Atorvastatin

Identification

Summary

Atorvastatin 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

Atorvaliq, Caduet, Lipitor, Lypqozet

Generic Name

Atorvastatin

DrugBank Accession Number

DB01076

Background

Atorvastatin (Lipitor®), is a lipid-lowering drug included in the statin class of medications. By inhibiting the endogenous production of cholesterol in 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,⁸ which catalyzes the conversion of HMG-CoA to mevalonic acid. This conversion is a critical metabolic reaction 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 statins is considered standard practice for patients following any cardiovascular event, and for people who are at moderate to high risk of developing cardiovascular disease. The evidence supporting statin use, coupled with minimal side effects and long term benefits, has resulted in wide use of this medication in North America.^9,10

Atorvastatin and other statins including lovastatin, pravastatin, rosuvastatin, fluvastatin, and simvastatin are considered first-line treatment options for dyslipidemia.^9,10 The increasing use of this class of drugs is largely attributed to the rise in cardiovascular diseases (CVD) (such as heart attack, atherosclerosis, angina, peripheral artery disease, and stroke) in many countries.¹¹ An elevated cholesterol level (elevated low-density lipoprotein (LDL) levels in particular) is a significant risk factor for the development of CVD.^9,12 Several landmark studies demonstrate that the use of statins is associated with both a reduction in LDL levels and CVD risk.^{13,14,15,16,17,18} Statins were shown to reduce the incidences of all-cause mortality, including fatal and non-fatal CVD, as well as the need for surgical revascularization or angioplasty following a heart attack.^9,10 Some evidence has shown that even for low-risk individuals (with <10% risk of a major vascular event occurring within five years) statin use leads to a 20%-22% relative reduction in the number of 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.^19,20

Atorvastatin was first synthesized in 1985 by Dr. Bruce Roth and approved by the FDA in 1996.³⁴ It is a pentasubstituted pyrrole ³ formed by two contrasting moieties with an achiral heterocyclic core unit and a 3,5-dihydroxypentanoyl side chain identical to its parent compound.³⁵ Unlike other members of the statin group, atorvastatin is an active compound and therefore does not require activation.⁴

Type

Small Molecule

Groups

Approved

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Atorvastatin (DB01076)

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Weight

Average: 558.6398
Monoisotopic: 558.253000445

Chemical Formula

C₃₃H₃₅FN₂O₅

Synonyms

• Atorvastatin
• atorvastatina
• atorvastatine
• atorvastatinum

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Pharmacology

Indication

Atorvastatin is indicated for the treatment of several types of dyslipidemias, including primary hyperlipidemia and mixed dyslipidemia in adults, hypertriglyceridemia, primary dysbetalipoproteinemia, homozygous familial hypercholesterolemia, and heterozygous familial hypercholesterolemia in adolescent patients with failed dietary modifications.²

Dyslipidemia describes an elevation of plasma cholesterol, triglycerides or both as well as to the presence of low levels of high-density lipoprotein. This condition represents an increased risk for the development of atherosclerosis.³⁶

Atorvastatin is indicated, in combination with dietary modifications, to prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles.²

Atorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.²

Atorvastatin may be used as a preventive agent for non-fatal myocardial infarction, fatal and non-fatal stroke, revascularization procedures, hospitalization for congestive heart failure and angina in patients with coronary heart disease.²

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.^9,10

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Used in combination to prevent	Angina	Combination Product in combination with: Amlodipine (DB00381)	••••••••••••	•••••	•••••••• •••• ••••••• ••• •••••••• ••••• •••••••
Used in combination to prevent	Angina	Combination Product in combination with: Amlodipine (DB00381)	••••••••••••	•••••	•••••••••• ••••••• •••••••• ••••• •••••••
Used in combination to prevent	Cardiovascular complications	Combination Product in combination with: Acetylsalicylic acid (DB00945)	••••••••••••		•••••••••••••• ••••	•••••••
Prevention of	Cardiovascular disease		••••••••••••		••• •••• •••••••• •••••••• ••••• •••••••• ••••••• •••••••••••••	••••••
Used in combination to manage	Coronary artery disease (cad)	Combination Product in combination with: Perindopril (DB00790), Amlodipine (DB00381)	••••••••••••	•••••	••••• •••••••• •••••••••• •••••••••• •••• ••••••••••• ••••• ••••• •••••••••••••	••••••• ••••••• •••• ••••••

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Contraindications & Blackbox Warnings

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Pharmacodynamics

Atorvastatin is an oral antilipemic agent that reversibly inhibits HMG-CoA reductase. It lowers total cholesterol, low-density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apo B), non-high density lipoprotein-cholesterol (non-HDL-C), and triglyceride (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 a 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, atorvastatin reduces the risk of cardiovascular morbidity and mortality.^21,9,10,27

Elevated cholesterol levels (and high low-density lipoprotein (LDL) levels in particular) are an important risk factor for the development of CVD.⁹ Clinical studies have shown that atorvastatin reduces LDL-C and total cholesterol by 36-53%.³ In patients with dysbetalipoproteinemia, atorvastatin reduced the levels of intermediate-density lipoprotein cholesterol.² It has also been suggested that atorvastatin can limit the extent of angiogenesis, which can be useful in the treatment of chronic subdural hematoma.¹

Myopathy/Rhabdomyolysis

Atorvastatin, like other HMG-CoA reductase inhibitors, is associated with a risk of drug-induced myopathy characterized by muscle pain, tenderness, or weakness in conjunction with elevated levels of creatine kinase (CK). Myopathy often manifests as rhabdomyolysis with or without acute renal failure secondary to myoglobinuria. The risk of statin-induced myopathy is dose-related, and the symptoms of myopathy are typically resolved upon drug discontinuation. Results from observational studies suggest that 10-15% of people taking statins may experience muscle aches at some point during treatment.³⁰

