pravastatin profile

Pravastatin is a synthetic HMG-CoA reductase inhibitor, commonly known as a statin, that is used to lower cholesterol levels. It was originally developed in the early 1980s by Sankyo, and was approved by the FDA in 1988. Pravastatin is produced through a fermentation process using the fungus *Monascus purpureus*. Its mechanism of action involves blocking the synthesis of cholesterol in the liver. This reduction in cholesterol levels leads to a decrease in the risk of cardiovascular disease, including heart attacks and strokes. Pravastatin is generally well-tolerated, with the most common side effects being muscle pain, headaches, and gastrointestinal disturbances. Its effectiveness in reducing cholesterol and preventing heart disease has made it a widely prescribed medication. Ongoing research focuses on its potential benefits in treating other conditions such as Alzheimer's disease and cancer.'

Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES). [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

pravastatin : A carboxylic ester resulting from the formal condensation of (S)-2-methylbutyric acid with the hydroxy group adjacent to the ring junction of (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6,8-dihydroxy-2-methyl-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid. Derived from microbial transformation of mevastatin, pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA). The sodium salt is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

acanthoside D: from Salsola collina [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	54687
CHEMBL ID	1144
CHEBI ID	63618
SCHEMBL ID	1117
MeSH ID	M0025879
PubMed CID	71312557
CHEMBL ID	2442731
CHEBI ID	144389
MeSH ID	M0025879

Synonym
BIDD:GT0773
BRD-K60511616-236-01-4
chebi:63618 ,
pravator
c10aa03
gtpl2953
eptastatin
(3r,5r)-3,5-dihydroxy-7-[(1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-{[(2s)-2-methylbutanoyl]oxy}-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]heptanoic acid
pravastatina [spanish]
pravastatin [inn:ban]
pravastatine [french]
1-naphthaleneheptanoic acid, 1,2,6,7,8,8a-hexahydro-beta,delta,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-, (1s-(1alpha(betas,deltas),2alpha,6alpha,8beta(r*),8aalpha))-
pravastatinum [latin]
ccris 7557
1-naphthaleneheptanoic acid, 1,2,6,7,8,8a-hexahydro-beta,delta,6-trihydroxy-2-methyl-8-((2s)-2-methyl-1-oxobutoxy)-, (betar,deltar,1s,2s,6s,8s,8ar)-
1,2,6,7,8,8a-hexahydro-beta,delta,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-, (1s-(1alpha(betas,deltas),2alpha,6alpha,8beta(r*),8aalpha))-1-naphthaleneheptanoic acid
bdbm20688
chembl1144 ,
(3r,5r)-7-[(1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-{[(2s)-2-methylbutanoyl]oxy}-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid
C01844
pravastatin
81093-37-0
pravastatin acid
(+)-(3r,5r)-3,5-dihydroxy-7-[(1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-{[(s)-2-methylbutyryl]oxy}-1,2,6,7,8,8a-hexahydro-1-naphthyl]heptanoic acid
DB00175
pravastatin (inn)
D08410
pravator (tn)
(3r,5r)-7-[(1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-[(2s)-2-methylbutanoyl]oxy-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid
(3r,5r)-3,5-dihydroxy-7-[(1s,2s,6s,8s)-6-hydroxy-2-methyl-8-[(2s)-2-methylbutanoyl]oxy-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]heptanoic acid
A840039
NCGC00188962-01
unii-kxo2kt9n0g
kxo2kt9n0g ,
pravastatina
pravastatine
hsdb 8368
pravastatinum
NCGC00188962-02
pravastatin [ema epar]
pravastatin [inn]
pravastatin [vandf]
pravastatin [who-dd]
AKOS015895229
S5713
CCG-221195
HY-B0165
SCHEMBL1117
KS-5015 ,
TUZYXOIXSAXUGO-PZAWKZKUSA-N
1,4-butanedisulfonicaciddisodiumsalt
mevalothin
DTXSID6023498 ,
LMFA05000695
SR-01000781259-2
sr-01000781259
3beta-hydroxycompactin
HMS3715P11
(3r,5r)-3,5-dihydroxy-7-((1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-((s)-2-methylbutanoyloxy)-1,2,6,7,8,8a-hexahydronaphthalen-1-yl)heptanoic acid
Q1240093
(betar,deltar,1s,2s,6s,8s,8ar)-1,2,6,7,8,8a-hexahydro-beta,delta,6-trihydroxy-2-methyl-8-[(2s)-2-methyl-1-oxobutoxy]-1-naphthaleneheptanoic acid
BRD-K60511616-236-08-9
BRD-K60511616-236-02-2
H12037
pravastatin-3h
1-naphthaleneheptanoic acid, 1,2,6,7,8,8a-hexahydro-.beta.,.delta.,6-trihydroxy-2-methyl-8-[(2s)-2-methyl-1-oxobutoxy]-, (.beta.r,.delta,r,1s,2s,6s,8s,8ar)-
EN300-6481366
dtxcid003498
(+)-(3r,5r)-3,5-dihydroxy-7-((1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-(((s)-2-methylbutyryl)oxy)-1,2,6,7,8,8a-hexahydro-1-naphthyl)heptanoic acid
(3r,5r)-3,5-dihydroxy-7-((1s,2s,6s,8s,8ar)-6-hydroxy-2-methyl-8-(((2s)-2-methylbutanoyl)oxy)-1,2,6,7,8,8a-hexahydronaphthalen-1-yl)heptanoic acid
(1s-(1alpha(betas,deltas),2alpha,6alpha,8beta(r*),8aalpha))-1,2,6,7,8,8a-hexahydro-beta,!d,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-1-naphthaleneheptanoic acid
pravastatinum (latin)
8jp2p44h3z ,
beta-d-glucopyranoside, ((1r,3ar,4s,6as)-tetrahydro-1h,3h-furo(3,4-c)furan-1,4-diyl)bis(2,6-dimethoxy-4,1-phenylene) bis-
unii-8jp2p44h3z
acanthoside d
CHEBI:144389
(2s,3r,4s,5s,6r)-2-[4-[(3s,3ar,6r,6as)-6-[3,5-dimethoxy-4-[(2s,3r,4s,5s,6r)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]-1,3,3a,4,6,6a-hexahydrouro[3,4-c]uran-3-yl]-2,6-dimethoxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol
CHEMBL2442731
CS-5288
HY-N0272
C20786
4-((1r,3as,4s,6ar)-4-(4-(.beta.-l-glucopyranosyloxy)-3,5-dimethoxyphenyl)tetrahydro-1h,3h-furo(3,4-c)furan-1-yl)-2,6-dimethoxyphenyl .beta.-d-glucopyranoside
.beta.-d-glucopyranoside, ((1r,3ar,4s,6as)-tetrahydro-1h,3h-furo(3,4-c)furan-1,4-diyl)bis(2,6-dimethoxy-4,1-phenylene) bis-
eleutheroside e [usp-rs]
eleutheroside e (constituent of eleuthero) [dsc]
AKOS030526142
[(1r,3ar,4s,6as)-tetrahydro-1h,3h-furo[3,4-c]furan-1,4-diyl]bis(2,6-dimethoxy-4,1-phenylene) bis-beta-d-glucopyranoside
(2s,3r,4s,5s,6r)-2-[4-[(3s,3ar,6r,6as)-6-[3,5-dimethoxy-4-[(2s,3r,4s,5s,6r)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-3-yl]-2,6-dimethoxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol
Q27270642
AS-56698
DTXSID801316969

Excerpt	Reference	Relevance
"Pravastatin sodium (PVS) is a hypolipidemic drug which suffers from extensive first-pass metabolism and short half-life. "	( Formulation and Evaluation of Pravastatin Sodium-Loaded PLGA Nanoparticles: In vitro-in vivo Studies Assessment. El-Dahan, MS; Elsayed, SI; Girgis, GNS, 2023)	2.64
"Pravastatin acts as a protector on myocardial ischemia reperfusion injury by regulating miR-93/Nrf2/ARE signaling pathway."	( Protective Effect of Pravastatin on Myocardial Ischemia Reperfusion Injury by Regulation of the miR-93/Nrf2/ARE Signal Pathway. Li, Y; Liu, L; Liu, Z; Zhang, F; Zhang, X; Zhao, L, 2020)	2.32
"Pravastatin is an effective agent to slow progression of structural kidney disease in children and young adults with ADPKD. "	( Effect of pravastatin on total kidney volume, left ventricular mass index, and microalbuminuria in pediatric autosomal dominant polycystic kidney disease. Cadnapaphornchai, MA; George, DM; Gitomer, B; McFann, K; Schrier, RW; Strain, JD; Wang, W, 2014)	2.25
"Pravastatin sodium is an [HMG-CoA] reductase inhibitor and is a lipid-regulating drug. "	( Pravastatin sodium. Al-Badr, AA; Mostafa, GA, 2014)	3.29
"Pravastatin sodium (PVS) is a hydrophilic HMG-CoA reductase inhibitor that is mainly absorbed from duodenum. "	( Duodenum-triggered delivery of pravastatin sodium via enteric surface-coated nanovesicular spanlastic dispersions: development, characterization and pharmacokinetic assessments. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2015)	2.15
"1. Pravastatin is a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor used for the treatment of hyperlipidaemia. "	( Mixed effects of OATP1B1, BCRP and NTCP polymorphisms on the population pharmacokinetics of pravastatin in healthy volunteers. Bi, KS; Chen, XH; Lu, XF; Zhou, Y, 2016)	1.28
"Pravastatin is a lipid-lowering agent that attenuates atherosclerosis. "	( Pravastatin and Sarpogrelate Synergistically Ameliorate Atherosclerosis in LDLr-Knockout Mice. Heo, TH; Jun, HS; Kwak, MK; Oh, E; Park, KY, 2016)	3.32
"Pravastatin sodium (PVS) is a freely water-soluble HMG-CoA inhibitor that suffers from instability at gastric pH, extensive first pass metabolism, short elimination half-life (1-3 h) and low oral bioavailability (18%)."	( Duodenum-triggered delivery of pravastatin sodium: II. Design, appraisal and pharmacokinetic assessments of enteric surface-decorated nanocubosomal dispersions. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2016)	2.16
"Pravastatin is an important therapeutic drug to treat hypercholesterolemia, which was described to be produced by oxyfunctionlization of mevastatin (compactin) by members of CYP105 family."	( Identification of a new plasmid-encoded cytochrome P450 CYP107DY1 from Bacillus megaterium with a catalytic activity towards mevastatin. Abdulmughni, A; Bernhardt, R; Hartz, P; Kern, F; Milhim, M; Putkaradze, N, 2016)	1.16
"Pravastatin is a potent cholesterol-lowering agent; ~34% of an oral dose of pravastatin is eliminated unchanged through biliary and urinary excretion. "	( Effects of a concomitant single oral dose of rifampicin on the pharmacokinetics of pravastatin in a two-phase, randomized, single-blind, placebo-controlled, crossover study in healthy Chinese male subjects. Cao, D; Chen, XP; Dai, ZY; Deng, S; Li, YJ; Luo, J; Tang, L; Yin, T, 2009)	2.02
"Pravastatin is a well-known drug with anti-inflammatory and immunomodulatory properties that may modulate host defense mechanisms against Leishmania."	( Influence of long-term treatment with pravastatin on the survival, evolution of cutaneous lesion and weight of animals infected by Leishmania amazonensis. Kückelhaus, CS; Kückelhaus, SA; Muniz-Junqueira, MI, 2011)	1.36
"Pravastatin is an effective medication to activate PPARs (especially PPARgamma) in the liver and the gallbladder epithelium of hamsters, and contributes to the prevention of gallstone formation."	( Pravastatin activates PPARalpha/PPARgamma expression in the liver and gallbladder epithelium of hamsters. Choi, MH; Dong, SH; Jang, HJ; Kae, SH; Koh, DH; Lee, J, 2011)	3.25
"Pravastatin is a hydrophilic statin that is selectively taken up by a sodium-independent organic anion transporter protein-1B1 (OATP1B1) exclusively expressed in liver."	( Differential effects of pravastatin and simvastatin on the growth of tumor cells from different organ sites. Chakraborty, K; Harirforoosh, S; Hsi, L; Krishnan, K; Menter, DG; Newman, RA; Ramsauer, VP; Yang, P, 2011)	1.4
"Pravastatin has shown to be an effective and safe therapy in dyslipidemic cardiac transplant patients."	( [Utility of pravastin in cardiac transplant dyslipidemia]. Almenar Bonet, L; Arnau Vives, MA; Dicenta Gisbert, F; Martínez-Dolz, L; Osa Sáez, A; Palencia Pérez, M; Rueda Soriano, J, 2002)	1.04
"Pravastatin is a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor often prescribed for the treatment of hypercholesterolemia."	( Massive postoperative rhabdomyolysis following combined CABG/abdominal aortic replacement: a possible association with HMG-CoA reductase inhibitors. Fischer, S; Haverich, A; Strüber, M; Walles, T; Wilhelmi, M; Winterhalter, M; Zuk, J, 2002)	1.04
"Pravastatin is a widely used statin in adults, but its pharmacokinetics in children is not known. "	( Pharmacokinetics and pharmacodynamics of pravastatin in children with familial hypercholesterolemia. Antikainen, M; Hedman, M; Neuvonen, M; Neuvonen, PJ, 2003)	2.03
"Pravastatin (Pravachol) is a competitive, reversible HMG-CoA reductase inhibitor that lowers serum cholesterol levels by inhibiting de novo cholesterol synthesis and has antiatherogenic effects that appear to be partially independent of its lipid-lowering effects. "	( Pravastatin: a review of its use in elderly patients. Bang, LM; Goa, KL, 2003)	3.2
"Pravastatin (PRA) is an inhibitor of HMG-CoA reductase enzyme, which is clinically used as a hypolipidemic agent to reduce cholesterol level. "	( Determination of pravastatin in tablets by capillary electrophoresis. Aboul-Enein, HY; Kircali, K; Tunçel, M, 2004)	2.11
"Pravastatin is a well known 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor. "	( Bile salt export pump (BSEP/ABCB11) can transport a nonbile acid substrate, pravastatin. Hayashi, H; Hirano, M; Kusuhara, H; Maeda, K; Sugiyama, Y, 2005)	2
"Pravastatin is a commonly used statin after cardiac transplantation, with favorable outcome and acceptable side-effect profile."	( Localized rhabdomyolysis after exertion in a cardiac transplant recipient on statin therapy. Biggs, MJ; Bonser, RS; Cram, R, 2006)	1.06
"Pravastatin is a hydrophilic substrate and fluvastatin a lipophilic substrate of the hepatic uptake transporter organic anion transporting polypeptide 1B1 encoded by SLCO1B1. "	( SLCO1B1 polymorphism and sex affect the pharmacokinetics of pravastatin but not fluvastatin. Neuvonen, PJ; Niemi, M; Pasanen, MK, 2006)	2.02
"Pravastatin treatment is an independent predictor for improvement of post-loaded hyperglycemia (odds ratio; 5.7; 95% confidence interval 1.7-19.3; p=0.003) and achieved beneficial conversion from IGT to normal glucose tolerance (40%; p=0.03)."	( Pravastatin improved glucose metabolism associated with increasing plasma adiponectin in patients with impaired glucose tolerance and coronary artery disease. Fukushima, H; Funahashi, T; Horibata, Y; Koga, H; Kojima, S; Kugiyama, K; Maruyoshi, H; Ogawa, H; Otsuka, F; Sakamoto, T; Shimomura, I; Sugamura, K; Sugiyama, S; Watanabe, K, 2007)	2.5
"Pravastatin is a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, which is widely used both in primary and secondary prevention of coronary heart disease (CHD). "	( SLCO1B1 521T-->C functional genetic polymorphism and lipid-lowering efficacy of multiple-dose pravastatin in Chinese coronary heart disease patients. Chen, BL; Deng, S; Fan, L; He, YJ; Ozdemir, V; Peng, DD; Wang, A; Wang, LC; Xie, QY; Xie, W; Xu, LY; Zhang, W; Zhou, G; Zhou, HH, 2007)	2
"Pravastatin is a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor (statin) and is hydrophilic."	( Effective uptake of N-acetylglucosamine-conjugated liposomes by cardiomyocytes in vitro. Aso, S; Goto, M; Ikeda, U; Ise, H; Izawa, A; Kobayashi, S; Morimoto, H; Takahashi, M, 2007)	1.06
"Pravastatin appears to be an effective and safe lipid-lowering agent and is the first 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor to be studied extensively in this underrepresented population."	( Efficacy and safety of pravastatin in African Americans with primary hypercholesterolemia. Chin, MM; Curry, CL; Jacobson, TA; LaRosa, JC; Miller, V; Papademetriou, V; Schlant, RC, 1995)	2.04
"Pravastatin is a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor that reduces plasma cholesterol levels. "	( High-performance liquid chromatography determination of pravastatin in plasma. Buggia, I; Fiorito, V; Guarnone, E; Iacona, I; Molinaro, M; Regazzi, MB; Villani, P, 1994)	1.98
"Pravastatin is a new potent cholesterol-lowering agent, which selectively inhibits hepatic HMG-CoA-reductase."	( [Pravastatin in the treatment of primary hypercholesterolemia: a Swiss multicenter study]. Erne, P; Ferrari, P; Fragiacomo, C; Luban, S; Martius, F; Noseda, G; Pasotti, E; Reutter, F; Riesen, WF; Weidmann, P, 1993)	1.92
"Pravastatin is an effective and safe drug."	( [Cholesterol and vascular disease. Study of pravastatin ]. Bellandi, F; Cantini, F; Palchetti, R; Pedone, T, 1993)	1.27
"Pravastatin is a new lipid-lowering drug belonging to the class of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitors. "	( Long-term experience with pravastatin in clinical research trials. McGovern, ME; Mellies, MJ, )	1.87
"Pravastatin is a much weaker inhibitor of cholesterol synthesis (IC50-value of 977.8 nM) in these cells."	( Vastatins have a distinct effect on sterol synthesis and progesterone secretion in human granulosa cells in vitro. Cohen, LH; Naaktgeboren, N; van Thiel, GC; van Vliet, AK, 1996)	1.02
"Pravastatin is a weaker inhibitor of sterol synthesis (IC50 value of 110 +/- 38 nM)."	( Action of lovastatin, simvastatin, and pravastatin on sterol synthesis and their antiproliferative effect in cultured myoblasts from human striated muscle. Bolhuis, PA; Cohen, LH; Nègre-Aminou, P; van Thiel, GC; van Vliet, AK, 1996)	1.28
"Pravastatin is an HMG-CoA reductase inhibitor which lowers plasma cholesterol levels by inhibiting de novo cholesterol synthesis. "	( Pravastatin. A reappraisal of its pharmacological properties and clinical effectiveness in the management of coronary heart disease. Haria, M; McTavish, D, 1997)	3.18
"Pravastatin is an HMG CoA reductase inhibitor used in the treatment of hypercholesterolaemia. "	( Steady state serum concentrations of pravastatin and digoxin when given in combination. Cohen, AI; Devault, A; Pan, HY; Swanson, BN; Triscari, J; Willard, DA, 1993)	2
"Pravastatin, which is a structural analogue of mevalonic acid and is absorbed via proton-coupled transport like mevalonic acid, did not."	( Intestinal brush-border membrane transport of monocarboxylic acids mediated by proton-coupled transport and anion antiport mechanisms. Maeda, H; Sai, Y; Suzuki, Y; Takanaga, H; Tamai, I; Tsuji, A; Yabuuchi, H, 1997)	1.02
"Pravastatin is a hydrophilic liver-specific inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase. "	( Determination of pravastatin by high performance liquid chromatography. Gross, W; März, W; Siekmeier, R, 2000)	2.09
"Pravastatin is a potent inhibitor of HMG-CoA reductase and is effective in lowering serum lipid levels. "	( Pravastatin suppress superoxide and fibronectin production of glomerular mesangial cells induced by oxidized-LDL and high glucose. Chen, HC; Guh, JY; Lai, YH; Shin, SJ, 2002)	3.2
"Pravastatin is a potent inhibitor of HMG-CoA reductase and is effective in lowering serum lipid levels. "	( Effects of pravastatin on superoxide and fibronectin production of mesangial cells induced by low-density lipoprotein. Chen, HC; Guh, JY; Lai, YH; Shin, SJ; Tomino, Y, 2002)	2.15
"Pravastatin is a new drug that inhibits 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the key enzyme in cholesterol synthesis. "	( [Evaluation of the therapeutic efficacy of pravastatin in monothereapy and in association with gemfibrozil in hypercholesterolemia associated with moderate hyperglyceridemia]. Ambrosio, G; Chiariello, M; Lepore, S; Napoli, C, 1992)	1.99
"Pravastatin was found to be a relatively effective, safe and well tolerated lipid-lowering drug. "	( Treatment of primary hypercholesterolaemia with pravastatin: efficacy and safety over three years. Clifton, P; Janus, ED; Nestel, PJ; Parfitt, A; Simons, J; Simons, LA, 1992)	1.98
"Pravastatin sodium is a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment of hypercholesterolemia."	( Pravastatin: a new drug for the treatment of hypercholesterolemia. Cantral, KA; Jungnickel, PW; Maloley, PA, 1992)	2.45
"Pravastatin seems to be a highly effective, well tolerated drug for severe hypercholesterolaemia. "	( Treatment of familial hypercholesterolaemia. United Kingdom lipid clinics study of pravastatin and cholestyramine. Betteridge, DJ; Bhatnager, D; Bing, RF; Durrington, PN; Evans, GR; Flax, H; Jay, RH; Lewis-Barned, N; Mann, J; Matthews, DR, 1992)	1.95
"Pravastatin is a foreign substrate of a sodium-independent transport system for bile acids. "	( Tissue-selective action of pravastatin due to hepatocellular uptake via a sodium-independent bile acid transporter. Stünkel, W; Ziegler, K, 1992)	2.02
"Pravastatin sodium (PV) is a potent cholesterol-lowering agent that acts by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase. "	( Biotransformation of pravastatin sodium in humans. Chando, TJ; Didonato, GC; Everett, DW; Pan, HY; Singhvi, SM; Weinstein, SH, )	1.89
"Pravastatin is an HMG-CoA reductase inhibitor which reduces plasma cholesterol levels by inhibiting de novo cholesterol synthesis and increasing the receptor-mediated catabolism of low density lipoprotein (LDL). "	( Pravastatin. A review of its pharmacological properties and therapeutic potential in hypercholesterolaemia. McTavish, D; Sorkin, EM, 1991)	3.17
"Pravastatin appears to be a safe and efficacious method of treating hyperlipidemia in renal transplant recipients."	( The effects of pravastatin on hyperlipidemia in renal transplant recipients. Ohmori, Y; Oka, T; Okamoto, M; Yoshimura, N, 1992)	1.36
"Pravastatin (CS-514) is a tissue selective inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.34), a key enzyme in cholesterol biosynthesis. "	( A two component-type cytochrome P-450 monooxygenase system in a prokaryote that catalyzes hydroxylation of ML-236B to pravastatin, a tissue-selective inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Matsuoka, T; Serizawa, N, 1991)	1.93
"Pravastatin is a metabolic product of mevastatin and a potent inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. "	( The effect of pravastatin on plasma lipoprotein and apolipoprotein levels in primary hypercholesterolemia. The Southeastern Michigan Collaborative Group. Blevins, RD; Kobylak, L; Maciejko, JJ; Orringer, C; Rosman, H; Rubenfire, M, 1991)	2.08

Excerpt	Reference	Relevance
"Pravastatin has a predominantly delayed antiatherogenic effect, and aspirin has an immediate antiplatelet effect, raising the possibility of additive clinical benefits."	( Additive benefits of pravastatin and aspirin to decrease risks of cardiovascular disease: randomized and observational comparisons of secondary prevention trials and their meta-analyses. Belder, R; Berry, DA; Berry, SM; Byington, RP; Fiedorek, FT; Ford, NF; Hennekens, CH; Jukema, JW; Natarajan, K; Pitt, B; Sacks, FM; Sheng-Lin, C; Tonkin, A; Walker, AJ, 2004)	1.36
"Pravastatin has a neutral drug interaction profile relative to cytochrome P450-3A4 inhibitors, but these substrates markedly increase systemic exposure to simvastatin and atorvastatin."	( Comparative pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with cytochrome P450 inhibitors. Jacobson, TA, 2004)	1.3
"Pravastatin also has an antithrombotic action."	( Pravastatin (mevalotin) restenosis trial after percutaneous transluminal coronary angioplasty. Cholesterol reduction rate determines the restenosis rate. Hosoda, S; Kawai, C; Yui, Y, 1995)	2.46
"Pravastatin has a moderate effect in reducing the risk of stroke from any cause and the risk of nonhemorrhagic stroke in patients with previous myocardial infarction or unstable angina."	( Pravastatin therapy and the risk of stroke. Anderson, NE; Colquhoun, DM; Glasziou, P; Hankey, GJ; Hunt, D; Kirby, AC; MacMahon, S; Simes, RJ; Tonkin, AM; Watson, JD; West, MJ; White, HD, 2000)	3.19
"Pravastatin has been demonstrated to have preventative effects in preeclampsia model mice, and a large volume of human data from pregnant women taking statins supports the safety of these drugs."	( Pravastatin for preeclampsia: From animal to human. Fujii, T; Iriyama, T; Kumasawa, K; Nagamatsu, T; Osuga, Y, 2020)	2.72
"Pravastatin has emerged for prevention and treatment of preeclampsia; no reports are available on pravastatin and HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome."	( Pravastatin for prevention of HELLP syndrome: A case report. Gembruch, U; Kühr, M; Merz, WM; Otten, LA; van der Ven, K, 2017)	3.34
"Pravastatin has shown efficacy and to be safe during hypertension in pregnancy."	( Placental nitric oxide formation and endothelium-dependent vasodilation underlie pravastatin effects against angiogenic imbalance, hypertension in pregnancy and intrauterine growth restriction. Chimini, JS; da Silva, MLS; Dias-Junior, CA; Possomato-Vieira, JS, 2019)	1.46
"Pravastatin has been reported to elevate circulating adiponectin levels in patients with various insulin resistant state, hypertension, coronary artery disease, and hypercholesterolemia. "	( Effects of pravastatin on serum adiponectin levels in female patients with type 2 diabetes mellitus. Chang, SA; Kim, JH; Lee, JM; Lee, MR; Lee, SS; Shin, JA; Yoon, KH; You, SJ, 2013)	2.22
"Pravastatin has been shown to prevent preeclampsia in animal models."	( The effect of prenatal pravastatin treatment on altered fetal programming of postnatal growth and metabolic function in a preeclampsia-like murine model. Costantine, MM; Gamble, P; Hankins, GD; Kechichian, T; Longo, M; McDonnold, M; Saade, GR; Tamayo, E, 2014)	1.43
"Pravastatin has been demonstrated to be useful in preventing steroid-induced ONFH in animal models."	( Pravastatin prevents steroid-induced osteonecrosis in rats by suppressing PPARγ expression and activating Wnt signaling pathway. Chen, W; Jiang, Y; Li, P; Lin, N; Lu, C; Xu, Y; Zhang, H; Zhang, Y; Zhu, B, 2014)	2.57
"Pravastatin has neuroprotective effects against aging but its role in brain injury remains unclear. "	( Effects of pravastatin on cellular ultrastructure and hemorheology in rats after traumatic head injury. Basak, AT; Berker, M; Dikmenoglu, N; Hazer, DB; Ileri-Gurel, E; Kaymaz, F; Narin, F; Seringec, N; Tuncel, M, 2010)	2.19
"Pravastatin has favorable safety and pharmacokinetic profiles."	( Pravastatin for the prevention of preeclampsia in high-risk pregnant women. Cleary, K; Costantine, MM, 2013)	2.55
"Pravastatin has shown to be an effective and safe therapy in dyslipidemic cardiac transplant patients."	( [Utility of pravastin in cardiac transplant dyslipidemia]. Almenar Bonet, L; Arnau Vives, MA; Dicenta Gisbert, F; Martínez-Dolz, L; Osa Sáez, A; Palencia Pérez, M; Rueda Soriano, J, 2002)	1.04
"Pravastatin (P) has been shown to be effective in adult renal Tx recipients, not only in reducing serum cholesterol, but possibly also in decreasing graft rejection."	( Pilot study describing the use of pravastatin in pediatric renal transplant recipients. Butani, L; Makker, SP; Pai, MV, 2003)	1.32
"Pravastatin has a predominantly delayed antiatherogenic effect, and aspirin has an immediate antiplatelet effect, raising the possibility of additive clinical benefits."	( Additive benefits of pravastatin and aspirin to decrease risks of cardiovascular disease: randomized and observational comparisons of secondary prevention trials and their meta-analyses. Belder, R; Berry, DA; Berry, SM; Byington, RP; Fiedorek, FT; Ford, NF; Hennekens, CH; Jukema, JW; Natarajan, K; Pitt, B; Sacks, FM; Sheng-Lin, C; Tonkin, A; Walker, AJ, 2004)	1.36
"Pravastatin has a neutral drug interaction profile relative to cytochrome P450-3A4 inhibitors, but these substrates markedly increase systemic exposure to simvastatin and atorvastatin."	( Comparative pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with cytochrome P450 inhibitors. Jacobson, TA, 2004)	1.3
"Pravastatin has been reported to reduce cardiovascular events and mortality in patients with coronary artery disease (CAD). "	( The effect of 6 months of treatment with pravastatin on serum adiponection concentrations in Japanese patients with coronary artery disease and hypercholesterolemia: a pilot study. Ogawa, H; Sakamoto, K; Sakamoto, T, 2006)	2.04
"Pravastatin also has an antithrombotic action."	( Pravastatin (mevalotin) restenosis trial after percutaneous transluminal coronary angioplasty. Cholesterol reduction rate determines the restenosis rate. Hosoda, S; Kawai, C; Yui, Y, 1995)	2.46
"pravastatin) has gradually increased in the treatment of hypercholesterolaemia."	( Changes in biliary lipid output after interruption of pravastatin treatment in humans. Einarsson, K; Eriksson, M; Hillebrant, CG; Nyberg, B, 1996)	1.26
"Pravastatin has been found to have clinical benefits beyond those predicted by its actions in reducing plasma low density lipoprotein cholesterol (LDL). "	( Pravastatin sodium activates endothelial nitric oxide synthase independent of its cholesterol-lowering actions. Caldwell, RB; Caldwell, RW; Huang, J; Kaesemeyer, WH, 1999)	3.19
"Pravastatin has a moderate effect in reducing the risk of stroke from any cause and the risk of nonhemorrhagic stroke in patients with previous myocardial infarction or unstable angina."	( Pravastatin therapy and the risk of stroke. Anderson, NE; Colquhoun, DM; Glasziou, P; Hankey, GJ; Hunt, D; Kirby, AC; MacMahon, S; Simes, RJ; Tonkin, AM; Watson, JD; West, MJ; White, HD, 2000)	3.19
"Pravastatin has been shown, in an experimental model of ischemia reperfusion, to increase adenosine levels, which exert a potent and protective effect on the heart. "	( Effect of pravastatin on myocardial protection during coronary angioplasty and the role of adenosine. Chou, TF; Lee, TM; Su, SF; Tsai, CH, 2001)	2.16
"Pravastatin has been demonstrated to reduce cholesterol in patients with familial and nonfamilial polygenic hypercholesterolemia and patients with diabetes mellitus."	( Pravastatin: a new drug for the treatment of hypercholesterolemia. Cantral, KA; Jungnickel, PW; Maloley, PA, 1992)	2.45
"Pravastatin has no affinity to other transport systems in liver cells such as those for long-chain fatty acids, amino acids, rifampicin and bivalent organic cations."	( Tissue-selective action of pravastatin due to hepatocellular uptake via a sodium-independent bile acid transporter. Stünkel, W; Ziegler, K, 1992)	1.3

Excerpt	Reference	Relevance
"Pravastatin can inhibit these pathways and suppress the apoptosis and necrosis of IMECs to relieve the cell inflammatory injuries."	( [Protective effects of pravastatin against P38MAPK signaling pathway-mediated inflammatory toxicity in islet micro-endothelial cells]. Cai, D; Chen, J; Chen, S; Hu, N; Kang, Y; Luo, L; Sun, J; Zhang, J, 2013)	1.42
"Pravastatin can inhibit dendritic cell activation, which is independent of plasma cholesterol lowering."	( Effects of pravastatin on the function of dendritic cells in patients with coronary heart disease. Cheng, JL; Cui, J; Dong, M; Jiang, SL; Li, QS; Li, X; Liu, C; Peng, CH; Tian, Y, 2009)	1.46
"Both Pravastatin and G-CSF can enhance EPC mobilization from the bone marrow and VEGF release, but G-CSF produces a stronger effect on EPC mobilization in association of VEGF release."	( [Effects of pravastatin and granulocyto-colony stimulating factor in mobilizing endothelial progenitor cells in mice with myocardial ischemia]. Chen, TT; Gao, CQ; Li, LB; Mi, WD; Wang, G, 2009)	1.19
"Pravastatin did not increase the rate of cancer incidence or cancer death in a large population of Japanese patients followed for >70,000 patient-years."	( Pravastatin use and cancer risk: a meta-analysis of individual patient data from long-term prospective controlled trials in Japan. Hattori, Y; Iwashita, M; Kaburagi, J; Matsushita, Y; Ozawa, M; Saito, H; Sugihara, M; Yoshida, S, 2010)	3.25
"Pravastatin can inhibit the proliferation and invasion of HepG2 cells."	( [Effects of pravastatin on the proliferation and invasion of human hepatocarcinoma HepG2 cell line]. Gong, YX; Li, ZX; Mao, WW; Qu, Y; Tian, SJ; Yang, SH; Zhang, WJ, 2010)	2.18
"Pravastatin can inhibit the proliferation and syndean-4 protein expression in rat VSMCs induced by TNF-alpha in vitro."	( [Pravastatin inhibits the expression of syndecan-4 protein in tumor necrosis factor-alpha-induced rat vascular smooth muscle cells in vitro]. Lai, WY; Luo, Y; Ouyang, P; Xu, DL; Zhang, Y, 2010)	2.71
"Pravastatin-induced increase in insulin sensitivity is mediated by elevation of 1,25-(OH)(2)-D(3)."	( Opposite effects of pravastatin and atorvastatin on insulin sensitivity in the rat: role of vitamin D metabolites. Atanassova, P; Bełtowski, J; Chaldakov, GN; Jamroz-Wiśniewska, A; Kula, W; Rusek, M, 2011)	1.41
"Pravastatin may inhibit the secretion and activation of MMP-2."	( [Effects of interaction between vascular endothelial cells and monocytes on expression of matrix metalloproteinase-2 and of tissue inhibitor of metalloproteinases 2 and regulation of pravastatin]. Yang, XH; Zheng, W, 2005)	1.24
"The pravastatin-induced increase in TM expression in TNFalpha-treated HAECs was mediated through inhibition of NF-kappaB activation."	( Pravastatin induces thrombomodulin expression in TNFalpha-treated human aortic endothelial cells by inhibiting Rac1 and Cdc42 translocation and activity. Chen, JW; Chen, YH; Chen, YL; Hsieh, LY; Ku, HH; Lin, CY; Lin, FY; Lin, SJ; Wang, SH; Wang, YC, 2007)	2.26
"Pravastatin appears to inhibit the synthesis and subsequent degradation of extracellular matrix proteins and block the infiltration of macrophages to the graft, which emphasizes that this inflammatory cell plays a major role in the pathogenesis of transplant chronic rejection."	( Effects of pravastatin on chronic rejection of rat cardiac allografts. Busuttil, RW; Imagawa, DK; Kaldas, F; Ke, B; Maggard, MA; Seu, P; Wang, T, 1998)	1.41
"Pravastatin could inhibit over-expression of PAI-1 mRNA in the rabbit liver with hyperlipidemia and fatty liver, and reduce its plasma PAI-1 activity."	( [Effects of pravastatin on hepatic plasminogen activator inhibitor 1 mRNA expression in rabbits with fatty liver]. Chen, L; Fan, J; Zeng, M, 2000)	2.13
"5. Pravastatin inhibit the activator protein-1 activity, but did not inhibit the activation of IkappaB-alpha."	( Pravastatin suppresses the interleukin-8 production induced by thrombin in human aortic endothelial cells cultured with high glucose by inhibiting the p44/42 mitogen activated protein kinase. Kishida, M; Kobayashi, M; Nakamura, N; Nobata, Y; Sato, A; Takata, M; Temaru, R; Urakaze, M; Yamazaki, K, 2001)	2.27
"Pravastatin did not inhibit aortic ring contraction."	( Inhibition of smooth muscle cell calcium mobilization and aortic ring contraction by lactone vastatins. Altieri, PI; Crespo, MJ; Escobales, N; Furilla, RA, 1996)	1.02
"Pravastatin lead to an increase of the HDL concentration of approximately 8%, gemfibrocil to approximately 13%, whilst cholestyramine alone did not change this lipid fraction."	( [Pravastatin, cholestyramine and gemfibrozil in long-term therapy of primary hypercholesterolemia. An open randomized comparative study]. Dammann, HG; Ditschuneit, H; Ditschuneit, HH; Dreyer, M, 1991)	1.91

