Rosuvastatin

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Identification

Summary

Rosuvastatin 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

Crestor, Ezallor, Roszet

Generic Name

Rosuvastatin

DrugBank Accession Number

DB01098

Background

Rosuvastatin, also known as the brand name product Crestor, is a lipid-lowering drug that belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage elevated lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase,²⁴ which catalyzes the conversion of HMG-CoA to mevalonic acid and 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.^15,21

Rosuvastatin and other drugs from the statin class of medications including atorvastatin, pravastatin, simvastatin, fluvastatin, and lovastatin are considered first-line options for the treatment of dyslipidemia.^15,21 This 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.¹⁴ Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.^15,38 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.^{16,17,18,26,31,42} 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.^15,21 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.^19,20

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% decreases in LDL cholesterol levels, which is about three-fold more potent than atorvastatin's effects on LDL cholesterol.^22,4 However, the results of the SATURN trial²⁶ concluded that despite this difference in potency, there was no difference in their effect on the progression of coronary atherosclerosis.

Rosuvastatin is also a unique member of the class of statins due to its high hydrophilicity which increases hepatic uptake at the site of action, low bioavailability, and minimal metabolism via the Cytochrome P450 system.³⁷ This last point results in less risk of drug-drug interactions compared to atorvastatin, lovastatin, and simvastatin, which are all extensively metabolized by Cytochrome P450 (CYP) 3A4, an enzyme involved in the metabolism of many commonly used drugs.²⁹ Drugs such as ciclosporin, gemfibrozil, and some antiretrovirals are more likely to interact with this statin through antagonism of OATP1B1 organic anion transporter protein 1B1-mediated hepatic uptake of rosuvastatin.^46,47

Type

Small Molecule

Groups

Approved

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Rosuvastatin (DB01098)

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Weight

Average: 481.538
Monoisotopic: 481.168284538

Chemical Formula

C₂₂H₂₈FN₃O₆S

Synonyms

• (3R,5S,6E)-7-(4-(4-fluorophenyl)-6-(1-methylethyl)-2-(ethyl(methylsulfonyl)amino)-5-pyrimidinyl)-3,5-dihydroxy-6-heptenoic acid
• (3R,5S,6E)-7-{4-(4-fluorophenyl)-6-isopropyl-2-[methyl(methylsulfonyl)amino]pyrimidin-5-yl}-3,5-dihydroxyhept-6-enoic acid
• Rosuvastatin
• Rosuvastatina

External IDs

• ZD-4522
• ZD4522

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Pharmacology

Indication

The FDA monograph states that rosuvastatin is indicated as an adjunct to diet in the treatment of triglyceridemia, Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia), and Homozygous Familial Hypercholesterolemia.⁴⁶

The Health Canada monograph for rosuvastatin further specifies that rosuvastatin is indicated for the reduction of elevated total cholesterol (Total-C), LDL-C, ApoB, the Total-C/HDL-C ratio and triglycerides (TG) and for increasing HDL-C in hyperlipidemic and dyslipidemic conditions when response to diet and exercise alone has been inadequate. It is also indicated for the prevention of major cardiovascular events (including risk of myocardial infarction, nonfatal stroke, and coronary artery revascularization) in adult patients without documented history of cardiovascular or cerebrovascular events, but with at least two conventional risk factors for cardiovascular disease.⁴⁷

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.^15,21

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Management of	Atherosclerosis		••••••••••••
Prevention of	Atherosclerotic cardiovascular disease		••••••••••••
Prevention of	Cardiovascular disease		••••••••••••
Used in combination to prevent	Cardiovascular events	Combination Product in combination with: Acetylsalicylic acid (DB00945)	••••••••••••		•••• •••••••••••••• ••••	••••••• ••••••••••••
Used in combination to prevent	Cardiovascular events	Combination Product in combination with: Amlodipine (DB00381)	••••••••••••			••••••• ••••••

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Associated Therapies

• Lipid-Lowering Therapy
• Primary Prevention of Cardiovascular Diseases

Contraindications & Blackbox Warnings

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Pharmacodynamics

Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. 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.^15,21

Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.¹⁵ 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.^{16,17,18,26,31} 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.^15,21 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.^19,20

Skeletal Muscle Effects

Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. These risks can occur at any dose level, but are increased at the highest dose (40 mg). Rosuvastatin should be prescribed with caution in patients with predisposing factors for myopathy (e.g., age ≥ 65 years, inadequately treated hypothyroidism, renal impairment).