Liver Dysfunction

Statins, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (> 3 times the upper limit of normal [ULN] occurring on two or more occasions) in serum transaminases occurred in 0.7% of patients who received atorvastatin in clinical trials. This effect appears to be dose-related.^41,42

Endocrine Effects

Statins are associated with a risk of increased serum HbA1c and glucose levels. An in vitro study demonstrated a dose-dependent cytotoxic effect on human pancreatic islet β cells following treatment with atorvastatin. Moreover, insulin secretion rates decreased relative to control.⁷

HMG-CoA reductase inhibitors interfere with cholesterol synthesis and may theoretically interfere with the production of adrenal and/or gonadal steroids. Clinical studies with atorvastatin and other HMG-CoA reductase inhibitors have suggested that these agents do not affect plasma cortisol concentrations, basal plasma testosterone concentration, or adrenal reserve. However, the effect of statins on male fertility has not been fully investigated. The effects of statins on the pituitary-gonadal axis in premenopausal women are unknown.⁴²

Cardiovascular

Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure.⁴²

Lipoprotein A

In some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by the concomitant increase in Lp(a) lipoprotein concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for coronary heart disease.⁴² Further studies have demonstrated statins affect Lp(a) levels differently in patients with dyslipidemia depending on their apo(a) phenotype; statins increase Lp(a) levels exclusively in patients with the low molecular weight apo(a) phenotype.²⁸

Mechanism of action

Atorvastatin 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.^1,8 Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL. Atorvastatin also reduces Very-Low-Density Lipoprotein-Cholesterol (VLDL-C), serum triglycerides (TG) and Intermediate Density Lipoproteins (IDL), as well as the number of apolipoprotein B (apo B) containing particles, but increases High-Density Lipoprotein Cholesterol (HDL-C).

In vitro and in vivo animal studies also demonstrate that atorvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins.²⁵ These effects include improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response. Statins were also found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an essential role in leukocyte trafficking and T cell activation.²⁹

Target	Actions	Organism
A3-hydroxy-3-methylglutaryl-coenzyme A reductase	inhibitor	Humans
UDipeptidyl peptidase 4	inhibitor	Humans
UAryl hydrocarbon receptor	agonist	Humans
UHistone deacetylase 2	inhibitor	Humans
UNuclear receptor subfamily 1 group I member 3	ligand	Humans

Absorption

Atorvastatin presents a dose-dependent and non-linear pharmacokinetic profile.⁴ It is very rapidly absorbed after oral administration. After the administration of a dose of 40 mg, its peak plasma concentration of 28 ng/ml is reached 1-2 hours after initial administration with an AUC of about 200 ng∙h/ml.⁶ Atorvastatin undergoes extensive first-pass metabolism in the wall of the gut and the liver, resulting in an absolute oral bioavailability of 14%.² Plasma atorvastatin concentrations are lower (approximately 30% for Cmax and AUC) following evening drug administration compared with morning. However, LDL-C reduction is the same regardless of the time of day of drug administration.⁴¹

Administration of atorvastatin with food results in prolonged Tmax and a reduction in Cmax and AUC.³

Breast Cancer Resistance Protein (BCRP) is a membrane-bound protein that plays an important role in the absorption of atorvastatin.²⁶ Evidence from pharmacogenetic studies of c.421C>A single nucleotide polymorphisms (SNPs) in the gene for BCRP has demonstrated that individuals with the 421AA genotype have reduced functional activity and 1.72-fold higher AUC for atorvastatin compared to study individuals with the control 421CC genotype. This has important implications for the variation in response to the drug in terms of efficacy and toxicity, particularly as the BCRP c.421C>A polymorphism occurs more frequently in Asian populations than in Caucasians.^31,32 Other statin drugs impacted by this polymorphism include fluvastatin, simvastatin, and rosuvastatin.³¹

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 atorvastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C single nucleotide polymorphism (SNP) in the gene encoding OATP1B1 (SLCO1B1) demonstrated that atorvastatin AUC was increased 2.45-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals.³³ Other statin drugs impacted by this polymorphism include simvastatin, pitavastatin, rosuvastatin, and pravastatin.²⁶

Volume of distribution

The reported volume of distribution of atorvastatin is of 380 L.^41,42

Protein binding

Atorvastatin is highly bound to plasma proteins and over 98% of the administered dose is found in a bound form.^41,42

Metabolism

Atorvastatin is highly metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products, primarily by Cytochrome P450 3A4 in the intestine and liver.^41,42 Atorvastatin's metabolites undergo further lactonization via the formation of acyl glucuronide intermediates by the enzymes UGT1A1 and UGT1A3. These lactones can be hydrolyzed back to their corresponding acid forms and exist in equilibirum.^5,26

In vitro inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites.^41,42

Hover over products below to view reaction partners

• Atorvastatin
  • para-hydroxyatorvastatin
    • para-hydroxyatorvastatin glucuronide
    • para-hydroxyatorvastatin lactone
  • ortho-hydroxyatorvastatin
    • ortho-hydroxyatorvastatin glucuronide
    • ortho-hydroxyatorvastatin lactone
  • Atorvastatin lactone

Route of elimination

Atorvastatin and its metabolites are mainly eliminated in the bile without enterohepatic recirculation. The renal elimination of atorvastatin is very minimal and represents less than 1% of the eliminated dose.^41,42

Half-life

The half-life of atorvastatin is 14 hours while the half-life of its metabolites can reach up to 30 hours.^41,42

Clearance

The registered total plasma clearance of atorvastatin is of 625 ml/min.⁵

Adverse Effects

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Toxicity

The reported LD50 of oral atorvastatin in mice is higher than 5000 mg/kg.^MSDS In cases of overdose with atorvastatin, there is reported symptoms of complicated breathing, jaundice, liver damage, dark urine, muscle pain, and seizures.³⁸ In case of overdose, symptomatic treatment is recommended and due to the high plasma protein binding, hemodialysis is not expected to generate significant improvement.^Label