Excerpt	Reference	Relevance
"Pravastatin treatment ameliorated the remodeling and improved cardiac output postpartum."	( Statins Reverse Postpartum Cardiovascular Dysfunction in a Rat Model of Preeclampsia. Birukov, A; Dechend, R; Geisberger, S; Golic, M; Haase, N; Herse, F; Heuser, A; Kräker, K; Müller, DN; O'Driscoll, JM; Patey, O; Schütte, T; Thilaganathan, B; Verlohren, S, 2020)	1.28
"Pravastatin treatment for 6 months, but not for 2 days, inhibited leukocyte activation and improved hemorheological parameters."	( Pravastatin improves postprandial endothelial dysfunction and hemorheological deterioration in patients with effort angina pectoris. Arao, K; Fujita, H; Horie, Y; Ikeda, N; Kawakami, M; Momomura, SI; Sugimura, H; Umemoto, T; Yasu, T, 2017)	2.62
"Pravastatin-treated individuals lived RMST 2,088.1 days), on average, 18.7 more days free of CHD over 6 years than those receiving usual care (RMST 2,069.4 days), but this difference was not statistically significant (difference 18.7 days, 95% CI=-10.4-47.8 days, p=.21)."	( Pravastatin for Primary Prevention in Older Adults: Restricted Mean Survival Time Analysis. Kim, DH; Lux, E; Orkaby, AR; Rich, MW; Sun, R; Wei, LJ, 2018)	2.64
"Pravastatin pretreatment ameliorates the intestinal microvascular oxygenation in sepsis and thus seems to prevent intestinal hypoxia. "	( Effect of Pravastatin Pretreatment and Hypercapnia on Intestinal Microvascular Oxygenation and Blood Flow During Sepsis. Bauer, I; Beck, C; Herminghaus, A; Picker, O; Schulz, J; Truse, R; Vollmer, C, 2020)	2.4
"Pravastatin treatment had no effect on the glycemic status of patients with T2DM and hypercholesterolemia, but may reduce the percentage changes in the plasma HMW-adiponectin concentrations."	( [Effect of Statins on Glycemic Status and Plasma Adiponectin Concentrations in Patients with Type 2 Diabetes Mellitus and Hypercholesterolemia]. Hori, E; Imaeda, K; Kikuchi, C; Matsunaga, T; Okayama, N; Suzuki, T, 2019)	1.24
"Pravastatin treatment did not improve angiogenic potential in RUPP serum and decreased (P<0.05) endothelial tube formation in NP rats."	( Pravastatin attenuates hypertension, oxidative stress, and angiogenic imbalance in rat model of placental ischemia-induced hypertension. Banek, CT; Bauer, AJ; Capoccia, S; Gilbert, JS; Gillham, H; Needham, K; Regal, JF, 2013)	2.55
"Pravastatin treatment for 3.2 years reduced CHD death in the full cohort, hazard ratio (HR) 0.80, 95% confidence interval (CI) 0.68-0.95, p=0.0091 and fatal coronary events or coronary hospitalisations in the Scottish cohort (HR 0.81, 95% CI 0.69-0.95, p=0.0081) over 8.6 years. "	( Long-term effects of statin treatment in elderly people: extended follow-up of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). Briggs, A; Buckley, BM; Comber, H; de Craen, AJ; Ford, I; Jukema, JW; Kearney, PM; Lloyd, SM; Marchbank, L; Packard, CJ; Perry, I; Sattar, N; Stott, DJ; Trompet, S; Westendorp, RG, 2013)	2.05
"Pravastatin treatment of elderly high-risk subjects for 3.2 years provided long-term protection against CHD events and CHD mortality. "	( Long-term effects of statin treatment in elderly people: extended follow-up of the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). Briggs, A; Buckley, BM; Comber, H; de Craen, AJ; Ford, I; Jukema, JW; Kearney, PM; Lloyd, SM; Marchbank, L; Packard, CJ; Perry, I; Sattar, N; Stott, DJ; Trompet, S; Westendorp, RG, 2013)	2.05
"With pravastatin treatment, this group has the highest absolute risk reduction and the lowest NNT to prevent fatal and nonfatal CHD."	( Homocysteine levels and treatment effect in the PROspective Study of Pravastatin in the Elderly at Risk. Assendelft, WJ; Blom, HJ; Blom, JW; de Craen, AJ; de Ruijter, W; Drewes, YM; Ford, I; Gussekloo, J; Poortvliet, RK; Sattar, N; Stott, DJ; Westendorp, RG; Wouter Jukema, J, 2014)	1.09
"Pravastatin-treated animals reached preimplant insulin requirements on days 22, 27, and 50."	( Pravastatin improves glucose regulation and biocompatibility of agarose encapsulated porcine islets following transplantation into pancreatectomized dogs. Carraway, JW; Gazda, LS; Hall, RD; Laramore, MA; Smith, BH; Vinerean, HV, 2014)	2.57
"Pravastatin treatment produced similar results and normalized the lipid alteration."	( Does combined peroxisome proliferator-activated receptors-agonist and pravastatin therapy attenuate the onset of diabetes-induced experimental nephropathy? Gad, HI, 2014)	1.36
"The pravastatin treatment was less effective on plaque inflammation than pitavastatin treatment. "	( Anti-inflammatory and morphologic effects of pitavastatin on carotid arteries and thoracic aorta evaluated by integrated backscatter trans-esophageal ultrasound and PET/CT: a prospective randomized comparative study with pravastatin (EPICENTRE study). Arai, M; Kako, N; Kawasaki, M; Minatoguchi, S; Miwa, H; Nagaya, M; Noda, T; Onishi, N; Ono, K; Saeki, M; Sato, N; Tanaka, R; Watanabe, S; Watanabe, T, 2015)	1.16
"Pravastatin treatment significantly improved the pathology of the lung after HILI (reduction in thickness of alveolar septum, attenuation of lung edema, fracturing of alveolar septa and decrease in infiltrated leukocytes); reduced the number of apoptotic cells; inhibited lung MPO activity; and regulated the balance between pro-inflammatory and anti-inflammatory cytokines."	( Pravastatin protects hyperbaric hyperoxia-induced lung injury via inhibiting inflammation in mice. Cai, Z; Cao, D; Chen, H; Li, R; Lin, F; Liu, W; Peng, Z; Xu, W; Zheng, J, )	2.3
"Pravastatin treatment significantly enhanced LDL receptor (LDLR) and PCSK9 mRNA gene expression, as well as PCSK9 secretion and LDL uptake in both control and S127R HLCs."	( Urine-sample-derived human induced pluripotent stem cells as a model to study PCSK9-mediated autosomal dominant hypercholesterolemia. Arnaud, L; Caillaud, A; Cariou, B; Champon, B; Idriss, S; Le May, C; Lemarchand, P; Pichelin, M; Si-Tayeb, K; Zibara, K, 2016)	1.16
"Pravastatin treatment reduced PAR-1 expression in a concentration-dependent manner."	( Pravastatin and C reactive protein modulate protease- activated receptor-1 expression in vitro blood platelets. Chu, LX; He, LP; Liang, ZS; Mo, CG; Qin, YQ; Wang, XD; Xie, J; Yang, F; Zhou, SX, 2016)	2.6
"Pravastatin treatment induced a significant decrease in the TC, LDL-c, and ApoB levels in patients expressing the ApoA1 AA+GA genotype (P < 0.05), and not in those expressing the GG genotype (P > 0.05)."	( Relationship between the G75A polymorphism in the apolipoprotein A1 (ApoA1) gene and the lipid regulatory effects of pravastatin in patients with hyperlipidemia. He, F; Li, HW; Li, SX; Liu, TN; Wu, CT; Wu, M; Yu, HY; Yuan, W, 2016)	1.36
"Pravastatin treatment combined with LDA+LMWH was also associated with live births that occurred close to full term in all patients."	( Pravastatin improves pregnancy outcomes in obstetric antiphospholipid syndrome refractory to antithrombotic therapy. Dagklis, T; Girardi, G; Lefkou, E; Mamopoulos, A; Rousso, D; Vosnakis, C, 2016)	2.6
"The pravastatin treatment was effective for reducing the risk of CHD, regardless of the presence of risk factors."	( The relationship between the effect of pravastatin and risk factors for coronary heart disease in Japanese patients with hypercholesterolemia. Ishikawa, T; Kushiro, T; Mizuno, K; Nakamura, H; Nakaya, N; Ohashi, Y; Tajima, N; Teramoto, T; Uchiyama, S, 2008)	1.1
"Pravastatin-treated TAC mice also showed less cardiac apoptosis."	( Inhibition of cardiac remodeling by pravastatin is associated with amelioration of endoplasmic reticulum stress. Asakura, M; Asano, Y; Asanuma, H; Hori, M; Kim, J; Kitakaze, M; Liao, Y; Minamino, T; Takashima, S; Zhao, H, 2008)	1.34
"Pravastatin treatments upregulated expressions of Cx43 at mRNA and protein levels and improved the INF-gamma/IL-10 balance which might be the working mechanisms for pravastatin-mediated anti-VMC and anti-arrhythmia effects in this VMC model."	( [Effects of pravastatin on myocardial connexin 43, IFN-gamma and IL-10 expressions in a murine model of viral myocarditis induced by Coxsackievirus B3]. Fang, HY; Wu, SY, 2008)	2.17
"Pravastatin treatment prevents the development of obesity and diabetes in DIO mice. "	( Effects of pravastatin on obesity, diabetes, and adiponectin in diet-induced obese mice. Araki, K; Kakuma, T; Katsuragi, I; Masaki, T; Yoshimatsu, H, 2008)	2.18
"Pravastatin treatment in old age did not affect cognitive decline during a 3 year follow-up period."	( Pravastatin and cognitive function in the elderly. Results of the PROSPER study. Blauw, GJ; Bollen, EL; Buckley, BM; de Craen, AJ; Ford, I; Jolles, J; Jukema, JW; Macfarlane, PW; Murphy, MB; Packard, CJ; Sattar, N; Shepherd, J; Stott, DJ; Trompet, S; van Vliet, P; Westendorp, RG, 2010)	2.52
"Pravastatin treatment before CABG may decrease the incidence of postoperative AF."	( Pravastatin treatment before coronary artery bypass grafting for reduction of postoperative atrial fibrillation. Arai, H; Ito, F; Miyagi, N; Someya, T; Tamura, K; Ushiyama, T, 2010)	3.25
"Pravastatin treatment decreased the incidence of ventricular premature complexes by 22.5 + or - 3.4% (n = 20, p <0.05), couplets, and runs of 3 to 6 beats of nonsustained ventricular tachycardia from 9.8 + or - 2.67 to 3.9 + or - 1.25 events/patient/24 hours (n = 12, p <0.05)."	( Differential effects of statins (pravastatin or simvastatin) on ventricular ectopic complexes: Galpha(i2), a possible molecular marker for ventricular irritability. Confalone, D; Estes, NA; Galper, JB; Karas, RH; Naggar, J; Park, HJ; Rhofiry, J; Shea, J; Welzig, CM, 2010)	1.36
"Pravastatin treatment decreased weight loss in Leishmania-infected C57BL6 mice and Syrian hamsters, but not infected BALB/c mice."	( Influence of long-term treatment with pravastatin on the survival, evolution of cutaneous lesion and weight of animals infected by Leishmania amazonensis. Kückelhaus, CS; Kückelhaus, SA; Muniz-Junqueira, MI, 2011)	1.36
"Pravastatin treatment led to inhibition of Rac-GTPase activity and integrin signaling."	( Cardiac remodeling caused by transgenic overexpression of a corn Rac gene. Abouelnaga, ZA; Alhaj, MA; Awad, MM; Citro, LA; El-Sayed, O; Elnakish, MT; Hassanain, HH; Hassona, MD; Khan, M; Kulkarni, A; Kuppusamy, P; Moldovan, L; Sayyid, M, 2011)	1.09
"Pravastatin treatment reduced hypertension (change in mean arterial pressure: 1±1 versus 18±3 mm Hg in C1q(-/-) untreated mice), and albuminuria (of creatinine) was reduced from 820±175 to 117±45 μg/mg (both P<0.01)."	( Role of complement component C1q in the onset of preeclampsia in mice. Ahmed, A; Girardi, G; Singh, J, 2011)	1.09
"Pravastatin treatment was associated with a significantly reduced late in-stent neointima formation as assessed at IVUS."	( The extent of late in-stent neointima formation is modified by treatment with pravastatin: a preliminary study with intravascular ultrasound. Bernardi, G; Boccanelli, A; Fioretti, P; Morocutti, G; Pagano, A; Parma, A; Prati, F; Sommariva, L; Tomai, F, 2002)	1.99
"Pravastatin treatment significantly reduced plasma total and low-density lipoprotein cholesterol levels, as well as increased high-density lipoprotein cholesterol."	( Association of pravastatin and left ventricular mass in hypercholesterolemic patients: role of 8-iso-prostaglandin f2alpha formation. Chou, TF; Lee, TM; Tsai, CH, 2002)	1.39
"pravastatin treatment inhibits the prothrombogenic effects of hypercholesterolemia via an action on both endothelial cells and platelets; and 3)."	( HMG-CoA reductase inhibitor attenuates platelet adhesion in intestinal venules of hypercholesterolemic mice. Granger, DN; Lefer, DJ; Tailor, A, 2004)	1.04
"Pravastatin treatment reduced total cholesterol LDL-C and triglycerides significantly more in the highest CETP quartile."	( Cholesteryl ester transfer protein concentration is associated with progression of atherosclerosis and response to pravastatin in men with coronary artery disease (REGRESS). de Grooth, GJ; Jukema, JW; Kastelein, JJ; Klerkx, AH; Kuivenhoven, JA; Zwinderman, AH, 2004)	1.25
"Pravastatin treatment prevented cardiomyocyte cell death following simulated hypoxia and reoxygenation (P < 0.01)."	( Novel cardioprotective effects of pravastatin in human ventricular cardiomyocytes subjected to hypoxia and reoxygenation: beneficial effects of statins independent of endothelial cells. Fedak, PW; Li, RK; Li, SH; Miriuka, S; Rao, V; Verma, S; Weisel, RD, 2004)	1.32
"Pravastatin treatment, resulting in decreased LDL oxidation, did not improve myocardial perfusion reserve in subjects with type 1 diabetes."	( Effect of pravastatin on low-density lipoprotein oxidation and myocardial perfusion in young adults with type 1 diabetes. Ahotupa, M; Janatuinen, T; Knuuti, J; Nuutila, P; Raitakari, OT; Rönnemaa, T; Toikka, JO, 2004)	2.17
"Pravastatin treatment alone led to a significant, but partial improvement of hyperlipidemia and renal disease."	( AT-1 receptor blockade prevents proteinuria, renal failure, hyperlipidemia, and glomerulosclerosis in the Imai rat. Quiroz, Y; Rodríguez-Iturbe, B; Sato, T; Vaziri, ND, 2004)	1.04
"Pravastatin treatment inhibits early plaque rupture and is also effective when begun after unstable plaques have developed."	( Plaque rupture after short periods of fat feeding in the apolipoprotein E-knockout mouse: model characterization and effects of pravastatin treatment. Angelini, G; Carson, K; George, S; Jackson, C; Johnson, J; Karanam, S; Newby, A; Williams, H, 2005)	1.26
"Pravastatin treatment lowered the incidence of major adverse cardiac events in subjects with the metabolic syndrome after adjustment for age and sex (hazard ratio=0.39; 95% CI 0.17-0.89; P=0.025)."	( Impact of statins in microalbuminuric subjects with the metabolic syndrome: a substudy of the PREVEND Intervention Trial. Asselbergs, FW; Bakker, SJ; de Jong, PE; Geluk, CA; Hillege, HL; van Gilst, WH; Zijlstra, F, 2005)	1.05
"Pravastatin treatment decreased total cholesterol, low-density lipoprotein cholesterol, and triglycerides levels by 24%, 32%, and 14%, respectively ( P < .05 for all), but did not affect glucose and insulin levels, the (QUICKI) index, and adiponectin and leptin levels. "	( Pravastatin does not affect insulin sensitivity and adipocytokines levels in healthy nondiabetic patients. Amm-Azar, M; Azar, RR; Gannagé-Yared, MH; Germanos-Haddad, M; Halaby, G; Khalifé, S; Neemtallah, R, 2005)	3.21
"Pravastatin treatment reduced endothelial nitric oxide synthase protein levels and reversed the renal dysfunction caused by CsA."	( Inhibitory effect of pravastatin on transforming growth factor beta1-inducible gene h3 expression in a rat model of chronic cyclosporine nephropathy. Cha, JH; Choi, BS; Kim, IS; Kim, J; Lee, SH; Li, C; Lim, SW; Yang, CW, )	1.17
"The pravastatin-treated rabbits showed, compared with untreated rabbits, a significantly reduced LOX-1 protein and mRNA expression in the aortic arch."	( Pravastatin inhibits expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in Watanabe heritable hyperlipidemic rabbits: a new pleiotropic effect of statins. Eschert, H; Hofnagel, O; Luechtenborg, B; Robenek, H; Severs, NJ; Weissen-Plenz, G, 2006)	2.26
"Pravastatin treatment was continued or started in the remaining members of group A and group B, but not in group C."	( [The effects of pravastatin on platelet-derived nitric oxide system in rabbits]. Feng, JH; Kang, MF; Li, YQ; Ma, LP; Nie, DN; Wu, YD; Xie, SF; Xu, LZ; Yin, SM, 2005)	1.4
"Pravastatin treatment increases the markers of cholesterol absorption and decreases those of cholesterol synthesis in HeFH during simultaneous inhibition of cholesterol absorption. "	( Serum noncholesterol sterols in children with heterozygous familial hypercholesterolemia undergoing pravastatin therapy. Antikainen, M; Gylling, H; Hedman, M; Ketomäki, A; Miettinen, TA, 2006)	1.99
"Pravastatin treatment also significantly increased neurite length and branching but did not affect cellular cholesterol levels."	( The 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitor pravastatin enhances neurite outgrowth in hippocampal neurons. Pooler, AM; Wurtman, RJ; Xi, SC, 2006)	1.29
"Pravastatin pretreatment resulted in a significantly better neurological outcome and reduced infarct size (15 +/- 0.5 and 59 +/- 10 mm(3), respectively) compared with controls (12.25 +/- 0.4 and 167 +/- 13 mm(3), respectively, P < 0.01 for both)."	( Pravastatin reduces microvascular basal lamina damage following focal cerebral ischemia and reperfusion. Dichgans, M; Hamann, GF; Trinkl, A; Vosko, MR; Wunderlich, N, 2006)	2.5
"Pravastatin treatment significantly reduced systolic BP (SBP) in the HT group (134+/-16 to 130+/-13 mmHg, p<0.005) but not in the NT group (124+/-10 to 123+/-9 mmHg, p=0.52), despite the fact that treatment significantly reduced low-density lipoprotein cholesterol in both groups (HT group 178+/-27 to 132+/-17 mg/dl, p<0.0001; NT group 169+/-27 to 125+/-21 mg/dl, p<0.0001)."	( Pravastatin decreases blood pressure in hypertensive and hypercholesterolemic patients receiving antihypertensive treatment. Kawano, H; Yano, K, 2006)	2.5
"Pravastatin treatment significantly decreased levels of total cholesterol (16%), low-density lipoprotein cholesterol (23%) and high-sensitivity C-reactive protein (37%) (p<0.01, respectively)."	( Pravastatin improved glucose metabolism associated with increasing plasma adiponectin in patients with impaired glucose tolerance and coronary artery disease. Fukushima, H; Funahashi, T; Horibata, Y; Koga, H; Kojima, S; Kugiyama, K; Maruyoshi, H; Ogawa, H; Otsuka, F; Sakamoto, T; Shimomura, I; Sugamura, K; Sugiyama, S; Watanabe, K, 2007)	2.5
"The pravastatin-treated mice had delayed onset of CIA compared with the controls."	( Effects of pravastatin in murine collagen-induced arthritis. Funauchi, M; Ikoma, S; Kinoshita, K; Nozaki, Y; Sugiyama, M; Yamagata, T, 2007)	1.21
"Pravastatin treatment attenuated the development of diabetes in db/db and high fat/high sucrose diet-fed C57BL/6J mice."	( Effect of pravastatin on the development of diabetes and adiponectin production. Abe, M; Caslake, MJ; Fukuhara, A; Funahashi, T; Kihara, S; Kobayashi, H; Komuro, R; Matsuda, M; McMahon, A; Shepherd, J; Shimomura, I; Takagi, T, 2008)	1.47
"Pravastatin treatment significantly decreased plasma lipids in all patients (P < 0.001). "	( SLCO1B1 521T-->C functional genetic polymorphism and lipid-lowering efficacy of multiple-dose pravastatin in Chinese coronary heart disease patients. Chen, BL; Deng, S; Fan, L; He, YJ; Ozdemir, V; Peng, DD; Wang, A; Wang, LC; Xie, QY; Xie, W; Xu, LY; Zhang, W; Zhou, G; Zhou, HH, 2007)	2
"Pravastatin treatment restored these sub-clinical abnormalities towards normal levels."	( Two-week treatment with pravastatin improves ventriculo-vascular haemodynamic interactions in young men with type 1 diabetes. Bouchier-Hayes, DJ; Casey, RG; Fitzgerald, P; Joyce, M; Moore, K; Thompson, C, 2007)	1.37
"The pravastatin treatment effectively lowered low-density lipoprotein cholesterol (LDL-C) levels in the hyperlipidemic diabetic patients to levels nearly to those in 11 non-hyperlipidemic type 2 diabetic patients with normoalbuminuria."	( Effects of long-term pravastatin treatment on serum and urinary monocyte chemoattractant protein-1 levels and renal function in type 2 diabetic patients with normoalbuminuria. Fujita, H; Ito, S; Kakei, M; Koshimura, J; Miura, T; Morii, T; Narita, T; Sasaki, H; Sato, T; Yamada, Y, 2007)	1.14
"Pravastatin treatment, at 10 mg or 40 mg daily for 8 weeks, reduced serum lipids and some inflammatory markers in nondiabetic hypercholesterolemic subjects. "	( Early Improvements in insulin sensitivity and inflammatory markers are induced by pravastatin in nondiabetic subjects with hypercholesterolemia. Chien, YH; Lee, WJ; Lee, WL; Liang, KW; Sheu, WH; Tang, YJ; Tsou, SS, 2008)	2.01
"Pravastatin-treated patients with a greater percent decrease in hs-CRP had a significant improvement in exercise time compared with those without hs-CRP decrease."	( Usefulness of C-reactive protein and interleukin-6 as predictors of outcomes in patients with chronic obstructive pulmonary disease receiving pravastatin. Chang, NC; Lee, TM; Lin, MS, 2008)	1.27
"Pravastatin treatment significantly reduced plasma levels of total cholesterol and LDL-cholesterol by 15.6 mg/dl (38.8%) and 12.7 mg/dl (42.9%), respectively."	( Pravastatin-induced changes in receptor-mediated metabolism of low density lipoprotein in guinea pigs. Arakawa, K; Araki, K; Hidaka, K; Matsunaga, A; Moriyama, K; Sasaki, J; Takada, Y, 1994)	2.45
"Pravastatin treatment reduced plasma total cholesterol (-20 +/- 3%), LDL cholesterol (-30 +/- 3%), triacylglycerols (-17 +/- 6%), and apoB levels (-25 +/- 4%) and simultaneously decreased platelet [Ca2+]i measured in a low-Ca2+ medium by 14 +/- 6% (P = .03)."	( Platelet cytosolic Ca2+ and membrane dynamics in patients with primary hypercholesterolemia. Effects of pravastatin. Devynck, MA; Le Quan Sang, KH; Levenson, J; Megnien, JL; Simon, A, 1995)	1.23
"Pravastatin treatment attenuated the increase in both malondialdehyde, beta-thromboglobulin and the prostanoids, but not to the level of normal subjects."	( Effects of acute exercise on the changes of lipid profiles and peroxides, prostanoids, and platelet activation in hypercholesterolemic patients before and after treatment. Chen, MF; Hsu, HC; Lee, YT, 1994)	1.01
"Pravastatin treatment, which continued for 4 weeks, significantly decreased LDL cholesterol (P < 0.01); however, before LDL-apheresis pravastatin treatment significantly increased Lp(a) levels (P < 0.05) in a small number (n = 6) of the FH patients, who had been regularly treated with LDL-apheresis."	( Reduction of lipoprotein(a) by LDL-apheresis using a dextran sulfate cellulose column in patients with familial hypercholesterolemia. Haraki, T; Inazu, A; Kajinami, K; Kamon, N; Koizumi, I; Koizumi, J; Miyamoto, S; Takegoshi, T; Uno, Y; Yagi, K, 1993)	1.01
"Pravastatin treatment of hypercholesterolemia is highly effective and well tolerated alone and in combination with bile acid-binding resin and shows no tendency to increase muscle enzyme levels."	( Comparative efficacy and safety of pravastatin and cholestyramine alone and combined in patients with hypercholesterolemia. Pravastatin Multicenter Study Group II. , 1993)	2.01
"Pravastatin-treated rats never showed signs of myopathy."	( Differential effects of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors on the development of myopathy in young rats. Bär, PR; Bredman, JJ; Joles, JA; Koot, RW; Reijneveld, JC, 1996)	1.02
"Pravastatin treatment (20 mg/day) was started at the 8th week of the study and its dose was doubled 4 weeks later if needed."	( Combined treatment with captopril, hydrochlorothiazide and pravastatin in dyslipidemic hypertensive patients. Darioli, R; Greminger, P; Riesen, W; Simeon-Dubach, D; Waeber, B; Wunderlin, R, 1995)	1.26
"Pravastatin-treatment for 1, 7 and 28 days did not affect the recovery of cholesterol and triacylglycerols during 24 h after the lipid administration: the recovery was 52-59% and 82-93% for cholesterol and triacylglycerols, respectively."	( Lymphatic transport of cholesterol in normocholesterolemic rats treated with pravastatin, an inhibitor of HMG-CoA reductase. Ibi, T; Ikeda, I; Imaizumi, K; Nagao, K; Sakono, M; Yamamoto, K, 1996)	1.24
"Pravastatin treatment of combined hyperlipidemia lowers low-density lipoprotein effectively; nicotinic acid lowers remnant cholesterol and raises high-density lipoprotein. "	( Comparison of pravastatin with crystalline nicotinic acid monotherapy in treatment of combined hyperlipidemia. Grundy, SM; Mostaza, JM; Schulz, I; Vega, GL, 1997)	2.1
"Pravastatin- and placebo-treated patients were classified as having progressing, regressing or stable CAD, and median lipoprotein(a) concentrations were compared."	( Modulation of lipoprotein(a) atherogenicity by high density lipoprotein cholesterol levels in middle-aged men with symptomatic coronary artery disease and normal to moderately elevated serum cholesterol. Regression Growth Evaluation Statin Study (REGRESS) Bruschke, AV; Cobbaert, C; Jukema, JW; Lindemans, J; Withagen, AJ; Zwinderman, AH, 1997)	1.02
"Pravastatin treatment did not affect serum apolipoprotein(a) levels. "	( Modulation of lipoprotein(a) atherogenicity by high density lipoprotein cholesterol levels in middle-aged men with symptomatic coronary artery disease and normal to moderately elevated serum cholesterol. Regression Growth Evaluation Statin Study (REGRESS) Bruschke, AV; Cobbaert, C; Jukema, JW; Lindemans, J; Withagen, AJ; Zwinderman, AH, 1997)	1.74
"Pravastatin treatment did not induce a significant change in high-density (HDL) cholesterol levels."	( Pravastatin in diabetes-associated hypercholesterolemia. Janssens, EN; Rustemeijer, C; Schouten, JA; Spooren, PF; van Doormaal, JJ, 1997)	2.46
"The pravastatin-treated groups also had fewer graft-infiltrating macrophages, specifically within the arterial intima and perivascular areas."	( Effects of pravastatin on chronic rejection of rat cardiac allografts. Busuttil, RW; Imagawa, DK; Kaldas, F; Ke, B; Maggard, MA; Seu, P; Wang, T, 1998)	1.17
"Pravastatin-treated heart transplant recipients exhibited a decrease in natural killer cell cytotoxicity (9.8% mean natural killer cell cytotoxicity vs 22.1% in the control group, p < 0.01). "	( The inhibitory effects of pravastatin on natural killer cell activity in vivo and on cytotoxic T lymphocyte activity in vitro. Chia, D; Hirata, M; Katznelson, S; Kobashigawa, JA; Ozawa, M; Terasaki, PI; Wang, XM; Zhong, HP, 1998)	2.04
"Pravastatin treatment effect was defined as the difference in progression of the combined intima-media thicknesses (IMT) between treatment groups."	( B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). Ackerstaff, RG; Bom, N; Bruschke, AV; de Groot, E; Jukema, JW; Lie, KI; Montauban van Swijndregt, AD; van der Steen, AF; Zwinderman, AH, 1998)	1.31
"Pravastatin treatment effects were highly significant (combined IMT: p = 0.0085; combined far wall IMT: p < 0.0001; common femoral artery far wall IMT: p = 0.004). "	( B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). Ackerstaff, RG; Bom, N; Bruschke, AV; de Groot, E; Jukema, JW; Lie, KI; Montauban van Swijndregt, AD; van der Steen, AF; Zwinderman, AH, 1998)	2.03
"Pravastatin treatment effects on carotid and femoral artery walls were observed. "	( B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). Ackerstaff, RG; Bom, N; Bruschke, AV; de Groot, E; Jukema, JW; Lie, KI; Montauban van Swijndregt, AD; van der Steen, AF; Zwinderman, AH, 1998)	2.03
"Pravastatin treatment reduced the absolute risk of coronary events for the diabetic and nondiabetic patients by 8.1% and 5.2% and the relative risk by 25% (P=0.05) and 23% (P<0.001), respectively."	( Cardiovascular events and their reduction with pravastatin in diabetic and glucose-intolerant myocardial infarction survivors with average cholesterol levels: subgroup analyses in the cholesterol and recurrent events (CARE) trial. The Care Investigators. Braunwald, E; Cole, TG; Davis, BR; Goldberg, RB; Howard, BV; Howard, WJ; Mellies, MJ; Moyé, LA; Pfeffer, MA; Sacks, FM, 1998)	1.28
"Pravastatin treatment at 100 mg/kg did not produce any alteration of excitation-contraction coupling since the rheobase voltage was similar to that of controls."	( Effects of HMG-CoA reductase inhibitors on excitation-contraction coupling of rat skeletal muscle. Camerino, C; Conte Camerino, D; De Luca, A; Liantonio, A; Pierno, S, 1999)	1.02
"Pravastatin treatment did not affect IS or the effect of IP under normocholesterolemia."	( Pravastatin restored the infarct size-limiting effect of ischemic preconditioning blunted by hypercholesterolemia in the rabbit model of myocardial infarction. Asanuma, H; Hori, M; Kitakaze, M; Komamura, K; Kuzuya, T; Minamino, T; Sato, H; Takeda, H; Ueda, Y, 1999)	2.47
"Pravastatin treatment was more effective in reducing total cholesterol, LDL-cholesterol, LDL-triglycerides, LDL-ApoB and LDL/HDL-cholesterol ratio (all p<0.001 between groups) and total/HDL-cholesterol and ApoA1/LDL-ApoB ratios (both p<0.01) and always induced a decrease in LDL-cholesterol concentrations and LDL/HDL-cholesterol ratio irrespective of baseline triglyceride concentration. "	( Pravastatin compared to bezafibrate in the treatment of dyslipidemia in insulin-treated patients with type 2 diabetes mellitus. Donker, AJ; Heine, RJ; Hensgens, HE; Rustemeijer, C; Schouten, JA; Voerman, HJ, )	3.02
"Pravastatin treatment is superior in lowering cholesterol-enriched lipoprotein subpopulations and improving cardiovascular risk factors. "	( Pravastatin compared to bezafibrate in the treatment of dyslipidemia in insulin-treated patients with type 2 diabetes mellitus. Donker, AJ; Heine, RJ; Hensgens, HE; Rustemeijer, C; Schouten, JA; Voerman, HJ, )	3.02
"Pravastatin-treated patients were grouped according to the LDL-C reduction at 6 months; (i) "adequate LDL-C reduction": LDL-C reduction >30% from baseline or LDL-C<125 mg/dl (n = 38; LDL-C reduction 74 +/- 4 mg/dl; 6-month LDL-C 119 +/- 5 mg/dl); (ii) "inadequate LDL-C reduction": neither of the above criteria (n = 19; LDL-C reduction 31 +/- 5 mg/dl; 6-month LDL-C 158 +/- 6 mg/dl)."	( Pravastatin: an antithrombotic effect independent of the cholesterol-lowering effect. Ambrose, JA; Badimon, JJ; Cohen, AM; Dangas, G; Fallon, JT; Fier, C; Meraj, P; Shao, JH; Smith, DA; Unger, AH, 2000)	2.47
"the pravastatin treated group was stratified into quartiles of LDL-C reduction."	( Intima-media thickness after pravastatin stabilizes also in patients with moderate to no reduction in LDL-cholesterol levels: the carotid atherosclerosis Italian ultrasound study. Baldassarre, D; Bong, MG; Collatina, S; Crepaldi, G; Fisicaro, M; Gallus, G; Gobbi, C; Mancini, M; Ricci, G; Rimondi, S; Sirtori, CR; Veglia, F; Ventura, A, 2000)	1.08
"Pravastatin treatment is effective in reducing coronary heart disease events in patients with high or low risk factor status and across a wide range of pretreatment lipid concentrations."	( Effect of pravastatin on coronary disease events in subgroups defined by coronary risk factors: the Prospective Pravastatin Pooling Project. Braunwald, E; Byington, R; Cobbe, S; Furberg, CD; Hawkins, CM; Keech, A; Packard, C; Sacks, FM; Shepherd, J; Simes, J; Tonkin, AM, 2000)	2.15
"Pravastatin treatment did not significantly affect PChE activity."	( Is pseudocholinesterase activity related to markers of triacylglycerol synthesis in Type II diabetes mellitus? Beynen, AC; Donker, AJ; Heine, RJ; Rustemeijer, C; Schouten, JA; Voerman, HJ, 2001)	1.03
"Pravastatin treatment increased PINP levels, a marker of bone formation, in hypercholesterolemic, post-menopausal women, without affecting bone resorption. "	( Pravastatin therapy increases procollagen I N-terminal propeptide (PINP), a marker of bone formation in post-menopausal women. Curiel, MD; De la Piedra, C; Lahoz, C; Mostaza, JM; Peña, R, 2001)	3.2
"As pravastatin treatment had no effect on LDL size, it is suggested that the additional effect of fenofibrate therapy on LDL size may contribute to reduce the risk of coronary heart disease (CHD) beyond what can be expected from the reduction in LDL cholesterol concentration in type IIa dyslipidemic patients."	( A 16-week fenofibrate treatment increases LDL particle size in type IIA dyslipidemic patients. Bourgeois, J; Després, JP; Dzavik, V; Laperrière, L; Lemieux, I; Tremblay, G, 2002)	0.94
"Pravastatin treatment results in a 43% decrease in plasma triglycerides in NAR, but not in Sprague-Dawley (SDR) rats, and had no significant effect on plasma total cholesterol, phospholipids apolipoproteins A-I, A-IV, B, or E, as well as on plasma LCAT activity levels in NAR or SDR."	( Hyperlipoproteinemia in Nagase analbuminemic rats: effects of pravastatin on plasma (apo)lipoproteins and lecithin:cholesterol acyltransferase activity. Jansen, EH; Joles, JA; Koomans, HA; Van Tol, A, 1991)	1.24
"Pravastatin treatment did not adversely affect serum glucose levels."	( The effect of pravastatin on serum cholesterol levels in hypercholesterolemic diabetic rabbits. Arbeeny, CM; Bergquist, KE, 1991)	1.36
"Pravastatin treatment however, did not result in a reduction in the LDL esterified/free cholesterol ratio or in the changes in cellular cholesterol synthesis and its regulation by LDL which accompanied simvastatin treatment."	( Hypercholesterolaemia: simvastatin and pravastatin alter cholesterol metabolism by different mechanisms. Collins, P; Johnson, A; Owens, D; Robinson, K; Tighe, O; Tomkin, GH, 1991)	1.27
"Pravastatin treatment (n = 6) decreased LDL cholesterol (-27%), lathosterol (-46%), and ubiquinone (-29%)."	( Effects of pravastatin and cholestyramine on products of the mevalonate pathway in familial hypercholesterolemia. Angelin, B; Berglund, L; Dallner, G; Elmberger, PG; Eriksson, M; Kalén, A; Lund, E; Reihnér, E, 1991)	1.39
"Pravastatin treatment also significantly decreased concentrations of apo B in LDL, IDL, and VLDL."	( Pravastatin therapy in primary moderate hypercholesterolaemia: changes in metabolism of apolipoprotein B-containing lipoproteins. Grundy, SM; Krauss, RM; Vega, GL, 1990)	2.44
"Pravastatin treatment resulted in lowering serum total cholesterol by 22.1% on the average (p less than 0.001), and led to a significant reduction in urinary excretion of albumin and beta 2-microglobulin in patients with an elevated urinary protein excretion rate at the baseline period."	( Amelioration of proteinuria with pravastatin in hypercholesterolemic patients with diabetes mellitus. Ikeda, Y; Kurata, H; Nomura, K; Sasaki, T; Utsunomiya, K, )	1.13
"35 pravastatin-treated patients with familial hypercholesterolemia were included in an ocular drug-safety study. "	( Ocular drug-safety study with the HMG-CoA reductase inhibitor pravastatin. Hockwin, O; Schmidt, J; Schmitt, C, 1990)	1.14
"Treatment with pravastatin did not reduce sPLA2-IIA mass or sPLA2 activity levels, as compared to placebo."	( Statin therapy and secretory phospholipase A₂ in children with heterozygous familial hypercholesterolemia. Braamskamp, MJ; Hutten, BA; Kastelein, JJ; Tsimikas, S; Wiegman, A, 2013)	0.73
"Treatment with pravastatin plus ezetimibe decreases the CIMT with improvement in the concentration of total cholesterol, LDL-C and CRP levels with good toleration."	( [Effect of pravastatine plus ezetimibe on carotid intima media thickness in patients with lupus erythematosus]. Ángeles-Garay, U; Carrillo-González, AL; Hernández, C; Jara, L; Medina, G; Olvera-Acevedo, A; Peralta-Amaro, AL; Vera-Lastra, OL, 2015)	1.16
"Upon treatment with Pravastatin reduced platelet LOX-1 expression induced by ADP."	( Pravastatin and C reactive protein modulate protease- activated receptor-1 expression in vitro blood platelets. Chu, LX; He, LP; Liang, ZS; Mo, CG; Qin, YQ; Wang, XD; Xie, J; Yang, F; Zhou, SX, 2016)	2.19
"Treatment with pravastatin (100mg/kg) decreased total and LDL cholesterol only in the LCHP group, but displayed a pronounced anti-atherosclerotic effect in BCA and abdominal aorta. "	( Anti-atherosclerotic effects of pravastatin in brachiocephalic artery in comparison with en face aorta and aortic roots in ApoE/LDLR Baranska, M; Chlopicki, S; Czyzynska-Cichon, I; Drahun, A; Franczyk-Zarow, M; Gasior-Glogowska, M; Jasztal, A; Kostogrys, RB; Kus, E; Manterys, A; Wrobel, TP, 2017)	1.09
"Pretreatment with pravastatin significantly ameliorated renal dysfunction and apoptosis and improved renal morphology and survival."	( Pravastatin attenuates carboplatin-induced nephrotoxicity in rodents via peroxisome proliferator-activated receptor alpha-regulated heme oxygenase-1. Chen, HH; Chen, TW; Lin, H, 2010)	2.13
"Treatment with pravastatin decreased the contractile responses to phenylephrine (maximal effect [mean+/-standard error of the mean] 137.35+/- 27.70 compared with 42.24+/-8.76; P=.006) for sFlt-1 compared with sFlt-1-pravastatin, respectively."	( Using pravastatin to improve the vascular reactivity in a mouse model of soluble fms-like tyrosine kinase-1-induced preeclampsia. Bytautiene, E; Costantine, MM; Hankins, GDV; Longo, M; Lu, F; Saade, GR; Tamayo, E, 2010)	1.18
"Treatment with pravastatin or fenofibrate improves the atherogenic lipid profile within the first 12 weeks and is sustained through 48 weeks with combination therapy. "	( Treatment with pravastatin and fenofibrate improves atherogenic lipid profiles but not inflammatory markers in ACTG 5087. Aberg, JA; Evans, SR; Fichtenbaum, CJ; Yeh, TM, )	0.84
"Treatment with pravastatin markedly increased aggregation amplitude and γIsc max values and significantly decreased erythrocyte deformability but did not change plasma viscosity in 2 weeks time."	( Effects of pravastatin on cellular ultrastructure and hemorheology in rats after traumatic head injury. Basak, AT; Berker, M; Dikmenoglu, N; Hazer, DB; Ileri-Gurel, E; Kaymaz, F; Narin, F; Seringec, N; Tuncel, M, 2010)	1.09
"Treatment with pravastatin reduced the frequency and duration of ventricular tachycardia and fibrillation (VT/VF) and improved the arrhythmia score after reperfusion."	( Cardioprotective effects of pravastatin against lethal ventricular arrhythmias induced by reperfusion in the rat heart. Ezaki, K; Fukui, A; Hara, M; Kume, O; Miyazaki, H; Nakagawa, M; Nishio, S; Saikawa, T; Takahashi, N; Teshima, Y; Thuc, LC; Yufu, K, 2011)	1
"Pretreatment with pravastatin (25 mg/kg) for 5 days significantly decreased both CTS and PTS."	( Pravastatin attenuates noise-induced cochlear injury in mice. Choung, YH; Jou, I; Kim, SW; Park, JS; Park, K; Park, SM, 2012)	2.15
"Treatment with pravastatin of stimulated human chondrocytes leads to significant down-regulation of selected MMP genes and a non-significant reduction in MMP enzyme activity. "	( Pravastatin suppresses matrix metalloproteinase expression and activity in human articular chondrocytes stimulated by interleukin-1β. Baker, JF; Byrne, DP; Mulhall, KJ; Walsh, PM, 2012)	2.17
"Treatment with pravastatin reduced the combined risk of fatal and nonfatal myocardial infarction by 31%. "	( The anatomy of a clinical trial. The West of Scotland Coronary Prevention Study. Gaw, A; Shepherd, J, 2002)	0.67
"Treatment with pravastatin reduced non-haemorrhagic stroke by 23% (P = 0.016) when considered alone, and 21% (P = 0.024) after adjustment for other risk factors."	( Risk factors for non-haemorrhagic stroke in patients with coronary heart disease and the effect of lipid-modifying therapy with pravastatin. Anderson, NE; Hankey, GJ; Hunt, D; Kirby, A; Simes, RJ; Tonkin, AM; Watson, JD; West, MJ; White, HD; Wonders, S, 2002)	0.86
"Treatment with pravastatin resulted in significant additional benefit after allowance for risk factors."	( Risk factors for non-haemorrhagic stroke in patients with coronary heart disease and the effect of lipid-modifying therapy with pravastatin. Anderson, NE; Hankey, GJ; Hunt, D; Kirby, A; Simes, RJ; Tonkin, AM; Watson, JD; West, MJ; White, HD; Wonders, S, 2002)	0.86
"Treatment with pravastatin was associated with the development of collateral circulation in patients with CAD, suggesting that such action constitutes part of the pleiotropic effects of statin."	( Pravastatin promotes coronary collateral circulation in patients with coronary artery disease. Arai, H; Miura, S; Nishikawa, H; Saku, K; Shimomura, H; Tsuchiya, Y; Zhang, B, 2002)	2.11
"Treatment with pravastatin (20-40 mg/day for 3 months) resulted in normalization of fasting levels of blood lipids and decreased postprandial hyperlipidemia due to of enhanced removal of triglyceride-rich atherogenic lipoproteins from blood and their diminished secretion in response to fat load."	( [Correction of atherogenic exogenously-induced postprandial hyperlipidemia with pravastatin]. Aronov, DM; Bubnova, MG; Golubev, MA; Mel'kina, OE; Olfer'ev, AM; Perova, NV; Zhasminova, VG, 2002)	0.88
"Treatment with pravastatin 40 mg/day for 8 weeks had no effect on the levels of ADMA in hypercholesterolemic men."	( Increased levels of asymmetric dimethylarginine in populations at risk for atherosclerotic disease. Effects of pravastatin. Arnesen, H; Eid, HM; Eritsland, J; Larsen, J; Seljeflot, I, 2003)	0.87
"Treatment with pravastatin (10 mg/day) was continued for 3 years."	( Preventing angiographic progression of coronary atherosclerosis with pravastatin. Ako, JY; Daida, H; Eto, M; Kurata, T; Mokuno, H; Nishide, T; Ouchi, Y; Saito, Y; Sato, H; Tango, T; Yamada, N; Yamaguchi, H, 2003)	0.89
"Treatment with pravastatin did not show any significant changes."	( Antioxidative potential of fluvastatin via the inhibition of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. Bandoh, T; Hoshi, K; Inoue, M; Mitani, H; Nakashima, A; Sato, EF, 2003)	0.66
"Treatment with pravastatin in patients with both low LDL-C and low HDL-C significantly reduced major coronary events, stroke, and all-cause mortality. "	( Effects of pravastatin on coronary events in 2073 patients with low levels of both low-density lipoprotein cholesterol and high-density lipoprotein cholesterol: results from the LIPID study. Barter, P; Colquhoun, D; Glasziou, P; Hunt, D; Keech, A; Marschner, I; Simes, J; Tonkin, A; White, H, 2004)	1.07
"Treatment with pravastatin did not result in a significant reduction in urinary albumin excretion or cardiovascular events."	( Effects of fosinopril and pravastatin on cardiovascular events in subjects with microalbuminuria. Asselbergs, FW; de Jong, PE; de Zeeuw, D; Diercks, GF; Hillege, HL; Janssen, WM; van Boven, AJ; van Gilst, WH; van Veldhuisen, DJ; Voors, AA, 2004)	0.96
"Treatment with pravastatin (1 mmol/L) not only prevented the inhibition of endothelial function but also reversed the decrease of DDAH activity induced by AGE-BSA and normalized the alterations in nitrite/nitrate and MDA contents."	( Pravastatin restores DDAH activity and endothelium-dependent relaxation of rat aorta after exposure to glycated protein. Xiong, Y; Yin, QF, 2005)	2.11
"Pretreatment with pravastatin significantly attenuated LPS-induced leucocyte-endothelial cell interactions (rolling velocity 89(6) per cent at 10 min, P = 0.038; adherent leucocytes 3.0(0.5) per 100 microm at 10 min, P = 0.038; migrating leucocytes 1.9(0.5) per field at 30 min, P = 0.001)."	( Hydroxymethylglutaryl co-enzyme A reductase inhibition attenuates endotoxin-mediated inflammatory responses. Bouchier-Hayes, DJ; Casey, R; Gang, C; Joyce, M; Kelly, CJ; Winter, D, 2005)	0.65
"Pretreatment with pravastatin at 20 microM for 16 h substantially attenuated ceramide cytotoxicity in mouse CECs."	( Pravastatin attenuates ceramide-induced cytotoxicity in mouse cerebral endothelial cells with HIF-1 activation and VEGF upregulation. Chen, H; Chen, SD; Hsu, CY; Hu, CJ; Nassief, A; Xu, J; Yang, DI; Yin, K, 2005)	2.09
"Treatment with pravastatin significantly reduced the incidence of transplant CAD (p = 0.05)."	( Survival, graft atherosclerosis, and rejection incidence in heart transplant recipients treated with statins: 5-year follow-up. Frazier, OH; Radovancevic, B; Radovancevic, R; Stojanovic, I; Thomas, CD; Vrtovec, B; Yazdanbakhsh, AP, 2005)	0.67
"The treatment with pravastatin 40 mg once a day for 6 months does not affect brain cholesterol metabolism as judged by plasma concentrations of 24(S)-hydroxycholesterol."	( Effect of pravastatin on plasma sterols and oxysterols in men. Janatuinen, T; Knuuti, J; Laaksonen, R; Lehtimäki, T; Lütjohann, D; Thelen, KM; Vesalainen, R; von Bergmann, K, 2006)	1.06
"Treatment with pravastatin at low to average dosages does not result in improved blood pressure regulation after kidney transplantation."	( Effects of pravastatin treatment on blood pressure regulation after renal transplantation. Lopau, K; Spindler, K; Wanner, C, 2006)	1.08
"Treatment with pravastatin in women with elevated cholesterol but no history of cardiovascular disease provides a benefit similar to that seen in men, and this benefit is more marked in older women. "	( Usefulness of pravastatin in primary prevention of cardiovascular events in women: analysis of the Management of Elevated Cholesterol in the Primary Prevention Group of Adult Japanese (MEGA study). Kushiro, T; Mizuno, K; Nakamura, H; Nakaya, N; Ohashi, Y; Tajima, N; Teramoto, T; Uchiyama, S, 2008)	1.06
"Treatment with pravastatin significantly reduced the incidence of myocardial infarction and death from cardiovascular causes without adversely affecting the risk of death from noncardiovascular causes in men with moderate hypercholesterolemia and no history of myocardial infarction."	( Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. Cobbe, SM; Ford, I; Isles, CG; Lorimer, AR; MacFarlane, PW; McKillop, JH; Packard, CJ; Shepherd, J, 1995)	0.91
"The treatment with pravastatin did not alter the FCR of the LDL receptor-independent pathway."	( Pravastatin-induced changes in receptor-mediated metabolism of low density lipoprotein in guinea pigs. Arakawa, K; Araki, K; Hidaka, K; Matsunaga, A; Moriyama, K; Sasaki, J; Takada, Y, 1994)	2.05
"Treatment with pravastatin significantly reduced total-c (23.8%, p < 0.001), LDL-c (31.9%, p < 0.001) and triglyceride (16.9%, p < 0.001) levels, concomitantly those of HDL-c were significantly raised (15%, p < 0.001)."	( The RED-LIP study--pravastatin in primary isolated hypercholesterolemia--an open, prospective, multicenter trial. Pirich, C; Sinzinger, H, 1994)	0.96
"Rats treated with pravastatin for 28 days had a higher lymphatic recovery of the lipids during 3-6 h after the lipid administration than did control rats."	( Lymphatic transport of cholesterol in normocholesterolemic rats treated with pravastatin, an inhibitor of HMG-CoA reductase. Ibi, T; Ikeda, I; Imaizumi, K; Nagao, K; Sakono, M; Yamamoto, K, 1996)	0.85
"Treatment with pravastatin normalized thrombin generation."	( Platelet-dependent thrombin generation in patients with hyperlipidemia. Aoki, I; Aoki, N; Homori, M; Ishikawa, K; Kawai, Y; Kawano, K; Maki, A; Shimoyama, K; Yamamoto, M; Yanagisawa, A, 1997)	0.64
"Treatment with pravastatin in a dose of 5 mg twice daily for 4 weeks resulted in lowering plasma total and LDL cholesterol levels by 17.0% and 22.9%, respectively."	( Short-term treatment with low-dose pravastatin attenuates oxidative susceptibility of low-density lipoprotein in hypercholesterolemic patients. Chen, MF; Hsu, HC; Lee, YT, 1997)	0.91
"Treatment with pravastatin reduced the levels of total cholesterol by 19%, LDL cholesterol by 27%, apolipoprotein B by 19%, and triglycerides by 13% (all 2P<.0001) and increased apolipoprotein A1 and HDL cholesterol levels by 4% (both 2P<.0005), in comparison with placebo."	( Effects of lowering average of below-average cholesterol levels on the progression of carotid atherosclerosis: results of the LIPID Atherosclerosis Substudy. LIPID Trial Research Group. Gamble, G; Hart, H; MacMahon, S; Scott, J; Sharpe, N; Simes, J; White, H, 1998)	0.64
"Treatment with pravastatin reduced the development of carotid atherosclerosis among patients with coronary heart disease and a wide range of pretreatment cholesterol levels. "	( Effects of lowering average of below-average cholesterol levels on the progression of carotid atherosclerosis: results of the LIPID Atherosclerosis Substudy. LIPID Trial Research Group. Gamble, G; Hart, H; MacMahon, S; Scott, J; Sharpe, N; Simes, J; White, H, 1998)	0.65
"Treatment with pravastatin did not affect serum cholesterol levels or systolic blood pressure but did reduce the L-NAME induced inflammatory and proliferative changes."	( Pravastatin attenuates cardiovascular inflammatory and proliferative changes in a rat model of chronic inhibition of nitric oxide synthesis by its cholesterol-lowering independent actions. Egashira, K; Inoue, S; Kataoka, C; Kitamoto, S; Koyanagi, M; Ni, W; Takeshita, A, 2000)	2.09
"Treatment with pravastatin, but not fluvastatin, preserved interstitial collagen content in vivo (detected by picrosirius red polarization)."	( Statins alter smooth muscle cell accumulation and collagen content in established atheroma of watanabe heritable hyperlipidemic rabbits. Aikawa, M; Enomoto, M; Fukumoto, Y; Hill, CC; Hirouchi, Y; Libby, P; Rabkin, E; Shiomi, M, 2001)	0.65
"Pre-treatment with pravastatin attenuated this neutrophil infiltration and microvascular leakage."	( Pravastatin attenuates lower torso ischaemia-reperfusion-induced lung injury by upregulating constitutive endothelial nitric oxide synthase. Bouchier-Hayes, DJ; Chen, G; Joyce, M; Kelly, CJ, 2001)	2.07
"Rats treated with pravastatin had a 22% reduction in GVD that did not reach statistical significance."	( Fluvastatin in combination with rad significantly reduces graft vascular disease in rat cardiac allografts. Berryman, ER; Gregory, CR; Griffey, SM; Katznelson, S; Kyles, AE, 2001)	0.63
"Pretreatment with pravastatin significantly attenuated IR-induced renal injury, improving urine production to 0.62 (0.2) ml/h and GFR to 0.14 (0.02) ml/min and diminishing protein leakage to 3.76 (0.7) g/L at the 2-h time point."	( Pravastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, attenuates renal injury in an experimental model of ischemia-reperfusion. Bouchier-Hayes, D; Chen, G; Joyce, M; Kelly, C; Leahy, A; Winter, D, 2001)	2.08
"Treatment with pravastatin over 5 years reduces all-cause mortality and coronary mortality in patients with and those without a history of coronary heart disease. "	( Effects of pravastatin on mortality in patients with and without coronary heart disease across a broad range of cholesterol levels. The Prospective Pravastatin Pooling project. Braunwald, E; Davis, BR; Ford, I; Furberg, CD; Shepherd, J; Simes, J; Tonkin, A, 2002)	1.06
"Treatment with pravastatin 40 mg once daily reduced total and LDL cholesterol (LDL-C) after 6 months by 19.7% and 25.4%, respectively (P less than .001)."	( Pravastatin in heterozygous familial hypercholesterolemia: low-density lipoprotein (LDL) cholesterol-lowering effect and LDL receptor activity on skin fibroblastS. Arca, M; Calandra, S; Ciarrocchi, A; D'Alò, G; Descovich, GC; Fazio, S; Gaddi, A; Tiozzo, R, 1991)	2.06
"Treatment with pravastatin resulted in a significant decrease in plasma cholesterol caused by a decrease in low density lipoprotein cholesterol (LDL-c) of 30% (p less than 0.005)."	( Effect of pravastatin on biliary lipid composition and bile acid synthesis in familial hypercholesterolaemia. de Rooy, FW; Hoogerbrugge-vd Linden, N; Jansen, H; van Blankenstein, M, 1990)	1.02

