U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

Details

Stereochemistry ABSOLUTE
Molecular Formula C25H38O5
Molecular Weight 418.5672
Optical Activity UNSPECIFIED
Defined Stereocenters 7 / 7
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of SIMVASTATIN

SMILES

CCC(C)(C)C(=O)O[C@@]1([H])C[C@@]([H])(C)C=C2C=C[C@]([H])(C)[C@]([H])(CC[C@]3([H])C[C@]([H])(CC(=O)O3)O)[C@]21[H]

InChI

InChIKey=RYMZZMVNJRMUDD-HGQWONQESA-N
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

HIDE SMILES / InChI
Molecular Formula C25H38O5
Molecular Weight 418.5672
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 7 / 7
E/Z Centers 0
Optical Activity UNSPECIFIED

Description
Curator's Comment:: description was created based on several sources, including: https://www.drugs.com/simvastatin.html http://www.rxlist.com/zocor-drug.htm http://www.wikidoc.org/index.php/Simvastatin

Simvastatin is a HMG-CoA Reductase Inhibitor that is FDA approved for the treatment of hypercholesterolemia and for the reduction in the risk of cardiac heart disease mortality and cardiovascular events. It reduces levels of "bad" cholesterol (low-density lipoprotein, or LDL) and triglycerides in the blood, while increasing levels of "good" cholesterol (high-density lipoprotein, or HDL). Common adverse reactions include abdominal pain, constipation, nausea, headache, upper respiratory infection. Cases of myopathy/rhabdomyolysis have been observed with simvastatin co-administered with lipid-modifying doses ( ≥ 1 g/day niacin) of niacin-containing products. The risk of myopathy, including rhabdomyolysis, is increased by concomitant administration of amiodarone, dronedarone, ranolazine, or calcium channel blockers such as verapamil, diltiazem, or amlodipine.

CNS Activity

Originator

Merck
91
Curator's Comment:: # Merck & Co., Inc.

Approval Year

1991
52
Targets

Targets

Primary TargetPharmacologyConditionPotency
Substrate
261
Inhibitor
3315
 4.0 nM [IC50]
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Preventing
Approved
4033
ZOCOR

Approved Use

Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate. In patients with coronary heart disease (CHD) or at high risk of CHD, simvastatin tablets, USP can be started simultaneously with diet. Simvastatin tablets, USP are an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of total mortality by reducing CHD deaths and reduce the risk of non-fatal myocardial infarction, stroke, and the need for revascularization procedures in patients at high risk of coronary events. (1.1) Reduce elevated total-C, LDL-C, Apo B, TG and increase HDL-C in patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia. (1.2) Reduce elevated TG in patients with hypertriglyceridemia and reduce TG and VLDL-C in patients with primary dysbeta­lipoproteinemia. (1.2) Reduce total-C and LDL-C in adult patients with homozygous familial hypercholesterolemia. (1.2) Reduce elevated total-C, LDL-C, and Apo B in boys and postmenarchal girls, 10 to 17 years of age with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. (1.2, 1.3) Limitations of Use Simvastatin tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. (1.4) 1.1 Reductions in Risk of CHD Mortality and Cardiovascular Events 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, simvastatin tablets, USP are indicated to: Reduce the risk of total mortality by reducing CHD deaths. Reduce the risk of non-fatal myocardial infarction and stroke. Reduce the need for coronary and non-coronary revascularization procedures. 1.2 Hyperlipidemia Simvastatin tablets, USP are indicated 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) in patients with primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIb). Reduce elevated TG in patients with hypertriglyceridemia (Fredrickson type IV hyperlipidemia). Reduce elevated TG and VLDL-C in patients with primary dysbetalipoproteinemia (Fredrickson type III hyperlipidemia). Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable. 1.3 Adolescent Patients with Heterozygous Familial Hypercholesterolemia (HeFH) Simvastatin tablets, USP are indicated as an adjunct to diet to reduce total-C, LDL-C, and Apo B levels in adolescent boys and girls who are at least one year post-menarche, 10 to 17 years of age, with HeFH, if after an adequate trial of diet therapy the following findings are present: 1. LDL cholesterol remains ≥190 mg/dL; or 2. LDL cholesterol remains ≥160 mg/dL and There is a positive family history of premature cardiovascular disease (CVD) or Two or more other CVD risk factors are present in the adolescent patient. The minimum goal of treatment in pediatric and adolescent patients is to achieve a mean LDL-C <130 mg/dL. The optimal age at which to initiate lipid-lowering therapy to decrease the risk of symptomatic adulthood CAD has not been determined. 1.4 Limitations of Use Simvastatin tablets, USP have not been studied in conditions where the major abnormality is elevation of chylomicrons (i.e., hyperlipidemia Fredrickson types I and V).