The risk of myopathy during treatment with rosuvastatin may be increased with concurrent administration of some other lipid-lowering therapies (such as fenofibrate or niacin), gemfibrozil, cyclosporine, atazanavir/ritonavir, lopinavir/ritonavir, or simeprevir. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors, including rosuvastatin, coadministered with colchicine, and caution should therefore be exercised when prescribing these two medications together.⁴⁶

Real-world data from observational studies has suggested that 10-15% of people taking statins may experience muscle aches at some point during treatment.⁴¹

Liver Enzyme Abnormalities

Increases in serum transaminases have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. In most cases, the elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy. There were two cases of jaundice, for which a relationship to rosuvastatin therapy could not be determined, which resolved after discontinuation of therapy. There were no cases of liver failure or irreversible liver disease in these trials.⁴⁶

Endocrine Effects

Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including rosuvastatin calcium tablets. Based on clinical trial data with rosuvastatin, in some instances these increases may exceed the threshold for the diagnosis of diabetes mellitus.⁴⁶

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.⁴⁰

HMG-CoA reductase inhibitors interfere with cholesterol synthesis and lower cholesterol levels and, as such, might theoretically blunt adrenal or gonadal steroid hormone production. Rosuvastatin demonstrated no effect upon nonstimulated cortisol levels and no effect on thyroid metabolism as assessed by TSH plasma concentration. In rosuvastatin treated patients, there was no impairment of adrenocortical reserve and no reduction in plasma cortisol concentrations. Clinical studies with other HMG-CoA reductase inhibitors have suggested that these agents do not reduce plasma testosterone concentration. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied. The effects, if any, on the pituitarygonadal axis in premenopausal women are unknown.⁴⁷

Cardiovascular

Ubiquinone levels were not measured in rosuvastatin clinical trials, however significant decreases in circulating ubiquinone levels in patients treated with 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.⁴⁷

Lipoprotein A

In some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by a concomitant increase in the Lipoprotein(a) [Lp(a)] concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for coronary heart disease. It is thus desirable to maintain and reinforce lifestyle changes in high-risk patients placed on rosuvastatin therapy.⁴⁷ 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.²³

Mechanism of action

Rosuvastatin 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.²⁴ Rosuvastatin 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. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL).⁴⁶ The overall effect is a decrease in plasma LDL and VLDL.

In vitro and in vivo animal studies also demonstrate that rosuvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins.²⁵ 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.³⁹

Rosuvastatin exerts an anti-inflammatory effect on rat mesenteric microvascular endothelium by attenuating leukocyte rolling, adherence and transmigration.¹¹ The drug also modulates nitric oxide synthase (NOS) expression and reduces ischemic-reperfusion injuries in rat hearts.¹ Rosuvastatin increases the bioavailability of nitric oxide^11,7,1 by upregulating NOS³ and by increasing the stability of NOS through post-transcriptional polyadenylation.⁶ It is unclear as to how rosuvastatin brings about these effects though they may be due to decreased concentrations of mevalonic acid.

Target	Actions	Organism
A3-hydroxy-3-methylglutaryl-coenzyme A reductase	inhibitor	Humans
UIntegrin alpha-L	inhibitory allosteric modulator	Humans

Absorption

In a study of healthy white male volunteers, the absolute oral bioavailability of rosuvastatin was found to be approximately 20% while absorption was estimated to be 50%, which is consistent with a substantial first-pass effect after oral dosing.^27,28 Another study in healthy volunteers found that the peak plasma concentration (Cmax) of rosuvastatin was 6.06ng/mL and was reached at a median of 5 hours following oral dosing.³⁰ Both Cmax and AUC increased in approximate proportion to dose. Neither food nor evening versus morning administration was shown to have an effect on the AUC of rosuvastatin.^46,47 Many statins are known to interact with hepatic uptake transporters and thus reach high concentrations at their site of action in the liver.

Breast Cancer Resistance Protein (BCRP) is a membrane-bound protein that plays an important role in the absorption of rosuvastatin, particularly as CYP3A4 has minimal involvement in its metabolism.²⁹ 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 2.4-fold higher AUC and Cmax values for rosuvastatin 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.^32,33 Other statin drugs impacted by this polymorphism include fluvastatin and atorvastatin.³²

Genetic differences in the OATP1B1 (organic-anion-transporting polypeptide 1B1) hepatic transporter have also been shown to impact rosuvastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C SNP showed that rosuvastatin AUC was increased 1.62-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals.³⁶ Other statin drugs impacted by this polymorphism include simvastatin, pitavastatin, atorvastatin, and pravastatin.²⁹

For patients known to have the above-mentioned c.421AA BCRP or c.521CC OATP1B1 genotypes, a maximum daily dose of 20mg of rosuvastatin is recommended to avoid adverse effects from the increased exposure to the drug, such as muscle pain and risk of rhabdomyolysis.⁴⁷

Volume of distribution

Rosuvastatin undergoes first-pass extraction in the liver, which is the primary site of cholesterol synthesis and LDL-C clearance. The mean volume of distribution at steady-state of rosuvastatin is approximately 134 litres.^46,47

Protein binding

Rosuvastatin is 88% bound to plasma proteins, mostly albumin. This binding is reversible and independent of plasma concentrations.^46,47

Metabolism

Rosuvastatin is not extensively metabolized, as demonstrated by the small amount of radiolabeled dose that is recovered as a metabolite (~10%). Cytochrome P450 (CYP) 2C9 is primarily responsible for the formation of rosuvastatin's major metabolite, N-desmethylrosuvastatin, which has approximately 20-50% of the pharmacological activity of its parent compound in vitro.^46,47 However, this metabolic pathway isn't deemed to be clinically significant as there were no observable effects found on rosuvastatin pharmacokinetics when rosuvastatin was coadministered with fluconazole, a potent CYP2C9 inhibitor.³⁴

