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

Details

Stereochemistry ABSOLUTE
Molecular Formula C23H36O7
Molecular Weight 424.5277
Optical Activity UNSPECIFIED
Defined Stereocenters 8 / 8
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of PRAVASTATIN

SMILES

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

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

Molecular Formula C23H36O7
Molecular Weight 424.5277
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 8 / 8
E/Z Centers 0
Optical Activity UNSPECIFIED

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.

Approval Year

Targets

Targets

Primary TargetPharmacologyConditionPotency
1370.0 nM [IC50]
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
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

1991
Primary
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

1991
Primary
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

1991
Primary
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

1991
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
27.4 μg/L
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
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
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
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
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
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
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

Drug as perpetrator​Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
no
no (co-administration study)
Comment: see https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/019898s060lbl.pdf#page=19
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes
yes (co-administration study)
Comment: Coadministration with cyclosporine (inhibitor): AUC increased 5-10 fold
PubMed

PubMed

TitleDatePubMed
Baseline characteristics of the diabetic participants in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
2001 Apr
Therapeutic change of HMG-CoA reductase inhibitors in patients with coronary artery disease.
2001 Apr
Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice.
2001 Apr
A new simvastatin (mevinolin)-resistance marker from Haloarcula hispanica and a new Haloferax volcanii strain cured of plasmid pHV2.
2001 Apr
Recent clinical trial highlights in hypertension.
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
New pharmacologic aspects of CS-866, the newest angiotensin II receptor antagonist.
2001 Apr 19
Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial.
2001 Apr 6
Safety of statins (hydroxymethyl glutaryl coenzyme a reductase inhibitors): different mechanisms of metabolism and drug transport may have clinical relevance.
2001 Apr 9
Clinical relevance of statins: their role in secondary prevention.
2001 Feb
Antioxidative effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on peroxidation of phospholipid liposomes.
2001 Feb
Safety and efficacy of pravastatin therapy for the prevention of hyperlipidemia in pediatric and adolescent cardiac transplant recipients.
2001 Jun
HMG-CoA reductase inhibitors prevent migration of human coronary smooth muscle cells through suppression of increase in oxidative stress.
2001 Jun
Effect of lovastatin, an HMG CoA reductase inhibitor, on acute renal allograft rejection.
2001 Jun
Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site.
2001 Jun
Fluvastatin suppresses oxidative stress and fibrosis in the interstitium of mouse kidneys with unilateral ureteral obstruction.
2001 Jun
Randomized clinical trials and recent patterns in the use of statins.
2001 Jun
The pravastatin inflammation CRP evaluation (PRINCE): rationale and design.
2001 Jun
PRINCE's prospects: statins, inflammation, and coronary risk.
2001 Jun
Compactin enhances osteogenesis in murine embryonic stem cells.
2001 Jun 8
[PATE Study [Pravastatin anti-Atherosclerosis Trial in the Elderly Study]].
2001 Mar
[CARE[ Cholesterol and Recurrent Events Trial]].
2001 Mar
[LIPID study [Long-term Intervention with Pravastatin in Ischaemic Disease study]].
2001 Mar
[WOSCOPS [West of Scotland Coronary Prevention Study]].
2001 Mar
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
[Effects of pravastatin in 3260 patients with unstable angina: results from the LIPID study].
2001 Mar
[Treatment with statins for the reduction of cardiovascular risk].
2001 Mar
Medical-economical aspects of high sensitivity C-reactive protein assay for the prediction of coronary heart disease. An analysis in Germany and Italy.
2001 Mar
Statin-fibrate combinations in patients with combined hyperlipedemia.
2001 Mar
Statin therapy--what now?
2001 Mar
Inhibition of human tumor cell growth in vivo by an orally bioavailable inhibitor of human farnesyltransferase, BIM-46228.
2001 Mar 1
Dementia and statins.
2001 Mar 17
Dementia and statins. PROSPER study group.
2001 Mar 17
Pravastatin and coronary heart disease.
2001 Mar 31
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
2001 Mar 8
New OTC drugs and devices 2000: a selective review.
2001 Mar-Apr
Protective effects of Saiko-ka-ryukotsu-borei-to (Chai-Hu-Jia-Long-Gu-Mu-Li-Tang) against atherosclerosis in Kurosawa and Kusanagi-hypercholesterolemic (KHC) rabbits.
2001 May
Statin induced myopathy does not show up in MIBI scintigraphy.
2001 May
[Pravastatin and the development of diabetes mellitus. Evidence for a protective treatment effect in the West of Scotland Coronary Prevention Study].
2001 May
What do the statin trials tell us?
2001 May
Interactions of leptin and thyrotropin 24-hour secretory profiles in short normal children.
2001 May
Effects of 1-year treatment with fluvastatin or pravastatin on bone.
2001 May
Cost-effectiveness of pravastatin therapy for survivors of myocardial infarction with average cholesterol levels.
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
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
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