In carcinogenic studies with high doses of atorvastatin, evidence of rhabdomyosarcoma, fibrosarcoma, liver adenoma, and liver carcinoma were observed.^Label

In fertility studies with high doses of atorvastatin, there were events of aplasia, aspermia, low testis and epididymal weight, decreased sperm motility, decreased spermatid head concentration and increased abnormal sperm.^Label

Atorvastatin was shown to not be mutagenic in diverse mutagenic assays.^Label

Pathways

Not Available

Pharmacogenomic Effects/ADRs Browse all" title="About SNP Mediated Effects/ADRs" id="snp-actions-info" class="drug-info-popup" href="javascript:void(0);">

Interacting Gene/Enzyme	Allele name	Genotype(s)	Defining Change(s)	Type(s)	Description	Details
Kinesin-like protein KIF6	---	(C;C) / (C;T)	C Allele	Effect Directly Studied	Patients with this genotype have a greater reduction in risk of a major cardiovascular event with high dose atorvastatin.	Details
3-hydroxy-3-methylglutaryl-coenzyme A reductase	---	(A;T)	T Allele	Effect Directly Studied	Patients with this genotype have a lesser reduction in LDL cholesterol with atorvastatin.	Details
Cytochrome P450 3A4	CYP3A4*1B	(G;G) / (A;G)	A > G	Effect Directly Studied	Patients with this genotype have an greater reduction in LDL cholesterol with atorvastatin.	Details

Interactions

Drug Interactions Learn More" title="About Drug Interactions" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">

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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Abametapir	The serum concentration of Atorvastatin can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Atorvastatin can be increased when combined with Abatacept.
Abiraterone	The metabolism of Atorvastatin can be decreased when combined with Abiraterone.
Acalabrutinib	The metabolism of Atorvastatin can be decreased when combined with Acalabrutinib.
Acenocoumarol	The risk or severity of bleeding can be increased when Atorvastatin is combined with Acenocoumarol.

Food Interactions

• Avoid grapefruit products. Grapefruit products may increase the risk for atorvastatin related adverse effects such as myopathy and rhabdomyolysis.
• Take with or without food. Food decreases absorption but not to a clinically significant extent.

Products

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Atorvastatin calcium	C0GEJ5QCSO	134523-03-8	FQCKMBLVYCEXJB-MNSAWQCASA-L
Atorvastatin calcium trihydrate	48A5M73Z4Q	344423-98-9	SHZPNDRIDUBNMH-NIJVSVLQSA-L

Product Images

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International/Other Brands

Atogal (Ingers (Czech Republic)) / Cardyl (Pfizer (Spain)) / Faboxim (Fabop (Argentina)) / Hipolixan (Pasteur (Chile)) / Lipotropic (Drugtech (Chile)) / Liprimar (Pfizer (Hungary, Ukraine), Goedecke (Russia)) / Lowden (Saval (Chile)) / Normalip (Quesada (Argentina)) / Sincol (Indeco (Argentina)) / Sortis (Pfizer (Austria, Czech Republic, Germany, Hungary, Poland, Portugal, Switzerland), Godecke (Germany), Parke, Davis (Germany)) / Torvacard (Zentiva (Czech Republic, Hungary, Poland, Russia, Ukraine)) / Torvast (Pfizer (Italy)) / Totalip (Guidotti (Italy)) / Tulip (Lek (Czech Republic, Russia), Wermar (Mexico), Sandoz (Poland, Ukraine), Pharmacia (Spain)) / Vastina (Penn (Argentina)) / Xanator (Sieger (Greece)) / Xarator (Parke, Davis (Italy)) / Zurinel (Prater (Chile))

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Atorvaliq	Suspension	20 mg/5mL	Oral	Cmp Pharma, Inc.	2023-03-01	Not applicable
Atorvastatin	Tablet	40 mg	Oral	Pro Doc Limitee	2010-05-21	Not applicable
Atorvastatin	Tablet	40 mg	Oral	Nora Pharma Inc	Not applicable	Not applicable
Atorvastatin	Tablet	20 mg	Oral	Sivem Pharmaceuticals Ulc	2012-06-26	2017-11-15
Atorvastatin	Tablet	80 mg	Oral	Sanis Health Inc	2010-05-27	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Ach-atorvastatin Calcium	Tablet	10 mg	Oral	Accord Healthcare Inc	2019-10-18	Not applicable
Ach-atorvastatin Calcium	Tablet	20 mg	Oral	Accord Healthcare Inc	2019-10-18	Not applicable
Ach-atorvastatin Calcium	Tablet	40 mg	Oral	Accord Healthcare Inc	2019-10-18	Not applicable
Ach-atorvastatin Calcium	Tablet	80 mg	Oral	Accord Healthcare Inc	2019-10-18	Not applicable
Ag-atorvastatin	Tablet	10 mg	Oral	Angita Pharma Inc.	2018-09-27	Not applicable

Over the Counter Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Coffeerazzi Minerang Dutchcoffee	Liquid	3 g/100mL	Oral	AML Bio Co., Ltd.	2022-08-17	Not applicable
Dengue Kill	Liquid	3 g/100mL	Oral	AML Bio Co., Ltd.	2022-08-17	Not applicable

