Simvastatin

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Identification

Summary

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

Brand Names

Cholib, FloLipid, Simcor, Vytorin, Zocor

Generic Name

Simvastatin

DrugBank Accession Number

DB00641

Background

Simvastatin, also known as the brand name product Zocor, is a lipid-lowering drug derived synthetically from a fermentation product of Aspergillus terreus. It belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage abnormal 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,² 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.^3,4

Simvastatin and other drugs from the statin class of medications including atorvastatin, pravastatin, rosuvastatin, fluvastatin, and lovastatin are considered first-line options for the treatment of dyslipidemia.^3,4 Increasing use of the statin class of drugs is largely due to the fact that cardiovascular disease (CVD), which includes heart attack, atherosclerosis, angina, peripheral artery disease, and stroke, has become a leading cause of death in high-income countries and a major cause of morbidity around the world.⁵ Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.^3,16 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.^{6,7,8,9,10,14} 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.^3,4 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.^11,12

While all statin medications are considered equally effective from a clinical standpoint, rosuvastatin is considered the most potent; doses of 10 to 40mg rosuvastatin per day were found in clinical studies to result in a 45.8% to 54.6% decrease in LDL cholesterol levels, while simvastatin has been found to have an average decrease in LDL-C of ~35%.^27,13,14,18 Potency is thought to correlate to tissue permeability as the more lipophilic statins such as simvastatin are thought to enter endothelial cells by passive diffusion, as opposed to hydrophilic statins such as pravastatin and rosuvastatin which are taken up into hepatocytes through OATP1B1 (organic anion transporter protein 1B1)-mediated transport.^15,20 Despite these differences in potency, several trials have demonstrated only minimal differences in terms of clinical outcomes between statins.⁹

Type

Small Molecule

Groups

Approved

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Simvastatin (DB00641)

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Weight

Average: 418.5662
Monoisotopic: 418.271924326

Chemical Formula

C₂₅H₃₈O₅

Synonyms

• 2,2-dimethylbutyric acid, 8-ester with (4R,6R)-6-(2-((1S,2S,6R,8S,8aR)-1,2,6,7,8,8a-hexahydro-8-hydroxy-2,6-dimethyl-1-naphthyl)ethyl)tetrahydro-4-hydroxy-2H-pyran-2-one
• Simvastatin
• Simvastatina
• Simvastatine
• Simvastatinum

External IDs

• MK 733
• MK-0733
• MK-733

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Pharmacology

Indication

Simvastatin is indicated for the treatment of hyperlipidemia to reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL‑C), apolipoprotein B (Apo B), and triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C).^29,30

This includes the treatment of primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial), mixed dyslipidemia (Fredrickson type IIb), hypertriglyceridemia (Fredrickson type IV hyperlipidemia), primary dysbetalipoproteinemia (Fredrickson type III hyperlipidemia), homozygous familial hypercholesterolemia (HoFH) as an adjunct to other lipid-lowering treatments, as well as adolescent patients with Heterozygous Familial Hypercholesterolemia (HeFH).^29,30

Simvastatin is also indicated to reduce the risk of cardiovascular morbidity and mortality including myocardial infarction, stroke, and the need for revascularization procedures. It is primarily used in patients at high risk of coronary events because of existing coronary heart disease, diabetes, peripheral vessel disease, history of stroke or other cerebrovascular disease.^29,30

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.^3,4

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Prevention of	Cardiovascular event		••••••••••••
Prevention of	Cardiovascular event		••••••••••••
Prevention of	Cardiovascular events		••• •••••
Treatment of	Diabetes mellitus		••• •••••
Used as adjunct in combination to manage	Heterozygous familial hypercholesterolemia	Combination Product in combination with: Ezetimibe (DB00973)	••••••••••••

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Pharmacodynamics

Simvastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality.^3,4

Elevated cholesterol levels, and in particular, elevated low-density lipoprotein (LDL) levels, are an important risk factor for the development of CVD.³ 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.^6,7,8,9,10 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.^3,4 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.^11,12

Skeletal Muscle Effects

Simvastatin occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase (CK) above ten times the upper limit of normal (ULN). Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and rare fatalities have occurred. Predisposing factors for myopathy include advanced age (≥65 years), female gender, uncontrolled hypothyroidism, and renal impairment. Chinese patients may also be at increased risk for myopathy. In most cases, muscle symptoms and CK increases resolved when treatment was promptly discontinued.^29,30

In a clinical trial database of 41,413 patients, the incidence of myopathy was approximately 0.03% and 0.08% at 20 and 40 mg/day, respectively, while the risk of myopathy with simvastatin 80 mg (0.61%) was disproportionately higher than that observed at the lower doses. It's therefore recommended that the 80mg dose of simvastatin should be used only in patients who have been taking simvastatin 80 mg chronically (e.g., for 12 months or more) without evidence of muscle toxicity. As well, patients already stabilized on simvastatin 80mg should be monitored closely for evidence of muscle toxicity; if they need to be initiated on an interacting drug that is contraindicated or is associated with a dose cap for simvastatin, that patient should be switched to an alternative statin with less potential for the drug-drug interaction.^29,30

The risk of myopathy during treatment with simvastatin may be increased with concurrent administration of interacting drugs such as fenofibrate, niacin, gemfibrozil, cyclosporine, and strong inhibitors of the CYP3A4 enzyme. Cases of myopathy, including rhabdomyolysis, have been reported with HMG-CoA reductase inhibitors coadministered with colchicine, and caution should therefore be exercised when prescribing these two medications together.^29,30