Excerpt	Reference	Relevance
"4%) developed adverse reactions, but interruption of the treatment was necessary in only 18 (0."	( [An evaluation of the efficacy and safety of pravastatin in patients with primary hypercholesterolemia. A Brazilian open multicenter study]. Giannini, SD, 1992)	0.54
" Adverse events were monitored."	( Treatment of primary hypercholesterolaemia with pravastatin: efficacy and safety over three years. Clifton, P; Janus, ED; Nestel, PJ; Parfitt, A; Simons, J; Simons, LA, 1992)	0.54
" Eight subjects allocated to pravastatin and seven allocated to resin withdrew (one and two subjects respectively because of drug-induced adverse events)."	( Treatment of primary hypercholesterolaemia with pravastatin: efficacy and safety over three years. Clifton, P; Janus, ED; Nestel, PJ; Parfitt, A; Simons, J; Simons, LA, 1992)	0.83
"Pravastatin was found to be a relatively effective, safe and well tolerated lipid-lowering drug."	( Treatment of primary hypercholesterolaemia with pravastatin: efficacy and safety over three years. Clifton, P; Janus, ED; Nestel, PJ; Parfitt, A; Simons, J; Simons, LA, 1992)	1.98
" Pravastatin was well tolerated and was associated with a low incidence of adverse events."	( Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. II. Once-daily versus twice-daily dosing. Goldberg, AC; Hunninghake, DB; Insull, W; Kostis, JB; Kuo, PT; Mellies, MJ; Pan, HY; Schrott, HG, 1990)	1.5
"Pravastatin appears to be an effective and safe lipid-lowering agent and is the first 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor to be studied extensively in this underrepresented population."	( Efficacy and safety of pravastatin in African Americans with primary hypercholesterolemia. Chin, MM; Curry, CL; Jacobson, TA; LaRosa, JC; Miller, V; Papademetriou, V; Schlant, RC, 1995)	2.04
" No adverse effects requiring treatment discontinuation were observed for both drugs."	( [Randomized, double-blind comparative study between pravastatin and lovastatin. Evaluation of efficacy and safety]. Bertolami, MC; Diament, J; Faludi, AA; Forti, N; Giannini, SD; Schölz, J, 1994)	0.54
" Adverse events observed in 5 cases were always mild and reversible."	( A multi-centre study of the efficacy and safety of pravastatin in hypercholesterolaemic patients with non-insulin-dependent diabetes mellitus. Ando, S; Fujii, S; Hatao, K; Hatao, M; Inoue, Y; Kaku, K; Kaneko, T; Matsumura, S; Okubo, M, 1994)	0.54
" Pravastatin was well tolerated, with an overall incidence of adverse events nearly identical to that of placebo."	( Efficacy and safety of pravastatin in the long-term treatment of elderly patients with hypercholesterolemia. Behounek, BD; Kobylak, L; Maciejko, JJ; McGovern, ME; Rosman, HS; Rubenfire, M; Santinga, JT, 1994)	1.51
" The drug was very well tolerated, with an incidence of adverse events of only 10."	( [Pravastatin: efficacy and safety in elderly patients with primary hypercholesterolemia. Open multicenter study]. Diament, J; Giannini, SD, 1993)	1.2
" The effects on the lipid fractions are significant, adverse effects are rare and the drug is very well tolerated."	( [Pravastatin: efficacy and safety in elderly patients with primary hypercholesterolemia. Open multicenter study]. Diament, J; Giannini, SD, 1993)	1.2
" No other significant differences were observed between the pravastatin and the placebo-treated groups with regard to other adverse effects and to patient compliance and withdrawal."	( Efficacy and safety of pravastatin once daily in primary moderate hypercholesterolemia: the Israeli experience. Beigel, Y; Brook, G; Eisenberg, S; Fainaru, M; Harats, D; Levy, Y; Rubinstein, A; Skurnik, Y, 1993)	0.84
" Adverse experiences were mild and did not differ between treatment groups; in each group, one subject discontinued medication because of complaints of dizziness."	( Treatment of primary hypercholesterolaemia. Short-term efficacy and safety of increasing doses of simvastatin and pravastatin: a double-blind comparative study. De Haan, AF; Kastelein, JJ; Kortmann, B; Kroon, AA; Lansberg, PJ; Stalenhoef, AF; Stuyt, PM, 1993)	0.5
"Between December 1989 and December 1992, the Netherlands Centre for Monitoring of Adverse Reactions to Drugs received 142 reports of suspected adverse reactions to simvastatin or pravastatin."	( [Side effects of cholesterol synthesis inhibitors]. Stricker, BH; Wolterbeek, R, 1993)	0.48
" There was no significant difference between groups in the frequency of drug-related adverse experiences."	( Comparison of the efficacy, safety and tolerability of simvastatin and pravastatin for hypercholesterolemia. The Simvastatin Pravastatin Study Group. , 1993)	0.52
" Relevant data on the incidence of adverse effects are presented."	( Comparative evaluation of the safety and efficacy of HMG-CoA reductase inhibitor monotherapy in the treatment of primary hypercholesterolemia. Hsu, I; Johnson, NE; Spinler, SA, )	0.13
" Results from this study confirmed that a low dose (10 mg) of pravastatin daily is a safe and effective method of reducing plasma total and LDL-cholesterol in hypercholesterolemic, hypertensive elderly patients who are on concurrent antihypertensive drug therapy."	( The effectiveness and safety of low dose pravastatin in elderly hypertensive hypercholesterolemic subjects on antihypertensive therapy. Chan, P; Ko, JT; Lee, CB; Lee, YS; Lin, TS; Pan, WH, 1995)	0.8
" The results show that pravastatin was well tolerated and that adverse events were mild and equally distributed among the three treatment groups."	( Short-term efficacy and safety of pravastatin in 72 children with familial hypercholesterolemia. Bakker, HD; Boelen, CC; Büller, HR; Groenemeijer, BE; Kastelein, JJ; Knipscheer, HC; van den Ende, A; van Diermen, DE, 1996)	0.88
" Adverse events and clinical laboratory abnormalities were generally mild and transient in all groups, and all but two patients finished the study."	( Effectiveness and safety of low-dose pravastatin and squalene, alone and in combination, in elderly patients with hypercholesterolemia. Chan, P; Lee, CB; Lee, YS; Tomlinson, B, 1996)	0.57
" Safety was assessed by recording adverse events and measuring clinical laboratory parameters."	( Efficacy and safety of atorvastatin compared to pravastatin in patients with hypercholesterolemia. Bertolini, S; Bon, GB; Campbell, LM; Egros, F; Farnier, M; Fayyad, R; Langan, J; Mahla, G; Nawrocki, JW; Pauciullo, P; Sirtori, C, 1997)	0.55
" Physical and laboratory investigations for adverse effects were performed every month for the first 3 months and every 3 months thereafter."	( Safety and efficacy of long-term statin-fibrate combinations in patients with refractory familial combined hyperlipidemia. Athyros, VG; Carina, MV; Didangelos, TP; Hatzikonstandinou, HA; Kontopoulos, AG; Kranitsas, DF; Papageorgiou, AA, 1997)	0.3
"To assess the additional benefit gained from high compliance in the West of Scotland Coronary Prevention Study and to examine cases where withdrawal from trial medication was due to an adverse event."	( Compliance and adverse event withdrawal: their impact on the West of Scotland Coronary Prevention Study. , 1997)	0.3
" The adverse events associated with withdrawal were coded by body system."	( Compliance and adverse event withdrawal: their impact on the West of Scotland Coronary Prevention Study. , 1997)	0.3
" Atorvastatin was well-tolerated, and no serious or medically important adverse events were observed."	( Efficacy and safety of a new cholesterol synthesis inhibitor, atorvastatin, in comparison with simvastatin and pravastatin, in subjects with hypercholesterolemia. Black, DM; Mahla, G; Muller, D; Pentrup, A; Wolffenbuttel, BH, 1998)	0.51
"We conclude that atorvastatin is a safe and very efficacious cholesterol-lowering agent, which also possesses significant triglyceride-lowering properties."	( Efficacy and safety of a new cholesterol synthesis inhibitor, atorvastatin, in comparison with simvastatin and pravastatin, in subjects with hypercholesterolemia. Black, DM; Mahla, G; Muller, D; Pentrup, A; Wolffenbuttel, BH, 1998)	0.51
" There was no significant difference between the incidence of adverse effects with cerivastatin and comparator statins or between cerivastatin and other statins with respect to clinically significant increases in either hepatic enzymes or creatine phosphokinase."	( Clinical efficacy and safety of cerivastatin: summary of pivotal phase IIb/III studies. Davignon, J; Hanefeld, M; Hunninghake, DB; Insull, W; Nakaya, N; Ose, L, 1998)	0.3
"Pravastatin and gemfibrozil therapy is safe and efficacious in patients with mixed hyperlipidemia."	( Long-term safety of pravastatin-gemfibrozil therapy in mixed hyperlipidemia. Iliadis, EA; Rosenson, RS, 1999)	2.07
" The frequency of treatment-associated adverse events (AEs) in the atorvastatin LDL-C < or =80 mg/dl (2."	( Safety profile of atorvastatin-treated patients with low LDL-cholesterol levels. Bakker-Arkema, RG; Black, DM; Nawrocki, JW, 2000)	0.31
" Both drugs were well tolerated, with most adverse events being mild."	( Efficacy and safety of cerivastatin and pravastatin in the treatment of primary hypercholesterolemia. Ferdinand, K; Krug-Gourley, S; Poland, M; Saunders, E; Tonkon, MJ; Yellen, LG, 2000)	0.57
" Overall, compliance was high and few adverse effects were reported."	( Effective and safe modification of multiple atherosclerotic risk factors in patients with peripheral arterial disease. Applegate, WB; Crouse, JR; Davis, KB; Egan, D; Elam, MB; Garg, R; Herd, JA; Hunninghake, DB; Johnson, WC; Kennedy, JW; Kostis, JB; Sheps, DS, 2000)	0.31
"ADMIT demonstrates that it is both feasible and safe to modify multiple atherosclerotic disease risk factors effectively with intensive combination therapy in patients with PAD."	( Effective and safe modification of multiple atherosclerotic risk factors in patients with peripheral arterial disease. Applegate, WB; Crouse, JR; Davis, KB; Egan, D; Elam, MB; Garg, R; Herd, JA; Hunninghake, DB; Johnson, WC; Kennedy, JW; Kostis, JB; Sheps, DS, 2000)	0.31
" Cerivastatin is safe and effective for patients with hypercholesterolemia who require aggressive LDL cholesterol lowering to achieve NCEP-recommended targets."	( Randomized comparison of the efficacy and safety of cerivastatin and pravastatin in 1,030 hypercholesterolemic patients. The Cerivastatin Study Group. Dujovne, CA; Hunninghake, D; Knopp, R; Kwiterovich, P; McBride, TA; Poland, M, 2000)	0.54
" Pravastatin, a HMG-CoA reductase inhibitor, has been shown to be effective and safe for cholesterol reduction in adult heart transplant recipients."	( Safety and efficacy of pravastatin therapy for the prevention of hyperlipidemia in pediatric and adolescent cardiac transplant recipients. Fricker, FJ; Harker, K; Kahler, DA; Penson, MG; Schowengerdt, KO; Thompson, JR; Williams, BJ, 2001)	1.53
"Pravastatin therapy is effective and safe when used in pediatric and adolescent cardiac transplant recipients."	( Safety and efficacy of pravastatin therapy for the prevention of hyperlipidemia in pediatric and adolescent cardiac transplant recipients. Fricker, FJ; Harker, K; Kahler, DA; Penson, MG; Schowengerdt, KO; Thompson, JR; Williams, BJ, 2001)	2.06
"Muscle symptoms are known as adverse effects of HMG-CoA reductase inhibitors but their incidence is reported to be low."	( Shoulder stiffness: a common adverse effect of HMG-CoA reductase inhibitors in women? Fujimura, A; Harada, K; Tsuruoka, S, 2001)	0.31
"Potential cost differences between statins are driven primarily by drug costs, differential lowering effects on low-density lipoprotein cholesterol (LDL-C) levels, and adverse drug interactions and reactions."	( Cerivastatin versus branded pravastatin in the treatment of primary hypercholesterolemia in primary care practice in Canada: a one-year, open-label, randomized, comparative study of efficacy, safety, and cost-effectiveness. Agro, A; Braeken, A; Hanna, K; McPherson, R, 2001)	0.6
"6%) because of an adverse event."	( Cerivastatin versus branded pravastatin in the treatment of primary hypercholesterolemia in primary care practice in Canada: a one-year, open-label, randomized, comparative study of efficacy, safety, and cost-effectiveness. Agro, A; Braeken, A; Hanna, K; McPherson, R, 2001)	0.6
" Cerivastatin was well tolerated; the most commonly reported adverse events were arthralgia, headache, pharyngitis, and rhinitis."	( Long-term efficacy and safety of cerivastatin 0.8 mg in patients with primary hypercholesterolemia. Brazg, R; Dujovne, CA; Insull, W; Isaacsohn, J; Kwiterovich, P; Patrick, MA; Ripa, S; Shan, M; Shugrue-Crowley, E; Stein, E; Tota, R, 2001)	0.31
"Data from 185 patients were retrospectively evaluated for adverse events, duration of exposure (person-days), and the mean atorvastatin dose exposure."	( Safety and efficacy of atorvastatin in heart transplant recipients. Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002)	0.31
"Data from 185 patients were retrospectively evaluated for adverse events, duration of exposure (person-days), and the mean atorvastatin dose exposure."	( Safety and efficacy of atorvastatin in heart transplant recipients. Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002)	0.31
"Atorvastatin, when used at moderate doses and with close biochemical and clinical monitoring, appears to be safe and is effective in aggressively lowering LDL in heart transplant recipients when treatment with other statins has failed to achieve LDL goals."	( Safety and efficacy of atorvastatin in heart transplant recipients. Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002)	0.31
" Major cardiovascular events and adverse events were compared according to initial treatment assignment."	( Long-term effectiveness and safety of pravastatin in 9014 patients with coronary heart disease and average cholesterol concentrations: the LIPID trial follow-up. , 2002)	0.59
" Pravastatin had no significant adverse effects."	( Long-term effectiveness and safety of pravastatin in 9014 patients with coronary heart disease and average cholesterol concentrations: the LIPID trial follow-up. , 2002)	1.5
" Safety was assessed by monitoring adverse events and measuring clinical laboratory parameters."	( A randomized, double-blind trial comparing the efficacy and safety of pitavastatin versus pravastatin in patients with primary hypercholesterolemia. Goto, Y; Hata, Y; Itakura, H; Mabuchi, H; Nakaya, N; Ogawa, N; Saito, Y; Sasaki, J; Teramoto, T; Tushima, M; Yamada, N, 2002)	0.54
" No differences in noncardiovascular serious adverse events were detected."	( Safety and tolerability of pravastatin in long-term clinical trials: prospective Pravastatin Pooling (PPP) Project. Braunwald, E; Byington, RP; Cobbe, SM; Davis, BR; Friedman, CP; Keech, A; Pfeffer, MA; Sacks, FM; Tonkin, A, 2002)	0.61
"This prospective analysis indicates that during prolonged exposure, 40 mg of pravastatin is well tolerated, with no excess of noncardiovascular serious adverse events, including liver function abnormalities and laboratory and clinical evidence for myositis."	( Safety and tolerability of pravastatin in long-term clinical trials: prospective Pravastatin Pooling (PPP) Project. Braunwald, E; Byington, RP; Cobbe, SM; Davis, BR; Friedman, CP; Keech, A; Pfeffer, MA; Sacks, FM; Tonkin, A, 2002)	0.84
" No significant adverse effects were noted, and no complications with drug withdrawals occurred."	( Comparison of the efficacy and safety of pravastatin and simvastatin in heart transplantation. DeGruiter, H; Lavie, CJ; Mehra, MR; Milani, RV; Uber, PA; Vivekananthan, K, 2002)	0.58
"Simvastatin and pravastatin are safe and very effective in total cholesterol and LDL cholesterol lowering in heart transplant recipients, with simvastatin being more efficacious than pravastatin in lipid lowering in this group of patients."	( Comparison of the efficacy and safety of pravastatin and simvastatin in heart transplantation. DeGruiter, H; Lavie, CJ; Mehra, MR; Milani, RV; Uber, PA; Vivekananthan, K, 2002)	0.93
" Data included medication use, clinic visits, adverse events, LDL-C and other laboratory measures."	( An economic analysis of the Atorvastatin Comparative Cholesterol Efficacy and Safety Study (ACCESS). McBurney, CR; Smith, DG, 2003)	0.32
"Two years of pravastatin therapy induced a significant regression of carotid atherosclerosis in children with familial hypercholesterolemia, with no adverse effects on growth, sexual maturation, hormone levels, or liver or muscle tissue."	( Efficacy and safety of statin therapy in children with familial hypercholesterolemia: a randomized controlled trial. Bakker, HD; Büller, HR; de Groot, E; Hutten, BA; Kastelein, JJ; Rodenburg, J; Sijbrands, EJ; Wiegman, A, 2004)	0.69
" When multiple doses of PV were given to EHBR without co-administration of any other compound, drug-induced skeletal muscle toxicity (myopathy/rhabdomyolysis) and increased creatine phosphokinase (CPK) level were observed, whereas a control experiment using SDR did not show any toxic change."	( Eisai hyperbilirubinemic rat (EHBR) as an animal model affording high drug-exposure in toxicity studies on organic anions. Kakinuma, C; Kuwayama, C; Naba, H; Ogihara, T; Ohnishi, S, 2004)	0.32
" In conclusion, pravastatin treatment was safe and well tolerated."	( Efficacy and safety of pravastatin in children and adolescents with heterozygous familial hypercholesterolemia: a prospective clinical follow-up study. Antikainen, M; Föhr, A; Hedman, M; Lappi, M; Matikainen, T; Nuutinen, M; Piippo, S, 2005)	0.99
" There were no severe adverse events caused by pravastatin."	( A prospective trial to evaluate the safety and efficacy of pravastatin for the treatment of refractory chronic graft-versus-host disease. Chiba, S; Goyama, S; Hamaki, T; Hirai, H; Hori, A; Imataki, O; Kami, M; Kanda, Y; Kishi, Y; Kojima, R; Komeno, Y; Makimoto, A; Mitani, K; Ogawa, S; Onishi, Y; Sakiyama, M; Takaue, Y; Tanosaki, R, 2005)	0.83
"The authors reviewed adverse events (AEs) reported to the United States Food and Drug Administration to determine the percentage of statin-associated AE reports with concurrent amiodarone use for simvastatin, atorvastatin, and pravastatin."	( Adverse events with concomitant amiodarone and statin therapy. Alsheikh-Ali, AA; Karas, RH, 2005)	0.51
" There were few adverse events and no rhabdomyolysis reported."	( A randomized trial of the efficacy and safety of fenofibrate versus pravastatin in HIV-infected subjects with lipid abnormalities: AIDS Clinical Trials Group Study 5087. Aberg, JA; Alston, BL; Brobst, SW; Evans, SR; Fichtenbaum, CJ; Glesby, MJ; Henry, WK; Owens, SI; Torriani, FJ; Yang, Y; Zackin, RA, 2005)	0.56
"Compared with patients treated with an accepted LDL goal (80 to 100 mg/dl), there was no adverse effect on safety with lower achieved LDL levels, and apparent improved clinical efficacy."	( Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy. Braunwald, E; Cannon, CP; Morrow, DA; Pfeffer, MA; Ray, KK; Wiviott, SD, 2005)	0.33
" Adverse effects have been related to the use of certain statins, high statin dosages, comorbidities, and coadministration with cyclosporine."	( Safety of statins when response is carefully monitored: a study of 336 heart recipients. Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005)	0.33
"Between April 1991 and December 2003, we retrospectively evaluated 336 heart transplant patients (including 55 women) with regard to the occurrence of possible adverse effects of statins (rhabdomyolysis, myalgia, hepatotoxicity, high CK without muscle symptoms, and others)."	( Safety of statins when response is carefully monitored: a study of 336 heart recipients. Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005)	0.33
"Possible adverse events of statins were suffered by 60 patients, all of them men."	( Safety of statins when response is carefully monitored: a study of 336 heart recipients. Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005)	0.33
"Some 10% to 20% of HT patients appear to suffer adverse side effects of initial statin therapy."	( Safety of statins when response is carefully monitored: a study of 336 heart recipients. Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005)	0.33
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."	( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling. Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004)	0.32
" Pravastatin was not toxic up to 1 mmol/l."	( Toxicity of statins on rat skeletal muscle mitochondria. Brecht, K; Kaufmann, P; Krähenbühl, S; Török, M; Waldhauser, KM; Zahno, A, 2006)	1.24
" Current drug labeling warns of an increased risk of adverse events with statin and niacin combinations."	( Safety of lovastatin/extended release niacin compared with lovastatin alone, atorvastatin alone, pravastatin alone, and simvastatin alone (from the United States Food and Drug Administration adverse event reporting system). Alsheikh-Ali, AA; Karas, RH, 2007)	0.56
"High-dose pravastatin (80 mg/day) administered to hypercholesterolemic subjects with chronic liver disease significantly lowered LDL-C, TC, and TGs in comparison with the placebo and was safe and well tolerated."	( Efficacy and safety of high-dose pravastatin in hypercholesterolemic patients with well-compensated chronic liver disease: Results of a prospective, randomized, double-blind, placebo-controlled, multicenter trial. Belder, R; Fusco, MJ; Lewis, JH; Medoff, JR; Mortensen, ME; Zweig, S, 2007)	1.02
" The purpose of this study was to explore documented adverse effects of liver transplant recipients receiving lipid-lowering therapies."	( Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients. Aranda-Michel, J; Bass, M; Cavanaugh, TM; Hanaway, M; Martin, JE; Rudich, S; Trumbull, L; Weber, F, )	0.13
"A retrospective chart review of 69 liver transplant patients was conducted to evaluate the incidence of adverse effects, especially rhabdomyolysis and liver function abnormalities, in liver transplant patients treated with a lipid lowering agent (LLA)."	( Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients. Aranda-Michel, J; Bass, M; Cavanaugh, TM; Hanaway, M; Martin, JE; Rudich, S; Trumbull, L; Weber, F, )	0.13
" Six patients studied had adverse effects, five (7."	( Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients. Aranda-Michel, J; Bass, M; Cavanaugh, TM; Hanaway, M; Martin, JE; Rudich, S; Trumbull, L; Weber, F, )	0.13
"Overall, there was a general tolerability with a low incidence of adverse events, no incidence of severe complications, and no alterations in liver function tests in the study population with the use of LLA."	( Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients. Aranda-Michel, J; Bass, M; Cavanaugh, TM; Hanaway, M; Martin, JE; Rudich, S; Trumbull, L; Weber, F, )	0.13
"There is a discrepancy in the adverse effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, statins between the clinical reports and the studies using skeletal muscle cell models."	( Involvement of organic anion transporting polypeptides in the toxicity of hydrophilic pravastatin and lipophilic fluvastatin in rat skeletal myofibres. Kimura, J; Mikami, H; Sakamoto, K, 2008)	0.57
" CPK surveillance is recommended because of a slight continued risk of adverse effects."	( The efficacy and safety of ezetimibe for treatment of dyslipidemia after heart transplantation. Castro-Beiras, A; Crespo-Leiro, MG; Flores, X; Franco, R; Grille, Z; Marzoa, R; Mosquera, V; Naya, C; Paniagua, MJ; Rodriguez, JA, 2008)	0.35
"3-Hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are safe and well-tolerated therapeutic drugs."	( Possible mechanisms underlying statin-induced skeletal muscle toxicity in L6 fibroblasts and in rats. Ichihara, K; Itagaki, M; Kaneta, S; Kano, S; Satoh, K; Takaguri, A, 2009)	0.35
" We defined a composite adverse event (CAE) as discontinuation for any side effect, myalgia, or CK >3x upper limit of normal during follow-up."	( The SLCO1B1*5 genetic variant is associated with statin-induced side effects. Ali, S; Ginsburg, GS; Reed, CR; Salisbury, BA; Shah, SH; Spasojevic, I; Voora, D, 2009)	0.35
" Our findings thereby reveal a safe and efficient therapeutic opportunity for the abrogation of late thoracic radiation injury, potentially usable either before or after radiation exposure; this approach is especially attractive in (1) the radiation oncology setting, as it does not interfere with prior anti-cancer treatment and in (2) radioprotection, as applicable to the treatment of established radiation injury, for example in the case of radiation accidents or acts of terrorism."	( Modulation of the Rho/ROCK pathway in heart and lung after thorax irradiation reveals targets to improve normal tissue toxicity. Monceau, V; Opolon, P; Pasinetti, N; Pouzoulet, F; Schupp, C; Vozenin, MC, 2010)	0.36
" Combination therapy was generally well tolerated with incidences of clinical and laboratory adverse experiences similar between the 2 groups."	( Efficacy and safety of adding fenofibrate 160 mg in high-risk patients with mixed hyperlipidemia not controlled by pravastatin 40 mg monotherapy. Bryniarski, L; Ducobu, J; Farnier, M, 2010)	0.57
" Adverse event (AE) profiles of FF/PRA 160 mg/40 mg (n=645 in the double-blind cohort) were evaluated relative to comparators (statins, n=519 or fenofibrate, n=122)."	( Safety of a fixed-dose combination of fenofibrate/pravastatin 160 mg/40 mg in patients with mixed hyperlipidaemia: a pooled analysis from a database of clinical trials. Bryniarski, L; Császár, A; De Niet, S; Ducobu, J; Farnier, M; Marcereuil, D; Retterstøl, K; Steinmetz, A; Vanderbist, F, 2012)	0.63
" These adverse events (AEs) can have serious impact, and form a significant barrier to therapy adherence."	( A survey of the FDA's AERS database regarding muscle and tendon adverse events linked to the statin drug class. Dimbil, M; Golomb, BA; Hoffman, KB; Kraus, C, 2012)	0.38
" However, this combination is often associated with adverse eff ects, especially muscular and hepatic."	( [Combination of pravastatin and fenofibrate (Pravafenix ®). Safety studies]. Hernández Mijares, A, 2014)	0.75
" We studied whether concurrent use of clarithromycin and a statin not metabolized by CYP3A4 was associated with an increased frequency of serious adverse events."	( Risk of adverse events among older adults following co-prescription of clarithromycin and statins not metabolized by cytochrome P450 3A4. Bailey, DG; Dixon, S; Fleet, JL; Gandhi, S; Garg, AX; Gomes, T; Juurlink, D; Kim, R; Li, DQ; Mamdani, M; McArthur, E; Shariff, SZ, 2015)	0.42
"Among older adults taking a statin not metabolized by CYP3A4, co-prescription of clarithromycin versus azithromycin was associated with a modest but statistically significant increase in the 30-day absolute risk of adverse outcomes."	( Risk of adverse events among older adults following co-prescription of clarithromycin and statins not metabolized by cytochrome P450 3A4. Bailey, DG; Dixon, S; Fleet, JL; Gandhi, S; Garg, AX; Gomes, T; Juurlink, D; Kim, R; Li, DQ; Mamdani, M; McArthur, E; Shariff, SZ, 2015)	0.42
" There were no differences between the 2 groups in rates of study drug side effects, congenital anomalies, or other adverse or serious adverse events."	( Safety and pharmacokinetics of pravastatin used for the prevention of preeclampsia in high-risk pregnant women: a pilot randomized controlled trial. Ahmed, MS; Brown, LM; Caritis, SN; Cleary, K; Costantine, MM; D'Alton, M; Easterling, TR; Haas, DM; Haneline, LS; Hankins, G; Hebert, MF; Ren, Z; Venkataramanan, R; West, H, 2016)	0.72
"Many adverse drug reactions are caused by the cytochrome P450 (CYP)-dependent activation of drugs into reactive metabolites."	( Development of a cell viability assay to assess drug metabolite structure-toxicity relationships. Jones, LH; Nadanaciva, S; Rana, P; Will, Y, 2016)	0.43
" Safety outcomes were evaluated by the risk of adverse events (AE)."	( Efficacy and safety of long-term treatment with statins for coronary heart disease: A Bayesian network meta-analysis. Bai, Y; Chan, C; Chang, X; Cheng, N; Cheng, Z; Lu, Y; Zhao, Y, 2016)	0.43
" Statins are generally well tolerated, but adverse reactions may occur, particularly myopathy and new onset of diabetes."	( Diabetogenic effect of pravastatin is associated with insulin resistance and myotoxicity in hypercholesterolemic mice. Favero, BC; García-Arevalo, M; Gomes-Marcondes, MCC; Lorza-Gil, E; Oliveira, HCF, 2019)	0.82
" Myotoxicity of statins in certain individuals is often a severe side effect leading to withdrawal."	( Resveratrol for protection against statin toxicity in C2C12 and H9c2 cells. Attalah Nee Rezkallah, C; Chen, QM; Thongkum, A; Zhu, C, 2020)	0.56
" There were no clinically important differences in statin-related adverse events between groups."	( Efficacy and safety profile of statins in patients with cancer: a systematic review of randomised controlled trials. Alexandre, L; Loke, YK; Thomas, JP, 2020)	0.56
" Subjects diagnosed with any type of dyslipidemia (population 4804) and received pitavastatin (interventions) versus comparator (comparison) with the primary efficacy endpoint of minimization of LDL-C and non- HDL-C, had an increase in HDL-C and/or reduction in major adverse cardiac events (MACE, cardiovascular death, myocardial infarction (fatal/nonfatal), and stroke (fatal/nonfatal) and/or their composite (outcomes)."	( A Systematic Review of Randomized Clinical Trials on the Efficacy and Safety of Pitavastatin. Alkaabi, M; Amoodi, AA; Baraka, MA; Don, J; Elnour, AA; Farah, FH; Mazrouei, NA; Ramadan, A; Sadeq, A; Sam, KG, 2023)	0.91

