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pitavastatin

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Description

pitavastatin : A dihydroxy monocarboxylic acid that is (6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]hept-6-enoic acid in which the two hydroxy groups are located at positions 3 and 5 (the 3R,5S-stereoisomer). Used as its calcium salt for treatment of hypercholesterolemia (elevated levels of cholesterol in the blood) on patients unable to sufficiently lower their cholesterol levels by diet and exercise. [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]

Cross-References

ID SourceID
PubMed CID5282452
CHEMBL ID1201753
CHEBI ID32020
SCHEMBL ID3369
SCHEMBL ID464781
MeSH IDM0422150

Synonyms (55)

Synonym
6-heptenoic acid, 7-(2-cyclopropyl-4-(4-fluorophenyl)-3-quinolinyl)-3,5-dihydroxy-, (s-(r*,s*-(e)))-
6-heptenoic acid, 7-(2-cyclopropyl-4-(4-fluorophenyl)-3-quinolinyl)-3,5-dihydroxy-, (3r,5s,6e)-
p 872441
(3r,5s,6e)-7-(2-cyclopropyl-4-(p-fluorophenyl)-3-quinolyl)-3,5-dihydroxy-6-heptenoic acid
itavastatin
( )-(3r,5s,6e)-7-(2-cyclopropyl-4-(4-fluorophenyl)-3-quinolyl)-3,5-dihydroxy-6-heptenoic acid
(3r,5s,6e)-7-(2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl)-3,5-dihydroxyhept-6-enoic acid
pitavastatin [inn]
(e,3r,5s)-7-(2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl)-3,5-dihydroxyhept-6-enoic acid
pitavastatin
AKOS005145916
(e,3r,5s)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxyhept-6-enoic acid
CHEMBL1201753
nsc-760423
chebi:32020 ,
bdbm86707
cas_147511-69-1
nsc 760423
m5681q5f9p ,
(+)-(3r,5s,6e)-7-(2-cyclopropyl-4-(4-fluorophenyl)-3-quinolyl)-3,5-dihydroxy-6-heptenoic acid
unii-m5681q5f9p
hsdb 8367
pitavastatin [vandf]
nikita
pitavastatin [mi]
pitavastatin [mart.]
pitavastatin [who-dd]
AM84440
(3r,5s,6e)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxyhept-6-enoic acid
pitavastatinum
pitavastatine
pitavastatia
gtpl3035
DB08860
HY-B0144A
MLS006010096
smr003965244
SCHEMBL3369
(3r,5s,6e)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]-3,5-dihydroxy hept-6-enoic acid
(e)-(3r,5s)-7-[2-cyclopropyl-4-(4-fluoro-phenyl)-quinolin-3-yl]-3,5-dihydroxy-hept-6enoic acid
e-(3r,5s)-7-[2-cyclopropyl-4-(4fluoro-phenyl)quinolin-3-yl]-3,5-dihydroxy-hept-6-enoic acid
(e)-(3r,5s)-7-[2-cyclopropyl-4-(4-fluoro-phenyl)-quinolin-3-yl]-3,5-dihydroxy-hept-6-enoic acid
VGYFMXBACGZSIL-MCBHFWOFSA-N
DTXSID1048384 ,
SCHEMBL464781
(3r,5s,e)-7-(2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl)-3,5-dihydroxyhept-6-enoic acid
Q412677
BRD-K75958547-001-01-2
(3r,5s,6e)-7-[2-cyclopropyl-4-(p-fluorophenyl)-3-quinolyl]-3,5-dihydroxy-6-heptenoic acid
6-heptenoic acid, 7-[2-cyclopropyl-4-(4-fluorophenyl)-3-quinolinyl]-3,5-dihydroxy-, (3r,5s,6e)-
EN300-25660282
c10aa08
pitavastatin (mart.)
dtxcid2028357
pitavastatina

Research Excerpts

Toxicity

Pitavastatin was associated with a low discontinuation rate, fewer adverse events, and very limited cases of new-onset diabetes. Most treatment emergent adverse events were mild or moderate and their frequency was not different from other statins. Known adverse effects do not include angioedema.

ExcerptReferenceRelevance
" 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
)
0.31
" At least 1 clinical adverse event and at least 1 adverse drug reaction were observed in 25."( A randomized, open-label study to evaluate the efficacy and safety of pitavastatin compared with simvastatin in Korean patients with hypercholesterolemia.
Cho, SY; Chung, N; Ha, JW; Kang, HJ; Oh, BH; Park, S; Rim, SJ, 2005
)
0.33
" Pitavastatin 1 mg once daily may be an alternative regimen with cost-saving benefits but without a significant decrease in therapeutic benefit or increase in adverse events in patients with hypercholesterolemia."( Comparative efficacy and safety of low-dose pitavastatin versus atorvastatin in patients with hypercholesterolemia.
Dhumma-Upakorn, R; Putwai, P; Sansanayudh, N; Wongwiwatthananukit, S, 2010
)
0.36
" Safety was assessed in terms of adverse event rates, including abnormal clinical laboratory variables related to liver and kidney function and skeletal muscle."( Randomized head-to-head comparison of pitavastatin, atorvastatin, and rosuvastatin for safety and efficacy (quantity and quality of LDL): the PATROL trial.
Noda, K; Saku, K; Zhang, B, 2011
)
0.37
" We investigated changes of lipid profiles, biochemical markers, adverse events, and clinical outcomes up to 12 months."( Long-term safety and efficacy of Pitavastatin in patients with acute myocardial infarction (from the Livalo Acute Myocardial Infarction Study [LAMIS]).
Ahn, TH; Bae, JH; Chae, IH; Choi, CU; Hong, YJ; Hur, SH; Jeong, MH; Kim, JH; Kim, KS; Kim, SW; Oh, DJ; Oh, SK; Rha, SW; Shin, EK; Suh, SY; Yoon, KH; Yun, KH, 2011
)
0.37
" Although statins have a favorable risk-to-benefit ratio, they have the potential to cause adverse events which can result in muscular inflammation (myositis), muscle breakdown (rhabdomyolysis) and, ultimately, kidney failure."( Statin-induced myotoxicity: pharmacokinetic differences among statins and the risk of rhabdomyolysis, with particular reference to pitavastatin.
Catapano, AL, 2012
)
0.38
" Pitavastatin was well tolerated: the most common treatment-emergent adverse events were nasopharyngitis, mild/moderate myalgia and hypertension."( Pitavastatin demonstrates long-term efficacy, safety and tolerability in elderly patients with primary hypercholesterolaemia or combined (mixed) dyslipidaemia.
Budinski, D; Hounslow, N; Stender, S, 2013
)
0.39
" There were no severe treatment-emergent adverse events (AEs), serious AEs, deaths, or treatment-emergent AEs leading to study drug discontinuation."( Comparison of the safety, tolerability, and pharmacokinetic profile of a single oral dose of pitavastatin 4 mg in adult subjects with severe renal impairment not on hemodialysis versus healthy adult subjects.
Campbell, SE; Morgan, RE; Muster, HA; Sponseller, CA; Yu, CY, 2012
)
0.38
" The adverse events mainly included vomiting, myalgia and the elevations of aspartate transaminase (AST), alanine transaminase (ALT) and creatine kinase (CK), etc."( [Safety and efficacy of pitavastatin in patients with hypercholesterolemia: a multicenter study].
Ding, RJ; Hu, DY; Jia, GX; Kong, QY; Li, SC; Lin, FL; Mao, Y; Yu, JM; Zhan, YQ; Zhang, F, 2012
)
0.38
" Treatment-emergent adverse events (TEAEs) are presented as risk ratio (RR)."( Efficacy and safety of pitavastatin versus simvastatin: a meta-analysis of randomized controlled trials.
Fang, DZ; Gong, RR; Hu, MS; Jiang, Z; Lin, J; Liu, XJ; Qiu, L; Su, M; Wang, Q, 2014
)
0.4
" Adverse events rates, including abnormal clinical laboratory variables, vital signs, and physical examination were assessed."( Efficacy and Safety of Pitavastatin in Children and Adolescents at High Future Cardiovascular Risk.
Braamskamp, MJ; Drogari, E; Hounslow, N; Kastelein, JJ; Langslet, G; Stefanutti, C; Wiegman, A, 2015
)
0.42
" 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
" The incidence rates of adverse events and adverse drug reactions in K-877 combination therapy groups were comparable to those in statin-monotherapy groups without any noteworthy event in both studies."( Efficacy and safety of K-877, a novel selective peroxisome proliferator-activated receptor α modulator (SPPARMα), in combination with statin treatment: Two randomised, double-blind, placebo-controlled clinical trials in patients with dyslipidaemia.
Arai, H; Araki, E; Ishibashi, S; Suganami, H; Yamashita, S; Yokote, K, 2017
)
0.46
" Pitavastatin was generally well tolerated in these studies and most treatment emergent adverse events were mild or moderate and their frequency was not different from other statins."( [The efficacy and safety of pitavastatin].
Sansoy, V, 2017
)
0.46
" Pitavastatin was well tolerated without any difference in the frequency or nature of adverse events between the treatment groups, or between the studies."( Efficacy and Safety of Pitavastatin in Children and Adolescents with Familial Hypercholesterolemia in Japan and Europe.
Arisaka, O; Harada-Shiba, M; Hovingh, GK; Kastelein, JJP; Ohta, T; Ohtake, A; Okada, T; Ray, KK; Suganami, H; Wiegman, A, 2018
)
0.48
" Known adverse effects of Pitavastatin do not include angioedema."( Angioedema; An Unreported Adverse Effect Of Pitavastatin.
Haider, AW; Naz, S; Saleem, MW,
)
0.13
" Safety was reported with respect to the incidence of adverse events occurring with the use of pitavastatin and the development of new-onset diabetes."( A Multicenter Prospective Hospital-based Cohort Study on the Efficacy and Safety of Pitavastatin.
Al-Rasadi, K; AlZaabi, S; Bhagavathula, AS; Elnour, AA; Gilbert, H; Hassan, G; Kurian, JP; Shehab, A, 2021
)
0.62
"7%) who reported various adverse events such as myalgia (7."( A Multicenter Prospective Hospital-based Cohort Study on the Efficacy and Safety of Pitavastatin.
Al-Rasadi, K; AlZaabi, S; Bhagavathula, AS; Elnour, AA; Gilbert, H; Hassan, G; Kurian, JP; Shehab, A, 2021
)
0.62
" The use of pitavastatin was associated with a low discontinuation rate, fewer adverse events, and very limited cases of new-onset diabetes."( A Multicenter Prospective Hospital-based Cohort Study on the Efficacy and Safety of Pitavastatin.
Al-Rasadi, K; AlZaabi, S; Bhagavathula, AS; Elnour, AA; Gilbert, H; Hassan, G; Kurian, JP; Shehab, A, 2021
)
0.62
" 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
" Adverse events (AEs), clinical laboratory data, and vital signs were assessed in all patients."( A Multicenter, Randomized, Double-blind, Active-controlled, Factorial Design, Phase III Clinical Trial to Evaluate the Efficacy and Safety of Combination Therapy of Pitavastatin and Ezetimibe Versus Monotherapy of Pitavastatin in Patients With Primary Hyp
Ahn, JC; Cha, DH; Cho, EJ; Cho, JM; Choi, CU; Choi, SY; Gwon, HC; Han, KH; Han, KR; Hong, SJ; Hong, YJ; Jeong, HS; Jeong, YH; Jo, SH; Kang, HJ; Kim, BK; Kim, SH; Kim, WS; Lee, SY; Park, TH; Woo, SI, 2022
)
0.72
" There were no significant differences in the incidence of overall AEs and adverse drug reactions."( A Multicenter, Randomized, Double-blind, Active-controlled, Factorial Design, Phase III Clinical Trial to Evaluate the Efficacy and Safety of Combination Therapy of Pitavastatin and Ezetimibe Versus Monotherapy of Pitavastatin in Patients With Primary Hyp
Ahn, JC; Cha, DH; Cho, EJ; Cho, JM; Choi, CU; Choi, SY; Gwon, HC; Han, KH; Han, KR; Hong, SJ; Hong, YJ; Jeong, HS; Jeong, YH; Jo, SH; Kang, HJ; Kim, BK; Kim, SH; Kim, WS; Lee, SY; Park, TH; Woo, SI, 2022
)
0.72
" The incidence of adverse events and adverse drug reactions was not significantly different between the two groups receiving the fixed-dose combination and monotherapy."( Efficacy and Safety of Pitavastatin/Ezetimibe Fixed-Dose Combination vs. Pitavastatin: Phase III, Double-Blind, Randomized Controlled Trial.
Ako, J; Suganami, H; Tajima, S; Tanigawa, R; Tsujita, K; Yokote, K, 2023
)
0.91

Pharmacokinetics

2 mg of pitavastatin was administered to 38 healthy volunteers. Pharmacokinetic parameters were compared among the following groups. Geometric mean ratios (GMRs) demonstrated bioequivalence of the EU and JP formulations. GMRs and 90% confidence intervals (CIs) fell within the range 80-125% in Caucasian men.