In vitro and in vivo data indicate that rosuvastatin has no clinically significant cytochrome P450 interactions (as substrate, inhibitor or inducer). Consequently, there is little potential for drug-drug interactions upon coadministration with agents that are metabolized by cytochrome P450.⁴⁷

Hover over products below to view reaction partners

• Rosuvastatin
  • N-Desmethylrosuvastatin
  • Rosuvastatin 5 S-lactone

Route of elimination

Rosuvastatin is not extensively metabolized; approximately 10% of a radiolabeled dose is recovered as metabolite. Following oral administration, rosuvastatin and its metabolites are primarily excreted in the feces (90%). After an intravenous dose, approximately 28% of total body clearance was via the renal route, and 72% by the hepatic route.^46,47,27

A study in healthy adult male volunteers found that approximately 90% of the rosuvastatin dose was recovered in feces within 72 hours after dose, while the remaining 10% was recovered in urine. The drug was completely excreted from the body after 10 days of dosing. They also found that approximately 76.8% of the excreted dose was unchanged from the parent compound, with the remaining dose recovered as the metabolites n-desmethyl rosuvastatin and rosuvastatin-5S-lactone.³⁰

Renal tubular secretion is responsible for >90% of total renal clearance, and is believed to be mediated primarily by the uptake transporter OAT3 (Organic anion transporter 1), while OAT1 had minimal involvement.³⁵

Half-life

The elimination half-life (t½) of rosuvastatin is approximately 19 hours and does not increase with increasing doses.^46,47

Clearance

Not Available

Adverse Effects

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Toxicity

Generally well-tolerated. Side effects may include myalgia, constipation, asthenia, abdominal pain, and nausea. Other possible side effects include myotoxicity (myopathy, myositis, rhabdomyolysis) and hepatotoxicity. To avoid toxicity in Asian patients, lower doses should be considered. Pharmacokinetic studies show an approximately two-fold increase in peak plasma concentration and AUC in Asian patients (Philippino, Chinese, Japanese, Korean, Vietnamese, or Asian-Indian descent) compared to Caucasian patients.

Pathways

Pathway	Category
Rosuvastatin Action Pathway	Drug action

Pharmacogenomic Effects/ADRs

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 rosuvastatin.	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 rosuvastatin.	Details
ATP-binding cassette sub-family G member 2	---	(A;A) / (A;C)	G > T	Effect Directly Studied	Patients with this genotype have a greater reduction in LDL cholesterol with rosuvastatin.	Details

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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Abametapir	The serum concentration of Rosuvastatin can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Rosuvastatin can be increased when combined with Abatacept.
Abemaciclib	The metabolism of Abemaciclib can be decreased when combined with Rosuvastatin.
Abrocitinib	The metabolism of Abrocitinib can be decreased when combined with Rosuvastatin.
Acalabrutinib	The metabolism of Acalabrutinib can be decreased when combined with Rosuvastatin.

Food Interactions

• Take with or without food. Co-administration with food does not affect absorption.

Products

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Rosuvastatin calcium	83MVU38M7Q	147098-20-2	LALFOYNTGMUKGG-JGMJEEPBSA-L
Rosuvastatin zinc	70VE4E19Z7	953412-08-3	KUQHZGJLQWUFPU-BGRFNVSISA-L

Product Images

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International/Other Brands

Astende (Lazar (Argentina)) / Cirantan (AstraZeneca (Netherlands)) / Cresadex (Drugtech (Chile)) / Provisacor (AstraZeneca (Italy, Netherlands) ) / Razel (Glenmark (India)) / Rosedex (Roux-Ocefa (Argentina)) / Rosimol (Sandoz (Argentina)) / Rosumed (Labomed (Chile)) / Rosustatin (Montpellier (Argentina)) / Rosuvas (Ranbaxy (India)) / Rosuvast (Bago (Argentina)) / Rosvel (Laboratorios Chile (Chile)) / Rovartal (Roemmers (Argentina)) / Simestat (Simesa (Italy)) / Sinlip (Gador (Argentina)) / Visacor (AstraZeneca (Portugal)) / Vivacor (AstraZeneca (Brazil))

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Act Rosuvastatin	Tablet	40 mg	Oral	Actavis Pharma Company	2012-03-16	2019-07-09
Act Rosuvastatin	Tablet	5 mg	Oral	Actavis Pharma Company	2012-03-16	2019-07-09
Act Rosuvastatin	Tablet	20 mg	Oral	Actavis Pharma Company	2012-03-16	2019-07-09
Act Rosuvastatin	Tablet	10 mg	Oral	Actavis Pharma Company	2012-03-16	2019-07-09
Crestor	Tablet, film coated	10 mg/1	Oral	bryant ranch prepack	2003-08-18	Not applicable

