Page last updated: 2024-11-06

atorvastatin

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Atorvastatin is a synthetic lipid-lowering drug that belongs to the class of statins. It is a potent inhibitor of the enzyme HMG-CoA reductase, which is responsible for the synthesis of cholesterol in the liver. Atorvastatin lowers cholesterol levels by inhibiting the production of mevalonate, a precursor to cholesterol. This reduction in cholesterol levels can help to prevent heart disease and stroke. Atorvastatin is widely studied due to its effectiveness in lowering cholesterol levels and reducing the risk of cardiovascular events. Research focuses on its effects on different patient populations, optimal dosage, long-term safety, and its role in combination therapies. The synthesis of atorvastatin involves a multi-step process that starts with a chiral building block and proceeds through several functional group transformations.'

Cross-References

ID SourceID
PubMed CID60823
CHEMBL ID1487
CHEBI ID39548
SCHEMBL ID3831
MeSH IDM0179294

Synonyms (95)

Synonym
BIDD:GT0336
xavator
(betar,deltar)-2-(p-fluorophenyl)-beta,delta-dihydroxy-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)pyrrole-1-heptanoic acid
tozalip
hsdb 7039
atorvastatin [inn:ban]
ccris 7159
1h-pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-, (betar,deltar)-
cardyl
gtpl2949
bdbm22164
(3r,5r)-7-[2-(4-fluorophenyl)-5-(1-methylethyl)-3-phenyl-4-(phenylcarbamoyl)-1h-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
chembl1487 ,
(3r,5r)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-(propan-2-yl)-1h-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
sortis (tn)
D07474
atorvastatin (inn)
C06834
134523-00-5
atorvastatin ,
atorvastatine
atorlip
atorvastatina
(3r,5r)-7-[3-(anilinocarbonyl)-5-(4-fluorophenyl)-4-phenyl-2-(propan-2-yl)-1h-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
CHEBI:39548 ,
7-[2-(4-fluoro-phenyl)-5-isopropyl-3-phenyl-4-phenylcarbamoyl-pyrrol-1-yl]-3,5-dihydroxy-heptanoic acid
atorvastatinum
(r-(r*,r*))-2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-1h-pyrrole-1-heptanoic acid
DB01076
NCGC00159458-02
7-[2-(4-fluoro-phenyl)-5-isopropyl-3-phenyl-4-phenylcarbamoyl-pyrrol-1-yl]- 3,5-dihydroxy-heptanoic acid
lipitor(tm)
1h-pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-, (r-(r*,r*))-
(3r,5r)-7-[2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)pyrrol-1-yl]-3,5-dihydroxy-heptanoic acid
atrovastin
(3r,5r)-7-[3-(anilinocarbonyl)-5-(4-fluorophenyl)-2-isopropyl-4-phenyl-1h-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
AKOS000281127
(3s,5s)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid
(3r,5r)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid
A802259
(3r,5r)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-yl-pyrrol-1-yl]-3,5-dihydroxy-heptanoic acid
sodium 7-[5-(4-fluorophenyl)-2-isopropyl-4-phenyl-3-(phenylcarbamoyl)-2,3-dihydropyrrol-1-yl]-3,5-dihydroxy-heptanoate
A806791
A806793
NCGC00255181-01
dtxcid509868
tox21_302417
cas-134523-00-5
dtxsid8029868 ,
lipinon
a0jwa85v8f ,
ator
unii-a0jwa85v8f
lipilou
atorcor
atofast
atorin
atorvastatin [vandf]
atorvastatin [hsdb]
atorvastatin [who-dd]
atorvastatin [mi]
1h-pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-.beta.,.delta.-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-, (r-(r*,r*))-
atorvastatin [inn]
(.beta.r,.delta.r)-2-(p-fluorophenyl)-.beta.,.delta.-dihydroxy-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)pyrrole-1-heptanoic acid
S5715
BRD-K69726342-001-02-6
CCG-221172
HY-B0589
(3r,5r)-7-(2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)-1h-pyrrol-1-yl)-3,5-dihydroxyheptanoic acid
SCHEMBL3831
(3r,5r)-7-[2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-phenylcarbamoyl-pyrrol-1-yl]-3,5-dihydroxy-heptanoic acid
XUKUURHRXDUEBC-KAYWLYCHSA-N
mfcd00899261
AC-9386
SR-01000872702-1
sr-01000872702
atorvastatin & primycin
MRF-0000761
HMS3715L05
NCGC00159458-20
atorvastatin (relative stereo)
DTXSID60274003
lipilou; tozalip; torvast; cardyl
rel-atorvastatin
AS-35260
Q668093
(3r,5r)-7-[2-(4-fluorophenyl)-5-isopropyl-3-phenyl-4-phenylcarbamoylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid
HMS3886C20
atorvastatin is known as an hmg-coa reductase inhibitor.
EN300-18527331
(betar,deltar)-2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-1h-pyrrole-1-heptanoic acid
7-(2-(4-fluoro-phenyl)-5-isopropyl-3-phenyl-4-phenylcarbamoyl-pyrrol-1-yl)-3,5-dihydroxy-heptanoic acid
(3r,5r)-7-(3-(anilinocarbonyl)-5-(4-fluorophenyl)-4-phenyl-2-(propan-2-yl)-1h-pyrrol-1-yl)-3,5-dihydroxyheptanoic acid
(betar,deltar)-2-(p-fluorophenyl)-beta,delta-dihydroxy-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)-pyrrole-1-heptanoic acid
c10aa05

Research Excerpts

Overview

Atorvastatin (AVA) is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. It is a potent lipid-lowering drug with poor solubility and high presystemic clearance that limits its therapeutic efficacy.