ExcerptReferenceRelevance
"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
" These results were compared with the single-dose pharmacokinetic results obtained from six male volunteers without liver disease."( Pharmacokinetics of pitavastatin in subjects with Child-Pugh A and B cirrhosis.
Cheung, BM; Hui, CK; Lau, GK, 2005
)
0.33
"Twenty-four healthy Korean volunteers who had previously participated in a pharmacokinetic study of pitavastatin (single oral dose, 1--8 mg) were further investigated."( Effect of OATP1B1 (SLCO1B1) variant alleles on the pharmacokinetics of pitavastatin in healthy volunteers.
Cho, JY; Chung, JY; Jang, IJ; Jung, HR; Kim, JR; Lim, KS; Moon, KH; Oh, DS; Shin, SG; Yu, KS, 2005
)
0.33
"To investigate the contribution of genetic polymorphisms of SLCO1B1 and ABCG2 to the pharmacokinetics of a dual substrate, pitavastatin, 2 mg of pitavastatin was administered to 38 healthy volunteers and pharmacokinetic parameters were compared among the following groups: 421C/C(*)1b/(*)1b (group 1), 421C/C(*)1b/(*)15 (group 2), 421C/C(*)15/(*)15 and 421C/A(*)15/(*)15 (group 3), 421C/A(*)1b/(*)1b (group 4), 421A/A(*)1b/(*)1b (group 5), and 421C/A(*)1b/(*)15 (group 6)."( SLCO1B1 (OATP1B1, an uptake transporter) and ABCG2 (BCRP, an efflux transporter) variant alleles and pharmacokinetics of pitavastatin in healthy volunteers.
Fujino, H; Hashimoto, K; Higuchi, S; Hirano, M; Ieiri, I; Irie, S; Kimura, M; Kusuhara, H; Maeda, K; Sugiyama, Y; Suwannakul, S; Uchimaru, H, 2007
)
0.34
" The developed method was successfully applied to determine pitavastatin in human plasma and urine, and was proved to be suitable for use in Phase I clinical pharmacokinetic study after oral administration of pitavastatin (1, 2 and 4 mg) in healthy Chinese volunteers."( Solid-phase extraction and liquid chromatography/tandem mass spectrometry assay for the determination of pitavastatin in human plasma and urine for application to Phase I clinical pharmacokinetic studies.
Cheng, MC; Di, B; He, LP; Qu, LJ; Su, MX; Yu, F; Zhao, LP, 2008
)
0.35
"The pharmacokinetic parameters of pitavastatin were significantly different between the two genotyped groups."( OATP1B1 388A>G polymorphism and pharmacokinetics of pitavastatin in Chinese healthy volunteers.
Wen, J; Xiong, Y, 2010
)
0.36
" The objectives of the present study were to evaluate the pharmacokinetic bioequivalence of the European (EU) and Japanese (JP) formulations of pitavastatin 2 mg in healthy Japanese and Caucasian men, and to assess whether the bioavailability of each formulation was similar in the two ethnic groups."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 2011
)
0.37
"In this open-label, single-dose, two-way crossover pharmacokinetic study, healthy men aged 18-45 years were randomized to receive: the JP formulation of pitavastatin 2 mg followed by the EU formulation; or the EU formulation of pitavastatin 2 mg followed by the JP formulation."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 2011
)
0.37
" Geometric mean ratios (GMRs) of the pharmacokinetic parameters of pitavastatin demonstrated bioequivalence of the EU and JP formulations: GMRs and 90% confidence intervals (CIs) fell within the range 80-125% in Caucasian men and in Caucasian and Japanese groups combined for pitavastatin C(max) (combined analysis: GMR 103."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 2011
)
0.37
"The EU and JP formulations of pitavastatin showed pharmacokinetic bioequivalence, and there were no clinically relevant differences in exposure to pitavastatin between Caucasian and Japanese participants when differences in body weight were taken into account."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 2011
)
0.37
" 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
)
0.37
"The aim of this study was to investigate the potential pharmacokinetic interaction between pitavastatin and valsartan in healthy male volunteers in Korea."( Pharmacokinetic interaction between pitavastatin and valsartan: a randomized, open-labeled crossover study in healthy male Korean volunteers.
Bae, KS; Jin, S; Jung, JA; Kim, MJ; Kim, YH; Lim, HS; Noh, YH, 2012
)
0.38
" Plasma samples were obtained at steady state for the pharmacokinetic evaluation of pitavastatin and valsartan."( Pharmacokinetic interaction between pitavastatin and valsartan: a randomized, open-labeled crossover study in healthy male Korean volunteers.
Bae, KS; Jin, S; Jung, JA; Kim, MJ; Kim, YH; Lim, HS; Noh, YH, 2012
)
0.38
"The pharmacokinetic profiles of pitavastatin and valsartan administered as monotherapy were comparable to combination treatment in these healthy male Korean volunteers, suggesting that individual pharmacokinetic properties are not significantly affected by concurrent administration."( Pharmacokinetic interaction between pitavastatin and valsartan: a randomized, open-labeled crossover study in healthy male Korean volunteers.
Bae, KS; Jin, S; Jung, JA; Kim, MJ; Kim, YH; Lim, HS; Noh, YH, 2012
)
0.38
" On day 1, the subjects received a single oral dose of pitavastatin 4 mg and remained in the clinic on days 1-3 for safety and pharmacokinetic assessments."( Comparison of the safety, tolerability, and pharmacokinetic profile of a single oral dose of pitavastatin 4 mg in adult subjects with severe renal impairment not on hemodialysis versus healthy adult subjects.
Campbell, SE; Morgan, RE; Muster, HA; Sponseller, CA; Yu, CY, 2012
)
0.38
" The primary objective was to investigate pharmacokinetic (PK) effects of lopinavir/ritonavir 400 mg/100 mg twice daily on pitavastatin 4 mg when coadministered."( Effects of steady-state lopinavir/ritonavir on the pharmacokinetics of pitavastatin in healthy adult volunteers.
Campbell, SE; Medlock, MM; Morgan, RE; Sponseller, CA; Suehira, K; Yu, CY, 2012
)
0.38
" To investigate the impact of influx (OATP1B1) and efflux (MRP2, BCRP) transporter alleles on its disposition, the pharmacokinetic (PK) parameters were compared among the following groups: SLCO1B1 (*15 carrier and non-carrier), ABCC2 (G1249A, C3972T, C-24T, G1549A, and G1774T), and ABCG2 (C421A) single nucleotide polymorphisms in 45 healthy Korean volunteers."( Impact of ABCC2, ABCG2 and SLCO1B1 polymorphisms on the pharmacokinetics of pitavastatin in humans.
Cho, SK; Chung, JY; Kim, CO; Oh, ES; Park, MS, 2013
)
0.39
" Compared to CYP2C9*1/*1 carriers, CYP2C9*1/*3 carriers had higher AUC(0-infinity) and Cmax of pitavastatin acid and AUC(0-infinity) of pitavastatin lactone (P<0."( CYP2C9*3(1075A > C), ABCB1 and SLCO1B1 genetic polymorphisms and gender are determinants of inter-subject variability in pitavastatin pharmacokinetics.
Chen, QX; Ruan, ZR; Xu, HM; Yuan, H; Zeng, S; Zhou, Q, 2013
)
0.39
"The effect of pitavastatin and SLCO1B1 genetic background on the pharmacokinetic and pharmacodynamic properties of repaglinide was investigated."( Effect of pitavastatin in different SLCO1B1 backgrounds on repaglinide pharmacokinetics and pharmacodynamics in healthy Chinese males.
Chen, XP; Fu, ZM; Huang, LH; Huang, YY; Huang, ZJ; Liu, C; Song, M; Tan, HY; Tan, ZR; Yang, GP; Yuan, H; Zhu, J, 2013
)
0.39
"A single dose of rifampin significantly increased the mean area under the plasma concentration-time curve(AUC)(0-48 h) and Cmax of pitavastatin by 573."( Effect of a single-dose rifampin on the pharmacokinetics of pitavastatin in healthy volunteers.
Chen, Y; Huang, WH; Huang, X; Tan, ZR; Wang, YC; Zhang, W; Zhou, HH, 2013
)
0.39
"Rosuvastatin and pitavastatin have favorable pharmacokinetic and safety profiles as their disposition does not depend on or is only marginally influenced by cytochrome P450 (CYP) enzymes, thus potentially reducing the risk of drug-drug interactions of these two statins with other drugs known to inhibit CYP enzymes."( Evaluation of the pharmacokinetics and drug interactions of the two recently developed statins, rosuvastatin and pitavastatin.
Hu, M; Tomlinson, B, 2014
)
0.4
" We verified if the pharmacodynamic effects of CYP3A4-metabolized statins (atorvastatin) and non-CYP3A4-metabolized statins (pitavastatin) differ in patients with coronary artery disease (CAD) treated with DAPT."( Pharmacodynamic comparison of pitavastatin versus atorvastatin on platelet reactivity in patients with coronary artery disease treated with dual antiplatelet therapy.
Franzoni, F; Gaudio, C; Greco, C; Marazzi, G; Pelliccia, F; Polacco, M; Rosano, G; Speziale, G; Spoletini, I; Vitale, C, 2014
)
0.4
" Pharmacokinetic blood sampling was performed on days 5, 11 and 16."( Steady-state pharmacokinetics of darunavir/ritonavir and pitavastatin when co-administered to healthy adult volunteers.
Campbell, SE; Medlock, MM; Morgan, RE; Small, DS; Sponseller, CA; Yu, CY, 2014
)
0.4
"5 years) were enrolled, and pharmacokinetic data were available for 27 subjects."( Steady-state pharmacokinetics of darunavir/ritonavir and pitavastatin when co-administered to healthy adult volunteers.
Campbell, SE; Medlock, MM; Morgan, RE; Small, DS; Sponseller, CA; Yu, CY, 2014
)
0.4
"The drug-drug interactions between pitavastatin and darunavir/ritonavir (DRV/r) as well as pitavastatin and efavirenz (EFV) were examined in an open-label, parallel-arm, pharmacokinetic (PK) study in HIV-uninfected healthy volunteers."( Lack of pharmacokinetic interactions between pitavastatin and efavirenz or darunavir/ritonavir.
Aberg, JA; Ma, Q; Malvestutto, CD; Morse, GD; Underberg, JA, 2014
)
0.4
"In the EFV arm, the geometric mean area under the concentration time curve (AUC0-τ) and Cmax of pitavastatin were 85."( Lack of pharmacokinetic interactions between pitavastatin and efavirenz or darunavir/ritonavir.
Aberg, JA; Ma, Q; Malvestutto, CD; Morse, GD; Underberg, JA, 2014
)
0.4
" The aim of the present study was to investigate the effect of food on the pharmacokinetic properties and bioequivalence of the original, branded, formulation of pitavastatin calcium and a new generic formulation in healthy Chinese male subjects under fasting and fed conditions."( The effect of food on the pharmacokinetic properties and bioequivalence of two formulations of pitavastatin calcium in healthy Chinese male subjects.
Deng, S; Hu, J; Huang, W; Lu, H; Ni, X; Qiu, C; Shang, D; Wang, Z; Wen, Y; Yao, Z; Zhang, M; Zhu, X, 2016
)
0.43
"To investigate the pharmacokinetic (PK) interaction between telmisartan (Tel) and pitavastatin (Pit), a rapid and sensitive ultra performance liquid chromatography-tandem mass spectrometric assay method had been successfully established and fully validated for the simultaneous quantification of Tel and Pit in rat plasma."( Simultaneous determination of telmisartan and pitavastatin in rat plasma by UPLC-MS/MS: Application to pharmacokinetic interaction study.
Chen, X; Fang, D; Fu, C; Gu, Y; Jian, Z; Jiang, C; Liu, J; Song, X; Tang, M; Xu, B; Yang, J; Zhang, Z, 2016
)
0.43
" Physiologically based pharmacokinetic (PBPK) models have, however, demonstrated ability to predict complex DDIs."( Physiologically Based Pharmacokinetic (PBPK) Modeling of Pitavastatin and Atorvastatin to Predict Drug-Drug Interactions (DDIs).
Duan, P; Zhang, L; Zhao, P, 2017
)
0.46
" 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
)
0.48
" The method was successfully applied to investigate pharmacokinetic interaction between PIT and CAN in wistar rats."( Quantitative bio-analysis of pitavastatin and candesartan in rat plasma by HPLC-UV: Assessment of pharmacokinetic drug-drug interaction.
Kothari, C; Patel, M, 2020
)
0.56
" Systemic concentrations of these flavonolignans can influence the potential biologic effects of silymarin and the risk for pharmacokinetic silymarin-drug interactions."( Hepatic organic anion transporting polypeptides mediate disposition of milk thistle flavonolignans and pharmacokinetic silymarin-drug interactions.
Arman, T; Bechtold, BJ; Clarke, JD; Graf, TN; Lynch, KD; Montonye, ML; Oberlies, NH; Oyanna, VO; Paine, MF; Tian, DD, 2021
)
0.62
"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
" The pharmacokinetic herb-disease-drug interaction found in this research will help inform the clinical administration of EGB or Oatp1b2 substrates."( Pharmacokinetic herb-disease-drug interactions: Effect of ginkgo biloba extract on the pharmacokinetics of pitavastatin, a substrate of Oatp1b2, in rats with non-alcoholic fatty liver disease.
Huang, Y; Lei, L; Li, Y; Li, Z; Tian, S; Wang, B; Wu, Z; Xu, X, 2021
)
0.62

Compound-Compound Interactions

Pitavastatin is a tool to be used in transporter-mediated drug-drug interaction studies. It was not associated with clinically significant increases in the incidence of adverse drug reactions (ADRs)

ExcerptReferenceRelevance
" Then, to explore the possibility of OATP1B1-mediated drug-drug interaction, we checked the inhibitory effects of various drugs on the pitavastatin uptake in OATP1B1-expressing cells and evaluated whether the in vitro inhibition was clinically significant or not."( Drug-drug interaction between pitavastatin and various drugs via OATP1B1.
Hirano, M; Maeda, K; Shitara, Y; Sugiyama, Y, 2006
)
0.33
" No drug-drug interaction between pitavastatin and warfarin was demonstrated."( Drug-drug interaction study to assess the effects of multiple-dose pitavastatin on steady-state warfarin in healthy adult volunteers.
Arana, B; Gosho, M; Hunt, T; Inagaki, Y; Morgan, R, 2011
)
0.37
"As the clinical complexity of patients at high cardiovascular risk and with multiple comorbid conditions increases, so does the potential for drug-drug interactions (DDIs)."( Drug-drug interactions with statins: will pitavastatin overcome the statins' Achilles' heel?
Ceska, R; Corsini, A, 2011
)
0.37
" 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
)
0.37
"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 investigate the effects of bisphosphonates (Bis) (etidronate, alendronate, and risedronate), alone and in combination with statin, on the BMD (bone mineral density) and bone metabolism of rheumatoid arthritis (RA) patients."( Osteogenesis and osteoclast inhibition in rheumatoid arthritis patients treated with bisphosphonates alone or in combination with pitavastatin over an 18-month follow-up after more than 4 years of treatment with bisphosphonates.
Nagase, Y; Nagashima, M; Shimane, K; Takahashi, H; Wauke, K, 2012
)
0.38
" In conclusion, pharmacokinetic studies using pitavastatin as a probe in combination with drug candidates in cynomolgus monkeys are useful to support the assessment of potential clinical DDIs involving hepatic uptake transporters."( Pitavastatin as an in vivo probe for studying hepatic organic anion transporting polypeptide-mediated drug-drug interactions in cynomolgus monkeys.
Kume, T; Ohtsuka, T; Takahashi, T; Tatekawa, I; Uno, Y; Utoh, M; Yamazaki, H; Yoshikawa, T, 2013
)
0.39
"Rosuvastatin and pitavastatin have favorable pharmacokinetic and safety profiles as their disposition does not depend on or is only marginally influenced by cytochrome P450 (CYP) enzymes, thus potentially reducing the risk of drug-drug interactions of these two statins with other drugs known to inhibit CYP enzymes."( Evaluation of the pharmacokinetics and drug interactions of the two recently developed statins, rosuvastatin and pitavastatin.
Hu, M; Tomlinson, B, 2014
)
0.4
"Medications that interact with the pathways responsible for statin metabolism may increase the risk of statin-associated myalgia."( Pitavastatin therapy in polymedicated patients is associated with a low risk of drug-drug interactions: analysis of real-world and phase 3 clinical trial data.
Gosho, M; Hounslow, N; Tanahashi, M; Teramoto, T, 2015
)
0.42
" Adverse events were classified according to the Medical Dictionary for Regulatory Activities (Med-DRA) and whether they occurred in patients taking medications that interact with hepatocyte organic anion-transporting polypeptide or cytochrome P450 (CYP) isoenzyme pathways."( Pitavastatin therapy in polymedicated patients is associated with a low risk of drug-drug interactions: analysis of real-world and phase 3 clinical trial data.
Gosho, M; Hounslow, N; Tanahashi, M; Teramoto, T, 2015
)
0.42
"Concomitant administration of pitavastatin with other medications was not associated with clinically significant increases in the incidence of adverse drug reactions (ADRs), even when given with medications that interact with CYP2C9, responsible for the minimal CYP metabolism of pitavastatin."( Pitavastatin therapy in polymedicated patients is associated with a low risk of drug-drug interactions: analysis of real-world and phase 3 clinical trial data.
Gosho, M; Hounslow, N; Tanahashi, M; Teramoto, T, 2015
)
0.42
" The objective of the present study was to identify the mechanism of clopidogrel-mediated drug-drug interactions (DDIs) on the pharmacokinetics of OATP1B1 and/or CYP2C8 substrates in vivo."( Clarification of the Mechanism of Clopidogrel-Mediated Drug-Drug Interaction in a Clinical Cassette Small-dose Study and Its Prediction Based on In Vitro Information.
Ieiri, I; Irie, S; Kim, SJ; Kimura, M; Kusuhara, H; Maeda, K; Sugiyama, Y; Yoshikado, T, 2016
)
0.43
"The disposition of statins varies and involves both metabolizing enzymes and transporters, making predictions of statin drug-drug interactions (DDIs) challenging."( Physiologically Based Pharmacokinetic (PBPK) Modeling of Pitavastatin and Atorvastatin to Predict Drug-Drug Interactions (DDIs).
Duan, P; Zhang, L; Zhao, P, 2017
)
0.46
"These results strongly support the favourable benefit-to-risk ratio of K-877 add-on therapy in combination with statin treatment."( Efficacy and safety of K-877, a novel selective peroxisome proliferator-activated receptor α modulator (SPPARMα), in combination with statin treatment: Two randomised, double-blind, placebo-controlled clinical trials in patients with dyslipidaemia.
Arai, H; Araki, E; Ishibashi, S; Suganami, H; Yamashita, S; Yokote, K, 2017
)
0.46
"Coproporphyrin (CP) I and III have recently been proposed as endogenous clinical biomarkers to predict organic anion-transporting polypeptide 1B (OATP1B)-mediated drug-drug interactions (DDIs)."( Clinical Investigation of Coproporphyrins as Sensitive Biomarkers to Predict Mild to Strong OATP1B-Mediated Drug-Drug Interactions.
Dillen, L; Ediage, EN; Kunze, A; Monshouwer, M; Snoeys, J, 2018
)
0.48
" Furthermore, CPI and CPIII plasma concentrations were determined from participants of three independent clinical trials who were administered with either a strong, moderate, or mild clinical OATP1B inhibitor."( Clinical Investigation of Coproporphyrins as Sensitive Biomarkers to Predict Mild to Strong OATP1B-Mediated Drug-Drug Interactions.
Dillen, L; Ediage, EN; Kunze, A; Monshouwer, M; Snoeys, J, 2018
)
0.48
"As a tool to be used in transporter-mediated drug-drug interaction studies, a sensitive LC-MS/MS method for the simultaneous quantification of adefovir and pitavastatin in human plasma and adefovir in urine was developed and successfully validated."( Quantification of adefovir and pitavastatin in human plasma and urine by LC-MS/MS: A useful tool for drug-drug interaction studies.
Fuhr, U; Kinzig, M; Scherf-Clavel, O; Sörgel, F; Stoffel, MS, 2019
)
0.51
" Hence, there is no evidence for a potential drug-drug interaction between PIT and CAN."( Quantitative bio-analysis of pitavastatin and candesartan in rat plasma by HPLC-UV: Assessment of pharmacokinetic drug-drug interaction.
Kothari, C; Patel, M, 2020
)
0.56
" A semimechanistic physiologically-based pharmacokinetic (PBPK) model was developed to evaluate the potential for clinical drug-drug interactions (DDIs)."( Prediction of Clinical Transporter-Mediated Drug-Drug Interactions via Comeasurement of Pitavastatin and Eltrombopag in Human Hepatocyte Models.
Carter, SJ; Chappell, MJ; Chouhan, B; Sharma, P, 2020
)
0.56
"The results mentioned above suggested that pitavastatin combined with ezetimibe was an effective approach for STEMI patients with non-IRA disease undergoing primary PCI."( Pitavastatin Combined with Ezetimibe Treatment was an Effective Approach to Non-IRA Lesion of ST-segment Elevation Myocardial Infarction Patients with Primary Percutaneous Coronary Intervention.
Lei, LC; Li, GP; Peng, JJ; Ren, LH; Wang, ZY; Ye, HM; Zhao, B; Zhao, S, 2021
)
0.62
" 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
)
0.62
" Based on the different effects of statin members, this study aims to evaluate the effect of two of the most promising lipophilic statins, Simvastatin and Pitavastatin, and their combination with a conventional chemotherapeutic regimen of doxorubicin and cyclophosphamide on breast cancer cells."( Enhanced therapeutic efficacy of doxorubicin/cyclophosphamide in combination with pitavastatin or simvastatin against breast cancer cells.
Dewidar, SA; El Gayar, AM; El-Mesery, M; Hamdy, O; Soliman, MM, 2023
)
0.91

