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

Details

Stereochemistry ABSOLUTE
Molecular Formula C25H38O5
Molecular Weight 418.5662
Optical Activity UNSPECIFIED
Defined Stereocenters 7 / 7
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of SIMVASTATIN

SMILES

[H][C@]12[C@H](C[C@@H](C)C=C1C=C[C@H](C)[C@@H]2CC[C@@H]3C[C@@H](O)CC(=O)O3)OC(=O)C(C)(C)CC

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 418.5662
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

Tenivastatin (well known as simvastatin acid or simvastatin hydroxy acid) is a pharmacologically active metabolite, which is formed in the mammalian organism from lactone prodrug, simvastatin. Tenivastatin is a potent reversible inhibitor of HMGCR (HMG-CoA reductase), reduces cholesterol synthesis and increases low-density lipoprotein (LDL) receptors on cell membranes of liver and extrahepatic tissues. It is also a substrate of organic anion transporting polypeptide 1B1 (OATP1B1/Oatp2), an influx transporter expressed on the sinusoidal membrane of hepatocytes. Recent studies have shown that OATP1B1 plays a clinically important role in the hepatic elimination of several drugs including statins, via mediating the hepatic uptake. In addition, was discovered, that the tenivastatin was a substrate of another transporter protein, human organic anion transporting polypeptide 3A1 (OATP3A1), which is predominately expressed in the heart. Presence of OATP3A1 in cardiomyocytes suggested that transporter could modulate the exposure of cardiac tissue to simvastatin acid due to its enrichment in cardiomyocytes. Increases in the uptake of simvastatin acid by OATP3A1 when combined with OATP substrates suggest the potential for drug-drug interactions that could influence clinical outcomes.

Originator

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

Approval Year

Targets

Targets

Primary TargetPharmacologyConditionPotency
Target ID: Q9UIG8
Gene ID: 28232.0
Gene Symbol: SLCO3A1
Target Organism: Homo sapiens (Human)
Target ID: Q9Y6L6
Gene ID: 10599.0
Gene Symbol: SLCO1B1
Target Organism: Homo sapiens (Human)
Target ID: P04035
Gene ID: 3156.0
Gene Symbol: HMGCR
Target Organism: Homo sapiens (Human)
4.0 nM [IC50]
Conditions

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

1991
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

1991
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

1991
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
Two different types of exercise-induced muscle pain without myopathy and CK-elevation during HMG-Co-enzyme-A-reductase inhibitor treatment.
1999 Apr
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
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
Inhibitors of sterol biosynthesis and amphotericin B reduce the viability of pneumocystis carinii f. sp. carinii.
2000 Jun
Simvastatin modulates cytokine-mediated endothelial cell adhesion molecule induction: involvement of an inhibitory G protein.
2000 Sep 1
Involvement of Rho GTPases in the transcriptional inhibition of preproendothelin-1 gene expression by simvastatin in vascular endothelial cells.
2000 Sep 29
Advantages of lipid-lowering therapy in cerebral ischemia: role of HMG-CoA reductase inhibitors.
2001
Clinical relevance of statins: their role in secondary prevention.
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
Preoperative lipid control with simvastatin reduces the risk for graft failure already 1 year after myocardial revascularization.
2001 Feb
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
Protective effects of fluvastatin against reactive oxygen species induced DNA damage and mutagenesis.
2001 Jan
Hypolipidemic effect of NK-104 and other 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in guinea pigs.
2001 Jan
Simvastatin inhibits noradrenaline-induced hypertrophy of cultured neonatal rat cardiomyocytes.
2001 Jan
Simvastatin has anti-inflammatory and antiatherosclerotic activities independent of plasma cholesterol lowering.
2001 Jan
Effects of initial and long-term lipid-lowering therapy on vascular wall characteristics.
2001 Jan
Statins in children: what do we know and what do we need to do?
2001 Jan
New statins and new doses of older statins.
2001 Jan
Simvastatin and Ca(2+) signaling in endothelial cells: involvement of rho protein.
2001 Jan 19
Statins for stroke: the second story?
2001 Jan 23
High-dose simvastin (80 mg/day) decreases plasma concentrations of total homocyst(e)ine in patients with hypercholesteromia.
2001 Mar
Statin therapy--what now?
2001 Mar
HMG-CoA reductase inhibitors and P-glycoprotein modulation.
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
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
The influences of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of simvastatin, in relation to CYP3A4 inhibition.
2017 Apr
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 Sat Dec 16 17:27:52 GMT 2023
Edited
by admin
on Sat Dec 16 17:27:52 GMT 2023
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 [WHO-DD]
Common Name English
SIMVASTATIN [USAN]
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 Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-ATC C10BA04
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-VATC QC10BA04
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
NCI_THESAURUS C1655
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-ATC A10BH51
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
NDF-RT N0000175589
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
LIVERTOX NBK548720
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-VATC QC10BA02
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
WHO-VATC QC10AA01
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
WHO-VATC QA10BH51
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
WHO-ATC C10BA02
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
NDF-RT N0000000121
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-ATC C10AA01
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-VATC QC10BX01
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
WHO-ATC C10BX01
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
WHO-ESSENTIAL MEDICINES LIST 12.6
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
WHO-VATC QC10BX04
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
Code System Code Type Description
DAILYMED
AGG2FN16EV
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
EPA CompTox
DTXSID0023581
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
HSDB
7208
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
LACTMED
Simvastatin
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
ChEMBL
CHEMBL1064
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
NCI_THESAURUS
C29454
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
USAN
Y-41
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY
INN
6147
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
RS_ITEM_NUM
1612700
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY
MERCK INDEX
m9947
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY Merck Index
MESH
D019821
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
CHEBI
9150
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
CAS
79902-63-9
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
WIKIPEDIA
SIMVASTATIN
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY
DRUG BANK
DB00641
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
EVMPD
SUB10529MIG
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
DRUG CENTRAL
2445
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
FDA UNII
AGG2FN16EV
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
PUBCHEM
54454
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY
RXCUI
36567
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY RxNorm
NSC
758706
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
SMS_ID
100000091786
Created by admin on Sat Dec 16 17:27:54 GMT 2023 , Edited by admin on Sat Dec 16 17:27:54 GMT 2023
PRIMARY
IUPHAR
2955
Created by admin on Sat Dec 16 17:27:53 GMT 2023 , Edited by admin on Sat Dec 16 17:27:53 GMT 2023
PRIMARY
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