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

Details

Stereochemistry ABSOLUTE
Molecular Formula C23H36O7
Molecular Weight 424.5286
Optical Activity UNSPECIFIED
Defined Stereocenters 8 / 8
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of PRAVASTATIN

SMILES

CC[C@]([H])(C)C(=O)O[C@@]1([H])C[C@@]([H])(C=C2C=C[C@]([H])(C)[C@]([H])(CC[C@]([H])(C[C@]([H])(CC(=O)O)O)O)[C@]21[H])O

InChI

InChIKey=TUZYXOIXSAXUGO-PZAWKZKUSA-N
InChI=1S/C23H36O7/c1-4-13(2)23(29)30-20-11-17(25)9-15-6-5-14(3)19(22(15)20)8-7-16(24)10-18(26)12-21(27)28/h5-6,9,13-14,16-20,22,24-26H,4,7-8,10-12H2,1-3H3,(H,27,28)/t13-,14-,16+,17+,18+,19-,20-,22-/m0/s1

HIDE SMILES / InChI

Description
Curator's Comment:: description was created based on several sources, including https://www.drugs.com/pravastatin.html | https://www.ncbi.nlm.nih.gov/pubmed/16960448 | http://reference.medscape.com/drug/pravachol-pravastatin-342460 | https://www.drugbank.ca/drugs/DB00175

Pravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used in combination with diet, exercise, and weight loss for lowering cholesterol and preventing cardiovascular disease. Pravastatin acts as a lipoprotein-lowering drug through two pathways. In the major pathway, pravastatin inhibits the function of hydroxymethylglutaryl-CoA (HMG-CoA) reductase. As a reversible competitive inhibitor, pravastatin sterically hinders the action of HMG-CoA reductase by occupying the active site of the enzyme. Taking place primarily in the liver, this enzyme is responsible for the conversion of HMG-CoA to mevalonate in the rate-limiting step of the biosynthetic pathway for cholesterol. Pravastatin also inhibits the synthesis of very-low-density lipoproteins, which are the precursor to low-density lipoproteins (LDL). These reductions increase the number of cellular LDL receptors, thus LDL uptake increases, removing it from the bloodstream. Pravastatin is primarily used for the treatment of dyslipidemia and the prevention of cardiovascular disease. It is recommended to be used only after other measures, such as diet, exercise, and weight reduction, have not improved cholesterol levels. The evidence for the use of pravastatin is generally weaker than for other statins. The antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT), failed to demonstrate a difference in all-cause mortality or nonfatal myocardial infarction/fatal coronary heart disease rates between patients receiving pravastatin 40 mg daily (a common starting dose) and those receiving usual care. Pravastatin is generally well tolerated; adverse reactions have usually been mild and transient. In 4-month-long placebo-controlled trials, 1.7% of Pravastatin-treated patients and 1.2% of placebo-treated patients were discontinued from treatment because of adverse experiences attributed to study drug therapy; this difference was not statistically significant.

CNS Activity

Originator

Approval Year

1991
105
Targets

Targets

Primary TargetPharmacologyConditionPotency
Inhibitor
7728
 1370.0 nM [IC50]
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Approved
8043
PRAVACHOL

