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:: 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.

Originator

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

Approval Year

TargetsConditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Preventing
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

693446400000
Primary
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

693446400000
Primary
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

693446400000
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
54.711 ng/mL
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
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
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
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
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
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
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
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
OverviewDrug as perpetrator​Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
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
minor
no
no
no
no
no
no
no
yes
yes
yes
yes (co-administration study)
Comment: Administered with cyclosporine: AUC of Simvastatin increased 2.6 fold
Tox targets

Tox targets

TargetModalityActivityMetaboliteClinical evidence
PubMed

PubMed

TitleDatePubMed
Rhabdomyolysis and acute renal failure after changing statin-fibrate combinations.
2000
Advantages of lipid-lowering therapy in cerebral ischemia: role of HMG-CoA reductase inhibitors.
2001
Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice.
2001 Apr
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
LpAI in HDL subfractions: serum levels in men and women with coronary heart disease and changes under hypolipemic therapy.
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
Cost-minimization analysis of simvastatin versus atorvastatin for maintenance therapy in patients with coronary or peripheral vascular disease.
2001 Feb
Clinical relevance of statins: their role in secondary prevention.
2001 Feb
Myositis, microvesicular hepatitis, and progression to cirrhosis from troglitazone added to simvastatin.
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
Anti-inflammatory effects of simvastatin in subjects with hypercholesterolemia.
2001 Feb
Fats, lipids and blood coagulation.
2001 Feb
Another reason to take your statin.
2001 Feb
Effect of simvastatin on micropulmonary red cell mass in patients with hyperlipoproteinemia.
2001 Feb 1
Fibrinogen response with simvastatin versus atorvastatin in familial hypercholesterolemia.
2001 Feb 1
Vascular effects of HMG CoA-reductase inhibitors (statins) unrelated to cholesterol lowering: new concepts for cardiovascular disease.
2001 Feb 1
Sildenafil-simvastatin interaction: possible cause of rhabdomyolysis?
2001 Feb 15
Hypolipidemic effect of NK-104 and other 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in guinea pigs.
2001 Jan
Simvastatin: building on success.
2001 Jan
Similar effects of atorvastatin, simvastatin and pravastatin on thrombogenic and inflammatory parameters in patients with hypercholesterolemia.
2001 Jan
[Antioxidative effects of fluvastatin, and its major metabolites [II]].
2001 Jan
Rhabdomyolysis secondary to a drug interaction between simvastatin and clarithromycin.
2001 Jan
How cost-effective is the treatment of dyslipidemia in patients with diabetes but without cardiovascular disease?
2001 Jan
Fragmentation study of simvastatin and lovastatin using electrospray ionization tandem mass spectrometry.
2001 Jan
Effective use of statins to prevent coronary heart disease.
2001 Jan 15
[The role of HDL in the prevention of cardiovascular events].
2001 Jan 21
Use of the statins in patients after acute myocardial infarction: does evidence change practice?
2001 Jan 22
Simvastatin promotes osteoblast differentiation and mineralization in MC3T3-E1 cells.
2001 Jan 26
The HMG-CoA reductase inhibitor simvastatin inhibits IFN-gamma induced MHC class II expression in human vascular endothelial cells.
2001 Jan 27
[Influence of FH Valencia 1 and 2 mutations of the LDL receptor gene on the response to simvastatin in subjects with molecularly defined heterozygous familial hypercholesterolemia in Spain].
2001 Jan 27
[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
The influence of short-term treatment with simvastatin on the inflammatory profile of patients with hypercholesterolaemia.
2001 Mar
Effect of simvastatin on vascular smooth muscle responsiveness: involvement of Ca(2+) homeostasis.
2001 Mar
Simvastatin treatment on postprandial hypertriglyceridemia in type 2 diabetes mellitus patients with combined hyperlipidemia.
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
Coronary artery reactivity after treatment with simvastatin.
2001 Mar
Magnetic resonance detects changes in phosphocholine associated with Ras activation and inhibition in NIH 3T3 cells.
2001 Mar 2
Pro and con: low-density lipoprotein cholesterol lowering is and will be the key to the future of lipid management.
2001 Mar 8
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
2001 Mar 8
An omega-3 polyunsaturated fatty acid concentrate administered for one year decreased triglycerides in simvastatin treated patients with coronary heart disease and persisting hypertriglyceridaemia.
2001 May
3-Hydroxy-3-methylglutaryl-CoA reductase inhibitors block calcium-dependent tyrosine kinase Pyk2 activation by angiotensin II in vascular endothelial cells. involvement of geranylgeranylation of small G protein Rap1.
2001 May 11
Cost effectiveness of HMG-CoA reductase inhibition in Canada.
2001 Spring
Patents

Sample Use Guides

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
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
TARGET -> INHIBITOR
TRANSPORTER -> INHIBITOR
METABOLIC ENZYME -> SUBSTRATE
BASIS OF STRENGTH->SUBSTANCE
ASSAY (HPLC)
USP
TRANSPORTER -> INHIBITOR
TRANSPORTER -> INHIBITOR
SUBSTRATE USED: ESTRONE-3-SULFATE
TRANSPORTER -> SUBSTRATE
TRANSPORTER -> INHIBITOR
BASIS OF STRENGTH->SUBSTANCE
ASSAY (HPLC)
EP
METABOLIC ENZYME -> SUBSTRATE
Related Record Type Details
METABOLITE ACTIVE -> PARENT
METABOLITE -> PARENT
PLASMA
METABOLITE ACTIVE -> PRODRUG
MAJOR
METABOLITE ACTIVE -> PARENT
MAJOR
METABOLITE ACTIVE -> PARENT
MAJOR
Related Record Type Details
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
IMPURITY -> PARENT
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
IMPURITY -> PARENT
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
IMPURITY -> PARENT
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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
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