Launch Date

6.9344638E11
Primary
Approved
4033
ZOCOR

Approved Use

Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate. In patients with coronary heart disease (CHD) or at high risk of CHD, simvastatin tablets, USP can be started simultaneously with diet. Simvastatin tablets, USP are an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of total mortality by reducing CHD deaths and reduce the risk of non-fatal myocardial infarction, stroke, and the need for revascularization procedures in patients at high risk of coronary events. (1.1) Reduce elevated total-C, LDL-C, Apo B, TG and increase HDL-C in patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia. (1.2) Reduce elevated TG in patients with hypertriglyceridemia and reduce TG and VLDL-C in patients with primary dysbeta­lipoproteinemia. (1.2) Reduce total-C and LDL-C in adult patients with homozygous familial hypercholesterolemia. (1.2) Reduce elevated total-C, LDL-C, and Apo B in boys and postmenarchal girls, 10 to 17 years of age with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. (1.2, 1.3) Limitations of Use Simvastatin tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. (1.4) 1.1 Reductions in Risk of CHD Mortality and Cardiovascular Events 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, simvastatin tablets, USP are indicated to: Reduce the risk of total mortality by reducing CHD deaths. Reduce the risk of non-fatal myocardial infarction and stroke. Reduce the need for coronary and non-coronary revascularization procedures. 1.2 Hyperlipidemia Simvastatin tablets, USP are indicated 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) in patients with primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIb). Reduce elevated TG in patients with hypertriglyceridemia (Fredrickson type IV hyperlipidemia). Reduce elevated TG and VLDL-C in patients with primary dysbetalipoproteinemia (Fredrickson type III hyperlipidemia). Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable. 1.3 Adolescent Patients with Heterozygous Familial Hypercholesterolemia (HeFH) Simvastatin tablets, USP are indicated as an adjunct to diet to reduce total-C, LDL-C, and Apo B levels in adolescent boys and girls who are at least one year post-menarche, 10 to 17 years of age, with HeFH, if after an adequate trial of diet therapy the following findings are present: 1. LDL cholesterol remains ≥190 mg/dL; or 2. LDL cholesterol remains ≥160 mg/dL and There is a positive family history of premature cardiovascular disease (CVD) or Two or more other CVD risk factors are present in the adolescent patient. The minimum goal of treatment in pediatric and adolescent patients is to achieve a mean LDL-C <130 mg/dL. The optimal age at which to initiate lipid-lowering therapy to decrease the risk of symptomatic adulthood CAD has not been determined. 1.4 Limitations of Use Simvastatin tablets, USP have not been studied in conditions where the major abnormality is elevation of chylomicrons (i.e., hyperlipidemia Fredrickson types I and V).

Launch Date

6.9344638E11
Primary
Approved
4033
ZOCOR

Approved Use

Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate. In patients with coronary heart disease (CHD) or at high risk of CHD, simvastatin tablets, USP can be started simultaneously with diet. Simvastatin tablets, USP are an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of total mortality by reducing CHD deaths and reduce the risk of non-fatal myocardial infarction, stroke, and the need for revascularization procedures in patients at high risk of coronary events. (1.1) Reduce elevated total-C, LDL-C, Apo B, TG and increase HDL-C in patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia. (1.2) Reduce elevated TG in patients with hypertriglyceridemia and reduce TG and VLDL-C in patients with primary dysbeta­lipoproteinemia. (1.2) Reduce total-C and LDL-C in adult patients with homozygous familial hypercholesterolemia. (1.2) Reduce elevated total-C, LDL-C, and Apo B in boys and postmenarchal girls, 10 to 17 years of age with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. (1.2, 1.3) Limitations of Use Simvastatin tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. (1.4) 1.1 Reductions in Risk of CHD Mortality and Cardiovascular Events 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, simvastatin tablets, USP are indicated to: Reduce the risk of total mortality by reducing CHD deaths. Reduce the risk of non-fatal myocardial infarction and stroke. Reduce the need for coronary and non-coronary revascularization procedures. 1.2 Hyperlipidemia Simvastatin tablets, USP are indicated 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) in patients with primary hyperlipidemia (Fredrickson type IIa, heterozygous familial and nonfamilial) or mixed dyslipidemia (Fredrickson type IIb). Reduce elevated TG in patients with hypertriglyceridemia (Fredrickson type IV hyperlipidemia). Reduce elevated TG and VLDL-C in patients with primary dysbetalipoproteinemia (Fredrickson type III hyperlipidemia). Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable. 1.3 Adolescent Patients with Heterozygous Familial Hypercholesterolemia (HeFH) Simvastatin tablets, USP are indicated as an adjunct to diet to reduce total-C, LDL-C, and Apo B levels in adolescent boys and girls who are at least one year post-menarche, 10 to 17 years of age, with HeFH, if after an adequate trial of diet therapy the following findings are present: 1. LDL cholesterol remains ≥190 mg/dL; or 2. LDL cholesterol remains ≥160 mg/dL and There is a positive family history of premature cardiovascular disease (CVD) or Two or more other CVD risk factors are present in the adolescent patient. The minimum goal of treatment in pediatric and adolescent patients is to achieve a mean LDL-C <130 mg/dL. The optimal age at which to initiate lipid-lowering therapy to decrease the risk of symptomatic adulthood CAD has not been determined. 1.4 Limitations of Use Simvastatin tablets, USP have not been studied in conditions where the major abnormality is elevation of chylomicrons (i.e., hyperlipidemia Fredrickson types I and V).