ExcerptReferenceRelevance
"Atorvastatin (AVA) is a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. "( Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
Almeras, L; Amalvict, R; Baret, E; Briolant, S; Fusaï, T; Henry, M; Parquet, V; Pradines, B; Rogier, C; Torrentino-Madamet, M, 2009
)
3.24
"Atorvastatin (AVA) is a pentasubstituted pyrrole, which has been tested as an adjuvant in the treatment of cerebral malaria."( New pentasubstituted pyrrole hybrid atorvastatin-quinoline derivatives with antiplasmodial activity.
Bastos, MM; Boechat, N; Carvalho, RC; Kaiser, CR; Krettli, AU; Martins, WA; Pinheiro, LC; Silva, TP, 2016
)
1.43
"Atorvastatin is a potential OA-modifying drug that warrants further clinical investigation."( Standardized study of atorvastatin possible osteoarthritis disease-modifying effect in a rat model of osteoarthritis.
El-Hawwary, AA; Elmasry, A; Gaballah, A; Genedy, D; Ghayaty, E, 2022
)
1.76
"Atorvastatin ester (Ate) is a structural trim of atorvastatin that can regulate hyperlipidemia. "( Atorvastatin Ester Regulates Lipid Metabolism in Hyperlipidemia Rats via the PPAR-signaling Pathway and HMGCR Expression in the Liver.
Chen, C; Hu, N; Huang, J; Li, C; Wang, J; Yao, D, 2021
)
3.51
"Atorvastatin is a statin known to influence both the cholesterol content and the organization of actin."( Atorvastatin Modulates the Efficacy of Electroporation and Calcium Electrochemotherapy.
Kiełbik, A; Kulbacka, J; Novickij, V; Rembiałkowska, N; Saczko, J; Szewczyk, A; Szlasa, W; Tarek, M; Łapińska, Z, 2021
)
2.79
"Atorvastatin is an effective therapeutic drug for patients with ED."( Impact of atorvastatin on erectile dysfunction: A meta-analysis and systematic review.
Li, H; Lu, Y; Ma, C; Su, H; Su, X, 2022
)
1.85
"Atorvastatin is a member of statin family, with cholesterol-lowering properties."( Atorvastatin induces downregulation of matrix metalloproteinase-2/9 in MDA-MB-231 triple negative breast cancer cells.
Bakar-Ates, F; Ozkan, E, 2022
)
2.89
"Atorvastatin is a potent lipid-lowering drug with poor solubility and high presystemic clearance that limits its therapeutic efficacy. "( Solid dispersions of atorvastatin with Kolliphor RH40: Enhanced supersaturation and improvement in a hyperlipidemic rat model.
de la Torre-Iglesias, PM; Guarnizo-Herrero, V; Peña, MÁ; Torrado, G; Torrado-Salmerón, C; Torrado-Santiago, S, 2023
)
2.67
"Atorvastatin calcium (ATV) is a well-known anti-hyperlipidemic drug currently being recognized for possessing an anti-inflammatory effect. "( Syringeable atorvastatin loaded eugenol enriched PEGylated cubosomes in-situ gel for the intra-pocket treatment of periodontitis: statistical optimization and clinical assessment.
Elakkad, YE; Elgendy, HA; Ismail, RM; Makky, AMA; Younes, NF, 2023
)
2.73
"Atorvastatin (AVA) is a third-generation statin with several pleiotropic effects, considered the last synthetic pharmaceutical blockbuster. "( In silico and in vitro assessment of anti-Trypanosoma cruzi efficacy, genotoxicity and pharmacokinetics of pentasubstituted pyrrolic Atorvastatin-aminoquinoline hybrid compounds.
Araujo-Lima, CF; Bastos, MM; Boechat, N; Carvalho, RCC; Castelo-Branco, FS; Felzenszwalb, I; Fiuza, LFA; Galvão, BVD; Peres, RB; Soeiro, MNC, 2023
)
2.56
"Atorvastatin is a commonly used statin for the treatment of hypercholesterolemia in people at high risk for coronary, cerebrovascular, and peripheral artery disease. "( Fatal hepatic failure following atorvastatin treatment: A case report.
Fu, Y; Liu, S; Wang, H; Zhou, C, 2023
)
2.64
"Atorvastatin is a statin commonly applied to treat hypercholesterolemia."( Simultaneous quantification of atorvastatin, erlotinib and OSI-420 in rat serum and liver microsomes using a novel liquid chromatography-mass spectrometry method.
In-Albon, K; Kinzi, J; Meyer Zu Schwabedissen, HE; Ricklin, D; Rysz, MA; Schäfer, AM; Schmidlin, S; Schwardt, O; Seibert, I; Zürcher, S, 2023
)
1.92
"Atorvastatin is a substrate of cytochrome P450 3a (CYP3a), organic anion-transporting polypeptides (OATPs), breast cancer-resistance protein (BCRP), and P-glycoprotein (P-gp). "( Prediction of Atorvastatin Pharmacokinetics in High-Fat Diet and Low-Dose Streptozotocin-Induced Diabetic Rats Using a Semiphysiologically Based Pharmacokinetic Model Involving Both Enzymes and Transporters.
Chen, N; Chen, Y; Geng, D; Li, P; Liang, L; Liu, L; Liu, X; Wang, Z; Xu, J; Yang, H; Zhang, X; Zhao, K, 2019
)
2.32
"Atorvastatin (ATO) is a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor widely used to treat hypercholesterolemia. "( Atorvastatin induces mitochondrial dysfunction and cell apoptosis in HepG2 cells via inhibition of the Nrf2 pathway.
Guo, JB; He, J; Li, LZ; Peng, SQ; Yu, L; Yuan, XY; Zhang, L; Zhang, TF; Zhao, J; Zhao, ZM, 2019
)
3.4
"Atorvastatin is a commonly prescribed statin drug for the control of lipid synthesis and recent studies have shown the cardiac protection potential of atorvastatin. "( Suppression of miR-143-3p contributes to the anti-fibrosis effect of atorvastatin on myocardial tissues via the modulation of Smad2 activity.
Nie, W; Shi, K; Xie, D; Yu, B; Yu, M; Zhang, H, 2020
)
2.24
"Atorvastatin is a lipid-lowering drug in clinical treatment."( Atorvastatin attenuates obese-induced kidney injury and impaired renal organic anion transporter 3 function through inhibition of oxidative stress and inflammation.
Chatsudthipong, V; Cherngwelling, R; Jaikumkao, K; Lungkaphin, A; Pengrattanachot, N; Pongchaidecha, A; Swe, MT; Thongnak, L, 2020
)
2.72
"Atorvastatin calcium (AT) is an ocular anti-inflammatory with limited bioavailability when taken orally due to its low solubility in low pH and extensive first-pass effect. "( Chitosan-Coated PLGA Nanoparticles for Enhanced Ocular Anti-Inflammatory Efficacy of Atorvastatin Calcium.
Arafa, MG; El-Dahan, MS; Girgis, GNS, 2020
)
2.22
"Atorvastatin calcium is a case in point, where confusing terminology, absence of a proper anhydrate form, and loss of water on heating lead to several doubtful conclusions in the literature."( Does the trihydrate of atorvastatin calcium possess a melting point?
Barrio, M; Clevers, S; Coquerel, G; Couvrat, N; Dupray, V; Galai, H; Rietveld, IB; Tamarit, JL; Tizaoui, C, 2020
)
1.59
"Atorvastatin is a widely prescribed lipid-lowering agent metabolized by cytochrome P450 (CYP) 3A4, whose hepatocyte uptake is facilitated by organic anion transporting polypeptide (OATP) 1B1/1B3."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.52
"Atorvastatin is a statin with the potential to cross the blood-brain barrier; however, the concentrations necessary for a cytotoxic effect against cancer cells exceed the concentrations achievable via oral administration, which made the development of a novel atorvastatin formulation necessary."(
Appelt-Menzel, A; Cubukova, A; Gohla, A; Haider, MS; Jeanclos, E; Kataoka, K; Kinoh, H; Krafft, M; Lübtow, MM; Luxenhofer, R; Meier, L; Oerter, S; Quader, S; Rist, M; Sampetrean, O; Schulte, C, 2020
)
1.28
"Atorvastatin is a pleiotropic agent with proven anti-inflammatory effects."( Atorvastatin protects against postoperative neurocognitive disorder via a peroxisome proliferator-activated receptor-gamma signaling pathway in mice.
Lin, D; Liu, J; Ma, D; Wei, C; Wu, A; Xiong, C; Yang, Y, 2020
)
2.72
"Atorvastatin (ATV) is a blood cholesterol-lowering drug used to prevent cardiovascular events, the leading cause of death worldwide. "( The atorvastatin metabolic phenotype shift is influenced by interaction of drug-transporter polymorphisms in Mexican population: results of a randomized trial.
Bamford, AD; Barrera-Saldaña, HA; Bustos, MFG; Gómez-Silva, M; León-Cachón, RBR; Meester, I, 2020
)
2.56
"Atorvastatin is a statin drug that presents antifungal activity. "( Antifungal efficacy of atorvastatin-containing emulgel in the treatment of oral and vulvovaginal candidiasis.
Amorim, MES; de Freitas Araújo, MG; de Freitas Souza, T; de Oliveira Neto, AS; do Couto, RO; Fabri, RL; Rocha, VN; Souza, ILA, 2021
)
2.37
"Atorvastatin is a member of statins, which has shown positive vascular effects, anti-oxidant, anti-platelet, and anti-apoptotic properties."( Atorvastatin Prevents the Neuron Loss in the Hippocampal Dentate Gyrus Region through its Anti-Oxidant and Anti-Apoptotic Activities.
Arani, HZ; Jangholi, E; Karimi, A; Movassaghi, S; Parsa, Y; Sharifi, ZN; Yadollah-Damavandi, S, 2021
)
3.51
"Atorvastatin (ATR) is a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor approved for control of plasma cholesterol levels."( Pretreatment with atorvastatin ameliorates cobra venom factor-induced acute lung inflammation in mice.
Guo, J; Li, M; Sun, QY; Yang, Y; Zhang, L; Zhang, LW, 2020
)
1.61
"Atorvastatin (ATR) is a poorly water-soluble drug and it has strong anti-hyperlipidemia activity, and it is usually used in combination with lisinopril (LNP), an anti-hypertension drug."( Co-amorphization of atorvastatin by lisinopril as a co-former for solubility improvement.
Fu, Q; He, Z; Li, J; Li, M; Li, W; Liu, X; Song, J; Tian, B, 2021
)
1.67
"Atorvastatin is a strong inhibitor of inflammation-induced osteoclastogenesis in inflammatory joint diseases."( Atorvastatin inhibits osteoclast differentiation by suppressing NF-κB and MAPK signaling during IL-1β-induced osteoclastogenesis.
Choi, YJ; Lee, EG; Lee, WS; Sung, MS; Yoo, WH, 2018
)
3.37
"Atorvastatin known to be a potential inhibitor of HMG-CoA reductase involved in the synthesis of cholesterol. "( Preparation and characterisation of atorvastatin and curcumin-loaded chitosan nanoformulations for oral delivery in atherosclerosis.
J B, VK; Madhusudhan, B; Ramakrishna, S, 2017
)
2.17
"Atorvastatin is a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor with cholesterol-lowering, anti-inflammatory, and antioxidant properties. "( Atorvastatin Prevents Early Oxidative Events and Modulates Inflammatory Mediators in the Striatum Following Intranasal 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) Administration in Rats.
Castro, AA; De Bem, AF; Mancini, G; Marques, NF; Prediger, RD; Rocha, FL; Santos, ARS; Tasca, CI, 2018
)
3.37
"Atorvastatin is a member of the statin class of drugs, which competitively inhibit the activity of 5‑hydroxy‑3‑methylglutaryl‑coenzyme A reductase. "( Atorvastatin protects BV‑2 mouse microglia and hippocampal neurons against oxygen‑glucose deprivation‑induced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NF‑κB pathway.
Fang, Y; Guo, FQ; Han, J; Shou, WQ; Yin, QH; Zhang, CC, 2018
)
3.37
"Atorvastatin is a synthetic statin commonly used in the treatment of hypercholesterolemia. "( Atorvastatin-loaded lipid nanoparticles: antitumor activity studies on MCF-7 breast cancer cells.
Gambhire, MS; Gambhire, VM; Salunkhe, SM, 2018
)
3.37
"Atorvastatin is a lipid lowering agent with poor oral bioavailability (12%) because of poor solubility and extensive first pass hepatic metabolism. "( Systematic approach for the formulation and optimization of atorvastatin loaded solid lipid NANOAPARTICLES using response surface methodology.
Jana, U; Manna, PK; Mohanta, GP; Sahoo, J; Sarangi, B, 2018
)
2.17
"Atorvastatin is a lipid-regulating drug that is commonly used in clinical practice and can stabilize plaques. "( Atorvastatin Improves Doxorubicin-Induced Cardiac Dysfunction by Modulating Hsp70, Akt, and MAPK Signaling Pathways.
Chen, W; Gao, G; Ge, L; Jiang, S; Sui, S; Zhai, C; Zhang, S, 2019
)
3.4
"Atorvastatin (Lipitor™) is a lipid‑lowering agent that is widely used in the treatment of cardiovascular diseases. "( Effects of various doses of atorvastatin on vascular endothelial cell apoptosis and autophagy in vitro.
Chang, F; Fu, H; Li, F; Liu, J; Wang, J; Zhao, J; Zhao, WB, 2019
)
2.25
"Atorvastatin is a cholesterol-lowering statin that possesses pleiotropic effects including neuroprotective and antidepressant actions."( Atorvastatin prevents lipopolysaccharide-induced depressive-like behaviour in mice.
Buss, ZS; Doneda, DL; Ferreira, YS; Fraga-Junior, EB; Lima, E; Lopes, L; Rios-Santos, F; Stupp, IJV; Taniguti, EH; Vandresen-Filho, S; Viola, GG, 2019
)
2.68
"Atorvastatin is a carboxylic acid that exists in equilibrium with a lactone form in vivo."( Physiologically-Based Pharmacokinetic Modeling of Atorvastatin Incorporating Delayed Gastric Emptying and Acid-to-Lactone Conversion.
Alberts, JJ; Dickinson, GL; Hall, SD; Hillgren, KM; Kolur, A; Loghin, C; Morse, BL; Posada, MM; Rehmel, J; Tham, LS, 2019
)
1.49
"Atorvastatin is a lipid lowering agent that is widely used worldwide. "( Rhabdomyolysis developing secondary to atorvastatin therapy in a patient with liver cirrhosis.