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. Pravastatin sodium tablet, USP is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of MI, revascularization, and cardiovascular mortality in hypercholesterolemic patients without clinically evident CHD. ( 1.1) Reduce the risk of total mortality by reducing coronary death, MI, revascularization, stroke/TIA, and the progression of coronary atherosclerosis in patients with clinically evident CHD. ( 1.1) Reduce elevated Total-C, LDL-C, ApoB, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia. ( 1.2) Reduce elevated serum TG levels in patients with hypertriglyceridemia. ( 1.2) Treat patients with primary dysbetalipoproteinemia who are not responding to diet. ( 1.2) Treat children and adolescent patients ages 8 years and older with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. ( 1.2) Limitations of use: Pravastatin sodium tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. ( 1.3) 1.1 Prevention of Cardiovascular Disease In hypercholesterolemic patients without clinically evident coronary heart disease (CHD), pravastatin sodium tablets, USP are indicated to: reduce the risk of myocardial infarction (MI). reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of cardiovascular mortality with no increase in death from non-cardiovascular causes. In patients with clinically evident CHD, pravastatin sodium tablet is indicated to: reduce the risk of total mortality by reducing coronary death. reduce the risk of MI. reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of stroke and stroke/transient ischemic attack (TIA). slow the progression of coronary atherosclerosis. 1.2 Hyperlipidemia Pravastatin sodium tablet is indicated: as an adjunct to diet to reduce elevated total cholesterol (Total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and triglyceride (TG) levels and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hypercholesterolemia and mixed dyslipidemia ( Fredrickson Types IIa and IIb). 1 as an adjunct to diet for the treatment of patients with elevated serum TG levels ( Fredrickson Type IV). for the treatment of patients with primary dysbetalipoproteinemia ( Fredrickson Type III) who do not respond adequately to diet. as an adjunct to diet and lifestyle modification for treatment of heterozygous familial hypercholesterolemia (HeFH) in children and adolescent patients ages 8 years and older if after an adequate trial of diet 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 (CVD) or two or more other CVD risk factors are present in the patient. 1.3 Limitations of Use Pravastatin sodium has not been studied in conditions where the major lipoprotein abnormality is elevation of chylomicrons (Fredrickson Types I and V).

Launch Date

6.8886718E11
Primary
Approved
8043
PRAVACHOL

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. Pravastatin sodium tablet, USP is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of MI, revascularization, and cardiovascular mortality in hypercholesterolemic patients without clinically evident CHD. ( 1.1) Reduce the risk of total mortality by reducing coronary death, MI, revascularization, stroke/TIA, and the progression of coronary atherosclerosis in patients with clinically evident CHD. ( 1.1) Reduce elevated Total-C, LDL-C, ApoB, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia. ( 1.2) Reduce elevated serum TG levels in patients with hypertriglyceridemia. ( 1.2) Treat patients with primary dysbetalipoproteinemia who are not responding to diet. ( 1.2) Treat children and adolescent patients ages 8 years and older with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. ( 1.2) Limitations of use: Pravastatin sodium tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. ( 1.3) 1.1 Prevention of Cardiovascular Disease In hypercholesterolemic patients without clinically evident coronary heart disease (CHD), pravastatin sodium tablets, USP are indicated to: reduce the risk of myocardial infarction (MI). reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of cardiovascular mortality with no increase in death from non-cardiovascular causes. In patients with clinically evident CHD, pravastatin sodium tablet is indicated to: reduce the risk of total mortality by reducing coronary death. reduce the risk of MI. reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of stroke and stroke/transient ischemic attack (TIA). slow the progression of coronary atherosclerosis. 1.2 Hyperlipidemia Pravastatin sodium tablet is indicated: as an adjunct to diet to reduce elevated total cholesterol (Total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and triglyceride (TG) levels and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hypercholesterolemia and mixed dyslipidemia ( Fredrickson Types IIa and IIb). 1 as an adjunct to diet for the treatment of patients with elevated serum TG levels ( Fredrickson Type IV). for the treatment of patients with primary dysbetalipoproteinemia ( Fredrickson Type III) who do not respond adequately to diet. as an adjunct to diet and lifestyle modification for treatment of heterozygous familial hypercholesterolemia (HeFH) in children and adolescent patients ages 8 years and older if after an adequate trial of diet 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 (CVD) or two or more other CVD risk factors are present in the patient. 1.3 Limitations of Use Pravastatin sodium has not been studied in conditions where the major lipoprotein abnormality is elevation of chylomicrons (Fredrickson Types I and V).

