Details
Stereochemistry | ABSOLUTE |
Molecular Formula | C33H35FN2O5 |
Molecular Weight | 558.6398 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 2 / 2 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)C1=C(C(=O)NC2=CC=CC=C2)C(=C(N1CC[C@@H](O)C[C@@H](O)CC(O)=O)C3=CC=C(F)C=C3)C4=CC=CC=C4
InChI
InChIKey=XUKUURHRXDUEBC-KAYWLYCHSA-N
InChI=1S/C33H35FN2O5/c1-21(2)31-30(33(41)35-25-11-7-4-8-12-25)29(22-9-5-3-6-10-22)32(23-13-15-24(34)16-14-23)36(31)18-17-26(37)19-27(38)20-28(39)40/h3-16,21,26-27,37-38H,17-20H2,1-2H3,(H,35,41)(H,39,40)/t26-,27-/m1/s1
Molecular Formula | C33H35FN2O5 |
Molecular Weight | 558.6398 |
Charge | 0 |
Count |
|
Stereochemistry | ABSOLUTE |
Additional Stereochemistry | No |
Defined Stereocenters | 2 / 2 |
E/Z Centers | 0 |
Optical Activity | UNSPECIFIED |
DescriptionCurator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/mesh/2009919
Curator's Comment: description was created based on several sources, including
https://www.ncbi.nlm.nih.gov/mesh/2009919
Atorvastatin calcium (LIPITOR®) is a pyrrole and heptanoic acid derivative, a synthetic lipid-lowering agent. Atorvastatin is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. Atorvastatin is used to reduce serum levels of LDL(low-density lipoprotein)-cholesterol; apolipoprotein B; and triglycerides and to increase serum levels of HDL(high-density lipoprotein)-cholesterol in the treatment of hyperlipidemias and prevention of cardiovascular disease in patients with multiple risk factors.
CNS Activity
Originator
Sources: https://www.ncbi.nlm.nih.gov/pubmed/2166504
Curator's Comment: In 2000 Pfizer bought Warner-Lambert along with all of its subsidiary companies.
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL402 |
14.0 nM [Ki] |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Preventing | LIPITOR 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 recommended 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 CHD or multiple risk factors for CHD, atorvastatin calcium tablets can be started simultaneously with diet. Atorvastatin calcium tablets are an inhibitor of HMG-CoA reductase (statin) indicated as an adjunct therapy to diet to: Reduce the risk of MI, stroke, revascularization procedures, and angina in patients without CHD, but with multiple risk factors (1.1). Reduce the risk of MI and stroke in patients with type 2 diabetes without CHD, but with multiple risk factors (1.1). Reduce the risk of non-fatal MI, fatal and non-fatal stroke, revascularization procedures, hospitalization for CHF, and angina in patients with CHD (1.1). Reduce elevated total-C, LDL-C, apo B, and TG levels and increase HDL-C in adult patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (1.2). Reduce elevated TG in patients with hypertriglyceridemia and primary dysbetalipoproteinemia (1.2). Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia (HoFH) (1.2). Reduce elevated total-C, LDL-C, and apo B levels 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). Limitations of Use Atorvastatin calcium tablets have not been studied in Fredrickson Types I and V dyslipidemias. 1.1 Prevention of Cardiovascular Disease In adult patients without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as age, smoking, hypertension, low HDL-C, or a family history of early coronary heart disease, atorvastatin calcium tablets are indicated to: Reduce the risk of myocardial infarction Reduce the risk of stroke Reduce the risk for revascularization procedures and angina In patients with type 2 diabetes, and without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as retinopathy, albuminuria, smoking, or hypertension, atorvastatin calcium tablets are indicated to: Reduce the risk of myocardial infarction Reduce the risk of stroke In patients with clinically evident coronary heart disease, atorvastatin calcium tablets are indicated to: Reduce the risk of non-fatal myocardial infarction Reduce the risk of fatal and non-fatal stroke Reduce the risk for revascularization procedures Reduce the risk of hospitalization for CHF Reduce the risk of angina 1.2 Hyperlipidemia Atorvastatin calcium tablets are indicated: As an adjunct to diet to reduce elevated total-C, LDL-C, apo B, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia ( Types IIa and IIb); Fredrickson As an adjunct to diet for the treatment of patients with elevated serum TG levels ( Type IV); Fredrickson For the treatment of patients with primary dysbetalipoproteinemia ( Type III) who do not respond adequately to diet; Fredrickson To 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; As an adjunct to diet to reduce total-C, LDL-C, and apo B levels in boys and postmenarchal girls, 10 to 17 years of age, with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C remains ≥ 190 mg/dL or LDL-C remains ≥ 160 mg/dL and: there is a positive family history of premature cardiovascular disease or two or more other CVD risk factors are present in the pediatric patient. Launch Date1996 |