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Ach-rosuvastatin	Tablet	10 mg	Oral	Accord Healthcare, S.L.U.	2019-05-23	Not applicable
Ach-rosuvastatin	Tablet	40 mg	Oral	Accord Healthcare, S.L.U.	2019-05-23	Not applicable
Ach-rosuvastatin	Tablet	5 mg	Oral	Accord Healthcare, S.L.U.	2019-05-23	Not applicable
Ach-rosuvastatin	Tablet	20 mg	Oral	Accord Healthcare, S.L.U.	2019-05-23	Not applicable
Ag-rosuvastatin	Tablet	10 mg	Oral	Angita Pharma Inc.	2018-12-28	2024-07-09

Mixture Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
ACIDO FENOFIBRICO / ROSUVASTATINA 135 MG/10 MG	Rosuvastatin calcium (10 mg) + Fenofibrate (135 mg)	Capsule, coated	Oral	TECNOQUIMICAS S.A.	2019-03-19	Not applicable
Arosuva plus Ezetimib 10 mg/10 mg Filmtabletten	Rosuvastatin (10 mg) + Ezetimibe (10 mg)	Tablet, film coated	Oral	Gebro Pharma Gmb H	2019-11-04	Not applicable
Arosuva plus Ezetimib 20 mg/10 mg Filmtabletten	Rosuvastatin (20 mg) + Ezetimibe (10 mg)	Tablet, film coated	Oral	Gebro Pharma Gmb H	2019-11-04	Not applicable
Arosuva plus Ezetimib 40 mg/10 mg Filmtabletten	Rosuvastatin (40 mg) + Ezetimibe (10 mg)	Tablet, film coated	Oral	Gebro Pharma Gmb H	2019-11-04	Not applicable
Arosuva plus Ezetimib 5 mg/10 mg Filmtabletten	Rosuvastatin (5 mg) + Ezetimibe (10 mg)	Tablet, film coated	Oral	Gebro Pharma Gmb H	2019-11-04	Not applicable

Categories

ATC Codes

C10BX10 — Rosuvastatin and valsartan

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

C10BX05 — Rosuvastatin and acetylsalicylic acid

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

C10BX07 — Rosuvastatin, amlodipine and lisinopril

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

C10AA07 — Rosuvastatin

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

A10BH52 — Gemigliptin and rosuvastatin

• A10BH — Dipeptidyl peptidase 4 (DPP-4) inhibitors
• A10B — BLOOD GLUCOSE LOWERING DRUGS, EXCL. INSULINS
• A10 — DRUGS USED IN DIABETES
• A — ALIMENTARY TRACT AND METABOLISM

G01AE10 — Combinations of sulfonamides

• G01AE — Sulfonamides
• G01A — ANTIINFECTIVES AND ANTISEPTICS, EXCL. COMBINATIONS WITH CORTICOSTEROIDS
• G01 — GYNECOLOGICAL ANTIINFECTIVES AND ANTISEPTICS
• G — GENITO URINARY SYSTEM AND SEX HORMONES

C10BX13 — Rosuvastatin, perindopril and indapamide

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

C10BX09 — Rosuvastatin and amlodipine

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

C10BA09 — Rosuvastatin and fenofibrate

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

C10BX20 — Rosuvastatin and telmisartan

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

C10BX21 — Rosuvastatin and perindopril

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

C10BX16 — Rosuvastatin and fimasartan

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

C10BX17 — Rosuvastatin and ramipril

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

C10BX14 — Rosuvastatin, amlodipine and perindopril

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

C10BA06 — Rosuvastatin and ezetimibe

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

Drug Categories

• Agents Causing Muscle Toxicity
• Alimentary Tract and Metabolism
• Amides
• Anticholesteremic Agents
• BCRP/ABCG2 Substrates
• BSEP/ABCB11 Substrates
• Cytochrome P-450 CYP2C9 Substrates
• Cytochrome P-450 CYP3A Inhibitors
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A4 Substrates (strength unknown)
• Cytochrome P-450 CYP3A5 Inhibitors
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Drugs Used in Diabetes
• Enzyme Inhibitors
• Fluorobenzenes
• Genito Urinary System and Sex Hormones
• Gynecological Antiinfectives and Antiseptics
• Hydrocarbons, Fluorinated
• Hydrocarbons, Halogenated
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Hypolipidemic Agents
• Hypolipidemic Agents Indicated for Hyperlipidemia
• Lipid Modifying Agents
• Lipid Modifying Agents, Plain
• Lipid Regulating Agents
• OAT3/SLC22A8 Inhibitors
• OAT3/SLC22A8 Substrates
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B1/SLCO1B1 Substrates
• Pyrimidines
• Sulfonamides
• Sulfones
• Sulfur Compounds

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as phenylpyrimidines. These are polycyclic aromatic compounds containing a benzene ring linked to a pyrimidine ring through a CC or CN bond. Pyrimidine is a 6-membered ring consisting of four carbon atoms and two nitrogen centers at the 1- and 3- ring positions.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Diazines