Liver Enzyme Abnormalities

Persistent increases (to more than 3X the ULN) in serum transaminases have occurred in approximately 1% of patients who received simvastatin in clinical studies. When drug treatment was interrupted or discontinued in these patients, the transaminase levels usually fell slowly to pretreatment levels. The increases were not associated with jaundice or other clinical signs or symptoms. ^29,30

In the Scandinavian Simvastatin Survival Study (4S),¹⁴ the number of patients with more than one transaminase elevation to >3 times the ULN, over the course of the study, was not significantly different between the simvastatin and placebo groups (14 [0.7%] vs. 12 [0.6%]). The frequency of single elevations of ALT to 3 times the ULN was significantly higher in the simvastatin group in the first year of the study (20 vs. 8, p=0.023), but not thereafter. In the HPS (Heart Protection Study),¹⁰ in which 20,536 patients were randomized to receive simvastatin 40 mg/day or placebo, the incidences of elevated transaminases (>3X ULN confirmed by repeat test) were 0.21% (n=21) for patients treated with simvastatin and 0.09% (n=9) for patients treated with placebo.^29,30

Endocrine Effects

Increases in HbA1c and fasting serum glucose levels have been reported with HMG-CoA reductase inhibitors, including simvastatin.²⁹

Although cholesterol is the precursor of all steroid hormones, studies with simvastatin have suggested that this agent has no clinical effect on steroidogenesis. Simvastatin caused no increase in biliary lithogenicity and, therefore, would not be expected to increase the incidence of gallstones.³⁰

Mechanism of action

Simvastatin is a prodrug in which the 6-membered lactone ring of simvastatin is hydrolyzed in vivo to generate the beta,delta-dihydroxy acid, an active metabolite structurally similar to HMG-CoA (hydroxymethylglutaryl CoA). Once hydrolyzed, simvastatin competes with HMG-CoA for HMG-CoA reductase, a hepatic microsomal enzyme, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.² Simvastatin 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. Simvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL).^29,30 The overall effect is a decrease in plasma LDL and VLDL.

At therapeutic doses, the HMG-CoA enzyme is not completely blocked by simvastatin activity, thereby allowing biologically necessary amounts of mevalonate to remain available. As mevalonate is an early step in the biosynthetic pathway for cholesterol, therapy with simvastatin would also not be expected to cause any accumulation of potentially toxic sterols. In addition, HMG-CoA is metabolized readily back to acetyl-CoA, which participates in many biosynthetic processes in the body.³⁰

In vitro and in vivo animal studies also demonstrate that simvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins.¹⁵ 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.¹⁷

Target	Actions	Organism
A3-hydroxy-3-methylglutaryl-coenzyme A reductase	inhibitor	Humans
UIntegrin alpha-L	inhibitory allosteric modulator	Humans
UHistone deacetylase 2	inhibitor	Humans

Absorption

Peak plasma concentrations of both active and total inhibitors were attained within 1.3 to 2.4 hours post-dose. While the recommended therapeutic dose range is 10 to 40 mg/day, there was no substantial deviation from linearity of AUC with an increase in dose to as high as 120 mg. Relative to the fasting state, the plasma profile of inhibitors was not affected when simvastatin was administered immediately before a test meal.^29,30

In a pharmacokinetic study of 17 healthy Chinese volunteers, the major PK parameters were as follows: Tmax 1.44 hours, Cmax 9.83 ug/L, t1/2 4.85 hours, and AUC 40.32ug·h/L.¹⁹

Simvastatin undergoes extensive first-pass extraction in the liver, the target organ for the inhibition of HMG-CoA reductase and the primary site of action. This tissue selectivity (and consequent low systemic exposure) of orally administered simvastatin has been shown to be far greater than that observed when the drug is administered as the enzymatically active form, i.e. as the open hydroxyacid.³⁰

In animal studies, after oral dosing, simvastatin achieved substantially higher concentrations in the liver than in non-target tissues. However, because simvastatin undergoes extensive first-pass metabolism, the bioavailability of the drug in the systemic system is low. In a single-dose study in nine healthy subjects, it was estimated that less than 5% of an oral dose of simvastatin reached the general circulation in the form of active inhibitors.³⁰

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 simvastatin pharmacokinetics. Evidence from pharmacogenetic studies of the c.521T>C single nucleotide polymorphism (SNP) showed that simvastatin plasma concentrations were increased on average 3.2-fold for individuals homozygous for 521CC compared to homozygous 521TT individuals.^22,21 The 521CC genotype is also associated with a marked increase in the risk of developing myopathy, likely secondary to increased systemic exposure.²³ Other statin drugs impacted by this polymorphism include rosuvastatin, pitavastatin, atorvastatin, lovastatin, and pravastatin.²⁰

For patients known to have the above-mentioned c.521CC OATP1B1 genotype, a maximum daily dose of 20mg of simvastatin is recommended to avoid adverse effects from the increased exposure to the drug, such as muscle pain and risk of rhabdomyolysis.³⁰

Evidence has also been obtained with other statins such as rosuvastatin that concurrent use of statins and inhibitors of Breast Cancer Resistance Protein (BCRP) such as elbasvir and grazoprevir increased the plasma concentration of these statins. Further evidence is needed, however a dose adjustment of simvastatin may be necessary. Other statin drugs impacted by this polymorphism include fluvastatin and atorvastatin.²¹