Launch Date

6.9344638E11
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
54.711 ng/mL
REVIEW
https://www.accessdata.fda.gov/drugsatfda_docs/nda/2016/206679Orig1s000ClinPharmR.pdf
80 mg single, oral
dose: 80 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
5.006 ng/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT01979185
20 mg single, oral
dose: 20 mg
route of administration: oral
experiment type: single
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: healthy
age: Adults
sex:
food status:
6.85 ng/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT01960140
40 mg single, oral
dose: 40 mg
route of administration: oral
experiment type: single
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status:
1.93 ng/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT01960140
40 mg single, oral
dose: 40 mg
route of administration: oral
experiment type: single
co-administered:
TENIVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status:
AUC

AUC

ValueDoseCo-administeredAnalytePopulation
235.795 ng × h/mL
REVIEW
https://www.accessdata.fda.gov/drugsatfda_docs/nda/2016/206679Orig1s000ClinPharmR.pdf
80 mg single, oral
dose: 80 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
34.3509999999999 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT01979185
20 mg single, oral
dose: 20 mg
route of administration: oral
experiment type: single
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: healthy
age: Adults
sex:
food status:
38.142 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT01979185
20 mg single, oral
dose: 20 mg
route of administration: oral
experiment type: single
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: healthy
age: Adults
sex:
food status:
T1/2

T1/2

ValueDoseCo-administeredAnalytePopulation
6.87 h
REVIEW
https://www.accessdata.fda.gov/drugsatfda_docs/nda/2016/206679Orig1s000ClinPharmR.pdf
80 mg single, oral
dose: 80 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
SIMVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: FASTED
Overview

Overview

CYP3A4CYP2C9CYP2D6hERG
substrate
882

inhibitor
753
substrate
530

inhibitor
825
substrate
610

inhibitor
894
inhibitor
775

OverviewOther

Other InhibitorOther SubstrateOther Inducer
BSEP
185

CYP2C8
417

CYP2C19
700

P-gp
666
CYP3A5
203

CYP2A6
266

CYP2C8
354

CYP2C19
500

CYP1A2
526

CYP2E1
332

OATP2
5

OATP1B1
155

OATP1B3
130
Drug as perpetrator​

Drug as perpetrator​

TargetModalityActivityMetaboliteClinical evidence
CYP3A4
920
 moderate [Ki 10 uM]
CYP2C8
448
 moderate [Ki 7.1 uM]
CYP2C9
851
 moderate
CYP2D6
908
 moderate
CYP2C19
738
 no
P-gp
754
 yes [IC50 9 uM]
BSEP
186
 yes
Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
CYP3A4
882
 major
yes (co-administration study)
Comment: cyclosporine has been shown to increase the AUC of statins. The increase in AUC for simvastatin acid is presumably due, in part, to inhibition of CYP3A4
CYP3A5
203
 minor
CYP1A2
526
 no
CYP2A6
266
 no
CYP2C19
500
 no
CYP2C8
354
 no
CYP2C9
530
 no
CYP2D6
610
 no
CYP2E1
332
 no
OATP1B3
130
 yes
OATP2
5
 yes
OATP1B1
155
 yes
yes (co-administration study)
Comment: Administered with cyclosporine: AUC of Simvastatin increased 2.6 fold
Tox targets