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Primary | LIPITOR 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 recommended 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 CHD or multiple risk factors for CHD, atorvastatin calcium tablets can be started simultaneously with diet. Atorvastatin calcium tablets are an inhibitor of HMG-CoA reductase (statin) indicated as an adjunct therapy to diet to: Reduce the risk of MI, stroke, revascularization procedures, and angina in patients without CHD, but with multiple risk factors (1.1). Reduce the risk of MI and stroke in patients with type 2 diabetes without CHD, but with multiple risk factors (1.1). Reduce the risk of non-fatal MI, fatal and non-fatal stroke, revascularization procedures, hospitalization for CHF, and angina in patients with CHD (1.1). Reduce elevated total-C, LDL-C, apo B, and TG levels and increase HDL-C in adult patients with primary hyperlipidemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (1.2). Reduce elevated TG in patients with hypertriglyceridemia and primary dysbetalipoproteinemia (1.2). Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia (HoFH) (1.2). Reduce elevated total-C, LDL-C, and apo B levels 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). Limitations of Use Atorvastatin calcium tablets have not been studied in Fredrickson Types I and V dyslipidemias. 1.1 Prevention of Cardiovascular Disease In adult patients without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as age, smoking, hypertension, low HDL-C, or a family history of early coronary heart disease, atorvastatin calcium tablets are indicated to: Reduce the risk of myocardial infarction Reduce the risk of stroke Reduce the risk for revascularization procedures and angina In patients with type 2 diabetes, and without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as retinopathy, albuminuria, smoking, or hypertension, atorvastatin calcium tablets are indicated to: Reduce the risk of myocardial infarction Reduce the risk of stroke In patients with clinically evident coronary heart disease, atorvastatin calcium tablets are indicated to: Reduce the risk of non-fatal myocardial infarction Reduce the risk of fatal and non-fatal stroke Reduce the risk for revascularization procedures Reduce the risk of hospitalization for CHF Reduce the risk of angina 1.2 Hyperlipidemia Atorvastatin calcium tablets are indicated: As an adjunct to diet to reduce elevated total-C, LDL-C, apo B, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia ( Types IIa and IIb); Fredrickson As an adjunct to diet for the treatment of patients with elevated serum TG levels ( Type IV); Fredrickson For the treatment of patients with primary dysbetalipoproteinemia ( Type III) who do not respond adequately to diet; Fredrickson To 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; As an adjunct to diet to reduce total-C, LDL-C, and apo B levels in boys and postmenarchal girls, 10 to 17 years of age, with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C remains ≥ 190 mg/dL or LDL-C remains ≥ 160 mg/dL and: there is a positive family history of premature cardiovascular disease or two or more other CVD risk factors are present in the pediatric patient. Launch Date1996 |
Cmax
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
8.8 ng/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29683561 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED |
|
9.52 ng/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/31450089 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
|
33.24 ng/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT00844376 |
80 mg single, oral dose: 80 mg route of administration: oral experiment type: single co-administered: |
ATORVASTATIN plasma | Homo sapiens |
AUC
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
45 ng × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29683561 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED |
|
35.04 ng × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/31450089 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
|
140.79 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT00844376 |
80 mg single, oral dose: 80 mg route of administration: oral experiment type: single co-administered: |
ATORVASTATIN plasma | Homo sapiens |
|
137.49 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT00844376 |
80 mg single, oral dose: 80 mg route of administration: oral experiment type: single co-administered: |
ATORVASTATIN plasma | Homo sapiens |
|
142.86 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT00844376 |
80 mg single, oral dose: 80 mg route of administration: oral experiment type: single co-administered: |
ATORVASTATIN plasma | Homo sapiens |
T1/2
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
6.2 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29683561 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE food status: FASTED |
|
16.57 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/31450089 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ATORVASTATIN blood | Homo sapiens population: HEALTHY age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
|
7.21 h Clinical Trial https://clinicaltrials.gov/ct2/show/NCT00844376 |
80 mg single, oral dose: 80 mg route of administration: oral experiment type: single co-administered: |
ATORVASTATIN plasma | Homo sapiens |
PubMed
Title | Date | PubMed |
---|---|---|
Atorvastatin-induced cholestatic hepatitis in a young woman with systemic lupus erythematosus. Grupo Lupus Virgen de las Nieves. | 1999 Aug 9-23 |
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Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl-CoA reductase activity and mRNA abundance in the guinea pig. | 1999 Dec |