Launch Date

6.8886718E11
Primary
Approved
8043
PRAVACHOL

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. Pravastatin sodium tablet, USP is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of MI, revascularization, and cardiovascular mortality in hypercholesterolemic patients without clinically evident CHD. ( 1.1) Reduce the risk of total mortality by reducing coronary death, MI, revascularization, stroke/TIA, and the progression of coronary atherosclerosis in patients with clinically evident CHD. ( 1.1) Reduce elevated Total-C, LDL-C, ApoB, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia. ( 1.2) Reduce elevated serum TG levels in patients with hypertriglyceridemia. ( 1.2) Treat patients with primary dysbetalipoproteinemia who are not responding to diet. ( 1.2) Treat children and adolescent patients ages 8 years and older with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. ( 1.2) Limitations of use: Pravastatin sodium tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. ( 1.3) 1.1 Prevention of Cardiovascular Disease In hypercholesterolemic patients without clinically evident coronary heart disease (CHD), pravastatin sodium tablets, USP are indicated to: reduce the risk of myocardial infarction (MI). reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of cardiovascular mortality with no increase in death from non-cardiovascular causes. In patients with clinically evident CHD, pravastatin sodium tablet is indicated to: reduce the risk of total mortality by reducing coronary death. reduce the risk of MI. reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of stroke and stroke/transient ischemic attack (TIA). slow the progression of coronary atherosclerosis. 1.2 Hyperlipidemia Pravastatin sodium tablet is indicated: as an adjunct to diet to reduce elevated total cholesterol (Total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and triglyceride (TG) levels and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hypercholesterolemia and mixed dyslipidemia ( Fredrickson Types IIa and IIb). 1 as an adjunct to diet for the treatment of patients with elevated serum TG levels ( Fredrickson Type IV). for the treatment of patients with primary dysbetalipoproteinemia ( Fredrickson Type III) who do not respond adequately to diet. as an adjunct to diet and lifestyle modification for treatment of heterozygous familial hypercholesterolemia (HeFH) in children and adolescent patients ages 8 years and older if after an adequate trial of diet 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 (CVD) or two or more other CVD risk factors are present in the patient. 1.3 Limitations of Use Pravastatin sodium has not been studied in conditions where the major lipoprotein abnormality is elevation of chylomicrons (Fredrickson Types I and V).

Launch Date

6.8886718E11
Primary
Approved
8043
PRAVACHOL

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. Pravastatin sodium tablet, USP is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce the risk of MI, revascularization, and cardiovascular mortality in hypercholesterolemic patients without clinically evident CHD. ( 1.1) Reduce the risk of total mortality by reducing coronary death, MI, revascularization, stroke/TIA, and the progression of coronary atherosclerosis in patients with clinically evident CHD. ( 1.1) Reduce elevated Total-C, LDL-C, ApoB, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia. ( 1.2) Reduce elevated serum TG levels in patients with hypertriglyceridemia. ( 1.2) Treat patients with primary dysbetalipoproteinemia who are not responding to diet. ( 1.2) Treat children and adolescent patients ages 8 years and older with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy. ( 1.2) Limitations of use: Pravastatin sodium tablets, USP have not been studied in Fredrickson Types I and V dyslipidemias. ( 1.3) 1.1 Prevention of Cardiovascular Disease In hypercholesterolemic patients without clinically evident coronary heart disease (CHD), pravastatin sodium tablets, USP are indicated to: reduce the risk of myocardial infarction (MI). reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of cardiovascular mortality with no increase in death from non-cardiovascular causes. In patients with clinically evident CHD, pravastatin sodium tablet is indicated to: reduce the risk of total mortality by reducing coronary death. reduce the risk of MI. reduce the risk of undergoing myocardial revascularization procedures. reduce the risk of stroke and stroke/transient ischemic attack (TIA). slow the progression of coronary atherosclerosis. 1.2 Hyperlipidemia Pravastatin sodium tablet is indicated: as an adjunct to diet to reduce elevated total cholesterol (Total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (ApoB), and triglyceride (TG) levels and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hypercholesterolemia and mixed dyslipidemia ( Fredrickson Types IIa and IIb). 1 as an adjunct to diet for the treatment of patients with elevated serum TG levels ( Fredrickson Type IV). for the treatment of patients with primary dysbetalipoproteinemia ( Fredrickson Type III) who do not respond adequately to diet. as an adjunct to diet and lifestyle modification for treatment of heterozygous familial hypercholesterolemia (HeFH) in children and adolescent patients ages 8 years and older if after an adequate trial of diet 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 (CVD) or two or more other CVD risk factors are present in the patient. 1.3 Limitations of Use Pravastatin sodium has not been studied in conditions where the major lipoprotein abnormality is elevation of chylomicrons (Fredrickson Types I and V).