Tox targets

TargetModalityActivityMetaboliteClinical evidence
hERG
796
Sourcing

Sourcing

Vendor/AggregatorIDURL
ChEBI
CHEBI:9150
https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:9150
MolPort
MolPort-002-507-345
https://www.molport.com/shop/molecule-link/MolPort-002-507-345
Selleck Chemicals
Simvastatin(Zocor)
http://www.selleckchem.com/products/Simvastatin(Zocor).html
ZINC
ZINC000003780893
http://zinc15.docking.org/substances/ZINC000003780893
eMolecules
11021557
https://www.emolecules.com/cgi-bin/more?vid=11021557
eMolecules
2724261
https://www.emolecules.com/cgi-bin/more?vid=2724261
eMolecules
36754543
https://www.emolecules.com/cgi-bin/more?vid=36754543
PubMed

PubMed

TitleDatePubMed
Angioedema due to losartan.
1999 Jan
[Simvastatin and ischemia-reperfusion damage: its effects on apoptotic myocyte death and on the endothelial expression of nitric-oxide synthetase in an experimental model of the isolated rat heart].
1999 Jan
Statins and peripheral neuropathy.
1999 Jan
Effect of simvastatin on proliferative nephritis and cell-cycle protein expression.
1999 Jul
Nephrotic syndrome and acute interstitial nephritis associated with the use of diclofenac.
1999 Jul 9
Effect of simvastatin treatment on the electronegative low-density lipoprotein present in patients with heterozygous familial hypercholesterolemia.
1999 Sep 15
Differences in the effects of HMG-CoA reductase inhibitors on proliferation and viability of smooth muscle cells in culture.
2000 Jun
Inhibitors of sterol biosynthesis and amphotericin B reduce the viability of pneumocystis carinii f. sp. carinii.
2000 Jun
Simvastatin attenuates vascular hypercoagulability in cardiac transplant recipients.
2000 May 15
A new simvastatin (mevinolin)-resistance marker from Haloarcula hispanica and a new Haloferax volcanii strain cured of plasmid pHV2.
2001 Apr
Clinical and biochemical features, molecular diagnosis and long-term management of a case of cerebrotendinous xanthomatosis.
2001 Apr
Rhabdomyolysis due to simvastatin in a transplant patient: Are some statins safer than others?
2001 Apr
Efficacy and safety of combination simvastatin and colesevelam in patients with primary hypercholesterolemia.
2001 Apr 1
Differential effect of simvastatin on various signal transduction intermediates in cultured human smooth muscle cells.
2001 Apr 15
Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive C-reactive protein levels.
2001 Apr 17
Clinical relevance of statins: their role in secondary prevention.
2001 Feb
The effects of lacidipine on the steady/state plasma concentrations of simvastatin in healthy subjects.
2001 Feb
Treatment with simvastatin and low-dose aspirin depresses thrombin generation in patients with coronary heart disease and borderline-high cholesterol levels.
2001 Feb
[Statins: intervention studies, facts and perspectives].
2001 Feb
Anti-inflammatory effects of simvastatin in subjects with hypercholesterolemia.
2001 Feb
Preoperative lipid control with simvastatin reduces the risk for graft failure already 1 year after myocardial revascularization.
2001 Feb
Safety and efficacy of simvastatin for hyperlipidemia in renal transplant recipients: a double-blind, randomized, placebo-controlled study.
2001 Feb-Mar
Simvastatin: building on success.
2001 Jan
How cost-effective is the treatment of dyslipidemia in patients with diabetes but without cardiovascular disease?
2001 Jan
Simvastatin preserves coronary endothelial function in hypercholesterolemia in the absence of lipid lowering.
2001 Jan
Statin trials in progress: unanswered questions.
2001 Jan
Simvastatin and Ca(2+) signaling in endothelial cells: involvement of rho protein.
2001 Jan 19
[The role of HDL in the prevention of cardiovascular events].
2001 Jan 21
[Treatment with statins for the reduction of cardiovascular risk].
2001 Mar
High-dose simvastin (80 mg/day) decreases plasma concentrations of total homocyst(e)ine in patients with hypercholesteromia.
2001 Mar
Statin-fibrate combinations in patients with combined hyperlipedemia.
2001 Mar
Statin therapy--what now?
2001 Mar
Making the most of cholesterol-lowering margarines.
2001 Mar
HMG-CoA reductase inhibitors and P-glycoprotein modulation.
2001 Mar
Simvastatin improves arterial compliance in the lower limb but not in the aorta.
2001 Mar
Effects of simvastatin treatment on sICAM-1 and sE-selectin levels in hypercholesterolemic subjects.
2001 Mar
A comparison of the effects of 3-hydroxy-3-methylglutaryl-coenzyme a (HMG-CoA) reductase inhibitors on the CYP3A4-dependent oxidation of mexazolam in vitro.
2001 Mar
Pro and con: low-density lipoprotein cholesterol lowering is and will be the key to the future of lipid management.
2001 Mar 8
Patents