Excerpt	Reference	Relevance
" The area under the serum concentration-time curve and maximum serum concentration of pravastatin showed dose-proportionality; time to maximum serum concentration and serum elimination half-life were independent of dose."	( Pharmacokinetics and pharmacodynamics of pravastatin alone and with cholestyramine in hypercholesterolemia. Brescia, D; DeVault, AR; Ivashkiv, E; Pan, HY; Swites, BJ; Whigan, D; Willard, DA, 1990)	0.77
"The maximum plasma pravastatin concentration (Cmax), time required for that concentration to develop (Tmax), and the elimination half-life (beta t1/2)."	( Pharmacokinetics of pravastatin in elderly versus young men and women. Funke, PT; Pan, HY; Waclawski, AP; Whigan, D, 1993)	0.94
"The pharmacokinetic profiles of pravastatin and SQ 31,906 in young and elderly subjects of men and women differed little."	( Pharmacokinetics of pravastatin in elderly versus young men and women. Funke, PT; Pan, HY; Waclawski, AP; Whigan, D, 1993)	0.89
" There are no simple methods to investigate the concentration-dependent inhibition of HMG-CoA reductase in human pharmacodynamic studies."	( Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences. Fager, G; Lennernäs, H, 1997)	0.3
" The pharmacokinetic parameters of pravastatin and SQ 31,906 were similar to those of healthy volunteers."	( The pharmacokinetics of pravastatin in patients on chronic hemodialysis. Ford, NF; Gehr, TW; Hammett, JL; Raymond, R; Sica, DA; Slugg, PH, 1997)	0.88
" Pharmacokinetic and pharmacodynamic parameters were determined after 8 hours of serum sampling on the final day of therapy."	( Effects of extensive and poor gastrointestinal metabolism on the pharmacodynamics of pravastatin. Ito, MK, 1998)	0.52
" Cmax was 48."	( A pharmacokinetic evaluation of pravastatin in middle-aged and elderly volunteers. Jóhannsson, M; Kjartansdóttir, T; Kristinsson, J; Sigurbjörnsson, S; Sigurdsson, G, )	0.41
" The inhibitory activity of pravastatin against cholesterol synthesis in liver could be related to the concentration in the shallow compartment via a sigmoidal Emax model and the obtained pharmacodynamic parameters were comparable to those in vitro."	( Pharmacokinetic and pharmacodynamic evaluation for tissue-selective inhibition of cholesterol synthesis by pravastatin. Hatanaka, T; Honda, S; Katayama, K; Koizumi, T; Sasaki, S, 1998)	0.81
" time curve (AUC0-infinity) and Cmax in the absence of mibefradil on day 1 (170 [117 to 395] ng h/mL and 91 [72 to 200] ng/mL respectively, geometric mean [95% confidence intervals]) were not significantly altered in the presence of mibefradil on day 8 (224 [174 to 381] ng h/mL and 124 [72 to 200] ng/mL) and on day 16 (200 [137 to 555] ng h/mL and 91 [74 to 184] ng/mL)."	( Mibefradil, a potent CYP3A inhibitor, does not alter pravastatin pharmacokinetics. Becquemont, L; Funck-Brentano, C; Jaillon, P, 1999)	0.55
"This study was conducted to evaluate the potential pharmacokinetic interaction between fenofibrate and pravastatin."	( Lack of a clinically significant pharmacokinetic interaction between fenofibrate and pravastatin in healthy volunteers. Achari, R; Gustavson, LE; Gutterman, C; Pan, WJ; Rieser, MJ; Wallin, BA; Ye, X, 2000)	0.75
" Pharmacokinetic parameters [AUC(0-infinity), AUC(0-tn), peak concentration (Cmax), time to reach Cmax (tmax), and half-life (t1/2)] were determined for parent statins and major metabolites."	( Itraconazole alters the pharmacokinetics of atorvastatin to a greater extent than either cerivastatin or pravastatin. Agarwal, V; Lasseter, KC; Lettieri, J; Mazzu, AL; Shamblen, EC; Sundaresen, P, 2000)	0.52
" However, itraconazole dramatically increased atorvastatin AUC (150%), Cmax (38%), and t1/2 (30%) (P < ."	( Itraconazole alters the pharmacokinetics of atorvastatin to a greater extent than either cerivastatin or pravastatin. Agarwal, V; Lasseter, KC; Lettieri, J; Mazzu, AL; Shamblen, EC; Sundaresen, P, 2000)	0.52
"Pravastatin, one of the 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) widely used in the management of hypercholesterolaemia, has unique pharmacokinetic characteristics among the members of this class."	( Clinical pharmacokinetics of pravastatin: mechanisms of pharmacokinetic events. Hatanaka, T, 2000)	2.04
" Unusual pharmacokinetic profiles were obtained, including high binding percentage with plasma protein (> 99%), a short elimination half-life (< 4 hr) and a relatively large Vd-area (0."	( Possible active transport mechanism in pharmacokinetics of flunixin-meglumin in rabbits. Horii, Y; Ikenaga, N; Kokue, E; Miyazaki, Y; Shimoda, M, 2001)	0.31
"The authors assessed the mutual influence of the immunosuppressant everolimus (Certican) and the HMG-CoA reductase inhibitors atorvastatin and pravastatin when coadministered based on pharmacokinetic and pharmacodynamic measures."	( Pharmacokinetic and pharmacodynamic assessments of HMG-CoA reductase inhibitors when coadministered with everolimus. Berthier, S; Hartmann, S; Hubert, M; Kovarik, JM; Rordorf, C; Rosenkranz, B; Schneider, W, 2002)	0.52
"Fifty-six subjects completed both pharmacokinetic study days."	( Pharmacokinetic interactions between protease inhibitors and statins in HIV seronegative volunteers: ACTG Study A5047. Aberg, JA; Alston, B; Aweeka, F; Blaschke, T; Fang, F; Fichtenbaum, CJ; Gerber, JG; Kosel, B; Rosenkranz, SL; Segal, Y, 2002)	0.31
"Aim of our study was to obtain pharmacokinetic data on pravastatin whilst monitoring the safety and efficiency of the lipid lowering therapy in heart-transplant recipients under immunosuppression with CsA and to compare these data to those of a healthy control group."	( Pharmacokinetics of pravastatin in heart-transplant patients taking cyclosporin A. Gross, W; Harder, S; Krell, B; März, W; Merz, M; Park, JW; Schüler, S; Seidel, D; Siekmeier, R, 2002)	0.89
" Blood was sampled for pharmacokinetic profiling (maximum concentration of the drug (Cmax), time to reach Cmax (tmax), area under the concentration vs."	( Pharmacokinetics of pravastatin in heart-transplant patients taking cyclosporin A. Gross, W; Harder, S; Krell, B; März, W; Merz, M; Park, JW; Schüler, S; Seidel, D; Siekmeier, R, 2002)	0.64
" Mean values for Cmax of pravastatin were 384."	( Pharmacokinetics of pravastatin in heart-transplant patients taking cyclosporin A. Gross, W; Harder, S; Krell, B; März, W; Merz, M; Park, JW; Schüler, S; Seidel, D; Siekmeier, R, 2002)	0.94
" The pharmacokinetic data obtained indicate that there is no significant cumulation of the drug following multiple dosages in spite of increased drug concentrations after a single oral dosage."	( Pharmacokinetics of pravastatin in heart-transplant patients taking cyclosporin A. Gross, W; Harder, S; Krell, B; März, W; Merz, M; Park, JW; Schüler, S; Seidel, D; Siekmeier, R, 2002)	0.64
"05), but there was no difference in the half-life between the phases."	( Gemfibrozil increases plasma pravastatin concentrations and reduces pravastatin renal clearance. Backman, JT; Kyrklund, C; Neuvonen, M; Neuvonen, PJ, 2003)	0.61
"The pharmacokinetic and pharmacodynamic profile of pravastatin in children is similar to that reported for adults."	( Pharmacokinetics and pharmacodynamics of pravastatin in children with familial hypercholesterolemia. Antikainen, M; Hedman, M; Neuvonen, M; Neuvonen, PJ, 2003)	0.84
"The purpose of this investigation was to determine whether there were individual pharmacokinetic differences of a drug, pravastatin."	( Individual difference in the pharmacokinetics of a drug, pravastatin, in healthy subjects. Hasegawa, S; Iwai, S; Nara, K; Ogawa, K; Oguchi, K; Udaka, Y, 2003)	0.77
" Rifampicin had no significant effect on the peak concentration, elimination half-life or renal clearance of pravastatin."	( Effect of rifampicin on pravastatin pharmacokinetics in healthy subjects. Backman, JT; Kyrklund, C; Neuvonen, M; Neuvonen, PJ, 2004)	0.84
" No significant changes were detected in any pravastatin pharmacokinetic parameter examined when pravastatin was taken with GFJ."	( Effects of grapefruit juice on pharmacokinetics of atorvastatin and pravastatin in Japanese. Fukazawa, I; Uchida, E; Uchida, N; Yasuhara, H, 2004)	0.82
" Studies compared the multiple-dose pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with 4 inhibitors of cytochrome P450-3A4 isoenzymes in healthy subjects."	( Comparative pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with cytochrome P450 inhibitors. Jacobson, TA, 2004)	0.8
"Statins (HMG-CoA reductase inhibitors) are one of the most widely prescribed classes of drugs throughout the world, because of their excellent cholesterol-lowering effect and overall safety profile except for rare but fatal rhabdomyolysis arising either directly or indirectly by pharmacokinetic interactions with certain other drugs."	( A literature search on pharmacokinetic drug interactions of statins and analysis of how such interactions are reflected in package inserts in Japan. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M; Urano, T, 2005)	0.33
"A MEDLINE search from 1996 to June 2004 was carried out to identify studies on clinical pharmacokinetic drug interactions for the five statins."	( A literature search on pharmacokinetic drug interactions of statins and analysis of how such interactions are reflected in package inserts in Japan. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M; Urano, T, 2005)	0.33
"All pharmacokinetic drug interactions including relevant quantitative data for potential effectors and details on mechanisms of interaction need to be given in package inserts as soon as the information becomes available, to ensure safe and proper use of the drugs concerned."	( A literature search on pharmacokinetic drug interactions of statins and analysis of how such interactions are reflected in package inserts in Japan. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M; Urano, T, 2005)	0.33
"Data from 14 subjects with complete pharmacokinetic samples were available for analysis."	( Pharmacokinetic interaction between nelfinavir and pravastatin in HIV-seronegative volunteers: ACTG Study A5108. Aberg, JA; Alston, BL; Brobst, SW; Fichtenbaum, CJ; Gerber, JG; Rosenkranz, SL; Segal, Y, 2006)	0.59
"012) and the mean peak concentration in plasma was 231% higher (174."	( Impact of the SLCO1B1 polymorphism on the pharmacokinetics and lipid-lowering efficacy of multiple-dose pravastatin. Arnold, KA; Eichelbaum, M; Hofmann, U; Igel, M; Kivistö, KT; Lütjohann, D; Niemi, M; Schwab, M; von Bergmann, K, 2006)	0.55
"7 years and receiving triple immunosuppressive medication) who had participated in previous pharmacokinetic and pharmacodynamic studies with pravastatin were genotyped for the -11187G > A and 521T > C SNPs in the SLCO1B1 gene and for the 2677G > T/A and 3435C > T SNPs in the ABCB1 gene."	( Pharmacokinetics and response to pravastatin in paediatric patients with familial hypercholesterolaemia and in paediatric cardiac transplant recipients in relation to polymorphisms of the SLCO1B1 and ABCB1 genes. Antikainen, M; Eichelbaum, M; Hedman, M; Holmberg, C; Kivistö, KT; Neuvonen, M; Neuvonen, PJ; Niemi, M, 2006)	0.82
" The cardiac transplant recipients with the SLCO1B1 521TC genotype (n = 3) had a 46% lower Cmax (-67."	( Pharmacokinetics and response to pravastatin in paediatric patients with familial hypercholesterolaemia and in paediatric cardiac transplant recipients in relation to polymorphisms of the SLCO1B1 and ABCB1 genes. Antikainen, M; Eichelbaum, M; Hedman, M; Holmberg, C; Kivistö, KT; Neuvonen, M; Neuvonen, PJ; Niemi, M, 2006)	0.62
"521CC genotype, the mean peak concentration in plasma and area under the plasma concentration-time curve from time 0 to infinity of pravastatin were 274% (95% confidence interval [CI], 92%-456%; P = ."	( SLCO1B1 polymorphism and sex affect the pharmacokinetics of pravastatin but not fluvastatin. Neuvonen, PJ; Niemi, M; Pasanen, MK, 2006)	0.78
" Each study participant had ingested a single 40-mg dose of pravastatin followed by blood sampling for pharmacokinetic characterization in standardized conditions."	( Association of genetic polymorphism in ABCC2 with hepatic multidrug resistance-associated protein 2 expression and pravastatin pharmacokinetics. Arnold, KA; Backman, JT; Eichelbaum, M; Gödtel-Armbrust, U; Kivistö, KT; Lang, T; Neuvonen, PJ; Niemi, M; Pasanen, MK; Wojnowski, L; Zanger, UM, 2006)	0.79
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."	( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds. Lombardo, F; Obach, RS; Waters, NJ, 2008)	0.35
"The impact of SLCO1B1 polymorphism on the pharmacokinetics of olmesartan and on the pharmacokinetic interaction between pravastatin and olmesartan was investigated."	( Pharmacokinetic interaction between pravastatin and olmesartan in relation to SLCO1B1 polymorphism. Higuchi, S; Hirota, T; Ieiri, I; Irie, S; Kawabata, K; Kimura, M; Kusuhara, H; Sugiyama, Y; Suwannakul, S, 2008)	0.83
" The present study examined the effects of changes in the transporter activities on the systemic and liver exposure of pravastatin using a physiologically based pharmacokinetic model."	( Physiologically based pharmacokinetic modeling to predict transporter-mediated clearance and distribution of pravastatin in humans. Kusuhara, H; Maeda, K; Shitara, Y; Sugiyama, Y; Watanabe, T, 2009)	0.77
"Intra- and inter-ethnic differences in pharmacokinetic and pharmacodynamic profiles of clinically relevant drugs are important issues not only for scenes of appropriate drug use in clinical settings but also for those of the drug development."	( [Pharmacogenomics: inter-ethnic and intra-ethnic differences in pharmacokinetic and pharmacodynamic profiles of clinically relevant drugs]. Higuchi, S; Ieiri, I, 2009)	0.35
" The mean pharmacokinetic parameters for pravastatin that changed significantly were as follows (rifampicin and placebo groups, respectively): C(max) (315."	( Effects of a concomitant single oral dose of rifampicin on the pharmacokinetics of pravastatin in a two-phase, randomized, single-blind, placebo-controlled, crossover study in healthy Chinese male subjects. Cao, D; Chen, XP; Dai, ZY; Deng, S; Li, YJ; Luo, J; Tang, L; Yin, T, 2009)	0.84
"The aims of this study were to develop a population pharmacokinetic (PPK) model for pravastatin pharmacokinetics with regard to enterohepatic circulation (EHC) and to evaluate effects of polymorphisms in SLCO1B1 and ABCC2 on the pharmacokinetic (PK) profile of pravastatin quantitatively."	( Quantitative population pharmacokinetic analysis of pravastatin using an enterohepatic circulation model combined with pharmacogenomic Information on SLCO1B1 and ABCC2 polymorphisms. Higuchi, S; Ide, T; Ieiri, I; Maeda, K; Sasaki, T; Sugiyama, Y, 2009)	0.83
" We demonstrate the feasibility of our approach with the development of a system that synthesizes pharmacokinetic pathways."	( Synthesis of pharmacokinetic pathways through knowledge acquisition and automated reasoning. Anwar, S; Baral, C; Hakenberg, J; Liang, S; Tari, L, 2010)	0.36
" Clearance and drug-drug interaction (DDI) of candidate drugs in animal and human could be predicted based on the pharmacokinetic data obtained from in vitro and in vivo experiments."	( [Prediction of the pharmacokinetic drug-drug interaction of pravastatin and pitavastatin with cyclosporine by a digital liver model based on metabolism and transporter]. Lin, ZQ; Yang, J; Yin, XF, 2011)	0.61
" Tissue-specific mRNA expression is used as a surrogate for protein abundance and activity and is integrated into physiologically based pharmacokinetic (PBPK) models that already represent detailed anatomical and physiological information."	( Using expression data for quantification of active processes in physiologically based pharmacokinetic modeling. Kuepfer, L; Lippert, J; Ludewig, B; Meyer, M; Schneckener, S, 2012)	0.38
"Although organic anion transporting polypeptide (OATP)-mediated hepatic uptake is generally conserved between rodents and humans at a gross pharmacokinetic level, the presence of three major hepatic OATPs with broad overlap in substrate and inhibitor affinity, and absence of rodent-human orthologs preclude clinical translation of single-gene knockout/knockin findings."	( Utility of Oatp1a/1b-knockout and OATP1B1/3-humanized mice in the study of OATP-mediated pharmacokinetics and tissue distribution: case studies with pravastatin, atorvastatin, simvastatin, and carboxydichlorofluorescein. Bao, JQ; Fallon, JK; Higgins, JW; Ke, AB; Manro, JR; Smith, PC; Zamek-Gliszczynski, MJ, 2014)	0.6
"The study aims to establish a method for simultaneous determination of repaglinide and pravastatin sodium in rat plasma by LC-MS/MS and to study its pharmacokinetic interactions."	( [Simultaneous determination of repaglinide and pravastatin sodium in rat plasma by LC-ms/MS and its application on pharmacokinetic interactions study]. Huang, J; Ma, YR; Rao, Z; Wei, YH; Wu, XA; Zhang, GQ; Zhou, Y, 2014)	0.88
"In pharmacokinetic evaluation of mice, using serial sampling methods rather than a terminal blood sampling method could reduce the number of animals needed and lead to more reliable data by excluding individual differences."	( Using improved serial blood sampling method of mice to study pharmacokinetics and drug-drug interaction. Nezasa, K; Ogawa, K; Shimizu, R; Takai, N; Tanaka, Y; Watanabe, A; Watari, R; Yamaguchi, Y, 2015)	0.42
" PVS has a short elimination half-life (1-3 h), suffers from instability at gastric pH, extensive hepatic first-pass metabolism and low absolute bioavailability (18%)."	( Duodenum-triggered delivery of pravastatin sodium via enteric surface-coated nanovesicular spanlastic dispersions: development, characterization and pharmacokinetic assessments. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2015)	0.7
"Volume of distribution is one of the most important pharmacokinetic properties of a drug candidate."	( Volume of Distribution in Drug Design. Beaumont, K; Di, L; Maurer, TS; Smith, DA, 2015)	0.42
"As an initial step in evaluating the utility of pravastatin in preventing preeclampsia and after consultation with the US Food and Drug Administration, we undertook a pilot randomized controlled trial with the objective to determine pravastatin safety and pharmacokinetic parameters when used in pregnant women at high risk of preeclampsia."	( Safety and pharmacokinetics of pravastatin used for the prevention of preeclampsia in high-risk pregnant women: a pilot randomized controlled trial. Ahmed, MS; Brown, LM; Caritis, SN; Cleary, K; Costantine, MM; D'Alton, M; Easterling, TR; Haas, DM; Haneline, LS; Hankins, G; Hebert, MF; Ren, Z; Venkataramanan, R; West, H, 2016)	0.98
" Primary outcomes were maternal-fetal safety and pharmacokinetic parameters of pravastatin during pregnancy."	( Safety and pharmacokinetics of pravastatin used for the prevention of preeclampsia in high-risk pregnant women: a pilot randomized controlled trial. Ahmed, MS; Brown, LM; Caritis, SN; Cleary, K; Costantine, MM; D'Alton, M; Easterling, TR; Haas, DM; Haneline, LS; Hankins, G; Hebert, MF; Ren, Z; Venkataramanan, R; West, H, 2016)	0.95
"This study provides preliminary safety and pharmacokinetic data regarding the use of pravastatin for preventing preeclampsia in high-risk pregnant women."	( Safety and pharmacokinetics of pravastatin used for the prevention of preeclampsia in high-risk pregnant women: a pilot randomized controlled trial. Ahmed, MS; Brown, LM; Caritis, SN; Cleary, K; Costantine, MM; D'Alton, M; Easterling, TR; Haas, DM; Haneline, LS; Hankins, G; Hebert, MF; Ren, Z; Venkataramanan, R; West, H, 2016)	0.94
" The method was successfully applied to the investigation of pharmacokinetic properties of pravastatin and its metabolites in children after an oral dose of 20-40mg."	( Quantification of pravastatin acid, lactone and isomers in human plasma by UHPLC-MS/MS and its application to a pediatric pharmacokinetic study. Gibson, KT; Leeder, JS; van Haandel, L; Wagner, JB, 2016)	0.99
"Pravastatin sodium (PVS) is a freely water-soluble HMG-CoA inhibitor that suffers from instability at gastric pH, extensive first pass metabolism, short elimination half-life (1-3 h) and low oral bioavailability (18%)."	( Duodenum-triggered delivery of pravastatin sodium: II. Design, appraisal and pharmacokinetic assessments of enteric surface-decorated nanocubosomal dispersions. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2016)	2.16
" A new model was developed for the prediction of AUC of statins that utilized the slopes of the above 2 models, with pharmacokinetic (Cmax) and a pharmacodynamic (IC50 value) components for the statins."	( Dual Incorporation of the in vitro Data (IC50) and in vivo (Cmax) Data for the Prediction of Area Under the Curve (AUC) for Statins using Regression Models Developed for Either Pravastatin or Simvastatin. Srinivas, NR, 2016)	0.63
" As a validation, we perform mechanistic pharmacokinetic modeling for SLCO1B1 (encoding OATP1B1) and ABCG2 (encoding BCRP) genotyped pharmacokinetic data from 18 clinical studies with healthy Caucasian and/or Asian subjects."	( Explaining Ethnic Variability of Transporter Substrate Pharmacokinetics in Healthy Asian and Caucasian Subjects with Allele Frequencies of OATP1B1 and BCRP: A Mechanistic Modeling Analysis. Barton, HA; Li, R, 2018)	0.48
"Simulations based on the current hypothesis reasonably describe SLCO1B1 and ABCG2 genotyped pharmacokinetic time course data for five transporter substrates (atorvastatin, pitavastatin, pravastatin, repaglinide, and rosuvastatin) in Caucasian and Asian populations."	( Explaining Ethnic Variability of Transporter Substrate Pharmacokinetics in Healthy Asian and Caucasian Subjects with Allele Frequencies of OATP1B1 and BCRP: A Mechanistic Modeling Analysis. Barton, HA; Li, R, 2018)	0.67
" Values for total clearance of compounds from plasma should be one of the most important pharmacokinetic parameters for predictions."	( Predicted values for human total clearance of a variety of typical compounds with differently humanized-liver mouse plasma data. Ito, S; Iwamoto, K; Kamimura, H; Mizunaga, M; Nakayama, K; Negoro, T; Nishiwaki, M; Nomura, Y; Suemizu, H; Yamazaki, H; Yoneda, N, 2020)	0.56
"Accurately predicting the pharmacokinetics of compounds that are transporter substrates has been notoriously challenging using traditional in vitro systems and physiologically based pharmacokinetic (PBPK) modeling."	( Improving the Translation of Organic Anion Transporting Polypeptide Substrates using HEK293 Cell Data in the Presence and Absence of Human Plasma via Physiologically Based Pharmacokinetic Modeling. Bowman, CM; Chen, B; Chen, Y; Cheong, J; Liu, L; Mao, J, 2021)	0.62
" Serial pharmacokinetic blood samples were collected, and safety was assessed."	( Assessment of the Effect of Filgotinib on the Pharmacokinetics of Atorvastatin, Pravastatin, and Rosuvastatin in Healthy Adult Participants. Alani, M; Anderson, K; Gong, Q; Nelson, CH; Othman, AA; Tarnowski, T, 2022)	0.95
" We developed a physiologically based pharmacokinetic (PBPK) model to assess drug-drug interaction (DDI) potential between dasatinib and known substrates for these transporters in a virtual population."	( Prediction of drug-drug interaction potential mediated by transporters between dasatinib and metformin, pravastatin, and rosuvastatin using physiologically based pharmacokinetic modeling. Bathena, S; Chang, M; Christopher, LJ; Roy, A; Shen, H, 2022)	0.94

Excerpt	Reference	Relevance
"Pravastatin sodium (pravastatin), a tissue-selective inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was administered alone (50 mg/kg) or in combination with cholestyramine, a bile acid sequestrant resin, at the level of 2% in the diet to homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits for 4 weeks."	( Effects of pravastatin sodium alone and in combination with cholestyramine on hepatic, intestinal and adrenal low density lipoprotein receptors in homozygous Watanabe heritable hyperlipidemic rabbits. Fukami, M; Fukushige, J; Itakura, H; Ito, T; Kuroda, M; Matsumoto, A; Nara, F; Shiomi, M; Tsujita, Y; Watanabe, Y, 1992)	2.12
" The treated rabbits were given pravastatin sodium (50 mg/kg/day), an HMG-CoA reductase inhibitor, in combination with cholestyramine (2% in diet), a bile acid sequestrant, for 36 weeks."	( Suppression of established atherosclerosis and xanthomas in mature WHHL rabbits by keeping their serum cholesterol levels extremely low. Effect of pravastatin sodium in combination with cholestyramine. Arai, M; Fukami, M; Fukushige, J; Ito, T; Kuroda, M; Shiomi, M; Tamura, A; Tsujita, Y; Watanabe, Y, 1990)	0.76
"The effects of the two HMG CoA reductase inhibitors lovastatin and pravastatin in combination with 12-16 g cholestyramine on serum lipids were studied in 18 patients with severe primary hypercholesterolemia."	( Long-term treatment (2 years) with the HMG CoA reductase inhibitors lovastatin or pravastatin in combination with cholestyramine in patients with severe primary hypercholesterolemia. Jacob, BG; Richter, WO; Schwandt, P, 1993)	0.75
"This randomized, open-label study compared the cost efficiency of low-dose pravastatin combined with low-dose cholestyramine with high-dose pravastatin monotherapy in 59 patients with moderate hypercholesterolemia and coronary disease."	( Pravastatin alone and in combination with low-dose cholestyramine in patients with primary hypercholesterolemia and coronary artery disease. Ito, MK; Shabetai, R, 1997)	1.97
" Pravastatin combined with HRT was therefore suggested to lower serum lipid concentrations earlier than pravastatin alone."	( Effect of a HMG-CoA reductase inhibitor combined with hormone replacement therapy on lipid metabolism in Japanese women with hypoestrogenic lipidemia: a multicenter double-blind controlled prospective study. Fuyuki, T; Horiguchi, F; Komukai, S; Makita, K; Nozawa, S; Ohta, H; Sugimoto, I; Takamatsu, K, 1998)	1.21
"To elucidate the effect on blood pressure and blood lipids of an angiotensin converting enzyme inhibitor (captopril), and a beta-receptor blocking agent (atenolol), given alone or in combination with a cholesterol reducing drug, the beta-hydroxy-methylglutaryl-coenzyme A reductase inhibitor pravastatin, in patients who were also encouraged to improve their lifestyle."	( Treatment of hypertensive and hypercholesterolaemic patients in general practice. The effect of captopril, atenolol and pravastatin combined with life style intervention. Foss, OP; Graff-Iversen, S; Graving, B; Istad, H; Søyland, E; Tjeldflaat, L, 1999)	0.69
" II: Continued lifestyle intervention combined with captopril or atenolol."	( Treatment of hypertensive and hypercholesterolaemic patients in general practice. The effect of captopril, atenolol and pravastatin combined with life style intervention. Foss, OP; Graff-Iversen, S; Graving, B; Istad, H; Søyland, E; Tjeldflaat, L, 1999)	0.51
"Pravastatin can be used in combination with captopril or atenolol in the treatment of hypertensive and hypercholesterolaemic patients."	( Treatment of hypertensive and hypercholesterolaemic patients in general practice. The effect of captopril, atenolol and pravastatin combined with life style intervention. Foss, OP; Graff-Iversen, S; Graving, B; Istad, H; Søyland, E; Tjeldflaat, L, 1999)	1.95
"The objectives of this review are to discuss the role of cytochrome P450 (CYP450) isoforms in drug metabolism, to explain differences in metabolism among the HMG-CoA reductase inhibitors (HMGs, statins), to review drug-drug and drug-food interaction studies dealing with the HMGs, to present case reports dealing with HMG-related myopathy, to discuss major clinical implications of these case reports and to express an opinion of use of HMGs in clinical practice."	( The role of cytochrome P450-mediated drug-drug interactions in determining the safety of statins. Bottorff, M; Worz, CR, 2001)	0.31
" Therefore, we determined the effect of SCH 48461 and ezetimibe in combination with 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors in chow-fed dogs."	( The synergistic hypocholesterolemic activity of the potent cholesterol absorption inhibitor, ezetimibe, in combination with 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors in dogs. Alton, KB; Burrier, RE; Davis, HR; Pula, KK; Watkins, RW, 2001)	0.31
"To evaluate the efficacy and safety of ezetimibe 10 mg administered with pravastatin in patients with primary hypercholesterolemia."	( Efficacy and safety of ezetimibe coadministered with pravastatin in patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Hassman, D; LeBeaut, A; Lipetz, R; Lipka, L; Melani, L; Mills, R; Mukhopadhyay, P; Suresh, R; Veltri, E, 2003)	0.8
" Since DDIs are associated with adverse reactions, we performed a cross-sectional study to assess the prevalence of potentially critical drug-drug and drug-statin interactions in an outpatient adult population with dyslipidaemia."	( Prevalence of potentially severe drug-drug interactions in ambulatory patients with dyslipidaemia receiving HMG-CoA reductase inhibitor therapy. Hess, L; Krähenbühl, S; Krähenbühl-Melcher, A; Rätz Bravo, AE; Schlienger, RG; Tchambaz, L, 2005)	0.33
" This study examined the use of the CETP inhibitor JTT-705 combined with pravastatin."	( Effectiveness of inhibition of cholesteryl ester transfer protein by JTT-705 in combination with pravastatin in type II dyslipidemia. de Grooth, GJ; Kastelein, JJ; Kawamura, H; Klerkx, AH; Kuivenhoven, JA; Trip, MD; Wilhelm, F, 2005)	0.78
"Hepatic uptake carriers of the organic anion-transporting peptide (OATP) family of solute carriers are more and more recognized as being involved in hepatic elimination of many drugs and potentially associated drug-drug interactions."	( Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3. Brun, ME; Funk, C; Noé, J; Portmann, R, 2007)	0.34
"To evaluate the therapeutic potential of an apolipoprotein A-1 (apoA-1) mimetic peptide, D-4F, in combination with pravastatin in collagen-induced arthritis (CIA), syngeneic Louvain rats were immunized with type II collagen and randomized to vehicle control, D-4F monotherapy, pravastatin monotherapy, or D-4F + pravastatin combination therapy."	( Treatment with an apolipoprotein A-1 mimetic peptide in combination with pravastatin inhibits collagen-induced arthritis. Banquerigo, ML; Brahn, E; Charles-Schoeman, C; Fogelman, AM; Hama, S; Navab, M; Park, GS; Van Lenten, BJ; Wagner, AC, 2008)	0.79
"In this study, a sensitive and selective method based on liquid chromatography combined with diode array and tandem mass spectrometry detection (LC-DAD-MS/MS) was developed for the simultaneous quantitative determination of fenofibric acid, pravastatin and its main metabolites in human plasma."	( An automated method for the simultaneous determination of pravastatin, 3-hydroxy isomeric metabolite, pravalactone and fenofibric acid in human plasma by sensitive liquid chromatography combined with diode array and tandem mass spectrometry detection. Cahay, B; Klinkenberg, R; Mertens, B; Streel, B, 2008)	0.77
" Fifty-two patients received TACE combined with pravastatin (20-40 mg/day) and 131 patients received chemoembolization alone."	( Chemoembolization combined with pravastatin improves survival in patients with hepatocellular carcinoma. Dogan, S; Goke, B; Graf, H; Helmberger, T; Hoffmann, RT; Jakobs, T; Jüngst, C; Jüngst, D; Reiser, M; Seidel, D; Straub, G; Waggershauser, T; Walli, A; Walter, A, 2008)	0.89
" The current review focuses distinctly on three aspects: (a) an in-depth coverage on the bioanalytical methods for the quantification of clopidogrel and its inactive carboxylic acid metabolite as well as the active metabolite in pre-clinical and clinical samples; (b) an overview of the pharmacokinetic/pharmacodynamic aspects of clopidogrel; and (c) enumerating the key findings from drug-drug interaction studies of clopidogrel with various co-substrates such as lanzoprazole, fluvastatin, atorvastatin, pravastatin, digoxin, ketoconazole, donezepil and theophylline."	( Clopidogrel: review of bioanalytical methods, pharmacokinetics/pharmacodynamics, and update on recent trends in drug-drug interaction studies. Mullangi, R; Srinivas, NR, 2009)	0.51
"To evaluate the long-term therapeutic effects of atorvastatin via cytochrome P450 (CYP)3A4 pathway or a non-CYP 3A4 pathway statin, pravastatin, combined with clopidogrel for the patients undergoing coronary stenting."	( [Comparison on long-term effects of atorvastatin or pravastatin combined with clopidogrel for patients undergoing coronary stenting: a randomized controlled trial]. Han, YL; Jing, QM; Li, Y; Wang, DM; Wang, SL; Wang, ZL; Zhang, ZL, 2009)	0.81
"The 12 month clinical outcomes were similar between patients receiving atorvastatin 20 mg/d or pravastatin 20 mg/d combined with clopidogrel after coronary stenting."	( [Comparison on long-term effects of atorvastatin or pravastatin combined with clopidogrel for patients undergoing coronary stenting: a randomized controlled trial]. Han, YL; Jing, QM; Li, Y; Wang, DM; Wang, SL; Wang, ZL; Zhang, ZL, 2009)	0.82
"To evaluate the potential drug-drug interaction between raltegravir and pravastatin."	( Drug-drug interactions between raltegravir and pravastatin in healthy volunteers. Burger, DM; Colbers, A; da Silva, HG; Hoitsma, A; Schouwenberg, B; van Ewijk-Beneken Kolmer, EW; van Luin, M; Verweij-van Wissen, CP, 2010)	0.85
" It is in clinical development for the prevention of cardiovascular events and will likely be used in combination with standard of care, including statins."	( Coadministration of dalcetrapib with pravastatin, rosuvastatin, or simvastatin: no clinically relevant drug-drug interactions. Abt, M; Bech, N; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Turnbull, L; White, AM, 2010)	0.63
" Clearance and drug-drug interaction (DDI) of candidate drugs in animal and human could be predicted based on the pharmacokinetic data obtained from in vitro and in vivo experiments."	( [Prediction of the pharmacokinetic drug-drug interaction of pravastatin and pitavastatin with cyclosporine by a digital liver model based on metabolism and transporter]. Lin, ZQ; Yang, J; Yin, XF, 2011)	0.61
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."	( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions. Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012)	0.38
"To develop physiologically based pharmacokinetic (PBPK) model to predict the pharmacokinetics and drug-drug interactions (DDI) of pravastatin, using the in vitro transport parameters."	( Physiologically based modeling of pravastatin transporter-mediated hepatobiliary disposition and drug-drug interactions. Bergman, A; Feng, B; Goosen, TC; Lai, Y; Litchfield, J; Varma, MV, 2012)	0.86
" The organic anion-transporting polypeptide (OATP)1B1 and OATP1B3 isoforms are selectively expressed in the human liver and are known to cause significant drug-drug interactions (DDIs), as observed with an increasing number of drugs."	( Model-based approaches to predict drug-drug interactions associated with hepatic uptake transporters: preclinical, clinical and beyond. Barton, HA; El-Kattan, AF; Goosen, TC; Gosset, JR; Jones, HM; Lai, Y; Lin, J; Varma, MV, 2013)	0.39
" These findings indicate that only fexofenadine is expected to interact with GFJ on OATP2B1 at therapeutic concentrations, in accordance with the clinical observations."	( Substrate- and dose-dependent drug interactions with grapefruit juice caused by multiple binding sites on OATP2B1. Mori, T; Murata, Y; Nakanishi, T; Shirasaka, Y; Tamai, I, 2014)	0.4
" A Phase 1 study demonstrated the safety of high dose pravastatin given with idarubicin and cytarabine in patients with AML and also demonstrated an encouraging response rate."	( SWOG0919: a Phase 2 study of idarubicin and cytarabine in combination with pravastatin for relapsed acute myeloid leukaemia. Advani, AS; Appelbaum, FR; Copelan, E; List, AF; McDonough, S; Mulford, DA; Othus, M; Sekeres, MA; Willman, C, 2014)	0.88
" In addition, using serial sampling methods can be valuable for evaluation of the drug-drug interaction (DDI) potential of drug candidates."	( Using improved serial blood sampling method of mice to study pharmacokinetics and drug-drug interaction. Nezasa, K; Ogawa, K; Shimizu, R; Takai, N; Tanaka, Y; Watanabe, A; Watari, R; Yamaguchi, Y, 2015)	0.42
"Quantitative assessment of potential drug-drug interactions (DDIs) is one of the major focuses in drug development."	( Characterization of Long-Lasting Oatp Inhibition by Typical Inhibitor Cyclosporine A and In Vitro-In Vivo Discrepancy in Its Drug Interaction Potential in Rats. Kato, Y; Kogi, T; Masuo, Y; Nakamichi, N; Taguchi, T, 2016)	0.43
" The purpose of this study is to elucidate the role of hyperlipidaemia alone or in combination with acidosis/alkalosis in the development and potentiation of statin-induced myotoxicity."	( Hyperlipidaemia alone and in combination with acidosis can increase the incidence and severity of statin-induced myotoxicity. Barrett, DA; Bruce, KD; de Moor, CH; Eckel, RH; Gershkovich, P; Lee, JB; Sungelo, M; Taha, DA; Zgair, A, 2017)	0.46
" A Phase 2 study of high dose pravastatin given in combination with idarubicin and cytarabine demonstrated an impressive response rate [75% complete remission (CR), CR with incomplete count recovery (CRi)]."	( Report of the relapsed/refractory cohort of SWOG S0919: A phase 2 study of idarubicin and cytarabine in combination with pravastatin for acute myelogenous leukemia (AML). Advani, AS; Appelbaum, FR; Erba, HP; Li, H; Liedtke, M; List, AF; Medeiros, BC; Michaelis, LC; O'Dwyer, K; Othus, M, 2018)	0.98
" As the management of drug-drug interactions (DDIs) constitutes a key aspect of the care of PLWH, the magnitude of pharmacokinetic DDIs between cardiovascular and anti-HIV drugs needs to be more thoroughly characterized."	( UHPLC-MS/MS assay for simultaneous determination of amlodipine, metoprolol, pravastatin, rosuvastatin, atorvastatin with its active metabolites in human plasma, for population-scale drug-drug interactions studies in people living with HIV. Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Desfontaine, V; Marzolini, C; Spaggiari, D, 2019)	0.74
" In this study, we evaluated the drug-drug interaction potential of the hepatitis C virus inhibitors elbasvir (EBR) and grazoprevir (GZR) with statins."	( Evaluation of Pharmacokinetic Drug Interactions of the Direct-Acting Antiviral Agents Elbasvir and Grazoprevir with Pitavastatin, Rosuvastatin, Pravastatin, and Atorvastatin in Healthy Adults. Butterton, JR; Caro, L; Fandozzi, CM; Feng, HP; Fraser, IP; Guo, Z; Iwamoto, M; Levine, V; Panebianco, D; Prueksaritanont, T; Swearingen, D; Wolford, D; Yeh, WW, 2021)	0.82
"This study aimed to assess the effect of folic acid combined with pravastatin on atherosclerosis-related indexes in elderly patients with hypertension complicated with lacunar cerebral infarction."	( Effect of folic acid combined with pravastatin on arteriosclerosis in elderly hypertensive patients with lacunar infarction. Bu, X; Li, C; Liu, Y, 2021)	1.14
" We developed a physiologically based pharmacokinetic (PBPK) model to assess drug-drug interaction (DDI) potential between dasatinib and known substrates for these transporters in a virtual population."	( Prediction of drug-drug interaction potential mediated by transporters between dasatinib and metformin, pravastatin, and rosuvastatin using physiologically based pharmacokinetic modeling. Bathena, S; Chang, M; Christopher, LJ; Roy, A; Shen, H, 2022)	0.94

Excerpt	Reference	Relevance
" Radiolabelled studies demonstrated oral absorption and bioavailability values of 34% and 17%, respectively."	( Clinical pharmacology of pravastatin, a selective inhibitor of HMG-CoA reductase. Pan, HY, 1991)	0.58
" The oral absorption of [14C] activity from pravastatin sodium was about 34% and the oral bioavailability was about 18%, suggesting first-pass metabolism of pravastatin."	( Disposition of pravastatin sodium, a tissue-selective HMG-CoA reductase inhibitor, in healthy subjects. Morrison, RA; Pan, HY; Singhvi, SM; Willard, DA, 1990)	0.89
"The oral bioavailability of two HMG-CoA reductase inhibitors, pravastatin and lovastatin, was investigated in this randomized, two-way crossover study."	( Comparative pharmacokinetics and pharmacodynamics of pravastatin and lovastatin. DeVault, AR; Ivashkiv, E; Pan, HY; Sugerman, AA; Swanson, BN; Wang-Iverson, D, 1990)	0.77
" The results imply a decreased bioavailability of SLS in the statin-treated group, while no evidence for an altered permeability barrier to water was found."	( Effect of systemic treatment with cholesterol-lowering drugs on the skin barrier function in humans. Agner, E; Agner, T; Malinowski, J; Meibom, J; Ramsing, D, 1995)	0.29
"The bioavailability of pravastatin, a hypocholesterolmic agent, may be enhanced by decreasing its exposure to stomach contents, where it may be converted nonenzymatically to a relatively inactive metabolite."	( Gastrointestinal absorption of pravastatin in healthy subjects. O'Donnell, D; Pan, HY; Triscari, J; Zinny, M, 1995)	0.89
" An enteric formulation of pravastatin should increase the bioavailability of pravastatin and enhanced lipid-lowering efficacy."	( Effects of extensive and poor gastrointestinal metabolism on the pharmacodynamics of pravastatin. Ito, MK, 1998)	0.82
"Grapefruit juice greatly increases the bioavailability of lovastatin and simvastatin."	( Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin. Kivistö, KT; Lilja, JJ; Neuvonen, PJ, 1999)	0.53
" Compared with lovastatin, the cytochrome P-450-dependent intestinal intrinsic clearance of pravastatin was >5000-fold lower and cannot be expected to significantly affect its oral bioavailability or to be a significant site of drug interactions."	( Small intestinal metabolism of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin and comparison with pravastatin. Baner, K; Benet, LZ; Christians, U; Deters, M; Hackbarth, I; Hallensleben, K; Jacobsen, W; Kirchner, G; Mancinelli, L; Sewing, KF, 1999)	0.73
" Pharmacokinetic parameters of these three compounds were calculated using noncompartmental methods and compared by analyses of variance and bioavailability assessments."	( Lack of a clinically significant pharmacokinetic interaction between fenofibrate and pravastatin in healthy volunteers. Achari, R; Gustavson, LE; Gutterman, C; Pan, WJ; Rieser, MJ; Wallin, BA; Ye, X, 2000)	0.53
" The oral bioavailability of pravastatin is low because of incomplete absorption and a first-pass effect."	( Clinical pharmacokinetics of pravastatin: mechanisms of pharmacokinetic events. Hatanaka, T, 2000)	0.89
" Lovastatin, Atorvastatin, Pravastatin and Simvastatin demonstrate variable potency to enhance the NO/O2- concentration ratio after stimulation of NOS, resulting in an increase of NO bioavailability in endothelial cells."	( Statin-stimulated nitric oxide release from endothelium. Dobrucki, IT; Dobrucki, LW; Kalinowski, L; Malinski, T, )	0.43
" As statin treatment is known to increase nitric oxide bioavailability and enhance myocardial function, we tested whether ADMA concentration modifies the effect of pravastatin on myocardial blood flow in young adults with mild hypercholesterolemia."	( Plasma asymmetric dimethylarginine modifies the effect of pravastatin on myocardial blood flow in young adults. Janatuinen, T; Knuuti, J; Laakso, J; Laaksonen, R; Lehtimäki, T; Nuutila, P; Raitakari, OT; Vesalainen, R, 2003)	0.76
" Dose optimization and use of novel controlled drug delivery systems may help in increasing the bioavailability and distribution of statins to the bone microenvironment."	( Statins and osteoporosis: new role for old drugs. Jadhav, SB; Jain, GK, 2006)	0.33
" In conclusion, orange juice increases the bioavailability of pravastatin administered orally."	( Orange juice increased the bioavailability of pravastatin, 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, in rats and healthy human subjects. Kobayashi, S; Koitabashi, Y; Kumai, T; Matsumoto, N; Sekine, S; Watanabe, M; Yanagida, Y, 2006)	0.83
"An open-label, randomised, crossover single-dose study, using two periods, two sequences, with a minimum washout period of 7 days, was conducted in order to assess the comparative bioavailability of a pravastatin (CAS 81131-70-6) 40 mg formulation and that of a reference formulation."	( Comparative study on the bioequivalence of two formulations of pravastatin. Data from a crossover, randomised, open-label bioequivalence study in healthy volunteers. Almeida, A; Almeida, S; Antonijoan, R; Barbanoj, M; Cruz Caturla, M; Filipe, A; Gich, I; Puntes, M, 2006)	0.76
" Human oral bioavailability is an important pharmacokinetic property, which is directly related to the amount of drug available in the systemic circulation to exert pharmacological and therapeutic effects."	( Hologram QSAR model for the prediction of human oral bioavailability. Andricopulo, AD; Moda, TL; Montanari, CA, 2007)	0.34
"Reduction in evoked flow velocity responses reflects reduced nitric oxide bioavailability and therefore supports molecular findings of acute statin withdrawal."	( Effects of initiation and acute withdrawal of statins on the neurovascular coupling mechanism in healthy, normocholesterolemic humans. Auch, D; Kaps, M; Rosengarten, B, 2007)	0.34
"Various mechanisms can influence the intestinal absorption and oral bioavailability of drugs."	( Contribution of multidrug resistance-associated protein 2 to secretory intestinal transport of organic anions. Chiba, M; Hirano, T; Iseki, K; Itagaki, S; Kobayashi, M, 2008)	0.35
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."	( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination. Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010)	0.36
" Cyclosporin, pravastatin, and azithromycin are known to inhibit P-glycoprotein, which will enhance the intracellular colchicine level by acting in its bioavailability and moderating hepatic and renal excretion."	( Colchicine-induced rhabdomyolysis in a heart/lung transplant patient with concurrent use of cyclosporin, pravastatin, and azithromycin. Bouquié, R; Dailly, E; Deslandes, G; Haloun, A; Jolliet, P; Renaud, C, 2011)	0.94
" The bioavailability of statin drugs is low due the effects of P-glycoprotein in the gastro-intestinal tract as well as the first-pass metabolism."	( Characterization of human erythrocytes as potential carrier for pravastatin: an in vitro study. Alanazi, FK; Harisa, Gel-D; Ibrahim, MF, 2011)	0.61
" Maximal superoxide scavenging with polyethylene glycol-superoxide dismutase (PEG-SOD), 150 U/ml did not influence phenylephrine constrictor responses but potentiated pravastatin's effect, suggesting that the statin did not increase NO bioavailability merely via an antioxidant mechanism."	( Acute modulation of vasoconstrictor responses by pravastatin in small vessels. Ball, C; Beltrame, JF; Ghaffari, N; Kennedy, JA; Stafford, I, 2011)	0.82
"In small vessels, pravastatin inhibits constrictor responses by increasing endothelial NO bioavailability via the Akt pathway."	( Acute modulation of vasoconstrictor responses by pravastatin in small vessels. Ball, C; Beltrame, JF; Ghaffari, N; Kennedy, JA; Stafford, I, 2011)	0.96
"The purpose of research was to develop a mucoadhesive multiparticulate sustained drug delivery system of pravastatin sodium, a highly water-soluble and poorly bioavailable drug, unstable at gastric pH."	( Design and in vitro performance evaluation of purified microparticles of pravastatin sodium for intestinal delivery. Garg, Y; Pathak, K, 2011)	0.81
" Bioavailability studies in rabbits demonstrated that [F9 (P3)] significantly higher C(max) (67."	( Bilayered transmucosal drug delivery system of pravastatin sodium: statistical optimization, in vitro, ex vivo, in vivo and stability assessment. Bali, V; Maurya, SK; Pathak, K, 2012)	0.64
"Mucoadhesive bilayer buccal patch has been developed to improve the bioavailability and therapeutic efficacy along with providing sustained release of pravastatin sodium."	( Biopolymeric mucoadhesive bilayer patch of pravastatin sodium for buccal delivery and treatment of patients with atherosclerosis. Dhiman, MK; Petkar, K; Sawant, K; Yedurkar, P, 2013)	0.85
" Based on the above results, since the original drug has a slower dissolution rate than the generic drugs, it is necessary to be cautious about the degradation of pravastatin in the stomach and the bioavailability of pravastatin due to the different dissolution rates and the different residual amount of pravastatin in the stomach."	( [Equivalence studies of pravastatin original and generic drugs by dissolution test]. Hashimoto, N; Katakawa, J; Nakauchi, T; Nozaki, A; Okamoto, T; Seko, F; Takeuchi, E; Teramoto, K; Yuminoki, K, 2012)	0.88
" Ritonavir dramatically increases the bioavailability of a variety of concurrently administered drugs by inhibition of metabolic enzymes and drug transporters."	( Analysis of the pharmacokinetic boosting effects of ritonavir on oral bioavailability of drugs in mice. Banba, H; Takayama, K; Takeda-Morishita, M; Tomaru, A, 2013)	0.39
" Consequently, the absolute bioavailability (AB) of nimodipine with pravastatin (1 mg/kg) was 31."	( Effects of pravastatin on the pharmacokinetic parameters of nimodipine after oral and intravenous administration in rats: possible role of CYP3A4 inhibition by pravastatin. Choi, DH; Choi, JS; Lee, CK, )	0.76
"The enhanced oral bioavailability of nimodipine might be mainly due to inhibition of the CYP3A-mediated metabolism of nimodipine in the small intestine and/or in the liver and due to reduction of the total body clearance rather than both to inhibition of the P-gp efflux transporter in the small intestine and reduction of renal elimination of nimodipine by pravastatin."	( Effects of pravastatin on the pharmacokinetic parameters of nimodipine after oral and intravenous administration in rats: possible role of CYP3A4 inhibition by pravastatin. Choi, DH; Choi, JS; Lee, CK, )	0.69
" Knockin of OATP1B1 or OATP1B3 partially restored control clearance, volume, and bioavailability values (24%-142% increase, ≤47% increase, and ≤77% decrease vs."	( Utility of Oatp1a/1b-knockout and OATP1B1/3-humanized mice in the study of OATP-mediated pharmacokinetics and tissue distribution: case studies with pravastatin, atorvastatin, simvastatin, and carboxydichlorofluorescein. Bao, JQ; Fallon, JK; Higgins, JW; Ke, AB; Manro, JR; Smith, PC; Zamek-Gliszczynski, MJ, 2014)	0.6
"OATP2B1-mediated grapefruit juice (GFJ)-drug interactions are substrate-dependent; for example, GFJ ingestion significantly reduces bioavailability of fexofenadine, but not pravastatin."	( Substrate- and dose-dependent drug interactions with grapefruit juice caused by multiple binding sites on OATP2B1. Mori, T; Murata, Y; Nakanishi, T; Shirasaka, Y; Tamai, I, 2014)	0.6
" PVS has a short elimination half-life (1-3 h), suffers from instability at gastric pH, extensive hepatic first-pass metabolism and low absolute bioavailability (18%)."	( Duodenum-triggered delivery of pravastatin sodium via enteric surface-coated nanovesicular spanlastic dispersions: development, characterization and pharmacokinetic assessments. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2015)	0.7
"Pravastatin sodium (PVS) is a freely water-soluble HMG-CoA inhibitor that suffers from instability at gastric pH, extensive first pass metabolism, short elimination half-life (1-3 h) and low oral bioavailability (18%)."	( Duodenum-triggered delivery of pravastatin sodium: II. Design, appraisal and pharmacokinetic assessments of enteric surface-decorated nanocubosomal dispersions. Abd-Elsalam, WH; El-Nabarawi, MA; Tadros, MI; Tayel, SA, 2016)	2.16
" Impaired nitric oxide (NO) bioavailability seems to be involved in these pathophysiological changes observed in hypertensive pregnancy."	( Placental nitric oxide formation and endothelium-dependent vasodilation underlie pravastatin effects against angiogenic imbalance, hypertension in pregnancy and intrauterine growth restriction. Chimini, JS; da Silva, MLS; Dias-Junior, CA; Possomato-Vieira, JS, 2019)	0.74
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51