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Differential regulation of apolipoprotein B secretion from HepG2 cells by two HMG-CoA reductase inhibitors, atorvastatin and simvastatin. | 1999 Jun |
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Atorvastatin-induced acute hepatitis with absence of cross-toxicity with simvastatin. | 1999 May 22 |
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Atorvastatin increases ecNOS levels in human platelets of hyperlipidemic subjects. | 1999 Nov |
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Hypertriglyceridemia: a review of clinical relevance and treatment options: focus on cerivastatin. | 2001 |
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Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in hypercholesterolaemic rabbits. | 2001 |
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Therapeutic change of HMG-CoA reductase inhibitors in patients with coronary artery disease. | 2001 Apr |
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Linear IgA bullous dermatosis induced by atorvastatin. | 2001 Apr |
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Comparative study of HMG-CoA reductase inhibitors on fibrinogen. | 2001 Apr |
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Lipid-lowering therapy in acute coronary syndromes. | 2001 Apr 4 |
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[Prevention in coronary heart disease. Can a CSE inhibitor arrest calcium deposits?]. | 2001 Apr 5 |
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Human breath isoprene and its relation to blood cholesterol levels: new measurements and modeling. | 2001 Aug |
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Effect of niacin and atorvastatin on lipoprotein subclasses in patients with atherogenic dyslipidemia. | 2001 Aug 1 |
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Treatment of heterozygous familial hypercholesterolemia: atorvastatin vs simvastatin. | 2001 Feb |
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A four-column parallel chromatography system for isocratic or gradient LC/MS analyses. | 2001 Feb 1 |
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Effect of atorvastatin 15 mg/week on serum lipids in patients with hypercholesterolemia. | 2001 Feb 1 |
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[Atorvastatin (Lipitor): a review of its pharmacological and clinical profile]. | 2001 Jan |
|
[Lymphocyte infiltration in superficial dermis]. | 2001 Jan |
|
[Cost-effectiveness of atorvastatin against simvastatin as hypolipemic treatment in hypercholesterolemic patients in primary care]. | 2001 Jan |
|
Hypolipidemic effect of NK-104 and other 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in guinea pigs. | 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 |
|
Statin trials in progress: unanswered questions. | 2001 Jan |
|
[The role of HDL in the prevention of cardiovascular events]. | 2001 Jan 21 |
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The effects of converting from simvastatin to atorvastatin on plasminogen activator inhibitor type-1. | 2001 Jul |
|
HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species. | 2001 Jun |
|
Rationale, design, methods and baseline demography of participants of the Anglo-Scandinavian Cardiac Outcomes Trial. ASCOT investigators. | 2001 Jun |
|
Growth hormone reduces plasma cholesterol in LDL receptor-deficient mice. | 2001 Jun |
|
Efficacy of atorvastatin in achieving National Cholesterol Education Program low-density lipoprotein targets in women with severe dyslipidemia and cardiovascular disease or risk factors for cardiovascular disease: The Women's Atorvastatin Trial on Cholesterol (WATCH). | 2001 Jun |
|
Atorvastatin-induced dermatomyositis. | 2001 Jun 1 |
|
Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease. | 2001 Jun 19 |
|
[Atorvastatin]. | 2001 Mar |
|
[AVERT [The Atorvastatin versus Revascularization Treatment]]. | 2001 Mar |
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HMG-CoA reductase inhibitors and P-glycoprotein modulation. | 2001 Mar |
|
Design and rationale of the ARBITER trial (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol)--a randomized trial comparing the effects of atorvastatin and pravastatin on carotid artery intima-media thickness. | 2001 Mar |
|
F 12511, a novel ACAT inhibitor, and atorvastatin regulate endogenous hypercholesterolemia in a synergistic manner in New Zealand rabbits fed a casein-enriched diet. | 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 |
|
Tachyphylaxis and statin drugs. | 2001 Mar 1 |
|
Comparison of efficacy and safety of atorvastatin (10mg) with simvastatin (10mg) at six weeks. ASSET Investigators. | 2001 Mar 1 |
|
A cost-effectiveness model of alternative statins to achieve target LDL-cholesterol levels. | 2001 May |
|
Statin induced myopathy does not show up in MIBI scintigraphy. | 2001 May |
|
Determinants of variable response to statin treatment in patients with refractory familial hypercholesterolemia. | 2001 May |
|
Structural mechanism for statin inhibition of HMG-CoA reductase. | 2001 May 11 |
|
Cost effectiveness of HMG-CoA reductase inhibition in Canada. | 2001 Spring |
Patents
Sample Use Guides