Launch Date

6.8886718E11
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
27.4 μg/L
EXPERIMENT
https://link.springer.com/article/10.2165/00003088-200039060-00002
19.2 mg single, oral
dose: 19.2 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: UNKNOWN
AUC

AUC

ValueDoseCo-administeredAnalytePopulation
66.2 μg × h/mL
EXPERIMENT
https://link.springer.com/article/10.2165/00003088-200039060-00002
19.2 mg single, oral
dose: 19.2 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: UNKNOWN
241.29 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT00829309
80 mg single, oral
dose: 80 mg
route of administration: oral
experiment type: single
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status: Fed
251.86 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT00829309
80 mg single, oral
dose: 80 mg
route of administration: oral
experiment type: single
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status: Fed
273.32 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT00829309
80 mg single, oral
dose: 80 mg
route of administration: oral
experiment type: single
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status: Fed
299.56 ng*h/mL
Clinical Trial
https://clinicaltrials.gov/ct2/show/NCT00829309
80 mg single, oral
dose: 80 mg
route of administration: oral
experiment type: single
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: healthy
age:
sex:
food status: Fed
T1/2

T1/2

ValueDoseCo-administeredAnalytePopulation
1.77 h
EXPERIMENT
https://link.springer.com/article/10.2165/00003088-200039060-00002
19.2 mg single, oral
dose: 19.2 mg
route of administration: Oral
experiment type: SINGLE
co-administered:
PRAVASTATIN plasma
Homo sapiens
population: HEALTHY
age: ADULT
sex: MALE
food status: UNKNOWN
Overview

Overview

CYP3A4CYP2C9CYP2D6hERG
substrate
1601

OverviewOther

Other InhibitorOther SubstrateOther Inducer
Kv1.3
16

OAT1
554

OAT2
131

OAT3
588

OAT4
131

P-gp
1330
OATP1B1
370

OATP1B3
319

OATP2B1
101

BCRP
515

MRP1
97

MRP5
39

MRP2
182

P-gp
1400

MRP4
73

MRP3
46

OATP2
6
Drug as perpetrator​

Drug as perpetrator​

TargetModalityActivityMetaboliteClinical evidence
P-gp
1514
 no
OAT2
133
 weak [IC50 352 uM]
OAT1
558
 weak [IC50 408 uM]
OAT4
131
 weak [IC50 591 uM]
OAT3
590
 yes [IC50 13.7 uM]
Kv1.3
31
 yes
Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
CYP3A4
1601
 no
no (co-administration study)
Comment: see https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/019898s060lbl.pdf#page=19
BCRP
515
 yes
MRP1
97
 yes
MRP2
182
 yes
MRP3
46
 yes
MRP4
73
 yes
MRP5
39
 yes
OATP1B3
319
 yes
OATP2
6
 yes
OATP2B1
101
 yes
P-gp
1400
 yes
OATP1B1
370
 yes
yes (co-administration study)
Comment: Coadministration with cyclosporine (inhibitor): AUC increased 5-10 fold
Sourcing

Sourcing

Vendor/AggregatorIDURL
ChEBI
CHEBI:63618
https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:63618
ChemicalBook
CB92544321
https://www.chemicalbook.com/ChemicalProductProperty_EN_CB92544321
MolPort
MolPort-006-167-482
https://www.molport.com/shop/molecule-link/MolPort-006-167-482
ZINC
ZINC000003798763
http://zinc15.docking.org/substances/ZINC000003798763
eMolecules
3716196
https://www.emolecules.com/cgi-bin/more?vid=3716196
PubMed

