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Details

Stereochemistry ABSOLUTE
Molecular Formula C33H35FN2O5.C6H14N2O2
Molecular Weight 704.8274
Optical Activity UNSPECIFIED
Defined Stereocenters 3 / 3
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of ATORVASTATIN LYSINE

SMILES

NCCCC[C@H](N)C(O)=O.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=OGVHFUBTPHZMJC-KLMFVFGRSA-N
InChI=1S/C33H35FN2O5.C6H14N2O2/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;7-4-2-1-3-5(8)6(9)10/h3-16,21,26-27,37-38H,17-20H2,1-2H3,(H,35,41)(H,39,40);5H,1-4,7-8H2,(H,9,10)/t26-,27-;5-/m10/s1

HIDE SMILES / InChI
Molecular Formula C6H14N2O2
Molecular Weight 146.1876
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 1 / 1
E/Z Centers 0
Optical Activity UNSPECIFIED
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

Description
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

Parke Davis|Warner-Lambert
10
Curator's Comment: In 2000 Pfizer bought Warner-Lambert along with all of its subsidiary companies.

Approval Year

1996
225
Targets

Targets

Primary TargetPharmacologyConditionPotency
Inhibitor
8297
 14.0 nM [Ki]
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Preventing
Approved
8429
LIPITOR

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 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 Date

1996
Primary
Approved
8429
LIPITOR

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 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 Date

1996
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
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

AUC

ValueDoseCo-administeredAnalytePopulation
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

T1/2

ValueDoseCo-administeredAnalytePopulation
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
Sourcing

Sourcing

Vendor/AggregatorIDURL
ChEBI
CHEBI:39548
https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:39548
ChemicalBook
CB4239912
https://www.chemicalbook.com/ChemicalProductProperty_EN_CB4239912
ChemicalBook
CB81269853
https://www.chemicalbook.com/ChemicalProductProperty_EN_CB81269853
MolPort
MolPort-000-883-773
https://www.molport.com/shop/molecule-link/MolPort-000-883-773
ZINC
ZINC000003920719
http://zinc15.docking.org/substances/ZINC000003920719
eMolecules
877278
https://www.emolecules.com/cgi-bin/more?vid=877278
PubMed

PubMed

TitleDatePubMed
Effects of statins on biomarkers of bone metabolism: a randomised trial.
2001 Apr
Therapeutic change of HMG-CoA reductase inhibitors in patients with coronary artery disease.
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
Assessing the results: phase 1 hyperlipidemia outcomes in 27 health plans.
2001 Apr 16
Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive C-reactive protein levels.
2001 Apr 17
Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial.
2001 Apr 4
Effect of atorvastatin on low-density lipoprotein subtypes in patients with different forms of hyperlipoproteinemia and control subjects.
2001 Aug
The effect of aggressive versus standard lipid lowering by atorvastatin on diabetic dyslipidemia: the DALI study: a double-blind, randomized, placebo-controlled trial in patients with type 2 diabetes and diabetic dyslipidemia.
2001 Aug
Heart rate variability after long-term treatment with atorvastatin in hypercholesterolaemic patients with or without coronary artery disease.
2001 Aug
Human breath isoprene and its relation to blood cholesterol levels: new measurements and modeling.
2001 Aug
Effects of atorvastatin and omega-3 fatty acids on LDL subfractions and postprandial hyperlipemia in patients with combined hyperlipemia.
2001 Feb
Treatment of heterozygous familial hypercholesterolemia: atorvastatin vs simvastatin.
2001 Feb
Cost-minimization analysis of simvastatin versus atorvastatin for maintenance therapy in patients with coronary or peripheral vascular disease.
2001 Feb
[Statins and diabetic hyperlipidemia].
2001 Feb
Do HMG-CoA reductase inhibitors affect fibrinogen?
2001 Feb
Drug therapy or coronary angioplasty for the treatment of coronary artery disease: new insights.
2001 Feb
Aggressive LDL-cholesterol lowering with atorvastatin results in regression of atherosclerosis.
2001 Feb-Mar
[Lymphocyte infiltration in superficial dermis].
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
Rhabdomyolysis secondary to a drug interaction between simvastatin and clarithromycin.
2001 Jan
Statins in children: what do we know and what do we need to do?
2001 Jan
[Disturbances in cholesterol metabolism].
2001 Jan 19
Hydroxy-methylglutaryl-coenzyme A reductase inhibition promotes endothelial nitric oxide synthase activation through a decrease in caveolin abundance.
2001 Jan 2
[The role of HDL in the prevention of cardiovascular events].
2001 Jan 21
Cerivastatin triggers tumor-specific apoptosis with higher efficacy than lovastatin.
2001 Jul
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
HMG-CoA reductase inhibitors (statins) characterized as direct inhibitors of P-glycoprotein.
2001 Jun
Low-density lipoprotein apheresis in a patient aged 3.5 years.
2001 Jun
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
Effect of atorvastatin on plasminogen activator inhibitor type-1 synthesis in human monocytes/macrophages.
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
Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease.
2001 Jun 19
HMG-CoA reductase inhibitors and P-glycoprotein modulation.
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
Tachyphylaxis and statin drugs.
2001 Mar 1
[Decreasing blood lipids for prevention of coronary heart disease--discussion of the "permissive LDL level". Diagnostic imaging facilitates therapeutic decision].
2001 Mar 29
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
2001 Mar 8
Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes. The MIRACL study.
2001 Mar-Apr
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
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
Genetic analysis of digestive physiology using fluorescent phospholipid reporters.
2001 May 18
Patents