Eshraghian, A; Kamyab, AA, 2013
)
2.1
"Atorvastatin is a hypolipidemic drug that may have a role in treatment of cancer."( Effect of atorvastatin and methotrexate on solid Ehrlich tumor.
Abdel-Rahman, MN; El Rashidy, MA; El-Sisi, Ael-D; Ezzat, NM; Haleem, MS; Kabel, AM, 2013
)
1.51
"Atorvastatin is a 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitor used in treatment of hypercholesterolemia and prevention of coronary heart disease. "( Antihyperalgesic and anti-inflammatory effects of atorvastatin in chronic constriction injury-induced neuropathic pain in rats.
Balaganur, V; Kant, V; Kumar, D; Lingaraju, MC; More, AS; Pathak, NN; Tandan, SK, 2013
)
2.09
"Atorvastatin is a 3 hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitor that lowers blood cholesterol levels."( The effect of atorvastatin on P wave dispersion in hyperlipidemic patients.
Akın, F; Avcı, II; Ayça, B; Can, MM; Çelik, Ö; Dinçkal, MH; Okuyan, E; Şahin, I; Yıldız, SS, 2013
)
1.47
"Atorvastatin is a potent immunomodulatory agent that holds promise as a novel and safe agent for acute GVHD prophylaxis."( Sibling donor and recipient immune modulation with atorvastatin for the prophylaxis of acute graft-versus-host disease.
Brundage, KM; Bunner, P; Craig, MD; Cumpston, A; Gibson, LF; Hamadani, M; Petros, W; Remick, SC; Tse, W; Vos, JA; Wen, S, 2013
)
1.36
"Atorvastatin is a statin group medicine that reduces the level of serum cholesterol; thus it is used to treat hypercholesterolaemia. "( The effect of atorvastatin on lung histopathology in a murine model of chronic asthma.
Bagrıyanık, A; Cilaker-Mıcılı, S; Fırıncı, F; Karaman, M; Karaman, O; Uzuner, N,
)
1.93
"Atorvastatin is an HMG-CoA reductase inhibitor used in the treatment of hypercholesterolemia and prevention of coronary heart disease. "( Atorvastatin attenuates neuropathic pain in rat neuropathy model by down-regulating oxidative damage at peripheral, spinal and supraspinal levels.
Balaganur, V; Kant, V; Kumar, D; Latief, N; Lingaraju, MC; More, AS; Pathak, NN; Tandan, SK, 2014
)
3.29
"Atorvastatin is a statin largely used in the treatment of hypercholesterolemia and recently revealed as a neuroprotective agent. "( Atorvastatin evokes a serotonergic system-dependent antidepressant-like effect in mice.
Binder, LB; Constantino, LC; Cunha, MP; Dal-Cim, T; Kuminek, G; Ludka, FK; Rodrigues, AL; Tasca, CI; Zomkowski, AD, 2014
)
3.29
"Atorvastatin is a common statin with greater LDL-C lowering efficacy than most other statins; its availability in generic form will likely increase its use."( Limitations of real-world treatment with atorvastatin monotherapy for lowering LDL-C in high-risk cardiovascular patients in the US.
Marrett, E; Neff, DR; Ramey, DR; Tershakovec, AM; Tomassini, JE; Zhang, NJ; Zhang, Q; Zhao, C, 2014
)
1.39
"Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke."( Atorvastatin protects GABAergic and dopaminergic neurons in the nigrostriatal system in an experimental rat model of transient focal cerebral ischemia.
Arango, CA; Cardona, GP; Céspedes, ÁE; Sabogal, AM,
)
2.3
"Atorvastatin is a member of the drug class known as statins, which is used for lowering blood cholesterol."( Inhibition of neointimal hyperplasia in rats treated with atorvastatin after carotid artery injury may be mainly associated with down-regulation of survivin and Fas expression.
Fang, Z; Huang, D; Li, X; Liu, Q; Xu, Y; Zheng, C; Zhou, S, 2014
)
2.09
"Atorvastatin is a 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitor used in the treatment of atherosclerosis and dyslipidemia. "( Topical atorvastatin ameliorates 12-O-tetradecanoylphorbol-13-acetate induced skin inflammation by reducing cutaneous cytokine levels and NF-κB activation.
Jaji, MS; Krishnan, UM; Kulkarni, NM; Mookkan, J; Muley, MM; Narayanan, S; Raghul, J; Rajesh, NB; Reddy, NK; Vijaykanth, G; Vishwakarma, SL, 2015
)
2.29
"Atorvastatin is a potent inhibitor of the mevalonate pathway and widely used as a hypolipidemic drug. "( Chemically induced mouse liver tumors are resistant to treatment with atorvastatin.
Braeuning, A; Bucher, P; Buchmann, A; Hofmann, U; Schwarz, M, 2014
)
2.08
"Atorvastatin is a synthetic and lipophilic statin which has been reported to have a positive role in reducing depression. "( Antidepressant-like effect of atorvastatin in the forced swimming test in mice: the role of PPAR-gamma receptor and nitric oxide pathway.
Dehpour, A; Jahanabadi, S; Javadi, S; Khoshnoodi, M; Mehr, SE; Shafaroodi, H; Shahsavarian, A; Shamsaee, J, 2014
)
2.13
"Atorvastatin is a synthetic statin characterized by a high efficacy, in part due to its longer half-life compared to other molecules of the same group."( Pleiotropic effects of statins in atherosclerotic disease: focus on the antioxidant activity of atorvastatin.
Buttari, B; Profumo, E; Rigano, R; Saso, L, 2014
)
1.34
"Atorvastatin is a reversible and competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, decreasing the de novo cholesterol synthesis. "( Use of atorvastatin in lipid disorders and cardiovascular disease in Chinese patients.
Ye, YC; Zhang, SY; Zhao, XL, 2015
)
2.31
"Atorvastatin is a beneficial pharmacological modulator of impaired antiinflammatory HDL-C levels, endothelial functions, and oxidative status against atherosclerosis indicating pleiotropic effects of statins."( The effects of atorvastatin on antioxidant/antiinflammatory properties of HDLs in hypercholesterolemics.
Akalin Çiftçi, G; Akalin, A; Alataş, İÖ; Ertorun, İ; Musmul, A, 2015
)
1.49
"Atorvastatin which functions as a potent antioxidant agent may inhibit this LDL-C oxidation by increasing PON-1 activity in atherogenesis."( Ameliorative effect of statin therapy on oxidative damage in heart tissue of hypercholesterolemic rabbits.
Sozer, V, 2015
)
1.14
"Atorvastatin calcium (AC) is a BCS class II drug which shows poor bioavailability due to inadequate dissolution. "( Dissolution enhancement of atorvastatin calcium by co-grinding technique.
Patravale, V; Prabhu, P, 2016
)
2.17
"Atorvastatin is a cholesterol-lowering statin that has been shown to exert several pleiotropic effects in the nervous system as a neuroprotective and antidepressant-like agent. "( Involvement of PI3K/Akt/GSK-3β and mTOR in the antidepressant-like effect of atorvastatin in mice.
Binder, LB; Constantino, LC; Dal-Cim, T; Ludka, FK; Rodrigues, AL; Tasca, CI; Zomkowski, A, 2016
)
2.11
"Atorvastatin is a 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor widely used in treatment of hypercholesterolemia and prevention of coronary heart disease and has various pleiotropic effects. "( Effects of Topical Atorvastatin (2 %) on Posthemorrhoidectomy Pain and Wound Healing: A Randomized Double-Blind Placebo-Controlled Clinical Trial.
Ala, S; Alvandipour, M; Faramarzi, F; Hamidian, M; Rahmani, N; Saeedi, M; Shiva, A, 2017
)
2.23
"Atorvastatin is a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor that is mainly metabolized by cytochrome P450 (CYP) 3A4. "( Contribution of cytochrome P450 3A4 and 3A5 to the metabolism of atorvastatin.
Bae, SK; Kim, KB; Liu, KH; Moon, BS; Park, JE; Shin, JG, 2008
)
2.03
"Atorvastatin, which is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, is prescribed to decrease high cholesterol levels, and it has anti-inflammation and anti-oxidization activities."( Atorvastatin inhibits renal crystal retention in a rat stone forming model.
Momohara, C; Nonomura, N; Okuyama, A; Tsujihata, M; Tsujimura, A; Yoshioka, I, 2008
)
2.51
"Atorvastatin is a widely-used therapeutic statin given for hypercholesterolaemia and for prevention of cardiovascular events. "( [Atorvastatin-induced drug reaction with eosinophilia and systemic symptoms (DRESS)].
Dubertret, L; Gressier, L; Pruvost-Balland, C; Viguier, M, 2009
)
2.71
"Atorvastatin is a highly effective 3-hydroxy-3 methylglutamyl- coenzyme A reductase (statin) used to lower low-density lipoprotein."( Severe acute cholestatic hepatitis with prolonged cholestasis and bile-duct injury following atorvastatin therapy: a case report.
Geubel, AP; Leclercq, I; Rahier, J; Rahier, JF,
)
1.07
"Atorvastatin is a potential candidate for the prevention and therapy of diseases associated with insulin resistance such as type 2 diabetes mellitus and cardiovascular disease. "( Atorvastatin improves insulin sensitivity in mice with obesity induced by monosodium glutamate.
Huan, Y; Huang, H; Shen, ZF; Song, GM; Sun, SJ; Zhang, N, 2010
)
3.25
"Atorvastatin calcium is a synthetic HMG-CoA reductase inhibitor that is used as a cholesterol-lowering agent. "( Development and validation of a reversed-phase high-performance thin-layer chromatography-densitometric method for determination of atorvastatin calcium in bulk drug and tablets.
Shirkhedkar, AA; Surana, SJ,
)
1.78
"Atorvastatin calcium is a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor indicated for the prevention of cardiovascular disease and for the treatment of dyslipidemia. "( Pharmacokinetics and bioequivalence evaluation of two different atorvastatin calcium 10-mg tablets: A single-dose, randomized-sequence, open-label, two-period crossover study in healthy fasted Chinese adult males.
Jia, JY; Li, GX; Liu, GY; Liu, YM; Lu, C; Pu, HH; Wang, W; Weng, LP; Xu, RJ; Yu, C; Zhang, MQ, 2010
)
2.04
"Atorvastatin proved to be an immunomodulatory agent, significantly decreasing lymphocyte proliferation by 15% (p = 0.001), increasing ATP levels by 16% (p = 0.0004), and showing a trend toward increasing T(reg) cells in hypercholesterolemic patients (p = 0.09). "( Biomarker assessment of the immunomodulator effect of atorvastatin in stable renal transplant recipients and hypercholesterolemic patients.
Brunet, M; Cofán, F; Cofán, M; Guillén, D; Millán, O; Ros, E, 2010
)
2.05
"Atorvastatin is a statin used for lowering LDL-C concentrations."( Efficacy and tolerability of a generic and a branded formulation of atorvastatin 20 mg/d in hypercholesterolemic Korean adults at high risk for cardiovascular disease: a multicenter, prospective, randomized, double-blind, double-dummy clinical trial.
Cho, YS; Hong, SJ; Hyon, MS; Kim, DW; Kim, HS; Kim, SH; Lee, MY; Moon, GW; Park, K; Sung, JD; Yoon, MH, 2010
)
1.32
"Atorvastatin is a selective HMG-CoA reductase competitive inhibitor, used for the treatment of hyperlipidaemia. "( Influence of atorvastatin on the pharmacokinetics and pharmacodynamics of glyburide in normal and diabetic rats.
Gade, J; Neerati, P, 2011
)
2.18
"Atorvastatin is a statin that inhibits the 3-hydroxy-methyl-glutaryl coenzyme A (HMG-CoA) reductase. "( Antinociception induced by atorvastatin in different pain models.
Garcia, GG; Miranda, HF; Noriega, V; Olavarría, L; Prieto, JC; Sierralta, F; Zepeda, RJ, 2011
)
2.11
"Atorvastatin is an HMG-CoA reductase inhibitor used to treat hypercholesterolemic conditions associated with hypertension. "( Neuroprotective and anti-inflammatory activities of atorvastatin in a rat chronic constriction injury model.
Chen, JY; Cheng, KI; Chu, LW; Wu, BN; Wu, PC; Yu, KL,
)
1.82
"Atorvastatin is a synthetic and lipophilic statin that presents a good effect in decreasing cholesterol levels and is safe and well tolerated. "( Acute atorvastatin treatment exerts antidepressant-like effect in mice via the L-arginine-nitric oxide-cyclic guanosine monophosphate pathway and increases BDNF levels.
Cunha, MP; Dal-Cim, T; Ludka, FK; Rodrigues, AL; Tasca, CI; Zeni, AL; Zomkowski, AD, 2013
)
2.31
"Atorvastatin (ATV) is a specific competitive inhibitor of 3-hydroxy-2-methyl-glutaryl coenzyme A reductase. "( Clinical efficacy of subgingivally delivered 1.2% atorvastatin in chronic periodontitis: a randomized controlled clinical trial.
Kumari, M; Martande, SS; Naik, SB; Pradeep, AR; Rao, NS, 2013
)
2.09
"Atorvastatin is an antilipemic drug belonging to the statins class, whose reference drug is Pfizer's Lipitor®. "( Degradation kinetics of atorvastatin under stress conditions and chemical analysis by HPLC.
Belinelo, VJ; Oliveira, MA; Valotto, RS; Yoshida, MI, 2013
)
2.14
"Atorvastatin is a drug of choice in the treatment of coronary heart disease, because this hepatic 3-hydroxy-3-methylglutaryl coenzyme reductase inhibitor significantly decreases plasma cholesterol and triglyceride levels. "( Induction of lipoprotein lipase gene expression in 3T3-L1 preadipocytes by atorvastatin, a cholesterol- and triglyceride-lowering drug.
Bey, L; Hamilton, MT; Laouenan, H; Maigret, P, 2002
)
1.99
