PRAVASTATIN

First approved in 1991

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 Search

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

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019898s066lbl.pdf
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

Targets

Primary Target	Pharmacology	Condition	Potency
HMG-CoA reductase 47 Target ID: CHEMBL402 Sources: https://www.ncbi.nlm.nih.gov/pubmed/11392538	Inhibitor 8297		1370.0 nM [IC50]

Conditions

Condition	Modality	Highest Phase	Product
Coronary heart disease 41 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019898s066lbl.pdf	Primary	Approved 8429	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
Hypercholesterolemia 47 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019898s066lbl.pdf	Primary	Approved 8429	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
Mixed dyslipidemia 8 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019898s066lbl.pdf	Primary	Approved 8429	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
Dysbetalipoproteinemia 6 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/019898s066lbl.pdf	Primary	Approved 8429	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

C_max

Value	Dose	Co-administered	Analyte	Population
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

Value	Dose	Analyte	Population
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

T_1/2

Value	Dose	Co-administered	Analyte	Population
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

CYP3A4	CYP2C9	CYP2D6	hERG
substrate 1737

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
Kv1.3 17 OAT1 599 OAT2 145 OAT3 642 OAT4 146 P-gp 1461	OATP1B1 406 OATP1B3 350 OATP2B1 104 BCRP 561 MRP1 107 MRP5 40 MRP2 205 P-gp 1537 MRP4 77 MRP3 50 OATP2 11

Drug as perpetrator

Target	Modality	Activity
P-gp 1650	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/11250868/ \| https://pubmed.ncbi.nlm.nih.gov/17064205/	no
OAT2 147	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/14978359/	weak [IC50 352 uM]
OAT1 603	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/14978359/	weak [IC50 408 uM]
OAT4 146	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/14978359/	weak [IC50 591 uM]
OAT3 644	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/14978359/	yes [IC50 13.7 uM]
Kv1.3 32	inhibitor 3277 Sources: https://pubmed.ncbi.nlm.nih.gov/33437096/	yes

Drug as victim

Target	Modality	Activity	Clinical evidence
CYP3A4 1737	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/019898s060lbl.pdf	no	no (co-administration study) Comment: see https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/019898s060lbl.pdf#page=19 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/019898s060lbl.pdf
BCRP 561	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/ \| https://pubmed.ncbi.nlm.nih.gov/15901800/	yes
MRP1 107	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/	yes
MRP2 205	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/ \| https://pubmed.ncbi.nlm.nih.gov/15901800/	yes
MRP3 50	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/	yes
MRP4 77	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/	yes
MRP5 40	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/	yes
OATP1B3 350	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/19785645/	yes
OATP2 11	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/11356905/ \| https://pubmed.ncbi.nlm.nih.gov/10601278/	yes
OATP2B1 104	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/19785645/	yes
P-gp 1537	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/30217571/ \| https://pubmed.ncbi.nlm.nih.gov/15901800/	yes
OATP1B1 406	substrate 3367 Sources: https://pubmed.ncbi.nlm.nih.gov/19785645/ \| https://pubmed.ncbi.nlm.nih.gov/15901800/	yes	yes (co-administration study) Comment: Coadministration with cyclosporine (inhibitor): AUC increased 5-10 fold Sources: https://pubmed.ncbi.nlm.nih.gov/19785645/ \| https://pubmed.ncbi.nlm.nih.gov/15901800/