Patents

07175854
9
EP 33538
1
JP2001507331A
1
JP2002145770A
1
JP2002501887A
7
JP2002543189A
1
JP2003515526A
221
JP2005200419A
1
JP2006335658A
2
JP2006512417A
3
JP2006521825A
1
JP2007500677A
7
JP2007529285A
8
JP2008539832A
39
JP2009235105A
1
JP2009511496A
1
JP2009521905A
1
JP2009536078A
1
JP2010090094A
3
JP2010150288A
1
JP2011510067A
26
JP2011524897A
2
JP2011525181A
1
JP2011529067A
15
JP4078300B2
1
JP4708327B2
30
JP4832303B2
4
JP4833840B2
7
JPH0334934A
1
US 4444784
1

Sample Use Guides

In Vivo Use Guide
Dose range is 5 to 40 mg/day. Recommended usual starting dose is 10 or 20 mg once a day in the evening (for patients at high risk of Coronary heart defect is 40 mg/day). Due to the increased risk of myopathy, including rhabdomyolysis, use of the 80-mg dose of Simvastatin should be restricted to patients who have been taking simvastatin 80 mg chronically (e.g., for 12 months or more) without evidence of muscle toxicity.
Route of Administration: Oral
In Vitro Use Guide
Simvastatin (30 μM) significantly (P <0.01) inhibited the proliferative effect of H2O2 (0.5 mM) and its stimulatory actions on ERK1/2 phosphorylation, NF-κB activation and IL-8 production.
Substance Class Chemical
Created
by admin
on Fri Jun 25 21:02:49 UTC 2021
Edited
by admin
on Fri Jun 25 21:02:49 UTC 2021
Record UNII
AGG2FN16EV
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
SIMVASTATIN
EP   HSDB   INN   JAN   MART.   MI   ORANGE BOOK   USAN   USP   USP-RS   VANDF   WHO-DD  
INN   USAN  
Official Name English
SIMVASTATIN [MI]
Common Name English
SIMVASTATIN [JAN]
Common Name English
MK-0733
Code English
ZOCOR
Brand Name English
SIMVASTATIN [INN]
Common Name English
SIMVASTATIN COMPONENT OF SIMCOR
Common Name English
SIMVASTATIN [EP MONOGRAPH]
Common Name English
C10AA01
Code English
SIMCOR COMPONENT SIMVASTATIN
Common Name English
SIMVASTATIN [MART.]
Common Name English
SIMVASTATIN [USP MONOGRAPH]
Common Name English
SYNVINOLIN
Common Name English
SIMVASTATIN [ORANGE BOOK]
Common Name English
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
Common Name English
VYTORIN COMPONENT SIMVASTATIN
Common Name English
NSC-758706
Code English
SIMVASTATIN [VANDF]
Common Name English
MK-733
Code English
SIMVASTATIN [HSDB]
Common Name English
SIMVASTATIN [USAN]
Common Name English
SIMVASTATIN [WHO-DD]
Common Name English
POLYCAP COMPONENT SIMVASTATIN
Brand Name English
BUTANOIC ACID, 2,2-DIMETHYL-, 1,2,3,7,8,8A-HEXAHYDRO-3,7-DIMETHYL-8-(2-(TETRAHYDRO-4-HYDROXY-6-OXO-2H-PYRAN-2-YL)ETHYL)-1-NAPHTHALENYL ESTER, (1S-(1.ALPHA.,3.ALPHA.,7.BETA.,8.BETA.(2S*,4S*),8A.BETA.))-
Common Name English
SIMVASTATIN [USP-RS]
Common Name English
SIMVASTATIN COMPONENT OF VYTORIN
Common Name English
Classification Tree Code System Code
WHO-ATC C10BX04
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-ATC C10BA04
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-VATC QC10BA04
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
NCI_THESAURUS C1655
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-ATC A10BH51
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
NDF-RT N0000175589
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
LIVERTOX 888
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-VATC QC10BA02
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
WHO-VATC QC10AA01
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
WHO-VATC QA10BH51
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
WHO-ATC C10BA02
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
NDF-RT N0000000121
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-ATC C10AA01
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-VATC QC10BX01
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
WHO-ATC C10BX01
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
WHO-ESSENTIAL MEDICINES LIST 12.6
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
WHO-VATC QC10BX04
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
Code System Code Type Description
USP_CATALOG
1612700
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
PRIMARY USP-RS
EPA CompTox
79902-63-9
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