"Atorvastatin is a powerful new synthetic 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor currently in clinical use. "( Atorvastatin reduces plasma levels of factor VII activity and factor VII antigen in patients with hyperlipidemia.
Asakura, H; Ishino, C; Kanno, M; Matsuda, T; Minami, S; Morishita, E; Nakao, S; Uotani, C, 2002
)
3.2
"Atorvastatin is an HMG-CoA reductase inhibitor which across its dosage range (10-80 mg/day) has shown significantly greater lipid-lowering effects than all previously marketed statins."( Comparison of the efficacy and tolerability of policosanol with atorvastatin in elderly patients with type II hypercholesterolaemia.
Alvarez, E; Castaño, G; Fernández, L; Illnait, J; Lezcay, M; Mas, R; Mesa, M, 2003
)
1.28
"Atorvastatin is a synthetic inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. "( Efficacy of alternate-day dosing versus daily dosing of atorvastatin.
Ahmadi-Kashani, M; Balian, H; Bashir, M; Ebrahimi, R; Jafari, M, 2003
)
2.01
"Atorvastatin (Lipitor) is an HMG-CoA reductase inhibitor with well documented lipid-lowering effects. "( Atorvastatin: a review of its use in the primary prevention of cardiovascular events in patients with type 2 diabetes mellitus.
Croom, KF; Plosker, GL, 2005
)
3.21
"Atorvastatin is a statin drug that inhibits 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (the rate-limiting step of cholesterol production) and primarily lowers LDL-C levels."( Torcetrapib/atorvastatin combination therapy.
Bays, H; Davidson, M; McKenney, J, 2005
)
1.43
"Atorvastatin is a new 3-hydroxy-3-metylglutaryl coenzyme A reductase inhibitor that reduces lipid serum levels."( A pilot study of atorvastatin treatment in dyslipemid, non-alcoholic fatty liver patients.
García-Buey, L; Gisbert, JP; Gómez-Domínguez, E; Moreno-Monteagudo, JA; Moreno-Otero, R, 2006
)
1.39
"Atorvastatin is an inhibitor of the enzyme 3-hydroxyl-3-methylglutaryl coenzyme A reductase used to prevent coronary heart disease. "( Atorvastatin inhibits inflammatory hypernociception.
Cunha, FQ; Cunha, TM; Ferreira, SH; Parada, CA; Poole, S; Santodomingo-Garzón, T; Valério, DA; Verri, WA, 2006
)
3.22
"Atorvastatin is an effective lipid-lowering agent for dyslipidemic subjects with advanced and endstage renal failure, and was reasonably well tolerated."( Efficacy, safety and tolerability of atorvastatin in dyslipidemic subjects with advanced (non-nephrotic) and endstage chronic renal failure.
Healy, H; Morgan, C; Saltissi, D; Westhuyzen, J, 2006
)
2.05
"Atorvastatin is an inhibitor of HMG-CoA reductase, which is a key rate-limiting enzyme in the cholesterol biosynthesis."( Automated enzyme inhibition assay method for the determination of atorvastatin-derived HMG-CoA reductase inhibitors in human plasma using radioactivity detection.
Liu, L; Musson, DG; Valesky, RJ; Zhao, JJ,
)
1.09
"Atorvastatin is a lipid-lowering agent that has been evaluated in a number of primary and secondary intervention studies. "( Atorvastatin: a pharmacoeconomic review of its use in the primary and secondary prevention of cardiovascular events.
Lyseng-Williamson, KA; Plosker, GL, 2007
)
3.23
"Atorvastatin calcium (AC) is a second-generation 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor approved for clinical use as a lipid lowering agent. "( Oral nanoparticulate atorvastatin calcium is more efficient and safe in comparison to Lipicure in treating hyperlipidemia.
Ankola, DD; Chandraiah, G; Kumar, MN; Meena, AK; Rao, PR; Ratnam, DV, 2008
)
2.11
"Atorvastatin is a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor demonstrated to be effective in reducing both cholesterol (CHOL) and triglyceride (TG) levels in humans."( Atorvastatin monotherapy vs. combination therapy in the management of patients with combined hyperlipidemia.
Avisar, I; Brook, JG; Wolfovitz, E, 2008
)
2.51
"Atorvastatin is an adequate monotherapy for many mixed hyperlipidemia patients. "( Atorvastatin monotherapy vs. combination therapy in the management of patients with combined hyperlipidemia.
Avisar, I; Brook, JG; Wolfovitz, E, 2008
)
3.23
"Atorvastatin is a new 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor under development."( Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor.
Black, DM; Davidson, MH; Haber, HE; Jones, PH; Lupien, PJ; Nawrocki, JW; Schwartz, SL; Sprecher, DL; Weiss, SR, 1995
)
1.23
"Atorvastatin is a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor that reduces plasma cholesterol by inhibiting cholesterol synthesis and increasing cellular uptake of low density lipoproteins. "( Effect of age and gender on pharmacokinetics of atorvastatin in humans.
Bron, NJ; Gibson, DM; Hounslow, NJ; Richens, A; Sedman, AJ; Whitfield, LR, 1996
)
1.99
"Atorvastatin is a synthetic HMG-CoA reductase inhibitor which lowers plasma cholesterol levels by inhibiting endogenous cholesterol synthesis. "( Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias.
Lea, AP; McTavish, D, 1997
)
3.18
"Atorvastatin is a highly efficacious hydroxymethylglutaryl-coenzyme A reductase inhibitor that has been shown to reduce low-density lipoprotein cholesterol by 40% to 60%. "( Effectiveness of atorvastatin for reducing low-density lipoprotein cholesterol to National Cholesterol Education Program treatment goals.
Black, DM; Davidson, MH; Haber, HE; Jones, PH; Lupien, PJ; Nawrocki, JW; Schwartz, SL; Weiss, SR, 1997
)
2.08
"Atorvastatin is a powerful and safe lipid-modifying agent for LDL cholesterol; it also modifies HDL cholesterol and triglyceride concentrations, and may suffice as a single agent for many subjects with heterozygous FH."( Atorvastatin: an effective lipid-modifying agent in familial hypercholesterolemia.
Bateman, ME; Byrnes, P; Firth, JC; Marais, AD; Martens, C; Mountney, J, 1997
)
2.46
"Atorvastatin calcium is an HMG-coenzyme A (CoA) reductase inhibitor that was approved by the Food and Drug Administration on December 17, 1996. "( Atorvastatin calcium: an addition to HMG-CoA reductase inhibitors.
Chong, PH; Seeger, JD,
)
3.02
"Atorvastatin is a potent inhibitor of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to mevalonate and constitutes the rate-limiting step in the biosynthesis of cholesterol. "( Pre- and postnatal toxicity of the HMG-CoA reductase inhibitor atorvastatin in rats.
Anderson, JA; Black, A; Colgin, J; Craft, WR; Henck, JW, 1998
)
1.98
"Atorvastatin is a major addition to this class of drugs because of its high efficacy and large spectrum of action."( Advances in drug treatment of dyslipidemia: focus on atorvastatin.
Davignon, J, 1998
)
1.27
"Atorvastatin is a new member of the class of drugs which inhibit the enzyme Hydroxy-Methylglutaryl Co-A reductase, the rate limiting step in cholesterol biosynthesis."( Comparison of atorvastatin alone versus simvastatin +/- cholestyramine in the management of severe primary hypercholesterolaemia (the six cities study).
Simons, LA, 1998
)
2.1
"Atorvastatin is a recent hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment of primary hypercholesterolemia, mixed dyslipidemias, and homozygous familial hypercholesterolemia. "( Atorvastatin in the treatment of primary hypercholesterolemia and mixed dyslipidemias.
Fong, NT; Yee, HS, 1998
)
3.19
"Atorvastatin is a valuable addition to the treatment possibilities of patients with serious hypercholesterolaemia, like FH."( Effects of atorvastatin on serum lipids of patients with familial hypercholesterolaemia.
Hoogerbrugge, N, 1998
)
2.13
"Atorvastatin is a new potent HMG-CoA reductase inhibitor. "( Atorvastatin compared with simvastatin in patients with severe LDL hypercholesterolaemia treated by regular LDL apheresis.
Geiss, HC; Parhofer, KG; Schwandt, P, 1999
)
3.19
"Atorvastatin is a potent inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase, but its effect on bile acid synthesis is unknown. "( Effect of inhibiting HMG-CoA reductase on 7 alpha-hydroxy-4-cholesten-3-one, a marker of bile acid synthesis: contrasting findings in patients with and without prior up-regulation of the latter pathway.
Axelson, M; Dunn, S; Naoumova, RP; Neuwirth, CK; O'Neill, FH; Taylor, GW; Thompson, GR, 1999
)
1.75
"Atorvastatin (AT) is a second-generation potent inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, clinically approved for lowering plasma cholesterol. "( Metabolism and excretion of atorvastatin in rats and dogs.
Black, AE; Hayes, RN; Roth, BD; Woo, P; Woolf, TF, 1999
)
2.04
"Atorvastatin is a second generation synthetic statin, introduced in Belgium in May 1998. "( [Atorvastatin (Lipitor)].
Carpentier, Y; Ducobu, J; Sternon, J, 1999
)
2.66
"Atorvastatin is a new hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor that has been demonstrated to be efficacious in reducing both triglyceride (TG) and cholesterol (CHOL) levels in humans. "( Lipid and apolipoprotein levels and distribution in patients with hypertriglyceridemia: effect of triglyceride reductions with atorvastatin.
Bakker-Arkema, R; Black, D; Brown, WV; Innis-Whitehouse, W; Le, NA; Li, X, 2000
)
1.96
"Atorvastatin is an effective and safe lipid-lowering agent for peritoneal dialysis patients with mixed dyslipidaemia."( Effects of atorvastatin on dyslipidaemia in uraemic patients on peritoneal dialysis.
Hufnagel, G; Kossari, N; Michel, C; Mignon, F; Queffeulou, G; Vrtovsnik, F, 2000
)
2.14
"Atorvastatin is an established HMG-CoA reductase inhibitor which effectively reduces the plasma low density lipoprotein (LDL)-cholesterol level in hyperlipidemic patients. "( Effects of atorvastatin treatment on the oxidatively modified low density lipoprotein in hyperlipidemic patients.
Choy, PC; Dembinski, T; Hatch, G; Kroeger, EA; McMaster, J; Mymin, D; Zhu, Q, 2000
)
2.14
"Atorvastatin is a new HMG-CoA reductase inhibitor that has shown a favourable profile of lipid reduction when compared with other statins."( Short-term effect of atorvastatin in hypercholesterolaemic renal-transplant patients unresponsive to other statins.
Calviño, J; Rodriguez, J; Romero, R; Sánchez-Guisande, D, 2000
)
1.35
"Atorvastatin is a potent HMG-CoA reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and fasting triglyceride concentrations. "( Atorvastatin improves postprandial lipoprotein metabolism in normolipidemlic subjects.
Barrett, PH; Parhofer, KG; Schwandt, P, 2000
)
3.19
"Atorvastatin is a new HMG-CoA reductase inhibitor that strongly lowers plasma cholesterol and triglyceride (TG) levels in humans and animals. "( Prolonged inhibition of cholesterol synthesis by atorvastatin inhibits apo B-100 and triglyceride secretion from HepG2 cells.
Arai, Y; Funatsu, T; Goto, M; Ida, M; Kakuta, H; Miyata, K; Nishijima, S; Suzuki, K; Tanaka, H; Yasuda, S, 2001
)
2.01
"Atorvastatin is a potent hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and triglyceride concentrations, but little is known about its effects on LDL subtype distribution in different types of hyperlipoproteinemia. "( Effect of atorvastatin on low-density lipoprotein subtypes in patients with different forms of hyperlipoproteinemia and control subjects.
Geiss, HC; Otto, C; Parhofer, KG; Schwandt, P, 2001
)
2.16
"Atorvastatin is a synthetic hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. "( Atorvastatin: an updated review of its pharmacological properties and use in dyslipidaemia.
Goa, KL; Malhotra, HS, 2001
)
3.2
"Atorvastatin is an appropriate first-line lipid-lowering therapy in numerous groups of patients at low to high risk of CHD. "( Atorvastatin: an updated review of its pharmacological properties and use in dyslipidaemia.
Goa, KL; Malhotra, HS, 2001
)
3.2
"Atorvastatin is a recently introduced statin that lowers LDL-cholesterol (LDL-C) and triglycerides more than some of the older statins."( Effect of atorvastatin treatment on lipoprotein lipase mass in the pre-heparin plasma in Japanese hyperlipidemic subjects.
Kobayashi, J; Maruyama, T; Masuda, M; Shinomiya, M, 2001
)
2.16
"Atorvastatin is a common option among the HMG-CoA reductase inhibitors for the treatment of lipid disorders because of its excellent lipid-lowering efficacy and overall safety profile. "( A study of the interaction potential of azithromycin and clarithromycin with atorvastatin in healthy volunteers.
Amsden, GW; Kuye, O; Wei, GC, 2002
)
1.99
"Atorvastatin is a safe and effective drug that enables most patients requiring primary prevention to reach LDL-C goal levels, even with a low dose of 10 mg. "( Efficacy of atorvastatin in treating high risk patients to reach low density lipoprotein-cholesterol goals: the Treat to Target (TTT-Israel) Study.
Gavish, D; Harats, D; Leibovitz, E, 2002
)
2.14

