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
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
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 |
DescriptionCurator'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
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
Sources: https://www.google.com/patents/US4444784
Curator's Comment:: # Merck & Co., Inc.
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL340 |
|||
Target ID: CHEMBL402 |
4.0 nM [IC50] |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Preventing | ZOCOR Approved UseTherapy 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 Date6.9344638E11 |
|||
Primary | ZOCOR Approved UseTherapy 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 Date6.9344638E11 |
|||
Primary | ZOCOR Approved UseTherapy 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 Date6.9344638E11 |
Cmax
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
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 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
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
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 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
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
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 |
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
---|---|---|
Drug as perpetrator
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
moderate [Ki 10 uM] | ||||
moderate [Ki 7.1 uM] | ||||
moderate | ||||
moderate | ||||
no | ||||
yes [IC50 9 uM] | ||||
yes |
Drug as victim
Target | Modality | Activity | Metabolite | Clinical 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
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
PubMed
Title | Date | PubMed |
---|---|---|
[Rhabdomyolysis and cholestatic hepatitis under treatment with simvastatin and chlorzoxazone]. | 1999 Apr 3 |
|
Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl-CoA reductase activity and mRNA abundance in the guinea pig. | 1999 Dec |
|
Rhabdomyolysis and acute renal failure due to combination therapy with simvastatin and warfarin. | 1999 Dec |
|
[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 |
|
Direct inhibitory effects of simvastatin on matrix accumulation in cultured murine mesangial cells. | 1999 Jul |
|
Effect of simvastatin on proliferative nephritis and cell-cycle protein expression. | 1999 Jul |
|
Differential regulation of apolipoprotein B secretion from HepG2 cells by two HMG-CoA reductase inhibitors, atorvastatin and simvastatin. | 1999 Jun |
|
The type of mutation in the low density lipoprotein receptor gene influences the cholesterol-lowering response of the HMG-CoA reductase inhibitor simvastatin in patients with heterozygous familial hypercholesterolaemia. | 1999 Mar |
|
Effect of simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on alpha-fetoprotein gene expression through interaction with the ras-mediated pathway. | 1999 May |
|
Comparative effects of simvastatin and cholestyramine on plasma lipoproteins and CETP in humans. | 1999 Summer |
|
Calf and forearm blood flow in hypercholesterolemic patients. | 2000 Apr |
|
Inhibitors of sterol biosynthesis and amphotericin B reduce the viability of pneumocystis carinii f. sp. carinii. | 2000 Jun |
|
Does vitamin E beneficially affect muscle pains during HMG-Co-enzyme-A-reductase inhibitors without CK-elevation? | 2000 Mar |
|
Simvastatin attenuates vascular hypercoagulability in cardiac transplant recipients. | 2000 May 15 |
|
Compactin and simvastatin, but not pravastatin, induce bone morphogenetic protein-2 in human osteosarcoma cells. | 2000 May 19 |
|
Simvastatin modulates cytokine-mediated endothelial cell adhesion molecule induction: involvement of an inhibitory G protein. | 2000 Sep 1 |
|
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 |
|
Comparative study of HMG-CoA reductase inhibitors on fibrinogen. | 2001 Apr |
|
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 |
|
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 |
|
Fats, lipids and blood coagulation. | 2001 Feb |
|
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 |
|
Fragmentation study of simvastatin and lovastatin using electrospray ionization tandem mass spectrometry. | 2001 Jan |
|
Simvastatin inhibits noradrenaline-induced hypertrophy of cultured neonatal rat cardiomyocytes. | 2001 Jan |
|
Effective use of statins to prevent coronary heart disease. | 2001 Jan 15 |
|
Effectiveness of high doses of simvastatin as monotherapy in mixed hyperlipidemia. | 2001 Jan 15 |
|
Use of the statins in patients after acute myocardial infarction: does evidence change practice? | 2001 Jan 22 |
|
Statins for stroke: the second story? | 2001 Jan 23 |
|
Simvastatin promotes osteoblast differentiation and mineralization in MC3T3-E1 cells. | 2001 Jan 26 |
|
[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 |
|
Making the most of cholesterol-lowering margarines. | 2001 Mar |
|
Cholesterol metabolism in primary biliary cirrhosis during simvastatin and UDCA administration. | 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 |
|
Coronary artery reactivity after treatment with simvastatin. | 2001 Mar |
|
Comparison of efficacy and safety of atorvastatin (10mg) with simvastatin (10mg) at six weeks. ASSET Investigators. | 2001 Mar 1 |
|
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 |
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
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/25432084
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
Edited
Fri Jun 25 21:02:49 UTC 2021
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admin
on
Fri Jun 25 21:02:49 UTC 2021
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Record UNII |
AGG2FN16EV
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Record Status |
Validated (UNII)
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Record Version |
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WHO-ATC |
C10BX04
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WHO-ATC |
C10BA04
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WHO-VATC |
QC10BA04
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NCI_THESAURUS |
C1655
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WHO-ATC |
A10BH51
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NDF-RT |
N0000175589
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LIVERTOX |
888
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WHO-VATC |
QC10BA02
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WHO-VATC |
QC10AA01
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WHO-VATC |
QA10BH51
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WHO-ATC |
C10BA02
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NDF-RT |
N0000000121
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WHO-ATC |
C10AA01
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WHO-VATC |
QC10BX01
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WHO-ATC |
C10BX01
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WHO-ESSENTIAL MEDICINES LIST |
12.6
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WHO-VATC |
QC10BX04
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Code System | Code | Type | Description | ||
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1612700
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PRIMARY | USP-RS | ||
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79902-63-9
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7208
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Simvastatin
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PRIMARY | |||
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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
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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
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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
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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
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PRIMARY | Merck Index | ||
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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
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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
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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
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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
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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
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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
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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
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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
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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
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PRIMARY | RxNorm | ||
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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
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Related Record | Type | Details | ||
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TARGET -> INHIBITOR | |||
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TRANSPORTER -> INHIBITOR | |||
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METABOLIC ENZYME -> SUBSTRATE | |||
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BASIS OF STRENGTH->SUBSTANCE |
ASSAY (HPLC)
USP
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TRANSPORTER -> INHIBITOR | |||
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TRANSPORTER -> INHIBITOR |
SUBSTRATE USED: ESTRONE-3-SULFATE
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TRANSPORTER -> SUBSTRATE | |||
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TRANSPORTER -> INHIBITOR | |||
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BASIS OF STRENGTH->SUBSTANCE |
ASSAY (HPLC)
EP
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METABOLIC ENZYME -> SUBSTRATE |
Related Record | Type | Details | ||
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METABOLITE ACTIVE -> PARENT | |||
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METABOLITE -> PARENT |
PLASMA
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METABOLITE ACTIVE -> PRODRUG |
MAJOR
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METABOLITE ACTIVE -> PARENT |
MAJOR
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METABOLITE ACTIVE -> PARENT |
MAJOR
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Related Record | Type | Details | ||
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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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
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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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
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
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IMPURITY -> PARENT |
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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IMPURITY -> PARENT |
Epilovastatin and Lovastatin 1.0%
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
USP
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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
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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
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Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
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Biological Half-life | PHARMACOKINETIC |
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SIMVASTATIN ACID PHARMACOKINETIC |
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Tmax | PHARMACOKINETIC |
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ORAL BIOAVAILABILITY | PHARMACOKINETIC |
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