feb 15. [Article]
23. Teramoto T, Shimano H, Yokote K, Urashima M: Effects of pitavastatin (LIVALO Tablet) on high density lipoprotein cholesterol (HDL-C) in hypercholesterolemia. J Atheroscler Thromb. 2009 Oct;16(5):654-61. doi: 10.5551/jat.1719. [Article]
24. Zhao W, Zhao SP: Different effects of statins on induction of diabetes mellitus: an experimental study. Drug Des Devel Ther. 2015 Nov 24;9:6211-23. doi: 10.2147/DDDT.S87979. eCollection 2015. [Article]
25. Hoy SM: Pitavastatin: A Review in Hypercholesterolemia. Am J Cardiovasc Drugs. 2017 Apr;17(2):157-168. doi: 10.1007/s40256-017-0213-8. [Article]
26. Weitz-Schmidt G, Welzenbach K, Brinkmann V, Kamata T, Kallen J, Bruns C, Cottens S, Takada Y, Hommel U: Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. Nat Med. 2001 Jun;7(6):687-92. doi: 10.1038/89058. [Article]
27. Ieiri I, Suwannakul S, Maeda K, Uchimaru H, Hashimoto K, Kimura M, Fujino H, Hirano M, Kusuhara H, Irie S, Higuchi S, Sugiyama Y: SLCO1B1 (OATP1B1, an uptake transporter) and ABCG2 (BCRP, an efflux transporter) variant alleles and pharmacokinetics of pitavastatin in healthy volunteers. Clin Pharmacol Ther. 2007 Nov;82(5):541-7. doi: 10.1038/sj.clpt.6100190. Epub 2007 Apr 25. [Article]
28. Harper CR, Jacobson TA: The broad spectrum of statin myopathy: from myalgia to rhabdomyolysis. Curr Opin Lipidol. 2007 Aug;18(4):401-8. doi: 10.1097/MOL.0b013e32825a6773. [Article]
29. Kannel WB, Castelli WP, Gordon T, McNamara PM: Serum cholesterol, lipoproteins, and the risk of coronary heart disease. The Framingham study. Ann Intern Med. 1971 Jan;74(1):1-12. doi: 10.7326/0003-4819-74-1-1. [Article]
30. FDA Approved Drug Products: Livalo (pitavastatin) oral tablets [Link]
31. FDA Approved Drug Products: Zypitamag (pitavastatin magnesium) oral tablets [Link]
32. FDA Approved Drug Products: NIKITATM (pitavastatin) tablets, for oral use (November 2023) [Link]
33. FDA Label - Pitavastatin [File]

External Links

Human Metabolome Database

HMDB0041991

KEGG Drug

D01862

KEGG Compound

C13334

PubChem Compound

5282452

PubChem Substance

175427122

ChemSpider

4445604

BindingDB

86707

RxNav

861634

ChEBI

32020

ChEMBL

CHEMBL1201753

ZINC

ZINC000001534965

PharmGKB

PA142650384

PDBe Ligand

PV9

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

Wikipedia

Pitavastatin

PDB Entries

8ecg

MSDS

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Clinical Trials

Clinical Trials

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Phase	Status	Purpose	Conditions	Count	Start Date	Why Stopped	100+ additional columns
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4	Completed	Not Available	Healthy Volunteers (HV)	3	somestatus	stop reason	just information to hide
4	Completed	Not Available	Severe Renal Impairment	1	somestatus	stop reason	just information to hide
4	Completed	Basic Science	Healthy Volunteers (HV)	1	somestatus	stop reason	just information to hide
4	Completed	Other	Healthy Volunteers (HV)	1	somestatus	stop reason	just information to hide
4	Completed	Prevention	Decreased carbohydrate and glucose tolerance / Diabetes Mellitus	1	somestatus	stop reason	just information to hide

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Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral	1 mg/1
Tablet, film coated	Oral	2 mg/1
Tablet, film coated	Oral	4 mg/1
Tablet, film coated	Oral	2 mg
Tablet, film coated	Oral	4 mg
Tablet, film coated	Oral	1 MG
Tablet, effervescent
Tablet, film coated	Oral	1.045 mg/1
Tablet, film coated	Oral	2.09 mg/1
Tablet, film coated	Oral	4.18 mg/1
Tablet	Oral	1 mg/1
Tablet	Oral	2 mg/1
Tablet	Oral	4 mg/1
Tablet	Oral	2.090 mg
Tablet, film coated	Oral
Tablet, coated	Oral	2 mg

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US6465477	No	2002-10-15	2016-12-20
US5753675	No	1998-05-19	2015-05-19
US5856336	Yes	1999-01-05	2021-06-25
US7022713	Yes	2006-04-04	2024-08-19
US5854259	No	1998-12-29	2015-12-29
US8557993	Yes	2013-10-15	2024-08-02
US8829186	No	2014-09-09	2031-01-19