Bioavailability

Pitavastatin SNEDDS were prepared with a variety of oils, surfactants, co-surfactants, and solvents to improve the dissolution rate and bioavailability of HMG-CoA reductase inhibitor. Oatp1b2 gene expression in rat liver is hardly effected by CAP.

ExcerptReferenceRelevance
"Pitavastatin retards the progression of atherosclerosis formation and it improves NO bioavailability by eNOS up-regulation and decrease of O(2)(-)."( A new HMG-CoA reductase inhibitor, pitavastatin remarkably retards the progression of high cholesterol induced atherosclerosis in rabbits.
Fukatsu, A; Hayashi, T; Ignarro, LJ; Iguchi, A; Kano-Hayashi, H; Matsui-Hirai, H; Miyazaki, A; Osawa, M; Rani P, JA; Sumi, D; Tsunekawa, T, 2004
)
0.32
" 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
"We investigated the effects of co-administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor and angiotensin II type 1 receptor blocker (ARB) on nitric oxide (NO) bioavailability in genetically hyperlipidemic rabbits with our newly developed NO sensor."( Combined effects of an 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor and angiotensin II receptor antagonist on nitric oxide bioavailability and atherosclerotic change in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits.
Akasaka, T; Goto, M; Ikejima, H; Imanishi, T; Kobayashi, K; Kuroi, A; Mochizuki, S; Muragaki, Y; Shiomi, M; Tsujioka, A; Tsujioka, H; Yoshida, K, 2008
)
0.35
" The bioavailability of pitavastatin is, at 60%, higher than that of any other statin and the majority of the bioavailable fraction of an oral dose is excreted unchanged in the bile."( Pitavastatin - pharmacological profile from early phase studies.
Catapano, AL, 2010
)
0.36
" The objectives of the present study were to evaluate the pharmacokinetic bioequivalence of the European (EU) and Japanese (JP) formulations of pitavastatin 2 mg in healthy Japanese and Caucasian men, and to assess whether the bioavailability of each formulation was similar in the two ethnic groups."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 2011
)
0.37
" This process probably accounts for pitavastatin's increased bioavailability relative to most other statins and contributes to its prolonged duration of action."( Pitavastatin: an overview.
Saito, Y, 2011
)
0.37
" These results demonstrated that chronic ingestion of CAP increases the bioavailability of pitavastatin in rat and that Oatp1b2 gene expression in rat liver is hardly effected by CAP."( Effects of capsaicin on pharmacokinetics of pitavastatin in rats.
Chen, F; Lu, Y; Zhai, X; Zhu, C, 2015
)
0.42
" The mean (SD) relative bioavailability calculated from the ratios (T/R) of AUC0-t was 101."( Comparison of scaled-average, population, and individual bioequivalence on 2 tablets of pitavastatin calcium: a 3-period, reference-replicated, crossover study in healthy Chinese volunteers.
Gu, XF; Huang, YH; Li, N; Li, YF; Li, ZQ; Liu, Y; Pan, GX; Sun, JX; Wang, BH, 2014
)
0.4
"In mice, the bioavailability changes, which corrected the effect of systemic clearance by Bcrp knockout, correlated well with the AUC changes in humans, whereas the correlation was weak when AUC changes were directly compared."( Evaluation of the usefulness of breast cancer resistance protein (BCRP) knockout mice and BCRP inhibitor-treated monkeys to estimate the clinical impact of BCRP modulation on the pharmacokinetics of BCRP substrates.
Abe, K; Hagihara-Nakagomi, R; Hirouchi, M; Imaoka, T; Izumi, T; Karibe, T; Mikkaichi, T; Okudaira, N; Watanabe, N; Yasuda, S, 2015
)
0.42
"This study suggests that pharmacokinetics studies that use the correction of the bioavailability changes in Bcrp knockout mice are effective for estimating clinical AUC changes in ABCG2 421C>A variants for BCRP substrate drugs and those studies in monkeys that use a BCRP inhibitor serve for the assessment of BCRP impact on the gastrointestinal absorption in a non-rodent model."( Evaluation of the usefulness of breast cancer resistance protein (BCRP) knockout mice and BCRP inhibitor-treated monkeys to estimate the clinical impact of BCRP modulation on the pharmacokinetics of BCRP substrates.
Abe, K; Hagihara-Nakagomi, R; Hirouchi, M; Imaoka, T; Izumi, T; Karibe, T; Mikkaichi, T; Okudaira, N; Watanabe, N; Yasuda, S, 2015
)
0.42
"The effective permeability coefficient and the absorption rate constant of telmisartan were higher in the duodenum as compared to other intestinal segments."( Simultaneous Determination of Telmisartan and Pitavastatin Calcium in Intestinal Perfusate by HPLC: Application to Intestinal Absorption Interaction Study.
Fu, C; Liu, J; Song, X; Wang, J, 2020
)
0.56
"Pitavastatin SNEDDS were prepared with a variety of oils, surfactants, co-surfactants, and solvents to improve the dissolution rate and bioavailability of the HMG-CoA reductase inhibitor."( Formulation and Statistical Evaluation of Tablets Containing Pitavastatin- Self Nano Emulsifying Drug Delivery Systems.
Gowripattapu, S; Sathis Kumar, D; Selvamuthukumar, S, 2023
)
0.91

Dosage Studied

Pavastatin dosed at 1 to 4 mg daily showed similar efficacy in lowering low-density lipoprotein cholesterol (LDL-C) and altering other lipid parameters. Dose adjustments are not required for gender, age or race. The main outcome measures were maximum plasma concentration (C(max) and area under the plasma concentration-time curve (AUC)

ExcerptRelevanceReference
" These results indicate that NK-104 and simvastatin at 10 times the dosage of the former, similarly enhances hepatic LDL receptor; however, only NK-104 with prolonged action suppresses VLDL secretion to show higher cholesterol-lowering potency and triglyceride-reducing effect."( Hypolipidemic effect of NK-104, a potent HMG-CoA reductase inhibitor, in guinea pigs.
Aoki, T; Kitahara, M; Saito, Y; Sato, F; Suzuki, H; Tamaki, T, 1999
)
0.3
" No induction of the drug metabolizing enzymes (aniline hydroxylase, aminopyrine N-demethylase, 7-ethoxycoumarin O-deethylase and UDP-glucuronic acid transferase) was found in the pitavastatin group compared to the control after the multiple administrations of pitavastatin at the dosage of 1-10 mg/kg per day for 7 days."( Metabolic fate of pitavastatin (NK-104), a new inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase. Effects on drug-metabolizing systems in rats and humans.
Fujino, H; Nagao, T; Shimada, S; Yamada, I; Yoneda, M, 2002
)
0.31
" 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
" 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
"Two simple and accurate methods for the determination of pitavastatin calcium (PIT) in tablet dosage forms were developed and validated using column liquid chromatography (LC) and UV spectrophotometry."( Estimation of pitavastatin calcium in tablet dosage forms by column liquid chromatography and ultraviolet spectrophotometry.
Panchal, HJ; Patel, BH; Patel, MM; Suhagia, BN,
)
0.13
" Compared to other statins such as atorvastatin, simvastatin and pravastatin at specific doses, pitavastatin dosed at 1 to 4 mg daily showed similar efficacy in lowering low-density lipoprotein cholesterol (LDL-C) and altering other lipid parameters according to a number of studies."( Pitavastatin: a new HMG-CoA reductase inhibitor for the treatment of hypercholesterolemia.
Ahmad, H; Cheng-Lai, A,
)
0.13
"Dahl salt-sensitive rats fed a high-salt diet were treated from 12 to 20 weeks of age with vehicle, the reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin, the synthetic cathepsin inhibitor E64d, or a low or high dosage of pitavastatin (1 or 3 mg/kg daily)."( Inhibition of mineralocorticoid receptor is a renoprotective effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pitavastatin.
Cheng, XW; Hirashiki, A; Hu, L; Huang, Z; Inoue, A; Kuzuya, M; Li, P; Murohara, T; Okumura, K; Sasaki, T; Sato, K; Shi, GP; Song, H; Takeshita, K, 2011
)
0.37
" The safety, tolerability and pharmacokinetics of pitavastatin and its major metabolite, pitavastatin lactone, have been investigated in a variety of patient groups with similar results, which suggests dosage adjustments are not required for gender, age or race."( Pitavastatin - pharmacological profile from early phase studies.
Catapano, AL, 2010
)
0.36
" The main outcome measures were maximum plasma concentration (C(max)), area under the plasma concentration-time curve (AUC) during a dosage interval (τ) [AUC(τ)] and AUC from time zero to infinity (AUC(∞)) for pitavastatin and its main (inactive) metabolite pitavastatin lactone."( Comparison of the pharmacokinetics of pitavastatin by formulation and ethnic group: an open-label, single-dose, two-way crossover pharmacokinetic study in healthy Caucasian and Japanese men.
Hounslow, N; Nagakawa, S; Warrington, S, 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
)
0.37
" the area under the plasma concentration-time curve over a dosing interval at steady state (AUC(0-τ))] and for peak exposure [i."( Steady-state pharmacokinetics of darunavir/ritonavir and pitavastatin when co-administered to healthy adult volunteers.
Campbell, SE; Medlock, MM; Morgan, RE; Small, DS; Sponseller, CA; Yu, CY, 2014
)
0.4
" The results showed that our bottom-up models predicted systemic exposure (AUC0h-t), maximum plasma concentration (Cmax), plasma clearance and time to reach Cmax (Tmax) within two-fold of the observed data, with the exception of parameters associated with multiple oral pitavastatin dosing and single oral fluvastatin dosing."( Bottom-up physiologically-based biokinetic modelling as an alternative to animal testing.
Chan, ECY; Chan, JCY; Tan, SPF; Upton, Z, 2019
)
0.51
" Our findings contribute towards the design of controlled release with low drug dosing bone grafts: i-CPFs loaded with PITA as osteogenic and angiogenic agent."( Injectable calcium phosphate foams for the delivery of Pitavastatin as osteogenic and angiogenic agent.
Canal, C; Ginebra, MP; Guillem-Marti, J; Khurana, K; Mücklich, F; Soldera, F, 2020
)
0.56
" To investigate in vivo OATP induction, RIF (18 mg/kg per day) was orally dosed to cynomolgus monkeys for 7 days."( Organic Anion-Transporting Polypeptide Genes Are Not Induced by the Pregnane X Receptor Activator Rifampin: Studies in Hepatocytes In Vitro and in Monkeys In Vivo.
Lai, Y; Murakami, E; Niu, C; Smith, B; Subramanian, R; Tep, S; Wang, Y; Zhao, X, 2019
)
0.51
" Log dose-response data over doses of 1 mg to 16 mg revealed strong linear dose-related effects on blood total cholesterol and LDL cholesterol and triglycerides."( Pitavastatin for lowering lipids.
Adams, SP; Alaeiilkhchi, N; Wright, JM, 2020
)
0.56
"SNEDDS of Pitavastatin is a promising approach to achieving a solid dosage form of the liquid-loaded drug delivery systems for enhancing the solubility and dissolution rate of the drug, and hence also its bioavailability."( Formulation and Statistical Evaluation of Tablets Containing Pitavastatin- Self Nano Emulsifying Drug Delivery Systems.
Gowripattapu, S; Sathis Kumar, D; Selvamuthukumar, S, 2023
)
0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (1)

RoleDescription
antioxidantA substance that opposes oxidation or inhibits reactions brought about by dioxygen or peroxides.
[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]

Drug Classes (5)

ClassDescription
quinolinesA class of aromatic heterocyclic compounds each of which contains a benzene ring ortho fused to carbons 2 and 3 of a pyridine ring.
dihydroxy monocarboxylic acidAny hydroxy monocarboxylic acid carrying at least two hydroxy groups.
cyclopropanesCyclopropane and its derivatives formed by substitution.
statin (synthetic)A statin which does not occur naturally and which is not obtained by chemical transformation of a naturally occurring statin.
monofluorobenzenesAny member of the class of fluorobenzenes containing a mono- or poly-substituted benzene ring carrying a single fluorine substitutent.
[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]

Protein Targets (2)

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Nuclear receptor subfamily 4 group A member 2Homo sapiens (human)EC50 (µMol)0.12000.01002.89125.1000AID1885210
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)Km4.80000.00763.201810.0000AID1218862
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (37)

Processvia Protein(s)Taxonomy
negative regulation of transcription by RNA polymerase IINuclear receptor subfamily 4 group A member 2Homo sapiens (human)
response to hypoxiaNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
neuron migrationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
response to amphetamineNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
DNA-templated transcriptionNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
transcription by RNA polymerase IINuclear receptor subfamily 4 group A member 2Homo sapiens (human)
adult locomotory behaviorNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
post-embryonic developmentNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
central nervous system projection neuron axonogenesisNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
habenula developmentNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
intracellular receptor signaling pathwayNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
cellular response to oxidative stressNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
regulation of dopamine metabolic processNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
dopamine biosynthetic processNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
neuron maturationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
negative regulation of neuron apoptotic processNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
regulation of respiratory gaseous exchangeNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
fat cell differentiationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
positive regulation of transcription by RNA polymerase IINuclear receptor subfamily 4 group A member 2Homo sapiens (human)
neuron apoptotic processNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
general adaptation syndromeNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
canonical Wnt signaling pathwayNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
cellular response to corticotropin-releasing hormone stimulusNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
dopaminergic neuron differentiationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
midbrain dopaminergic neuron differentiationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
negative regulation of apoptotic signaling pathwayNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
regulation of transcription by RNA polymerase IINuclear receptor subfamily 4 group A member 2Homo sapiens (human)
central nervous system neuron differentiationNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (17)

Processvia Protein(s)Taxonomy
DNA-binding transcription factor activity, RNA polymerase II-specificNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
DNA bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nuclear receptor activityNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
protein bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
beta-catenin bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
zinc ion bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nuclear retinoid X receptor bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
protein heterodimerization activityNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
sequence-specific double-stranded DNA bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nuclear glucocorticoid receptor bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (11)