Effects

Atorvastatin has a dose-dependent risk of developing new-onset diabetes mellitus. It has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1)

Atorvastatin monotherapy has a better effect on LDL-C and apoprotein B than statin-fibrate combinations, but a lesser effect on HDL-C, TG and fibrinogen. Atorvstatin has been found to have neuroprotective effects in some nervous system diseases.

ExcerptReferenceRelevance
"Atorvastatin has a significant effect on P-gp mediated intestinal transport of daclatasvir; however, it did not affect the systemic bioavailability of a single oral dose of daclatasvir."( Effect of Atorvastatin on Single Oral Pharmacokinetics and Safety of Daclatasvir in Rats: Emphasis on P-glycoprotein and Cytochrome P450.
El-Demerdash, E; Elbadawy, HA; Wahdan, SA, 2022
)
2.57
"Atorvastatin has a dose-dependent risk of developing new-onset diabetes mellitus. "( Evaluation of glycemic status among hypercholesterolemic patients on atorvastatin in a tertiary care hospital - A retrospective study.
Karthick, R; Nalini, R; Ramya, JE,
)
1.81
"Atorvastatin has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1)."( Analysis of HMGB-1 level before and after providing atorvastatin standard therapy in coronary artery disease patients with type-2 diabetes mellitus compared to without type-2 diabetes mellitus.
Handayani, W; Yogiarto, M, 2021
)
1.59
"Atorvastatin has a limited advantage to formulate oral dosage forms."( Solid self microemulsification of Atorvastatin using hydrophilic carriers: a design.
Nanda Kishore, R; Rasheed, A; Sushma, M; Vadlamudi, HC; Vandana, KR; Yalavarthi, PR, 2015
)
2.14
"Atorvastatin has a protective effect on the myocardial injury in the myocardial ischemia and reperfusion rats. "( Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats.
Luo, YQ; Xu, Y; Yang, Y, 2014
)
2.25
"Atorvastatin has a beneficial effect on bone metabolism in patients with acute ischemic heart disease (mainly males) by incrementing bone mineral density in which vitamin D levels are required to be higher than 30 nmol/l for the drug to be effective."( Effect of atorvastatin on bone mineral density in patients with acute coronary syndrome.
Abad, L; Dueñas, A; García-Porrero, M; Pérez-Castrillón, JL; Pinacho, F; Sanz-Cantalapiedra, A; Vega, G,
)
1.98
"Atorvastatin 20 mg has a dramatic effect on the lipid but moderate effect on CRP. "( Effect of atorvastatin on LDL & hs-CRP in a selected Thai population.
Benjanuwatra, T; Boonbaichaiyapruck, S; Buakhamsri, A; Cheepudomwit, S; Moleelerkpoom, W; Panjavenin, P; Sukanandachai, B; Suthichaiyakul, T, 2008
)
2.19
"Atorvastatin has a beneficial effect on oxidative stress in rats fed with high-cholesterol diet. "( Effect of atorvastatin and ezetimibe treatment on serum lipid profile and oxidative state in rats fed with a high-cholesterol diet.
Ciralik, H; Gümüşalan, Y; Kilinc, M; Ozbag, D; Toru, H; Yasim, A, 2010
)
2.21
"Atorvastatin has a significant effect on lowering of PRA in sensitized hemodialysis patients waiting for kidney transplantation. "( Alteration of panel-reactive antibodies following treatment with either atorvastatin or low-dose mycophenolate mofetil in sensitized hemodialysis patients.
Aref, A; Ehsanpour, A; Ghorbani, A; Shahbazian, H, 2011
)
2.04
"Atorvastatin has a further sympatholytic effect in CKD patients, who are on chronic aliskiren, which is independent of blood pressure and heart rate."( Atorvastatin reduces sympathetic activity in patients with chronic kidney disease.
Blankestijn, PJ; Joles, JA; Oey, PL; Siddiqi, L, 2011
)
3.25
"Atorvastatin has an anti-inflammatory action benefiting the alleviation of secondary inflammatory damaged in acute cerebral infarction that is independent of lipid lowering."( [Effects of atorvastatin on plasma hypersensitive C-reactive protein and interleukin-6 in patients with acute cerebral infarction].
Hu, ZP; Jiang, B; Nie, S; Tan, LM; Wu, J; Xiao, ZJ; Zhao, SP; Zhou, HN, 2005
)
2.15
"Atorvastatin has a parallel effect on systemic and local inflammatory process in patients with coronary artery disease."( Relation between local temperature and C-reactive protein levels in patients with coronary artery disease: effects of atorvastatin treatment.
Boudoulas, H; Stefanadi, E; Stefanadis, C; Toutouzas, K; Tsiamis, E; Tsioufis, C; Vavuranakis, M, 2007
)
1.27
"Atorvastatin monotherapy has a better effect on LDL-C and apoprotein B than statin-fibrate combinations, but a lesser effect on HDL-C, TG and in the case of ciprofibrate combinations, fibrinogen."( Atorvastatin versus four statin-fibrate combinations in patients with familial combined hyperlipidaemia.
Athyros, VG; Athyrou, VV; Demitriadis, DS; Kontopoulos, AG; Papageorgiou, AA; Pehlivanidis, AN, 2002
)
2.48
"Atorvastatin has been suggested to reduce hematoma volume and improve neurological outcomes in patients with chronic subdural hematoma (CSDH). "( Effects of postoperative atorvastatin use in elderly patients with chronic subdural hematoma.
Guan, JW; Sun, T; Wu, K; You, C; Yuan, YK, 2021
)
2.37
"Atorvastatin has been found to have neuroprotective effects in some nervous system diseases, but its role in regulating the pathogenesis of neonatal HIBD remains elusive."( Atorvastatin inhibits neuronal apoptosis via activating cAMP/PKA/p-CREB/BDNF pathway in hypoxic-ischemic neonatal rats.
Li, S; Liu, Q; Liu, S; Mu, D; Qu, Y; Su, X; Sun, H; Ying, J; Yu, L; Zhao, F; Zhou, R, 2022
)
2.89
"Atorvastatin has a significant effect on P-gp mediated intestinal transport of daclatasvir; however, it did not affect the systemic bioavailability of a single oral dose of daclatasvir."( Effect of Atorvastatin on Single Oral Pharmacokinetics and Safety of Daclatasvir in Rats: Emphasis on P-glycoprotein and Cytochrome P450.
El-Demerdash, E; Elbadawy, HA; Wahdan, SA, 2022
)
2.57
"Atorvastatin has been shown to inhibit inflammation and may be a suitable drug candidate."( Atorvastatin for unruptured intracranial vertebrobasilar dissecting aneurysm (ATREAT-VBD): protocol for a randomised, double-blind, blank-controlled trial.
Huang, J; Kang, H; Li, M; Liu, J; Turhon, M; Wang, K; Yang, X; Zhang, Y, 2022
)
2.89
"Atorvastatin has a dose-dependent risk of developing new-onset diabetes mellitus. "( Evaluation of glycemic status among hypercholesterolemic patients on atorvastatin in a tertiary care hospital - A retrospective study.
Karthick, R; Nalini, R; Ramya, JE,
)
1.81
"Atorvastatin (ATV) has attracted considerable attention as a potential therapeutic agent for cancer because it inhibits cancer cell proliferation by suppressing the mevalonate pathway. "( Enhancement of the anticancer effect of atorvastatin-loaded nanoemulsions by improving oral absorption via multivalent intestinal transporter-targeting lipids.
Byun, Y; Cho, SS; Khadka, B; Kim, KT; Kweon, S; Pandey, P; Park, JW; Shim, JH; Subedi, L, 2022
)
2.43
"Atorvastatin has been used in the management of dyslipidemia and little is known about the efficacy and safety of high-dose atorvastatin administration for secondary prevention of Major Cardiovascular Events (MACE)."( [Efficacy and safety of atorvastatin in major cardiovascular events: Meta-analysis].
García-Rivero, AA; González-Tovar, NB; Rivas-Ruíz, R; Rivera-Lara, P; Villegas-Quintero, VE, 2023
)
2.66
"Atorvastatin has been on the market for several years with a safety profile that is acceptable even in patients with liver disease."( Atorvastatin for prevention of disease progression and hospitalisation in liver cirrhosis: protocol for a randomised, double-blind, placebo-controlled trial.
Bendtsen, F; Deshmukh, AS; Fred, RG; Grønbæk, H; Hansen, T; Kimer, N; Mann, M, 2020
)
2.72
"Atorvastatin has beneficial effects in improving Cadmium chloride-induced antioxidative enzymes disturbance which may be contribute to improving liver function in male rats."( Hepatoprotective effect of atorvastatin on Cadmium chloride induced hepatotoxicity in rats.
Bandegi, AR; Dehdashti, A; Ghanbari, A; Goodarzi, Z; Karami, E; Yousefi, S, 2020
)
2.3
"Atorvastatin has certain efficacy in the treatment of heart failure."( Effectiveness of Atorvastatin in the Treatment of Asymptomatic Heart Failure After Myocardial Infarction: A Clinical Study.
Bai, L; Cui, XR; Wang, D; Yang, XH; Zhang, JD, 2020
)
1.62
"Atorvastatin (ATV) has been widely used to reduce serum lipids levels, but its synergistic effect with RAPA in CKD remains unclear."( Combined application of rapamycin and atorvastatin improves lipid metabolism in apolipoprotein E-deficient mice with chronic kidney disease.
Ahn, S; Ha, J; Min, SK; Oh, GT; Song, EJ, 2021
)
1.61
"Atorvastatin and aspirin have been used in treating different forms of epilepsy. "( Effects of atorvastatin and aspirin on post-stroke epilepsy and usage of levetiracetam.
Ding, Y; Feng, X; Lin, W; Zhao, T; Zhou, C, 2020
)
2.39
"Atorvastatin has beneficial effects on vessel remodeling due to its lipid-lowering capacity. "( Atorvastatin pleiotropically decreases intraplaque angiogenesis and intraplaque haemorrhage by inhibiting ANGPT2 release and VE-Cadherin internalization.
Baganha, F; de Jong, RCM; de Vries, MR; Delibegovic, M; Jukema, JW; Peters, EA; Quax, PHA; Voorham, W, 2021
)
3.51
"Atorvastatin has no statistically significant effect on the prevention of CSDH recurrence after surgery."( The effect of atorvastatin on recurrence of chronic subdural hematoma after novel YL-1 puncture needle surgery.
Chen, P; He, S; Wang, C; Wang, D; Wang, H; Wen, J; Xu, M; Yu, B; Zeng, W; Zhang, H, 2021
)
1.7
"Atorvastatin has been reported to alleviate early brain injury (EBI) following subarachnoid hemorrhage (SAH) via reducing reactive oxygen species, antiapoptosis, regulated autophagy, and neuroinflammation."( Atorvastatin ameliorates early brain injury after subarachnoid hemorrhage via inhibition of pyroptosis and neuroinflammation.
Chen, J; Chen, Q; Li, M; Shi, Z; Wang, Y; Yan, T; Yang, L; Zhang, C, 2021
)
2.79
"Atorvastatin (ATV) has been shown to play a protective role on endothelial cells."( Hsa_circ_0004831 downregulation is partially responsible for atorvastatinalleviated human umbilical vein endothelial cell injuries induced by ox-LDL through targeting the miR-182-5p/CXCL12 axis.
Liu, H; Lv, J; Su, G; Su, H; Sun, G; Tang, Y; Zhang, W, 2021
)
1.58
"Atorvastatin treatment has been suggested as a therapeutic method for women with polycystic ovary syndrome (PCOS) in many clinical studies. "( Effects of atorvastatin on the insulin resistance in women of polycystic ovary syndrome: A systematic review and meta-analysis.
Chen, LL; Zheng, JH, 2021
)
2.45
"Atorvastatin has a pleiotropic effect as anti-inflammatory through one of the target levels of High Mobility Group Box-1 (HMGB-1)."( Analysis of HMGB-1 level before and after providing atorvastatin standard therapy in coronary artery disease patients with type-2 diabetes mellitus compared to without type-2 diabetes mellitus.
Handayani, W; Yogiarto, M, 2021
)
1.59
"Atorvastatin, which has proven safe in NAFLD/NASH, reduces SUA levels, ameliorates NAFLD/NASH, prevents liver fibrosis, and above all substantially reduces CVD morbidity and mortality in comparison with those on statins but without NAFLD/NASH."( Can Serum Uric Acid Lowering Therapy Contribute to the Prevention or Treatment of Nonalcoholic Fatty Liver Disease?
Athyros, VG; Giouleme, O; Grammatikos, N; Katsoula, A; Paschos, P; Tsimperidis, A, 2018
)
1.2
"Atorvastatin (ATO) has anti-inflammatory and antioxidant properties."( Preconditioning with atorvastatin against renal ischemia-reperfusion injury in nondiabetic versus diabetic rats.
Abdelfattah, S; Ahmad, Z; Hassan, SS; Motawie, A; Rizk, A; Thomann, C, 2019
)
1.55
"Atorvastatin has pleiotropic actions, including increasing nitric oxide (NO) bioavailability and reducing inflammation and oxidative damage."( Atorvastatin protects against deleterious cardiovascular consequences induced by chronic intermittent hypoxia.
Baldazza, M; Cachot, S; Faury, G; Fhayli, W; Joyeux-Faure, M; Korichneva, I; Lévy, P; Pépin, JL; Ribuot, C; Totoson, P, 2013
)
2.55
"Atorvastatin (ATV) has bone anabolic properties, and alendronate (ALD) is an important antiresorptive drug. "( Low-dose combination of alendronate and atorvastatin reduces ligature-induced alveolar bone loss in rats.
Alencar, NM; Benevides, NM; Goes, P; Lima, V; Melo, IM; Ribeiro, RA; Silva, LM, 2014
)
2.11
"Atorvastatin has been shown to be neuroprotective after transient ischaemia or traumatic injury."( Atorvastatin is beneficial for muscle reinnervation after complete sciatic nerve section in rats.
Beaumont, E; Beaumont, PH; Cloutier, FC; Hébert-Davies, J; Rouleau, DM, 2013
)
2.55
"Oral atorvastatin has prevented or reversed paralysis in the multiple sclerosis (MS) model experimental autoimmune encephalomyelitis (EAE), and reduced development of new MS lesions in clinical trials. "( Neither T-helper type 2 nor Foxp3+ regulatory T cells are necessary for therapeutic benefit of atorvastatin in treatment of central nervous system autoimmunity.
Dunn, SE; Prod'homme, T; Steinman, L; Weber, MS; Youssef, S; Zamvil, SS, 2014
)
1.13
"Atorvastatin has pleiotropic effects on restraining inflammation and promoting angiogenesis besides its cholesterol-lowering function."( Effects of atorvastatin on the inflammation regulation and elimination of subdural hematoma in rats.
Chen, J; Cui, W; Jiang, R; Li, T; Quan, W; Tian, Y; Wang, D; Wang, Y; Yu, H; Zhang, J; Zhou, L, 2014
)
1.51
"Atorvastatin (AT) has been alternatively used for managing diabetic complications in clinic. "( Renoprotective effect of atorvastatin on STZ-diabetic rats through attenuating kidney-associated dysmetabolism.
Deng, T; Li, H; Li, Y; Tian, L; Zhao, P; Zhou, S, 2014
)
2.15
"Atorvastatin has a limited advantage to formulate oral dosage forms."( Solid self microemulsification of Atorvastatin using hydrophilic carriers: a design.
Nanda Kishore, R; Rasheed, A; Sushma, M; Vadlamudi, HC; Vandana, KR; Yalavarthi, PR, 2015
)
2.14
"Atorvastatin has a protective effect on the myocardial injury in the myocardial ischemia and reperfusion rats. "( Effect of atorvastatin on serum oxidative stress and N-terminal brain natriuretic peptide expression in rats.
Luo, YQ; Xu, Y; Yang, Y, 2014
)
2.25
"Atorvastatin has been demonstrated to reduce the incidence of postoperative atrial fibrillation (POAF) in patients undergoing cardiac surgery, but its effect on isolated heart valve surgery is unknown."( Atorvastatin Reduces the Incidence of Postoperative Atrial Fibrillation in Statin-Naive Patients Undergoing Isolated Heart Valve Surgery: A Double-Blind, Placebo-Controlled Randomized Trial.
Dehghani, MR; Kasianzadeh, M; Rezaei, Y; Sepehrvand, N, 2015
)
3.3
"Atorvastatin has been suggested to exhibit anti-cancer effects."( Atorvastatin induces autophagic cell death in prostate cancer cells in vitro.
He, Z; Qi, P; Wang, Z; Yuan, J; Zhang, L, 2015
)
2.58
"Atorvastatin 20 mg has no clinically relevant effect on the pharmacokinetics of raltegravir and vice versa. "( Pharmacokinetic Drug-Drug Interaction Study Between Raltegravir and Atorvastatin 20 mg in Healthy Volunteers.
Blonk, M; Burger, D; Colbers, A; Schouwenberg, B; van Beek, M, 2015
)
2.1
"Atorvastatin has antioxidant activity and has been reported to increase blood antioxidant capacity. "( Paradoxical effects of atorvastatin on renal tubular cells: an experimental investigation.
Ahmadi, A; Baradaran, A; Hasanpour, Z; Nasri, H; Nasri, P; Nematbakhsh, M; Rafieian-Kopaei, M, 2015
)
2.17
"Atorvastatin has been reported to ameliorate ischemic brain damage after stroke, but the underlying mechanisms are not clear. "( Neuroprotective effects and dynamic expressions of MMP9 and TIMP1 associated with atorvastatin pretreatment in ischemia-reperfusion rats.
Dong, X; Fang, X; Ji, X; Shen, J; Tao, D; Wang, Y, 2015
)
2.09
"Atorvastatin has protective effects against myocardial ischemia-reperfusion injuries and ischemia-reperfusion arrhythmia. "( Atorvastatin protects myocardium against ischemia-reperfusion arrhythmia by increasing Connexin 43 expression: A rat model.
Bian, B; Nie, J; Teng, T; Wang, Q; Yu, X, 2015
)
3.3