Mixture Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
Amlodipine and atorvastatin	Atorvastatin calcium trihydrate (20 mg/1) + Amlodipine besylate (10 mg/1)	Tablet, film coated	Oral	Zydus Lifesciences Limited	2019-05-30	Not applicable
Amlodipine and atorvastatin	Atorvastatin calcium trihydrate (10 mg/1) + Amlodipine besylate (10 mg/1)	Tablet, film coated	Oral	Mylan Pharmaceuticals Inc.	2014-11-06	Not applicable
Amlodipine and Atorvastatin	Atorvastatin calcium trihydrate (40 mg/1) + Amlodipine besylate (2.5 mg/1)	Tablet, coated	Oral	Prasco Laboratories	2022-03-14	Not applicable
Amlodipine and atorvastatin	Atorvastatin calcium trihydrate (40 mg/1) + Amlodipine besylate (5 mg/1)	Tablet, film coated	Oral	Zydus Lifesciences Limited	2019-05-30	Not applicable
Amlodipine and atorvastatin	Atorvastatin calcium trihydrate (20 mg/1) + Amlodipine besylate (5 mg/1)	Tablet, film coated	Oral	Mylan Pharmaceuticals Inc.	2014-05-21	Not applicable

Unapproved/Other Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
Coffeerazzi Minerang Dutchcoffee	Atorvastatin calcium (3 g/100mL)	Liquid	Oral	AML Bio Co., Ltd.	2022-08-17	Not applicable
Dengue Kill	Atorvastatin calcium (3 g/100mL)	Liquid	Oral	AML Bio Co., Ltd.	2022-08-17	Not applicable

Categories

ATC Codes

C10BA05 — Atorvastatin and ezetimibe

• C10BA — Combinations of various lipid modifying agents
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX11 — Atorvastatin, amlodipine and perindopril

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX12 — Atorvastatin, acetylsalicylic acid and perindopril

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX19 — Atorvastatin, amlodipine and candesartan

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX18 — Atorvastatin, amlodipine and ramipril

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10AA05 — Atorvastatin

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

C10BX15 — Atorvastatin and perindopril

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX03 — Atorvastatin and amlodipine

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX08 — Atorvastatin and acetylsalicylic acid

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

C10BX06 — Atorvastatin, acetylsalicylic acid and ramipril

• C10BX — Lipid modifying agents in combination with other drugs
• C10B — LIPID MODIFYING AGENTS, COMBINATIONS
• C10 — LIPID MODIFYING AGENTS
• C — CARDIOVASCULAR SYSTEM

Drug Categories

• Agents Causing Muscle Toxicity
• Anticholesteremic Agents
• BSEP/ABCB11 Substrates
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2C19 Inhibitors
• Cytochrome P-450 CYP2C19 inhibitors (strength unknown)
• Cytochrome P-450 CYP2C8 Inhibitors
• Cytochrome P-450 CYP2C8 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2D6 Inhibitors
• Cytochrome P-450 CYP2D6 Inhibitors (strength unknown)
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A5 Substrates
• Cytochrome P-450 CYP3A7 Substrates
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Enzyme Inhibitors
• Fatty Acids
• Heptanoic Acids
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Hypolipidemic Agents
• Hypolipidemic Agents Indicated for Hyperlipidemia
• Lipid Modifying Agents
• Lipid Modifying Agents, Plain
• Lipid Regulating Agents
• Lipids
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B1/SLCO1B1 Substrates
• OATP1B3 substrates
• OATP2B1/SLCO2B1 substrates
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• Toxic Actions
• UGT1A1 Substrates
• UGT1A3 substrates

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as diphenylpyrroles. These are aromatic heterocyclic compounds with a structure based on a pyrrole ring linked to exactly two phenyl groups.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Pyrroles

Sub Class

Substituted pyrroles

Direct Parent

Diphenylpyrroles

Alternative Parents

Aromatic anilides / Medium-chain hydroxy acids and derivatives / Pyrrole carboxamides / Medium-chain fatty acids / Beta hydroxy acids and derivatives / Fluorobenzenes / Halogenated fatty acids / Hydroxy fatty acids / Heterocyclic fatty acids / Aryl fluorides / Vinylogous amides / Heteroaromatic compounds / Secondary carboxylic acid amides / Secondary alcohols / Azacyclic compounds / Carboxylic acids / Monocarboxylic acids and derivatives / Organonitrogen compounds / Carbonyl compounds / Organofluorides / Organic oxides / Organopnictogen compounds / Hydrocarbon derivatives

show 13 more

Substituents

2,3-diphenylpyrrole / Alcohol / Aromatic anilide / Aromatic heteromonocyclic compound / Aryl fluoride / Aryl halide / Azacycle / Benzenoid / Beta-hydroxy acid / Carbonyl group / Carboxamide 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 / Pyrrole-3-carboxamide / Pyrrole-3-carboxylic acid or derivatives / Secondary alcohol / Secondary carboxylic acid amide / Vinylogous amide

show 30 more

Molecular Framework

Aromatic heteromonocyclic compounds

External Descriptors

statin (synthetic), aromatic amide, pyrroles, dihydroxy monocarboxylic acid, monofluorobenzenes (CHEBI:39548)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

A0JWA85V8F

CAS number

134523-00-5

InChI Key

XUKUURHRXDUEBC-KAYWLYCHSA-N

InChI

InChI=1S/C33H35FN2O5/c1-21(2)31-30(33(41)35-25-11-7-4-8-12-25)29(22-9-5-3-6-10-22)32(23-13-15-24(34)16-14-23)36(31)18-17-26(37)19-27(38)20-28(39)40/h3-16,21,26-27,37-38H,17-20H2,1-2H3,(H,35,41)(H,39,40)/t26-,27-/m1/s1

IUPAC Name

(3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-(propan-2-yl)-1H-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid

SMILES

CC(C)C1=C(C(=O)NC2=CC=CC=C2)C(=C(N1CC[C@@H](O)C[C@@H](O)CC(O)=O)C1=CC=C(F)C=C1)C1=CC=CC=C1

References

Synthesis Reference

US20020183527

General References

1. Qiu S, Zhuo W, Sun C, Su Z, Yan A, Shen L: Effects of atorvastatin on chronic subdural hematoma: A systematic review. Medicine (Baltimore). 2017 Jun;96(26):e7290. doi: 10.1097/MD.0000000000007290. [Article]
2. McIver LA, Siddique MS: Atorvastatin . [Article]
3. Ye YC, Zhao XL, Zhang SY: Use of atorvastatin in lipid disorders and cardiovascular disease in Chinese patients. Chin Med J (Engl). 2015 Jan 20;128(2):259-66. doi: 10.4103/0366-6999.149226. [Article]
4. Ray SK, Rege NN: Atorvastatin: in the management of hyperlipidaemia. J Postgrad Med. 2000 Jul-Sep;46(3):242-3. [Article]
5. Lennernas H: Clinical pharmacokinetics of atorvastatin. Clin Pharmacokinet. 2003;42(13):1141-60. [Article]
6. Lins RL, Matthys KE, Verpooten GA, Peeters PC, Dratwa M, Stolear JC, Lameire NH: Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients. Nephrol Dial Transplant. 2003 May;18(5):967-76. [Article]
7. 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]
8. 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]
9. 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]
10. 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]
11. 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]
12. 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]
13. 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]
14. 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]
15. 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]
16. 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]
17. 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]
18. 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]
19. 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]
20. 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]
21. Henwood JM, Heel RC: Lovastatin. A preliminary review of its pharmacodynamic properties and therapeutic use in hyperlipidaemia. Drugs. 1988 Oct;36(4):429-54. doi: 10.2165/00003495-198836040-00003. [Article]
22. 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]
23. 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]
24. 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]
25. 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]
26. 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]
27. Bradford RH, Shear CL, Chremos AN, Dujovne CA, Franklin FA, Grillo RB, Higgins J, Langendorfer A, Nash DT, Pool JL, et al.: Expanded Clinical Evaluation of Lovastatin (EXCEL) study results: two-year efficacy and safety follow-up. Am J Cardiol. 1994 Oct 1;74(7):667-73. doi: 10.1016/0002-9149(94)90307-7. [Article]
28. Yahya R, Berk K, Verhoeven A, Bos S, van der Zee L, Touw J, Erhart G, Kronenberg F, Timman R, Sijbrands E, Roeters van Lennep J, Mulder M: Statin treatment increases lipoprotein(a) levels in subjects with low molecular weight apolipoprotein(a) phenotype. Atherosclerosis. 2019 Jul 3. pii: S0021-9150(19)31392-9. doi: 10.1016/j.atherosclerosis.2019.07.001. [Article]
29. 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]
30. 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]
31. Keskitalo JE, Zolk O, Fromm MF, Kurkinen KJ, Neuvonen PJ, Niemi M: ABCG2 polymorphism markedly affects the pharmacokinetics of atorvastatin and rosuvastatin. Clin Pharmacol Ther. 2009 Aug;86(2):197-203. doi: 10.1038/clpt.2009.79. Epub 2009 May 27. [Article]
32. Lee E, Ryan S, Birmingham B, Zalikowski J, March R, Ambrose H, Moore R, Lee C, Chen Y, Schneck D: Rosuvastatin pharmacokinetics and pharmacogenetics in white and Asian subjects residing in the same environment. Clin Pharmacol Ther. 2005 Oct;78(4):330-41. doi: 10.1016/j.clpt.2005.06.013. [Article]
33. Pasanen MK, Fredrikson H, Neuvonen PJ, Niemi M: Different effects of SLCO1B1 polymorphism on the pharmacokinetics of atorvastatin and rosuvastatin. Clin Pharmacol Ther. 2007 Dec;82(6):726-33. doi: 10.1038/sj.clpt.6100220. Epub 2007 May 2. [Article]
34. Corey E., Czako B. and Kurti L. (2007). Molecules and medicine. John Wiley & Sons, Inc. [ISBN:978-0-470-26096-8]
35. Kumar R. and Bandichhor R. (2018). Hazardous reagent substitution. A pharmaceutical perspective. The Royal Society of Chemistry. [ISBN:978-1-78262-050-1]
36. Merck Manuals [Link]
37. Chemocare [Link]
38. Laguna Treatment [Link]
39. FDA Approved Drug Products: Lipitor (atorvastatin calcium) oral tablets [Link]
40. INVIMA Product Authorization: Lipomega (atorvastatin calcium/omega-3 ethyl esters) oral capsule [Link]
41. FDA Label - Atorvastatin [File]
42. Health Canada Monograph - Atorvastatin [File]

External Links

Human Metabolome Database

HMDB0005006

KEGG Drug

D07474

KEGG Compound

C06834

PubChem Compound

60823

PubChem Substance

46506188

ChemSpider

54810

BindingDB

22164

RxNav

1483793

ChEBI

39548

ChEMBL

CHEMBL1487

ZINC

ZINC000003920719

Therapeutic Targets Database

DAP000553

PharmGKB

PA448500

PDBe Ligand

117

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

PDRhealth

PDRhealth Drug Page

Wikipedia

Atorvastatin

PDB Entries

1hwk

FDA label

Download (387 KB)

MSDS

Download (56.5 KB)

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Active Not Recruiting	Prevention	Aging / Cognitive Deficits / Dementia of the Alzheimer's Type / Dementia, Mixed / Neurodegenerative Disorders / Vascular Dementia (VaD) / White Matter Hyperintensity	1
4	Active Not Recruiting	Prevention	Cardiovascular Disease (CVD)	1
4	Active Not Recruiting	Prevention	Disability Free Survival / Elderly / Healthy Subjects (HS) / Independent Living	1
4	Completed	Not Available	Cardiovascular Disease (CVD) / Cholesterol, LDL / Cognitive Functioning / Type 2 Diabetes Mellitus	1
4	Completed	Not Available	Chronic Stable Angina Pectoris / Coronary Heart Disease (CHD)	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