Processvia Protein(s)Taxonomy
nucleusNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nucleoplasmNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
cytoplasmNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nuclear speckNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
chromatinNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
protein-containing complexNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
transcription regulator complexNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
nucleusNuclear receptor subfamily 4 group A member 2Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (58)

Assay IDTitleYearJournalArticle
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1698004Fraction unbound in cynomolgus monkey plasma
AID1698001Lipophilicity, log D of the compound at pH 7.4 by by shake flask method
AID699541Inhibition 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 counting2012Journal 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.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1210301Apparent intrinsic clearance in Sprague-Dawley rat hepatocytes assessed per 10'6 cells at 0.1 to 10 uM up to 90 mins by media-loss method2012Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 40, Issue:8
Utility of drug depletion-time profiles in isolated hepatocytes for accessing hepatic uptake clearance: identifying rate-limiting steps and role of passive processes.
AID1283271Inhibition of HMGCoA reductase in Dhcr7-deficient mouse Neuro2a cells assessed as decrease in 7-DHC levels at 1 uM by LC-MS/GC-MS analysis2016Journal 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.
AID1698002Intrinsic clearance in cryopreserved human hepatocytes at 1 uM measured up to 120 mins by LC-MS/MS analysis
AID1220811Biliary clearance in BCRP-deficient Wistar rat day 6 sandwich-cultured hepatocytes at 5 uM after 10 mins by LC-MS/MS analysis relative to control2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Decreased hepatic breast cancer resistance protein expression and function in multidrug resistance-associated protein 2-deficient (TR⁻) rats.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1210299Apparent intrinsic clearance in Sprague-Dawley rat hepatocytes assessed per 10'6 cells at 0.1 to 10 uM up to 90 mins by conventional assay2012Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 40, Issue:8
Utility of drug depletion-time profiles in isolated hepatocytes for accessing hepatic uptake clearance: identifying rate-limiting steps and role of passive processes.
AID1698006Ratio of drug level in cynomolgus monkey blood to plasma administered through iv dosing by LC-MS/MS analysis
AID1698008Hepatic clearance in Wistar Hannover rat at 1 mg/kg, iv
AID1283247Inhibition of delta 8-7 isomerase in mouse Neuro2a cells assessed as decrease in 7-DHC levels at 1 uM by LC-MS/GC-MS analysis2016Journal 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.
AID1210302Drug metabolism in Sprague-Dawley rat hepatocytes assessed per 10'6 cells at 0.1 to 10 uM up to 90 mins by media-loss method2012Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 40, Issue:8
Utility of drug depletion-time profiles in isolated hepatocytes for accessing hepatic uptake clearance: identifying rate-limiting steps and role of passive processes.
AID1698005Ratio of drug level in Wistar Hannover rat blood to plasma administered through iv dosing by LC-MS/MS analysis
AID1698000Apparent permeability in dog MDCKII-LE cells at pH 7.4
AID1283275Inhibition of DR24 in mouse Neuro2a cells assessed as decrease in 7-DHC levels at 1 uM by LC-MS/GC-MS analysis2016Journal 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.
AID1698011Fraction unbound in human plasma
AID1079933Acute 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
AID1698010Hepatic clearance in human administered through iv dosing
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079938Chronic 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]
AID1220813Biliary excretion index in BCRP-deficient Wistar rat day 6 sandwich-cultured hepatocytes at 5 uM after 10 mins by LC-MS/MS analysis relative to control2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Decreased hepatic breast cancer resistance protein expression and function in multidrug resistance-associated protein 2-deficient (TR⁻) rats.
AID1079936Choleostatic 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]
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1311584Drug uptake in mouse hepatocytes measured at 30 secs relative to control2016Bioorganic & medicinal chemistry letters, 08-01, Volume: 26, Issue:15
Synthesis and evaluation of a series of 4-azaindole-containing p21-activated kinase-1 inhibitors.
AID1698007Ratio of drug level in human blood to plasma administered through iv dosing by LC-MS/MS analysis
AID1318771Inhibition of HMG-CoA reductase in rat liver microsomes assessed as reduction in [14C]-HMG-CoA conversion to [14C]-mevalonic acid after 15 mins by column filtration method2016Journal of medicinal chemistry, 10-13, Volume: 59, Issue:19
The "Cyclopropyl Fragment" is a Versatile Player that Frequently Appears in Preclinical/Clinical Drug Molecules.
AID1697999Dissociation constant, acidic pKa of compound measured up to 18 mins by capillary electrophoresis
AID1698003Fraction unbound in rat plasma
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1311581Drug uptake in mouse hepatocytes measured at 120 secs relative to control2016Bioorganic & medicinal chemistry letters, 08-01, Volume: 26, Issue:15
Synthesis and evaluation of a series of 4-azaindole-containing p21-activated kinase-1 inhibitors.
AID1218862Drug uptake in HEK293 cells expressing OATP1B1 (unknown origin) assessed as OATP1B1-mediated drug transport2012Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 40, Issue:8
The development, characterization, and application of an OATP1B1 inhibition assay in drug discovery.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug 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.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID699540Inhibition 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 counting2012Journal 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.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1218866Drug uptake in HEK293 cells expressing OATP1B1 (unknown origin) assessed as OATP1B1-mediated drug transport per mg protein2012Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 40, Issue:8
The development, characterization, and application of an OATP1B1 inhibition assay in drug discovery.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1885210Agonist activity at human Nurr1 measured by Gal4-Nurr1 hybrid reporter gene assay2022Journal of medicinal chemistry, 07-28, Volume: 65, Issue:14
Medicinal Chemistry and Chemical Biology of Nurr1 Modulators: An Emerging Strategy in Neurodegeneration.
AID679168TP_TRANSPORTER: cell accumulation in OATP2-expressing HEK293 cells2004The Journal of pharmacology and experimental therapeutics, Oct, Volume: 311, Issue:1
Contribution of OATP2 (OATP1B1) and OATP8 (OATP1B3) to the hepatic uptake of pitavastatin in humans.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug 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.
AID699539Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting2012Journal 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.
AID678974TP_TRANSPORTER: cell accumulation in OATP8-expressing HEK293 cells2004The Journal of pharmacology and experimental therapeutics, Oct, Volume: 311, Issue:1
Contribution of OATP2 (OATP1B1) and OATP8 (OATP1B3) to the hepatic uptake of pitavastatin in humans.
AID1079931Moderate 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]
AID1079935Cytolytic 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]
AID1698016Dissociation constant, basic pKa of compound measured up to 18 mins by capillary electrophoresis
AID1698009Hepatic clearance in cynomolgus monkey at < 1 mg/kg, iv administered as cassette dosing
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)2009Bioorganic & medicinal chemistry, Dec-01, Volume: 17, Issue:23
Synthesis and HMG-CoA reductase inhibition of 2-cyclopropyl-4-thiophenyl-quinoline mevalonolactones.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (714)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's11 (1.54)18.2507
2000's206 (28.85)29.6817
2010's399 (55.88)24.3611
2020's98 (13.73)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials192 (26.30%)5.53%
Reviews75 (10.27%)6.00%
Case Studies10 (1.37%)4.05%
Observational3 (0.41%)0.25%
Other450 (61.64%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (80)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Efficacy and Safety of Pitavastatin and PCSK9 Inhibitors in Liver Transplant Patients [NCT05537948]Phase 480 participants (Anticipated)Interventional2021-10-01Recruiting
Effects of Pitavastatin Treatments on the Plasma Lgi3 Level in the Patients With Dyslipidemia: A Randomized Crossover Trial [NCT03730038]50 participants (Actual)Interventional2019-02-18Completed
Thyroid Hormone Replacement for Subclinical Hypothyroidism and Dyslipidemia in Patients With Atherosclerotic Cardiovascular Diseases (ThyroHeart-Lipid Study) [NCT03606824]248 participants (Anticipated)Interventional2019-03-25Recruiting
An Open-Label, Fixed Sequence, Two-Period Study to Investigate the Effect of RO7049389 on the Pharmacokinetics of Pitavastatin in Healthy Volunteers [NCT03717064]Phase 118 participants (Actual)Interventional2018-11-07Completed
Effects of Pitavastatin or Combination of Pitavastatin and Ezetimibe on Glucose Metabolism Compared to AtoRvastatin in atheroscLerotic Cardiovascular Disease Patients With Metabolic Syndrome: The EZ-PEARL Randomized Trial [NCT05705804]250 participants (Anticipated)Interventional2023-06-13Recruiting
A Multicenter, Randomized, Double-blinded, Parallel, Therapeutic Confirmatory Clinical Trial to Evaluate the Efficacy and Safety of Pitavastatin Versus Pitavastatin/Fenofibrate in Complex-dyslipidemia Patients [NCT03618797]Phase 3347 participants (Actual)Interventional2015-11-30Completed
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)Observational2021-11-19Completed
A Prospective, Double-blind, Randomized, Parallel, Multiple-center Study to Compare the Efficacy and Safety of 1PC002 and Atorvastatin in Taiwanese Patients With Hypercholesterolemia [NCT01710007]Phase 3202 participants (Actual)Interventional2011-11-30Completed
Effect of Pitavastatin on Coronary Flow Reserve in Hypertensive Patients With Cardiovascular Risk [NCT02144922]Phase 485 participants (Actual)Interventional2014-05-31Completed
A Multi-center, Open-label, Randomized, 12-month, Parallel-group, Non-inferiority Study to Compare the Hemoglobin A1C Metabolism of Pitavastatin Therapy Versus Atorvastatin in Chinese Patients With Prediabetes and Hypertension [NCT03532620]Phase 4396 participants (Anticipated)Interventional2018-08-09Recruiting
A Study to Assess the Pharmacokinetics of Midazolam, Dabigatran, Pitavastatin, Atorvastatin, and Rosuvastatin Administered as Microdoses in Subjects With Varying Degrees of Renal Insufficiency in the Presence and Absence of Rifampin [NCT03311841]Phase 132 participants (Actual)Interventional2018-03-01Completed
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 4252 participants (Actual)Interventional2010-12-31Completed
Pitavastatin Evaluation of Atherosclerosis Regression by Intensive Cholesterol-Lowering Therapy [NCT00711919]300 participants (Anticipated)Interventional2007-07-31Active, not recruiting
A Phase 1, Open-label, Sequential Study to Investigate the Effect of JNJ 63623872 on Pitavastatin in Healthy Subjects [NCT02595268]Phase 114 participants (Actual)Interventional2015-11-30Completed
Randomized Evaluation of Aggressive or Moderate Lipid Lowering Therapy With Pitavastatin in Coronary Artery Disease (REAL-CAD) [NCT01042730]13,054 participants (Actual)Interventional2010-02-28Completed
Effect of Low-dose vs. High-dose Pitavastatin on In-stent Restenosis, Endothelial Function, Circulating microRNAs, and Cardiovascular Events in Patients With Coronary Artery Disease Requiring Stent Implantation: OCT and NIRS Comparison [NCT02545231]Phase 41,000 participants (Actual)Interventional2013-02-28Completed
Randomized, Open-label, Multi-centered Study to Evaluate the Safety and Efficacy of Pitavastatin in Patients With Impaired Fasting Glucose and Hyperlipidemia(Phase 4) [NCT02056847]Phase 4313 participants (Actual)Interventional2013-09-30Completed
Phase 0 lead-in Trial of Pitavastatin in Primary and Recurrent Glioblastoma Patients [NCT05977738]Early Phase 118 participants (Anticipated)Interventional2023-11-30Not yet recruiting
Randomized Trial to Prevent Vascular Events in HIV - REPRIEVE [NCT02344290]Phase 37,769 participants (Actual)Interventional2015-03-26Completed
Single Centre in Vivo Cocktail Phenotyping Study on OATP1B1, OCT1/2, MATE1/2K, OAT1/3, and P-gp Drug Transporters in Healthy Volunteers [NCT02743260]Phase 424 participants (Actual)Interventional2016-04-30Completed
[NCT02799758]Phase 30 participants (Actual)Interventional2016-02-29Withdrawn
Orient Pharma Co., Ltd. [NCT04643093]Phase 3390 participants (Actual)Interventional2020-08-01Completed
[NCT02670434]Phase 30 participants (Actual)Interventional2016-01-31Withdrawn
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 470 participants (Anticipated)Interventional2008-07-31Completed
Combination of Low Dose Antiestrogens With Omega-3 Fatty Acids for Prevention of Hormone-independent Breast Cancer [NCT00723398]266 participants (Actual)Interventional2009-03-31Completed
Effect of Pitavastatin on Erythrocyte Membrane Fatty Acid Contents in Patients With Chronic Kidney Disease [NCT02863185]Phase 445 participants (Actual)Interventional2016-05-01Completed
Effects of Three Statins, Simvastatin, Atorvastatin, and Pitavastatin, on the Pharmacokinetics for Midazolam in Healthy Volunteers [NCT00716846]11 participants (Actual)Interventional2006-06-30Completed
[NCT02634034]Phase 118 participants (Actual)Interventional2015-12-31Completed
Comparison of Pitavastatin With Atorvastatin in Increasing HDL-C and Adiponectin in Patients With Dyslipidemia and Coronary Artery Disease. [NCT00861861]Phase 4129 participants (Actual)Interventional2008-09-30Completed
Yokohama Assessment of Fluvastatin, Pravastatin, Pitavastatin and Atorvastatin in Acute Coronary Syndrome (Yokohama-ACS) [NCT00549926]Phase 4200 participants (Anticipated)Interventional2007-10-31Completed
A 12-week, Randomized, Multicenter, Double-blind, Active-controlled, Non-inferiority Study to Compare the Efficacy and Safety of Pitavastatin and Atorvastatin in High Risk Hypercholesterolemic Patients [NCT01386853]Phase 3200 participants (Anticipated)Interventional2011-07-31Not yet recruiting
Evaluation of Potential for Pharmacokinetic Drug Interaction Between SCH 58235 and Pitavastatin [NCT00653913]Phase 118 participants (Actual)Interventional2004-03-31Completed
[NCT00548145]38 participants (Actual)Interventional2007-11-30Terminated
A Randomized, Open Label, Comparative Study to Evaluate Effect of Pitavastatin for Reduction of Myocardial Damage in Patient Are Scheduled Elective PCI for Stable Angina Pectoris [NCT00786734]Phase 40 participants (Actual)Interventional2008-08-31Withdrawn
Effects of Pitavastatin on Insulin Sensitivity and Liver Fat [NCT02290106]50 participants (Actual)Interventional2015-03-02Completed
Study of Pitavastatin Vs. Simvastatin (Following Up-Titration) in Patients With Primary Hypercholesterolemia or Combined Dyslipidemia [NCT00309777]Phase 3857 participants (Actual)Interventional2005-09-30Completed
Multicenter Study for Anti-oxidative and Anti-inflammatory Effects of Pitavastatin in Hypercholesterolemic Patients With Metabolic Syndrome [NCT00444717]Phase 4100 participants (Actual)Interventional2007-04-30Completed
To Evaluate the Efficacy and Safety of Combination Therapy of Pitavastatin and Ezetimibe Versus Monotherapy of Pitavastatin in Patients With Primary Hypercholesterolemia [NCT04584736]Phase 3283 participants (Actual)Interventional2019-06-11Completed
Drug-Drug Interaction Study to Assess the Effects of Steady State Pitavastatin 4 mg or Rosuvastatin 40 mg on Steady-State Warfarin in Healthy Adult Volunteers [NCT01178853]Phase 448 participants (Actual)Interventional2010-07-31Completed
Pharmacodynamic Comparison of Pitavastatin Versus Atorvastatin on Platelet Reactivity in Patients With Coronary Artery Disease Treated With Dual Antiplatelet Therapy - The PORTO Trial [NCT01648829]Phase 4100 participants (Anticipated)Interventional2014-01-31Not yet recruiting
A Prospective Comparative Clinical Study to Identify Efficacy and Safety of Pitavastatin in Patients With a Metabolic Syndrome [NCT00640276]Phase 4187 participants (Actual)Interventional2008-04-30Completed
A Phase-1, Open-label, Four Group, Fixed-Sequence Study to Evaluate the Effect of AL-794 on the Pharmacokinetics of Oseltamivir, JNJ-63623872, and Probes for P-glycoprotein, CYP3A and OATP1B1 in Healthy Volunteers [NCT02888327]Phase 168 participants (Actual)Interventional2016-07-31Completed
A Phase 1 Open-Label, Dose Escalation Study of Pitavastatin in Combination With Venetoclax in Patients With Chronic Lymphocytic Leukemia or Acute Myeloid Leukemia [NCT04512105]Phase 115 participants (Anticipated)Interventional2020-12-02Recruiting
A Randomized, Double Blind, Double Dummy, Placebo Controlled Phase III Trial to Evaluate the Efficacy, Safety of Coadministered Pitavastatin and Valsartan in Patients With Hypertension and Dyslipidemia(COCTAIL Study) [NCT01402843]Phase 3150 participants (Anticipated)Interventional2011-06-30Completed