PubMed

TitleDatePubMed
Advantages of lipid-lowering therapy in cerebral ischemia: role of HMG-CoA reductase inhibitors.
2001
Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice.
2001 Apr
Recent clinical trial highlights in hypertension.
2001 Apr
Cell cycle-related changes in regulatory volume decrease and volume-sensitive chloride conductance in mouse fibroblasts.
2001 Apr
[Acute coronary syndrome. Early lipid reduction decreases risk of recurrence].
2001 Apr 19
Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial.
2001 Apr 6
[Statins: intervention studies, facts and perspectives].
2001 Feb
Protective effect of fluvastatin on degradation of apolipoprotein B by a radical reaction in human plasma.
2001 Feb
Do HMG-CoA reductase inhibitors affect fibrinogen?
2001 Feb
Operational aspects of terminating the doxazosin arm of The Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
2001 Feb
Statins alter smooth muscle cell accumulation and collagen content in established atheroma of watanabe heritable hyperlipidemic rabbits.
2001 Feb 20
[Acute coronary syndrome. Statins in the early phase save lives].
2001 Feb 8
Stimulation of inflammatory responses in vitro and in vivo by lipophilic HMG-CoA reductase inhibitors.
2001 Jan
Cholesterol-dependent modulation of tau phosphorylation in cultured neurons.
2001 Jan
Systolic and pulse blood pressures (but not diastolic blood pressure and serum cholesterol) are associated with alterations in carotid intima-media thickness in the moderately hypercholesterolaemic hypertensive patients of the Plaque Hypertension Lipid Lowering Italian Study. PHYLLIS study group.
2001 Jan
Statin trials in progress: unanswered questions.
2001 Jan
Effective use of statins to prevent coronary heart disease.
2001 Jan 15
Use of the statins in patients after acute myocardial infarction: does evidence change practice?
2001 Jan 22
Interim monitoring of clinical trials based on long-term binary endpoints.
2001 Jan 30
Beneficial effects of pravastatin in peri- and postmenopausal hyperlipidemic women: a 5-year study on serum lipid and sex hormone levels.
2001 Jan 31
Inflammation and coronary heart disease: an overview.
2001 Jan-Feb
Statin therapy and the prevention of dementia.
2001 Jun
Safety and efficacy of pravastatin therapy for the prevention of hyperlipidemia in pediatric and adolescent cardiac transplant recipients.
2001 Jun
Simvastatin-associated memory loss.
2001 Jun
HMG-CoA reductase inhibitors prevent migration of human coronary smooth muscle cells through suppression of increase in oxidative stress.
2001 Jun
Randomized clinical trials and recent patterns in the use of statins.
2001 Jun
Human liver-specific organic anion transporter, LST-1, mediates uptake of pravastatin by human hepatocytes.
2001 Jun
Limitation of heart growth in neonatal piglets by simvastatin and atorvastatin: comparison with pravastatin.
2001 Jun
Compactin enhances osteogenesis in murine embryonic stem cells.
2001 Jun 8
Is a statin a statin?
2001 Mar
Role of fibrates and HMG-CoA reductase inhibitors in gallstone formation: epidemiological study in an unselected population.
2001 Mar
Statin therapy--what now?
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
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
Effect of pravastatin on plasma markers of inflammation and peripheral endothelial function in male heart transplant recipients.
2001 Mar 15
What do the statin trials tell us?
2001 May
Cost-effectiveness of pravastatin therapy for survivors of myocardial infarction with average cholesterol levels.
2001 May
Cholesterol ester accumulation: an immediate consequence of acute in vivo ischemic renal injury.
2001 May
[Statins as new therapeutic possibility in osteoporosis?].
2001 May 11
Summaries for patients. Benefits of lowering cholesterol levels in older patients.
2001 May 15
Benefits of pravastatin on cardiovascular events and mortality in older patients with coronary heart disease are equal to or exceed those seen in younger patients: Results from the LIPID trial.
2001 May 15
Cost effectiveness of HMG-CoA reductase inhibition in Canada.
2001 Spring
Patents