• Advanced Pharmaceutical Services Inc.
• Apotheca Inc.
• A-S Medication Solutions LLC
• Atlantic Biologicals Corporation
• Bryant Ranch Prepack
• Cardinal Health
• Direct Pharmaceuticals Inc.
• Dispensing Solutions
• Diversified Healthcare Services Inc.
• Goedecke GmbH
• Healthcare Pharmacy
• Heartland Repack Services LLC
• Kaiser Foundation Hospital
• Lake Erie Medical and Surgical Supply
• Murfreesboro Pharmaceutical Nursing Supply
• Nucare Pharmaceuticals Inc.
• Orifice Medical AB
• PCA LLC
• PD-Rx Pharmaceuticals Inc.
• Pfizer Inc.
• Pharmaceutical Utilization Management Program VA Inc.
• Physicians Total Care Inc.
• Prepackage Specialists
• Prepak Systems Inc.
• Resource Optimization and Innovation LLC
• Sandhills Packaging Inc.
• Southwood Pharmaceuticals
• Tya Pharmaceuticals
• US Pharmaceutical Group
• Vangard Labs Inc.
• Vitrum Ab
• Warner Lambert Company LLC

Dosage Forms

Form	Route	Strength
Tablet	Oral	20 mg
Tablet	Oral	40 mg
Tablet	Oral	80 mg
Tablet, coated	Oral
Capsule
Tablet, film coated	Oral	30 MG
Tablet, film coated	Oral	60 MG
Tablet, coated	Oral	21.65 mg
Tablet, film coated	Oral	10.825 mg
Suspension	Oral	20 mg/5mL
Powder	Not applicable	1 kg/1kg
Tablet	Oral	10 mg/1
Tablet	Oral	20 mg/1
Tablet	Oral	40 mg/1
Tablet	Oral	80 mg/1
Tablet, coated	Oral	10 mg/1
Tablet, coated	Oral	20 mg/1
Tablet, coated	Oral	40 mg/1
Tablet, coated	Oral	80 mg/1
Tablet, film coated	Oral	10 mg/301
Tablet, film coated	Oral	10.36 MG
Tablet, film coated	Oral	80 mg/301
Powder	Not applicable	20 kg/20kg
Tablet, film coated	Oral	21.7 MG
Tablet, film coated	Oral	43.38 MG
Tablet	Oral	10 mg
Tablet, coated	Oral	10 mg
Tablet, coated	Oral	20 mg
Tablet, coated	Oral	20.7 mg
Tablet, film coated	Oral	20 mg
Tablet, film coated	Oral	10 MG
Tablet, film coated	Oral	80 mg
Capsule, liquid filled	Oral	10 mg
Capsule, liquid filled	Oral	80 mg
Capsule, liquid filled	Oral	8000000 mg
Capsule, liquid filled	Oral	43.376 mg
Capsule, liquid filled	Oral	20 mg
Tablet, film coated	Oral	40.00 mg
Tablet	Oral	40.000 mg
Tablet	Oral	10.00 mg
Tablet, film coated	Oral
Tablet, film coated	Oral	10 MG
Liquid	Oral	3 g/100mL
Tablet	Oral	20.0 mg
Tablet	Oral	21.640 mg
Tablet, film coated	Oral	4000000 mg
Tablet	Oral	10.000 mg
Tablet, film coated	Oral	40 mg
Capsule	Oral
Tablet	Oral
Tablet, film coated	Oral
Tablet	Oral	10.00 mg
Tablet	Oral	20.000 mg
Tablet, film coated	Oral	10.85 Mg
Tablet, film coated	Oral	21.69 Mg
Tablet	Oral
Tablet	Oral	80.000 mg
Tablet, chewable	Oral
Tablet, film coated	Oral	10 mg/1
Tablet, film coated	Oral	20 mg/1
Tablet, film coated	Oral	40 mg/1
Tablet, film coated	Oral	80 mg/1
Tablet, coated	Oral	2000000 mg
Tablet	Oral	4000000 mg
Tablet, coated	Oral	1000000 mg
Capsule, liquid filled	Oral
Tablet, coated	Oral	40 mg
Tablet, coated	Oral	80 mg
Tablet	Oral	21.649 mg
Tablet	Oral	10.825 mg
Tablet, chewable	Oral	10 MG
Tablet, chewable	Oral	20 MG
Tablet	Oral	40.000 mg
Tablet	Oral	21.648 mg
Tablet	Oral	86.800 mg
Tablet, chewable	Oral	40 MG
Tablet, chewable	Oral	5 MG
Tablet, film coated	Oral	10.000 mg
Tablet, film coated	Oral	20.000 mg
Tablet, film coated	Oral	40.000 mg
Tablet, film coated	Oral	80.000 mg
Tablet	Oral	10.341 mg

Prices

Unit description	Cost	Unit
Lipitor 20 mg tablet	5.0USD	tablet
Lipitor 40 mg tablet	5.0USD	tablet
Lipitor 80 mg tablet	5.0USD	tablet
Lipitor 10 mg tablet	3.5USD	tablet
Lipitor 40 mg Tablet	2.52USD	tablet
Lipitor 80 mg Tablet	2.52USD	tablet
Lipitor 20 mg Tablet	2.34USD	tablet
Lipitor 10 mg Tablet	1.87USD	tablet

DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US4681893	No	1987-07-21	2009-09-24
CA2521776	No	2006-04-25	2022-05-21
CA2220018	No	2001-04-17	2016-07-08
US5969156	Yes	1999-10-19	2017-01-08
USRE42461	Yes	2011-06-14	2017-04-25
US6455574	No	2002-09-24	2018-08-11
US11369567	No	2017-06-07	2037-06-07
US11654106	No	2017-06-07	2037-06-07

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	176 °C	'MSDS'
boiling point (°C)	722 ºC at 760 mmHg	'MSDS'
water solubility	Practically insoluble	'MSDS'
logP	6.36	'MSDS'
pKa	4.46	'MSDS'