Excerpt	Relevance	Reference
"The chemistry, pharmacology, pharmacokinetics, clinical trials, adverse effects, role in lipid-lowering therapy, and dosage and administration of pravastatin are reviewed."	( Pravastatin: a new drug for the treatment of hypercholesterolemia. Cantral, KA; Jungnickel, PW; Maloley, PA, 1992)	1.93
"This multicenter, double-blind, placebo-controlled study was conducted to evaluate dose-response effects and safety of once-daily administration of pravastatin, a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase."	( Once-daily pravastatin in patients with primary hypercholesterolemia: a dose-response study. Berkson, DM; Colfer, HT; Cressman, MD; Farmer, JA; Farnham, DJ; Jones, PH; McKenney, JM; Proctor, JD; Wolfson, PM; Wright, JT, 1991)	0.87
"The effects of long-term dosing with inhibitors of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase on the rate of cholesterol biosynthesis were examined in the lens and liver of rats and hamsters."	( Effects of long-term administration of HMG-CoA reductase inhibitors on cholesterol synthesis in lens. Kalinowski, SS; Mosley, ST; Tanaka, RD, 1991)	0.28
"The efficacy of once-daily versus twice-daily dosing of pravastatin was determined in men with primary hypercholesterolemia."	( Comparative efficacy of once-daily versus twice-daily pravastatin in primary hypercholesterolemia. Brescia, D; DeVault, AR; Pan, HY; Willard, DA, )	0.63
"This multicenter, double-blind, placebo-controlled, dose-response study was conducted in patients with primary hypercholesterolemia to examine the effects of pravastatin, a selective inhibitor of HMG-CoA reductase, on plasma lipids and lipoproteins."	( Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. I. A dose-response study. Brown, WV; Dobs, AS; Goldberg, AC; Hunninghake, DB; Insull, W; Knopp, RH; Margolis, S; Mellies, MJ; Schaefer, EJ; Schonfeld, G, 1990)	0.79
"Pravastatin sodium was orally administered to cynomolgus monkeys at dosage levels of 50, 200 and 800 mg/kg/day for 7 successive days."	( Preliminary dose finding study for subacute toxicological study of pravastatin sodium in monkeys. Manabe, S; Masuda, H; Matsunuma, N; Miyakoshi, N; Sudo, S; Yamashita, K, 1989)	1.96
"Pravastatin sodium was administered orally to cynomolgus monkeys at dosage levels of 50, 100, 200 and 400 mg/kg/day for 5 successive weeks."	( Subacute toxicological study in monkeys treated orally with pravastatin sodium for 5 weeks. Manabe, S; Masuda, H; Matsunuma, N; Miyakoshi, N; Sudo, S; Tanase, H; Yamashita, K, 1989)	1.96
" In rat liver slices, the dose-response curves for inhibition of [14C]acetate incorporation into cholesterol were similar for the active acid forms of lovastatin, simvastatin, and pravastatin."	( Tissue-selective acute effects of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase on cholesterol biosynthesis in lens. Kalinowski, SS; Mosley, ST; Schafer, BL; Tanaka, RD, 1989)	0.47
" Most of these drugs have side effects which, in the elderly, may necessitate lower dosing than usual."	( Treating hyperlipidemia, Part III: Drug therapy. Brown, WV; Karmally, W; Smith, DA, 1987)	0.27
" This difference is consistent throughout the dosage range."	( Pharmaco-economic assessment of the HMG-CoA reductase inhibitors. Smart, AJ; Walters, L, 1994)	0.29
"8% higher than an equivalent milligram dose of pravastatin, depending on the dosage used."	( Pharmaco-economic assessment of the HMG-CoA reductase inhibitors. Smart, AJ; Walters, L, 1994)	0.55
" Severe renal insufficiency may necessitate dosage modification in lovastatin recipients."	( Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Garnett, WR, 1995)	0.29
" The drug acquisition cost per year of therapy was calculated for each patient's most recent dosage of lovastatin and pravastatin as of April 1993."	( Replacing lovastatin with pravastatin: effect on serum lipids and costs. Borysiuk, L; Korman, L, 1995)	0.8
" The drugs were administered in dosages of 10 mg/kg from the fourth to seventh weeks; at the end of the seventh week, plasma cholesterol was determined, and the Pravastatin dosage adjusted to 15 mg/kg to obtain similar levels of plasma cholesterol for the two experimental groups."	( Effects of simvastatin and pravastatin on endothelium-dependent relaxation in hypercholesterolemic rabbits. Jorge, PA; Metze, K; Ozaki, MR, 1994)	0.78
" The smaller effect observed with the more commonly used dosage (10 mg/day) was most probably due to the characteristics of the sample with already established hypercholesterolemia, being thus dependent of higher concentrations of medications, as observed in previous treatments in our outpatient clinic."	( [Pravastatin effects on lipoproteins, Lp (a), apo B and apo A-1 in patients with primary hypercholesterolemia]. da Silva, RC; Feres, MC; Fonseca, FA; Lima, JC; Martinez, TL; Novazzi, JP, 1994)	1.2
"6%) received the standard dosage of 10 mg/day whereas 140 patients (19."	( The RED-LIP study--pravastatin in primary isolated hypercholesterolemia--an open, prospective, multicenter trial. Pirich, C; Sinzinger, H, 1994)	0.62
" Fourteen subjects were given simvastatin, and 12 were given pravastatin, both at the maximum therapeutic dosage of 40 mg/day."	( Sustained therapy with 3-hydroxy-3-methylglutaryl-coenzyme-A reductase inhibitors does not impair steroidogenesis by adrenals and gonads. Faccini, G; Moghetti, P; Muggeo, M; Negri, C; Tosi, F; Travia, D, 1995)	0.53
" Once daily dosing consisted of 10 mg pravastatin during the first month, 20 mg during the second month and 40 mg during an additional 4 months or matching placebos."	( Efficacy and safety of pravastatin in hypertensive hypercholesterolaemic patients on antihypertensive drug therapy. Amery, A; Celis, H; Fagard, R; Lijnen, P; Staessen, J; Thijs, L, 1994)	0.87
" The dual route of elimination reduces the need for dosage adjustment if the function of either of these organs is impaired."	( Clinical pharmacokinetics of pravastatin. Jones, PH; Quion, JA, 1994)	0.58
" Dosage could be doubled after 8 weeks, a bile acid-binding resin could be added after 16 weeks, and nicotinic acid or probucol could be added after 32 weeks, as needed, to adequately lower the low-density lipoprotein cholesterol (LDL-C) levels."	( Efficacy and safety of pravastatin in the long-term treatment of elderly patients with hypercholesterolemia. Behounek, BD; Kobylak, L; Maciejko, JJ; McGovern, ME; Rosman, HS; Rubenfire, M; Santinga, JT, 1994)	0.6
" To inhibit HMG-CoA reductase in liver, pravastatin sodium, a competitive inhibitor of HMG-CoA reductase, was administered to homozygous Watanabe heritable hyperlipidemic (WHHL) rabbits, a low-density lipoprotein receptor-deficient animal model, at a dosage of 50 mg/kg per day for 5 weeks."	( Pravastatin sodium, a competitive inhibitor of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreases the cholesterol content of newly secreted very-low-density lipoprotein in Watanabe heritable hyperlipidemic rabbits. Ito, T; Shiomi, M, 1994)	2
" Pravastatin, a well tolerated HMG CoA reductase inhibitor with a convenient once-daily dosing regimen, has been shown to effectively lower total and low density lipoprotein (LDL) cholesterol."	( Pravastatin experience in elderly and non-elderly patients. DeVault, AR; Kassler-Taub, K; McGovern, ME; Mellies, MJ; Pan, HY, 1993)	2.64
"The pharmacokinetics of pravastatin do not necessitate dosage adjustments in elderly men or women."	( Pharmacokinetics of pravastatin in elderly versus young men and women. Funke, PT; Pan, HY; Waclawski, AP; Whigan, D, 1993)	0.92
"Using various concentrations of the drugs, a dose-response curve was constructed for the inhibition of the cholesterol synthesis."	( Pravastatin and simvastatin differently inhibit cholesterol biosynthesis in human lens. Bloemendal, H; Cohen, LH; de Vries, AC; Vermeer, MA, 1993)	1.73
"A randomized, controlled, double-blind trial in 672 hypercholesterolemic patients evaluated the efficacy and safety profile of lovastatin and pravastatin across their usually recommended dosage ranges (lovastatin 20 to 80 mg/day and pravastatin 10 to 40 mg/day)."	( A multicenter comparative trial of lovastatin and pravastatin in the treatment of hypercholesterolemia. The Lovastatin Pravastatin Study Group. , 1993)	0.74
" Using various concentrations of the drugs, a dose-response curve was composed for the inhibition of the cholesterol synthesis."	( Different effects of the hypolipidemic drugs pravastatin and lovastatin on the cholesterol biosynthesis of the human ocular lens in organ culture and on the cholesterol content of the rat lens in vivo. Cohen, LH; de Vries, AC, 1993)	0.55
"After 8 weeks of therapy, pravastatin in a dosage of 20 mg twice daily reduced low-density lipoprotein cholesterol levels by 31%, whereas a dosage of 40 mg twice daily reduced low-density lipoprotein cholesterol levels by 38%."	( Comparative efficacy and safety of pravastatin and cholestyramine alone and combined in patients with hypercholesterolemia. Pravastatin Multicenter Study Group II. , 1993)	0.86
"The efficacy and safety profile of simvastatin and pravastatin across their most commonly recommended dosage ranges were compared in a double-blind, parallel, multicenter study in 550 patients with primary hypercholesterolemia."	( Comparison of the efficacy, safety and tolerability of simvastatin and pravastatin for hypercholesterolemia. The Simvastatin Pravastatin Study Group. , 1993)	0.77
" In posttransplant patients receiving cyclosporine, safety has been documented for low doses of lovastatin and simvastatin, but when a higher dosage of an HMG-CoA reductase inhibitor is warranted, pravastatin should be considered the drug of choice because of a lower incidence of myopathy."	( Comparative evaluation of the safety and efficacy of HMG-CoA reductase inhibitor monotherapy in the treatment of primary hypercholesterolemia. Hsu, I; Johnson, NE; Spinler, SA, )	0.32
" The dosage consisted of 10 mg of pravastatin daily during the 6-month trial."	( The effectiveness and safety of low dose pravastatin in elderly hypertensive hypercholesterolemic subjects on antihypertensive therapy. Chan, P; Ko, JT; Lee, CB; Lee, YS; Lin, TS; Pan, WH, 1995)	0.84
" Only 2 of the 90 patients were on maximal dosage regimens."	( Inadequate treatment with HMG-CoA reductase inhibitors by health care providers. Feingold, KR; Marcelino, JJ, 1996)	0.29
" It is likely that the magnitude of risk reduction produced by lipid-lowering therapy is proportional to the degree of cholesterol lowering achieved, which is an important consideration when selecting an agent and deciding the dosage to use."	( Benefits and risks of HMG-CoA reductase inhibitors in the prevention of coronary heart disease: a reappraisal. Pedersen, TR; Tobert, JA, 1996)	0.29
"In dogs, no significant difference in the reduction of serum cholesterol was observed among three dosing regimens of pravastatin: once in the morning (3 mg/kg), once in the evening (3 mg/kg), and twice-daily (1."	( The mechanism of comparable serum cholesterol lowering effects of pravastatin sodium, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor, between once- and twice-daily treatment regimens in beagle dogs and rabbits. Fujioka, T; Fukami, M; Fukushige, J; Nara, F; Shigehara, E; Shimada, Y; Shimotsu, H; Tsujita, Y, 1996)	0.74
"The aim of this study was to evaluate the cholesterol-lowering and antiatherosclerotic effect of the HMG-CoA reductase inhibitor pravastatin sodium at a dosage comparable to human therapy."	( Effects of low-dose pravastatin sodium on plasma cholesterol levels and aortic atherosclerosis of heterozygous WHHL rabbits fed a low cholesterol (0.03%) enriched diet for one year. Braesen, JH; Harsch, M; Niendorf, A, 1997)	0.83
" Over 2 weeks, patients' regimens were titrated to a maximal dosage of 500 mg tid."	( Combination of low-dose niacin and pravastatin improves the lipid profile in diabetic patients without compromising glycemic control. Fonseca, VA; Gardner, SF; Granberry, MC; Marx, MA; Skelton, DR; White, LM, 1997)	0.57
" At the dosage used pravastatin significantly lowered the total cholesterol and LDL-cholesterol levels and increased the HDL-cholesterol levels compared to placebo."	( Time course of serum lipids and apolipoproteins after acute myocardial infarction: modification by pravastatin. Blanckaert, N; Claeys, G; Kesteloot, H; Lesaffre, E, 1997)	0.84
" Micronised fenofibrate has improved absorption characteristics compared with the standard preparation, allowing a lower daily dosage and once-daily administration."	( Micronised fenofibrate: a review of its pharmacodynamic properties and clinical efficacy in the management of dyslipidaemia. Adkins, JC; Faulds, D, 1997)	0.3
" dose was employed, followed by daily oral dosing of 20 mg over four hemodialysis intervals."	( The pharmacokinetics of pravastatin in patients on chronic hemodialysis. Ford, NF; Gehr, TW; Hammett, JL; Raymond, R; Sica, DA; Slugg, PH, 1997)	0.6
"No statistical differences in the pharmacokinetics of pravastatin or SQ 31,906 were evident when comparing the first and last days of oral dosing with pravastatin."	( The pharmacokinetics of pravastatin in patients on chronic hemodialysis. Ford, NF; Gehr, TW; Hammett, JL; Raymond, R; Sica, DA; Slugg, PH, 1997)	0.85
"Pravastatin can be safely administered in the usual dosages to subjects with renal failure on hemodialysis and no change in dosing is necessary."	( The pharmacokinetics of pravastatin in patients on chronic hemodialysis. Ford, NF; Gehr, TW; Hammett, JL; Raymond, R; Sica, DA; Slugg, PH, 1997)	2.05
" Concomitant use of potent inhibitors of CYP3A with simvastatin should be avoided or its dosage should be greatly reduced."	( Simvastatin but not pravastatin is very susceptible to interaction with the CYP3A4 inhibitor itraconazole. Kantola, T; Kivistö, KT; Neuvonen, PJ, 1998)	0.62
" Nicotinamide did not show a synergistic effect with pravastatin at the dosage used in this study."	( Prevention of primary islet isograft nonfunction in mice with pravastatin. Arita, S; Atiya, A; Kasraie, A; Mullen, Y; Ohtsuka, S; Shevlin, L; Une, S, 1998)	0.79
" These two factors suggest that an increase in the dosage of the HMG-CoA reductase inhibitor may be appropriate."	( Compliance with and efficacy of treatment with pravastatin and cholestyramine: a randomized study on lipid-lowering in primary care. Eriksson, M; Hådell, K; Holme, I; Kjellström, T; Walldius, G, 1998)	0.56
" In animals receiving pravastatin and the enriched diet (verum group; n = 6), mean total serum cholesterol levels were consistently lowered at a dosage of 5 mg/kg pravastatin and with the combined treatment."	( Survival and cardiovascular pathology of heterozygous Watanabe heritable hyperlipidaemic rabbits treated with pravastatin and probucol on a low-cholesterol (0.03%)-enriched diet. Bräsen, JH; Harsch, M; Niendorf, A, 1998)	0.83
" The incidence of side effects with these agents increases as the dose increases within the recommended dosage range."	( Comparative efficacy and tolerability of low-dose pravastatin versus lovastatin in patients with hypercholesterolemia. Gaziano, JM; Lapsley, D; Strauss, WE, 1999)	0.56
" In particular, pravastatin at a dosage of 20 mg/ day significantly reduced only fibrinogen levels, while at a dosage of 40 mg/day significantly reduced factor VII, fibrinogen, prothrombin fragments 1 and 2, thrombin-antithrombin complexes, tissue plasminogen activator antigen (tPA:Ag) before venous occlusion (b."	( Non lipid, dose-dependent effects of pravastatin treatment on hemostatic system and inflammatory response. Avellone, G; Bono, M; De Simone, R; Di Garbo, V; Di Raimondo, D; Raneli, G, 2000)	0.93
"Niacin increased HDL cholesterol levels by 30%, with the majority of effect achieved at a dosage of 500 mg twice daily."	( Effective and safe modification of multiple atherosclerotic risk factors in patients with peripheral arterial disease. Applegate, WB; Crouse, JR; Davis, KB; Egan, D; Elam, MB; Garg, R; Herd, JA; Hunninghake, DB; Johnson, WC; Kennedy, JW; Kostis, JB; Sheps, DS, 2000)	0.31
" The dual routes of pravastatin elimination reduce the need for dosage adjustment if the function of either the liver or kidney is impaired, and also reduce the possibility of drug interactions compared with other statins."	( Clinical pharmacokinetics of pravastatin: mechanisms of pharmacokinetic events. Hatanaka, T, 2000)	0.92
" A dosage of 20 mg pravastatin (pravachol) and 1 g of fish oil (prolipid) were added to the diet after dinner, according to our protocol."	( Combined treatment with low-dose pravastatin and fish oil in post-renal transplantation dislipidemia. Bacharaki, D; Bamichas, G; Grekas, D; Kassimatis, E; Makedou, A; Tourkantonis, A, 2001)	0.92
" The dosage of simvastatin was based on the additional percent reduction in LDL cholesterol needed to achieve the goal specified by the National Cholesterol Education Program."	( Effect of pravastatin-to-simvastatin conversion on low-density-lipoprotein cholesterol. Dresselhaus, TR; Henry, RR; Ito, MK; Lin, JC; Marcus, DB; Morreale, AP; Shabetai, R, 2001)	0.71
" Dose-response curves of simvastatin for bone formation and resorption differed."	( Effect of statins on bone mineral density and bone histomorphometry in rodents. Conradie, MM; Gopal, R; Hough, S; Hulley, PA; Maritz, FJ, 2001)	0.31
" Six product brands encompassing 20 dosage strengths have been available during the past two years."	( Managed care trends in statin usage. Bazalo, GR, 2001)	0.31
" Trends in market share, mean daily dose, and dosage distribution of the six current statin brands were examined."	( Managed care trends in statin usage. Bazalo, GR, 2001)	0.31
"Fifty-three patients were randomized to group 1, for which the dosing frequency was changed from daily to every other day, and 51 patients were randomized to group 2, for which the daily dose was halved."	( Maintenance of low-density lipoprotein goal with step-down pravastatin therapy. Graham, MR; Kennedy, JA; Lindsey, CC, 2002)	0.56
" If a clinician decides, however, to attempt dosage reduction, the preferred regimen appears to be to halve the current dose once/day (vs administering the current dose every other day)."	( Maintenance of low-density lipoprotein goal with step-down pravastatin therapy. Graham, MR; Kennedy, JA; Lindsey, CC, 2002)	0.56
" To evaluate this effect further, dose-response curves with noradrenaline were measured in the presence and absence of 20 micromol/l simvastatin, lovastatin, mevastatin and pravastatin."	( Inhibition of smooth muscle cell calcium mobilization and aortic ring contraction by lactone vastatins. Altieri, PI; Crespo, MJ; Escobales, N; Furilla, RA, 1996)	0.49
" Oral dosing of pravastatin (0."	( Effects of pravastatin on the expression of ATP-binding cassette transporter A1. Ando, H; Fujimura, A; Kaneko, S; Takamura, T; Tsuruoka, S; Yamamoto, H, 2004)	1.06
" Instructions for dosage adjustment are seldom provided in the Japanese package inserts."	( A literature search on pharmacokinetic drug interactions of statins and analysis of how such interactions are reflected in package inserts in Japan. Hasegawa, R; Hirata-Koizumi, M; Miyake, S; Saito, M; Urano, T, 2005)	0.33
"The aim of this study was to test whether oral pre-treatment with rosuvastatin at a dosage giving clinically relevant plasma concentrations protects the myocardium against ischaemia/reperfusion injury and to investigate the involvement of nitric oxide (NO) and neutrophil infiltration."	( Oral pre-treatment with rosuvastatin protects porcine myocardium from ischaemia/reperfusion injury via a mechanism related to nitric oxide but not to serum cholesterol level. Bulhak, AA; Gonon, AT; Gourine, AV; Pernow, J; Sjöquist, PO; Valen, G, 2005)	0.33
"To investigate the effect of early intervention by pravastatin with two different dosage on inflammatory factors and endothelial vasodilator function in patients with unstable angina (UA)."	( [Clinical study of pravastatin with different dosage in early admission period in patients with unstable angina]. Han, ZH; Hu, R; Lü, Q; Ma, CS; Wu, XS; Zhao, Z, 2005)	0.91
" In the dosage of 20 mg pravastatin group non-endothelium-dependent vasodilation in brachial artery was also tested by ultrasound before and 8 weeks after the therapy."	( [Clinical study of pravastatin with different dosage in early admission period in patients with unstable angina]. Han, ZH; Hu, R; Lü, Q; Ma, CS; Wu, XS; Zhao, Z, 2005)	0.96
" Blood samples were collected for 24 hours after dosing on days 5, 6, and 15."	( The effects of multiple doses of fenofibrate on the pharmacokinetics of pravastatin and its 3alpha-hydroxy isomeric metabolite. Achari, R; Chira, TO; Esslinger, HU; Gustavson, LE; Koehne-Voss, S; Schweitzer, SM; Yannicelli, HD, 2005)	0.56
" Moreover, it is unclear if the cardiovascular disease history length was similar in the two treatment groups as well as the length and dosage of statin treatment of the about 25% of patients taking statins before the enrollment."	( REVERSAL and PROVE-IT: are clinically oriented trials really better than "pure" scientific studies? Cicero, AF; Gaddi, A, 2005)	0.33
" Group I-treated with pravastatin, group II--with simvastatin--both drugs in a dosage of 40 mg/kg daily, 5 days/week for a total of 3 weeks."	( Effect of pravastatin, simvastatin and atorvastatin on the phagocytic activity of mouse peritoneal macrophages. Bergman, M; Bessler, H; Djaldetti, M; Salman, H, 2006)	1.05
" Application of the square-wave voltammetric method to determination of pravastatin in a pharmaceutical dosage form, without sample pretreatment, resulted in acceptable deviation from the stated concentration."	( Electrochemical properties and square-wave voltammetric determination of pravastatin. Nigović, B, 2006)	0.8
" Resolution on reduction of dosage or discontinuance and/or change of statin were deemed to constitute confirmation of cause."	( Safety of statins when response is carefully monitored: a study of 336 heart recipients. Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005)	0.33
"We searched Medline, the international medical database, to conduct a systematic review of the literature on the efficacy and tolerability of statins in CKD and renal transplant patients and on specific recommendations for dosage adjustments in this population."	( [Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant]. Deray, G; Isnard-Bagnis, C; Karie, S; Launay-Vacher, V, 2006)	0.33
" Although most statins are not excreted by the kidneys, the dosage of some must be adapted in CKD patients because of pharmacokinetic modifications induced by renal impairment."	( [Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant]. Deray, G; Isnard-Bagnis, C; Karie, S; Launay-Vacher, V, 2006)	0.33
" Control mice received an equimolar dosage of the parent statin compound, pravastatin."	( Nitropravastatin stimulates reparative neovascularisation and improves recovery from limb Ischaemia in type-1 diabetic mice. Campesi, I; Emanueli, C; Gadau, S; Kraenkel, N; Madeddu, P; Meloni, M; Monopoli, A; Ongini, E, 2007)	1.08
" The results suggest that the effect of hydrophobic statins on the engulfing capacity of human peripheral blood phagocytes and apoptosis is dependent on their dosage and physiochemical properties."	( Hydrophobic but not hydrophilic statins enhance phagocytosis and decrease apoptosis of human peripheral blood cells in vitro. Bergman, M; Bessler, H; Djaldetti, M; Salman, H, 2008)	0.35
" Our objective was to explore how differences in prevalences of use, dosing characteristics, choice of statin and continuity of therapy in individual patients adds new information to previous results."	( Aspects of statin prescribing in Norwegian counties with high, average and low statin consumption - an individual-level prescription database study. Eggen, AE; Engeland, A; Furu, K; Hartz, I; Njølstad, I; Sakshaug, S; Skurtveit, S, 2007)	0.34
" Patients were excluded if the dosage of their antidiabetic drugs was changed, if their drug therapy was altered within 3 months before starting statin therapy, or if events occurred that could affect glycemic control such as hospitalization."	( Influence of pitavastatin on glucose tolerance in patients with type 2 diabetes mellitus. Kadonosono, K; Takano, T; Tanaka, S; Terauchi, Y; Yamakawa, T, 2008)	0.35
" The anti-inflammatory effect of pravastatin showed no obvious difference between the two dosage groups."	( Effects of pravastatin on the function of dendritic cells in patients with coronary heart disease. Cheng, JL; Cui, J; Dong, M; Jiang, SL; Li, QS; Li, X; Liu, C; Peng, CH; Tian, Y, 2009)	1.02
" Recent studies have shown statins prevented CIN after contrast media exposure, but optimal statin type and dosage are still unknown."	( Prevention of contrast-induced nephropathy by chronic pravastatin treatment in patients with cardiovascular disease and renal insufficiency. Iwasaka, T; Kamihata, H; Manabe, K; Motohiro, M; Nakamura, S; Senoo, T; Sugiura, T; Yoshida, S, 2009)	0.6
" In this study, increasing the dosage of pravastatin was investigated to determine whether it had a clearly favorable effect on the adiponectin level in hypercholesterolemic patients."	( Effects of increasing the dose of pravastatin on serum adiponectin level in Japanese mild hypercholesterolemic and hypertensive patients. Kai, T; Kanamasa, K, 2009)	0.9
"Treatment with a low dosage of fluvastatin sodium or pravastatin sodium reduced the lipid build-up as well as the macrophages in the choroid and restored the vascular lumens of choroidal vessels independently of the cholesterol effect."	( Low-dosage statins reduce choroidal damage in hypercholesterolemic rabbits. de Hoz, R; Mendez, T; Ramírez, AI; Ramírez, JM; Raposo, R; Redondo, A; Rojas, B; Salazar, JJ; Tejerina, T; Triviño, A, 2011)	0.62
" We proposed a systematic classification scheme using FDA-approved drug labeling to assess the DILI potential of drugs, which yielded a benchmark dataset with 287 drugs representing a wide range of therapeutic categories and daily dosage amounts."	( FDA-approved drug labeling for the study of drug-induced liver injury. Chen, M; Fang, H; Liu, Z; Shi, Q; Tong, W; Vijay, V, 2011)	0.37
" The program's successful prediction in DDI tendency might indicate its application in optimizing the dosage regimen and reducing the risk of clinical trial."	( [Prediction of the pharmacokinetic drug-drug interaction of pravastatin and pitavastatin with cyclosporine by a digital liver model based on metabolism and transporter]. Lin, ZQ; Yang, J; Yin, XF, 2011)	0.61
"38 times higher than the oral dosage form, indicating its therapeutic potential in the treatment of atherosclerosis."	( Biopolymeric mucoadhesive bilayer patch of pravastatin sodium for buccal delivery and treatment of patients with atherosclerosis. Dhiman, MK; Petkar, K; Sawant, K; Yedurkar, P, 2013)	0.65
" This study shows a simple and fast method validation by reversed-phase high-performance liquid chromatography in the linear range 28 to 52 µg/mL to quantify lovastatin, pravastatin sodium or simvastatin in bulk drug or dosage forms."	( Development and validation of a simple and fast HPLC method for determination of lovastatin, pravastatin and simvastatin. de Oliveira, RB; Oliveira, MA; Silva, TD; Vianna-Soares, CD, 2012)	0.79
" The type and dosage of concomitant drugs were not changed during the study periods."	( Association of cholesteryl ester transfer protein mass with peripheral leukocyte count following statin therapy: a pilot study. Hirayama, A; Nagao, K; Tani, S, 2012)	0.38
" Micro/small dosing is useful for examining the mechanism of drug interactions without safety concern."	( Mechanisms of pharmacokinetic enhancement between ritonavir and saquinavir; micro/small dosing tests using midazolam (CYP3A4), fexofenadine (p-glycoprotein), and pravastatin (OATP1B1) as probe drugs. Ando, Y; Deguchi, M; Hirota, T; Ieiri, I; Irie, S; Izumi, N; Kanda, E; Kimura, M; Kotani, N; Kusuhara, H; Maeda, K; Matsuguma, K; Matsuki, S; Morishita, M; Okuzono, T; Sugiyama, Y; Tsunemitsu, S; Yamane, N, 2013)	0.59
" This dosage was selected on the basis of its expected -20% efficacy in reducing low-density lipoprotein-cholesterol."	( Nutraceutical approach to moderate cardiometabolic risk: results of a randomized, double-blind and crossover study with Armolipid Plus. Arnoldi, A; Bosisio, R; Calabresi, L; Gomaraschi, M; Macchi, C; Magni, P; Mombelli, G; Pavanello, C; Pazzucconi, F; Ruscica, M; Sirtori, CR, )	0.13
"These results suggest that a randomized trial with a larger sample size and a higher dosage of pravastatin would be helpful in further evaluating the anti-inflammatory properties of pravastatin, its association with improvements in cognitive symptoms, and its potential to reduce positive and negative symptoms associated with schizophrenia or schizoaffective disorders."	( A randomized placebo-controlled pilot study of pravastatin as an adjunctive therapy in schizophrenia patients: effect on inflammation, psychopathology, cognition and lipid metabolism. Borba, CP; Cather, C; Cleary, SM; Copeland, PM; Fan, X; Freudenreich, O; Henderson, DC; Oppenheim, CE; Petruzzi, LJ; Stock, S; Vincenzi, B, 2014)	0.88
" It is a major determinant of half-life and dosing frequency of a drug."	( Volume of Distribution in Drug Design. Beaumont, K; Di, L; Maurer, TS; Smith, DA, 2015)	0.42
" Selection criteria comprised 28 subcriteria under the following main criteria: clinical efficacy, best publish evidence and experience, adverse effects, drug interaction, dosing time, and fixed dose combination availability."	( Statin Selection in Qatar Based on Multi-indication Pharmacotherapeutic Multi-criteria Scoring Model, and Clinician Preference. Al-Badriyeh, D; Al-Khal, A; Alabbadi, I; Fahey, M; Zaidan, M, 2015)	0.42
"We have used three dimensional (3D) extrusion printing to manufacture a multi-active solid dosage form or so called polypill."	( 3D printing of five-in-one dose combination polypill with defined immediate and sustained release profiles. Alexander, MR; Burley, JC; Khaled, SA; Roberts, CJ; Yang, J, 2015)	0.42
"Extemporaneously prepared liquid dosage forms are needed to administer required medications in infants and young children."	( Stability of Levothyroxine, Doxycycline, Hydrocortisone, and Pravastatin in Liquid Dosage Forms Stored at Two Temperatures. Nahata, MC, )	0.37
" We considered any type and dosage of statin as eligible, as long as the control and experimental arms differed only in the timing of the administration of the same statin."	( Chronotherapy versus conventional statins therapy for the treatment of hyperlipidaemia. Añino Alba, A; Fernandez-Esteban, I; Fernandez-Tabera, JM; Gómez Álvarez, P; Izquierdo-Palomares, JM; Martin-Carrillo, P; Pinar López, Ó; Plana, MN; Saiz, LC, 2016)	0.43
" Electronic pharmacy records were used to abstract information on the type, length, and dosage of statin exposures starting in the year prior to diagnosis."	( Influence of Statins and Cholesterol on Mortality Among Patients With Pancreatic Cancer. Chang, JI; Huang, BZ; Li, E; Wu, BU; Xiang, AH, 2017)	0.46
" Using the median of the first year cumulative statin dosage as a cut-off point, patients were classified into either a high-dose or low-dose group."	( Intensive statin regimens for reducing risk of cardiovascular diseases among human immunodeficiency virus-infected population: A nation-wide longitudinal cohort study 2000-2011. Chang, KC; Ko, NY; Li, CY; Ou, HT; Yang, CY, 2017)	0.46
" No consistent differences in plasma exposure of atorvastatin or M1 were observed in mice after single or repeat dosing of atorvastatin with or without mineral oil."	( Effects of mineral oil administration on the pharmacokinetics, metabolism and pharmacodynamics of atorvastatin and pravastatin in mice and dogs. Abrahamsson, B; Agrawal, R; Bergenholm, L; Björkbom, A; Bright, J; Cavallin, A; Gopaul, VS; Hammarberg, M; Hawthorne, G; Hurt-Camejo, E; Jansson-Löfmark, R; Jarke, A; Johansson, MJ; Li, X; Lundborg, E; Pieterman, EJ; Princen, HMG; Svensson, L, 2021)	0.83
" Twice-weekly dosing with VSW1198 at the previously established maximally tolerated dose in combination with a statin led to hepatotoxicity, while once-weekly VSW1198-based combinations were feasible."	( In vivo evaluation of combination therapy targeting the isoprenoid biosynthetic pathway. Chhonker, Y; Haney, SL; Holstein, SA; Murry, DJ; Smith, LM; Talmon, G; Varney, ML, 2021)	0.62
" Only rosuvastatin was assessed in a repeated dosing PK study."	( A systematic review on pharmacokinetics, cardiovascular outcomes and safety profiles of statins in cirrhosis. Abraldes, JG; Al-Karaghouli, M; Cabrera Garcia, L; Kalainy, S; Sung, S, 2021)	0.62
" We report the pravastatin pharmacokinetic parameters including pravastatin area under the curve (total drug exposure over a dosing interval), apparent oral clearance, half-life, and others during pregnancy and compare it with those values measured during the postpartum period."	( A randomized pilot clinical trial of pravastatin versus placebo in pregnant patients at high risk of preeclampsia. Ahmed, MS; Caritis, S; Clark, S; Costantine, MM; Rytting, E; Stika, CS; Venkataramanan, R; Wang, X; West, H; Wisner, KL, 2021)	1.25
" A dose-response relationship was also found, with higher cumulative defined daily doses and higher daily intensity of statin use associated with lower mortality."	( Statin Use During Concurrent Chemoradiotherapy With Improved Survival Outcomes in Esophageal Squamous Cell Carcinoma: A Propensity Score-Matched Nationwide Cohort Study. Chen, M; Chen, WM; Shia, BC; Wu, SY; Yu, YH, 2023)	0.91
" Furthermore, we found a dose-response relationship of statin use associated with lower ESCC-specific mortality."	( Statin Use During Concurrent Chemoradiotherapy With Improved Survival Outcomes in Esophageal Squamous Cell Carcinoma: A Propensity Score-Matched Nationwide Cohort Study. Chen, M; Chen, WM; Shia, BC; Wu, SY; Yu, YH, 2023)	0.91
" Log dose-response data over the doses of 5 mg to 160 mg revealed strong linear dose-related effects on blood total cholesterol and LDL cholesterol, and a weak linear dose-related effect on blood triglycerides."	( Pravastatin for lowering lipids. Adams, SP; Alaeiilkhchi, N; Tasnim, S; Wright, JM, 2023)	2.35

Role	Description
metabolite	Any intermediate or product resulting from metabolism. The term 'metabolite' subsumes the classes commonly known as primary and secondary metabolites.
anticholesteremic drug	A substance used to lower plasma cholesterol levels.
xenobiotic	A xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
environmental contaminant	Any minor or unwanted substance introduced into the environment that can have undesired effects.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Class	Description
3-hydroxy carboxylic acid	Any hydroxy carboxylic acid which contains a hydroxy group located beta- to the carboxylic acid group.
hydroxy monocarboxylic acid	Any monocarboxylic acid which also contains a separate (alcoholic or phenolic) hydroxy substituent.
carboxylic ester	An ester of a carboxylic acid, R(1)C(=O)OR(2), where R(1) = H or organyl and R(2) = organyl.
secondary alcohol	A secondary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has two other carbon atoms attached to it.
carbobicyclic compound	A bicyclic compound in which all the ring atoms are carbon.
statin (semi-synthetic)	A statin that is derived from a naturally occurring statin by partial chemical synthesis.
lignan	Any phenylpropanoid derived from phenylalanine via dimerization of substituted cinnamic alcohols, known as monolignols, to a dibenzylbutane skeleton. Note that while individual members of the class have names ending ...lignane, ...lignene, ...lignadiene, etc., the class names lignan, neolignan, etc., do not end with an "e".
glycoside	A glycosyl compound resulting from the attachment of a glycosyl group to a non-acyl group RO-, RS-, RSe-, etc. The bond between the glycosyl group and the non-acyl group is called a glycosidic bond. By extension, the terms N-glycosides and C-glycosides are used as class names for glycosylamines and for compounds having a glycosyl group attached to a hydrocarbyl group respectively. These terms are misnomers and should not be used. The preferred terms are glycosylamines and C-glycosyl compounds, respectively.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathway	Proteins	Compounds
Pravastatin Action Pathway	21	43