"Atorvastatin has prevented or limited LDL oxidation and has showed constitutively beneficial effects in group 4."( Ameliorative effect of statin therapy on oxidative damage in heart tissue of hypercholesterolemic rabbits.
Sozer, V, 2015
)
1.14
"Atorvastatin has been reported to ameliorate ischemic brain damage after ischemia reperfusion (I/R)."( Atorvastatin attenuates cognitive deficits through Akt1/caspase-3 signaling pathway in ischemic stroke.
Li, X; Pan, Y; Wang, X; Yang, J, 2015
)
2.58
"Atorvastatin (ATV) has been reported to improve AD, however, it is unclear how the anti-inflammatory mechanism is linked with its protection against the impairment of spatial cognitive function in AD."( Atorvastatin in improvement of cognitive impairments caused by amyloid β in mice: involvement of inflammatory reaction.
Chen, L; Chen, T; Li, G; Wan, Q; Wang, C; Yin, J; Zhao, L; Zhi, W, 2016
)
2.6
"Atorvastatin 80 mg/day has significant benefits for the primary and secondary prevention of cardiovascular and cerebrovascular disease. "( Safety Profile of Atorvastatin 80 mg: A Meta-Analysis of 17 Randomized Controlled Trials in 21,910 Participants.
Cheng, G; Li, H; Li, R; Sun, S; Wang, C; Zhang, S; Zou, M, 2016
)
2.21
"Atorvastatin has preliminarily been proved to be safe and effective for chronic subdural hematomas in both conservative and surgical patients and can provide a drug treatment strategy for neurosurgeons."( Effects of Atorvastatin on Conservative and Surgical Treatments of Chronic Subdural Hematoma in Patients.
Chen, P; Shi, X; Wang, C; Xu, M; Yu, B; Zhu, X, 2016
)
2.27
"Atorvastatin has been shown to exert a neuroprotective action by counteracting glutamatergic toxicity. "( Atorvastatin and Fluoxetine Prevent Oxidative Stress and Mitochondrial Dysfunction Evoked by Glutamate Toxicity in Hippocampal Slices.
Binder, LB; Constantino, LC; Dal-Cim, T; Ludka, FK; Massari, C; Tasca, CI, 2017
)
3.34
"Atorvastatin (ATV) has shown pleiotropic effects on bone tissue, and osteoporosis can aggravate periodontitis. "( Effects of Atorvastatin on Periodontitis of Rats Subjected to Glucocorticoid-Induced Osteoporosis.
Alexandre, JT; Brito, GA; Chaves, HV; Freitas, R; Furlaneto, F; Goes, P; Linhares, EV; Lisboa, MR; Marques, M; Martins, C; Ribeiro, I; Sousa, LH; Val, D, 2016
)
2.27
"Atorvastatin has been shown to affect cognitive functions in rodents and humans. "( Atorvastatin enhances kainate-induced gamma oscillations in rat hippocampal slices.
Guo, FL; Li, C; Liu, Z; Lu, CB; Vreugdenhil, M; Wang, J; Wang, XF; Wang, Y; Zhao, J, 2016
)
3.32
"Atorvastatin (ATV) has been reported to attenuate cognitive deficits after stroke, but precise mechanism for neuroprotection remains unknown."( Atorvastatin Attenuates Ischemia/Reperfusion-Induced Hippocampal Neurons Injury Via Akt-nNOS-JNK Signaling Pathway.
Chen, G; Ge, X; Guo, L; Li, K; Luo, L; Shao, S; Xu, M; Zhang, F; Zhou, J; Zhu, Z, 2017
)
2.62
"Atorvastatin has favorable effects on biochemical markers of oxidative stress in SCI."( Effects of Atorvastatin on Experimental Spinal Cord Ischemia-Reperfusion Injury in Rabbits.
Aykol, S; Civi, S; Kardes, O; Omeroglu, S; Oyar, EO; Tufan, K, 2017
)
1.57
"Atorvastatin has become a cornerstone in the prevention and treatment of atherosclerosis."( Atorvastatin inhibits insulin synthesis by inhibiting the Ras/Raf/ERK/CREB pathway in INS-1 cells.
Chang, B; Chen, L; Hou, N; Li, Y; Shan, C; Sun, B; Sun, H; Wang, J; Xu, J; Yang, J; Zeng, X; Zhang, Y; Zheng, M, 2016
)
2.6
"Atorvastatin (Atv) has been shown to protect against atherosclerosis, cardiac fibrosis, ischemia/reperfusion injury, etc."( Attenuation of Low Ambient Temperature-Induced Myocardial Hypertrophy by Atorvastatin via Promoting Bcl-2 Expression.
Bi, C; Cao, X; Ding, F; Feng, D; Han, Z; Huang, Q; Liang, J; Liu, Y; Ma, W; Pan, Z; Yin, K; Zhang, L, 2017
)
1.41
"Atorvastatin has a beneficial effect on bone metabolism in patients with acute ischemic heart disease (mainly males) by incrementing bone mineral density in which vitamin D levels are required to be higher than 30 nmol/l for the drug to be effective."( Effect of atorvastatin on bone mineral density in patients with acute coronary syndrome.
Abad, L; Dueñas, A; García-Porrero, M; Pérez-Castrillón, JL; Pinacho, F; Sanz-Cantalapiedra, A; Vega, G,
)
1.98
"Atorvastatin has previously been shown to reduce the endogenous angiogenic response to chronic ischemia in a porcine model. "( Atorvastatin increases myocardial indices of oxidative stress in a porcine model of hypercholesterolemia and chronic ischemia.
Bianchi, C; Boodhwani, M; Clements, RT; Feng, J; Mieno, S; Ramlawi, B; Sellke, FW; Sodha, NR; Xu, SH,
)
3.02
"Atorvastatin has been widely investigated among the older subjects and has the greatest magnitude of favorable effects on clinical outcomes of CHD."( Atorvastatin and cardiovascular risk in the elderly--patient considerations.
Acharjee, S; Welty, FK, 2008
)
2.51
"Atorvastatin has cardioprotective effects in acute reperfusion injury. "( Evaluation cardioprotective effects of atorvastatin in rats by real time myocardial contrast echocardiography.
Buss, S; Filusch, A; Hansen, A; Hardt, S; Katus, HA; Kuecherer, HF, 2008
)
2.06
"Atorvastatin 20 mg has a dramatic effect on the lipid but moderate effect on CRP. "( Effect of atorvastatin on LDL & hs-CRP in a selected Thai population.
Benjanuwatra, T; Boonbaichaiyapruck, S; Buakhamsri, A; Cheepudomwit, S; Moleelerkpoom, W; Panjavenin, P; Sukanandachai, B; Suthichaiyakul, T, 2008
)
2.19
"Atorvastatin has previously been implicated in various cutaneous adverse events."( [Atorvastatin-induced drug reaction with eosinophilia and systemic symptoms (DRESS)].
Dubertret, L; Gressier, L; Pruvost-Balland, C; Viguier, M, 2009
)
1.98
"Atorvastatin has thus to be added to the list of medication potentially responsible for bile duct injury."( Severe acute cholestatic hepatitis with prolonged cholestasis and bile-duct injury following atorvastatin therapy: a case report.
Geubel, AP; Leclercq, I; Rahier, J; Rahier, JF,
)
1.07
"Atorvastatin therapy has substantially beneficial effects on oxidative protein and DNA damage in hypercholesterolemic rabbits."( Effects of atorvastatin therapy on protein oxidation and oxidative DNA damage in hypercholesterolemic rabbits.
Altug, T; Aydin, S; Sozer, V; Uzun, H, 2009
)
1.46
"Atorvastatin has been shown to reduce resistin expression in macrophages after pro-inflammatory stimulation. "( Mechanism of inhibitory effect of atorvastatin on resistin expression induced by tumor necrosis factor-alpha in macrophages.
Chua, SK; Kuan, P; Shyu, KG; Wang, BW, 2009
)
2.07
"Atorvastatin has been shown to have an inhibitory effect on cardiac fibroblasts in vitro."( Mechanism of the inhibitory effect of atorvastatin on endoglin expression induced by transforming growth factor-beta1 in cultured cardiac fibroblasts.
Chen, WJ; Hung, CR; Kuan, P; Shyu, KG; Wang, BW, 2010
)
1.35
"Atorvastatin has a beneficial effect on oxidative stress in rats fed with high-cholesterol diet. "( Effect of atorvastatin and ezetimibe treatment on serum lipid profile and oxidative state in rats fed with a high-cholesterol diet.
Ciralik, H; Gümüşalan, Y; Kilinc, M; Ozbag, D; Toru, H; Yasim, A, 2010
)
2.21
"Atorvastatin has been employed as standard agent."( Role of glucagon-like peptide- 1 in vascular endothelial dysfunction.
Bijjem, KV; Goyal, S; Kumar, S; Singh, M, 2010
)
1.08
"Atorvastatin has been associated with liver injury. "( Atorvastatin-induced acute elevation of hepatic enzymes and the absence of cross-toxicity of pravastatin.
Cheng, KA; Cheng, Z; Ding, L; Fang, F; Fang, Q; Liu, Y; Shi, GP, 2010
)
3.25
"Atorvastatin has dramatic antiatherosclerotic effects, part of which seems to be due to the antioxidant features of the parent drug and/or its metabolites, favoring inhibition of LDL oxidation."( Effect of atorvastatin therapy on oxidant-antioxidant status and atherosclerotic plaque formation.
Nart, D; Onat, T; Sezer, ED; Sozmen, EY, 2011
)
2.21
"Atorvastatin has anti-inflammatory and angioprotective effects in SS patients."( [Pleiotropic effects of statins in systemic sclerosis].
Alekperov, RT; Aleksandrova, EN; Anan'eva, LP; Korzeneva, EG; Novikov, AA, 2011
)
1.81
"Atorvastatin has a significant effect on lowering of PRA in sensitized hemodialysis patients waiting for kidney transplantation. "( Alteration of panel-reactive antibodies following treatment with either atorvastatin or low-dose mycophenolate mofetil in sensitized hemodialysis patients.
Aref, A; Ehsanpour, A; Ghorbani, A; Shahbazian, H, 2011
)
2.04
"Atorvastatin has a further sympatholytic effect in CKD patients, who are on chronic aliskiren, which is independent of blood pressure and heart rate."( Atorvastatin reduces sympathetic activity in patients with chronic kidney disease.
Blankestijn, PJ; Joles, JA; Oey, PL; Siddiqi, L, 2011
)
3.25
"Atorvastatin pretreatment has been reported to reduce myocardial damage in patients undergoing percutaneous coronary intervention (PCI). "( Effects of atorvastatin pretreatment on infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.
Ahn, KJ; Choi, JH; Choi, SH; Choi, YJ; Gwon, HC; Hahn, JY; Jo, SH; Kim, HJ; Lee, KH; Lee, S; Lee, SH; Song, YB, 2011
)
2.2
"Atorvastatin (AVA) has shown in vitro anti-malarial activity and has improved the activity of mefloquine (MQ) and quinine."( Atorvastatin treatment is effective when used in combination with mefloquine in an experimental cerebral malaria murine model.
Amalvict, R; Baret, E; Briolant, S; Dormoi, J; Mosnier, J; Pradines, B; Rogier, C; Savini, H; Soulard, R; Souraud, JB, 2012
)
2.54
"Atorvastatin 10 mg daily has no beneficial effect on the natural history of PAH or CTEPH over 6 months."( Atorvastatin in pulmonary arterial hypertension (APATH) study.
Cheng, XS; Gu, Q; He, JG; Liu, ZH; Ni, XH; Shan, GL; Wilkins, MR; Xiong, CM; Xue, F; Zeng, WJ; Zhao, L; Zhao, ZH, 2012
)
2.54
"Atorvastatin has neuroprotective effects, and there is some evidence that nitric oxide is involved in atorvastatin effects. "( Chronic administration of atorvastatin induced anti-convulsant effects in mice: the role of nitric oxide.
Dehpour, AR; Fakhrzad, A; Hassanipour, M; Hassanpour, S; Moezi, L; Shafaroodi, H, 2012
)
2.12
"Atorvastatin has shown to possess neuroprotective, antiexcitotoxic, and antiepileptic effects besides its cholesterol-lowering properties. "( Anticonvulsive effect of atorvastatin on pentylenetetrazole-induced seizures in mice: the role of nitric oxide pathway.
Emamzadeh-Fard, S; Moazzami, K; Shabani, M, 2013
)
2.14
"Atorvastatin has been shown to reduce efficiently the levels of atherogenic lipoproteins also in patients with renal failure, but pharmacokinetic data in haemodialysis patients are lacking."( Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients.
Dratwa, M; Lameire, NH; Lins, RL; Matthys, KE; Peeters, PC; Stolear, JC; Verpooten, GA, 2003
)
1.36
"Atorvastatin has been shown to have pleiotropic immunomodulatory effects involving both antigen presenting cells and T cell compartment."( [Effects of atorvastatin in multiple sclerosis].
Koh, CS, 2003
)
1.42
"Atorvastatin has protective effects against membrane lipid peroxidation at pharmacologic concentrations."( Hypothesis: atorvastatin has pleiotropic effects that translate into early clinical benefits on cardiovascular disease.
Hennekens, CH; Novela, C, 2004
)
1.42
"Atorvastatin has promoted more beneficial effects on TC and LDL-c, whereas estradiol was responsible for an increase in HDL-c. "( Progesterone abolishes estrogen and/or atorvastatin endothelium dependent vasodilatory effects.
Abdalla, DS; Aldrighi, JM; Bertolami, MC; Faludi, AA; Nakamura, Y; Pereira, IR; Ramires, JA; Saleh, MH; Silva, RA; Sousa, JE, 2004
)
2.04
"Atorvastatin has also been shown to significantly reduce CHD events."( Torcetrapib/atorvastatin combination therapy.
Bays, H; Davidson, M; McKenney, J, 2005
)
1.43
"Atorvastatin has an anti-inflammatory action benefiting the alleviation of secondary inflammatory damaged in acute cerebral infarction that is independent of lipid lowering."( [Effects of atorvastatin on plasma hypersensitive C-reactive protein and interleukin-6 in patients with acute cerebral infarction].
Hu, ZP; Jiang, B; Nie, S; Tan, LM; Wu, J; Xiao, ZJ; Zhao, SP; Zhou, HN, 2005
)
2.15
"Atorvastatin has been shown to reduce coronary events and revascularization procedures in patients with multiple risk factors for coronary heart disease. "( Comparative safety of atorvastatin 80 mg versus 10 mg derived from analysis of 49 completed trials in 14,236 patients.
Gibson, E; Luo, D; Newman, C; Szarek, M; Tsai, J, 2006
)
2.09
"Atorvastatin has been employed in the present study as standard agent to improve vascular endothelial dysfunction."( Involvement of Rho-kinase in experimental vascular endothelial dysfunction.
Shah, DI; Singh, M, 2006
)
1.06
"Atorvastatin has lipid-lowering and pleiotropic properties, including a protective effect on endothelial function."( Early effects on endothelial function of atorvastatin 40 mg twice daily and its withdrawal.
Borucki, K; Luley, C; Makarova, R; Schmidt-Lucke, C; Taneva, E; Westphal, S; Wiens, L, 2006
)
1.32
"Atorvastatin has a parallel effect on systemic and local inflammatory process in patients with coronary artery disease."( Relation between local temperature and C-reactive protein levels in patients with coronary artery disease: effects of atorvastatin treatment.
Boudoulas, H; Stefanadi, E; Stefanadis, C; Toutouzas, K; Tsiamis, E; Tsioufis, C; Vavuranakis, M, 2007
)
1.27
"Atorvastatin has been extensively studied in the primary and secondary prevention of cardiovascular events, and may have some clinical advantages over various other statins in these respects. "( Atorvastatin efficacy in the primary and secondary prevention of cardiovascular events.
Arca, M; Gaspardone, A, 2007
)
3.23
"Atorvastatin has also been shown to reduce levels of the inflammatory marker C-reactive protein; in comparative studies, this effect proved to be superior to that of simvastatin or pravastatin and equivalent to that of rosuvastatin."( Effects of atorvastatin on the different phases of atherogenesis.
Rubba, P, 2007
)
1.45
"Atorvastatin has been found to be effective for reducing nonfatal myocardial infarctions and fatal CHD in hypertensive patients with three or more additional risk factors."( Cumulative clinical trial data on atorvastatin for reducing cardiovascular events: the clinical impact of atorvastatin.
Bybee, KA; Lee, JH; O'Keefe, JH, 2008
)
1.35
"Atorvastatin has differential effects on SREBF1a and SCAP mRNA expression in PBMC that are associated with baseline transcription levels, triglycerides response to atorvastatin and SCAP A2386G polymorphism."( Atorvastatin effects on SREBF1a and SCAP gene expression in mononuclear cells and its relation with lowering-lipids response.
Arazi, SS; Bernik, M; Dorea, EL; Genvigir, FD; Hirata, MH; Hirata, RD; Willrich, MA, 2008
)
3.23
"Atorvastatin has little or no ability to increase high density lipoprotein (HDL)-cholesterol, and this may be a disadvantage in patients with metabolic syndrome or diabetes, where low HDL-cholesterol is a key feature."( Is atorvastatin superior to other statins? Analysis of the clinical trials with atorvastatin having cardiovascular endpoints.
Doggrell, SA, 2006
)
1.68
"Atorvastatin has become a popular addition to hospital formularies, even though formal pharmacoeconomic analyses are lacking."( Atorvastatin: a hydroxymethylglutaryl-coenzyme A reductase inhibitor.
Malinowski, JM, 1998
)
2.46
"Atorvastatin has greater cholesterol-lowering efficacy than simvastatin in HFH."( Treatment of heterozygous familial hypercholesterolemia: atorvastatin vs simvastatin.
Bo, M; Fabris, F; Fiandra, U; Mercadante, G; Nicolello, MT; Piliego, T, 2001
)
2
"Atorvastatin monotherapy has a better effect on LDL-C and apoprotein B than statin-fibrate combinations, but a lesser effect on HDL-C, TG and in the case of ciprofibrate combinations, fibrinogen."( Atorvastatin versus four statin-fibrate combinations in patients with familial combined hyperlipidaemia.
Athyros, VG; Athyrou, VV; Demitriadis, DS; Kontopoulos, AG; Papageorgiou, AA; Pehlivanidis, AN, 2002
)
2.48