Volume of distribution

Rat studies indicate that when radiolabeled simvastatin was administered, simvastatin-derived radioactivity crossed the blood-brain barrier.²⁹

Protein binding

Both simvastatin and its β-hydroxyacid metabolite are highly bound (approximately 95%) to human plasma proteins.^29,30

Metabolism

Simvastatin is administered as the inactive lactone derivative that is then metabolically activated to its β-hydroxyacid form by a combination of spontaneous chemical conversion and enzyme-mediated hydrolysis by nonspecific carboxyesterases in the intestinal wall, liver, and plasma. Oxidative metabolism in the liver is primarily mediated by CYP3A4 and CYP3A5, with the remaining metabolism occurring through CYP2C8 and CYP2C9.²⁵

The major active metabolites of simvastatin are β-hydroxyacid metabolite and its 6'-hydroxy, 6'-hydroxymethyl, and 6'-exomethylene derivatives.^29,30

Polymorphisms in the CYP3A5 gene have been shown to affect the disposition of simvastatin and may provide a plausible explanation for interindividual variability of simvastatin disposition and pharmacokinetics.²⁴

Hover over products below to view reaction partners

• Simvastatin
  • simvastatin hydroxy acid
  • 6'-beta-Hydroxysimvastatin
  • 3', 5'-Dihydrodiol
  • 6'-exomethylene

Route of elimination

Following an oral dose of 14C-labeled simvastatin in man, 13% of the dose was excreted in urine and 60% in feces.^29,30

Half-life

4.85 hours¹⁹

Clearance

Not Available

Adverse Effects

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Toxicity

Not Available

Pathways

Pathway	Category
Simvastatin 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 simvastatin.	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 simvastatin.	Details
Solute carrier organic anion transporter family member 1B1	SLCO1B1*5	(C;C) / (C;T)	T > C	ADR Directly Studied	The presence of this genotype in SLCO1B1 is associated with an increased risk of myopathy when treated with simvastatin.	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 Simvastatin can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Simvastatin can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be increased when it is combined with Simvastatin.
Abiraterone	The metabolism of Simvastatin can be decreased when combined with Abiraterone.
Abrocitinib	The serum concentration of Simvastatin can be increased when it is combined with Abrocitinib.

Food Interactions

• Avoid grapefruit products. Co-administration with grapefruit products may increase the risk for adverse effects such as myalgia.

Products

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International/Other Brands

Cholestat (Kalbe) / Colemin (Biohorm) / Labistatin (Sandoz) / Lipex (Merck Sharp & Dohme) / Medipo (Mediolanum Farmaceutici) / Nivelipol (Temis-Lostalo) / Simovil (Merck Sharp & Dohme) / Sinvacor (Merck Sharp & Dohme) / Sivastin (Sigma-Tau) / Sivatin (Rowex) / Sivinar (Anfarm) / Sorfox (Galex) / Sotovastin (Bros) / Starezin (Leovan Pharmaceuticals) / Starstat (Lupin) / Starzoko (Daewoong) / Stasiva (Pharmanel) / Statex (Pliva) / Staticor (Darnitsa) / Statinal (Alet Pharmaceuticals) / Stativer (Iapharm) / Synvinolin

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Act Simvastatin	Tablet	5 mg	Oral	Actavis Pharma Company	2003-09-26	2018-06-11
Act Simvastatin	Tablet	20 mg	Oral	Actavis Pharma Company	2003-09-26	2018-06-11
Act Simvastatin	Tablet	80 mg	Oral	Actavis Pharma Company	2003-09-26	2018-06-11
Act Simvastatin	Tablet	10 mg	Oral	Actavis Pharma Company	2003-09-26	2018-06-11
Act Simvastatin	Tablet	40 mg	Oral	Actavis Pharma Company	2003-09-26	2018-06-11

Generic Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Ag-simvastatin	Tablet	80 mg	Oral	Angita Pharma Inc.	2018-09-06	Not applicable
Ag-simvastatin	Tablet	10 mg	Oral	Angita Pharma Inc.	2018-09-06	Not applicable
Ag-simvastatin	Tablet	20 mg	Oral	Angita Pharma Inc.	2018-09-06	Not applicable
Ag-simvastatin	Tablet	5 mg	Oral	Angita Pharma Inc.	2018-09-06	Not applicable
Ag-simvastatin	Tablet	40 mg	Oral	Angita Pharma Inc.	2018-09-06	Not applicable

Mixture Products

Name	Ingredients	Dosage	Route	Labeller	Marketing Start	Marketing End	Region	Image
AMISITELA	Simvastatin (20 MG) + Ezetimibe (10 MG)	Tablet	Oral	Pharmacare S.R.L.	2019-10-10	Not applicable
AMISITELA	Simvastatin (10 MG) + Ezetimibe (10 MG)	Tablet	Oral	Pharmacare S.R.L.	2019-10-10	Not applicable
AMISITELA	Simvastatin (40 MG) + Ezetimibe (10 MG)	Tablet	Oral	Pharmacare S.R.L.	2019-10-10	Not applicable
Cholib	Simvastatin (40 mg) + Fenofibrate (145 mg)	Tablet, film coated	Oral	Viatris Healthcare Limited	2016-09-08	Not applicable
CHOLIB	Simvastatin (40 MG) + Fenofibrate (145 MG)	Tablet, film coated	Oral	Viatris Healthcare Limited	2014-07-08	Not applicable