Sub Class

Pyrimidines and pyrimidine derivatives

Direct Parent

Phenylpyrimidines

Alternative Parents

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 / Aryl fluorides / Unsaturated fatty acids / Organosulfonamides / Organic sulfonamides / Heteroaromatic compounds / Aminosulfonyl compounds / Secondary alcohols / Azacyclic compounds / Carboxylic acids / Monocarboxylic acids and derivatives / Organonitrogen compounds / Hydrocarbon derivatives / Organopnictogen compounds / Carbonyl compounds / Organofluorides / Organic oxides

show 13 more

Substituents

4-phenylpyrimidine / 5-phenylpyrimidine / Alcohol / Aminosulfonyl compound / Aromatic heteromonocyclic 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 / Organic sulfonic acid amide / Organic sulfonic acid or derivatives / Organofluoride / Organohalogen compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Organosulfonic acid amide / Organosulfonic acid or derivatives / Organosulfur compound / Secondary alcohol / Sulfonyl / Unsaturated fatty acid

show 33 more

Molecular Framework

Aromatic heteromonocyclic compounds

External Descriptors

statin (synthetic), sulfonamide, pyrimidines, dihydroxy monocarboxylic acid, monofluorobenzenes (CHEBI:38545)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

413KH5ZJ73

CAS number

287714-41-4

InChI Key

BPRHUIZQVSMCRT-VEUZHWNKSA-N

InChI

InChI=1S/C22H28FN3O6S/c1-13(2)20-18(10-9-16(27)11-17(28)12-19(29)30)21(14-5-7-15(23)8-6-14)25-22(24-20)26(3)33(4,31)32/h5-10,13,16-17,27-28H,11-12H2,1-4H3,(H,29,30)/b10-9+/t16-,17-/m1/s1

IUPAC Name

(3R,5S,6E)-7-[4-(4-fluorophenyl)-2-(N-methylmethanesulfonamido)-6-(propan-2-yl)pyrimidin-5-yl]-3,5-dihydroxyhept-6-enoic acid

SMILES

CC(C)C1=NC(=NC(C2=CC=C(F)C=C2)=C1\C=C\[C@@H](O)C[C@@H](O)CC(=O)O)N(C)S(C)(=O)=O

References

Synthesis Reference

Valerie Niddam-Hildesheim, Greta Sterimbaum, "Process for preparation of rosuvastatin calcium." U.S. Patent US20050080134, issued April 14, 2005.

US20050080134

General References

1. Di Napoli P, Taccardi AA, Grilli A, De Lutiis MA, Barsotti A, Felaco M, De Caterina R: Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts. Cardiovasc Res. 2005 Jun 1;66(3):462-71. Epub 2005 Mar 2. [Article]
2. Everett BM, Glynn RJ, MacFadyen JG, Ridker PM: Rosuvastatin in the prevention of stroke among men and women with elevated levels of C-reactive protein: justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER). Circulation. 2010 Jan 5;121(1):143-50. doi: 10.1161/CIRCULATIONAHA.109.874834. Epub 2009 Dec 21. [Article]
3. Jones SP, Gibson MF, Rimmer DM 3rd, Gibson TM, Sharp BR, Lefer DJ: Direct vascular and cardioprotective effects of rosuvastatin, a new HMG-CoA reductase inhibitor. J Am Coll Cardiol. 2002 Sep 18;40(6):1172-8. [Article]
4. 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]
5. Kilic E, Kilic U, Matter CM, Luscher TF, Bassetti CL, Hermann DM: Aggravation of focal cerebral ischemia by tissue plasminogen activator is reversed by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor but does not depend on endothelial NO synthase. Stroke. 2005 Feb;36(2):332-6. Epub 2004 Dec 29. [Article]
6. Kosmidou I, Moore JP, Weber M, Searles CD: Statin treatment and 3' polyadenylation of eNOS mRNA. Arterioscler Thromb Vasc Biol. 2007 Dec;27(12):2642-9. Epub 2007 Oct 4. [Article]
7. Laufs U, Gertz K, Dirnagl U, Bohm M, Nickenig G, Endres M: Rosuvastatin, a new HMG-CoA reductase inhibitor, upregulates endothelial nitric oxide synthase and protects from ischemic stroke in mice. Brain Res. 2002 Jun 28;942(1-2):23-30. [Article]
8. McKillop T: The statin wars. Lancet. 2003 Nov 1;362(9394):1498. [Article]
9. McTaggart F, Buckett L, Davidson R, Holdgate G, McCormick A, Schneck D, Smith G, Warwick M: Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Am J Cardiol. 2001 Mar 8;87(5A):28B-32B. [Article]
10. Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, Davignon J, Erbel R, Fruchart JC, Tardif JC, Schoenhagen P, Crowe T, Cain V, Wolski K, Goormastic M, Tuzcu EM: Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA. 2006 Apr 5;295(13):1556-65. Epub 2006 Mar 13. [Article]
11. Stalker TJ, Lefer AM, Scalia R: A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid. Br J Pharmacol. 2001 Jun;133(3):406-12. [Article]
12. Authors unspecified: The statin wars: why AstraZeneca must retreat. Lancet. 2003 Oct 25;362(9393):1341. [Article]
13. Ho RH, Tirona RG, Leake BF, Glaeser H, Lee W, Lemke CJ, Wang Y, Kim RB: Drug and bile acid transporters in rosuvastatin hepatic uptake: function, expression, and pharmacogenetics. Gastroenterology. 2006 May;130(6):1793-806. Epub 2006 Mar 6. [Article]
14. 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]
15. 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]
16. 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]
17. 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]
18. 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]
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. 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]
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. 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]
24. 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]
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. 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]
27. Martin PD, Warwick MJ, Dane AL, Brindley C, Short T: Absolute oral bioavailability of rosuvastatin in healthy white adult male volunteers. Clin Ther. 2003 Oct;25(10):2553-63. [Article]
28. Birmingham BK, Bujac SR, Elsby R, Azumaya CT, Zalikowski J, Chen Y, Kim K, Ambrose HJ: Rosuvastatin pharmacokinetics and pharmacogenetics in Caucasian and Asian subjects residing in the United States. Eur J Clin Pharmacol. 2015 Mar;71(3):329-40. doi: 10.1007/s00228-014-1800-0. Epub 2015 Jan 30. [Article]
29. 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]
30. Martin PD, Warwick MJ, Dane AL, Hill SJ, Giles PB, Phillips PJ, Lenz E: Metabolism, excretion, and pharmacokinetics of rosuvastatin in healthy adult male volunteers. Clin Ther. 2003 Nov;25(11):2822-35. [Article]
31. 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]
32. 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]
33. 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]
34. Cooper KJ, Martin PD, Dane AL, Warwick MJ, Schneck DW, Cantarini MV: The effect of fluconazole on the pharmacokinetics of rosuvastatin. Eur J Clin Pharmacol. 2002 Nov;58(8):527-31. doi: 10.1007/s00228-002-0508-8. Epub 2002 Oct 3. [Article]
35. Windass AS, Lowes S, Wang Y, Brown CD: The contribution of organic anion transporters OAT1 and OAT3 to the renal uptake of rosuvastatin. J Pharmacol Exp Ther. 2007 Sep;322(3):1221-7. doi: 10.1124/jpet.107.125831. Epub 2007 Jun 21. [Article]
36. 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]
37. Kostapanos MS, Milionis HJ, Elisaf MS: Rosuvastatin-associated adverse effects and drug-drug interactions in the clinical setting of dyslipidemia. Am J Cardiovasc Drugs. 2010;10(1):11-28. doi: 10.2165/13168600-000000000-00000. [Article]
38. 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]
39. 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]
40. 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]
41. 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]
42. 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]
43. Crestor (Rosuvastatin Calcium) FDA Label [Link]
44. FDA Approved Drug Products: Crestor (rosuvastatin) tablets for oral use (July 2023) [Link]
45. FDA Approved Drug Products: Ezallor Sprinkle (rosuvastatin) capsules for oral use [Link]
46. FDA Label - Rosuvastatin [File]
47. Health Canada Monograph - Rosuvastatin [File]