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Atorvastatin can activate AMPK and the phosphorylation of AMPK results in eNOS activated, which provides a novel explanation for the multi-effect of statins on cardiovascular system. Atorvstatin may inhibit the proliferation of HL-60 cells and induce apoptosis by inhibiting PI3K/ATK/mTOR signaling pathway.

ExcerptReferenceRelevance
"Atorvastatin can inhibit PAH in rats by suppressing the Notch pathway."( Effect of atorvastatin on pulmonary hypertension rats through regulating notch signaling pathway.
Cao, GQ; Liu, H; Liu, JY; Tang, MM; Zhang, XQ; Zhu, YT, 2020
)
2.4
"Atorvastatin could inhibit the proliferation of HL-60 cells. "( [Effects of Atorvastatin on Proliferation and Apoptosis of Leukemia Cell Line HL-60 and Its Mechanism of Signal Pathway].
Chen, ZZ; Dai, J; Liu, T; Pang, YX; Wang, K; Wang, Q, 2017
)
2.28
"Atorvastatin may inhibit the proliferation of HL-60 cells and induce apoptosis by inhibiting the PI3K/ATK/mTOR signaling pathway."( [Effects of Atorvastatin on Proliferation and Apoptosis of Leukemia Cell Line HL-60 and Its Mechanism of Signal Pathway].
Chen, ZZ; Dai, J; Liu, T; Pang, YX; Wang, K; Wang, Q, 2017
)
2.28
"Atorvastatin was found to inhibit ALT and AST activities and to reduce FBG levels in rats with STZ-induced diabetes."( Protective effect of atorvastatin on oxidative stress in streptozotocin-induced diabetic rats independently their lipid-lowering effects.
Aktay, G; Gürsoy, ŞÖ; İlhan, N; Ünüvar, S; Uyumlu, U, 2019
)
1.55
"Atorvastatin inhibit MMP-9 expression of aging myocytes by PPARalpha signal channel."( [The effect of PPARalpha signal channel on atorvastatin inhibiting MMP-9 expression in aging myocytes].
Han, L; Li, MG; Ye, P, 2013
)
2.1
"Atorvastatin can suppress cardiomyocyte apoptosis after I/R injury in rats, which may be related to the down-regulated expression of Mfn2."( [Atorvastatin inhibits cardiomyocyte apoptosis via down-cegulation the expression mitofusin 2 after myocardial ischemia/reperfusion injury in rats].
Chen, L; Chen, M; Zhou, W, 2014
)
2.76
"Atorvastatin did not lower plasma total cholesterol levels or affect plaque progression at this dosage; however, vulnerable plaque numbers were significantly reduced in the atorvastatin-treated group compared to control."( Atorvastatin improves plaque stability in ApoE-knockout mice by regulating chemokines and chemokine receptors.
Cai, Z; He, B; Hu, L; Jin, S; Li, D; Nie, P; Shao, Q; Shen, J; Shen, L; Xiao, H; Yi, J; Yu, Y, 2014
)
2.57
"Atorvastatin can inhibit neointimal hyperplasia and promote SMCs apoptosis in neointimal layers, which may be mainly associated with down-regulation of survivin and Fas expression after CAI of rat."( Inhibition of neointimal hyperplasia in rats treated with atorvastatin after carotid artery injury may be mainly associated with down-regulation of survivin and Fas expression.
Fang, Z; Huang, D; Li, X; Liu, Q; Xu, Y; Zheng, C; Zhou, S, 2014
)
2.09
"Atorvastatin could inhibit neuronal apoptosis and alleviate the cerebral I/R injury."( Protection effect of atorvastatin in cerebral ischemia-reperfusion injury rats by blocking the mitochondrial permeability transition pore.
Deng, JG; Liu, J; Song, T; Tao, X, 2014
)
1.44
"Atorvastatin may primarily inhibit the nuclear translocation of pNFκB to prevent CCI-induced peripheral neuropathic pain."( Atorvastatin prevents neuroinflammation in chronic constriction injury rats through nuclear NFκB downregulation in the dorsal root ganglion and spinal cord.
Chen, JY; Chu, LW; Wu, BN; Wu, PC, 2015
)
2.58
"Atorvastatin can inhibit VEGI and vascular endothelial growth factor expression to protect rats from diabetic retinopathy."( Effect of atorvastatin on diabetic rat endothelial cells and retinal lesions.
Bi, MC; Shi, H; Song, E; Song, XJ; Xu, CL; Xue, WX, 2015
)
1.54
"Atorvastatin can enhance the existing effects of MSCs transplantation, and this combinational therapy is a superior cell/pharmacological therapeutic approach that merits future preclinical and clinical studies."( Atorvastatin treatment improves effects of implanted mesenchymal stem cells: meta-analysis of animal models with acute myocardial infarction.
Chen, H; Dai, G; Deng, Y; Gao, J; Li, Y; Luo, R; Wang, Y; Wu, X; Xu, Q; Yuan, W, 2015
)
3.3
"Atorvastatin may inhibit Hcy-induced ROS accumulation and endothelium cell apoptosis through an NADPH oxidase and/or p38MAPK-dependent mechanisms, all of which may contribute to atorvastatin-induced beneficial effect on endothelial function."( Atorvastatin attenuates homocysteine-induced apoptosis in human umbilical vein endothelial cells via inhibiting NADPH oxidase-related oxidative stress-triggered p38MAPK signaling.
Bao, XM; Lu, GP; Wu, CF, 2009
)
3.24
"Atorvastatin could inhibit tau hyperphosphorylation and decrease Abeta generation."( Inhibition of tau hyperphosphorylation and beta amyloid production in rat brain by oral administration of atorvastatin.
Li, X; Lu, F; Suo, AQ; Zhang, JW, 2010
)
1.3
"Atorvastatin can activate AMPK and the phosphorylation of AMPK results in eNOS activated, which provides a novel explanation for the multi-effect of statins on cardiovascular system."( Atorvastatin prevents mesenchymal stem cells from hypoxia and serum-free injury through activating AMP-activated protein kinase.
Dong, Q; Qian, H; Song, L; Xu, Z; Yang, Y, 2011
)
3.25
"Atorvastatin use may also increase Cp levels although this effect appears to be independent of its anti-oxidant effects."( Effects of statin use on total oxidant and antoxidant capacity and ceruloplasmin activity.
Aksoy, N; Bas, M; Buyukhatıpoglu, H; Celik, H; Demirbag, R; Guntekin, U; Polat, M; Sezen, Y; Taskin, A; Yildiz, A, 2010
)
1.08
"Atorvastatin was able to activate all of the elements."( Atorvastatin activates heme oxygenase-1 at the stress response elements.
Handal, J; Kwok, SC; Samuel, SP, 2012
)
2.54
"Atorvastatin treatment promotes functional restoration after PDT, but does not promote glioma growth in vitro and in vivo."( Atorvastatin reduces functional deficits caused by photodynamic therapy in rats.
Chopp, M; Ding, C; Jiang, F; Jiang, J; Lu, Y; Yang, H; Zhang, L; Zhao, D; Zheng, X, 2011
)
2.53
"Atorvastatin can inhibit the signal transduction of TLR4 and reduce proinflammatory cytokines release induced by CRP on CD14 monocyte, and this might be one of the anti-inflammatory mechanisms of atorvastatin."( [The effects of atorvastatin on C-reactive protein induced Toll-like receptor 4 expression on CD14+ monocyte].
Liu, JL; Luo, YT; Peng, L, 2011
)
1.44
"Atorvastatin inhibited the increase in the production of IL-1β, PGE(2) and MMP-3 in submandibular glands treated with anti-M(3) peptide IgG."( Atorvastatin inhibits the inflammatory response caused by anti-M(3) peptide IgG in patients with primary Sjögren's syndrome.
Borda, E; Passafaro, D; Reina, S; Sterin-Borda, L, 2012
)
2.54
"Atorvastatin did not cause a deterioration in insulin sensitivity."( Effects of 90-day hypolipidemic treatment on insulin resistance, adipokines and proinflammatory cytokines in patients with mixed hyperlipidemia and impaired fasting glucose.
Buldak, L; Dulawa-Buldak, A; Labuzek, K; Okopien, B, 2012
)
1.1
"Atorvastatin pretreatment inhibit cellular apoptosis induced by H₂O₂ (39.45%, 20.53% and 7.83%)."( [Atorvastatin inhibits the H₂O₂-induced apoptosis of human vascular endothelial cells through a down-regulation of cleaved caspase-9/caspase-3].
Li, SJ; Wu, WZ; Xu, ZR; Yang, YM; Yao, HP, 2012
)
2.01
"Atorvastatin could inhibit the TLR4 expression and TLR4-dependent downstream signaling in THP-1 cells. "( Atorvastatin decreases Toll-like receptor 4 expression and downstream signaling in human monocytic leukemia cells.
Fang, W; Li, R; Qu, X; Quan, Z; Yang, SS, 2012
)
3.26
"Atorvastatin can increase eNOS synthesis in the vital organs of aging rats, which partially explains the organ-protective effect of atorvastatin against myocardial ischemia- reperfusion."( [Effect of atorvastatin on eNOS synthesis in organs of aging rats with myocardial ischemia-reperfusion].
Wang, H; Ye, P; Zhang, J, 2012
)
2.21
"Atorvastatin can inhibit IL-6 secretion in adipocytes possibly through upregulating PPARgamma, which may help to explain the anti-inflammatory effects of statins use."( Atorvastatin reduces interleukin-6 plasma concentration and adipocyte secretion of hypercholesterolemic rabbits.
Zhang, DQ; Zhao, SP, 2003
)
3.2
"The atorvastatin-mediated increase in S-nitrosylation was associated with an enhanced enzymatic activity of thioredoxin (atorvastatin, 157+/-9% increase)."( Antioxidant effects of statins via S-nitrosylation and activation of thioredoxin in endothelial cells: a novel vasculoprotective function of statins.
Dimmeler, S; Haendeler, J; Hoffmann, J; Zeiher, AM, 2004
)
0.8
"Atorvastatin can inhibit leptin release and mRNA expression, and reduces serum leptin level in hypercholesterolemic rabbits."( Atorvastatin reduces serum leptin concentration in hypercholesterolemic rabbits.
Wu, ZH; Zhao, SP, 2005
)
3.21
"As atorvastatin can enhance protective Th2 responses and has a different mechanism of action than glatiramer acetate (GA), a parenterally administered immunomodulatory agent approved for MS treatment, we tested whether the combination of these agents could be beneficial in EAE."( Immunomodulatory synergy by combination of atorvastatin and glatiramer acetate in treatment of CNS autoimmunity.
Hemmer, B; Nessler, S; Prod'homme, T; Sobel, RA; Steinman, L; Stüve, O; von Büdingen, HC; Weber, MS; Youssef, S; Zamvil, SS, 2006
)
1.11
"Atorvastatin did not cause a redistribution of triglycerides but consistently lowered triglycerides in all lipoprotein fractions."( Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia.
Bakker-Arkema, RG; Black, DM; Brown, WV; Davidson, MH; Davignon, J; Goldstein, RJ; Isaacsohn, JL; Keilson, LM; Miller, VT; Shurzinske, LJ; Weiss, SR, 1996
)
1.26
"Atorvastatin may allow patients with combined hyperlipidemia to be treated with monotherapy and offers an efficacious and well-tolerated alternative to niacin for the treatment of patients with isolated hypertriglyceridemia."( A randomized trial of the effects of atorvastatin and niacin in patients with combined hyperlipidemia or isolated hypertriglyceridemia. Collaborative Atorvastatin Study Group.
Black, DM; Kafonek, S; Koren, M; McCormick, LS; McKenney, JM; Weiss, S, 1998
)
2.02

Treatment

Atorvastatin treatment did not affect the duration of status epilepticus or the development of epilepsy. Treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537±0.427pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ML to 15.13 ± 7.61 ng/ ML; P = 0.002) serum levels in diabetic patients.