Sample Use Guides

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
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.
Substance Class Chemical
Created
by admin
on Sat Dec 16 16:54:46 GMT 2023
Edited
by admin
on Sat Dec 16 16:54:46 GMT 2023
Record UNII
KXO2KT9N0G
Record Status Validated (UNII)
Record Version
  • Download
Name Type Language
PRAVASTATIN
EMA EPAR   INN   VANDF   WHO-DD  
INN  
Official Name English
PRAVASTATIN [EMA EPAR]
Common Name English
Pravastatin [WHO-DD]
Common Name English
C10AA03
Code English
pravastatin [INN]
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 Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
NDF-RT N0000175589
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
WHO-VATC QC10BA03
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
WHO-VATC QC10AA03
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
WHO-ATC C10BA03
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
LIVERTOX NBK548653
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
WHO-ATC C10BX02
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
WHO-ATC C10AA03
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
NDF-RT N0000000121
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
NCI_THESAURUS C1655
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
EU-Orphan Drug EU/3/10/748
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
Code System Code Type Description
DRUG CENTRAL
2239
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
PUBCHEM
54687
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
FDA UNII
KXO2KT9N0G
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
CAS
81093-37-0
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
IUPHAR
2953
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
DRUG BANK
DB00175
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
WIKIPEDIA
PRAVASTATIN
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
MESH
D017035
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
SMS_ID
100000091161
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
EVMPD
SUB10004MIG
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
EPA CompTox
DTXSID6023498
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
INN
6070
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
ChEMBL
CHEMBL1144
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
DAILYMED
KXO2KT9N0G
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
LACTMED
Pravastatin
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
CHEBI
63660
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
RXCUI
42463
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY RxNorm
NCI_THESAURUS
C62070
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
CHEBI
63618
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
HSDB
8368
Created by admin on Sat Dec 16 16:54:48 GMT 2023 , Edited by admin on Sat Dec 16 16:54:48 GMT 2023
PRIMARY
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SALT/SOLVATE -> PARENT
TRANSPORTER -> INHIBITOR
TRANSPORTER -> SUBSTRATE
SALT/SOLVATE -> PARENT
Related Record Type Details
METABOLITE LESS ACTIVE -> PARENT
METABOLITE INACTIVE -> PARENT
MAJOR
METABOLITE LESS ACTIVE -> PARENT
MAJOR
METABOLITE INACTIVE -> PARENT
MAJOR
PARENT -> METABOLITE LESS ACTIVE
MAJOR
PARENT -> METABOLITE INACTIVE
MAJOR
Related Record Type Details
ACTIVE MOIETY
Name Property Type Amount Referenced Substance Defining Parameters References
PROTEIN BINDING PHARMACOKINETIC
Biological Half-life PHARMACOKINETIC
ORAL BIOAVAILABILITY PHARMACOKINETIC
Route of Elimination PHARMACOKINETIC RENAL
PHARMACOKINETIC
Tmax PHARMACOKINETIC