External Links

Human Metabolome Database

HMDB0015230

KEGG Drug

D08492

PubChem Compound

446157

PubChem Substance

46509022

ChemSpider

393589

BindingDB

18372

RxNav

301542

ChEBI

38545

ChEMBL

CHEMBL1496

ZINC

ZINC000001535101

Therapeutic Targets Database

DAP000555

PharmGKB

PA134308647

PDBe Ligand

FBI

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

Wikipedia

Rosuvastatin

MSDS

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Clinical Trials

Clinical Trials

Clinical Trial & Rare Diseases Add-on Data Package

Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package

Phase	Status	Purpose	Conditions	Count	Start Date	Why Stopped	100+ additional columns
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Not Available	Active Not Recruiting	Not Available	Dyslipidemia	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Dyslipidemia / Hypertension	1	somestatus	stop reason	just information to hide
Not Available	Active Not Recruiting	Not Available	Hyperlipidemias / Hypertension	1	somestatus	stop reason	just information to hide
Not Available	Available	Not Available	Cardiovascular Disease (CVD) / Diabetes	1	somestatus	stop reason	just information to hide
Not Available	Available	Not Available	Hyperlipidemias	1	somestatus	stop reason	just information to hide

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Pharmacoeconomics

Manufacturers

Not Available

Packagers

• A-S Medication Solutions LLC
• AstraZeneca Inc.
• Bryant Ranch Prepack
• Cardinal Health
• Corden Pharma GmbH
• IPR Pharmaceuticals Inc.
• Lake Erie Medical and Surgical Supply
• Murfreesboro Pharmaceutical Nursing Supply
• Nucare Pharmaceuticals Inc.
• PD-Rx Pharmaceuticals Inc.
• Physicians Total Care Inc.
• Prepak Systems Inc.
• Remedy Repack
• Resource Optimization and Innovation LLC
• Southwood Pharmaceuticals