Patents

JP2001270825A
2
JP2002020282A
2
JP2002121172A
2
JP2003506424A
2
JP2004002447A
2
JP2007524644A
41
JP2007534731A
2
JP2008044956A
2
JP2009161542A
2
JP2009268479A
2
JP2009525790A
92
JP4739217B2
37
JPH02235821A
2
JPH0320226A
2
JPH06298644A
2
JPH08291047A
2
JPH11240877A
5
JPS59186973A
2

Sample Use Guides

In Vivo Use Guide
May be beneficial for prophylaxis of cardiovascular events in at-risk patients, even if patients have normal levels of cholesterol. 10-40 mg PO qDay; not to exceed 80 mg/day Initiate with 10 mg qHS if taking immunosuppressants like cyclosporine concurrently; not to exceed 20 mg/day Limit maximum to 40 mg/day if taking concurrently with clarithromycin Dose adjustments should be made at intervals of 4 weeks or more; individualize dosing according to baseline LDL cholesterol levels
Route of Administration: Oral
In Vitro Use Guide
Pravastatin activity was evaluated using cellular steroidgenesis assay in Hep G2cells (human hepatoma cell line) cultured with 5% lipoprotein deficient serum containing medium for 48 h. The activities were determined by decreased incorporation of sodium [2-14C] acetate into non-saponifiable lipids.
Name Type Language
PRAVASTATIN
EMA EPAR   INN   VANDF   WHO-DD  
INN  
Official Name English
PRAVASTATIN [EMA EPAR]
Common Name English
C10AA03
Code English
PRAVASTATIN [INN]
Common Name English
PRAVASTATIN [WHO-DD]
Common Name English
PRAVASTATIN [VANDF]
Common Name English
PRAVATOR
Brand Name English
Classification Tree Code System Code
WHO-VATC QC10BX02
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
NDF-RT N0000175589
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
WHO-VATC QC10BA03
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
WHO-VATC QC10AA03
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
WHO-ATC C10BA03
Created by admin on Sat Jun 26 02:51:25 UTC 2021 , Edited by admin on Sat Jun 26 02:51:25 UTC 2021
LIVERTOX 791
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
WHO-ATC C10BX02
Created by admin on Sat Jun 26 02:51:25 UTC 2021 , Edited by admin on Sat Jun 26 02:51:25 UTC 2021
WHO-ATC C10AA03
Created by admin on Sat Jun 26 02:51:25 UTC 2021 , Edited by admin on Sat Jun 26 02:51:25 UTC 2021
NDF-RT N0000000121
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
NCI_THESAURUS C1655
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
EU-Orphan Drug EU/3/10/748
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
Code System Code Type Description
DRUG CENTRAL
2239
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
PUBCHEM
54687
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
FDA UNII
KXO2KT9N0G
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
CAS
81093-37-0
Created by admin on Sat Jun 26 02:51:25 UTC 2021 , Edited by admin on Sat Jun 26 02:51:25 UTC 2021
PRIMARY
IUPHAR
2953
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
DRUG BANK
DB00175
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
WIKIPEDIA
PRAVASTATIN
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
MESH
D017035
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
EVMPD
SUB10004MIG
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
EPA CompTox
81093-37-0
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
INN
6070
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
ChEMBL
CHEMBL1144
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
LACTMED
Pravastatin
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
RXCUI
42463
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY RxNorm
NCI_THESAURUS
C62070
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
HSDB
8368
Created by admin on Sat Jun 26 02:51:26 UTC 2021 , Edited by admin on Sat Jun 26 02:51:26 UTC 2021
PRIMARY
ACTIVE MOIETY
Structure of PRAVASTATIN
METABOLITE INACTIVE (PARENT)
Structure of 3''-HYDROXYPRAVASTATIN
METABOLITE INACTIVE (PARENT)
Structure of DESACYL-DEHYDROPRAVASTATIN
METABOLITE LESS ACTIVE (PARENT)
Structure of 3'.ALPHA.-ISOPRAVASTATIN
METABOLITE LESS ACTIVE (PARENT)
Structure of SQ-31945
PARENT (METABOLITE INACTIVE)
Structure of 6'-EPIPRAVASTATIN
SALT/SOLVATE (PARENT)
Structure of PRAVASTATIN SODIUM
NIH
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