Categories

ATC Codes

A10BH51 — Sitagliptin and simvastatin

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

C10AA01 — Simvastatin

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

C10BX04 — Simvastatin, 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

C10BA02 — Simvastatin and ezetimibe

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

C10BX01 — Simvastatin and acetylsalicylic acid

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

C10BA04 — Simvastatin and fenofibrate

• 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
• Anticholesteremic Agents
• BSEP/ABCB11 Substrates
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2B6 Inhibitors
• Cytochrome P-450 CYP2B6 Inhibitors (weak)
• Cytochrome P-450 CYP2C19 Substrates
• 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 Substrates
• Cytochrome P-450 CYP3A Inhibitors
• 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
• Drugs causing inadvertant photosensitivity
• Enzyme Inhibitors
• Hydroxymethylglutaryl-CoA Reductase Inhibitors
• Hypolipidemic Agents
• Hypolipidemic Agents Indicated for Hyperlipidemia
• Lipid Modifying Agents
• Lipid Modifying Agents, Plain
• Lipid Regulating Agents
• Naphthalenes
• Noxae
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B1/SLCO1B1 Substrates
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• Photosensitizing Agents
• UGT1A1 Substrates
• UGT1A3 substrates
• UGT2B7 substrates

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as delta valerolactones. These are cyclic organic compounds containing an oxan-2- one moiety.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Lactones

Sub Class

Delta valerolactones

Direct Parent

Delta valerolactones

Alternative Parents

Fatty acid esters / Oxanes / Dicarboxylic acids and derivatives / Secondary alcohols / Carboxylic acid esters / Oxacyclic compounds / Organic oxides / Hydrocarbon derivatives / Carbonyl compounds

Substituents

Alcohol / Aliphatic heteropolycyclic compound / Carbonyl group / Carboxylic acid derivative / Carboxylic acid ester / Delta valerolactone / Delta_valerolactone / Dicarboxylic acid or derivatives / Fatty acid ester / Fatty acyl

Molecular Framework

Aliphatic heteropolycyclic compounds

External Descriptors

statin (semi-synthetic), fatty acid ester, delta-lactone, carbobicyclic compound (CHEBI:9150)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

AGG2FN16EV

CAS number

79902-63-9

InChI Key

RYMZZMVNJRMUDD-HGQWONQESA-N

InChI

InChI=1S/C25H38O5/c1-6-25(4,5)24(28)30-21-12-15(2)11-17-8-7-16(3)20(23(17)21)10-9-19-13-18(26)14-22(27)29-19/h7-8,11,15-16,18-21,23,26H,6,9-10,12-14H2,1-5H3/t15-,16-,18+,19+,20-,21-,23-/m0/s1

IUPAC Name

(1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxooxan-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2,2-dimethylbutanoate

SMILES

[H][C@]12[C@H](C[C@@H](C)C=C1C=C[C@H](C)[C@@H]2CC[C@@H]1C[C@@H](O)CC(=O)O1)OC(=O)C(C)(C)CC

References

Synthesis Reference

Shieh-Shung J. Chen, Byron H. Arison, "Process for the preparation of 3-keto, 5-hydroxy simvastatin analogs." U.S. Patent US4965200, issued April, 1981.

US4965200

General References

1. Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE: Simvastatin is associated with a reduced incidence of dementia and Parkinson's disease. BMC Med. 2007 Jul 19;5:20. [Article]
2. 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]
3. 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]
4. 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]
5. 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]
6. 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]
7. 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]
8. 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]
9. 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]
10. 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]
11. 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]
12. 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]
13. 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]
14. 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]
15. 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]
16. 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]
17. 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]
18. Jones PH, Davidson MH, Stein EA, Bays HE, McKenney JM, Miller E, Cain VA, Blasetto JW: Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol. 2003 Jul 15;92(2):152-60. [Article]
19. Zhou Q, Ruan ZR, Jiang B, Yuan H, Zeng S: Simvastatin pharmacokinetics in healthy Chinese subjects and its relations with CYP2C9, CYP3A5, ABCB1, ABCG2 and SLCO1B1 polymorphisms. Pharmazie. 2013 Feb;68(2):124-8. [Article]
20. Elsby R, Hilgendorf C, Fenner K: Understanding the critical disposition pathways of statins to assess drug-drug interaction risk during drug development: it's not just about OATP1B1. Clin Pharmacol Ther. 2012 Nov;92(5):584-98. doi: 10.1038/clpt.2012.163. Epub 2012 Oct 10. [Article]
21. 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]
22. Pasanen MK, Neuvonen M, Neuvonen PJ, Niemi M: SLCO1B1 polymorphism markedly affects the pharmacokinetics of simvastatin acid. Pharmacogenet Genomics. 2006 Dec;16(12):873-9. doi: 10.1097/01.fpc.0000230416.82349.90. [Article]
23. Link E, Parish S, Armitage J, Bowman L, Heath S, Matsuda F, Gut I, Lathrop M, Collins R: SLCO1B1 variants and statin-induced myopathy--a genomewide study. N Engl J Med. 2008 Aug 21;359(8):789-99. doi: 10.1056/NEJMoa0801936. Epub 2008 Jul 23. [Article]
24. Kim KA, Park PW, Lee OJ, Kang DK, Park JY: Effect of polymorphic CYP3A5 genotype on the single-dose simvastatin pharmacokinetics in healthy subjects. J Clin Pharmacol. 2007 Jan;47(1):87-93. doi: 10.1177/0091270006295063. [Article]
25. Tubic-Grozdanis M, Hilfinger JM, Amidon GL, Kim JS, Kijek P, Staubach P, Langguth P: Pharmacokinetics of the CYP 3A substrate simvastatin following administration of delayed versus immediate release oral dosage forms. Pharm Res. 2008 Jul;25(7):1591-600. doi: 10.1007/s11095-007-9519-6. Epub 2008 Jan 24. [Article]
26. Kitzmiller JP, Mikulik EB, Dauki AM, Murkherjee C, Luzum JA: Pharmacogenomics of statins: understanding susceptibility to adverse effects. Pharmgenomics Pers Med. 2016 Oct 3;9:97-106. doi: 10.2147/PGPM.S86013. eCollection 2016. [Article]
27. 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]
28. FDA Approved Drug Products: Zocor (simvastatin) oral tablets [Link]
29. FDA Label - Simvastatin [File]
30. Health Canada Monograph - Simvastatin [File]