A Single Dose, Sequence-randomized, Open-label, 2x2 Crossover Study to Compare Pharmacokinetics Between Pitavastatin and Valsartan Co-administration and Livalo® Fixed Combination Drug in Healthy Male Subjects [NCT01406431]Phase 148 participants (Actual)Interventional2011-08-31Completed
Differential Intervention Trial by Standard Therapy Versus Pitavastatin in Patients With Chronic Hemodialysis. [NCT00846118]905 participants (Actual)Interventional2009-02-01Terminated
Preventive Effect of the PRetreatment With pItavastatiN on Contrast-Induced Nephropathy in Patients With RenaL Dysfunction UndErgoing Coronary Angiography/Intervention (PRINCIPLE-II Study) [NCT01871792]Phase 4404 participants (Anticipated)Interventional2013-06-30Not yet recruiting
Efficacy and Safety of Pitavastatin in a Real-wOrld Setting: Observational Study Evaluating saFety in Patient With Pitavastatin for Lipid Lowering Therapy in Korea [NCT04402112]28,343 participants (Actual)Observational2012-04-02Completed
A 12-month Open-label, Multicenter Observation Study on the Occurrence of Major Adverse Cardiac Events (MACE) in Patients With Acute Myocardial Infarction (AMI) Receiving Pitavastatin/Valsartan Treatment [NCT04270344]905 participants (Anticipated)Observational2018-07-01Recruiting
Drug-Drug Interaction Study to Assess the Effects of Steady-State Lopinavir/Ritonavir on Pitavastatin in Healthy Adult Volunteers [NCT01057433]Phase 424 participants (Actual)Interventional2010-01-31Completed
Open-Label, Long-Term (> 1 Year) Extension Study of Pitavastatin in Elderly Patients With Primary Hypercholesterolemia or Combined Dyslipidemia [NCT00330876]Phase 3545 participants (Actual)Interventional2006-06-30Completed
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 4328 participants (Actual)Interventional2010-10-31Completed
A Study to Compare the Safety, Tolerability, and Pharmacokinetic Profile of a Single Oral Dose of Pitavastatin 4 mg in Adult Volunteers With Severe Renal Impairment Who Are Not Being Treated With Hemodialysis Versus Healthy Adult Volunteers [NCT01043094]Phase 416 participants (Actual)Interventional2009-12-31Completed
the Long-term Effects of High-doSe pitavaStatin on Diabetogenicity in Comparison With Atorvastatin in Patients With Metabolic Syndrome (LESS-DM) Randomized Clinical Trial [NCT02940366]Phase 4500 participants (Anticipated)Interventional2016-12-01Recruiting
Double-blind follow-on Study of Pitavastatin (4mg) Versus Simvastatin (40mg and 80mg) With a Single-blind Extension of Treatment in Patients With Primary Hypercholesterolemia or Combined Dyslipidemia and 2 or More Risk Factors for Coronary Heart Disease [NCT00344175]Phase 3178 participants (Actual)Interventional2006-06-30Completed
A Clinical Study to Evaluate the Pharmacokinetics of Microdose Midazolam, Dabigatran, Pitavastatin, Atorvastatin and Rosuvastatin in Healthy Volunteers and Renal Impairment Patients [NCT05747768]Phase 460 participants (Anticipated)Interventional2022-07-15Recruiting
Efficacy of Statin Addition to Neoadjuvant Chemotherapy Protocols for Breast Cancer [NCT04705909]Phase 2/Phase 360 participants (Anticipated)Interventional2021-01-15Not yet recruiting
Study of Pitavastatin Vs. Atorvastatin (Following Up-Titration) in Patients With Type II Diabetes Mellitus and Combined Dyslipidemia [NCT00309751]Phase 3418 participants (Actual)Interventional2005-12-31Completed
Comparison of Atorvastatin and Pitavastatin on the Effect of HbA1c in Acute Myocardial Infarction (AMI) Patients With Abnormal Glucose Metabolism: a Multicenter Prospective Randomized Clinical Trial [NCT04945122]Phase 4900 participants (Anticipated)Interventional2015-10-01Recruiting
Japan Prevention Trial of Diabetes by Pitavastatin in Patients With Impaired Glucose Tolerance (J-PREDICT) [NCT00301392]Phase 41,240 participants (Actual)Interventional2006-04-30Completed
[NCT01502904]Phase 4120 participants (Actual)Interventional2010-07-31Completed
A Single Dose, Sequence-randomized, Open-label, 2x2 Crossover Study to Compare Pharmacokinetics Between Pitavastatn and Valsartan Co-administration and Livalo Complex Product in Healthy Male Subjects [NCT01764178]Phase 152 participants (Actual)Interventional2013-01-22Completed
Open-label, Randomized, Repeated Dosing Crossover Study to Evaluate the Pharmacokinetic Interaction Between Micronized Fenofibrate and Pitavastatin in Healthy Adult Subjects [NCT01767610]Phase 124 participants (Actual)Interventional2013-01-31Completed
Pitavastatin to REduce Physical Function Impairment and FRailty in HIV (PREPARE) [NCT03070223]602 participants (Actual)Observational2017-02-28Completed
Double-Blind, Follow-On Study of Pitavastatin (4 mg) Versus Atorvastatin (20 mg and 40 mg), With a Single-Blind Extension of Treatment, in Patients With Type II Diabetes Mellitus and Combined Dyslipidemia [NCT00344370]Phase 3214 participants (Actual)Interventional2006-08-31Completed
Drug-Drug Interaction Study to Assess the Effects of Steady-State Darunavir/Ritonavir on Steady-State Pitavastatin in Healthy Adult Volunteers [NCT01422369]Phase 428 participants (Actual)Interventional2011-04-30Completed
A Randomized, Open Label, Dose Titration Study to Evaluate the Efficacy and Safety of Pitavastatin Compared to atoRvastatin in Type 2 dIabeTes Mellitus With Hypercholesterolemia [NCT00889226]Phase 4161 participants (Actual)Interventional2008-04-30Completed
An Open Label Study of the Chronic and Acute Effects of Pitavastatin on Monocyte Phenotype, Endothelial Dysfunction and HDL Atheroprotective Function in Subjects With Metabolic Syndrome (CAPITAIN) [NCT01595828]Phase 114 participants (Actual)Interventional2010-10-31Completed
Study of Pitavastatin Vs. Simvastatin (Following Up-Titration) in Patients With Primary Hypercholesterolemia or Combined Dyslipidemia and 2 or More Risk Factors for Coronary Heart Disease [NCT00309738]Phase 3355 participants (Actual)Interventional2005-09-30Completed
Safety and Efficacy of Statins for Chinese Patients With Dyslipidemia: A Network Register-based Follow-up Study [NCT03418974]Phase 410,000 participants (Actual)Interventional2017-11-01Active, not recruiting
Dyslipidemia of Obesity Intervention in Teens Trial [NCT02956590]Phase 3122 participants (Actual)Interventional2018-05-01Completed
Study of Pitavastatin 2 mg vs. Atorvastatin 10 mg and Pitavastatin 4 mg vs. Atorvastatin 20 mg (Following Up Titration) in Patients With Primary Hypercholesterolemia or Combined Dyslipidemia [NCT00249249]Phase 3830 participants (Actual)Interventional2005-10-31Completed
Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome [NCT00242944]Phase 4307 participants (Actual)Interventional2005-11-30Completed
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 3962 participants (Actual)Interventional2005-09-30Completed
Open-Label, Long-Term (1 Year) Extension Study of Pitavastatin in Patients With Primary Hypercholesterolemia or Combined Dyslipidemia [NCT00325780]Phase 31,355 participants (Actual)Interventional2006-07-31Completed
A Phase 2 Efficacy and Safety Dose-Ranging Study of LY3015014 in Patients With Primary Hypercholesterolemia [NCT01890967]Phase 2527 participants (Actual)Interventional2013-06-30Completed
The Effect of Efavirenz and Ritonavir-boosted Darunavir on the Pharmacokinetics of the HMG CoA Reductase Inhibitor Pitavastatin [NCT01695954]Phase 134 participants (Actual)Interventional2012-05-31Completed
Drug-Drug Interaction Study to Assess the Effects of Steady-State Cardizem LA (Diltiazem Hydrochloride) and Steady-State Pitavastatin on Their Respective Pharmacokinetics in Healthy Adult Volunteers [NCT01422382]Phase 428 participants (Actual)Interventional2011-05-31Completed
A Randomized , Open Label, Dose Titration Study to Evaluate the Effect of Pitavastatin Versus Atorvastatin in Patients With Hypercholesterolemia and Mild to Moderate Hepatic Damage [NCT01166633]Phase 4200 participants (Actual)Interventional2009-06-30Completed
Effects of Pitavastatin on Lipid Profiles in HIV-infected Patients With Dyslipidemia and Receiving Atazanavir/Ritonavir: A Randomized, Double-blind, Crossover Study [NCT02442700]Phase 424 participants (Actual)Interventional2014-05-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00249249 (12) [back to overview]Triglycerides (TG)
NCT00249249 (12) [back to overview]TC:HDL-C Ratio
NCT00249249 (12) [back to overview]Percent Change From Baseline Low Density Lipoprotein-cholesterol (LDL-C) at Week 12
NCT00249249 (12) [back to overview]Percent Change From Baseline in Total Cholesterol (TC)
NCT00249249 (12) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C)
NCT00249249 (12) [back to overview]Oxidized LDL at 12 Weeks
NCT00249249 (12) [back to overview]Non-HDL:HDL Ratio
NCT00249249 (12) [back to overview]National Cholesterol Education Program [NCEP]LDL-C Target Attainment
NCT00249249 (12) [back to overview]High Sensitivity C-reactive Protein (Hs-CRP) at 12 Weeks
NCT00249249 (12) [back to overview]Apolipoprotein-A1 (Apo-A1)
NCT00249249 (12) [back to overview]Apolipoprotein B (Apo B)
NCT00249249 (12) [back to overview]Apo-B:Apo-A1 Ratio
NCT00257686 (2) [back to overview]Percent Change From Baseline in LDL-C
NCT00257686 (2) [back to overview]Percent Change From Baseline in TC
NCT00309738 (2) [back to overview]Percent Change From Baseline in LDL-C
NCT00309738 (2) [back to overview]Number of Patients Attaining NCEP LDL-C Target (< 160 mg/dL)
NCT00309751 (2) [back to overview]Number of Patients Attaining National Cholesterol Education Program (NCEP) LDL-C Target
NCT00309751 (2) [back to overview]Percent Change From Baseline Low Density Lipoprotein Cholesterol (LDL-C)
NCT00309777 (2) [back to overview]Percent Change From Baseline in Low Density Lipoprotein-cholesterol (LDL-C) at 12 Weeks
NCT00309777 (2) [back to overview]National Cholesterol Education Program (NCEP) LDL-C Target Attainment
NCT00325780 (2) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C)
NCT00325780 (2) [back to overview]Change From Baseline in Total Cholesterol
NCT00330876 (2) [back to overview]Change From Baseline in LDL-C
NCT00330876 (2) [back to overview]Change From Baseline in Total Cholesterol
NCT00344175 (3) [back to overview]Number of Patients Attaining NCEP LDL-C Target at Week 44
NCT00344175 (3) [back to overview]Number of Patients Attaining NCEP LDL-C Target at Week 16
NCT00344175 (3) [back to overview]Percent Change From Baseline in LDL-C
NCT00344370 (2) [back to overview]Percent Change From Baseline in LDL-C
NCT00344370 (2) [back to overview]NCEP LDL-C Target Attainment
NCT00548145 (1) [back to overview]Alzheimer's Disease Assessment Scale-cognitive Component-Japanese Version(ADAS-Jcog)
NCT00723398 (11) [back to overview]Changes in Insulin-like Growth Factor-1 (IGF-1) and Insulin-like Growth Factor-1 Binding Protein-3 (IGFBP-3)
NCT00723398 (11) [back to overview]Change in Absolute Breast Density
NCT00723398 (11) [back to overview]Changes in Biomarkers for Oxidative Stress: Urinary 8-hydroxy-deoxyguansine
NCT00723398 (11) [back to overview]Changes in Biomarkers for Oxidative Stress:Urinary 8-(Isoprostane) F-2α
NCT00723398 (11) [back to overview]Changes in Complete Blood Count: Hematocrit
NCT00723398 (11) [back to overview]Changes in Complete Blood Count: Hemoglobin
NCT00723398 (11) [back to overview]Changes in Complete Blood Count: Red Blood Cells
NCT00723398 (11) [back to overview]Changes in Complete Blood Count: White Blood Cells and Platelets
NCT00723398 (11) [back to overview]Changes in Serum Biomarkers for Inflammation From Levels of High Sensitivity C-reactive Protein (hsCRP) and Interleukin 6 (IL-6)
NCT00723398 (11) [back to overview]Changes in Serum Lipid Levels
NCT00723398 (11) [back to overview]Changes in Biomarkers for Estrogen Metabolism: 2-hydroxy Estrone (Urinary 2-OHE1) and 16-α-hydroxy Estrone (16α-OHE1)
NCT00889226 (2) [back to overview]Proportion of Patients Achieving LDL- C<100mg/dL
NCT00889226 (2) [back to overview]The Change of LDL-C
NCT01043094 (2) [back to overview]Number of Participants With Treatment Emergent Adverse Events
NCT01043094 (2) [back to overview]Area Under the Curve From 0 to Tau (AUC 0-t (ng*h/mL))
NCT01057433 (1) [back to overview]Area Under the Curve From Time 0 to Tau (AUC 0-τ)
NCT01178853 (1) [back to overview]Percent Mean Change From Baseline of International Normalized Ratio (INR)
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
NCT01422369 (2) [back to overview]Number of Participants With at Least One Adverse Event.
NCT01422369 (2) [back to overview]NK-104 AUC
NCT01422382 (2) [back to overview]NK-104 AUC
NCT01422382 (2) [back to overview]Number of Participants With at Least One Adverse Event.
NCT01695954 (3) [back to overview]AUC
NCT01695954 (3) [back to overview]GMR of Cmax of Pitavastatin When Coadministered With Efavirenz or With Darunavir/Ritonavir
NCT01695954 (3) [back to overview]GMR of 24- Hour AUC of Pitavastatin When Coadministered With Efavirenz or With Darunavir/Ritonavir Over 24 Hour AUC of Pitavastatin
NCT01710007 (4) [back to overview]Triglyceride
NCT01710007 (4) [back to overview]LDL-C
NCT01710007 (4) [back to overview]The Percentage Change From Baseline in LDL-C Level at Week 12.
NCT01710007 (4) [back to overview]HDL-C
NCT01890967 (10) [back to overview]Change From Baseline in High Sensitivity C-Reactive Protein (hsCRP)
NCT01890967 (10) [back to overview]Number of Participants Who Develop Treatment Emergent Anti-LY3015014 Antibodies
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 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]Percentage Change From Baseline in Total Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
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]Number of Participants With an Injection Site Reaction
NCT02290106 (7) [back to overview]Insulin-stimulated Glucose Uptake
NCT02290106 (7) [back to overview]Alanine Aminotransferase (ALT)
NCT02290106 (7) [back to overview]Hepatic Insulin Sensitivity
NCT02290106 (7) [back to overview]Aspartate Aminotransferase (AST)
NCT02290106 (7) [back to overview]Hemoglobin A1c (HbA1c)
NCT02290106 (7) [back to overview]Quantitative Insulin Sensitivity Check Index (QUICKI)
NCT02290106 (7) [back to overview]Liver Fat
NCT02442700 (2) [back to overview]Efficacy of Pitavastatin in HIV-infected Patients With Dyslipidemia and Receiving Atazanavir/Ritonavir
NCT02442700 (2) [back to overview]Safety of Pitavastatin in HIV-infected Patients
NCT03311841 (18) [back to overview]Effect of Rifampin on Tmax Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on t1/2 Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on Cmax Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on CL/F Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on C24 Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on AUC0-inf Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on AUC0-24 Post-dose Period 2
NCT03311841 (18) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to Last (AUC0-last) Post-dose Period 1
NCT03311841 (18) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to Infinity (AUC0-inf) Post-dose Period 1
NCT03311841 (18) [back to overview]Maximum Plasma Concentration (Cmax) Post-dose Period 1
NCT03311841 (18) [back to overview]Apparent Volume of Distribution During the Terminal Phase (Vz/F) Post-dose Period 1
NCT03311841 (18) [back to overview]Apparent Plasma Terminal Half-life (t1/2) Post-dose Period 1
NCT03311841 (18) [back to overview]Apparent Clearance After Extravascular Administration (CL/F) Post-dose Period 1
NCT03311841 (18) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to 24 Hours (AUC0-24) Post-dose Period 1
NCT03311841 (18) [back to overview]Effect of Rifampin on Vz/F Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on AUC0-last Post-dose Period 2
NCT03311841 (18) [back to overview]Time to Maximum Plasma Concentration (Tmax) Post-dose Period 1
NCT03311841 (18) [back to overview]Plasma Concentration at 24 Hours (C24) Post-dose Period 1
NCT03717064 (21) [back to overview]Period 2: Elimination Half-Life (T1/2) of Pitavastatin
NCT03717064 (21) [back to overview]Period 2: Cmax of RO7049389
NCT03717064 (21) [back to overview]Period 2: AUC-tau of RO7049389
NCT03717064 (21) [back to overview]Period 1: Cmax of Pitavastatin Lactone
NCT03717064 (21) [back to overview]Period 2: AUC Ratio of Pitavastatin Lactone to Pitavastatin
NCT03717064 (21) [back to overview]Period 2: AUC0-inf of Pitavastatin Lactone
NCT03717064 (21) [back to overview]Percentage of Participants With Adverse Events (AEs)
NCT03717064 (21) [back to overview]Period 2: Cmax of Pitavastatin Lactone
NCT03717064 (21) [back to overview]Period 2: Maximum Plasma Concentration (Cmax) of Pitavastatin
NCT03717064 (21) [back to overview]Period 2: Plasma Concentration Versus Time (Area Under the Curve, AUC0-inf) of Pitavastatin
NCT03717064 (21) [back to overview]Period 2: Time to Maximum Concentration (Tmax) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Volume of Distribution (V/F) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Time to Maximum Concentration (Tmax) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Plasma Concentration Versus Time (Area Under the Curve, AUC0-inf) of Pitavastatin
NCT03717064 (21) [back to overview]Period 2: Apparent Total Clearance (CL/F) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: AUC Ratio of Pitavastatin Lactone to Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Apparent Total Clearance (CL/F) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Maximum Plasma Concentration (Cmax) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: Elimination Half-Life (T1/2) of Pitavastatin
NCT03717064 (21) [back to overview]Period 2: Volume of Distribution (V/F) of Pitavastatin
NCT03717064 (21) [back to overview]Period 1: AUC0-inf of Pitavastatin Lactone