Dosage Forms

Form	Route	Strength
Tablet		5 mg
Tablet, coated	Oral	10 mg
Tablet, coated	Oral	20 mg
Tablet, film coated	Oral
Tablet, effervescent	Oral
Tablet, film coated	Oral	20.84 mg
Tablet	Oral; Sublingual	20 mg
Tablet, effervescent		10 mg
Tablet, effervescent		20 mg
Tablet, effervescent		40 mg
Tablet, effervescent
Tablet	Oral	10.000 mg
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	5 mg/1
Tablet	Oral	10 mg
Tablet	Oral	20 mg
Tablet	Oral	5 mg
Tablet	Oral	10.0000 mg
Tablet	Oral	40.000 mg
Tablet, coated	Oral	40 mg
Tablet	Oral	20.800 mg
Capsule	Oral	10 mg/1
Capsule	Oral	20 mg/1
Capsule	Oral	40 mg/1
Capsule	Oral	5 mg/1
Tablet, coated	Oral
Capsule, liquid filled	Oral
Tablet	Oral	20.860 mg
Tablet, coated	Oral	10.42 mg
Tablet, film coated	Oral	10419 MG
Tablet, film coated	Oral	20838 MG
Tablet, delayed release	Oral	10 mg
Tablet, coated	Oral	41.58 mg
Capsule	Oral	10.400 mg
Tablet	Oral	10.000 mg
Tablet	Oral	10.00 mg
Tablet	Oral
Tablet, film coated	Oral
Tablet, film coated	Oral	10.00 mg
Tablet, film coated	Oral	5.00 mg
Tablet, coated	Oral	30 MG
Tablet, coated	Oral	10.4 mg
Tablet, film coated	Oral	10.419 MG
Tablet, film coated	Oral	20.838 MG
Tablet	Oral	10.0 mg
Tablet	Oral	20.0 mg
Tablet	Oral	40.0 mg
Tablet	Oral	5.0 mg
Tablet	Oral	10 mg/1
Tablet	Oral	20 mg/1
Tablet	Oral	40 mg/1
Tablet	Oral	5 mg/1
Tablet, coated	Oral	10 mg/1
Tablet, coated	Oral	20 mg/1
Tablet, coated	Oral	40 mg/1
Tablet, coated	Oral	5 mg/1
Tablet, film coated	Oral	10.42 MG
Tablet, film coated	Oral	10.51 MG
Tablet, film coated	Oral	21.02 MG
Tablet, film coated	Oral	22.04 MG
Tablet, film coated	Oral	44.08 MG
Tablet, film coated	Oral	10.000 mg
Tablet, film coated	Oral	20.000 mg
Tablet, coated	Oral	1000000 mg
Capsule, liquid filled	Oral	2000000 mg
Tablet, coated	Oral	2000000 mg
Tablet, film coated	Oral	15 MG
Tablet, film coated	Oral	30 MG
Tablet, film coated	Oral	40 MG
Tablet, film coated	Oral	5 MG
Tablet	Oral	41.66 mg
Tablet, coated	Oral	4000000 mg
Tablet	Oral	40 mg
Tablet		20 mg
Tablet	Oral	10.400 mg
Tablet, film coated	Oral	42.04 MG
Tablet, film coated	Oral	10395 MG
Tablet, film coated	Oral	20.79 MG
Capsule, liquid filled	Oral	5 mg
Capsule, liquid filled	Oral	10 mg
Capsule, liquid filled	Oral	20 mg
Capsule, liquid filled	Oral	40 mg
Tablet, coated	Oral	20.84 mg
Tablet	Oral	10.400 mg
Tablet, film coated	Oral	21.4 MG
Tablet, film coated	Oral	10.4 MG
Tablet, film coated	Oral	20.8 MG
Tablet, film coated	Oral	41.58 MG
Tablet, film coated	Oral	41.6 MG
Tablet, coated	Oral	5 mg
Tablet	Oral	20.000 mg
Tablet, film coated	Oral	11.02 MG
Tablet, film coated	Oral	11 Mg
Tablet, film coated	Oral	22 Mg
Capsule, coated	Oral
Capsule, coated	Oral	20 mg
Capsule	Oral
Tablet	Oral	200.000 mg
Tablet	Oral	20.790 mg
Tablet		10 mg
Tablet	Oral
Tablet	Oral	5.200 mg
Tablet, film coated	Oral	10 mg
Tablet, film coated	Oral	20 mg

Prices

Unit description	Cost	Unit
Crestor 40 mg tablet	4.7USD	tablet
Crestor 20 mg tablet	4.69USD	tablet
Crestor 10 mg tablet	4.68USD	tablet
Crestor 5 mg tablet	4.68USD	tablet
Crestor 40 mg Tablet	2.24USD	tablet
Crestor 20 mg Tablet	1.91USD	tablet
Crestor 10 mg Tablet	1.53USD	tablet
Crestor 5 mg Tablet	1.45USD	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
CA2315141	No	2009-08-18	2020-08-04
CA2072945	No	2001-07-31	2012-07-02
US6858618	Yes	2005-02-22	2022-06-17
US7030152	Yes	2006-04-18	2018-10-02
US7964614	Yes	2011-06-21	2018-10-02
US6316460	Yes	2001-11-13	2021-02-04
USRE37314	Yes	2001-08-07	2016-07-08
US10413543	No	2019-09-17	2036-02-12
US10376470	No	2019-08-13	2033-05-01
US9763885	No	2017-09-19	2033-05-01

Properties

State

Solid

Experimental Properties

Property	Value	Source
water solubility	Sparingly soluble in water	FDA label
logP	0.13	FDA label