External Links

Human Metabolome Database

HMDB0005007

KEGG Drug

D00434

PubChem Compound

54454

PubChem Substance

46508654

ChemSpider

49179

BindingDB

50139181

RxNav

36567

ChEBI

9150

ChEMBL

CHEMBL1064

ZINC

ZINC000003780893

Therapeutic Targets Database

DAP001519

PharmGKB

PA451363

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

PDRhealth

PDRhealth Drug Page

Wikipedia

Simvastatin

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	Completed	Not Available	Atherosclerosis / Cardiovascular Disease (CVD) / Coronary Heart Disease (CHD) / Myocardial Infarction	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	Atherosclerosis / Carotid Artery Diseases / Coronary Artery Disease (CAD)	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	Cardiovascular Disease (CVD) / Diabetes Mellitus / Dyslipidemia / Hypertension / Myocardial Infarction / Stroke	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	Cardiovascular Disease (CVD) / Type 2 Diabetes Mellitus	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	High Cholesterol	5	somestatus	stop reason	just information to hide

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Pharmacoeconomics

Manufacturers

• Synthon pharmaceuticals ltd
• Accord healthcare inc
• Aurobindo pharma ltd
• Dr reddys laboratories inc
• Dr reddys laboratories ltd
• Ivax pharmaceuticals inc sub teva pharmaceuticals usa
• Lupin ltd
• Matrix laboratories ltd
• Perrigo r and d co
• Ranbaxy laboratories ltd
• Sandoz inc
• Watson laboratories inc
• Zydus pharmaceuticals usa inc
• Merck research laboratories div merck co inc

Packagers

• Abbott Laboratories Ltd.
• Accord Healthcare
• Advanced Pharmaceutical Services Inc.
• Aeropharm Technology LLC
• Amerisource Health Services Corp.
• AQ Pharmaceuticals Inc.
• A-S Medication Solutions LLC
• Atlantic Biologicals Corporation
• Aurobindo Pharma Ltd.
• Blenheim Pharmacal
• Blu Pharmaceuticals LLC
• Bryant Ranch Prepack
• Cadila Healthcare Ltd.
• Cardinal Health
• Cobalt Pharmaceuticals Inc.
• Comprehensive Consultant Services Inc.
• Corepharma LLC
• Coupler Enterprises Inc.
• Dept Health Central Pharmacy
• DHHS Program Support Center Supply Service Center
• Direct Dispensing Inc.
• DispenseXpress Inc.
• Dispensing Solutions
• Diversified Healthcare Services Inc.
• Doctor Reddys Laboratories Ltd.
• Intas Pharmaceuticals Ltd.
• Kaiser Foundation Hospital
• Laboratorios Belmac SA
• Lake Erie Medical and Surgical Supply
• Lupin Pharmaceuticals Inc.
• Major Pharmaceuticals
• Mallinckrodt Inc.
• Mckesson Corp.
• Medisca Inc.
• Medvantx Inc.
• Merck & Co.
• MSP Distribution Services LLC
• Murfreesboro Pharmaceutical Nursing Supply
• Mylan
• Northstar Rx LLC
• Nucare Pharmaceuticals Inc.
• Ohm Laboratories Inc.
• Palmetto Pharmaceuticals Inc.
• PCA LLC
• PD-Rx Pharmaceuticals Inc.
• Perrigo Co.
• Pharmaceutical Utilization Management Program VA Inc.
• Physicians Total Care Inc.
• Preferred Pharmaceuticals Inc.
• Prepackage Specialists
• Prepak Systems Inc.
• Ranbaxy Laboratories
• Rebel Distributors Corp.
• Remedy Repack
• Resource Optimization and Innovation LLC
• Sandhills Packaging Inc.
• Sandoz
• Southwood Pharmaceuticals
• Stat Rx Usa
• Stat Scripts LLC
• Teva Pharmaceutical Industries Ltd.
• UDL Laboratories
• Va Cmop Dallas
• Vangard Labs Inc.
• Zydus Pharmaceuticals