Properties

State

Solid

Experimental Properties

Property	Value	Source
water solubility	Very slightly soluble	FDA label

Predicted Properties

Property	Value	Source
Water Solubility	0.00394 mg/mL	ALOGPS
logP	3.75	ALOGPS
logP	2.92	Chemaxon
logS	-5	ALOGPS
pKa (Strongest Acidic)	4.13	Chemaxon
pKa (Strongest Basic)	4.86	Chemaxon
Physiological Charge	-1	Chemaxon
Hydrogen Acceptor Count	5	Chemaxon
Hydrogen Donor Count	3	Chemaxon
Polar Surface Area	90.65 Å2	Chemaxon
Rotatable Bond Count	8	Chemaxon
Refractivity	115.74 m3·mol-1	Chemaxon
Polarizability	43.76 Å3	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9735
Blood Brain Barrier	+	0.9296
Caco-2 permeable	+	0.5135
P-glycoprotein substrate	Substrate	0.5
P-glycoprotein inhibitor I	Non-inhibitor	0.9015
P-glycoprotein inhibitor II	Non-inhibitor	0.9672
Renal organic cation transporter	Non-inhibitor	0.9101
CYP450 2C9 substrate	Non-substrate	0.7757
CYP450 2D6 substrate	Non-substrate	0.7668
CYP450 3A4 substrate	Non-substrate	0.5634
CYP450 1A2 substrate	Non-inhibitor	0.6867
CYP450 2C9 inhibitor	Non-inhibitor	0.7168
CYP450 2D6 inhibitor	Non-inhibitor	0.8695
CYP450 2C19 inhibitor	Non-inhibitor	0.8563
CYP450 3A4 inhibitor	Non-inhibitor	0.6855
CYP450 inhibitory promiscuity	Low CYP Inhibitory Promiscuity	0.6481
Ames test	Non AMES toxic	0.837
Carcinogenicity	Non-carcinogens	0.9038
Biodegradation	Not ready biodegradable	0.997
Rat acute toxicity	3.1821 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.987
hERG inhibition (predictor II)	Non-inhibitor	0.926

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted GC-MS Spectrum - GC-MS	Predicted GC-MS	splash10-0uxr-8149500000-7a528b44f7ab848deb48
MS/MS Spectrum - DI-ESI-qTof , Negative	LC-MS/MS	splash10-0006-0095000000-052cbc222b6600555667
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0fe0-0007900000-2bb63235658aceafb061
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-1009100000-e0a8cad23f775b34848c
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0fe0-0009300000-5362f65145869bdf6bb1
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0bt9-2009000000-c7fb90c2c2217c08693d
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-03dl-0059000000-2f9d7b346af0853e6113
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-03ys-2069000000-ff586f4ac86690ac7b9a
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å2)	Source type	Source
[M-H]-	216.7849741	predicted	DarkChem Lite v0.1.0
[M-H]-	199.21974	predicted	DeepCCS 1.0 (2019)
[M+H]+	217.1742741	predicted	DarkChem Lite v0.1.0
[M+H]+	201.61531	predicted	DeepCCS 1.0 (2019)
[M+Na]+	216.8337741	predicted	DarkChem Lite v0.1.0
[M+Na]+	207.52785	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. 3-hydroxy-3-methylglutaryl-coenzyme A reductase

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Catalyzes the conversion of (3S)-hydroxy-3-methylglutaryl-CoA (HMG-CoA) to mevalonic acid, the rate-limiting step in the synthesis of cholesterol and other isoprenoids, thus plays a critical role in cellular cholesterol homeostasis (PubMed:21357570, PubMed:2991281, PubMed:36745799, PubMed:6995544). HMGCR is the main target of statins, a class of cholesterol-lowering drugs (PubMed:11349148, PubMed:18540668, PubMed:36745799)

Specific Function

Coenzyme a binding

Gene Name

HMGCR

Uniprot ID

P04035

Uniprot Name

3-hydroxy-3-methylglutaryl-coenzyme A reductase

Molecular Weight

97475.155 Da

References

1. Morgan RE, Campbell SE, Yu CY, Sponseller CA, Muster HA: Comparison of the safety, tolerability, and pharmacokinetic profile of a single oral dose of pitavastatin 4 mg in adult subjects with severe renal impairment not on hemodialysis versus healthy adult subjects. J Cardiovasc Pharmacol. 2012 Jul;60(1):42-8. doi: 10.1097/FJC.0b013e318256cdf0. [Article]
2. Hoy SM: Pitavastatin: A Review in Hypercholesterolemia. Am J Cardiovasc Drugs. 2017 Apr;17(2):157-168. doi: 10.1007/s40256-017-0213-8. [Article]
3. Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
4. FDA Label - Pitavastatin [File]

Details2. Integrin alpha-L

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

General Function

Integrin ITGAL/ITGB2 is a receptor for ICAM1, ICAM2, ICAM3 and ICAM4. Integrin ITGAL/ITGB2 is a receptor for F11R (PubMed:11812992, PubMed:15528364). Integrin ITGAL/ITGB2 is a receptor for the secreted form of ubiquitin-like protein ISG15; the interaction is mediated by ITGAL (PubMed:29100055). Involved in a variety of immune phenomena including leukocyte-endothelial cell interaction, cytotoxic T-cell mediated killing, and antibody dependent killing by granulocytes and monocytes. Contributes to natural killer cell cytotoxicity (PubMed:15356110). Involved in leukocyte adhesion and transmigration of leukocytes including T-cells and neutrophils (PubMed:11812992). Required for generation of common lymphoid progenitor cells in bone marrow, indicating a role in lymphopoiesis (By similarity). Integrin ITGAL/ITGB2 in association with ICAM3, contributes to apoptotic neutrophil phagocytosis by macrophages (PubMed:23775590)

Specific Function

Cell adhesion molecule binding

Gene Name

ITGAL

Uniprot ID

P20701

Uniprot Name

Integrin alpha-L

Molecular Weight

128768.495 Da

References

1. Weitz-Schmidt G, Welzenbach K, Brinkmann V, Kamata T, Kallen J, Bruns C, Cottens S, Takada Y, Hommel U: Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. Nat Med. 2001 Jun;7(6):687-92. doi: 10.1038/89058. [Article]
2. Liao JK, Laufs U: Pleiotropic effects of statins. Annu Rev Pharmacol Toxicol. 2005;45:89-118. doi: 10.1146/annurev.pharmtox.45.120403.095748. [Article]

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Drug created at March 03, 2013 23:50 / Updated at August 02, 2024 07:30