Triglycerides (TG)

mean triglycerides at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
Pitavastatin 2 mg QD132.4
Atorvastatin 10 mg QD122.2
Pitavastatin 4 mg QD124.4
Atorvastatin 20 mg QD122.6

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TC:HDL-C Ratio

Ratio of mean total cholesterol to mean HDL-C at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionratio (Mean)
Pitavastatin 2 mg QD4.018
Atorvastatin 10 mg QD3.763
Pitavastatin 4 mg QD3.583
Atorvastatin 20 mg QD3.79

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Percent Change From Baseline Low Density Lipoprotein-cholesterol (LDL-C) at Week 12

(NCT00249249)
Timeframe: Baseline to 12 weeks

Interventionpercent change (Mean)
Pitavastatin 2 mg QD-37.89
Atorvastatin 10 mg QD-38.76
Pitavastatin 4 mg QD-45.5
Atorvastatin 20 mg QD-43.9

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Percent Change From Baseline in Total Cholesterol (TC)

Percent change in total cholesterol from baseline to Week 12 (NCT00249249)
Timeframe: Baseline to 12 Weeks

Interventionpercent change (Mean)
Pitavastatin 2 mg QD-27.57
Atorvastatin 10 mg QD-28.92
Pitavastatin 4 mg QD-33.09
Atorvastatin 20 mg QD-32.99

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C)

percent change from baseline in high density lipoprotein-cholesterol (HDL-C) (NCT00249249)
Timeframe: Baseline to 12 weeks

Interventionpercent change (Mean)
Pitavastatin 2 mg QD4.28
Atorvastatin 10 mg QD3.42
Pitavastatin 4 mg QD4.93
Atorvastatin 20 mg QD2.63

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Oxidized LDL at 12 Weeks

oxidized low density lipoprotein at 12 weeks (NCT00249249)
Timeframe: 12 weeks

InterventionU/L (Mean)
Pitavastatin 2 mg QD59.93
Atorvastatin 10 mg QD58.59
Pitavastatin 4 mg QD54.32
Atorvastatin 20 mg QD54.70

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Non-HDL:HDL Ratio

Ratio of non-HDL to HDL at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Intervention (Mean)
Pitavastatin 2 mg QD2.993
Atorvastatin 10 mg QD2.770
Pitavastatin 4 mg QD2.601
Atorvastatin 20 mg QD2.710

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National Cholesterol Education Program [NCEP]LDL-C Target Attainment

Number of patients achieving NCEP LDL-C target (LDL-C less than or equal to 130 mg/dL) (NCT00249249)
Timeframe: up to 12 weeks

InterventionPatients (Number)
Pitavastatin 2 mg QD179
Atorvastatin 10 mg QD67
Pitavastatin 4 mg QD232
Atorvastatin 20 mg QD72

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High Sensitivity C-reactive Protein (Hs-CRP) at 12 Weeks

high sensitivity C-reactive protein (hs-CRP) at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionmg/L (Mean)
Pitavastatin 2 mg QD2.87
Atorvastatin 10 mg QD2.39
Pitavastatin 4 mg QD3.12
Atorvastatin 20 mg QD2.56

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Apolipoprotein-A1 (Apo-A1)

Apolipoprotein-A1 at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
Pitavastatin 2 mg QD164.6
Atorvastatin 10 mg QD166
Pitavastatin 4 mg QD166.9
Atorvastatin 20 mg QD160.9

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Apolipoprotein B (Apo B)

Apolipoprotein B at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
Pitavastatin 2 mg QD114.5
Atorvastatin 10 mg QD111.1
Pitavastatin 4 mg QD102.3
Atorvastatin 20 mg QD102.4

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Apo-B:Apo-A1 Ratio

Ratio of Apo-B to Apo-A1 at 12 weeks (NCT00249249)
Timeframe: 12 weeks

Interventionratio (Mean)
Pitavastatin 2 mg QD0.72
Atorvastatin 10 mg QD0.68
Pitavastatin 4 mg QD0.64
Atorvastatin 20 mg QD0.66

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Percent Change From Baseline in LDL-C

Percent change from baseline in low density cholesterol (LDL-C) (NCT00257686)
Timeframe: Baseline to 12 weeks

InterventionPercent 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

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Percent Change From Baseline in TC

Percent change from baseline in total cholesterol (TC) (NCT00257686)
Timeframe: Baseline to 12 weeks

InterventionPercent 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

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Percent Change From Baseline in LDL-C

Percent change from baseline in low density lipoprotein-cholesterol (LDL-C) (NCT00309738)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
Pitavastatin 4 mg QD-43.96
Simvastatin 40 mg QD-43.77

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Number of Patients Attaining NCEP LDL-C Target (< 160 mg/dL)

Number of patients attaining LDL-C target according to National Cholesterol Education Program (NCEP) criteria (< 160 mg/dL) (NCT00309738)
Timeframe: 12 weeks

Interventionparticipants (Number)
Pitavastatin 4 mg QD203
Simvastatin 40 mg QD101

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Number of Patients Attaining National Cholesterol Education Program (NCEP) LDL-C Target

Number of patients attaining National Cholesterol Education Program (NCEP)LDL-C target (LDL-C less than 160 mg/dL) at 12 weeks (NCT00309751)
Timeframe: 12 weeks

InterventionParticipants (Number)
Pitavastatin 4 mg QD212
Atorvastatin 20 mg QD111

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Percent Change From Baseline Low Density Lipoprotein Cholesterol (LDL-C)

Percent change from baseline to Week 12 low density lipoprotein cholesterol (LDL-C) (NCT00309751)
Timeframe: 12 weeks

Interventionpercent change (Mean)
Pitavastatin 4 mg QD-40.78
Atorvastatin 20 mg QD-43.25

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Percent Change From Baseline in Low Density Lipoprotein-cholesterol (LDL-C) at 12 Weeks

Percent change from baseline in low density lipoprotein-cholesterol (LDL-C)after 12 Weeks (NCT00309777)
Timeframe: Baseline to 12 weeks

InterventionPercent change (Mean)
Pitavastatin 2 mg-38.99
Simvastatin 20 mg-34.97
Pitavastatin 4 mg-43.97
Simvastatin 40 mg-42.84

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National Cholesterol Education Program (NCEP) LDL-C Target Attainment

Number of subjects achieving National Cholesterol Education Program (NCEP) LDL-C Target (LDL less than or equal to 130 mg/dL)at Week 12 (NCT00309777)
Timeframe: 12 week

InterventionParticipants (Number)
Pitavastatin 2 mg215
Simvastatin 20 mg69
Pitavastatin 4 mg253
Simvastatin 40 mg86

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C)

Mean percent change from baseline in low-density lipoprotein cholesterol (LDL-C) (NCT00325780)
Timeframe: Baseline to 52 Weeks

Interventionpercent change (Mean)
Pitavastatin 4 mg QD-42.89

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Change From Baseline in Total Cholesterol

Mean percent change from baseline in total cholesterol (NCT00325780)
Timeframe: Baseline to 52 weeks

Interventionpercent change (Mean)
Pitavastatin 4 mg QD-29.59

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Change From Baseline in LDL-C

percent change from baseline in low density lipoprotein-cholesterol (LDL-C) (NCT00330876)
Timeframe: Baseline to 60 weeks

Interventionpercent change (Mean)
Pitavastatin 2 mg QD-43.18
Pitavastatin 4 mg QD-44.26

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Change From Baseline in Total Cholesterol

Percent change from baseline in total cholesterol (TC) (NCT00330876)
Timeframe: Baseline to 60 weeks

Interventionpercent change (Mean)
Pitavastatin 2 mg QD-28.27
Pitavastatin 4 mg QD-30.54

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Number of Patients Attaining NCEP LDL-C Target at Week 44

Number of patients attaining National Cholesterol Education Program (NCEP) LDL-C target at Week 44. According to NCEP criteria the target LDL-C is 100 mg/dL. (NCT00344175)
Timeframe: 44 Weeks

InterventionParticipants (Number)
Pitavastatin 4 mg94
Simvastatin 40mg/80mg42

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Number of Patients Attaining NCEP LDL-C Target at Week 16

Number of patients attaining the National Cholesterol Education Program (NCEP) LDL-C target at Week 16. According to NCEP criteria the target LDL-C is 100 mg/dL. (NCT00344175)
Timeframe: 16 weeks

Interventionparticpants (Number)
Pitavastatin 4 mg98
Simvastatin 40mg/80mg45

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Percent Change From Baseline in LDL-C

(NCT00344175)
Timeframe: Baseline to 44 weeks

Interventionpercent change (Mean)
Pitavastatin 4 mg-41.81
Simvastatin 40mg/80mg-41.37

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Percent Change From Baseline in LDL-C

Percent change from baseline in LDL-C at 44 weeks (NCT00344370)
Timeframe: Basseline to 44 weeks

Interventionpercent change (Mean)
Pitavastatin 4 mg-40.98
Atorvastatin 40 mg-41.43

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NCEP LDL-C Target Attainment

Number of patients attaining National Cholesterol Education Program (NCEP) LDL-C target at 44 weeks. According to NCEP criteria the target LDL-C is 100 mg/dL for all patients in this study. (NCT00344370)
Timeframe: 44 weeks

InterventionParticipants (Number)
Pitavastatin 4 mg110
Atorvastatin 40 mg55

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Alzheimer's Disease Assessment Scale-cognitive Component-Japanese Version(ADAS-Jcog)

Alzheimer's Disease Assessment Scale-cognitive component-Japanese version is a cognitive test for Alzheimer's disease. This test includes some aspects that assess memory ,orientation, language, praxis, and so on. The possible range of this test is 0-70 points.Higher total points indicate more impairment. (NCT00548145)
Timeframe: baseline and 12 months

,
Interventionscores on a scale (Mean)
baseline12month
Cholesterol-lowering Medicine Other Than Statin19.5020.59
Pitavastatin18.5920.20

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Changes in Insulin-like Growth Factor-1 (IGF-1) and Insulin-like Growth Factor-1 Binding Protein-3 (IGFBP-3)

Changes in insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-1 binding protein-3 (IGFBP-3) obtained through blood sample. Specific time points for evaluation are baseline and Year +1 (only). (NCT00723398)
Timeframe: 1 year

,,,,
Interventionng/mL (Mean)
Baseline: IGF-11 year: IGF-1Baseline: IGFBP-31 year: IGFBP-3
Group 1: Control4.965.057.677.75
Group 2: Raloxifene 60 mg4.634.407.537.55
Group 3: Raloxifene 30 mg4.804.767.697.79
Group 4: Lovaza 4 gm4.954.967.837.83
Group 5: Lovaza 4 gm and Raloxifene 30 mg4.894.827.577.61

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Change in Absolute Breast Density

Change of absolute breast density as indicated by mammography from baseline to Year +1 and completion of study (Year +2). No other mammograms will be obtained or used for the purpose of this study. Absolute breast density volume is based on breast thickness and the x-ray attenuation at each pixel of the image. (NCT00723398)
Timeframe: 2 years

,,,,
Interventioncm squared (Mean)
Absolute density at baselineAbsolute density at 1 yearAbsolute density at 2 years
Group 1: Control65.5359.2954.34
Group 2: Raloxifene 60 mg64.3960.4860.57
Group 3: Raloxifene 30 mg65.0859.5358.86
Group 4: Lovaza 4 gm56.3558.8757.60
Group 5: Lovaza 4 gm and Raloxifene 30 mg63.8160.9328.53

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Changes in Biomarkers for Oxidative Stress: Urinary 8-hydroxy-deoxyguansine

Changes in biomarkers for oxidative stress. Specific time points for evaluation are baseline and Year +1 (only). Urinary 8-hydroxy-deoxyguansine as measured through urinary analysis. (NCT00723398)
Timeframe: 1 year

,,,,
Interventionng/mg creatinine (Mean)
Baseline1 year
Group 1: Control255224
Group 2: Raloxifene 60 mg285309
Group 3: Raloxifene 30 mg213246
Group 4: Lovaza 4 gm184177
Group 5: Lovaza 4 gm and Raloxifene 30 mg355297

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Changes in Biomarkers for Oxidative Stress:Urinary 8-(Isoprostane) F-2α

Changes in biomarkers for oxidative stress. Specific time points for evaluation are baseline and Year +1 (only). Urinary 8-(isoprostane) F-2α as measured through urine analysis. (NCT00723398)
Timeframe: 1 year

,,,,
Interventionpg/mg creatinine (Mean)
Baseline1 year
Group 1: Control544484
Group 2: Raloxifene 60 mg366360
Group 3: Raloxifene 30 mg530538
Group 4: Lovaza 4 gm440313
Group 5: Lovaza 4 gm and Raloxifene 30 mg444396

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Changes in Complete Blood Count: Hematocrit

Changes in complete blood count levels as measured through hematocrit percentage. Specific time points for evaluation are baseline, Year +1, and Year 2. (NCT00723398)
Timeframe: 2 years

,,,,
Interventionvolume percentage (Mean)
Baseline: Hematocrit1 year: Hematocrit2 year: Hematocrit
Group 1: Control39.1438.8339.00
Group 2: Raloxifene 60 mg38.9538.7938.86
Group 3: Raloxifene 30 mg38.7938.4338.31
Group 4: Lovaza 4 gm39.0939.5238.59
Group 5: Lovaza 4 gm and Raloxifene 30 mg39.2039.1439.14

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Changes in Complete Blood Count: Hemoglobin