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral	10.0 mg
Tablet, film coated	Oral	5.0 mg
Tablet	Oral	10.000 mg
Tablet, coated	Oral
Capsule, liquid filled	Oral
Tablet	Oral	10.000 mg
Suspension	Oral	20 mg/5mL
Suspension	Oral	40 mg/5mL
Tablet, film coated	Oral
Tablet, film coated	Oral
Tablet, film coated	Oral	20.000 mg
Tablet, film coated	Oral	40.000 mg
Tablet, film coated		80 mg
Tablet	Oral	5 mg
Tablet	Oral	80 mg
Tablet, film coated	Oral	10.00 mg
Tablet, film coated	Oral	20.00 mg
Tablet	Oral	20.000 mg
Tablet	Oral
Tablet, film coated, extended release	Oral
Tablet, film coated	Oral	30 MG
Tablet, film coated	Oral	60 MG
Tablet, film coated	Oral	80 MG
Tablet, film coated	Oral	5 MG
Tablet, film coated		10 mg
Tablet, film coated		20 mg
Tablet, film coated		40 mg
Tablet, film coated	Oral	10 mg
Tablet	Oral	10 mg/1
Tablet	Oral	20 mg/1
Tablet	Oral	40 mg/1
Tablet	Oral	5 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	5 mg/1
Tablet, coated	Oral	80 mg/1
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, film coated	Oral	80 mg/1
Tablet, film coated	Periarticular	80 mg/1
Tablet, orally disintegrating	Oral	10 mg/1
Tablet, orally disintegrating	Oral	20 mg/1
Tablet, orally disintegrating	Oral	40 mg/1
Tablet, orally disintegrating	Oral	80 mg/1
Tablet, film coated	Oral	40 mg
Tablet, film coated
Tablet, film coated	Oral	10000 Mg
Tablet, film coated	Oral	20 MG
Tablet	Oral
Capsule	Oral	20.000 mg
Tablet, coated	Oral	4000000 mg
Tablet	Oral	20 mg
Tablet	Oral	40 mg
Tablet, film coated	Oral	20.0 mg
Tablet, delayed release	Oral	20 mg
Tablet	Oral	10 mg
Tablet, coated	Oral	10 mg
Tablet, coated	Oral	20 mg
Tablet, coated	Oral	40 mg
Tablet, coated	Oral	80 mg

Prices

Unit description	Cost	Unit
Zocor 90 40 mg tablet Bottle	525.16USD	bottle
Simvastatin 100% powder	10.71USD	g
Vytorin 10-20 mg tablet	5.05USD	tablet
Vytorin 10-40 mg tablet	5.05USD	tablet
Vytorin 10-10 mg tablet	4.97USD	tablet
Zocor 20 mg tablet	4.69USD	tablet
Zocor 80 mg tablet	4.69USD	tablet
Vytorin 10-80 mg tablet	4.63USD	tablet
Zocor 40 mg tablet	4.11USD	tablet
Simvastatin 20 mg tablet	3.83USD	tablet
Simvastatin 40 mg tablet	3.83USD	tablet
Simvastatin 80 mg tablet	3.83USD	tablet
Zocor 10 mg tablet	2.89USD	tablet
Simvastatin 10 mg tablet	2.31USD	tablet
Zocor 5 mg tablet	1.99USD	tablet
Simvastatin 5 mg tablet	1.63USD	tablet
Phl-Simvastatin 40 mg Tablet	1.45USD	tablet
Phl-Simvastatin 80 mg Tablet	1.45USD	tablet
Pms-Simvastatin 20 mg Tablet	1.45USD	tablet
Pms-Simvastatin 40 mg Tablet	1.45USD	tablet
Pms-Simvastatin 80 mg Tablet	1.45USD	tablet
Ran-Simvastatin 20 mg Tablet	1.45USD	tablet
Ran-Simvastatin 40 mg Tablet	1.45USD	tablet
Ran-Simvastatin 80 mg Tablet	1.45USD	tablet
Ratio-Simvastatin 20 mg Tablet	1.45USD	tablet
Ratio-Simvastatin 40 mg Tablet	1.45USD	tablet
Ratio-Simvastatin 80 mg Tablet	1.45USD	tablet
Sandoz Simvastatin 20 mg Tablet	1.45USD	tablet
Sandoz Simvastatin 40 mg Tablet	1.45USD	tablet
Sandoz Simvastatin 80 mg Tablet	1.45USD	tablet
Apo-Simvastatin 20 mg Tablet	1.45USD	tablet
Apo-Simvastatin 40 mg Tablet	1.45USD	tablet
Apo-Simvastatin 80 mg Tablet	1.45USD	tablet
Co Simvastatin 20 mg Tablet	1.45USD	tablet
Co Simvastatin 40 mg Tablet	1.45USD	tablet
Co Simvastatin 80 mg Tablet	1.45USD	tablet
Jamp-Simvastatin 20 mg Tablet	1.45USD	tablet
Jamp-Simvastatin 40 mg Tablet	1.45USD	tablet
Jamp-Simvastatin 80 mg Tablet	1.45USD	tablet
Mylan-Simvastatin 20 mg Tablet	1.45USD	tablet
Mylan-Simvastatin 40 mg Tablet	1.45USD	tablet
Mylan-Simvastatin 80 mg Tablet	1.45USD	tablet
Novo-Simvastatin 20 mg Tablet	1.45USD	tablet
Novo-Simvastatin 40 mg Tablet	1.45USD	tablet
Novo-Simvastatin 80 mg Tablet	1.45USD	tablet
Phl-Simvastatin 20 mg Tablet	1.45USD	tablet
Apo-Simvastatin 10 mg Tablet	1.17USD	tablet
Co Simvastatin 10 mg Tablet	1.17USD	tablet
Jamp-Simvastatin 10 mg Tablet	1.17USD	tablet
Mylan-Simvastatin 10 mg Tablet	1.17USD	tablet
Novo-Simvastatin 10 mg Tablet	1.17USD	tablet
Phl-Simvastatin 10 mg Tablet	1.17USD	tablet
Pms-Simvastatin 10 mg Tablet	1.17USD	tablet
Ran-Simvastatin 10 mg Tablet	1.17USD	tablet
Ratio-Simvastatin 10 mg Tablet	1.17USD	tablet
Sandoz Simvastatin 10 mg Tablet	1.17USD	tablet
Apo-Simvastatin 5 mg Tablet	0.59USD	tablet
Co Simvastatin 5 mg Tablet	0.59USD	tablet
Jamp-Simvastatin 5 mg Tablet	0.59USD	tablet
Mylan-Simvastatin 5 mg Tablet	0.59USD	tablet
Novo-Simvastatin 5 mg Tablet	0.59USD	tablet
Phl-Simvastatin 5 mg Tablet	0.59USD	tablet
Pms-Simvastatin 5 mg Tablet	0.59USD	tablet
Ran-Simvastatin 5 mg Tablet	0.59USD	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
US5846966	No	1998-12-08	2013-09-21
US7326708	Yes	2008-02-05	2027-05-24
US6080428	No	2000-06-27	2017-05-27
US6469035	No	2002-10-22	2018-03-15
US6699871	Yes	2004-03-02	2023-01-26
US7125873	Yes	2006-10-24	2023-01-26
USRE37721	Yes	2002-05-28	2017-04-25
USRE42461	Yes	2011-06-14	2017-04-25
US6303661	No	2001-10-16	2017-04-24
US6890898	No	2005-05-10	2019-02-02
US7078381	No	2006-07-18	2019-02-02
US7459428	No	2008-12-02	2019-02-02
US8168637	No	2012-05-01	2022-06-26
US9597289	No	2017-03-21	2030-02-23
US10300041	No	2019-05-28	2027-04-26