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
EWS/FLI fusion protein	Homo sapiens (human)	Potency	27.0522	0.0013	10.1577	42.8575	AID1259253; AID1259256
Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus	Potency	31.6228	0.0096	10.5250	35.4813	AID1479145
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Solute carrier family 22 member 6	Rattus norvegicus (Norway rat)	Ki	601.0000	1.6000	5.7440	10.0000	AID598875; AID679489
Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)	IC50 (µMol)	190.0000	0.5500	3.7083	6.1000	AID699544
Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)	Ki	180.0000	0.5300	4.1157	8.4800	AID699544
3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)	IC50 (µMol)	0.1452	0.0000	0.7949	8.9000	AID1315659; AID625271; AID83165
Insulin receptor	Rattus norvegicus (Norway rat)	IC50 (µMol)	0.0056	0.0001	0.7846	3.3700	AID625271
Prostaglandin G/H synthase 2	Homo sapiens (human)	IC50 (µMol)	0.0056	0.0001	0.9950	10.0000	AID625271
3-hydroxy-3-methylglutaryl-coenzyme A reductase	Rattus norvegicus (Norway rat)	IC50 (µMol)	0.0254	0.0009	0.2094	9.0300	AID1798004; AID1798163; AID384740
Solute carrier family 22 member 6	Homo sapiens (human)	IC50 (µMol)	408.0000	0.2700	4.5306	9.9000	AID682026
Canalicular multispecific organic anion transporter 1	Rattus norvegicus (Norway rat)	Ki	172.0000	0.8400	4.9682	10.0000	AID679034
Solute carrier family 22 member 8	Homo sapiens (human)	IC50 (µMol)	13.7000	4.9300	7.3900	9.9200	AID678815
Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)	IC50 (µMol)	62.0000	0.1047	2.7195	7.0795	AID699543
Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)	Ki	57.0000	0.0800	2.4688	9.8000	AID699543
Solute carrier family 22 member 11	Homo sapiens (human)	IC50 (µMol)	591.0000	2.0300	4.6650	7.3000	AID678973
Solute carrier family 22 member 8	Rattus norvegicus (Norway rat)	IC50 (µMol)	15.6000	6.0300	6.0300	6.0300	AID678805
Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)	IC50 (µMol)	3.6000	0.0500	2.3797	9.7000	AID699542
Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)	Ki	3.4000	0.0440	1.3630	5.0000	AID699542
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Solute carrier organic anion transporter family member 1A4	Rattus norvegicus (Norway rat)	Km	37.5000	0.2400	3.2841	6.5300	AID681820
Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)	Km	2,250.0000	0.7000	5.0060	8.0900	AID679476
Solute carrier organic anion transporter family member 1A1	Rattus norvegicus (Norway rat)	Km	30.0000	0.0150	3.4996	7.0000	AID679967
Canalicular multispecific organic anion transporter 1	Rattus norvegicus (Norway rat)	Km	223.0000	1.5000	4.3420	6.9000	AID678896
Solute carrier family 22 member 8	Rattus norvegicus (Norway rat)	Km	13.4000	0.7390	1.5395	2.3400	AID681391
Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)	Km	59.7000	0.0076	3.2018	10.0000	AID678959; AID678960
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
xenobiotic metabolic process	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
monoatomic ion transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
organic anion transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
prostaglandin transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
heme catabolic process	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
sodium-independent organic anion transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
transmembrane transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
transport across blood-brain barrier	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
bile acid and bile salt transport	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
cholesterol biosynthetic process	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
visual learning	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
coenzyme A metabolic process	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
negative regulation of protein catabolic process	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
negative regulation of protein secretion	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
long-term synaptic potentiation	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
regulation of ERK1 and ERK2 cascade	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
negative regulation of amyloid-beta clearance	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
isoprenoid biosynthetic process	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
sterol biosynthetic process	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
prostaglandin biosynthetic process	Prostaglandin G/H synthase 2	Homo sapiens (human)
angiogenesis	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to oxidative stress	Prostaglandin G/H synthase 2	Homo sapiens (human)
embryo implantation	Prostaglandin G/H synthase 2	Homo sapiens (human)
learning	Prostaglandin G/H synthase 2	Homo sapiens (human)
memory	Prostaglandin G/H synthase 2	Homo sapiens (human)
regulation of blood pressure	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of cell population proliferation	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to xenobiotic stimulus	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to nematode	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to fructose	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to manganese ion	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of vascular endothelial growth factor production	Prostaglandin G/H synthase 2	Homo sapiens (human)
cyclooxygenase pathway	Prostaglandin G/H synthase 2	Homo sapiens (human)
bone mineralization	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of prostaglandin biosynthetic process	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of fever generation	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of synaptic plasticity	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of synaptic transmission, dopaminergic	Prostaglandin G/H synthase 2	Homo sapiens (human)
prostaglandin secretion	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to estradiol	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to lipopolysaccharide	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to vitamin D	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to heat	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to tumor necrosis factor	Prostaglandin G/H synthase 2	Homo sapiens (human)
maintenance of blood-brain barrier	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of protein import into nucleus	Prostaglandin G/H synthase 2	Homo sapiens (human)
hair cycle	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of apoptotic process	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of nitric oxide biosynthetic process	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of cell cycle	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of vasoconstriction	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of smooth muscle contraction	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of smooth muscle contraction	Prostaglandin G/H synthase 2	Homo sapiens (human)
decidualization	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of smooth muscle cell proliferation	Prostaglandin G/H synthase 2	Homo sapiens (human)
regulation of inflammatory response	Prostaglandin G/H synthase 2	Homo sapiens (human)
brown fat cell differentiation	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to glucocorticoid	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of calcium ion transport	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of synaptic transmission, glutamatergic	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to fatty acid	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to mechanical stimulus	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to lead ion	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to ATP	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to hypoxia	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to non-ionic osmotic stress	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to fluid shear stress	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of transforming growth factor beta production	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of cell migration involved in sprouting angiogenesis	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of fibroblast growth factor production	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of brown fat cell differentiation	Prostaglandin G/H synthase 2	Homo sapiens (human)
positive regulation of platelet-derived growth factor production	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular oxidant detoxification	Prostaglandin G/H synthase 2	Homo sapiens (human)
regulation of neuroinflammatory response	Prostaglandin G/H synthase 2	Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to osmotic stress	Prostaglandin G/H synthase 2	Homo sapiens (human)
cellular response to homocysteine	Prostaglandin G/H synthase 2	Homo sapiens (human)
response to angiotensin	Prostaglandin G/H synthase 2	Homo sapiens (human)
monoatomic anion transport	Solute carrier family 22 member 6	Homo sapiens (human)
response to organic cyclic compound	Solute carrier family 22 member 6	Homo sapiens (human)
inorganic anion transport	Solute carrier family 22 member 6	Homo sapiens (human)
organic anion transport	Solute carrier family 22 member 6	Homo sapiens (human)
prostaglandin transport	Solute carrier family 22 member 6	Homo sapiens (human)
alpha-ketoglutarate transport	Solute carrier family 22 member 6	Homo sapiens (human)
xenobiotic transport	Solute carrier family 22 member 6	Homo sapiens (human)
sodium-independent organic anion transport	Solute carrier family 22 member 6	Homo sapiens (human)
transmembrane transport	Solute carrier family 22 member 6	Homo sapiens (human)
metanephric proximal tubule development	Solute carrier family 22 member 6	Homo sapiens (human)
renal tubular secretion	Solute carrier family 22 member 6	Homo sapiens (human)
monoatomic ion transport	Solute carrier family 22 member 8	Homo sapiens (human)
response to toxic substance	Solute carrier family 22 member 8	Homo sapiens (human)
inorganic anion transport	Solute carrier family 22 member 8	Homo sapiens (human)
prostaglandin transport	Solute carrier family 22 member 8	Homo sapiens (human)
xenobiotic transport	Solute carrier family 22 member 8	Homo sapiens (human)
transmembrane transport	Solute carrier family 22 member 8	Homo sapiens (human)
transport across blood-brain barrier	Solute carrier family 22 member 8	Homo sapiens (human)
xenobiotic metabolic process	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
monoatomic ion transport	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
organic anion transport	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
bile acid and bile salt transport	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
heme catabolic process	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
sodium-independent organic anion transport	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
transmembrane transport	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
monoatomic ion transport	Solute carrier family 22 member 11	Homo sapiens (human)
inorganic anion transport	Solute carrier family 22 member 11	Homo sapiens (human)
organic anion transport	Solute carrier family 22 member 11	Homo sapiens (human)
prostaglandin transport	Solute carrier family 22 member 11	Homo sapiens (human)
urate metabolic process	Solute carrier family 22 member 11	Homo sapiens (human)
transmembrane transport	Solute carrier family 22 member 11	Homo sapiens (human)
xenobiotic metabolic process	Solute carrier family 22 member 7	Homo sapiens (human)
monoatomic ion transport	Solute carrier family 22 member 7	Homo sapiens (human)
organic anion transport	Solute carrier family 22 member 7	Homo sapiens (human)
prostaglandin transport	Solute carrier family 22 member 7	Homo sapiens (human)
alpha-ketoglutarate transport	Solute carrier family 22 member 7	Homo sapiens (human)
transmembrane transport	Solute carrier family 22 member 7	Homo sapiens (human)
xenobiotic metabolic process	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
monoatomic ion transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
organic anion transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
bile acid and bile salt transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
prostaglandin transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
heme catabolic process	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
sodium-independent organic anion transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
transmembrane transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
thyroid hormone transport	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
transmembrane transporter activity	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
bile acid transmembrane transporter activity	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
hydroxymethylglutaryl-CoA reductase (NADPH) activity	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
protein binding	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
GTPase regulator activity	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
NADPH binding	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
coenzyme A binding	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
peroxidase activity	Prostaglandin G/H synthase 2	Homo sapiens (human)
prostaglandin-endoperoxide synthase activity	Prostaglandin G/H synthase 2	Homo sapiens (human)
protein binding	Prostaglandin G/H synthase 2	Homo sapiens (human)
enzyme binding	Prostaglandin G/H synthase 2	Homo sapiens (human)
heme binding	Prostaglandin G/H synthase 2	Homo sapiens (human)
protein homodimerization activity	Prostaglandin G/H synthase 2	Homo sapiens (human)
metal ion binding	Prostaglandin G/H synthase 2	Homo sapiens (human)
oxidoreductase activity, acting on single donors with incorporation of molecular oxygen, incorporation of two atoms of oxygen	Prostaglandin G/H synthase 2	Homo sapiens (human)
solute:inorganic anion antiporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
protein binding	Solute carrier family 22 member 6	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
alpha-ketoglutarate transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
antiporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
chloride ion binding	Solute carrier family 22 member 6	Homo sapiens (human)
identical protein binding	Solute carrier family 22 member 6	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier family 22 member 6	Homo sapiens (human)
solute:inorganic anion antiporter activity	Solute carrier family 22 member 8	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 8	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier family 22 member 8	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Solute carrier family 22 member 8	Homo sapiens (human)
serine-type endopeptidase inhibitor activity	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
bile acid transmembrane transporter activity	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
solute:inorganic anion antiporter activity	Solute carrier family 22 member 11	Homo sapiens (human)
protein binding	Solute carrier family 22 member 11	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 11	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier family 22 member 11	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier family 22 member 11	Homo sapiens (human)
protein binding	Solute carrier family 22 member 7	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 7	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier family 22 member 7	Homo sapiens (human)
alpha-ketoglutarate transmembrane transporter activity	Solute carrier family 22 member 7	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier family 22 member 7	Homo sapiens (human)
transmembrane transporter activity	Solute carrier family 22 member 7	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
bile acid transmembrane transporter activity	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activity	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
thyroid hormone transmembrane transporter activity	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
plasma membrane	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
basal plasma membrane	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
apical plasma membrane	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
basolateral plasma membrane	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
apical plasma membrane	Solute carrier organic anion transporter family member 2B1	Homo sapiens (human)
peroxisomal membrane	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
endoplasmic reticulum	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
endoplasmic reticulum membrane	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
endoplasmic reticulum membrane	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
peroxisomal membrane	3-hydroxy-3-methylglutaryl-coenzyme A reductase	Homo sapiens (human)
nuclear inner membrane	Prostaglandin G/H synthase 2	Homo sapiens (human)
nuclear outer membrane	Prostaglandin G/H synthase 2	Homo sapiens (human)
cytoplasm	Prostaglandin G/H synthase 2	Homo sapiens (human)
endoplasmic reticulum	Prostaglandin G/H synthase 2	Homo sapiens (human)
endoplasmic reticulum lumen	Prostaglandin G/H synthase 2	Homo sapiens (human)
endoplasmic reticulum membrane	Prostaglandin G/H synthase 2	Homo sapiens (human)
caveola	Prostaglandin G/H synthase 2	Homo sapiens (human)
neuron projection	Prostaglandin G/H synthase 2	Homo sapiens (human)
protein-containing complex	Prostaglandin G/H synthase 2	Homo sapiens (human)
neuron projection	Prostaglandin G/H synthase 2	Homo sapiens (human)
cytoplasm	Prostaglandin G/H synthase 2	Homo sapiens (human)
virion membrane	Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus
plasma membrane	Solute carrier family 22 member 6	Homo sapiens (human)
caveola	Solute carrier family 22 member 6	Homo sapiens (human)
basal plasma membrane	Solute carrier family 22 member 6	Homo sapiens (human)
basolateral plasma membrane	Solute carrier family 22 member 6	Homo sapiens (human)
extracellular exosome	Solute carrier family 22 member 6	Homo sapiens (human)
protein-containing complex	Solute carrier family 22 member 6	Homo sapiens (human)
plasma membrane	Solute carrier family 22 member 8	Homo sapiens (human)
basolateral plasma membrane	Solute carrier family 22 member 8	Homo sapiens (human)
apical plasma membrane	Solute carrier family 22 member 8	Homo sapiens (human)
extracellular exosome	Solute carrier family 22 member 8	Homo sapiens (human)
plasma membrane	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
basal plasma membrane	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
basolateral plasma membrane	Solute carrier organic anion transporter family member 1B3	Homo sapiens (human)
plasma membrane	Solute carrier family 22 member 11	Homo sapiens (human)
external side of plasma membrane	Solute carrier family 22 member 11	Homo sapiens (human)
basal plasma membrane	Solute carrier family 22 member 11	Homo sapiens (human)
apical plasma membrane	Solute carrier family 22 member 11	Homo sapiens (human)
extracellular exosome	Solute carrier family 22 member 11	Homo sapiens (human)
cytosol	Solute carrier family 22 member 7	Homo sapiens (human)
plasma membrane	Solute carrier family 22 member 7	Homo sapiens (human)
basal plasma membrane	Solute carrier family 22 member 7	Homo sapiens (human)
membrane	Solute carrier family 22 member 7	Homo sapiens (human)
basolateral plasma membrane	Solute carrier family 22 member 7	Homo sapiens (human)
apical plasma membrane	Solute carrier family 22 member 7	Homo sapiens (human)
plasma membrane	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
basal plasma membrane	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
membrane	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
basolateral plasma membrane	Solute carrier organic anion transporter family member 1B1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID1698001	Lipophilicity, log D of the compound at pH 7.4 by by shake flask method
AID313917	Incidence of myalgia in human	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID682168	TP_TRANSPORTER: inhibition of benzylpenicillin uptake by Pravastatin at a concentration of 1000uM in Oat3-expressing oocyte cells	2004	The Journal of pharmacology and experimental therapeutics, Jun, Volume: 309, Issue:3	Mouse reduced in osteosclerosis transporter functions as an organic anion transporter 3 and is localized at abluminal membrane of blood-brain barrier.
AID1217707	Time dependent inhibition of CYP2C19 in human liver microsomes at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1217712	Time dependent inhibition of CYP2C8 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1079947	Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID588217	FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID682026	TP_TRANSPORTER: inhibition of PHA uptake (PHA: 5uM) in hOAT1-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID588211	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID588215	FDA HLAED, alkaline phosphatase increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID313915	Cmax in human	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID678966	TP_TRANSPORTER: Transepithelial Transport (basal to apical) in OATP1B1/BCRP double transfected MDCKII cells	2005	The Journal of pharmacology and experimental therapeutics, Sep, Volume: 314, Issue:3	Identification of the hepatic efflux transporters of organic anions using double-transfected Madin-Darby canine kidney II cells expressing human organic anion-transporting polypeptide 1B1 (OATP1B1)/multidrug resistance-associated protein 2, OATP1B1/multid
AID384762	Hepatotoxicity in guinea pig assessed as hepatocellular degeneration at 200 mg/kg	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID625282	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588214	FDA HLAED, liver enzyme composite activity	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1636440	Drug activation in human Hep3B cells assessed as human CYP2D6-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA	2016	Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16	Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID681391	TP_TRANSPORTER: uptake in Oat3-expressing LLC-PK1 cells	2002	The Journal of pharmacology and experimental therapeutics, Mar, Volume: 300, Issue:3	Functional involvement of rat organic anion transporter 3 (rOat3; Slc22a8) in the renal uptake of organic anions.
AID1217706	Time dependent inhibition of CYP2C9 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID312175	Ratio of IC50 for cholesterol synthesis in rat myocytes to rat hepatocytes	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID625291	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079934	Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID679136	TP_TRANSPORTER: Transepithelial Transport (basal to apical) in OATP1B1/MDR1 double transfected MDCKII cells	2005	The Journal of pharmacology and experimental therapeutics, Sep, Volume: 314, Issue:3	Identification of the hepatic efflux transporters of organic anions using double-transfected Madin-Darby canine kidney II cells expressing human organic anion-transporting polypeptide 1B1 (OATP1B1)/multidrug resistance-associated protein 2, OATP1B1/multid
AID1217710	Covalent binding in human liver microsomes measured per mg of protein using radiolabelled compound at 10 uM after 1 hr incubation by liquid scintillation counting	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID625284	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1315658	Inhibition of human HMGR catalytic domain at 1 uM using HMG-CoA as substrate measured every 20 secs for 10 mins relative to control	2016	Journal of natural products, 06-24, Volume: 79, Issue:6	Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID444057	Fraction escaping hepatic elimination in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1211548	In vivo apparent biliary clearance in iv dosed Sprague-Dawley rat by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID1398781	Inhibition of human HMG-CoA reductase catalytic domain at 1 uM using HMG-CoA as substrate measured every 20 secs for 10 mins relative to control	2018	Bioorganic & medicinal chemistry, 08-15, Volume: 26, Issue:15	Asperidines A-C, pyrrolidine and piperidine derivatives from the soil-derived fungus Aspergillus sclerotiorum PSU-RSPG178.
AID679887	TP_TRANSPORTER: uptake in OATP-A-expressing 293c18 cell	1999	The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52	A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID1698003	Fraction unbound in rat plasma
AID313913	Selectivity, ratio of IC50 for rat hepatocyte to IC50 for rat L6 myocyte	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID176793	In vivo ability to inhibit cholesterol biosynthesis from [14C]acetate after a single oral administration in female rats	1995	Journal of medicinal chemistry, Aug-18, Volume: 38, Issue:17	(Aryloxy)methylsilane derivatives as new cholesterol biosynthesis inhibitors: synthesis and hypocholesterolemic activity of a new class of squalene epoxidase inhibitors.
AID1217709	Time dependent inhibition of CYP3A4 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID625288	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID679967	TP_TRANSPORTER: uptake in Oatp1-expressing 293c18 cells	1999	The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52	A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID185290	The compound was tested in vivo for the inhibition of cholesterol biosynthesis in chow-fed rats at 1.0 mg/kg; not determined	1992	Journal of medicinal chemistry, May-29, Volume: 35, Issue:11	Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID444058	Volume of distribution at steady state in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID678805	TP_TRANSPORTER: inhibition of ES uptake (ES: 50nM) in rOAT3-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID384741	Inhibition of cholesterol synthesis in rat hepatocytes assessed as incorporation of [14C]acetate into cholesterol	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID681381	TP_TRANSPORTER: inhibition of calcein-AM efflux in MDR1-expressing MDCK cells	2005	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4	Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID386623	Inhibition of 4-(4-(dimethylamino)styryl)-N-methylpyridinium uptake at human OCT1 expressed in HEK293 cells at 100 uM by confocal microscopy	2008	Journal of medicinal chemistry, Oct-09, Volume: 51, Issue:19	Structural requirements for drug inhibition of the liver specific human organic cation transport protein 1.
AID625287	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID384758	Hepatotoxicity in guinea pig assessed as increase in aspartate aminotransferase level relative to control	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1217729	Intrinsic clearance for reactive metabolites formation assessed as summation of [3H]GSH adduct formation rate-based reactive metabolites formation and cytochrome P450 (unknown origin) inactivation rate-based reactive metabolites formation	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID444051	Total clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID444053	Renal clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1211870	Total biliary clearance in iv dosed rat	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID384750	Reduction in plasma total cholesterol level in guinea pig at 200 mg/kg after 10 days	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1212341	Cytotoxicity against human Fa2N-4 cells by lactate dehydrogenase assay	2013	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4	Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID679476	TP_TRANSPORTER: uptake (pH 5.0) in OATP-B-expressing HEK293 cells	2004	The Journal of pharmacology and experimental therapeutics, Feb, Volume: 308, Issue:2	Functional characterization of pH-sensitive organic anion transporting polypeptide OATP-B in human.
AID1697999	Dissociation constant, acidic pKa of compound measured up to 18 mins by capillary electrophoresis
AID1211849	Unbound biliary clearance in iv dosed human after 24 hrs by T-tube method	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID1474166	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID599893	Hypolipidemic activity in chow fed Hartley guinea pig assessed as reduction of LDL level administered orally for 7 days measured on day 8 after 2 hrs post dose	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID312180	Reduction of LDL level in po dosed Hartley guinea pig plasma after 7 days	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID1079933	Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID384744	Partition coefficient, log P by reverse phase HPLC method	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1217708	Time dependent inhibition of CYP2D6 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1079948	Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID699539	Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID681366	TP_TRANSPORTER: inhibition of estradiol-17beta-glucuronide uptake(estradiol-17beta-glucuronide:0.02uM) in OATP1B1-expressing HEK293 cells	2005	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4	Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID385189	Myotoxicity in po dosed weanling Sprague-Dawley rat assessed as drug dose causing >2.5 fold increase in plasma creatine kinase activity relative to control	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID600037	Drug uptake by rat hepatic OATP1A1 transporters expressed in CHO cells at 1 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID598875	Inhibition of rat Oat1 expressed in pig LLC-PK11 cells	2011	Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11	Elucidation of common pharmacophores from analysis of targeted metabolites transported by the multispecific drug transporter-Organic anion transporter1 (Oat1).
AID1211829	Total biliary clearance in iv dosed human after 24 hrs by T-tube method	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID1636356	Drug activation in human Hep3B cells assessed as human CYP2C9-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA	2016	Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16	Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID313912	Inhibition of cholesterol synthesis in rat L6 myocyte	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID83165	Tested in vitro for the inhibition of HMG-CoA reductase from partially purified microsomal preparations.	1992	Journal of medicinal chemistry, May-29, Volume: 35, Issue:11	Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID588219	FDA HLAED, gamma-glutamyl transferase (GGT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID384748	Reduction in plasma total cholesterol level in guinea pig after 10 days	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1217728	Intrinsic clearance for reactive metabolites formation per mg of protein based on cytochrome P450 (unknown origin) inactivation rate by TDI assay	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID23913	Calculated partition coefficient (clogP) (active dihydroxy acid form)	1992	Journal of medicinal chemistry, May-29, Volume: 35, Issue:11	Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID86224	In vitro ability to inhibit cholesterol biosynthesis in HepG2 cells in culture from [14C]mevalonate	1995	Journal of medicinal chemistry, Aug-18, Volume: 38, Issue:17	(Aryloxy)methylsilane derivatives as new cholesterol biosynthesis inhibitors: synthesis and hypocholesterolemic activity of a new class of squalene epoxidase inhibitors.
AID682067	TP_TRANSPORTER: transepithelial transport (basal to apical) in MRP2- and OATP-C-expressing MDCKII cells	2002	The Journal of biological chemistry, Feb-22, Volume: 277, Issue:8	Transcellular transport of organic anions across a double-transfected Madin-Darby canine kidney II cell monolayer expressing both human organic anion-transporting polypeptide (OATP2/SLC21A6) and Multidrug resistance-associated protein 2 (MRP2/ABCC2).
AID1079942	Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID678712	Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID496784	Induction of cell differentiation in mouse C2C12 cells assessed as myosin heavy chain expression at 10 uM in presence of 250 uM cholesterol	2010	Nature chemical biology, Mar, Volume: 6, Issue:3	Carbon metabolism-mediated myogenic differentiation.
AID204661	In vitro inhibitory activity against pig liver microsomal squalene epoxidase	1995	Journal of medicinal chemistry, Aug-18, Volume: 38, Issue:17	(Aryloxy)methylsilane derivatives as new cholesterol biosynthesis inhibitors: synthesis and hypocholesterolemic activity of a new class of squalene epoxidase inhibitors.
AID600043	Drug uptake by rat hepatic OATP1A1 transporters expressed in CHO cells at 10 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID567091	Drug absorption in human assessed as human intestinal absorption rate	2011	European journal of medicinal chemistry, Jan, Volume: 46, Issue:1	Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID1079931	Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID678716	Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID444054	Oral bioavailability in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID699544	Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID678960	TP_TRANSPORTER: uptake in OATP-C-expressing 293c18 cells	1999	The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52	A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID697693	Drug uptake in human hepatocytes in presence of pan OATP inhibitor rifamycin	2012	Journal of medicinal chemistry, Feb-09, Volume: 55, Issue:3	Discovery of (S)-6-(3-cyclopentyl-2-(4-(trifluoromethyl)-1H-imidazol-1-yl)propanamido)nicotinic acid as a hepatoselective glucokinase activator clinical candidate for treating type 2 diabetes mellitus.
AID588218	FDA HLAED, lactate dehydrogenase (LDH) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID679034	TP_TRANSPORTER: inhibition of DNP-SG uptake in bile canalicular membrane vesicles from SD rat	1997	Drug metabolism and disposition: the biological fate of chemicals, Oct, Volume: 25, Issue:10	Biliary excretion of pravastatin in rats: contribution of the excretion pathway mediated by canalicular multispecific organic anion transporter.
AID600044	Drug uptake by human hepatic OATP1B1 transporter expressed in HEK293 cells at 1 uM relative to wild type HEK293 cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID600039	Drug uptake by rat hepatic OATP1B2 transporters expressed in CHO cells at 1 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID600042	Drug uptake by rat hepatic OATP1A4 transporters expressed in CHO cells at 10 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID385211	Myotoxicity in guinea pig assessed as drug dose causing >10 fold increase in plasma creatine kinase activity relative to control	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID570995	Antimalarial activity against Plasmodium falciparum infected in mouse assessed as mouse survival at 200 mg/kg, ip, qd administered 5 days post infection for 3 days measured after 6 days relative to control	2008	Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11	Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID1698004	Fraction unbound in cynomolgus monkey plasma
AID1315661	Binding affinity to human HMGR catalytic domain at 0.225 uM in presence of 800 to 3200 uM HMG-CoA as substrate measured every 20 secs for 10 mins	2016	Journal of natural products, 06-24, Volume: 79, Issue:6	Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID1211810	Drug excretion in iv dosed human assessed as compound excreted into bile after 24 hrs by T-tube method	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID467613	Volume of distribution at steady state in human	2009	European journal of medicinal chemistry, Nov, Volume: 44, Issue:11	Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID678959	TP_TRANSPORTER: uptake in OATP1B1-expressing HEK293 cells	2005	Pharmacogenetics and genomics, Jul, Volume: 15, Issue:7	Functional characterization of SLCO1B1 (OATP-C) variants, SLCO1B15, SLCO1B115 and SLCO1B1*15+C1007G, by using transient expression systems of HeLa and HEK293 cells.
AID679431	TP_TRANSPORTER: uptake (pH 5.0) of Pravastatin at a concentration of 14.7 u M in OATP-B-expressing HEK293 cells	2004	The Journal of pharmacology and experimental therapeutics, Feb, Volume: 308, Issue:2	Functional characterization of pH-sensitive organic anion transporting polypeptide OATP-B in human.
AID679828	TP_TRANSPORTER: inhibition of PGF2alpha uptake (PGF2: 50nM) in rOAT2-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID625286	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID600335	Drug uptake by human hepatic OATP1B3 transporter expressed in HEK293 cells at 10 uM relative to wild-type HEK293 cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID625277	FDA Liver Toxicity Knowledge Base Benchmark Dataset (LTKB-BD) drugs of less concern for DILI	2011	Drug discovery today, Aug, Volume: 16, Issue:15-16	FDA-approved drug labeling for the study of drug-induced liver injury.
AID588216	FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase	2004	Current drug discovery technologies, Dec, Volume: 1, Issue:4	Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID385190	Safety index, ratio of ED50 for inhibition of hepatic cholesterol synthesis in Sprague-Dawley rat to drug dose not causing >2.5 fold increase in plasma creatine kinase level in weanling Sprague-Dawley rat	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID384756	Myotoxicity in guinea pig assessed as increase in plasma creatine kinase activity at >200 mg/kg after 10 days relative to control	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID699543	Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID540213	Half life in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID86692	In vitro inhibitory activity was evaluated on cholesterol biosynthesis in HepG2 cells	2004	Bioorganic & medicinal chemistry letters, Feb-09, Volume: 14, Issue:3	Synthesis and biological activity of a novel squalene epoxidase inhibitor, FR194738.
AID384742	Inhibition of cholesterol synthesis in rat L6 cells assessed as incorporation of [14C]acetate into cholesterol	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID678815	TP_TRANSPORTER: inhibition of ES uptake (ES: 50nM) in hOAT3-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID1698000	Apparent permeability in dog MDCKII-LE cells at pH 7.4
AID1079935	Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID697691	Drug uptake in human hepatocytes assessed per mg of protein	2012	Journal of medicinal chemistry, Feb-09, Volume: 55, Issue:3	Discovery of (S)-6-(3-cyclopentyl-2-(4-(trifluoromethyl)-1H-imidazol-1-yl)propanamido)nicotinic acid as a hepatoselective glucokinase activator clinical candidate for treating type 2 diabetes mellitus.
AID384757	Hepatotoxicity in guinea pig assessed as increase in alanine aminotransferase level relative to control	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID600041	Drug uptake by rat hepatic OATP1B2 transporters expressed in CHO cells at 10 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID444050	Fraction unbound in human plasma	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID699540	Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1211553	Drug uptake in iv dosed Sprague-Dawley rat liver after 5 hrs by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID1217727	Intrinsic clearance for reactive metabolites formation per mg of protein in human liver microsomes based on [3H]GSH adduct formation rate at 100 uM by [3H]GSH trapping assay	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID312173	Inhibition of cholesterol synthesis in rat hepatocytes	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID313916	Ratio of Cmax for human to IC50 for rat L6 myocyte	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID678715	Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1079949	Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID540209	Volume of distribution at steady state in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1217704	Time dependent inhibition of CYP1A2 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID600334	Drug uptake by human hepatic OATP1B1 transporter expressed in HEK293 cells at 10 uM relative to wild type HEK293 cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID496782	Induction of cell differentiation in mouse C2C12 cells assessed as myosin heavy chain expression at 5 uM	2010	Nature chemical biology, Mar, Volume: 6, Issue:3	Carbon metabolism-mediated myogenic differentiation.
AID678714	Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID540212	Mean residence time in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1079944	Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID600038	Drug uptake by rat hepatic OATP1A4 transporters expressed in CHO cells at 1 uM relative to wild type CHO cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID699542	Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID678896	TP_TRANSPORTER: uptake in bile canalicular membrane vesicles from SD rat	1997	Drug metabolism and disposition: the biological fate of chemicals, Oct, Volume: 25, Issue:10	Biliary excretion of pravastatin in rats: contribution of the excretion pathway mediated by canalicular multispecific organic anion transporter.
AID679421	TP_TRANSPORTER: uptake (pH 7.4) of Pravastatin at a concentration of 14.7 u M in OATP-B-expressing HEK293 cells	2004	The Journal of pharmacology and experimental therapeutics, Feb, Volume: 308, Issue:2	Functional characterization of pH-sensitive organic anion transporting polypeptide OATP-B in human.
AID444055	Fraction absorbed in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID384740	Inhibition of HMGR in rat hepatic microsomes assessed as conversion of [14C]HMG-CoA to [14C]mevalonic acid	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID625281	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID697692	Drug uptake in rat hepatocytes in presence of pan OATP inhibitor rifamycin	2012	Journal of medicinal chemistry, Feb-09, Volume: 55, Issue:3	Discovery of (S)-6-(3-cyclopentyl-2-(4-(trifluoromethyl)-1H-imidazol-1-yl)propanamido)nicotinic acid as a hepatoselective glucokinase activator clinical candidate for treating type 2 diabetes mellitus.
AID1211550	In vivo intrinsic biliary clearance in iv dosed Sprague-Dawley rat by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID496783	Induction of cell differentiation in mouse C2C12 cells assessed as myosin heavy chain expression at 10 uM	2010	Nature chemical biology, Mar, Volume: 6, Issue:3	Carbon metabolism-mediated myogenic differentiation.
AID1698009	Hepatic clearance in cynomolgus monkey at < 1 mg/kg, iv administered as cassette dosing
AID678717	Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1698006	Ratio of drug level in cynomolgus monkey blood to plasma administered through iv dosing by LC-MS/MS analysis
AID1698005	Ratio of drug level in Wistar Hannover rat blood to plasma administered through iv dosing by LC-MS/MS analysis
AID1079946	Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID592682	Apparent permeability from apical to basolateral side of human Caco2 cells after 2 hrs by LC/MS/MS analysis	2011	Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8	QSAR-based permeability model for drug-like compounds.
AID313911	Inhibition of cholesterol synthesis in rat hepatocyte	2008	Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3	Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID1079940	Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1636357	Drug activation in human Hep3B cells assessed as human CYP3A4-mediated drug metabolism-induced cytotoxicity measured as decrease in cell viability at 300 uM pre-incubated with BSO for 18 hrs followed by incubation with compound for 3 hrs in presence of NA	2016	Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16	Development of a cell viability assay to assess drug metabolite structure-toxicity relationships.
AID1212314	Drug uptake in lysosomes of human Fa2N-4 cells assessed as inhibition of LysoTracker Red fluorescence after 30 mins	2013	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4	Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID1211551	Drug uptake in sandwich cultured Sprague-Dawley rat hepatocytes by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID625289	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625290	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1474167	Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status	2016	Drug discovery today, Apr, Volume: 21, Issue:4	DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID588976	Substrates of transporters of clinical importance in the absorption and disposition of drugs, BSEP	2010	Nature reviews. Drug discovery, Mar, Volume: 9, Issue:3	Membrane transporters in drug development.
AID1232319	Volume of distribution at steady state in wild type mouse	2015	Journal of medicinal chemistry, Aug-13, Volume: 58, Issue:15	Volume of Distribution in Drug Design.
AID1217705	Time dependent inhibition of CYP2B6 (unknown origin) at 100 uM by LC/MS system	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1283271	Inhibition of HMGCoA reductase in Dhcr7-deficient mouse Neuro2a cells assessed as decrease in 7-DHC levels at 1 uM by LC-MS/GC-MS analysis	2016	Journal of medicinal chemistry, Feb-11, Volume: 59, Issue:3	The Effect of Small Molecules on Sterol Homeostasis: Measuring 7-Dehydrocholesterol in Dhcr7-Deficient Neuro2a Cells and Human Fibroblasts.
AID625279	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID679489	TP_TRANSPORTER: inhibition of PAH uptake in Oat1-expressing LLC-PK1 cells	2002	The Journal of pharmacology and experimental therapeutics, Mar, Volume: 300, Issue:3	Functional involvement of rat organic anion transporter 3 (rOat3; Slc22a8) in the renal uptake of organic anions.
AID678713	Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID444056	Fraction escaping gut-wall elimination in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1079937	Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID540210	Clearance in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1211549	Unbound fraction in Sprague-Dawley rat plasma at 100 uM by equilibrium dialysis method	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID625283	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID503308	Antiproliferative activity against human PC3 cells at 30 uM after 120 hrs by MTT assay relative to DMSO	2006	Nature chemical biology, Jun, Volume: 2, Issue:6	Identifying off-target effects and hidden phenotypes of drugs in human cells.
AID540211	Fraction unbound in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID86222	In vitro ability to inhibit cholesterol biosynthesis in HepG2 cells in culture from [14C]acetate	1995	Journal of medicinal chemistry, Aug-18, Volume: 38, Issue:17	(Aryloxy)methylsilane derivatives as new cholesterol biosynthesis inhibitors: synthesis and hypocholesterolemic activity of a new class of squalene epoxidase inhibitors.
AID588212	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079943	Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID384743	Selectivity index, ratio of IC50 for cholesterol synthesis in rat L6 cells to IC50 for cholesterol synthesis in rat hepatocytes	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID678985	TP_TRANSPORTER: Transepithelial Transport (basal to apical) in OATP1B1/MRP2 double transfected MDCKII cells	2005	The Journal of pharmacology and experimental therapeutics, Sep, Volume: 314, Issue:3	Identification of the hepatic efflux transporters of organic anions using double-transfected Madin-Darby canine kidney II cells expressing human organic anion-transporting polypeptide 1B1 (OATP1B1)/multidrug resistance-associated protein 2, OATP1B1/multid
AID681820	TP_TRANSPORTER: uptake in Xenopus laevis oocytes	1999	Pharmaceutical research, Jun, Volume: 16, Issue:6	Pravastatin, an HMG-CoA reductase inhibitor, is transported by rat organic anion transporting polypeptide, oatp2.
AID570990	Antimalarial activity against Plasmodium falciparum infected in mouse assessed as parasitemia at 40 mg/kg, ip, qd administered 5 days post infection for 3 days measured after 6 days (Rvb =9.9+/-2.2 %)	2008	Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11	Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID1079932	Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID312174	Inhibition of cholesterol synthesis in rat L6 cells	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID625285	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID444052	Hepatic clearance in human	2010	Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3	Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID681827	TP_TRANSPORTER: uptake in Oatp2-expressing 293c18 cells	1999	The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52	A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID697690	Drug uptake in rat hepatocytes assessed per mg of protein	2012	Journal of medicinal chemistry, Feb-09, Volume: 55, Issue:3	Discovery of (S)-6-(3-cyclopentyl-2-(4-(trifluoromethyl)-1H-imidazol-1-yl)propanamido)nicotinic acid as a hepatoselective glucokinase activator clinical candidate for treating type 2 diabetes mellitus.
AID1698010	Hepatic clearance in human administered through iv dosing
AID678722	Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH	2012	Chemical research in toxicology, Oct-15, Volume: 25, Issue:10	Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID312172	Inhibition of HMG-CoA reductase in Sprague-Dawley rat liver microsomes	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID570991	Antimalarial activity against Plasmodium falciparum infected in mouse assessed as parasitemia at 200 mg/kg, ip, qd administered 5 days post infection for 3 days measured after 6 days (Rvb =9.9+/-2.2 %)	2008	Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11	Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID680991	TP_TRANSPORTER: inhibition of E1S uptake by Pravastatin at a concentration of 200uM in membrane vesicles from ABCG2-expressing P388 cells	2003	The Journal of biological chemistry, Jun-20, Volume: 278, Issue:25	ABCG2 transports sulfated conjugates of steroids and xenobiotics.
AID680259	TP_TRANSPORTER: inhibition of Taurocholate uptake (Taurocholate: 0.5 uM, Pravastatin: 50 uM) in Oatp1-expressing 293c18 cells	1999	The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52	A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID570994	Antimalarial activity against Plasmodium falciparum infected in mouse assessed as mouse survival at 40 mg/kg, ip, qd administered 5 days post infection for 3 days measured after 6 days relative to control	2008	Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11	Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID1698007	Ratio of drug level in human blood to plasma administered through iv dosing by LC-MS/MS analysis
AID476929	Human intestinal absorption in po dosed human	2010	European journal of medicinal chemistry, Mar, Volume: 45, Issue:3	Neural computational prediction of oral drug absorption based on CODES 2D descriptors.
AID1698008	Hepatic clearance in Wistar Hannover rat at 1 mg/kg, iv
AID404304	Effect on human MRP2-mediated estradiol-17-beta-glucuronide transport in Sf9 cells inverted membrane vesicles relative to control	2008	Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11	Prediction and identification of drug interactions with the human ATP-binding cassette transporter multidrug-resistance associated protein 2 (MRP2; ABCC2).
AID1079936	Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1698011	Fraction unbound in human plasma
AID1315659	Inhibition of human HMGR catalytic domain using 800 uM HMG-CoA as substrate measured every 20 secs for 10 mins	2016	Journal of natural products, 06-24, Volume: 79, Issue:6	Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID311524	Oral bioavailability in human	2007	Bioorganic & medicinal chemistry, Dec-15, Volume: 15, Issue:24	Hologram QSAR model for the prediction of human oral bioavailability.
AID625292	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID699541	Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting	2012	Journal of medicinal chemistry, May-24, Volume: 55, Issue:10	Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID467612	Fraction unbound in human plasma	2009	European journal of medicinal chemistry, Nov, Volume: 44, Issue:11	Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID678973	TP_TRANSPORTER: inhibition of ES uptake (ES: 50nM) in hOAT4-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID312171	Lipophilicity, log P of the compound	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID1211554	Biliary excretion index in sandwich cultured Sprague-Dawley rat hepatocytes after 15 mins by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID1079938	Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID425652	Total body clearance in human	2009	Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15	Physicochemical determinants of human renal clearance.
AID185126	The compound form was tested in vivo for the inhibition of cholesterol biosynthesis in chow-fed rats at 1.0 mg/kg; not determined	1992	Journal of medicinal chemistry, May-29, Volume: 35, Issue:11	Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID467611	Dissociation constant, pKa of the compound	2009	European journal of medicinal chemistry, Nov, Volume: 44, Issue:11	Prediction of volume of distribution values in human using immobilized artificial membrane partitioning coefficients, the fraction of compound ionized and plasma protein binding data.
AID1217711	Metabolic activation in human liver microsomes assessed as [3H]GSH adduct formation rate measured per mg of protein at 100 uM by [3H]GSH trapping assay	2011	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7	Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID679430	TP_TRANSPORTER: uptake (pH 5.5) in OATP-B-expressing HEK293 cells	2003	The Journal of pharmacology and experimental therapeutics, Aug, Volume: 306, Issue:2	Involvement of human organic anion transporting polypeptide OATP-B (SLC21A9) in pH-dependent transport across intestinal apical membrane.
AID679512	TP_TRANSPORTER: inhibition of PGF2alpha uptake (PGF2: 50nM) in hOAT2-expressing S2 cells	2004	Journal of pharmacological sciences, Feb, Volume: 94, Issue:2	Interactions of human- and rat-organic anion transporters with pravastatin and cimetidine.
AID1211555	In vitro apparent biliary clearance in sandwich cultured Sprague-Dawley rat hepatocytes after 15 mins by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID1079941	Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID681370	TP_TRANSPORTER: inhibition of calcein-AM efflux in MRP2-expressing MDCK cells	2005	Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4	Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID425653	Renal clearance in human	2009	Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15	Physicochemical determinants of human renal clearance.
AID1079939	Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID384745	Partition coefficient, log P by octanol-water partitioning method	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1698002	Intrinsic clearance in cryopreserved human hepatocytes at 1 uM measured up to 120 mins by LC-MS/MS analysis
AID384747	Inhibition of hepatic cholesterol synthesis in po dosed Sprague-Dawley rat assessed as incorporation of [14C]acetate into hepatic sterols	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1211802	Drug excretion in iv dosed rat assessed as compound excreted into bile	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID625280	Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis	2011	PLoS computational biology, Dec, Volume: 7, Issue:12	Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID592683	Apparent permeability from basolateral side to apical side of human Caco2 cells by LC/MS/MS analysis	2011	Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8	QSAR-based permeability model for drug-like compounds.
AID588213	Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents	2010	Chemical research in toxicology, Jan, Volume: 23, Issue:1	Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079945	Animal toxicity known. [column 'TOXIC' in source]
AID1211552	In vitro intrinsic biliary clearance in sandwich cultured Sprague-Dawley rat hepatocytes by LC-MS/MS analysis	2012	Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 40, Issue:3	In vivo biliary clearance should be predicted by intrinsic biliary clearance in sandwich-cultured hepatocytes.
AID1211878	Unbound biliary clearance in iv dosed rat	2013	Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 41, Issue:2	Species differences in biliary clearance and possible relevance of hepatic uptake and efflux transporters involvement.
AID600045	Drug uptake by human hepatic OATP1B3 transporter expressed in HEK293 cells at 1 uM relative to wild-type HEK293 cells	2011	Bioorganic & medicinal chemistry letters, May-01, Volume: 21, Issue:9	Discovery of novel hepatoselective HMG-CoA reductase inhibitors for treating hypercholesterolemia: a bench-to-bedside case study on tissue selective drug distribution.
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1346822	Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	2001	Bioorganic & medicinal chemistry letters, May-21, Volume: 11, Issue:10	Synthesis and biological evaluations of condensed pyridine and condensed pyrimidine-based HMG-CoA reductase inhibitors.
AID1346838	Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	2001	Bioorganic & medicinal chemistry letters, May-21, Volume: 11, Issue:10	Synthesis and biological evaluations of condensed pyridine and condensed pyrimidine-based HMG-CoA reductase inhibitors.
AID1346822	Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	1992	Journal of medicinal chemistry, May-29, Volume: 35, Issue:11	Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID1346822	Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	2005	Biochemistry, Sep-06, Volume: 44, Issue:35	Binding thermodynamics of statins to HMG-CoA reductase.
AID1346838	Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID1346838	Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	1993	Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23	Inhibitors of cholesterol biosynthesis. 2. 3,5-Dihydroxy-7-(N-pyrrolyl)-6-heptenoates, a novel series of HMG-CoA reductase inhibitors.
AID1346838	Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)	2001	The American journal of cardiology, Mar-08, Volume: 87, Issue:5A	Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
AID1798163	HMG-CoA Reductase Enzyme Assay and Inhibition of Cellular Cholesterol Synthesis Assay from Article 10.1021/jm800001n: \\(3R,5S,E)-7-(4-(4-Fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1H-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic Aci	2008	Journal of medicinal chemistry, May-08, Volume: 51, Issue:9	(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1798004	HMG-CoA Reductase Enzyme Assay and Inhibition of Cellular Cholesterol Synthesis Assay from Article 10.1021/jm070849r: \\Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-meth	2008	Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1	Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID1802450	Oatp1d1 Transport Assay from Article 10.1074/jbc.M113.518506: \\Molecular characterization of zebrafish Oatp1d1 (Slco1d1), a novel organic anion-transporting polypeptide.\\	2013	The Journal of biological chemistry, Nov-22, Volume: 288, Issue:47	Molecular characterization of zebrafish Oatp1d1 (Slco1d1), a novel organic anion-transporting polypeptide.