The recommended starting dose of atorvastatin calcium (LIPITOR®) is 10 or 20 mg once daily. Patients who require a large reduction in LDL(low-density lipoprotein)-cholesterol (more than 45%) may be started at 40 mg once daily. The dosage range of atorvastatin calcium is 10 to 80 mg once daily. Atorvastatin calcium can be administered as a single dose at any time of the day, with or without food. The starting dose and maintenance doses of atorvastatin calcium should be individualized according to patient characteristics such as goal of therapy and response. After initiation and/or upon titration of atorvastatinc calcium, lipid levels should be analyzed within 2 to 4 weeks and dosage adjusted accordingly.
Route of Administration:
Oral
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/1739744
In vitro, atorvastatin (CI-981) was equipotent as HMG-CoA reductase inhibitor in rat liver, spleen, testis and adrenal tissue (IC50 38.7 nM, 29.5 nM, 36.4, and 100.4 nM, respectively).
Substance Class |
Chemical
Created
by
admin
on
Edited
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by
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on
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Record UNII |
A0JWA85V8F
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Record Status |
Validated (UNII)
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WHO-VATC |
QC10BX03
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WHO-ATC |
C10AA05
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WHO-VATC |
QC10AA05
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WHO-ATC |
C10BX08
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LIVERTOX |
NBK548236
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NDF-RT |
N0000175589
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NCI_THESAURUS |
C1655
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WHO-ATC |
C10BX11
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WHO-ATC |
C10BA05
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WHO-ATC |
C10BX03
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WHO-ATC |
C10BX06
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WHO-VATC |
QC10BA05
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WHO-ATC |
C10BX15
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NDF-RT |
N0000000121
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WHO-ATC |
C10BX12
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100000092373
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CHEMBL1487
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2949
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Atorvastatin
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C065179
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Atorvastatin
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DTXSID8029868
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Related Record | Type | Details | ||
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TRANSPORTER -> INHIBITOR | |||
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SALT/SOLVATE -> PARENT | |||
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TARGET -> INHIBITOR | |||
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SALT/SOLVATE -> PARENT | |||
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TRANSPORTER -> INHIBITOR | |||
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TRANSPORTER -> SUBSTRATE | |||
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SALT/SOLVATE -> PARENT |
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SALT/SOLVATE -> PARENT |
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SALT/SOLVATE -> PARENT | |||
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TARGET -> INHIBITOR |
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PARENT -> SALT/SOLVATE | |||
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METABOLIC ENZYME -> SUBSTRATE | |||
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BINDER->LIGAND |
BINDING
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TRANSPORTER -> SUBSTRATE |
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TRANSPORTER -> INHIBITOR | |||
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SALT/SOLVATE -> PARENT | |||
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SALT/SOLVATE -> PARENT | |||
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TARGET -> INHIBITOR |
Related Record | Type | Details | ||
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METABOLITE -> PARENT |
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METABOLITE -> PARENT |
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METABOLITE ACTIVE -> PARENT |
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ACTIVE MOIETY |
Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
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Biological Half-life | PHARMACOKINETIC |
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Volume of Distribution | PHARMACOKINETIC |
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Tmax | PHARMACOKINETIC |
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ORAL BIOAVAILABILITY | PHARMACOKINETIC |
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HMG-CoA REDUCTASE INHIBITORY ACTIVITY |
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Biological Half-life | PHARMACOKINETIC |
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