Sourcing

Vendor/Aggregator	ID	URL
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

Title	Date	PubMed
Baseline characteristics of the diabetic participants in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).	2001 Apr	11315826
Therapeutic change of HMG-CoA reductase inhibitors in patients with coronary artery disease.	2001 Apr	11310513
Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice.	2001 Apr	11283400
A new simvastatin (mevinolin)-resistance marker from Haloarcula hispanica and a new Haloferax volcanii strain cured of plasmid pHV2.	2001 Apr	11283291
Recent clinical trial highlights in hypertension.	2001 Apr	11276395
Comparative study of HMG-CoA reductase inhibitors on fibrinogen.	2001 Apr	11254918
[Effect on plasma fibrinogen of hypercholesterolaemia treatment with pravastatin].	2001 Apr 15	11334580
Assessing the results: phase 1 hyperlipidemia outcomes in 27 health plans.	2001 Apr 16	11311193
Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive C-reactive protein levels.	2001 Apr 17	11306519
[Acute coronary syndrome. Early lipid reduction decreases risk of recurrence].	2001 Apr 19	11368001
New pharmacologic aspects of CS-866, the newest angiotensin II receptor antagonist.	2001 Apr 19	11334766
Reassuring effect of pravastatin on natural killer cell activity in stable renal transplant patients.	2001 Apr 27	11374422
Effect of pravastatin on survival in patients with advanced hepatocellular carcinoma. A randomized controlled trial.	2001 Apr 6	11286466
Safety of statins (hydroxymethyl glutaryl coenzyme a reductase inhibitors): different mechanisms of metabolism and drug transport may have clinical relevance.	2001 Apr 9	11295969
Clinical relevance of statins: their role in secondary prevention.	2001 Feb	11286152
Clinical relevance of statins: instituting treatment early in acute coronary syndrome patients.	2001 Feb	11286151
Antioxidative effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on peroxidation of phospholipid liposomes.	2001 Feb	11273020
Simvastatin-associated memory loss.	2001 Jun	11401190
Human liver-specific organic anion transporter, LST-1, mediates uptake of pravastatin by human hepatocytes.	2001 Jun	11356905
Limitation of heart growth in neonatal piglets by simvastatin and atorvastatin: comparison with pravastatin.	2001 Jun	11356632
[PATE Study [Pravastatin anti-Atherosclerosis Trial in the Elderly Study]].	2001 Mar	11347113
[CARE[ Cholesterol and Recurrent Events Trial]].	2001 Mar	11347108
[REGRESS [The Regression Growth Evaluation Statin Study]].	2001 Mar	11347107
[LIPID study [Long-term Intervention with Pravastatin in Ischaemic Disease study]].	2001 Mar	11347106
[WOSCOPS [West of Scotland Coronary Prevention Study]].	2001 Mar	11347100
Is a statin a statin?	2001 Mar	11321864
Role of fibrates and HMG-CoA reductase inhibitors in gallstone formation: epidemiological study in an unselected population.	2001 Mar	11318529
[Effects of pravastatin in 3260 patients with unstable angina: results from the LIPID study].	2001 Mar	11307791
[Treatment with statins for the reduction of cardiovascular risk].	2001 Mar	11307779
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	11305529
Statin-fibrate combinations in patients with combined hyperlipedemia.	2001 Mar	11293392
Statin therapy--what now?	2001 Mar	11284361
HMG-CoA reductase inhibitors and P-glycoprotein modulation.	2001 Mar	11250868
Inhibition of human tumor cell growth in vivo by an orally bioavailable inhibitor of human farnesyltransferase, BIM-46228.	2001 Mar 1	11267986
Effect of pravastatin on plasma markers of inflammation and peripheral endothelial function in male heart transplant recipients.	2001 Mar 15	11249916
Dementia and statins.	2001 Mar 17	11265974
Dementia and statins. PROSPER study group.	2001 Mar 17	11265973
Pravastatin and coronary heart disease.	2001 Mar 31	11293615
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.	2001 Mar 8	11256847
Statin therapy: where are we? Where do we go next?	2001 Mar 8	11256844
New OTC drugs and devices 2000: a selective review.	2001 Mar-Apr	11297337
[Pravastatin and the development of diabetes mellitus. Evidence for a protective treatment effect in the West of Scotland Coronary Prevention Study].	2001 May	11388336
Interactions of leptin and thyrotropin 24-hour secretory profiles in short normal children.	2001 May	11344208
Effects of 1-year treatment with fluvastatin or pravastatin on bone.	2001 May	11343673
Cost-effectiveness of pravastatin therapy for survivors of myocardial infarction with average cholesterol levels.	2001 May	11320359
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	11320358
Cholesterol ester accumulation: an immediate consequence of acute in vivo ischemic renal injury.	2001 May	11318945
Summaries for patients. Benefits of lowering cholesterol levels in older patients.	2001 May 15	11357858
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	11352694
Cost effectiveness of HMG-CoA reductase inhibition in Canada.	2001 Spring	11283756

Patents

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

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