Patents

07534810
10
08822703
10
JP2002234871A
13
JP2002541106A
98
JP2003500487A
24
JP2003513036A
14
JP2003518130A
14
JP2004511521A
14
JP2005523255A
21
JP2006515186A
38
JP2007506649A
19
JP2007512228A
19
JP2009235100A
10
JP2009509013A
52
JP2009512711A
15
JP2009531466A
75
JP2009538831A
25
JP2010500290A
18
JP2011524416A
138
JP2011529928A
14
US5273995
10

Sample Use Guides

In Vivo Use Guide
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
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 Sat Dec 16 16:07:48 GMT 2023
Edited
by admin
on Sat Dec 16 16:07:48 GMT 2023
Record UNII
WK4UJ44C6N
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
ATORVASTATIN LYSINE
Common Name English
Atorvastatin l-lysine [WHO-DD]
Common Name English
L-LYSINE, (.BETA.R,.DELTA.R)-2-(4-FLUOROPHENYL)-.BETA.,.DELTA.-DIHYDROXY-5-(1-METHYLETHYL)-3-PHENYL-4-((PHENYLAMINO)CARBONYL)-1H-PYRROLE-1-HEPTANOATE (1:1)
Systematic Name English
ATORVASTATIN L-LYSINE
Common Name English
Code System Code Type Description
PUBCHEM
9939961
Created by admin on Sat Dec 16 16:07:48 GMT 2023 , Edited by admin on Sat Dec 16 16:07:48 GMT 2023
PRIMARY
CAS
609843-23-4
Created by admin on Sat Dec 16 16:07:48 GMT 2023 , Edited by admin on Sat Dec 16 16:07:48 GMT 2023
PRIMARY
SMS_ID
100000170402
Created by admin on Sat Dec 16 16:07:48 GMT 2023 , Edited by admin on Sat Dec 16 16:07:48 GMT 2023
PRIMARY
FDA UNII
WK4UJ44C6N
Created by admin on Sat Dec 16 16:07:48 GMT 2023 , Edited by admin on Sat Dec 16 16:07:48 GMT 2023
PRIMARY
Related Record Type Details
Structure of ATORVASTATIN
PARENT -> SALT/SOLVATE
Related Record Type Details
Structure of ATORVASTATIN
ACTIVE MOIETY
Name Property Type Amount Referenced Substance Defining Parameters References
Biological Half-life PHARMACOKINETIC
Tmax PHARMACOKINETIC
Volume of Distribution PHARMACOKINETIC
Biological Half-life PHARMACOKINETIC
ORAL BIOAVAILABILITY PHARMACOKINETIC HMG-CoA REDUCTASE INHIBITORY ACTIVITY

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