Predicted Properties

Property	Value	Source
Water Solubility	0.0886 mg/mL	ALOGPS
logP	1.47	ALOGPS
logP	1.92	Chemaxon
logS	-3.7	ALOGPS
pKa (Strongest Acidic)	4	Chemaxon
pKa (Strongest Basic)	-1.6	Chemaxon
Physiological Charge	-1	Chemaxon
Hydrogen Acceptor Count	8	Chemaxon
Hydrogen Donor Count	3	Chemaxon
Polar Surface Area	140.92 Å2	Chemaxon
Rotatable Bond Count	9	Chemaxon
Refractivity	121.44 m3·mol-1	Chemaxon
Polarizability	48.55 Å3	Chemaxon
Number of Rings	2	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9791
Blood Brain Barrier	-	0.6815
Caco-2 permeable	-	0.5818
P-glycoprotein substrate	Non-substrate	0.6962
P-glycoprotein inhibitor I	Non-inhibitor	0.5099
P-glycoprotein inhibitor II	Non-inhibitor	0.8987
Renal organic cation transporter	Non-inhibitor	0.9467
CYP450 2C9 substrate	Non-substrate	0.5544
CYP450 2D6 substrate	Non-substrate	0.8633
CYP450 3A4 substrate	Non-substrate	0.584
CYP450 1A2 substrate	Non-inhibitor	0.6896
CYP450 2C9 inhibitor	Non-inhibitor	0.5957
CYP450 2D6 inhibitor	Non-inhibitor	0.8609
CYP450 2C19 inhibitor	Non-inhibitor	0.6414
CYP450 3A4 inhibitor	Non-inhibitor	0.8308
CYP450 inhibitory promiscuity	Low CYP Inhibitory Promiscuity	0.6226
Ames test	Non AMES toxic	0.662
Carcinogenicity	Non-carcinogens	0.6578
Biodegradation	Not ready biodegradable	1.0
Rat acute toxicity	2.5599 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.9856
hERG inhibition (predictor II)	Non-inhibitor	0.8117

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	splash10-03dl-4024900000-6da5a329db1ec51e7329
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-001i-0000900000-26b4568a209a0f9ca797
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-067i-5003900000-1e54f4b5c5a578131b66
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-01pk-0003900000-6fc593c80bc67a4f7a62
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-00di-5009400000-d6af550a498ba542b65a
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0h3j-1049100000-d17a79f668861f817ffe
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-057v-7029300000-3d71a257f025972ec7d0
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]-	234.2873326	predicted	DarkChem Lite v0.1.0
[M-H]-	211.98924	predicted	DeepCCS 1.0 (2019)
[M+H]+	235.1144326	predicted	DarkChem Lite v0.1.0
[M+H]+	214.38481	predicted	DeepCCS 1.0 (2019)
[M+Na]+	234.3503326	predicted	DarkChem Lite v0.1.0
[M+Na]+	220.29735	predicted	DeepCCS 1.0 (2019)

Targets

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Binding Properties

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Property	Measurement	pH	Temperature (°C)	References
IC 50 (nM)	5.4	N/A	N/A	A28717
IC 50 (nM)	5	N/A	N/A	A28221
IC 50 (nM)	3.1	N/A	N/A	A28719
Ki (nM)	0.9	N/A	N/A	A28717
Ki (nM)	71000	N/A	N/A	A28717

Details

Binding Properties1. 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. Carbonell T, Freire E: Binding thermodynamics of statins to HMG-CoA reductase. Biochemistry. 2005 Sep 6;44(35):11741-8. [Article]
2. Chapman MJ, Caslake M, Packard C, McTaggart F: New dimension of statin action on ApoB atherogenicity. Clin Cardiol. 2003 Jan;26(1 Suppl 1):I7-10. [Article]
3. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
4. Davidson MH: Rosuvastatin: a highly efficacious statin for the treatment of dyslipidaemia. Expert Opin Investig Drugs. 2002 Jan;11(1):125-41. [Article]
5. Hanefeld M: Clinical rationale for rosuvastatin, a potent new HMG-CoA reductase inhibitor. Int J Clin Pract. 2001 Jul-Aug;55(6):399-405. [Article]
6. Holdgate GA, Ward WH, McTaggart F: Molecular mechanism for inhibition of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase by rosuvastatin. Biochem Soc Trans. 2003 Jun;31(Pt 3):528-31. [Article]
7. McTaggart F, Buckett L, Davidson R, Holdgate G, McCormick A, Schneck D, Smith G, Warwick M: Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Am J Cardiol. 2001 Mar 8;87(5A):28B-32B. [Article]
8. Olsson AG, McTaggart F, Raza A: Rosuvastatin: a highly effective new HMG-CoA reductase inhibitor. Cardiovasc Drug Rev. 2002 Winter;20(4):303-28. [Article]
9. 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]

Details2. Integrin alpha-L

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Inhibitory allosteric modulator

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. Katano H, Pesnicak L, Cohen JI: Simvastatin induces apoptosis of Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines and delays development of EBV lymphomas. Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4960-5. Epub 2004 Mar 23. [Article]
3. 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 June 13, 2005 13:24 / Updated at October 21, 2024 08:50