Predicted Properties

Property	Value	Source
Water Solubility	0.00063 mg/mL	ALOGPS
logP	4.24	ALOGPS
logP	5.39	Chemaxon
logS	-6	ALOGPS
pKa (Strongest Acidic)	4.31	Chemaxon
pKa (Strongest Basic)	-2.7	Chemaxon
Physiological Charge	-1	Chemaxon
Hydrogen Acceptor Count	5	Chemaxon
Hydrogen Donor Count	4	Chemaxon
Polar Surface Area	111.79 Å2	Chemaxon
Rotatable Bond Count	12	Chemaxon
Refractivity	158.2 m3·mol-1	Chemaxon
Polarizability	59.45 Å3	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	0	Chemaxon
Rule of Five	No	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.8947
Blood Brain Barrier	-	0.7825
Caco-2 permeable	-	0.8956
P-glycoprotein substrate	Substrate	0.5246
P-glycoprotein inhibitor I	Inhibitor	0.7164
P-glycoprotein inhibitor II	Inhibitor	0.8724
Renal organic cation transporter	Non-inhibitor	0.8131
CYP450 2C9 substrate	Non-substrate	0.7887
CYP450 2D6 substrate	Non-substrate	0.9116
CYP450 3A4 substrate	Substrate	0.6841
CYP450 1A2 substrate	Non-inhibitor	0.8551
CYP450 2C9 inhibitor	Non-inhibitor	0.719
CYP450 2D6 inhibitor	Non-inhibitor	0.9042
CYP450 2C19 inhibitor	Non-inhibitor	0.6191
CYP450 3A4 inhibitor	Non-inhibitor	0.6675
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.6894
Ames test	Non AMES toxic	0.9133
Carcinogenicity	Non-carcinogens	0.7777
Biodegradation	Not ready biodegradable	0.9974
Rat acute toxicity	2.5686 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9904
hERG inhibition (predictor II)	Non-inhibitor	0.5101

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	splash10-000f-5100950000-b76d194b9679e4b35417
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-0a4i-0000090000-ae5c999b091a2bc93933
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-0a4i-0000190000-dd563e18b1f0f74aadd5
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-0zfs-0007960000-cb66a18d2f0a687261ba
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-002b-0059000000-0942bc1e35434cd7d0d3
LC-MS/MS Spectrum - LC-ESI-QTOF , negative	LC-MS/MS	splash10-004i-0093000000-f42ba46820a3cf3295c5
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udj-0005910000-b09ba5f3b86948c7f3cb
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0a4i-0000090000-6f297ca79ae1761aac33
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0002-1009300000-9479520f395dcdd585e7
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0092000000-9b561b8d35c3bdc5e46a
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0090000000-3aad87273e7f9942a50f
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-01t9-1090000000-3f0efff41ebdb5320ce4
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-03di-2090000000-0227638704b90c4249d0
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0a4i-0000090000-65c729c6734f6533c431
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0002-1009300000-9122e4479d8c0c32bb0d
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0092000000-22d639a8882509e1bcdb
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-004i-0090000000-30a0198165bae85fa258
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-01t9-1090000000-cb3feea45f5280f05c37
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-03di-2090000000-8db2f70b373277f143c0
LC-MS/MS Spectrum - LC-ESI-ITFT , negative	LC-MS/MS	splash10-0udj-0005910000-a63c845ca248d958068d
LC-MS/MS Spectrum - LC-ESI-QFT , negative	LC-MS/MS	splash10-0a6s-1085190000-9e43612012842effca5a
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0006-0031900000-4081fba1ae61b0d871cf
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-052f-0000980000-6751fefdee0a257e52f8
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0006-0000900000-4009a70e947dcceb6e0f
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0006-0085900000-e1a4447e4c9a4bda83b2
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0udi-0092100000-4a5517154ad5f7375ea2
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0a4i-0000090000-e741fcb91eb29d1032cb
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-00kf-0000900000-fdd41dae94afd3f4d3c5
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4i-0000490000-25199beeece682c7de9e
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0006-0020900000-71cacdfc979c4386762b
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udi-0092000000-38374b1412250df34777
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udi-0090000000-87710909ebad67c88f3b
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udj-0190000000-60e7ef3dc3f76db11c5f
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0f72-0290000000-e8c2cda8588874b2aaa5
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0a4i-0000490000-a5ee6b466e73e9e72383
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0006-0011900000-b8fc562d4be5ffb07f59
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udi-0092000000-df78998b01951a3dd03a
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udi-0090000000-19c391db652668c97d59
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0udj-0190000000-931a1911dcd7ec9dbbc8
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-0f72-0290000000-6157ef91cb98aeef5cf7
LC-MS/MS Spectrum - LC-ESI-ITFT , positive	LC-MS/MS	splash10-00kf-0000900000-cd6fb2c00146543cbb47
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0f6x-0092420000-fb2c084ecdd5af8f6f7b
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0000190000-24684d99b986505a11da
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4j-0001590000-21281180bb7119e07111
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0abc-1100790000-3d316b7077d264af3a30
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0kc2-3101960000-218b21ca3eff177c6c5a
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0aov-1224940000-646210e933a7e341ef0b
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-054o-6136980000-139f2fd8be199a634435

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å2)	Source type	Source
[M-H]-	241.651896	predicted	DarkChem Lite v0.1.0
[M-H]-	235.525296	predicted	DarkChem Lite v0.1.0
[M-H]-	224.32292	predicted	DeepCCS 1.0 (2019)
[M+H]+	239.832996	predicted	DarkChem Lite v0.1.0
[M+H]+	233.413296	predicted	DarkChem Lite v0.1.0
[M+H]+	226.14781	predicted	DeepCCS 1.0 (2019)
[M+Na]+	239.696196	predicted	DarkChem Lite v0.1.0
[M+Na]+	232.943296	predicted	DarkChem Lite v0.1.0
[M+Na]+	231.75365	predicted	DeepCCS 1.0 (2019)

Targets

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Binding Properties

×

Property	Measurement	pH	Temperature (°C)	References
IC 50 (nM)	6	N/A	N/A	A28221
IC 50 (nM)	13	N/A	N/A	A27467

Details

Binding Properties1. 3-hydroxy-3-methylglutaryl-coenzyme A reductase

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Nadph binding

Specific Function

Transmembrane glycoprotein that is the rate-limiting enzyme in cholesterol biosynthesis as well as in the biosynthesis of nonsterol isoprenoids that are essential for normal cell function including...