Changes in complete blood count levels as measured through hemoglobin. Specific time points for evaluation are baseline, Year +1, and Year 2. (NCT00723398)
Timeframe: 2 years

,,,,
Interventiong/dL (Mean)
Baseline: Hemoglobin1 year: Hemoglobin2 year: Hemoglobin
Group 1: Control13.0912.9713.10
Group 2: Raloxifene 60 mg13.1112.9713.07
Group 3: Raloxifene 30 mg12.7312.9512.82
Group 4: Lovaza 4 gm13.2513.3313.16
Group 5: Lovaza 4 gm and Raloxifene 30 mg13.3513.1013.22

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Changes in Complete Blood Count: Red Blood Cells

Changes in complete blood count levels as measured through red blood cells (RBC). Specific time points for evaluation are baseline, Year +1, and Year 2. (NCT00723398)
Timeframe: 2 years

,,,,
Interventionmillions of cells per microliter (Mean)
Baseline: RBC1 year: RBC2 year: RBC
Group 1: Control4.314.274.32
Group 2: Raloxifene 60 mg4.254.194.20
Group 3: Raloxifene 30 mg4.304.254.24
Group 4: Lovaza 4 gm4.334.364.33
Group 5: Lovaza 4 gm and Raloxifene 30 mg4.244.204.23

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Changes in Complete Blood Count: White Blood Cells and Platelets

Changes in complete blood count levels as measured through white blood cells (WBC) and platelets. Specific time points for evaluation are baseline, Year +1, and Year 2. (NCT00723398)
Timeframe: 2 years

,,,,
Interventionthousand cells/mL (Mean)
Baseline: WBC1 year: WBC2 year: WBCBaseline: Platelets1 year: Platelets2 year: Platelets
Group 1: Control5.135.155.14270.70237.02234.02
Group 2: Raloxifene 60 mg5.475.515.42235.22228.02226.16
Group 3: Raloxifene 30 mg5.004.784.90240.42230.61232.09
Group 4: Lovaza 4 gm5.044.954.90237.33231.42232.47
Group 5: Lovaza 4 gm and Raloxifene 30 mg5.274.914.91235.76221.49223.27

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Changes in Serum Biomarkers for Inflammation From Levels of High Sensitivity C-reactive Protein (hsCRP) and Interleukin 6 (IL-6)

Changes in serum biomarkers for inflammation including highly sensitive C-reactive protein and IL-6 obtained through a blood draw. Specific time points for evaluation are baseline and Year +1 (only). (NCT00723398)
Timeframe: 1 Year

,,,,
Interventionpg/ml (Mean)
Baseline: Serum hsCRP1 year: Serum hsCRPBaseline: Serum IL-61 year: Serum IL-6
Group 1: Control2.392.191.271.03
Group 2: Raloxifene 60 mg0.911.041.141.13
Group 3: Raloxifene 30 mg1.671.341.041.11
Group 4: Lovaza 4 gm1.221.691.321.49
Group 5: Lovaza 4 gm and Raloxifene 30 mg4.282.591.841.32

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Changes in Serum Lipid Levels

Changes in serum lipid levels as measured through total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides. Specific time points for evaluation are baseline, Year +1, and Year 2. (NCT00723398)
Timeframe: 2 years

,,,,
Interventionmg/dL (Mean)
Baseline: Total Cholesterol1 year: Total Cholestrol2 year: Total CholesterolBaseline: LDL Cholesterol1 year: LDL Cholesterol2 year: LDL CholesterolBaseline: HDL Cholesterol1 year: HDL Cholesterol2 year: HDL CholestrolBaseline: Triglycerides1 year: Triglycerides2 year: Triglycerides
Group 1: Control207.3208.8207.5114115.1115.368.7570.7170.19122.7114.5110.1
Group 2: Raloxifene 60 mg203.6198.3196.6114.7106.8104.766.1868.8868.63113.2113.2116.9
Group 3: Raloxifene 30 mg204.3199.6202.3111.2106.2106.170.9270.5973.17110.6113.7115.8
Group 4: Lovaza 4 gm197.7199.6200.2106.6109.7110.468.0670.5970.67115.196.2295.41
Group 5: Lovaza 4 gm and Raloxifene 30 mg197.6189.4192.6108.196.5899.4868.976.1175.77103.683.7186.43

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Changes in Biomarkers for Estrogen Metabolism: 2-hydroxy Estrone (Urinary 2-OHE1) and 16-α-hydroxy Estrone (16α-OHE1)

Changes in biomarkers for estrogen metabolism: 2-hydroxy estrone (Urinary 2-OHE1) and 16-α-hydroxy estrone (16α-OHE1) as measured by urinary analysis. Specific time points for evaluation are baseline and Year +1 (only). (NCT00723398)
Timeframe: 1 year

,,,,
Interventionng/mg creatinine (Mean)
Baseline: Urinary 2-OHE11 year: Urinary 2-OHE1Baseline: 16α-OHE11 year: 16α-OHE1
Group 1: Control10.577.466.225.68
Group 2: Raloxifene 60 mg8.5810.035.084.35
Group 3: Raloxifene 30 mg8.829.106.867.46
Group 4: Lovaza 4 gm7.157.495.244.79
Group 5: Lovaza 4 gm and Raloxifene 30 mg15.613.26.65.68

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Proportion of Patients Achieving LDL- C<100mg/dL

compare the proportion of patients achieving LDL- C<100mg/dL (NCT00889226)
Timeframe: After 16wk drug administration

InterventionParticipants (Count of Participants)
Pitavastatin Group61
Atorvastatin Group54

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The Change of LDL-C

The change of LDL-C between at 16-week and baseline (NCT00889226)
Timeframe: After 16wk drug administration

Interventionmg/dl (Mean)
Pitavastatin Group-69.8
Atorvastatin Group-70.9

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Number of Participants With Treatment Emergent Adverse Events

(NCT01043094)
Timeframe: 3 Days

InterventionParticipants (Number)
Pitavastatin 4mg Renal Impaired3
Pitavastatin 4mg Healthy Subjects3

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Area Under the Curve From 0 to Tau (AUC 0-t (ng*h/mL))

Area under the curve from start to elimination for Pitavastatin. (NCT01043094)
Timeframe: 48 hours

Interventionnanogram hour per milliliter (ng•h/mL) (Mean)
Pitavastatin 4mg Renal Impaired175
Pitavastatin 4mg Healthy Subjects145

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Area Under the Curve From Time 0 to Tau (AUC 0-τ)

Area under the curve from start to elimination. (NCT01057433)
Timeframe: 0, 1, 2, 3, 4, 5, 6, 8, and 12 hours after dosing on days 19 and 24

Interventionng•h/mL (Mean)
All Subjects113.92

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Percent Mean Change From Baseline of International Normalized Ratio (INR)

INR is the ratio of a patient's prothrombin time to a standard, raised to the power of the ISI value for the tissue factor reagent used (INR = (PT-Test/PT-Normal)^ISI) (NCT01178853)
Timeframe: 22 Days

Interventionpercent change (Mean)
Warfarin + Pitavastatin0.0452
Warfarin + Rosuvastatin0.1605

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Mean Percent Change in Low Density Lipoprotein Cholesterol(LDL-C) From Baseline to Week 12

(NCT01256476)
Timeframe: Baseline and 12 weeks

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

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Change of Fasting Serum Low-density Lipoprotein Cholesterol (LDL-C) at 12 Weeks

(NCT01301066)
Timeframe: 12 weeks minus baseline

Interventionmg/dL (Mean)
Pitavastatin 4 mg QD155.1
Pravastatin 40 mg QD154.6

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Number of Participants With at Least One Adverse Event.

(NCT01422369)
Timeframe: 16 Days

InterventionParticipants (Number)
All Subjects2

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NK-104 AUC

(NCT01422369)
Timeframe: 16 Days

Interventionng * h/mL (Mean)
NK-104192.00

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NK-104 AUC

(NCT01422382)
Timeframe: 15 Days

Interventionng * h/mL (Mean)
All Subjects208.92

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Number of Participants With at Least One Adverse Event.

(NCT01422382)
Timeframe: 24 Days

InterventionParticipants (Number)
All Subjects12

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AUC

24-hour area under the curve (AUC) for pitavastatin when coadministered with efavirenz and with darunavir/ritonavir and 24-hour AUC for efavirenz or darunavir when coadministered with pitavastatin (NCT01695954)
Timeframe: 0 to 24 hours

Interventionng*hr/mL (Mean)
Arm A: (Pitavastatin and Efavirenz)85.3
Arm B: (Pitavastatin and Darunavir)62.8

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GMR of Cmax of Pitavastatin When Coadministered With Efavirenz or With Darunavir/Ritonavir

Geometric Mean Ratio (GMR) of Cmax for pitavastatin with Efavirenz vs. alone and GMR of Cmax for pitavastatin with darunavir/ritonavir vs. alone was reported. (NCT01695954)
Timeframe: Day 18

Interventionng/mL (Geometric Mean)
Arm A: (Pitavastatin and Efavirenz)1.20
Arm B: (Pitavastatin and Ritonavir-boosted Darunavir)0.93

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GMR of 24- Hour AUC of Pitavastatin When Coadministered With Efavirenz or With Darunavir/Ritonavir Over 24 Hour AUC of Pitavastatin

Geometric Mean Ratio (GMR) of 24- Hour Area under the plasma drug concentration-time curve (AUC) of pitavastatin when coadministered with efavirenz or with darunavir/ritonavir over 24 Hour (AUC) of pitavastatin (NCT01695954)
Timeframe: 0 to 24 hours

,
InterventionRatio (Geometric Mean)
GMR of Pitavastatin with (EFV or DRV)/PitavastatinGMR of (EFV or DRV) with Pitavastatin/(EFV or DRV)
Arm A: (Pitavastatin and Efavirenz).89.90
Arm B: (Pitavastatin and Darunavir).911.08

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Triglyceride

Percent change from baseline in TG level at Week 4 (NCT01710007)
Timeframe: week 4

InterventionPercent change from baseline (Mean)
1PC002-18.75
Lipitor-19.5

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LDL-C

Percent change from baseline in LDL-C level at Week 4 (NCT01710007)
Timeframe: week 4

InterventionPercent change from baseline (Mean)
1PC002-39.01
Lipitor-40.07

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The Percentage Change From Baseline in LDL-C Level at Week 12.

The study aimed to test that the efficacy of 1PC002 group was non-inferior to Atorvastatin group in percent change from baseline of LDL-C level at Week 12. (NCT01710007)
Timeframe: 12 weeks

InterventionPercent change from baseline (Mean)
Lipitor-42.89
1PC002-37.43

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HDL-C

Percent change from baseline in HDL-C level at Week 4 (NCT01710007)
Timeframe: week 4

InterventionPercent change from baseline (Mean)
1PC0020.06
Lipitor-1.64

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Change From Baseline in High Sensitivity C-Reactive Protein (hsCRP)

LS Mean was calculated using MMRM analysis with baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included in the model. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

InterventionPercentage change (Least Squares Mean)
Placebo Q4W0.5
20 mg LY3015014 Q4W-0.2
120 mg LY3015014 Q4W1.6
300 mg LY3015014 Q4W-0.3
100 mg LY3015014 Q8W-0.3
300 mg LY3015014 Q8W-0.7

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Number of Participants Who Develop Treatment Emergent Anti-LY3015014 Antibodies

(NCT01890967)
Timeframe: Baseline through Week 24

InterventionParticipants (Number)
Placebo Q4W4
20 mg LY3015014 Q4W6
120 mg LY3015014 Q4W10
300 mg LY3015014 Q4W5
100 mg LY3015014 Q8W4
300 mg LY3015014 Q8W3

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Percentage Change From Baseline in Free Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels

LS Mean was calculated using MMRM analysis with baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included in the model. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

InterventionPercentage change (Least Squares Mean)
Placebo Q4W9.9
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

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Percentage Change From Baseline in Lipoprotein(a) [Lp(a)]

Data was log-transformed for MMRM analysis, with change from baseline as the dependent variable, and baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included as independent variables. Percentage change from baseline in the original scale was then back-calculated from the log-transformed MMRM analysis. (NCT01890967)
Timeframe: Baseline, Week 16

InterventionPercentage 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

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Percentage Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C)

Least square (LS) Means was calculated using analysis of covariance (ANCOVA) adjusted for disease classification, statin dose, baseline LDL-C measurement. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

InterventionPercentage change (Least Squares Mean)
Placebo Q4W7.6
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

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Percentage Change From Baseline in Total Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels

LS Mean was calculated using MMRM analysis with baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included in the model. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

InterventionPercentage change (Least Squares Mean)
Placebo Q4W14.6
20 mg LY3015014 Q4W9.1
120 mg LY3015014 Q4W86.4
300 mg LY3015014 Q4W130.6
100 mg LY3015014 Q8W21.8
300 mg LY3015014 Q8W41.0

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Pharmacokinetics (PK): Area Under the Concentration-Time Curve at Steady-State (AUC,ss) for LY3015014

(NCT01890967)
Timeframe: Week 12-16 (Q4W) - Predose, Week 8-16 (Q8W) - Predose

Interventionμg∙hr/mL (Geometric Mean)
20 mg LY3015014 Q4W1590
120 mg LY3015014 Q4W9670
300 mg LY3015014 Q4W27300
100 mg LY3015014 Q8W7800
300 mg LY3015014 Q8W26600

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Percentage Change From Baseline in Apolipoprotein A1 (Apo A1), Apolipoprotein B (Apo B)

LS Mean was calculated using MMRM analysis with baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included in the model. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

,,,,,
InterventionPercentage change (Least Squares Mean)
Apo A1Apo B
100 mg LY3015014 Q8W3.8-16.0
120 mg LY3015014 Q4W6.5-34.9
20 mg LY3015014 Q4W2.4-16.6
300 mg LY3015014 Q4W6.2-46.8
300 mg LY3015014 Q8W5.8-31.9
Placebo Q4W0.34.2

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Percentage Change From Baseline in LDL-C, Total Cholesterol (TC), High-Density Lipoprotein Cholesterol (HDL-C), Triglycerides (TG), Non-HDL-C

LS Mean was calculated using mixed model repeated measures (MMRM) analysis with baseline measurement, disease classification, statin dose, treatment, visit, and treatment by visit interaction included in the model. Percent change from baseline response is the dependent variable. (NCT01890967)
Timeframe: Baseline, Week 16

,,,,,
InterventionPercentage change (Least Squares Mean)
LDL-CTGTCHDL-CNon-HDL-C
100 mg LY3015014 Q8W-18.4-7.2-11.04.5-16.1
120 mg LY3015014 Q4W-46.4-7.2-27.87.3-39.3
20 mg LY3015014 Q4W-18.0-6.1-10.54.5-16.1
300 mg LY3015014 Q4W-56.5-15.1-34.18.8-48.9
300 mg LY3015014 Q8W-42.2-10.6-24.68.4-35.8
Placebo Q4W5.93.53.51.64.9

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Number of Participants With an Injection Site Reaction

(NCT01890967)
Timeframe: Baseline through Week 24

InterventionParticipants (Number)
Placebo Q4W26
20 mg LY3015014 Q4W42
120 mg LY3015014 Q4W57
300 mg LY3015014 Q4W51
100 mg LY3015014 Q8W36
300 mg LY3015014 Q8W41

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Insulin-stimulated Glucose Uptake

insulin-stimulated glucose uptake measured by euglycemic hyperinsulinemic clamp (NCT02290106)
Timeframe: 6 months

Interventionmg/kg/minute (Mean)
Pitavastatin5.9
Placebo5.9

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Alanine Aminotransferase (ALT)

alanine aminotransferase at the 6 month timepoint (NCT02290106)
Timeframe: 6 months

InterventionU/L (Mean)
Pitavastatin37
Placebo27

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Hepatic Insulin Sensitivity

"hepatic insulin sensitivity assessed by glucose infusion rate corrected for fluctuations in serum glucose (M) during low-dose insulin clamp" (NCT02290106)
Timeframe: 6 months

Interventionmg/kg/minute (Mean)
Pitavastatin1.5
Placebo1.6

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Aspartate Aminotransferase (AST)

aspartate aminotransferase at 6 month timepoint (NCT02290106)
Timeframe: 6 months

InterventionU/L (Mean)
Pitavastatin31
Placebo26

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Hemoglobin A1c (HbA1c)