AID1159607	Screen for inhibitors of RMI FANCM (MM2) intereaction	2016	Journal of biomolecular screening, Jul, Volume: 21, Issue:6	A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1700793	Protective activity against radioactive-induced Caenorhabditis elegans N2 assessed as head thrashes preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700810	Memory enhancement effect in radioactive-induced Caenorhabditis elegans MT1434 harboring egl-30(n686) mutant assessed as memory index preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700805	Inhibition of Gs-apha-coupled PKA pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of gsa-1 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700804	Inhibition of Gq-alpha-coupled PLC pathway in radioactive-induced Caenorhabditis elegans N2 assessed as up regulation of goa-1 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700818	Activation of CREB in radioactive-induced Caenorhabditis elegans MY36 harboring [crh-1(tz2); Pmbr-1-mcherry::crh-1(mtIs18)] mutant assessed as increase in long-term memory preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700794	Protective activity against radioactive-induced Caenorhabditis elegans N2 assessed as body bends preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700797	Inhibition of neuropeptide pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of npr-2 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700801	Inhibition of Gq-alpha-coupled PLC pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of egl-30 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700802	Inhibition of Gs-apha-coupled PKA pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of kin-2 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700803	Inhibition of Gq-alpha-coupled PLC pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of egl-8 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700817	Activation of CREB in radioactive-induced Caenorhabditis elegans YT17 harboring crh-1(tz2) mutant assessed as reduction radiation-induced damage preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700796	Inhibition of neuropeptide signaling pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of npr-11 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700792	Protective activity against radioactive-induced Caenorhabditis elegans N2 at 0.05 to 0.2 mg/ml preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700807	Inhibition of cGMP signaling pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of daf-11 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700809	Inhibition of cGMP signaling pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of tax-4 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700795	Protective activity against Butanone-induced Caenorhabditis elegans N2 assessed as chemotaxis index incubated for 1 hr	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700815	Memory enhancement effect in radioactive-induced Caenorhabditis elegans assessed as increase in cAMP level preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700814	Memory enhancement effect in radioactive-induced Caenorhabditis elegans harboring RNAi podr-1::unc-31 mutant assessed as memory index preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700813	Memory enhancement effect in radioactive-induced Caenorhabditis elegans RB1341 harboring npl-1(ok1470) mutant assessed as memory index preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700791	Memory enhancement effect in Caenorhabditis elegans N2 assessed as increase in long-term memory index at 0.1 mg/ml preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700812	Memory enhancement effect in radioactive-induced Caenorhabditis elegans harboring RNAi egl8;egl-30(n686)ls(Podr-1-mcherry::egl-30) mutant assessed as memory index preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700799	Inhibition of neuropeptide pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of nlp-5 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700800	Inhibition of neuropeptide pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of nlp-1 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700798	Inhibition of neuropeptide pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of nlp-23 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700806	Inhibition of cGMP signaling pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of odr-1 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700811	Memory enhancement effect in radioactive-induced Caenorhabditis elegans MY66 harboring egl-30(n686);Podr-1-mcherry::egl-30(mtIs35)] mutant assessed as memory index preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700808	Inhibition of cGMP signaling pathway in radioactive-induced Caenorhabditis elegans N2 assessed as down regulation of tax-2 mRNA expression preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs qRT-PCR analysis	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID1700816	Activation of CREB in radioactive-induced Caenorhabditis elegans YT17 harboring crh-1(tz2) mutant assessed as increase in long-term memory preincubated for 24 hrs followed by gamma-radiation treatment and measured after 24 hrs	2020	Journal of natural products, 11-25, Volume: 83, Issue:11
AID779150	Inhibition of Wnt/beta-catenin signaling pathway in human HEK293 cells at 20 uM after 24 hrs by dual luciferase reporter gene assay relative to vehicle-treated control	2013	Bioorganic & medicinal chemistry letters, Oct-15, Volume: 23, Issue:20	Anti-proliferative activity of hydnocarpin, a natural lignan, is associated with the suppression of Wnt/β-catenin signaling pathway in colon cancer cells.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	35 (1.02)	18.7374
1990's	930 (27.00)	18.2507
2000's	1541 (44.73)	29.6817
2010's	813 (23.60)	24.3611
2020's	126 (3.66)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	1,036 (28.98%)	5.53%
Trials	0 (0.00%)	5.53%
Reviews	316 (8.84%)	6.00%
Reviews	1 (14.29%)	6.00%
Case Studies	129 (3.61%)	4.05%
Case Studies	0 (0.00%)	4.05%
Observational	9 (0.25%)	0.25%
Observational	0 (0.00%)	0.25%
Other	2,085 (58.32%)	84.16%
Other	6 (85.71%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (157)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
S0919, A Phase II Study of Idarubicin and Ara-C in Combination With Pravastatin for Poor-Risk Acute Myelogenous Leukemia [NCT00840177]	Phase 2	115 participants (Actual)	Interventional	2009-12-10	Completed
Phase II Randomized Trial Evaluating the Administration of Sorafenib or Pravastatin or Association Sorafenib-pravastatin or Best Supportive Care for the Palliative Treatment of Hepatocellular Carcinoma in Patient With CHILD B Cirrhosis [NCT01357486]	Phase 2	160 participants (Actual)	Interventional	2011-11-14	Completed
Statin Therapeutic Interchange by Pharmacist Collaborative Practice Process [NCT01222182]		260 participants (Actual)	Observational	2009-09-30	Completed
A Randomized, Double-Blind, Placebo-Controlled Study Followed by an Open Label Treatment Period to Evaluate the Efficacy and Safety of Alirocumab in Children and Adolescents With Heterozygous Familial Hypercholesterolemia [NCT03510884]	Phase 3	153 participants (Actual)	Interventional	2018-05-31	Completed
Curative Efficacy of Pravastatine in Patients Presented Delayed Cutaneous and Subcutaneous Radio-induced Fibrosis [NCT01268202]	Phase 2	61 participants (Actual)	Interventional	2010-12-17	Completed
Pravastatin to Prevent Preeclampsia and Reduce Maternal-Neonatal Mortality and Morbidity in High Risk Preeclampsia Patients [NCT03648970]	Phase 2	280 participants (Anticipated)	Interventional	2018-03-01	Recruiting
Single Dose Two-Way Crossover Fed Bioequivalence Study of Pravastatin 80 mg Tablets in Healthy Volunteers [NCT01146093]	Phase 1	24 participants (Actual)	Interventional	2002-11-30	Completed
Primary Prevention of MACE With Standard and Intensive Statin Treatment in Hypercholesterolemia Patients With Concomitant Diabetes and Hypertension [NCT01173939]		10,000 participants (Anticipated)	Interventional	2010-07-31	Terminated(stopped due to With recommendation from IDMC, Steering Committee terminated this trial due to ethical concerns raised by J-ART study.)
"Improving Theempowerment in Patients With Severe Breast Fibrosis Radio-induced Treated by Pravastatin : Benefit of e-PROs (Electronic Patient Reported Outcome ) on Breast-related Quality of Life" [NCT04356209]	Phase 2	105 participants (Anticipated)	Interventional	2020-09-28	Recruiting
Pravastatin and Alkali Therapy in Patients With Autosomal Dominant Polycystic Kidney Disease [NCT04284657]	Phase 2	30 participants (Anticipated)	Interventional	2019-01-30	Enrolling by invitation
Statins: A New Therapeutic Option for Treatment of Patients With Endometriosis [NCT02079974]		0 participants (Actual)	Interventional	2014-07-31	Withdrawn
Single Dose Two-Way Crossover Fasting Bioequivalence Study of Pravastatin 80 mg Tablets in Healthy Volunteers [NCT01146106]	Phase 1	43 participants (Actual)	Interventional	2002-12-31	Completed
Pharmacodynamics, Preliminary Pharmacokinetics and Tolerability After Multiple Oral Doses of 2.5 mg o.d. BIBB 515 BS (Capsule) or Pravastatin 20 mg Over 2 Weeks in Hyperlipemic Healthy Male Subjects (Parallel Group Comparison, Randomized, Placebo Controll [NCT02266485]	Phase 1	60 participants (Actual)	Interventional	1998-07-31	Completed
StAT-TB (Statin Adjunctive Therapy for TB): A Phase 2b Dose-finding Study of Pravastatin in Adults With Tuberculosis [NCT03882177]	Phase 2	16 participants (Actual)	Interventional	2020-02-21	Completed
A Double-Blind, Randomized Study to Evaluate the Efficacy and Safety of Lapaquistat Acetate 50 mg or Placebo When Co-administered With Statins in Subjects With Hypercholesterolemia, With an Optional Open-Label Extension [NCT00532311]	Phase 3	411 participants (Actual)	Interventional	2007-07-31	Terminated(stopped due to Overall profile of the compound does not offer significant clinical advantage to patients over currently available lipid lowering agents)
Effects of Concomitant Administration of BMS-986195 on the Single-dose Pharmacokinetics of Methotrexate and Probe Substrates for Cytochrome P450 1A2, 2C8, 2C9, 2C19, 3A4, Organic Anion Transporter Polypeptide 1B1 and P-glycoprotein in Healthy Participants [NCT03131973]	Phase 1	26 participants (Actual)	Interventional	2017-05-13	Completed
A Single-Dose, Comparative, Bioavailability Study of Two Formulations of Pravastatin Sodium 80 mg Tablets Under Fasting Conditions [NCT00830258]	Phase 1	60 participants (Actual)	Interventional	2005-04-30	Completed
A Multicenter, Randomized, Double-blind, Placebo Controlled, Parallel Study to Determine the Efficacy and Safety of Pravastatin 80 mg Administered Once Daily to Hypercholesterolemic Subjects With Chronic, Well Compensated Liver Disease [NCT00529178]	Phase 4	232 participants (Anticipated)	Interventional	2002-12-31	Completed
Pravastatin or Atorvastatin Evaluation and Infection Therapy (TIMI22) [NCT00382460]	Phase 4	4,000 participants	Interventional	2000-11-30	Completed
Real World Evidence Study for Assessing Statin Use for Primary and Secondary Prevention of Cardiovascular Disease in Primary Care in Brazil [NCT05285085]		2,133,900 participants (Actual)	Observational	2021-11-19	Completed
[NCT02155530]		30 participants (Actual)	Interventional	2014-06-30	Completed
Prevention of Renal and Vascular Endstage Disease Intervention Trial [NCT03073018]	Phase 3	864 participants (Actual)	Interventional	1998-04-30	Completed
A Phase 1 Study to Evaluate OATP Transporter-Mediated Drug-Drug Interactions Between Filgotinib and Statins as Probe Drugs in Healthy Participants [NCT04608344]	Phase 1	27 participants (Actual)	Interventional	2020-11-04	Completed
Intensive Statin Treatment in Chinese Coronary Artery Disease Patients Undergoing Percutaneous Coronary Intervention(PCI) [NCT01293097]	Phase 4	2,884 participants (Actual)	Interventional	2010-06-30	Completed
A Phase I, Open Label, Randomised, Parallel Group Study of Repeated Oral Doses of AZD1981 (100 mg Twice Daily and 400 mg Twice Daily Via Tablet) for Eight Days and Single Doses of Pravastatin (Pravachol® Tablet 40 mg) to Evaluate the Pharmacokinetic Inter [NCT01254461]	Phase 1	30 participants (Anticipated)	Interventional	2011-02-28	Completed
Use of High Potency Statins and Rates of Admission for Acute Kidney Injury: Multicenter, Retrospective Observational Analysis of Administrative Databases [NCT02518516]		2,067,639 participants (Actual)	Observational	2011-01-31	Completed
Pravastatin Intervention to Delay Hepatocellular Carcinoma Recurrence [NCT03219372]	Phase 2	1 participants (Actual)	Interventional	2018-09-27	Terminated(stopped due to Study discontinued due to low accrual.)
An Open-Label Study to Evaluate the Efficacy and Safety of Alirocumab in Children and Adolescents With Homozygous Familial Hypercholesterolemia [NCT03510715]	Phase 3	18 participants (Actual)	Interventional	2018-08-31	Completed
A Phase 1, Single-center, Open-label, Sequential Study to Evaluate the Drug-drug Interaction Potential of BMS-986196 in Healthy Participants [NCT05852769]	Phase 1	18 participants (Actual)	Interventional	2023-05-31	Completed
A 12-Week, Randomized, Double-Blind, Active-Controlled, Parallel-Group Study Comparing Pitavastatin 4 mg vs. Pravastatin 40 mg in HIV-Infected Subjects With Dyslipidemia, Followed by a 40-Week Safety Extension Study [NCT01301066]	Phase 4	252 participants (Actual)	Interventional	2010-12-31	Completed
A 6 Week Open Label, Dose Comparison Study to Evaluate the Safety and Efficacy of Rosuvastatin Versus Atorvastatin, Pravastatin, and Simvastatin in Subjects With Hypercholesterolemia. [NCT00654537]	Phase 3	5,625 participants (Anticipated)	Interventional	2001-04-30	Completed
A Multicenter, Randomized, Open-labeled, Parallel Group Comparison Study to Evaluate the Efficacy, Safety and Tolerability of Ezetimibe Added to Ongoing Statin Therapy Versus Doubling the Dose of Ongoing Statin in the Treatment of Hypercholesterolemia. [NCT00652327]	Phase 4	83 participants (Actual)	Interventional	2005-12-31	Completed
Coadministration of Ezetimibe With Fenofibrate Versus Pravastatin Monotherapy for the Treatment of Hyperlipidaemia in HIV-infected Patients Receiving Protease Inhibitors: a Randomized, Prospective, Controlled Pilot Study. [NCT00843661]	Phase 4	60 participants (Anticipated)	Interventional	2009-03-31	Recruiting
A Relative Bioavailability Study of Pravastatin Sodium 40 mg Tablets Under Fasting Conditions [NCT00834379]	Phase 1	58 participants (Actual)	Interventional	2000-09-30	Completed
A Relative Bioavailability Food Challenge Study of Pravastatin Sodium 40 mg Tablets [NCT00834847]	Phase 1	24 participants (Actual)	Interventional	2000-08-31	Completed
A Study to Evaluate the Efficacy and Safety of Pravastatin/Fenofibrate Complex in Patients With Combined Dyslipidemia With Adequately Controlled LDL-C But Inadequately Controlled Triglyceride Level by Atorvastatin Monotherapy [NCT02166593]	Phase 3	302 participants (Actual)	Interventional	2014-05-31	Completed
A Relative Bioavailability Study of 80 mg Pravastatin Sodium Tablets Under Non-Fasting Conditions [NCT00829309]	Phase 1	16 participants (Actual)	Interventional	2005-03-31	Completed
A Multi-Center, Prospective, Longitudinal, Randomized, Double-Blind, Phase III Study to Evaluate the Efficacy and Safety of Daily Administration of Pravastatin 40 mg or Fenofibrate 160 mg or Pravafen (the Combination of Pravastatin and Fenofibrate 40/160 [NCT00459745]	Phase 3	481 participants (Actual)	Interventional	2007-04-30	Completed
Higher Potency Statins and the Risk of New Diabetes: Multicentre, Observational Study of Administrative Databases [NCT02518503]		136,966 participants (Actual)	Observational	2012-07-31	Completed
A Comparative Study of Pravastatin vs Placebo as Primary Prevention of Severe Subcutaneous Breast Fibrosis in Hyper-radiosensitive Identified Patients With Breast Cancer [NCT04385433]	Phase 3	15 participants (Actual)	Interventional	2020-12-04	Terminated(stopped due to Not enough patients enrolled)
Randomized Controlled Study to Evaluate the Efficacy of Pravastatin on Survival and Recurrence of Advanced Gastroesophageal Cancer [NCT01038154]	Phase 4	146 participants (Anticipated)	Interventional	2009-11-30	Recruiting
A Stable-isotope Study in Healthy Normolipidemic Volunteers Comparing the Mechanisms of Action of Lifibrol and Pravastatin [NCT01057654]	Phase 3	18 participants (Actual)	Interventional	1996-01-31	Completed
The Effects of Pravastatin and Rosuvastatin on the Tissue Characteristics and Morphology of Coronary Plaques in Patients With Stable Angina Pectoris [NCT01325818]	Phase 4	150 participants (Anticipated)	Interventional	2011-03-31	Recruiting
[NCT01011127]		0 participants	Observational	2009-12-31	Completed
Pravastatin for Acute Myocardial Infarction With Minimally to Mildly Increased Levels of Serum Cholesterol Study That Evaluates the Effects of Pravastatin for Acute Myocardial Infarction With LDL-Cholesterol Levels of 70-129 mg/dl [NCT00688922]	Phase 4	400 participants (Anticipated)	Interventional	2008-07-31	Recruiting
The Influence of Raltegravir on Pravastatin Pharmacokinetics in Healthy Volunteers (GRAPPA) [NCT00665717]	Phase 1	24 participants (Actual)	Interventional	2008-05-31	Completed
A Phase 1, Open-Label Study to Evaluate the Effect of GDC-0810 on the Pharmacokinetics of Pravastatin in Healthy Female Subjects of Non-Childbearing Potential [NCT02621957]	Phase 1	15 participants (Actual)	Interventional	2015-12-31	Completed
Quality of Life and Metabolic Alterations in Patients With Statin-Associated Myopathy [NCT00850460]	Phase 4	14 participants (Actual)	Interventional	2009-02-28	Terminated(stopped due to Investigator left institution and no PI has been found to continue the study)
A Prospective, Randomized, Two Group Comparison Study to Evaluate the Effect of Statin on Heart Function in Patients With Chronic Ischemic Heart Failure. [NCT00701285]	Phase 4	70 participants (Anticipated)	Interventional	2008-07-31	Completed
A Two-Way Crossover, Open-Label, Single-Dose, Fasting, Bioequivalence Study of Pravastatin Sodium 80 mg Tablets Versus Pravachol® 80 mg Tablets In Normal Healthy Non-Smoking Male and Female Subjects [NCT00650221]	Phase 1	43 participants (Actual)	Interventional	2003-06-30	Completed
Treatment of the Hutchinson-Gilford Progeria Syndrome With a Combination of Pravastatin and Zoledronic Acid [NCT00731016]	Phase 2	15 participants (Actual)	Interventional	2008-10-31	Completed
Vytorin on Carotid Intima-media Thickness and Overall Rigidity [NCT00738296]	Phase 4	90 participants (Actual)	Interventional	2005-04-30	Completed
Yokohama Assessment of Fluvastatin, Pravastatin, Pitavastatin and Atorvastatin in Acute Coronary Syndrome (Yokohama-ACS) [NCT00549926]	Phase 4	200 participants (Anticipated)	Interventional	2007-10-31	Completed
Efficacy of WelChol as an Add-on to Pravastatin Therapy [NCT00755352]	Phase 4	67 participants (Actual)	Interventional	2002-11-30	Completed
European Society of Hypertension and Chinese Hypertension League Stroke in Hypertension Optimal Treatment Trial [NCT01563731]	Phase 4	200 participants (Actual)	Interventional	2013-04-30	Completed
An Open-Label, Multicenter Study to Assess the Efficacy of Switching to a Combination Tablet Ezetimibe/Simvastatin 10mg/40mg, Compared to Doubling the Dose of Statin in Patients Hospitalized With a Coronary Event [NCT00132717]	Phase 3	450 participants (Actual)	Interventional	2005-01-01	Completed
High Intensity Lipid Lowering Following Acute Coronary Syndromes for Persons Living With Human Immunodeficiency Virus (HILLCLIMBER) [NCT02841774]	Phase 2	10 participants (Actual)	Interventional	2016-11-30	Completed
An Open-label Exploratory Study of the Pharmacokinetic Interaction of CXA-10 Administered to Steady State With Pravastatin and Vytorin® (Simvastatin and Ezetimibe) in Healthy Males [NCT02547402]	Phase 1	10 participants (Actual)	Interventional	2015-12-31	Completed
A Prospective, Multicenter, Randomized Trial Comparing the Efficacy and Safety of Fenofibrate Versus Pravastatin in HIV-Infected Subjects With Lipid Abnormalities [NCT00006412]	Phase 3	630 participants	Interventional		Completed
The Effect of Efavirenz and Nelfinavir on the Pharmacokinetics of Hydroxymethylglutaryl Coenzyme A Reductase Inhibitors [NCT00017758]	Phase 1	56 participants	Interventional		Completed
Randomized Phase III Trial Sorafenib-Pravastatin Versus Sorafenib Alone for the Palliative Treatment of Child-Pugh A Hepatocellular Carcinoma [NCT01075555]	Phase 3	323 participants (Actual)	Interventional	2010-02-28	Completed
[NCT00546559]		0 participants	Observational	2004-01-31	Completed
[NCT01004237]	Phase 4	52 participants (Actual)	Interventional	2009-11-30	Completed
Secondary Prevention With HMG-CoA Reductase Inhibitor Against Stroke [NCT00221104]	Phase 3	1,578 participants (Actual)	Interventional	2004-03-01	Completed
Pilot Study of a Multi-Drug Regimen for Severe Pulmonary Fibrosis in Hermansky-Pudlak Syndrome [NCT00467831]	Phase 1/Phase 2	3 participants (Actual)	Interventional	2007-04-30	Terminated(stopped due to insufficient enrollment)
Effect of Statin Therapy on Disease Progression in Autosomal Dominant Polycystic Kidney Disease [NCT00456365]	Phase 3	110 participants (Actual)	Interventional	2006-11-30	Completed
[NCT01903694]	Phase 3	474 participants (Anticipated)	Interventional	2010-03-31	Completed
Evaluation Of The Effect Of PF-05089771 On The Metabolism Of Multiple Cytochrome P450 And OATP1B1 Transporter Substrates [NCT01934569]	Phase 1	17 participants (Actual)	Interventional	2013-09-30	Completed
An 18-week, Randomized, Multicenter, Phase 3b, Double-blind, Crossover Study, Followed by an 18-week Open-Label Period to Evaluate the Efficacy & Safety of the Lipid-Regulating Agents, Rosuvastatin & Pravastatin in the Treatment of Subjects With Dysbetali [NCT00214604]	Phase 3	30 participants	Interventional	2005-02-28	Completed
The Role of Androgen Deprivation Therapy In Cardiovascular Disease - A Longitudinal Prostate Cancer Study (RADICAL PC1) & A RAndomizeD Intervention for Cardiovascular and Lifestyle Risk Factors in Prostate Cancer Patients (RADICAL PC2) [NCT03127631]		6,000 participants (Anticipated)	Interventional	2015-10-21	Recruiting
Cyclosporine Modulation of Drug Resistance in Combination With Pravastatin, Mitoxantrone, and Etoposide for Adult Patients With Relapsed/Refractory Acute Myeloid Leukemia (AML): A Phase 1/2 Study [NCT01342887]	Phase 1/Phase 2	6 participants (Actual)	Interventional	2011-04-30	Terminated
Pravastatin Therapy in Patients With Active Crohn's Disease: A Pilot Study [NCT00599625]		40 participants (Anticipated)	Interventional	2004-10-31	Recruiting
Aggressive Treatment of Metabolic Syndrome in Patients Treated With Clozapine for Schizophrenia [NCT00794963]		8 participants (Actual)	Interventional	2008-11-30	Terminated(stopped due to Difficulty recruiting)
Naturopathic Treatment for the Prevention of Cardiovascular Disease: a Pragmatic Randomized Controlled Trial [NCT00718796]	Phase 3	300 participants (Anticipated)	Interventional	2008-04-30	Completed
A 4-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study Evaluating the Efficacy and Safety of JTT-705 (300 mg or 600 mg) Versus Placebo in Combination With Pravastatin 40 mg in Patients With Type II Hyperlipidemia [NCT00688896]	Phase 2	155 participants (Actual)	Interventional	2002-06-30	Completed
Effect of Pravastatin in the Subjects With Prediabetes or Early Diabetes [NCT02754739]	Phase 4	44 participants (Actual)	Interventional	2014-04-15	Completed
A Two-Way Crossover, Open-Label, Single-Dose, Fed, Bioequivalence Study of Pravastatin Sodium 80 mg Tablets Versus Pravachol® 80 mg Tablets In Normal Healthy Non-Smoking Male and Female Subjects [NCT00648544]	Phase 1	44 participants (Actual)	Interventional	2003-07-31	Completed
Pravastatin for the Prevention of Preeclampsia in High-Risk Women: A Phase I Pilot Study [NCT01717586]	Phase 1	48 participants (Actual)	Interventional	2012-08-31	Active, not recruiting
Statin Therapy in Patients With Early Stage ADPKD [NCT03273413]	Phase 4	150 participants (Actual)	Interventional	2017-08-31	Active, not recruiting
Statins and Noncardiovascular Endpoints [NCT00330980]	Phase 4	1,000 participants (Anticipated)	Interventional	2000-04-30	Completed
Phase-II, Multicenter, Randomized, Double-Blind, Parallel-Group Trial to Compare the Efficacy and Safety of Sorafenib Plus Pravastatin Against Sorafenib Plus Placebo in Patients With Advanced Hepatocarcinoma [NCT01418729]	Phase 2	216 participants (Actual)	Interventional	2011-09-30	Completed
Effects of GSK3640254 on the Single-Dose Pharmacokinetics of Probe Substrates (Caffeine, Metoprolol, Montelukast, Flurbiprofen, Omeprazole, Midazolam, Digoxin, and Pravastatin) in Healthy Subjects [NCT04425902]	Phase 1	20 participants (Actual)	Interventional	2020-12-16	Completed
The Effect of Pravastatin on the Incidence and in the Natural Course of Ventilatory Associated Pneumonia in the Intensive Care Unit Patients [NCT00702130]	Early Phase 1	152 participants (Actual)	Interventional	2008-06-30	Completed
Safety and Efficacy of Pravastatin in Relapsing-remitting MS: a Double Blind Placebo Controlled Study [NCT00200655]	Phase 3	40 participants (Actual)	Interventional	2004-12-31	Completed
[NCT01856374]	Phase 4	60 participants (Actual)	Interventional	2011-08-31	Completed
[NCT01857843]	Phase 4	160 participants (Actual)	Interventional	2009-11-30	Completed
[NCT01857921]		290 participants (Actual)	Interventional	2010-12-31	Completed
Pravastatin in HIV-Infected Patients Treated With Highly Active Antiretroviral Therapy [NCT00221754]	Phase 2	21 participants (Actual)	Interventional	2003-03-31	Completed
[NCT01872845]		671 participants (Actual)	Interventional	2013-06-12	Completed
A Randomized Controlled Trial of Pravastatin to Prevent Preeclampsia in High Risk Women [NCT03944512]	Phase 3	1,550 participants (Anticipated)	Interventional	2019-07-17	Active, not recruiting
Left Ventricular Hypertrophy Reduction With Statins in Hypertensives Patients. [NCT00738972]	Phase 3	12 participants (Actual)	Interventional	2008-01-31	Terminated(stopped due to Study terminated early due to sample size, not possible to perform further statistical analysis.)
A Single-dose Pilot Study to Evaluate the Pharmacokinetics of Pravastatin Given as an Oral Dose in Pediatric and Adolescent Subjects 12 Months to 16 Years of Age Receiving Continuous Cycling Peritoneal Dialysis [NCT00571194]	Phase 1	7 participants (Actual)	Interventional	2007-09-30	Terminated
A RANDOMIZED, DOUBLE-BLIND, ACTIVE CONTROLLED, PARALLEL GROUP STUDY OF PITAVASTATIN 4 MG VS. PRAVASTATIN 40 MG IN PATIENTS WITH PRIMARY HYPERLIPIDEMIA OR MIXED DYSLIPIDEMIA [NCT01256476]	Phase 4	328 participants (Actual)	Interventional	2010-10-31	Completed
Statin Recapture Therapy Before Coronary Artery Bypass Grafting [NCT01715714]	Phase 4	2,630 participants (Actual)	Interventional	2012-11-07	Completed
Red Yeast Rice vs. Pravastatin: A Double-Blind Randomized Comparative Study of Myopathic Symptoms [NCT00639223]	Phase 2	43 participants (Actual)	Interventional	2008-01-31	Completed
An Interventional Trial in Established Chronic Renal Allograft Rejection [NCT00005010]	Phase 3	0 participants	Interventional		Completed
Effect of an Oxidative-Stress-Reducing Strategy Consisting of Pravastatin, Vitamin E and Homocysteine-Lowering on Carotid Intima-Media Thickness in Patients With Mild-to-Moderate Chronic Kidney Disease [NCT00384618]	Phase 4	100 participants	Interventional	2001-05-31	Terminated
Effect of Pravastatin on Erythrocyte Membrane Fatty Acid Contents in Patients With Chronic Kidney Disease [NCT02992548]	Phase 4	62 participants (Actual)	Interventional	2015-09-30	Completed
The Reduction Effect of Oral Pravastatin on Acute Phase Response of Intravenous Zoledronic Acid: a Real-world Study [NCT04719481]	Phase 4	110 participants (Anticipated)	Interventional	2021-11-30	Not yet recruiting
A Phase I Trial Evaluating the Effect of the Addition of HMGCoA-Reductase Inhibition With Pravastatin to Salvage Chemotherapy Idarubicin-HDAC in Patients With Relapsed or Refractory Acute Myelogenous Leukemia [NCT00107523]	Phase 1	0 participants	Interventional	2005-01-31	Completed
Do HMG CoA Reductase Inhibitors Affect Abeta Levels? [NCT00303277]	Phase 4	35 participants (Actual)	Interventional	2002-08-31	Completed
A Multicentre Phase III Randomized Double Blind Placebo Controlled Trial of Pravastatin Added to First-Line Standard Chemotherapy in Patients With Small Lung Cancer [NCT00433498]	Phase 3	846 participants (Actual)	Interventional	2007-01-31	Completed
The Effect of Statins on the Urinary Proteome [NCT00464503]		7 participants (Actual)	Interventional	2007-09-30	Completed
Randomised Comparative Study of the Efficacy and Safety of Rosuvastatin and Pravastatin in Dyslipidemic Patients Treated With Antiretroviral Agents. Anrs 126 [NCT00117494]	Phase 4	86 participants	Interventional	2005-10-31	Completed
Effects of Atorvastatin Versus Pravastatin on Platelet Inhibition by Clopidogrel in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention [NCT00405717]	Phase 4	1,300 participants (Anticipated)	Interventional	2006-02-28	Completed
A Randomized Controlled Trial to Compare the Effects of Highly Active Antiretroviral Therapy (HAART) Versus Statin Therapy on Endothelial Function and Markers of Inflammation/Coagulation In HIV-Infected Individuals With High CD4 Cell Counts [NCT01515813]	Phase 2	0 participants (Actual)	Interventional	2011-11-30	Withdrawn(stopped due to On 05/08/12, team working on revising protocol and re-open study under version 2.0)
[NCT00000461]	Phase 2	0 participants	Interventional	1986-12-31	Completed
[NCT00000539]	Phase 3	0 participants	Interventional	1992-09-30	Completed
Evaluation of Potential Pharmacokinetic Interactions Between Protease Inhibitors and Lipid Lowering Agents [NCT00000941]	Phase 1	56 participants	Interventional		Completed
Pilot Study to Evaluate the Tolerability of Velcade (Bortezomib) and Pravastatin for the Treatment of Relapsed Leukemia Following Allogeneic Hematopoietic Stem Cell Transplantation in Children [NCT02484261]	Phase 1	10 participants (Actual)	Interventional	2015-05-31	Terminated(stopped due to Contractual/Funding/Accrual)
Endothelial Dysfunction as a Risk Factor in HIV Study [NCT00039663]	Phase 1	75 participants	Interventional	2002-05-31	Completed
Management of Elevated Cholesterol in the Primary Prevention Group of Adult Japanese(MEGA Study) [NCT00211705]	Phase 4	8,000 participants	Interventional	1994-02-28	Completed
Effects of Combined Ventricular Unloading and Pharmacological Therapy on Left Ventricular Metabolic Dysfunction in Heart Failure [NCT00402376]	Phase 4	20 participants (Anticipated)	Interventional	2007-04-30	Terminated
A Randomized Controlled Trial of Strategies for the Prevention of Accelerated Atherosclerosis in Systemic Lupus Erythematosus - A Pilot Study [NCT00054938]	Phase 2	150 participants	Interventional	2003-03-31	Completed
A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial of Adjunctive Treatment With Pravastatin in Partially Remitted Patients With Schizophrenia or Schizoaffective Disorder [NCT00177580]	Phase 4	72 participants (Anticipated)	Interventional	2003-07-31	Completed
A Randomised, Double-Blind Study of Pravastatin for the Treatment of Hyperlipidaemia in Patients With HIV [NCT00227500]	Phase 4	40 participants	Interventional	2001-07-31	Completed
Effect of Statin Use on Aldosterone Secretion [NCT02871687]	Phase 1	103 participants (Actual)	Interventional	2016-04-30	Completed
A Phase 1, Three-Part, Open-label Study in Healthy Adult Volunteers to Assess Vadadustat as a Perpetrator in Drug-Drug Interactions With Rosuvastatin, Sulfasalazine, Pravastatin, Atorvastatin and Simvastatin [NCT03801733]	Phase 1	134 participants (Actual)	Interventional	2018-06-17	Completed
Study Of Pitavastatin 1 Mg Vs. Pravastatin 10 Mg, Pitavastatin 2 Mg Vs. Pravastatin 20 Mg And Pitavastatin 4 Mg Vs. Pravastatin 40 Mg (Following Up-Titration) In Elderly Patients With Primary Hypercholesterolemia Or Combined Dyslipidemia [NCT00257686]	Phase 3	962 participants (Actual)	Interventional	2005-09-30	Completed
Incident Type II Diabetes Mellitus Among Patients Exposed to the Combination of Pravastatin and Paroxetine [NCT01602913]		1 participants (Actual)	Observational	2011-12-31	Completed
Cardiovascular Risk Markers Before and After Therapy With Statins in Patients With History of Kawasaki Disease [NCT00305201]	Phase 2	0 participants (Actual)	Interventional	2006-04-30	Withdrawn(stopped due to Withdrawn due to lack of study participants)
The Pharmacokinetic Interaction Between Pravastatin and Cyclosporine in Healthy Volunteers [NCT01497483]	Phase 1	21 participants (Actual)	Interventional	2011-12-31	Completed
[NCT01502904]	Phase 4	120 participants (Actual)	Interventional	2010-07-31	Completed
A Multicenter, Prospective, Non-interventional Observational Study to Investigate the Change in Blood Cholesterol With Mevalotin® Tablet Administration in Korean Menopausal Women Aged 50 Years or More Who Require Treatment of Dyslipidemia [NCT05120895]		2,467 participants (Anticipated)	Observational	2021-08-10	Recruiting
Open Label Study for the Functional Characterization of Drug Metabolism and Transport [NCT01788254]	Phase 1	144 participants (Actual)	Interventional	2012-01-31	Completed
The Influence of Statins on Glucose Homeostasis and the Biomarkers of Diabetes in Subjects With Impaired Fasting Glucose [NCT01816997]	Phase 4	160 participants (Anticipated)	Interventional	2012-01-31	Recruiting
Open Label Repeated Dose Study for the Evaluation of Heritability of and Genetic Influences on Drug Pharmacokinetics (TWINS II) [NCT01845194]	Phase 1	117 participants (Actual)	Interventional	2009-12-31	Completed
Assessment of the Efficacy of Lipid-lowering Agents to Limit Lipid Oxidation and Activation of the Clotting System in Patients With the Nephrotic Syndrome: a Pilot Study. [NCT01845428]	Phase 1	7 participants (Actual)	Interventional	2012-05-31	Completed
Effects of BMS-986142 on the Single-dose Pharmacokinetics of Methotrexate and Probe Substrates Montelukast (CYP2C8), Flurbiprofen (CYP2C9), Midazolam (CYP3A4), Digoxin (P-gp), and Pravastatin (OATP1B1) in Healthy Subjects [NCT02456844]	Phase 1	24 participants (Actual)	Interventional	2015-05-31	Completed
Idarubicin, Cytarabine and Pravastatin (IAP) for Induction of Newly Diagnosed Acute Myeloid Leukemia (AML) [NCT01831232]		24 participants (Actual)	Interventional	2013-05-31	Completed
Determining Cardiovascular Health Using a Multi-Analyte Profile in a Longitudinal Study of a Statin Intervention for Dyslipidemia [NCT01441908]		40 participants (Anticipated)	Interventional	2011-06-30	Active, not recruiting
Cardiovascular Disease Risk Reduction for Persons With HIV Infection: a Polypill Pilot Study [NCT00982189]		37 participants (Actual)	Interventional	2009-09-30	Completed
Pharmacodynamics, Preliminary Pharmacokinetics and Tolerability After Multiple Oral Doses of 0.25 mg, 0.5 mg and 1 mg o.d. BIBB 1464 (Tablet) or Pravastatin 20 mg Over 2 Weeks in Hyperlipemic Healthy Male Subjects (Parallel Group Comparison, Randomized, P [NCT02229773]	Phase 1	100 participants (Actual)	Interventional	2000-01-31	Completed
Evaluation of the Efficacy and Safety of Rosuvastatin 5 mg Versus Pravastatin 40 mg and Atorvastatin 10 mg in Subjects With Type IIa and IIb Hypercholesterolaemia [NCT00631189]	Phase 4	668 participants (Actual)	Interventional	2007-10-31	Completed
AuTophagy Activation for Cardiomyopathy Due to Anthracycline tReatment (ATACAR) Trial [NCT04190433]	Phase 2	0 participants (Actual)	Interventional	2020-09-01	Withdrawn(stopped due to Administratively closed due to low/no accrual)
Effects of High-dose Statin Treatments on Patients With Aspirin Mono Antiplatelet Therapy 12-months After Drug-eluting Stents Implantation: a Randomized Controlled Study [NCT01557075]	Phase 4	2,000 participants (Anticipated)	Interventional	2010-07-31	Recruiting
HDL Increased Plaque Stabilization in the Elderly [NCT00127218]	Phase 3	145 participants (Actual)	Interventional	2003-09-30	Completed
[NCT00000542]	Phase 3	0 participants	Interventional	1993-08-31	Completed
A Prospective, Randomized, Double-Blind, Multi-Center Study Comparing the Effects of Atorvastatin Versus Pravastatin on the Progression and Quantification of Coronary Atherosclerotic Lesions as Measured by Intravascular Ultrasound (REVERSAL) [NCT00380939]	Phase 4	600 participants	Interventional	1999-04-30	Completed
Statin Adjunctive Therapy for TB (StAT- TB) [NCT03456102]	Phase 2	16 participants (Actual)	Interventional	2020-03-09	Completed
Pharmacokinetics of Pravastatin and Simvastatin in Pediatric Dyslipidemia Patients: Clinical Impact of Genetic Variation in Statin Disposition [NCT02360826]	Phase 1	32 participants (Actual)	Interventional	2014-06-17	Completed
A Randomized, Open-label, Multiple-dose, Parallel Study to Investigate The Effect of Cilostazol on the Disposition of Simvastatin in Healthy Male Volunteers [NCT02431013]	Phase 1	20 participants (Anticipated)	Interventional	2015-04-30	Recruiting
An Open Label Phase II Trial of Zoledronic Acid, Pravastatin, and Lonafarnib for Patients With Hutchinson-Gilford Progeria Syndrome(HGPS) and Progeroid Laminopathies [NCT00916747]	Phase 2	85 participants (Actual)	Interventional	2009-08-31	Active, not recruiting
[NCT00005117]		0 participants	Interventional		Active, not recruiting
A Randomized, Double-blind Study of the Effect of RO4607381 in Combination With Pravastatin on HDL-cholesterol (HDL-C) Levels in Patients With Low or Average HDL-C Levels [NCT00697203]	Phase 2	292 participants (Actual)	Interventional	2005-07-31	Completed
Phase 4 Study of the Effects of Pravastatin on Cholesterol Levels, Inflammation and Cognition in Schizophrenia [NCT01082588]	Phase 4	60 participants (Actual)	Interventional	2010-06-30	Completed
Effect of Statins on Oxidative Stress and Endothelial Progenitor Cells: Comparison of Atorvastatin With Pravastatin [NCT00166036]	Phase 2	36 participants (Actual)	Interventional	2004-09-30	Completed
A Phase 2 Efficacy and Safety Dose-Ranging Study of LY3015014 in Patients With Primary Hypercholesterolemia [NCT01890967]	Phase 2	527 participants (Actual)	Interventional	2013-06-30	Completed
Effect of Evacetrapib on the Pharmacokinetics of Pravastatin in Healthy Japanese and Non-Japanese Subjects [NCT01958489]	Phase 1	24 participants (Actual)	Interventional	2013-10-31	Completed
A Phase II Pilot Study of Zoledronic Acid, Pravastatin, and Lonafarnib (SCH66336) for Patients With Hutchinson-Gilford Progeria Syndrome (HGPS) and Progeroid Laminopathies [NCT00879034]	Phase 2	5 participants (Actual)	Interventional	2009-03-31	Completed
A Multi-center, Prospective Observational Study to Investigate the Effectiveness of Pravastatin on Renal Function in Korean Dyslipidemic Patients With Type 2 Diabetes [NCT05107063]		2,972 participants (Actual)	Observational	2016-01-20	Completed
Genetic Predictors of Pharmacokinetic Variability in the Drug-drug Interaction Between Darunavir/Ritonavir and Pravastatin: the Role of SLCO1B1 Polymorphisms. [NCT00630734]	Phase 4	32 participants (Actual)	Interventional	2008-02-29	Completed
Dapagliflozin Effect in Cognitive Impairment in Stroke Trial [NCT05565976]	Phase 2/Phase 3	270 participants (Anticipated)	Interventional	2020-08-01	Recruiting
Pilot Trial of Pravastatin as a Novel Prophylactic Medicine to Reduce Endothelial Injury in Pediatric Patients With Elevated Body Mass Index [NCT05524246]	Phase 1	20 participants (Anticipated)	Interventional	2023-01-27	Recruiting
Efficacy and Safety of Prescription Omega-3 Fatty Acid Added to Stable Statin Therapy in Patients With Type 2 Diabetes and Hypertriglyceridemia [NCT02305355]	Phase 4	68 participants (Actual)	Interventional	2009-02-28	Completed
Impact of Metformin and Polysorbate 80 on Drug Absorption and Disposition [NCT04640571]	Phase 4	18 participants (Actual)	Interventional	2021-04-01	Completed
A Multicenter, Double-Blind, Randomized, Forced-Titration Study to Compare the Efficacy and Safety of the Combination of 145 mg Fenofibrate and 20 or 40 mg Simvastatin With 40 mg Pravastatin Monotherapy in Patients With Mixed Dyslipidemia at Risk of Cardi [NCT00362206]	Phase 3	423 participants (Actual)	Interventional	2006-09-30	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00127218 (2) [back to overview]	Multiple Combined Events ( Cardiovascular and Cerebrovascular Events as Well as Myocardial Revascularization)
NCT00127218 (2) [back to overview]	Changes in Plaque Architecture and Composition Directly Measured by Magnetic Resonance Imaging (MRI) in the Aorta and Carotid Arteries
NCT00166036 (2) [back to overview]	Change in Plasma Thiobarbituric Acid Reactive Substance (TBARS) Levels
NCT00166036 (2) [back to overview]	Change in Flow-mediated Dilatation (FMD)
NCT00221104 (5) [back to overview]	Incidence Rate of Stroke and TIA
NCT00221104 (5) [back to overview]	Incidence Rate of Lacunar Infarction
NCT00221104 (5) [back to overview]	Incidence Rate of Intracranial Hemorrhage
NCT00221104 (5) [back to overview]	Incidence Rate of Atherothrombotic Infarction
NCT00221104 (5) [back to overview]	Incidence Rate of Cardioembolic Infarction
NCT00257686 (2) [back to overview]	Percent Change From Baseline in TC
NCT00257686 (2) [back to overview]	Percent Change From Baseline in LDL-C
NCT00456365 (4) [back to overview]	Percent of Participants Demonstrating 20% or More Increase in Total Kidney Volume
NCT00456365 (4) [back to overview]	Urinary Albumin Excretion
NCT00456365 (4) [back to overview]	Percentage Change in Total Kidney Volume Corrected for Height
NCT00456365 (4) [back to overview]	Left Ventricular Mass Index
NCT00467831 (1) [back to overview]	Survival at 2 Years
NCT00630734 (10) [back to overview]	Darunavir Maximum Plasma Concentration (Cmax)
NCT00630734 (10) [back to overview]	Ritonavir Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval
NCT00630734 (10) [back to overview]	Relative Change in Pravastatin Maximum Plasma Concentration (Cmax)
NCT00630734 (10) [back to overview]	Relative Change in Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval
NCT00630734 (10) [back to overview]	Pravastatin Alone: Pravastatin Maximum Plasma Concentration (Cmax)
NCT00630734 (10) [back to overview]	Pravastatin Alone: Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval
NCT00630734 (10) [back to overview]	Darunavir Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval
NCT00630734 (10) [back to overview]	Pravastatin + Darunavir/Ritonavir: Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval
NCT00630734 (10) [back to overview]	Pravastatin + Darunavir/Ritonavir: Pravastatin Maximum Plasma Concentration (Cmax)
NCT00630734 (10) [back to overview]	Ritonavir Maximum Plasma Concentration (Cmax)
NCT00631189 (9) [back to overview]	Compare the Percentage of Variation From Baseline Apolipoprotein B/Apolipoprotein A1 Ratio and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]	To Evaluate Clinical and Laboratory Safety
NCT00631189 (9) [back to overview]	Compare the Percentage of Total Cholesterol Variation From Baseline and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]	Compare the Percentage of HDL-C (High Density Lipoprotein Cholesterol) Variation From Baseline and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]	Change in Low Density Lipoprotein Cholesterol (LDL-C) Level After 8 Weeks
NCT00631189 (9) [back to overview]	Compare the Numbers of Patients Achieving the LDL-C Goal According to the National Cholesterol Education Program Adult Treatment Panel III (NCEP) ATP III) Guidelines for the Management of Dyslipidaemic Patients
NCT00631189 (9) [back to overview]	Compare the Percentage of Variation of Phospholipase A2 (PLA2)
NCT00631189 (9) [back to overview]	Compare the Percentage of Variation of C-reactive Protein (CRP)
NCT00631189 (9) [back to overview]	Compare the Percentage of Variation From Baseline Triglycerides Values and After 8 Weeks
NCT00639223 (2) [back to overview]	Withdrawal of Therapy Due to Muscle Symptoms That Are Either Intolerable and/or Associated With a Creatine Kinase(CK) >500
NCT00639223 (2) [back to overview]	Change in LDL-Cholesterol Measured at the Beginning and End of the Study
NCT00652327 (1) [back to overview]	Percentage Change in Low Density Lipoprotein-Cholesterol (LDL-C) From Baseline at Study Endpoint, After 8 Weeks of Treatment
NCT00697203 (5) [back to overview]	Percent Change of Fasting Glucose Level
NCT00697203 (5) [back to overview]	Change From Baseline in: Total Cholesterol, Triglycerides, HDL-C, LDL-C, HDL-2, HDL-3, ApoA1, ApoA2, ApoB, LpAI
NCT00697203 (5) [back to overview]	Percent Change From Baseline in HDL-C Level\
NCT00697203 (5) [back to overview]	Absolute Change From Baseline in HDL-C Level\
NCT00697203 (5) [back to overview]	Ratios of Total HDL-C/LDL-C, HDL-2/HDL-3, ApoA1/ApoB
NCT00794963 (1) [back to overview]	Change in Weight
NCT00829309 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00829309 (3) [back to overview]	Cmax - Maximum Observed Concentration - Pravastatin in Plasma
NCT00829309 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00830258 (3) [back to overview]	AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)
NCT00830258 (3) [back to overview]	Cmax - Maximum Observed Concentration - Pravastatin in Plasma
NCT00830258 (3) [back to overview]	AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)
NCT00840177 (4) [back to overview]	Overall Survival (OS)
NCT00840177 (4) [back to overview]	Relapse-free Survival (RFS)
NCT00840177 (4) [back to overview]	Frequency and Severity of Toxicity as Assessed by NCI CTCAE Version 3.0
NCT00840177 (4) [back to overview]	Complete Remission (CR) Rate (Including CR With Incomplete Recovery)
NCT00850460 (2) [back to overview]	Individualized Short Form-36 (SF-36) Mean Scores (Physical Component) From Week 0 to Week 8
NCT00850460 (2) [back to overview]	Individualized Neuromuscular Quality of Life (INQoL) Mean Scores From Week 0 to Week 8
NCT00879034 (4) [back to overview]	The Primary Objective of This Study is to Evaluate the Feasibility of Administering Intravenous Zoledronic Acid, Oral Pravastatin and Oral Lonafarnib, to Patients With Progeria for a Minimum of 4 Weeks
NCT00879034 (4) [back to overview]	To Investigate Which Clinical and Laboratory Studies Are Needed to Monitor or Alter Therapy to Prevent Unacceptable Toxicity
NCT00879034 (4) [back to overview]	To Describe Any Acute and Chronic Toxicities Associated With Treating Progeria Patients With the Combination of Zoledronic Acid, Pravastatin and Lonafarnib
NCT00879034 (4) [back to overview]	To Obtain Baseline Clinical and Laboratory Data so That Longer-term Measures of Efficacy Will be Achievable if Treatment Continues Beyond the 4-week Feasibility Study Period.
NCT00982189 (9) [back to overview]	Change From Baseline to Month 4 in the Framingham Risk Score (FRS)
NCT00982189 (9) [back to overview]	Changes hsCRP (C-reactive Protein)
NCT00982189 (9) [back to overview]	Changes IL-6 (Interleukin-6)
NCT00982189 (9) [back to overview]	Changes in Small Artery Elasticity
NCT00982189 (9) [back to overview]	Changes TNFa (Tumor Necrosis Factor Alpha)
NCT00982189 (9) [back to overview]	Number of Participants Who Stated (by Self-report) That They Had Side Effects
NCT00982189 (9) [back to overview]	Number of Participants Who Took >90% of Their Doses (by Pill Count)
NCT00982189 (9) [back to overview]	Changes in Blood Lipids
NCT00982189 (9) [back to overview]	Changes in Blood Pressure
NCT01082588 (7) [back to overview]	Change in C-Reactive Protein (CRP) From Baseline to Week 12
NCT01082588 (7) [back to overview]	Change in LDL-cholesterol Between Baseline and Week 12
NCT01082588 (7) [back to overview]	Change in MATRICS Neuropsychological Battery Composite Score From Baseline to Week 12
NCT01082588 (7) [back to overview]	Change in Positive and Negative Syndrome Scale (PANSS) General Score From Baseline to Week 12
NCT01082588 (7) [back to overview]	Change in Positive and Negative Syndrome Scale (PANSS) Negative Score From Baseline to Week 12
NCT01082588 (7) [back to overview]	Change in Positive and Negative Syndrome Scale (PANSS) Positive Score From Baseline to Week 12
NCT01082588 (7) [back to overview]	Change in Positive and Negative Syndrome Scale (PANSS) Total Score From Baseline to Week 12
NCT01256476 (1) [back to overview]	Mean Percent Change in Low Density Lipoprotein Cholesterol(LDL-C) From Baseline to Week 12
NCT01301066 (1) [back to overview]	Change of Fasting Serum Low-density Lipoprotein Cholesterol (LDL-C) at 12 Weeks
NCT01342887 (1) [back to overview]	Maximum Tolerated Doses Mitoxantrone Hydrochloride and Etoposide When Combined With Cyclosporine and Pravastatin Sodium
NCT01831232 (6) [back to overview]	Number of Biomarker-positive Participants With Clinical Responses
NCT01831232 (6) [back to overview]	Number of Participants With Good Complete Remission (CR)
NCT01831232 (6) [back to overview]	Number of Participants With TRM.
NCT01831232 (6) [back to overview]	Overall Survival
NCT01831232 (6) [back to overview]	Rate of Complete Remission (CR), Remission With Incomplete Blood Count Recovery (CRi) and Partial Remission (PR)
NCT01831232 (6) [back to overview]	Progression Free Survival (PFS)
NCT01890967 (10) [back to overview]	Number of Participants With an Injection Site Reaction
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in Lipoprotein(a) [Lp(a)]
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C)
NCT01890967 (10) [back to overview]	Change From Baseline in High Sensitivity C-Reactive Protein (hsCRP)
NCT01890967 (10) [back to overview]	Pharmacokinetics (PK): Area Under the Concentration-Time Curve at Steady-State (AUC,ss) for LY3015014
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in Apolipoprotein A1 (Apo A1), Apolipoprotein B (Apo B)
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in LDL-C, Total Cholesterol (TC), High-Density Lipoprotein Cholesterol (HDL-C), Triglycerides (TG), Non-HDL-C
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in Free Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
NCT01890967 (10) [back to overview]	Percentage Change From Baseline in Total Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
NCT01890967 (10) [back to overview]	Number of Participants Who Develop Treatment Emergent Anti-LY3015014 Antibodies
NCT01958489 (3) [back to overview]	Pharmacokinetics (PK): Maximum Concentration (Cmax) of Pravastatin
NCT01958489 (3) [back to overview]	PK: Area Under the Concentration Versus Time Curve From Time Zero to Infinity [AUC(0-∞)] of Pravastatin
NCT01958489 (3) [back to overview]	PK: Time of Maximum Observed Concentration (Tmax) of Pravastatin
NCT02841774 (2) [back to overview]	Treatment-emergent Adverse Events
NCT02841774 (2) [back to overview]	Mean Percent Change in Fasting LDL-cholesterol
NCT03456102 (1) [back to overview]	Safety of Escalating Doses of Pravastatin as Assessed by Number of Adverse Events
NCT03510715 (13) [back to overview]	Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Lipoprotein a (Lp) (a) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Weeks 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Weeks 12, 24 and 48 - ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Total Cholesterol (Total-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percentage of Participants Reporting >=15 Percent (%) Reduction in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12: Intent-to-Treat (ITT) Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Week 12: On-treatment Analysis
NCT03510715 (13) [back to overview]	Absolute Change From Baseline in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Number of Participants With Tanner Staging at Baseline, Weeks 12, 24 and 48
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Apolipoprotein (Apo) B at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]	Percent Change From Baseline in Fasting Triglycerides (TG) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein A1 at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 110 mg/dL (2.84 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	Number of Participants With Tanner Staging at Baseline and Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]	DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved at Least 30 Percent (%) Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 130 mg/dL (3.37 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Achieved at Least 30% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Total Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Weeks 12, and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Lipoprotein (a) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Fasting Triglycerides at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein B at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Apolipoprotein A1 at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]	DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]	DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]	Change From Baseline in Cogstate Battery Test - Overall Composite Score at Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]	OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: On-treatment Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level Lower Than (<) 130 mg/dL (3.37 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level <130 mg/dL (3.37 mmol/L) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Total Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 24: Intent-to-treat (ITT) Estimand
NCT03510884 (44) [back to overview]	DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 24: ITT Estimand
NCT03882177 (2) [back to overview]	Number of Participants Who Permanently Discontinue Assigned Study Regimen for Any Reason
NCT03882177 (2) [back to overview]	Frequency of Grade 3 or Higher Adverse Events
NCT04425902 (171) [back to overview]	Cmax for Montelukast
NCT04425902 (171) [back to overview]	Cmax for Omeprazole
NCT04425902 (171) [back to overview]	Cmax for Pravastatin
NCT04425902 (171) [back to overview]	Maximum Observed Plasma Concentration (Cmax) for Caffeine
NCT04425902 (171) [back to overview]	Ratio of AUC(0-infinity) of 1-hydroxymidazolam to Midazolam
NCT04425902 (171) [back to overview]	Ratio of AUC(0-infinity) of 36-hydroxymontelukast to Montelukast
NCT04425902 (171) [back to overview]	Ratio of AUC(0-infinity) of 5-hydroxyomeprazole to Omeprazole
NCT04425902 (171) [back to overview]	Ratio of AUC(0-infinity) of Alpha-hydroxymetoprolol to Metoprolol
NCT04425902 (171) [back to overview]	Ratio of Cmax of 1-hydroxymidazolam to Midazolam
NCT04425902 (171) [back to overview]	Ratio of Cmax of 36-hydroxymontelukast to Montelukast
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Erythrocytes
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Hematocrit
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Hemoglobin
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Oral Temperature
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Pulse Rate
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment C: AUC From Time Zero to the End of the Dosing Interval at Steady State (AUC[0-tau]) for GSK3640254
NCT04425902 (171) [back to overview]	Treatment C: AUC(0-t) for GSK3640254
NCT04425902 (171) [back to overview]	Treatment C: Cmax for GSK3640254
NCT04425902 (171) [back to overview]	Treatment C: Plasma Concentration at the End of the Dosing Interval (Ctau) for GSK3640254
NCT04425902 (171) [back to overview]	Treatment C: t1/2 for GSK3640254
NCT04425902 (171) [back to overview]	Treatment C: Tmax for GSK3640254
NCT04425902 (171) [back to overview]	Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values for Electrocardiogram (ECG) Parameters: PR Interval, QRS Duration, QT Interval, Corrected QT Interval Using Fridericia's Formula (QTcF)
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Creatine Kinase, Lactate Dehydrogenase, Alanine Aminotransferase (ALT), Alkaline Phosphatase (ALP), Aspartate Aminotransferase (AST), Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Erythrocytes
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Hematocrit
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Hemoglobin
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Oral Temperature
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Pulse Rate
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
NCT04425902 (171) [back to overview]	Treatment A: Absolute Values of Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Creatine Kinase, Lactate Dehydrogenase, ALT, ALP, AST, Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in ECG Parameters: PR Interval, QRS Duration, QT Interval, QTcF
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in SBP and DBP
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values for ECG Parameters: PR Interval, QRS Duration, QT Interval, QTcF Interval
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Creatine Kinase, Lactate Dehydrogenase, ALT, ALP, AST, Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Erythrocytes
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Hematocrit
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Hemoglobin
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Oral Temperature
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Pulse Rate
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of SBP and DBP
NCT04425902 (171) [back to overview]	Treatment B: Absolute Values of Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Creatine Kinase, Lactate Dehydrogenase, ALT, ALP, AST, Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in ECG Parameters: PR Interval, QRS Duration, QT Interval, QTcF
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in SBP and DBP
NCT04425902 (171) [back to overview]	Treatment B: Change From Baseline in Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values for ECG Parameters: PR Interval, QRS Duration, QT Interval, QTcF Interval
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Creatine Kinase, Lactate Dehydrogenase, ALT, ALP, AST, Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Erythrocytes
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Hematocrit
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Hemoglobin
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Oral Temperature
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Pulse Rate
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of SBP and DBP
NCT04425902 (171) [back to overview]	Treatment C: Absolute Values of Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Albumin, Globulin, Protein
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Amylase, Lipase
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Creatine Kinase, Lactate Dehydrogenase, ALT, ALP, AST, Gamma-glutamyl Transferase
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in ECG Parameters: PR Interval, QRS Duration, QT Interval, QTcF
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Oral Temperature
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Glucose, Carbon Dioxide, Cholesterol, Triglycerides, Anion Gap, Calcium, Chloride, Phosphate, Potassium, Sodium, Urea
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Hematocrit
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Hemoglobin
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Oral Temperature
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Platelet Count, Leukocyte Count, Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Pulse Rate
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Respiratory Rate
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in SBP and DBP
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Urate, Creatinine, Bilirubin, Direct Bilirubin
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Hemoglobin
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Erythrocytes Mean Corpuscular Volume
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Erythrocytes Mean Corpuscular Hemoglobin
NCT04425902 (171) [back to overview]	Apparent Terminal Phase Half-life (t1/2) for Caffeine
NCT04425902 (171) [back to overview]	Area Under the Plasma Concentration-time Curve (AUC) From Time Zero to Time t (AUC[0-t]) for Caffeine
NCT04425902 (171) [back to overview]	AUC From Time Zero Extrapolated to Infinity (AUC[0-infinity]) for Caffeine
NCT04425902 (171) [back to overview]	AUC(0-infinity) for 1-hydroxymidazolam
NCT04425902 (171) [back to overview]	AUC(0-infinity) for 36-hydroxymontelukast
NCT04425902 (171) [back to overview]	AUC(0-infinity) for 5-hydroxyomeprazole
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Alpha-hydroxymetoprolol
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Digoxin
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Flurbiprofen
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Erythrocytes
NCT04425902 (171) [back to overview]	Tmax for Pravastatin
NCT04425902 (171) [back to overview]	Tmax for Omeprazole
NCT04425902 (171) [back to overview]	Tmax for Montelukast
NCT04425902 (171) [back to overview]	Tmax for Midazolam
NCT04425902 (171) [back to overview]	Tmax for Metoprolol
NCT04425902 (171) [back to overview]	Tmax for Flurbiprofen
NCT04425902 (171) [back to overview]	Tmax for Digoxin
NCT04425902 (171) [back to overview]	Tmax for Alpha-hydroxymetoprolol
NCT04425902 (171) [back to overview]	Tmax for 5-hydroxyomeprazole
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Pulse Rate
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Metoprolol
NCT04425902 (171) [back to overview]	Tmax for 36-hydroxymontelukast
NCT04425902 (171) [back to overview]	Tmax for 1-hydroxymidazolam
NCT04425902 (171) [back to overview]	Time to Cmax (Tmax) for Caffeine
NCT04425902 (171) [back to overview]	t1/2 for Pravastatin
NCT04425902 (171) [back to overview]	t1/2 for Omeprazole
NCT04425902 (171) [back to overview]	Treatment A: Change From Baseline in Hematocrit
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Midazolam
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Montelukast
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Omeprazole
NCT04425902 (171) [back to overview]	AUC(0-infinity) for Pravastatin
NCT04425902 (171) [back to overview]	AUC(0-t) for 1-hydroxymidazolam
NCT04425902 (171) [back to overview]	AUC(0-t) for 36-hydroxymontelukast
NCT04425902 (171) [back to overview]	t1/2 for Montelukast
NCT04425902 (171) [back to overview]	t1/2 for Midazolam
NCT04425902 (171) [back to overview]	AUC(0-t) for 5-hydroxyomeprazole
NCT04425902 (171) [back to overview]	AUC(0-t) for Alpha-hydroxymetoprolol
NCT04425902 (171) [back to overview]	AUC(0-t) for Digoxin
NCT04425902 (171) [back to overview]	AUC(0-t) for Flurbiprofen
NCT04425902 (171) [back to overview]	AUC(0-t) for Metoprolol
NCT04425902 (171) [back to overview]	AUC(0-t) for Midazolam
NCT04425902 (171) [back to overview]	AUC(0-t) for Montelukast
NCT04425902 (171) [back to overview]	AUC(0-t) for Omeprazole
NCT04425902 (171) [back to overview]	AUC(0-t) for Pravastatin
NCT04425902 (171) [back to overview]	Cmax for 1-hydroxymidazolam
NCT04425902 (171) [back to overview]	Cmax for 36-hydroxymontelukast
NCT04425902 (171) [back to overview]	Cmax for 5-hydroxyomeprazole
NCT04425902 (171) [back to overview]	Cmax for Alpha-hydroxymetoprolol
NCT04425902 (171) [back to overview]	Cmax for Digoxin
NCT04425902 (171) [back to overview]	Cmax for Flurbiprofen
NCT04425902 (171) [back to overview]	Cmax for Metoprolol
NCT04425902 (171) [back to overview]	Cmax for Midazolam
NCT04425902 (171) [back to overview]	t1/2 for Metoprolol
NCT04425902 (171) [back to overview]	t1/2 for Flurbiprofen
NCT04425902 (171) [back to overview]	t1/2 for Digoxin
NCT04425902 (171) [back to overview]	t1/2 for Alpha-hydroxymetoprolol
NCT04425902 (171) [back to overview]	t1/2 for 5-hydroxyomeprazole
NCT04425902 (171) [back to overview]	t1/2 for 36-hydroxymontelukast
NCT04425902 (171) [back to overview]	t1/2 for 1-hydroxymidazolam
NCT04425902 (171) [back to overview]	Ratio of Cmax of Alpha-hydroxymetoprolol to Metoprolol
NCT04425902 (171) [back to overview]	Ratio of Cmax of 5-hydroxyomeprazole to Omeprazole
NCT04425902 (171) [back to overview]	Treatment C: Change From Baseline in Erythrocytes
NCT04608344 (8) [back to overview]	Percentage of Participants With Severity Grade 3 or Above Treatment-Emergent Laboratory Abnormalities
NCT04608344 (8) [back to overview]	Percentage of Participants Experiencing Treatment Emergent Adverse Events (TEAEs)
NCT04608344 (8) [back to overview]	PK Parameter: Cmax of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]	PK Parameter: Cmax of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]	PK Parameter: AUCinf of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]	PK Parameter: AUCinf of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]	Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]	Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS

Multiple Combined Events ( Cardiovascular and Cerebrovascular Events as Well as Myocardial Revascularization)

Cerebrovascular events (newly diagnosed) such as Stroke and Myocardial revascularization (specifically coronary artery bypass grafting, percutaneous coronary interventions, carotid endarterectomy) were recorded (NCT00127218)
Timeframe: 18 months

Intervention	Participants (Count of Participants)
Any Statin Plus Niacin	6
Any Statin Plus Placebo	2

Intervention	Percent change (Mean)
Pitavastatin 1 mg	-22.19
Pravastatin 10 mg	-15.34
Pitavastatin 2 mg	-26.68
Pravastatin 20 mg	-20.61
Pitavastatin 4 mg	-30.75
Pravastatin 40 mg	-24.07

Intervention	Percent change (Mean)
Pitavastatin 1 mg	-31.43
Pravastatin 10 mg	-22.41
Pitavastatin 2 mg	-38.99
Pravastatin 20 mg	-28.83
Pitavastatin 4 mg	-44.31
Pravastatin 40 mg	-33.98

Intervention	ng*h/ml (Mean)
SLCO1B1 Group 1	58552
SLCO1B1 Group 2	63679
SLCO1B1 Group 3	60156

Intervention	Percent change in mg/dL (Least Squares Mean)
Dalcetrapib 300mg	3.61
Dalcetrapib 600mg	6.03
Dalcetrapib 900mg	5.42
Placebo	3.00

Intervention	Percent change in mg/dL (Least Squares Mean)
	Total Cholesterol	Triglycerides	HDL-C	LDL-C	HDL-2	HDL-3	ApoA1	ApoA2	ApoB	LpA1
Dalcetrapib 300mg	7.08	-5.95	17.18	8.51	52.10	11.95	7.03	3.82	2.66	15.06
Dalcetrapib 600mg	12.58	4.45	31.42	10.88	97.40	20.94	13.60	8.07	4.62	22.68
Dalcetrapib 900mg	9.36	-5.01	36.45	5.28	121.2	23.56	14.90	8.36	-1.64	24.76
Placebo	1.35	-4.25	2.31	3.84	10.54	0.68	1.01	0.72	-0.71	3.32

Intervention	Percent change in mg/dL (Least Squares Mean)
Dalcetrapib 300mg	6.58
Dalcetrapib 600mg	11.90
Dalcetrapib 900mg	13.92
Placebo	0.73

Intervention	Percent Change in Ratio (Least Squares Mean)
	HDL-C/LDL-C	ApoB/ApoA1	HDL-2/HDL-3
Dalcetrapib 300mg	-3.76	-4.97	35.18
Dalcetrapib 600mg	-16.0	-5.79	63.40
Dalcetrapib 900mg	-19.4	-12.7	76.38
Placebo	3.09	-1.84	8.89

Intervention	months (Median)
Initial Cohort: Relapsed AML With Previous Remission ≥ 3 Month	10
Poor-risk Cohort: MDS Transformed to AML	10
Poor-risk Cohort: Refractory/Relapsed AML, < 6 Mths Remission	4

Intervention	months (Median)
Initial Cohort: Relapsed AML With Previous Remission ≥ 3 Month	9
Poor-risk Cohort: MDS Transformed to AML	19.4
Poor-risk Cohort: Refractory/Relapsed AML, < 6 Mths Remission	2.7

Intervention	Participants (Number)
	ALT, SGPT (serum glutamic pyruvic transaminase)	AST, SGOT	Acidosis (metabolic or respiratory)	Albumin, serum-low (hypoalbuminemia)	Alkaline phosphatase	Alkalosis (metabolic or respiratory)	Anorexia	Bilirubin (hyperbilirubinemia)	Blood/Bone Marrow-Other (Specify)	Bone marrow cellularity	Calcium, serum-low (hypocalcemia)	Carbon monoxide diffusion capacity (DL(co))	Cardiac General-Other (Specify)	Cardiac-ischemia/infarction	Colitis, infectious (e.g., Clostridium difficile)	Conduction abnormality - Asystole	Confusion	Constitutional Symptoms-Other (Specify)	Creatinine	Diarrhea	Distention/bloating, abdominal	Dry mouth/salivary gland (xerostomia)	Dyspnea (shortness of breath)	Edema: limb	Esophagitis	Fatigue (asthenia, lethargy, malaise)	Febrile neutropenia	Glucose, serum-high (hyperglycemia)	Hemoglobin	Hemorrhage, GI - Duodenum	Hemorrhage, GU - Vagina	Hemorrhage, pulmo/upper resp- Bronchopulmonary NOS	Hemorrhage, pulmonary/upper respiratory - Nose	Hemorrhage/Bleeding-Other (Specify)	Hypertension	Hypotension	Hypoxia	Ileus, GI (functional obstruction of bowel)	Inf (clin/microbio) w/Gr 3-4 neuts - Blood	Inf (clin/microbio) w/Gr 3-4 neuts - Bronchus	Inf (clin/microbio) w/Gr 3-4 neuts - Kidney	Inf (clin/microbio) w/Gr 3-4 neuts - Lung	Inf (clin/microbio) w/Gr 3-4 neuts - Meninges	Inf (clin/microbio) w/Gr 3-4 neuts - Sinus	Inf (clin/microbio) w/Gr 3-4 neuts - Skin	Inf (clin/microbio) w/Gr 3-4 neuts - Small bowel	Inf (clin/microbio) w/Gr 3-4 neuts - Stomach	Infection with unknown ANC - Blood	Infection with unknown ANC - Lung (pneumonia)	Infection with unknown ANC - Mucosa	Infection with unknown ANC - Sinus	Infection with unknown ANC - Small bowel NOS	Infection-Other (Specify)	Left ventricular diastolic dysfunction	Leukocytes (total WBC)	Lipase	Lymphopenia	Magnesium, serum-high (hypermagnesemia)	Mental status	Mucositis/stomatitis (clinical exam) - Oral cavity	Mucositis/stomatitis (clinical exam) - Pharynx	Mucositis/stomatitis (functional/symp) - Oral cav	Musculoskeletal/Soft Tissue-Other (Specify)	Nausea	Necrosis, GI - Small bowel NOS	Neutrophils/granulocytes (ANC/AGC)	Obstruction, GI - Small bowel NOS	Ocular/Visual-Other (Specify)	Opportunistic inf associated w/gt=Gr 2 lymphopenia	Pain - Abdomen NOS	Pain - Bone	Pain - Esophagus	Pain - Extremity-limb	Pain - Oral cavity	Pain - Peritoneum	Phosphate, serum-low (hypophosphatemia)	Platelets	Pleural effusion (non-malignant)	Potassium, serum-high (hyperkalemia)	Potassium, serum-low (hypokalemia)	Pulmonary hypertension	Pulmonary/Upper Respiratory-Other (Specify)	Rash/desquamation	Renal failure	Renal/Genitourinary-Other (Specify)	SVT and nodal arrhythmia - Atrial fibrillation	SVT and nodal arrhythmia - Atrial flutter	Sodium, serum-high (hypernatremia)	Sodium, serum-low (hyponatremia)	Syncope (fainting)	Typhlitis (cecal inflammation)	Ulcer, GI - Duodenum	Ulceration	Vomiting	Weight loss
Initial Cohort: Relapsed AML With Previous Remission ≥ 3 Month	0	0	0	1	0	0	1	2	2	1	2	1	1	0	0	1	1	0	0	3	0	0	2	0	1	3	20	1	11	0	1	0	0	1	1	1	1	1	4	1	0	5	0	1	0	1	0	1	0	0	1	0	1	2	16	1	6	0	1	0	0	1	0	2	0	14	0	1	0	1	0	0	0	0	0	2	17	0	0	6	1	0	0	0	0	1	1	1	1	1	0	0	0	2	0
Poor-risk Cohort: MDS Transformed to AML	2	3	1	3	0	1	1	2	1	0	5	4	0	1	1	0	0	2	3	4	2	1	1	2	0	2	18	2	14	1	0	0	0	0	0	2	2	2	4	0	0	2	0	0	1	0	0	2	1	0	0	1	1	0	11	0	5	1	0	0	0	0	1	1	1	15	1	0	0	3	0	0	0	0	1	4	16	1	2	3	0	1	0	0	1	1	0	0	0	0	0	1	0	2	0
Poor-risk Cohort: Refractory/Relapsed AML, < 6 Mths Remission	2	1	0	6	1	0	0	0	0	0	3	1	0	0	1	0	0	0	2	8	0	0	2	0	0	2	32	0	21	0	0	1	1	0	0	1	3	0	7	1	1	6	1	0	0	0	1	4	0	1	0	0	0	0	17	0	9	0	0	1	1	1	0	3	0	16	0	0	2	0	1	1	1	3	0	2	19	0	0	3	0	0	1	2	0	0	0	0	1	0	1	0	1	0	2

Intervention	Percent probability of CHD event in 10yr (Median)
Lisinopril/P-placebo	-1.6
L-placebo/Pravastatin	-0.7
Lisinopril/Pravastatin	-1.5
L-placebo/P-placebo	-0.3

Intervention	(mmHG) (Mean)
	Systolic BP	Diastolic BP
Lisinopril/L-placebo Treatment Effect	-1.8	-3.3

Intervention	percent (Mean)
Pitavastatin 4 mg Once Daily (QD)	-34.8
Pravastatin 40 mg Once Daily (QD)	-22.7

Intervention	Participants (Count of Participants)
	CR	CRi	PR
Treatment (Pravastatin Sodium, Idarubicin, and Cytarabine)	15	2	0

Intervention	Participants (Number)
Placebo Q4W	26
20 mg LY3015014 Q4W	42
120 mg LY3015014 Q4W	57
300 mg LY3015014 Q4W	51
100 mg LY3015014 Q8W	36
300 mg LY3015014 Q8W	41

Intervention	Percentage Change (Least Squares Mean)
Placebo Q4W	-0.31
20 mg LY3015014 Q4W	-16.63
120 mg LY3015014 Q4W	-19.02
300 mg LY3015014 Q4W	-37.29
100 mg LY3015014 Q8W	-7.54
300 mg LY3015014 Q8W	-21.01

Intervention	Percentage change (Least Squares Mean)
Placebo Q4W	7.6
20 mg LY3015014 Q4W	-14.9
120 mg LY3015014 Q4W	-40.5
300 mg LY3015014 Q4W	-50.5
100 mg LY3015014 Q8W	-14.9
300 mg LY3015014 Q8W	-37.1

Intervention	Percentage change (Least Squares Mean)
Placebo Q4W	0.5
20 mg LY3015014 Q4W	-0.2
120 mg LY3015014 Q4W	1.6
300 mg LY3015014 Q4W	-0.3
100 mg LY3015014 Q8W	-0.3
300 mg LY3015014 Q8W	-0.7

Intervention	μg∙hr/mL (Geometric Mean)
20 mg LY3015014 Q4W	1590
120 mg LY3015014 Q4W	9670
300 mg LY3015014 Q4W	27300
100 mg LY3015014 Q8W	7800
300 mg LY3015014 Q8W	26600

Intervention	Percentage change (Least Squares Mean)
	Apo A1	Apo B
100 mg LY3015014 Q8W	3.8	-16.0
120 mg LY3015014 Q4W	6.5	-34.9
20 mg LY3015014 Q4W	2.4	-16.6
300 mg LY3015014 Q4W	6.2	-46.8
300 mg LY3015014 Q8W	5.8	-31.9
Placebo Q4W	0.3	4.2

pravastatin

Description

Cross-References

Synonyms (92)

Research Excerpts

Overview

Effects

Actions

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Roles (4)

Drug Classes (8)

Pathways (1)

Protein Targets (19)

Potency Measurements

Inhibition Measurements

Other Measurements

Biological Processes (88)

Molecular Functions (25)

Ceullar Components (19)

Bioassays (296)

Research

Studies (3,445)

Market Indicators

Research Demand Index: 95.62

Study Types

Clinical Trials (157)

Trial Overview

Trial Outcomes

Multiple Combined Events ( Cardiovascular and Cerebrovascular Events as Well as Myocardial Revascularization)

Changes in Plaque Architecture and Composition Directly Measured by Magnetic Resonance Imaging (MRI) in the Aorta and Carotid Arteries

Change in Plasma Thiobarbituric Acid Reactive Substance (TBARS) Levels

Change in Flow-mediated Dilatation (FMD)

Incidence Rate of Stroke and TIA

Incidence Rate of Lacunar Infarction

Incidence Rate of Intracranial Hemorrhage

Incidence Rate of Atherothrombotic Infarction

Incidence Rate of Cardioembolic Infarction

Percent Change From Baseline in TC

Percent Change From Baseline in LDL-C

Percent of Participants Demonstrating 20% or More Increase in Total Kidney Volume

Urinary Albumin Excretion

Percentage Change in Total Kidney Volume Corrected for Height

Left Ventricular Mass Index

Survival at 2 Years

Darunavir Maximum Plasma Concentration (Cmax)

Ritonavir Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval

Relative Change in Pravastatin Maximum Plasma Concentration (Cmax)

Relative Change in Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval

Pravastatin Alone: Pravastatin Maximum Plasma Concentration (Cmax)

Pravastatin Alone: Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval

Darunavir Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval

Pravastatin + Darunavir/Ritonavir: Pravastatin Area Under the Plasma Concentration-time Curve (AUC) Over the Dosing Interval

Pravastatin + Darunavir/Ritonavir: Pravastatin Maximum Plasma Concentration (Cmax)

Ritonavir Maximum Plasma Concentration (Cmax)

Compare the Percentage of Variation From Baseline Apolipoprotein B/Apolipoprotein A1 Ratio and After 8 Weeks of Treatment

To Evaluate Clinical and Laboratory Safety

Compare the Percentage of Total Cholesterol Variation From Baseline and After 8 Weeks of Treatment

Compare the Percentage of HDL-C (High Density Lipoprotein Cholesterol) Variation From Baseline and After 8 Weeks of Treatment

Change in Low Density Lipoprotein Cholesterol (LDL-C) Level After 8 Weeks

Compare the Numbers of Patients Achieving the LDL-C Goal According to the National Cholesterol Education Program Adult Treatment Panel III (NCEP) ATP III) Guidelines for the Management of Dyslipidaemic Patients

Compare the Percentage of Variation of Phospholipase A2 (PLA2)

Compare the Percentage of Variation of C-reactive Protein (CRP)

Compare the Percentage of Variation From Baseline Triglycerides Values and After 8 Weeks

Withdrawal of Therapy Due to Muscle Symptoms That Are Either Intolerable and/or Associated With a Creatine Kinase(CK) >500

Change in LDL-Cholesterol Measured at the Beginning and End of the Study

Percentage Change in Low Density Lipoprotein-Cholesterol (LDL-C) From Baseline at Study Endpoint, After 8 Weeks of Treatment

Percent Change of Fasting Glucose Level

Change From Baseline in: Total Cholesterol, Triglycerides, HDL-C, LDL-C, HDL-2, HDL-3, ApoA1, ApoA2, ApoB, LpAI

Percent Change From Baseline in HDL-C Level\

Absolute Change From Baseline in HDL-C Level\

Ratios of Total HDL-C/LDL-C, HDL-2/HDL-3, ApoA1/ApoB

Change in Weight

AUC0-t - Area Under the Concentration-time Curve From Time Zero to Time of Last Non-zero Concentration (Per Participant)

Cmax - Maximum Observed Concentration - Pravastatin in Plasma

AUC0-inf - Area Under the Concentration-time Curve From Time Zero to Infinity (Extrapolated)

Intervention	Percentage change (Least Squares Mean)
	LDL-C	TG	TC	HDL-C	Non-HDL-C
100 mg LY3015014 Q8W	-18.4	-7.2	-11.0	4.5	-16.1
120 mg LY3015014 Q4W	-46.4	-7.2	-27.8	7.3	-39.3
20 mg LY3015014 Q4W	-18.0	-6.1	-10.5	4.5	-16.1
300 mg LY3015014 Q4W	-56.5	-15.1	-34.1	8.8	-48.9
300 mg LY3015014 Q8W	-42.2	-10.6	-24.6	8.4	-35.8
Placebo Q4W	5.9	3.5	3.5	1.6	4.9

Intervention	Percentage change (Least Squares Mean)
Placebo Q4W	9.9
20 mg LY3015014 Q4W	-16.3
120 mg LY3015014 Q4W	-36.6
300 mg LY3015014 Q4W	-68.0
100 mg LY3015014 Q8W	-4.4
300 mg LY3015014 Q8W	-35.2

Intervention	Percentage change (Least Squares Mean)
Placebo Q4W	14.6
20 mg LY3015014 Q4W	9.1
120 mg LY3015014 Q4W	86.4
300 mg LY3015014 Q4W	130.6
100 mg LY3015014 Q8W	21.8
300 mg LY3015014 Q8W	41.0

Intervention	nanograms/milliliter (ng/mL) (Geometric Mean)
Pravastatin (Period 1)	142
Evacetrapib + Pravastatin (Period 2)	128

Intervention	hours (Median)
Pravastatin (Period 1)	1.00
Evacetrapib + Pravastatin (Period 2)	0.75

Intervention	Participants (Count of Participants)
	Baseline: Prepubescent	Baseline: Pubescent	Baseline: Post-pubescent	Week 12: Prepubescent	Week 12: Pubescent	Week 12: Post-pubescent	Week 24: Prepubescent	Week 24: Pubescent	Week 24: Post-pubescent	Week 48: Prepubescent	Week 48: Pubescent	Week 48: Post-pubescent
Alirocumab 150 mg Q2W	0	9	0	0	8	1	0	8	1	0	7	2
Alirocumab 75 mg Q2W/up to 150 mg Q2W	3	6	0	3	6	0	2	6	0	1	7	0

Intervention	percent change (Least Squares Mean)
DB Period: Placebo Q2W	-0.1
DB Period: Alirocumab Q2W	-1.7
DB Period: Placebo Q4W	-0.7
DB Period: Alirocumab Q4W	5.0

Intervention	percent change (Least Squares Mean)
DB Period: Placebo Q2W	10.4
DB Period: Alirocumab Q2W	-27.4
DB Period: Placebo Q4W	-3.6
DB Period: Alirocumab Q4W	-34.3

Intervention	percent change (Least Squares Mean)
DB Period: Placebo Q2W	8.9
DB Period: Alirocumab Q2W	-30.0
DB Period: Placebo Q4W	1.1
DB Period: Alirocumab Q4W	-31.7

Intervention	percent change (Mean)
DB Period: Placebo Q2W	6.5
DB Period: Alirocumab Q2W	-2.2
DB Period: Placebo Q4W	7.8
Db Period: Alirocumab Q4W	-0.3