HSDB
7208
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
LACTMED
Simvastatin
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
ChEMBL
CHEMBL1064
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
NCI_THESAURUS
C29454
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
INN
6147
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
MERCK INDEX
M9947
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY Merck Index
MESH
D019821
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
CAS
79902-63-9
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
WIKIPEDIA
SIMVASTATIN
Created by admin on Fri Jun 25 21:02:50 UTC 2021 , Edited by admin on Fri Jun 25 21:02:50 UTC 2021
PRIMARY
DRUG BANK
DB00641
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
EVMPD
SUB10529MIG
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
DRUG CENTRAL
2445
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
FDA UNII
AGG2FN16EV
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
PUBCHEM
54454
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
RXCUI
36567
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY RxNorm
IUPHAR
2955
Created by admin on Fri Jun 25 21:02:49 UTC 2021 , Edited by admin on Fri Jun 25 21:02:49 UTC 2021
PRIMARY
Related Record Type Details
3-HYDROXY-3-METHYLGLUTARYL-COENZYME A REDUCTASE
TARGET -> INHIBITOR
OAT-3
TRANSPORTER -> INHIBITOR
CYTOCHROME P450 3A4
METABOLIC ENZYME -> SUBSTRATE
Structure of SIMVASTATIN
BASIS OF STRENGTH->SUBSTANCE
ASSAY (HPLC)
USP
OCT-1
TRANSPORTER -> INHIBITOR
OATP-B
TRANSPORTER -> INHIBITOR
SUBSTRATE USED: ESTRONE-3-SULFATE
OATP1B1
TRANSPORTER -> SUBSTRATE
OAT-1
TRANSPORTER -> INHIBITOR
Structure of SIMVASTATIN
BASIS OF STRENGTH->SUBSTANCE
ASSAY (HPLC)
EP
CYTOCHROME P450 3A5
METABOLIC ENZYME -> SUBSTRATE
Related Record Type Details
Structure of 6-HYDROXYSIMVASTATIN, (6S)-
METABOLITE ACTIVE -> PARENT
Structure of 2,2-DIMETHYLBUTYRIC ACID
METABOLITE -> PARENT
PLASMA
Structure of TENIVASTATIN
METABOLITE ACTIVE -> PRODRUG
MAJOR
Structure of 6-EXOMETHYLENESIMVASTATIN
METABOLITE ACTIVE -> PARENT
MAJOR
Structure of 3-HYDROXYSIMVASTATIN
METABOLITE ACTIVE -> PARENT
MAJOR
Related Record Type Details
Structure of SIMVASTATIN DIMER
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of TENIVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of LOVASTATIN
IMPURITY -> PARENT
sum of impurities E and F: not more than twice the area of the principal peak in the chromatogram obtained with reference solution (b) (1.0 per cent)
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of SIMVASTATIN DIMER
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of METHYLENE SIMVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of TENIVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of EPILOVASTATIN
IMPURITY -> PARENT
sum of impurities E and F: not more than twice the area of the principal peak in the chromatogram obtained with reference solution (b) (1.0 per cent)
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of METHYLENE SIMVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of LOVASTATIN
IMPURITY -> PARENT
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of EPILOVASTATIN
IMPURITY -> PARENT
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of ACETYL SIMVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of ANHYDRO SIMVASTATIN
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
Structure of ANHYDRO SIMVASTATIN
IMPURITY -> PARENT
sum of impurities B and C: not more than 1.6 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.8 per cent);
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Structure of ACETYL SIMVASTATIN
IMPURITY -> PARENT
sum of impurities B and C: not more than 1.6 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.8 per cent);
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
Name Property Type Amount Referenced Substance Defining Parameters References
Biological Half-life PHARMACOKINETIC SIMVASTATIN ACID
PHARMACOKINETIC
Tmax PHARMACOKINETIC
ORAL BIOAVAILABILITY PHARMACOKINETIC
NIH
NCATS
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