(NCT02290106)
Timeframe: 6 months

Intervention% (hemoglobin A1c) (Mean)
Pitavastatin5.7
Placebo5.7

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Quantitative Insulin Sensitivity Check Index (QUICKI)

quantitative insulin sensitivity check index (QUICKI) at 6 months. Measure = 1/((log(glucose in mg/dL) + log(insulin in uU/mL)) (NCT02290106)
Timeframe: 6 months

InterventionQUICKI index (Mean)
Pitavastatin0.16
Placebo0.15

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Liver Fat

liver fat content as measured by 1H-magnetic resonance spectroscopy (NCT02290106)
Timeframe: 6 months

Intervention% liver fat (hepatic fat fraction) (Mean)
Pitavastatin17
Placebo14

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Efficacy of Pitavastatin in HIV-infected Patients With Dyslipidemia and Receiving Atazanavir/Ritonavir

Efficacy was measured by level of TC, TG, LDL, and HDL that decreased after pitavastatin treatment. Pitavastatin was considered efficient when it could decrease TC, TG, LDL, or HDL significantly compared to placebo. (NCT02442700)
Timeframe: 12 weeks

,
Interventionmg/dL (Mean)
TC at baselineTG at baselineLDL at baselineHDL at baselineTC at 4 weeks after treatmentTG at 4 weeks after treatmentLDL at 4 weeks after treatmentHDL at 4 weeks after treatmentTC at 8 weeks after treatmentTG at 8 weeks after treatmentLDL at 8 weeks after treatmentHDL at 8 weeks after treatmentTC at 12 weeks after treatmentTG at 12 weeks after treatmentLDL after 12 weeks of treatmentHDL after 12 weeks of treatment
Treatment A239.9282144.743201.3246.5111.643.5202.3250.8111.544.9207351.3113.245.3
Treatment B257.6350146.344.8246.6292.5142.543.5255.2334145.143.7246.3279.1145.644.2

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Safety of Pitavastatin in HIV-infected Patients

"Safety clinical was defined by FDA; grade 1 mild symptoms; grade 2 moderate symptoms with limiting age-appropriate IADL; grade 3 severe symptoms with limiting self-care ADL, But not immediately life-threatening; grade 4 life-threatening consequences; and grade 5 death related to adverse event.~Safety laboratory evaluation was determined safe if AST, ALT, and/or CPK level was not increased significantly comparing pitavastatin to placebo." (NCT02442700)
Timeframe: 12 weeks

,
InterventionU/L (Mean)
AST at baselineALT at baselineAST at 12 weeks after treatmentALT at 12 weeks after treatment
Treatment A38.264.639.564.2
Treatment B36.358.940.7572.5

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Effect of Rifampin on Tmax Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the Tmax of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. Tmax is the amount of time to reach maximum (peak) plasma drug concentration following drug administration. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionhours (Median)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)1.002.501.002.001.503.002.00
Mild Impairment (Period 2)0.502.501.003.001.001.751.00
Moderate Impairment (Period 2)0.753.001.004.001.502.502.00
Severe Impairment (Period 2)0.503.501.003.000.501.751.00

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Effect of Rifampin on t1/2 Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the t1/2 of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. T1/2 is the elimination half-life of study drug. T1/2 is the time it takes for half of the study drug in the blood plasma to dissipate. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionhours (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)4.976.486.5016.52.763.496.76
Mild Impairment (Period 2)4.127.578.4021.03.223.839.64
Moderate Impairment (Period 2)5.4911.311.517.72.994.257.48
Severe Impairment (Period 2)4.1419.46.9917.23.144.564.89

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Effect of Rifampin on Cmax Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the Cmax of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. Cmax is the peak plasma concentration of study drug after administration. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionpg/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)81.4351599102405198236
Mild Impairment (Period 2)73.0243819131505215254
Moderate Impairment (Period 2)92.5443860119508174396
Severe Impairment (Period 2)75.442298188.4531150208

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Effect of Rifampin on CL/F Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the CL/F of midazolam, dabigatran, pitavastatin, atorvastatin, and rosuvatatin. CL/F is the rate at which study drug was removed from the body. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionliters/hour (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinAtorvastatinRosuvastatin
Healthy Control (Period 2)41.885.65.2456.457.9
Mild Impairment (Period 2)53.092.83.9558.647.1
Moderate Impairment (Period 2)27.838.92.8641.128.9
Severe Impairment (Period 2)40.526.33.5744.238.6

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Effect of Rifampin on C24 Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the C24 of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. C24 is a measure of the plasma study drug concentration 24 hours post-dose. C24 is reported as median (minimum and maximum) in severe renal impairment arm due to zero values. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: 24 hours post-dose

,,,
Interventionpg/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)0.60127.54.7217.11.355.572.42
Mild Impairment (Period 2)0.0031.14.7020.71.766.284.18
Moderate Impairment (Period 2)1.4210010.534.02.989.966.97
Severe Impairment (Period 2)0.3941747.0121.32.987.234.47

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Effect of Rifampin on AUC0-inf Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the AUC0-inf of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. AUC0-inf is the area under the plasma concentration versus time curve from time zero (pre-dose) to extrapolated infinite time. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include data from the end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0 hour (pre-dose) and 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionpg*hr/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)23932901910134017701650830
Mild Impairment (Period 2)189304025301930171017601060
Moderate Impairment (Period 2)359724035002500243018701800
Severe Impairment (Period 2)2441070028501560224016201240

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Effect of Rifampin on AUC0-24 Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the AUC0-24 of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. AUC0-24 is the area under the plasma concentration-time curve from time 0 to 24 hours post-dose. This is a measure of the average amount of study drug in the blood plasma over a period of 24 hours after the dose. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, and 24 hours post-dose; rifampin: 0 hour (pre-dose) and 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionpg*hr/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)23430301860100017601620842
Mild Impairment (Period 2)186266024601490170017201010
Moderate Impairment (Period 2)346548033601780242018001670
Severe Impairment (Period 2)238654027601070223015801100

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Area Under the Plasma Concentration-time Curve From Time 0 to Last (AUC0-last) Post-dose Period 1

AUC0-last is the area under the plasma concentration-time curve from time zero to time of last measurable concentration. This is a measure of the amount of study drug in the blood plasma from pre-dose until the last measurable concentration of study drug could be determined. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionpg*hr/mL (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease10537406491060298126171
Healthy Control26414104831450255152181
Mild Impairment16714406431490295221231
Moderate Impairment34442309502020459256479
Severe Impairment24874506021570419176269

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Area Under the Plasma Concentration-time Curve From Time 0 to Infinity (AUC0-inf) Post-dose Period 1

AUC0-inf is the area under the plasma concentration versus time curve from time zero (pre-dose) to extrapolated infinite time. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease (ESRD) requiring hemodialysis. (NCT03311841)
Timeframe: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionpg*hr/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease11053706761100329163208
Healthy Control27315805201540292208292
Mild Impairment17616106881610329286262
Moderate Impairment364455010202240511273575
Severe Impairment26079006481680476226365

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Maximum Plasma Concentration (Cmax) Post-dose Period 1

Cmax is the peak plasma concentration of study drug after administration. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionpg/mL (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease39.913224278.563.78.5822.5
Healthy Control73.218316488.121.67.6721.5
Mild Impairment70.715324410531.98.5023.6
Moderate Impairment77.231230310655.09.5040.4
Severe Impairment68.431921895.446.77.2224.4

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Apparent Volume of Distribution During the Terminal Phase (Vz/F) Post-dose Period 1

Vz/F is the distribution of study drug between the plasma and the rest of the body after the dose. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. Vz/F was to be calculated for the parent plasma analytes only, midazolam, dabigatran, pitavastatin, atorvastatin, and rosuvastatin. (NCT03311841)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionliters (Geometric Mean)
MidazolamDabigatranPitavastatinAtorvastatinRosuvastatin
End-Stage Renal Disease579314025235204870
Healthy Control422173049573804010
Mild Impairment555212040573004270
Moderate Impairment409106031752403120
Severe Impairment433123045453103720

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Apparent Plasma Terminal Half-life (t1/2) Post-dose Period 1

T1/2 is the elimination half-life of study drug. T1/2 is the time it takes for half of the study drug in the blood plasma to dissipate. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionhours (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease4.4141.411.811.08.0312.414.0
Healthy Control7.996.7517.818.514.921.216.2
Mild Impairment6.768.4019.320.516.722.815.5
Moderate Impairment10.311.922.422.018.624.624.9
Severe Impairment7.7924.020.418.117.521.918.8

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Apparent Clearance After Extravascular Administration (CL/F) Post-dose Period 1

CL/F is the rate at which study drug was removed from the body. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. CL/F was to be calculated for the parent plasma analytes only, midazolam, dabigatran, pitavastatin, atorvastatin, and rosuvastatin. (NCT03311841)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionliters/hour (Geometric Mean)
MidazolamDabigatranPitavastatinAtorvastatinRosuvastatin
End-Stage Renal Disease90.852.514.8304240
Healthy Control36.617819.2343171
Mild Impairment56.917514.5304191
Moderate Impairment27.561.89.8419687.0
Severe Impairment38.535.715.4210137

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Area Under the Plasma Concentration-time Curve From Time 0 to 24 Hours (AUC0-24) Post-dose Period 1

AUC0-24 is the area under the plasma concentration-time curve from time 0 to 24 hours post-dose. This is a measure of the average amount of study drug in the blood plasma over a period of 24 hours after the dose. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, and 24 hours post-dose

,,,,
Interventionpg*hr/mL (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease1062100593858287115162
Healthy Control25214404151010198108153
Mild Impairment16813805431040219139191
Moderate Impairment31734407641280329143343
Severe Impairment23544705251100300112223

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Effect of Rifampin on Vz/F Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the Vz/F of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. Vz/F is the distribution of study drug between the plasma and the rest of the body after the dose. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionliters (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinAtorvastatinRosuvastatin
Healthy Control (Period 2)30080049.2225565
Mild Impairment (Period 2)315101047.8272654
Moderate Impairment (Period 2)22063247.3177313
Severe Impairment (Period 2)24273336.0200272

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Effect of Rifampin on AUC0-last Post-dose Period 2

To evaluate the effect of a single oral dose of rifampin on the AUC0-last of midazolam, dabigatran, pitavastatin, pitavastatin lactone, atorvastatin, ortho-hydroxyatorvastatin, and rosuvatatin. AUC0-last is the area under the plasma concentration-time curve from time zero to time of last measurable concentration. It is a measure of the amount of study drug in the blood plasma from pre-dose until the last measurable concentration of study drug could be determined. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail and rifampin in healthy participants and participants with renal impairment. As pre-specified in the protocol, this outcome measure does not include end-stage renal disease participants as they did not receive rifampin during Period 2. (NCT03311841)
Timeframe: Microdose cocktail: 0 hour (pre-dose) and 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose; rifampin: 0 hour (pre-dose) and 0.5, 1, 1.5, 2, 3, 4, 6, 12, and 24 hours post-dose

,,,
Interventionpg*hr/mL (Geometric Least Squares Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
Healthy Control (Period 2)23131401890127017601630854
Mild Impairment (Period 2)182283025101850169017501040
Moderate Impairment (Period 2)353683034802380242018501740
Severe Impairment (Period 2)2361040028501470222016101150

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Time to Maximum Plasma Concentration (Tmax) Post-dose Period 1

Tmax is the amount of time to reach maximum (peak) plasma drug concentration following drug administration. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 32, 48, and 72 hours post-dose

,,,,
Interventionhours (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease0.502.000.502.500.255.003.00
Healthy Control1.001.500.752.000.506.003.50
Mild Impairment0.501.500.522.000.256.002.00
Moderate Impairment0.502.501.002.500.256.004.00
Severe Impairment0.503.000.504.000.256.004.00

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Plasma Concentration at 24 Hours (C24) Post-dose Period 1

C24hr is a measure of the plasma study drug concentration 24 hours post-dose. Plasma pharmacokinetic data presented in the table below are following the administration of a single oral dose of a microdose cocktail in healthy participants, participants with renal impairment, and 24 hours prior to hemodialysis in participants with end-stage renal disease requiring hemodialysis. (NCT03311841)
Timeframe: 24 hours post-dose

,,,,
Interventionpg/mL (Geometric Mean)
MidazolamDabigatranPitavastatinPitavastatin lactone (metabolite)AtorvastatinOrtho-hydroxyatorvastatin (metabolite)Rosuvastatin
End-Stage Renal Disease0.28370.26.0712.94.283.672.64
Healthy Control1.577.704.1021.73.853.081.94
Mild Impairment0.73418.75.3222.45.045.023.59
Moderate Impairment2.6459.38.1332.86.034.436.01
Severe Impairment1.831074.0423.25.733.253.40

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Period 2: Elimination Half-Life (T1/2) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionh (Geometric Mean)
Pitavastatin/RO70493899.78

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Period 2: Cmax of RO7049389

(NCT03717064)
Timeframe: Period 2 Days 3-4

Interventionng/mL (Geometric Mean)
RO7049389RO7049389 + Pitavastatin
Pitavastatin/RO70493891540017600

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Period 2: AUC-tau of RO7049389

(NCT03717064)
Timeframe: Period 2 Days 3-4

Interventionh*ng/mL (Geometric Mean)
RO7049389RO7049389 + Pitavastatin
Pitavastatin/RO70493896270068500

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Period 1: Cmax of Pitavastatin Lactone

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionng/mL (Geometric Mean)
Pitavastatin/RO704938914.4

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Period 2: AUC Ratio of Pitavastatin Lactone to Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

InterventionRatio (Geometric Mean)
Pitavastatin/RO70493890.636

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Period 2: AUC0-inf of Pitavastatin Lactone

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionh*ng/mL (Geometric Mean)
Pitavastatin/RO704938981.7

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Percentage of Participants With Adverse Events (AEs)

An adverse event is any untoward medical occurrence in a participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with the treatment. An adverse event can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding, for example), symptom, or disease temporally associated with the use of a pharmaceutical product, whether or not considered related to the pharmaceutical product. Preexisting conditions which worsen during a study are also considered as adverse events. (NCT03717064)
Timeframe: From the start of Period 1 through safety follow-up (Period 2, Day 34)

InterventionPercentage of Participants (Number)
Pitavastatin/RO704938939

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Period 2: Cmax of Pitavastatin Lactone

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionng/mL (Geometric Mean)
Pitavastatin/RO70493896.39

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Period 2: Maximum Plasma Concentration (Cmax) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionng/mL (Geometric Mean)
Pitavastatin/RO704938933.5

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Period 2: Plasma Concentration Versus Time (Area Under the Curve, AUC0-inf) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionh*ng/mL (Geometric Mean)
Pitavastatin/RO7049389129

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Period 2: Time to Maximum Concentration (Tmax) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

Interventionh (Median)
Pitavastatin/RO70493892

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Period 1: Volume of Distribution (V/F) of Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

InterventionLiters (L) (Geometric Mean)
Pitavastatin/RO7049389525

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Period 1: Time to Maximum Concentration (Tmax) of Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionhours (h) (Median)
Pitavastatin/RO70493891.5

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Period 1: Plasma Concentration Versus Time (Area Under the Curve, AUC0-inf) of Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionh*ng/mL (Geometric Mean)
Pitavastatin/RO704938978.6

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Period 2: Apparent Total Clearance (CL/F) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

InterventionL/h (Geometric Mean)
Pitavastatin/RO704938915.6

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Period 1: AUC Ratio of Pitavastatin Lactone to Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

InterventionRatio (Geometric Mean)
Pitavastatin/RO70493892.45

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Period 1: Apparent Total Clearance (CL/F) of Pitavastatin

(NCT03717064)
Timeframe: Period 1

InterventionL/h (Geometric Mean)
Pitavastatin/RO704938925.4

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Period 1: Maximum Plasma Concentration (Cmax) of Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionng/mL (Geometric Mean)
Pitavastatin/RO704938923.8

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Period 1: Elimination Half-Life (T1/2) of Pitavastatin

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionh (Geometric Mean)
Pitavastatin/RO704938914.3

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Period 2: Volume of Distribution (V/F) of Pitavastatin

(NCT03717064)
Timeframe: Period 2 Day 4

InterventionL (Geometric Mean)
Pitavastatin/RO7049389220

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Period 1: AUC0-inf of Pitavastatin Lactone

(NCT03717064)
Timeframe: Period 1 Day 1

Interventionh*ng/mL (Geometric Mean)
Pitavastatin/RO7049389193

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