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	135-138 °C	PhysProp
water solubility	Insoluble	FDA label
logP	4.68	HANSCH,C ET AL. (1995)

Predicted Properties

Property	Value	Source
Water Solubility	0.0122 mg/mL	ALOGPS
logP	4.51	ALOGPS
logP	4.46	Chemaxon
logS	-4.5	ALOGPS
pKa (Strongest Acidic)	14.91	Chemaxon
pKa (Strongest Basic)	-2.8	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	3	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	72.83 Å2	Chemaxon
Rotatable Bond Count	7	Chemaxon
Refractivity	117.68 m3·mol-1	Chemaxon
Polarizability	47.88 Å3	Chemaxon
Number of Rings	3	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	0.9475
Blood Brain Barrier	+	0.9422
Caco-2 permeable	-	0.5951
P-glycoprotein substrate	Substrate	0.8508
P-glycoprotein inhibitor I	Inhibitor	0.7335
P-glycoprotein inhibitor II	Inhibitor	0.8387
Renal organic cation transporter	Non-inhibitor	0.8435
CYP450 2C9 substrate	Non-substrate	0.835
CYP450 2D6 substrate	Non-substrate	0.9254
CYP450 3A4 substrate	Substrate	0.7513
CYP450 1A2 substrate	Non-inhibitor	0.9045
CYP450 2C9 inhibitor	Non-inhibitor	0.9071
CYP450 2D6 inhibitor	Non-inhibitor	0.9307
CYP450 2C19 inhibitor	Non-inhibitor	0.9025
CYP450 3A4 inhibitor	Inhibitor	0.7959
CYP450 inhibitory promiscuity	Low CYP Inhibitory Promiscuity	0.8682
Ames test	Non AMES toxic	0.792
Carcinogenicity	Non-carcinogens	0.9408
Biodegradation	Not ready biodegradable	0.9657
Rat acute toxicity	2.0061 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.8921
hERG inhibition (predictor II)	Non-inhibitor	0.8573

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	splash10-0fk9-9154200000-9a8f0d47976b67e5c9d5
Mass Spectrum (Electron Ionization)	MS	splash10-0a4i-3900000000-d04758924bf88a90c017
LC-MS/MS Spectrum - LC-ESI-qTof , Positive	LC-MS/MS	splash10-0229-0967000000-6c51c479e90818ec703b
LC-MS/MS Spectrum - LC-ESI-qTof , Positive	LC-MS/MS	splash10-0229-0967000000-6c51c479e90818ec703b
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0fya-0988400000-d9778b2f11696b81fb07
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-006w-0790000000-4f23e0376d85845e0964
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-05i1-0940000000-058f6298af54c05532ed
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0092-0910000000-6ecd838b2f6fddf67dad
LC-MS/MS Spectrum - LC-ESI-QTOF , positive	LC-MS/MS	splash10-0597-0900000000-012d0d6fcabbd21d696d
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-000e-0590000000-7f99e0b9531d4f42831a
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0092-1960000000-e8429bbec985c5ecdd2d
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0592-1910000000-dc09a51ca37fe4d24a5a
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0abd-1900000000-9b55821f49270e5dd598
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-0536-1900000000-d8a41a97ccbdb30e5a5e
LC-MS/MS Spectrum - LC-ESI-QFT , positive	LC-MS/MS	splash10-002f-2900000000-abe04d7f99c3eb0f2fcb
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0udi-0429000000-7c1071c3498f1c95105d
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-03dr-4900000000-87bfa0125a9700ae0ca8
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-00kr-9400000000-787d54f349bd89491216
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0zg0-0539100000-b821c3b7774662423e94
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0gb9-0629100000-ea6604279b6bab6ea1f1
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0604-5983200000-6128e659d4c901fcea54
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]-	215.8726772	predicted	DarkChem Lite v0.1.0
[M-H]-	201.6614519	predicted	DarkChem Lite v0.1.0
[M-H]-	216.2593772	predicted	DarkChem Lite v0.1.0
[M-H]-	220.8756772	predicted	DarkChem Lite v0.1.0
[M-H]-	211.12212	predicted	DeepCCS 1.0 (2019)
[M+H]+	216.7115772	predicted	DarkChem Lite v0.1.0
[M+H]+	193.5600009	predicted	DarkChem Lite v0.1.0
[M+H]+	217.3793772	predicted	DarkChem Lite v0.1.0
[M+H]+	219.5544772	predicted	DarkChem Lite v0.1.0
[M+H]+	213.16254	predicted	DeepCCS 1.0 (2019)
[M+Na]+	216.0871772	predicted	DarkChem Lite v0.1.0
[M+Na]+	220.7065772	predicted	DarkChem Lite v0.1.0
[M+Na]+	216.4403772	predicted	DarkChem Lite v0.1.0
[M+Na]+	219.4337772	predicted	DarkChem Lite v0.1.0
[M+Na]+	219.03467	predicted	DeepCCS 1.0 (2019)

