Details
| Stereochemistry | ABSOLUTE |
| Molecular Formula | 2C33H34FN2O5.Sr.10H2O |
| Molecular Weight | 1383.04 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 4 / 4 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
O.O.O.O.O.O.O.O.O.O.[Sr++].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.CC(C)C5=C(C(=O)NC6=CC=CC=C6)C(=C(N5CC[C@@H](O)C[C@@H](O)CC([O-])=O)C7=CC=C(F)C=C7)C8=CC=CC=C8
InChI
InChIKey=BBDJXEPNNLXCKB-OIHIBBKGSA-L
InChI=1S/2C33H35FN2O5.10H2O.Sr/c2*1-21(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;;;;;;;;;;;/h2*3-16,21,26-27,37-38H,17-20H2,1-2H3,(H,35,41)(H,39,40);10*1H2;/q;;;;;;;;;;;;+2/p-2/t2*26-,27-;;;;;;;;;;;/m11.........../s1
| Molecular Formula | H2O |
| Molecular Weight | 18.0153 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | Sr |
| Molecular Weight | 87.62 |
| Charge | 2 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | C33H34FN2O5 |
| Molecular Weight | 557.6319 |
| Charge | -1 |
| 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
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 |
|||
| 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 |
|---|---|---|
| A comparison of simvastatin and atorvastatin up to maximal recommended doses in a large multicenter randomized clinical trial. | 2001 |
|
| Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in hypercholesterolaemic rabbits. | 2001 |
|
| The effect of atorvastatin on serum lipids, lipoprotein(a) and plasma fibrinogen levels in primary dyslipidaemia--a pilot study involving serial sampling. | 2001 |
|
| Effects of statins on biomarkers of bone metabolism: a randomised trial. | 2001 Apr |
|
| Possible short-term amelioration of basilar plaque by high-dose atorvastatin: use of reductase inhibitors for intracranial plaque stabilization. | 2001 Apr |
|
| Chitotriosidase genotype and serum activity in subjects with combined hyperlipidemia: effect of the lipid-lowering agents, atorvastatin and bezafibrate. | 2001 Apr |
|
| Linear IgA bullous dermatosis induced by atorvastatin. | 2001 Apr |
|
| Comparative study of HMG-CoA reductase inhibitors on fibrinogen. | 2001 Apr |
|
| Tachyphylaxis in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. | 2001 Apr 15 |
|
| Assessing the results: phase 1 hyperlipidemia outcomes in 27 health plans. | 2001 Apr 16 |
|
| Lipid-lowering therapy in acute coronary syndromes. | 2001 Apr 4 |
|
| Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial. | 2001 Apr 4 |
|
| [Prevention in coronary heart disease. Can a CSE inhibitor arrest calcium deposits?]. | 2001 Apr 5 |
|
| Effect of atorvastatin on low-density lipoprotein subtypes in patients with different forms of hyperlipoproteinemia and control subjects. | 2001 Aug |
|
| Heart rate variability after long-term treatment with atorvastatin in hypercholesterolaemic patients with or without coronary artery disease. | 2001 Aug |
|
| Cost-minimization analysis of simvastatin versus atorvastatin for maintenance therapy in patients with coronary or peripheral vascular disease. | 2001 Feb |
|
| [Statins and unstable angina: MIRACL]. | 2001 Feb |
|
| Elevated baseline triglyceride levels modulate effects of HMGCoA reductase inhibitors on plasma lipoproteins. | 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 |
|
| Efficacy and drug interactions of the new HMG-CoA reductase inhibitors cerivastatin and atorvastatin in CsA-treated renal transplant recipients. | 2001 Jan |
|
| Similar effects of atorvastatin, simvastatin and pravastatin on thrombogenic and inflammatory parameters in patients with hypercholesterolemia. | 2001 Jan |
|
| [The role of HDL in the prevention of cardiovascular events]. | 2001 Jan 21 |
|
| Prolonged inhibition of cholesterol synthesis by atorvastatin inhibits apo B-100 and triglyceride secretion from HepG2 cells. | 2001 Jul |
|
| Atorvastatin versus micronized fenofibrate in the treatment of patients with mixed hyperlipoproteinemia. | 2001 Jul 15 |
|
| Use of intravascular ultrasound to compare effects of different strategies of lipid-lowering therapy on plaque volume and composition in patients with coronary artery disease. | 2001 Jul 24 |
|
| Statin-stimulated nitric oxide release from endothelium. | 2001 Jul-Aug |
|
| The effect of atorvastatin on postprandial lipaemia in overweight or obese women homozygous for apo E3. | 2001 Jun |
|
| Effects of low doses of simvastatin and atorvastatin on high-density lipoprotein cholesterol levels in patients with hypercholesterolemia. | 2001 Jun |
|
| Low-density lipoprotein apheresis in a patient aged 3.5 years. | 2001 Jun |
|
| Is a mechanical or a metabolic approach superior in the treatment of coronary disease? Results of the atorvastatin versus revascularization (AVERT) trial. | 2001 Jun |
|
| Rationale, design, methods and baseline demography of participants of the Anglo-Scandinavian Cardiac Outcomes Trial. ASCOT investigators. | 2001 Jun |
|
| Effect of atorvastatin on plasminogen activator inhibitor type-1 synthesis in human monocytes/macrophages. | 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 |
|
| Limitation of heart growth in neonatal piglets by simvastatin and atorvastatin: comparison with pravastatin. | 2001 Jun |
|
| Atorvastatin-induced dermatomyositis. | 2001 Jun 1 |
|
| [Atorvastatin]. | 2001 Mar |
|
| [AVERT [The Atorvastatin versus Revascularization Treatment]]. | 2001 Mar |
|
| Statin therapy--what now? | 2001 Mar |
|
| [Decreasing blood lipids for prevention of coronary heart disease--discussion of the "permissive LDL level". Diagnostic imaging facilitates therapeutic decision]. | 2001 Mar 29 |
|
| Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes. The MIRACL study. | 2001 Mar-Apr |
|
| Dermographism: an adverse effect of atorvastatin. | 2001 Mar-Apr |
|
| 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 |
|
| Atorvastatin. | 2001 May |
|
| Aggressive versus moderate lipid-lowering therapy in postmenopausal women with hypercholesterolemia: Rationale and design of the Beyond Endorsed Lipid Lowering with EBT Scanning (BELLES) trial. | 2001 May |
|
| Repeated analysis of semen parameters in beagle dogs during a 2-year study with the HMG-CoA reductase inhibitor, atorvastatin. | 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
| Substance Class |
Chemical
Created
by
admin
on
Edited
Sat Dec 16 19:20:16 GMT 2023
by
admin
on
Sat Dec 16 19:20:16 GMT 2023
|
| Record UNII |
5F4N5Y2B7Y
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| Record Status |
Validated (UNII)
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| Record Version |
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-
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164888920
Created by
admin on Sat Dec 16 19:20:17 GMT 2023 , Edited by admin on Sat Dec 16 19:20:17 GMT 2023
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5F4N5Y2B7Y
Created by
admin on Sat Dec 16 19:20:17 GMT 2023 , Edited by admin on Sat Dec 16 19:20:17 GMT 2023
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1072903-93-5
Created by
admin on Sat Dec 16 19:20:17 GMT 2023 , Edited by admin on Sat Dec 16 19:20:17 GMT 2023
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PRIMARY |
| Related Record | Type | Details | ||
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PARENT -> SALT/SOLVATE |
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ANHYDROUS->SOLVATE |
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| Related Record | Type | Details | ||
|---|---|---|---|---|
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ACTIVE MOIETY |
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