Gene Name

HMGCR

Uniprot ID

P04035

Uniprot Name

3-hydroxy-3-methylglutaryl-coenzyme A reductase

Molecular Weight

97475.155 Da

References

1. Davidson MH: Rosuvastatin: a highly efficacious statin for the treatment of dyslipidaemia. Expert Opin Investig Drugs. 2002 Mar;11(3):125-41. [Article]
2. Jafari M, Ebrahimi R, Ahmadi-Kashani M, Balian H, Bashir M: Efficacy of alternate-day dosing versus daily dosing of atorvastatin. J Cardiovasc Pharmacol Ther. 2003 Jun;8(2):123-6. [Article]
3. Baxter JD, Webb P, Grover G, Scanlan TS: Selective activation of thyroid hormone signaling pathways by GC-1: a new approach to controlling cholesterol and body weight. Trends Endocrinol Metab. 2004 May-Jun;15(4):154-7. [Article]
4. Maejima T, Yamazaki H, Aoki T, Tamaki T, Sato F, Kitahara M, Saito Y: Effect of pitavastatin on apolipoprotein A-I production in HepG2 cell. Biochem Biophys Res Commun. 2004 Nov 12;324(2):835-9. [Article]
5. Bosel J, Gandor F, Harms C, Synowitz M, Harms U, Djoufack PC, Megow D, Dirnagl U, Hortnagl H, Fink KB, Endres M: Neuroprotective effects of atorvastatin against glutamate-induced excitotoxicity in primary cortical neurones. J Neurochem. 2005 Mar;92(6):1386-98. [Article]
6. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]

Details2. Dipeptidyl peptidase 4

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Inhibitor

General Function

Virus receptor activity

Specific Function

Cell surface glycoprotein receptor involved in the costimulatory signal essential for T-cell receptor (TCR)-mediated T-cell activation. Acts as a positive regulator of T-cell coactivation, by bindi...

Gene Name

DPP4

Uniprot ID

P27487

Uniprot Name

Dipeptidyl peptidase 4

Molecular Weight

88277.935 Da

References

1. Taldone T, Zito SW, Talele TT: Inhibition of dipeptidyl peptidase-IV (DPP-IV) by atorvastatin. Bioorg Med Chem Lett. 2008 Jan 15;18(2):479-84. Epub 2007 Dec 3. [Article]

Details3. Aryl hydrocarbon receptor

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Agonist

General Function

Transcription regulatory region dna binding

Specific Function

Ligand-activated transcriptional activator. Binds to the XRE promoter region of genes it activates. Activates the expression of multiple phase I and II xenobiotic chemical metabolizing enzyme genes...

Gene Name

AHR

Uniprot ID

P35869

Uniprot Name

Aryl hydrocarbon receptor

Molecular Weight

96146.705 Da

References

1. Hu W, Sorrentino C, Denison MS, Kolaja K, Fielden MR: Induction of cyp1a1 is a nonspecific biomarker of aryl hydrocarbon receptor activation: results of large scale screening of pharmaceuticals and toxicants in vivo and in vitro. Mol Pharmacol. 2007 Jun;71(6):1475-86. Epub 2007 Feb 27. [Article]
2. Chauvin B, Drouot S, Barrail-Tran A, Taburet AM: Drug-drug interactions between HMG-CoA reductase inhibitors (statins) and antiviral protease inhibitors. Clin Pharmacokinet. 2013 Oct;52(10):815-31. doi: 10.1007/s40262-013-0075-4. [Article]
3. Korhonova M, Doricakova A, Dvorak Z: Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. PLoS One. 2015 Sep 14;10(9):e0137720. doi: 10.1371/journal.pone.0137720. eCollection 2015. [Article]

Details4. Histone deacetylase 2

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Inhibitor

General Function

Transcription factor binding

Specific Function

Responsible for the deacetylation of lysine residues on the N-terminal part of the core histones (H2A, H2B, H3 and H4). Histone deacetylation gives a tag for epigenetic repression and plays an impo...

Gene Name

HDAC2

Uniprot ID

Q92769

Uniprot Name

Histone deacetylase 2

Molecular Weight

55363.855 Da

References

1. Lin YC, Lin JH, Chou CW, Chang YF, Yeh SH, Chen CC: Statins increase p21 through inhibition of histone deacetylase activity and release of promoter-associated HDAC1/2. Cancer Res. 2008 Apr 1;68(7):2375-83. doi: 10.1158/0008-5472.CAN-07-5807. [Article]

Details5. Nuclear receptor subfamily 1 group I member 3

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Ligand

General Function

Zinc ion binding

Specific Function

Binds and transactivates the retinoic acid response elements that control expression of the retinoic acid receptor beta 2 and alcohol dehydrogenase 3 genes. Transactivates both the phenobarbital re...

Gene Name

NR1I3

Uniprot ID

Q14994

Uniprot Name

Nuclear receptor subfamily 1 group I member 3

Molecular Weight

39942.145 Da

References

1. Rezen T, Hafner M, Kortagere S, Ekins S, Hodnik V, Rozman D: Rosuvastatin and Atorvastatin Are Ligands of the Human Constitutive Androstane Receptor/Retinoid X Receptor alpha Complex. Drug Metab Dispos. 2017 Aug;45(8):974-976. doi: 10.1124/dmd.117.075523. Epub 2017 May 23. [Article]

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Drug created at June 13, 2005 13:24 / Updated at February 20, 2024 23:55