Targets

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Binding Properties

×

Property	Measurement	pH	Temperature (°C)	References
IC 50 (nM)	12	N/A	N/A	A27462
IC 50 (nM)	11.2	N/A	N/A	A28717
IC 50 (nM)	11	N/A	N/A	A28221
IC 50 (nM)	49	N/A	N/A	A28718 / A28719
Ki (nM)	68000	N/A	N/A	A28717
Ki (nM)	2.6	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. Cenedella RJ, Kuszak JR, Al-Ghoul KJ, Qin S, Sexton PS: Discordant expression of the sterol pathway in lens underlies simvastatin-induced cataracts in Chbb: Thom rats. J Lipid Res. 2003 Jan;44(1):198-211. [Article]
2. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
3. Kocarek TA, Dahn MS, Cai H, Strom SC, Mercer-Haines NA: Regulation of CYP2B6 and CYP3A expression by hydroxymethylglutaryl coenzyme A inhibitors in primary cultured human hepatocytes. Drug Metab Dispos. 2002 Dec;30(12):1400-5. [Article]
4. Liu L, Zhang R, Zhao JJ, Rogers JD, Hsieh JY, Fang W, Matuszewski BK, Dobrinska MR: Determination of simvastatin-derived HMG-CoA reductase inhibitors in biomatrices using an automated enzyme inhibition assay with radioactivity detection. J Pharm Biomed Anal. 2003 Apr 24;32(1):107-23. [Article]
5. Pappu AS, Bacon SP, Illingworth DR: Residual effects of lovastatin and simvastatin on urinary mevalonate excretions in patients with familial hypercholesterolemia. J Lab Clin Med. 2003 Apr;141(4):250-6. [Article]
6. Stoebner PE, Michot C, Ligeron C, Durand L, Meynadier J, Meunier L: [Simvastatin-induced lichen planus pemphigoides]. Ann Dermatol Venereol. 2003 Feb;130(2 Pt 1):187-90. [Article]
7. Carbonell T, Freire E: Binding thermodynamics of statins to HMG-CoA reductase. Biochemistry. 2005 Sep 6;44(35):11741-8. [Article]
8. 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. 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]
2. 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]
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]
4. Fujii T, Masuyama K, Kawashima K: Simvastatin regulates non-neuronal cholinergic activity in T lymphocytes via CD11a-mediated pathways. J Neuroimmunol. 2006 Oct;179(1-2):101-7. Epub 2006 Jul 10. [Article]

Details3. Histone deacetylase 2

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Inhibitor

General Function

Histone deacetylase that catalyzes the deacetylation of lysine residues on the N-terminal part of the core histones (H2A, H2B, H3 and H4) (PubMed:28497810). Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression and developmental events (By similarity). Histone deacetylases act via the formation of large multiprotein complexes (By similarity). Forms transcriptional repressor complexes by associating with MAD, SIN3, YY1 and N-COR (PubMed:12724404). Component of a RCOR/GFI/KDM1A/HDAC complex that suppresses, via histone deacetylase (HDAC) recruitment, a number of genes implicated in multilineage blood cell development (By similarity). Acts as a component of the histone deacetylase NuRD complex which participates in the remodeling of chromatin (PubMed:16428440, PubMed:28977666). Component of the SIN3B complex that represses transcription and counteracts the histone acetyltransferase activity of EP300 through the recognition H3K27ac marks by PHF12 and the activity of the histone deacetylase HDAC2 (PubMed:37137925). Also deacetylates non-histone targets: deacetylates TSHZ3, thereby regulating its transcriptional repressor activity (PubMed:19343227). May be involved in the transcriptional repression of circadian target genes, such as PER1, mediated by CRY1 through histone deacetylation (By similarity). Involved in MTA1-mediated transcriptional corepression of TFF1 and CDKN1A (PubMed:21965678). In addition to protein deacetylase activity, also acts as a protein-lysine deacylase by recognizing other acyl groups: catalyzes removal of (2E)-butenoyl (crotonyl) and 2-hydroxyisobutanoyl (2-hydroxyisobutyryl) acyl groups from lysine residues, leading to protein decrotonylation and de-2-hydroxyisobutyrylation, respectively (PubMed:28497810, PubMed:29192674)

Specific Function

chromatin binding

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]

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Drug created at June 13, 2005 13:24 / Updated at October 21, 2024 12:37