ExcerptReferenceRelevance
"Atorvastatin treatment had the highest inverse-correlation with the UC gene signature among non-oncolytic FDA-approved therapies. "( Computational drug repositioning of atorvastatin for ulcerative colitis.
Bai, L; Habtezion, A; Kalesinskas, L; Khatri, P; Scott, MKD; Shah, NH; Steinberg, E, 2021
)
2.34
"Atorvastatin pretreatment exerted protective effect on CPB-associated kidney injury and inflammation in rats. "( Atorvastatin Exerts Protective Effect on Cardiopulmonary Bypass Induced Renal Injury in Rats via PPAR-γ.
Ge, J; Wei, C; Zhang, T, 2022
)
3.61
"Atorvastatin pretreatment prevented kidney damage following exposure to toxic doses of cadmium."( Atorvastatin prevents cadmium-induced renal toxicity in a rat model.
Bandegi, AR; Dehdashti, A; Ghanbari, A; Goodarzi, Z; Karami, E; Yosefi, S, 2023
)
3.07
"Atorvastatin treatment of HHcy in mice led to no changes in total cholesterol but decreases in total homocysteine in plasma. "( Atorvastatin rescues hyperhomocysteinemia-induced cognitive deficits and neuroinflammatory gene changes.
Bottiglieri, T; Fardo, DW; Johnson, SN; Qiao, Q; Rogers, CB; Sudduth, TL; Weekman, EM; Wilcock, DM; Xie, K, 2023
)
3.8
"In atorvastatin (ator)-treated high-fat diet-fed mice, we found reduced pancreatic β-cell size and β-cell mass, fewer mature insulin granules, and reduced insulin secretion and glucose tolerance."( Atorvastatin Targets the Islet Mevalonate Pathway to Dysregulate mTOR Signaling and Reduce β-Cell Functional Mass.
Cheng, T; Cui, C; Feng, B; Fu, C; Fu, L; Gu, Y; Li, T; Li, X; Ni, Q; Nie, A; Qiu, Y; Shen, L; Wang, Q; Wang, W; Wang, Y, 2020
)
2.51
"Atorvastatin treatment does not significantly affect circulating adiponectin. "( Effect of atorvastatin treatment on circulating adiponectin: a meta-analysis of randomized controlled trials.
Jia, G; Liu, X; Sun, R; Zhang, W; Zhao, M, 2019
)
2.36
"Atorvastatin treatment improved cognitive function in the mouse model, attenuated neuroinflammation, and increased PPARγ expression in the hippocampus."( Atorvastatin protects against postoperative neurocognitive disorder via a peroxisome proliferator-activated receptor-gamma signaling pathway in mice.
Lin, D; Liu, J; Ma, D; Wei, C; Wu, A; Xiong, C; Yang, Y, 2020
)
2.72
"Atorvastatin treatment provides significant benefits for dilated cardiomyopathy."( The Impact of Atorvastatin on Cardiac Performance for Dilated Cardiomyopathy: A Meta-analysis of Randomized Controlled Studies.
Fu, L; Shang, X; Zhang, X, 2020
)
2.36
"Atorvastatin treatment increased EPC VEGFA protein levels, proliferation, migration, and angiogenesis."( Atorvastatin improves the proliferation and migration of endothelial progenitor cells via the miR-221/VEGFA axis.
Sun, L; Wang, J; Xing, S; Zhang, J; Zhang, Y, 2020
)
2.72
"Atorvastatin treatment increased anti-oxidant enzyme levels (P<0.01)."( Atorvastatin Prevents the Neuron Loss in the Hippocampal Dentate Gyrus Region through its Anti-Oxidant and Anti-Apoptotic Activities.
Arani, HZ; Jangholi, E; Karimi, A; Movassaghi, S; Parsa, Y; Sharifi, ZN; Yadollah-Damavandi, S, 2021
)
2.79
"Atorvastatin treatment in I/R rats decreases oxidative stress, production of ROS, apoptosis rate in neuronal cells, and improves the mitochondrial function. "( Atorvastatin Prevents the Neuron Loss in the Hippocampal Dentate Gyrus Region through its Anti-Oxidant and Anti-Apoptotic Activities.
Arani, HZ; Jangholi, E; Karimi, A; Movassaghi, S; Parsa, Y; Sharifi, ZN; Yadollah-Damavandi, S, 2021
)
3.51
"Oral atorvastatin treatment in Göttingen Minipigs is associated with a reduced mitochondrial respiratory capacity in the liver that may be linked to increased content of atorvastatin in this organ."( Atorvastatin impairs liver mitochondrial function in obese Göttingen Minipigs but heart and skeletal muscle are not affected.
Christiansen, LB; Ciborowski, M; Desler, C; Dohlmann, TL; Kretowski, A; Larsen, S; Ludvigsen, TP; Martinussen, T; Olsen, LH; Orlando, P; Parfieniuk, E; Szczerbinski, L; Tiano, L, 2021
)
2.52
"Atorvastatin treatment reduced the presence of immature vessels by 34% vs."( Atorvastatin pleiotropically decreases intraplaque angiogenesis and intraplaque haemorrhage by inhibiting ANGPT2 release and VE-Cadherin internalization.
Baganha, F; de Jong, RCM; de Vries, MR; Delibegovic, M; Jukema, JW; Peters, EA; Quax, PHA; Voorham, W, 2021
)
2.79
"Atorvastatin treatment along with BaP in the embryonic period were able to bring the antioxidant status and sex hormones levels relatively close to normal."( Effect of prenatal exposure to Benzo[a]pyrene on ovarian toxicity and reproductive dysfunction: Protective effect of atorvastatin in the embryonic period.
Karimpour Malekshah, A; Rahmani, Z; Talebpour Amiri, F; Zargari, M, 2021
)
1.55
"Atorvastatin treatment has been suggested as a therapeutic method for women with polycystic ovary syndrome (PCOS) in many clinical studies. "( Effects of atorvastatin on the insulin resistance in women of polycystic ovary syndrome: A systematic review and meta-analysis.
Chen, LL; Zheng, JH, 2021
)
2.45
"Atorvastatin treatment resulted in enhanced graft take and wound closure of the full thickness wounds, faster resolution of neutrophils compared to all treatments and reduced alpha-smooth muscle actin positive cells compared to control treatment."( Differential effects of Losartan and Atorvastatin in partial and full thickness burn wounds.
Akershoek, JJ; Beelen, RHJ; Boekema, BKHL; Brouwer, KM; Middelkoop, E; Ulrich, MMW; Vlig, M, 2017
)
1.45
"Atorvastatin treatment may alleviate cerebral vasospasm and mediate structural and functional remodeling of vascular endothelial cells, in addition to promoting anti‑apoptotic signaling."( Protective effects of atorvastatin on cerebral vessel autoregulation in an experimental rabbit model of subarachnoid hemorrhage.
Chen, JH; Chen, L; Hu, X; Li, PP; Wang, YH; Wu, T; Yang, LK; Zhu, J, 2018
)
1.52
"Atorvastatin treatment and arsenic exposure alone are capable of generating apoptosis in pancreatic β-cells of Wistar rats with T2D. "( Apoptosis in pancreatic β-cells is induced by arsenic and atorvastatin in Wistar rats with diabetes mellitus type 2.
Cervantes-Flores, M; Delgado-León, TG; López-Guzmán, OD; Lozano-Guzmán, E; Martínez-Romero, A; Sálas-Pacheco, JM; Úrtiz-Estrada, N; Vazquez-Alaniz, F; Vértiz-Hernández, ÁA, 2018
)
2.17
"Atorvastatin treatment during epileptogenesis had slight beneficial effects on seizure susceptibility. "( Subtle improvement of seizure susceptibility by atorvastatin treatment during epileptogenesis.
Fighera, MR; Furian, AF; Oliveira, CV; Oliveira, MS; Royes, LFF; Zorzi, VN, 2018
)
2.18
"Atorvastatin treatment produces a relatively mild effect on sexual functioning and mood in women, affecting only selected elements of female sexual behaviour."( The effect of atorvastatin on sexual function and depressive symptoms in young women with elevated cholesterol levels - a pilot study.
Drosdzol-Cop, A; Krysiak, R; Okopień, B; Skrzypulec-Plinta, V, 2018
)
2.28
"Atorvastatin treatment works for patients with carotid plaque by reducing LDL-cholesterol and improving plaque regression. "( Evaluating the Efficacy of Atorvastatin on Patients with Carotid Plaque by an Innovative Ultrasonography.
Bai, QK; Deng, SH; Jiang, Q; Jiang, XZ; Zhang, Y; Zhang, ZP; Zhu, YC, 2019
)
2.25
"In atorvastatin-treated mice, total MK4 and percentage of deuterium-labeled MK4 in kidney were both approximately 45% lower compared to values in mice not given atorvastatin (all P < 0.05)."( Atorvastatin Decreases Renal Menaquinone-4 Formation in C57BL/6 Male Mice.
Booth, SL; Fu, X; Greenberg, A; Grusak, MA; Harshman, SG; Kuliopulos, A; Lamon-Fava, S; Shea, MK; Smith, D, 2019
)
2.47
"The atorvastatin treatments to mice with PF resulted in significant increases at the TGF-β activation, cell proliferation and kidney damage and decreases in the levels of p-SMAD2, p-ELK1, p-ATF2 and p-c-Jun, but not change the p-SMAD3, ELK1 and ATF2 in kidneys."( The effects of atorvastatin on the kidney injury in mice with pulmonary fibrosis.
Bolkent, S; Karatug Kacar, A; Oztay, F; Yildirim, M, 2019
)
1.35
"Atorvastatin treatment produced a significant decrease in MPV levels (9.3 ± 1.3 vs 9.1 ± 1.2 fL, P = .008) and platelet count (259 ± 61 vs 248 ± 51 10(9)/L, P = .005)."( Effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia.
Akin, F; Akin, MN; Ayça, B; Canbek, TD; Güngör, O; Köse, N; Sahin, I, 2013
)
1.51
"Atorvastatin pretreatment promoted increased cell viability after OGD and reoxygenation of hippocampal slices."( Atorvastatin prevents cell damage via modulation of oxidative stress, glutamate uptake and glutamine synthetase activity in hippocampal slices subjected to oxygen/glucose deprivation.
Bertoldo, DB; de Bem, AF; Herculano, BA; Mancini, G; Martins, WC; Tasca, CI; Vandresen-Filho, S, 2013
)
2.55
"Atorvastatin pretreatment restored part of the up or down regulations."( Altered microRNA expression in the ischemic-reperfusion spinal cord with atorvastatin therapy.
Hu, JR; Lv, GH; Yin, BL, 2013
)
1.34
"Atorvastatin treatment of HUVECs produced a time-dependent increase in GTP loading of all Rho GTPases, and induced the translocation of small Rho GTPases from the cellular membrane to the cytosol, which was reversed by 100 µM MVA and 10 µM GGPP, but not by 10 µM FPP."( Inhibition of Rho and Rac geranylgeranylation by atorvastatin is critical for preservation of endothelial junction integrity.
Ping, D; Qin, X; Xiao, H; Zuo, K, 2013
)
1.37
"Atorvastatin treatment significantly reduced the active form of RhoC in vitro and diminished cell motility, invasion, proliferation and colony formation. "( Atorvastatin inhibits RhoC function and limits head and neck cancer metastasis.
Islam, M; Kumar, B; Sharma, S; Teknos, TN, 2013
)
3.28
"Atorvastatin treatment was also associated with increased haemoglobin A1C levels from 7.45% to 7.77% (p = 0.008)."( Impaired endothelium-dependent skin microvascular function during high-dose atorvastatin treatment in patients with type 1 diabetes.
Adamson, U; Jörneskog, G; Lins, PE; Mobarrez, F; Tehrani, S; Wallén, HN, 2013
)
1.34
"Atorvastatin treatment appeared to facilitate to reduce all-cause mortality (lnRR = 0.61, p = 0.05) and rehospitalisation for heart failure (lnRR = 0.44, p = 0.04) compared with non-atorvastatin therapy."( Long-term clinical outcomes of statin use for chronic heart failure: a meta-analysis of 15 prospective studies.
Dai, XP; Li, XR; Wang, JQ; Wang, Z; Wu, GR, 2014
)
1.12
"Atorvastatin treatment increased cholesterol absorption by 52.3% in those with the lowest baseline campesterol levels, which attenuated the effect of LDL-C reduction."( Association between cholesterol synthesis/absorption markers and effects of cholesterol lowering by atorvastatin among patients with high risk of coronary heart disease.
Li, Y; Liu, J; Liu, X; Lv, Q; Ma, C; Qi, Y; Sun, J; Wang, M; Wang, W; Zhao, D, 2013
)
1.33
"Atorvastatin and HT treatments reduced the mRNA levels of APOA1 and SCARB1, respectively, whereas ABCA1 expression was reduced after all treatments. "( Atorvastatin and hormone therapy influence expression of ABCA1, APOA1 and SCARB1 in mononuclear cells from hypercholesterolemic postmenopausal women.
Bertolami, MC; Cavalli, SA; Cerda, A; Faludi, AA; Genvigir, FD; Hirata, MH; Hirata, RD; Issa, MH; Rohde, CB, 2013
)
3.28
"Atorvastatin treatment inhibited dose-dependently cell attachment to endothelium and differentiation."( Atorvastatin inhibited Rho-associated kinase 1 (ROCK1) and focal adhesion kinase (FAK) mediated adhesion and differentiation of CD133+CD44+ prostate cancer stem cells.
Chintala, M; Chintala, R; Guda, M; Komarraju, AL; Mangamoori, LN; Rentala, S, 2013
)
2.55
"Atorvastatin treatment significantly reduced serum total cholesterol levels while probucol treatment led to significant reduction of high-density lipoprotein cholesterol levels without changing total cholesterol levels compared with those in the control group. "( Probucol inhibits the initiation of atherosclerosis in cholesterol-fed rabbits.
Fan, J; Keyamura, Y; Kohashi, M; Koyama, T; Niimi, M; Nozako, M; Yasufuku, R; Yoshikawa, T, 2013
)
1.83
"Each atorvastatin-treated group demonstrated significant reductions in infarct and edema volumes compared with the vehicle-treated group 24h after reperfusion. "( Continuous oral administration of atorvastatin ameliorates brain damage after transient focal ischemia in rats.
Inaba, T; Kamiya, F; Katayama, Y; Katsura, K; Muraga, K; Nito, C; Saito, T; Ueda, M, 2014
)
1.2
"Atorvastatin treatment of fructose-fed rats increased vascular BH4 content, which was associated with an increase in endothelial NO synthase activity as well as a reduction in endothelial O2(-) production."( Effects of atorvastatin, amlodipine, and their combination on vascular dysfunction in insulin-resistant rats.
Geddawy, A; Imamura, T; Iwasaki, H; Masada, M; Okamura, T; Shimosato, T; Shinozaki, K; Shintaku, H; Tawa, M; Yoshida, Y, 2014
)
1.51
"Atorvastatin treatment failed to induce IL-4-producing Th2 cells in vivo; however, when T cells from atorvastatin-treated 4-GET mice were reactivated in vitro, T cells preferentially differentiated into Th2 cells, while antigen-specific T-cell proliferation and secretion of proinflammatory cytokines (interferon gamma, IL-17, tumor necrosis factor and IL-12) were reduced."( Neither T-helper type 2 nor Foxp3+ regulatory T cells are necessary for therapeutic benefit of atorvastatin in treatment of central nervous system autoimmunity.
Dunn, SE; Prod'homme, T; Steinman, L; Weber, MS; Youssef, S; Zamvil, SS, 2014
)
1.34
"Atorvastatin treatment resulted in behavioral deficits as measured in paradigms for basic exploration (open field activity) and cognitive function (Barnes maze, startle response) without impairment in global motor function (Rotor Rod)."( Long-term atorvastatin treatment leads to alterations in behavior, cognition, and hippocampal biochemistry.
Cui, W; Drummond, JC; Godoy, JC; Head, BP; Niesman, IR; Patel, HH; Patel, PM; Risbrough, VB; Roth, DM; Schilling, JM; Zemljic-Harpf, AE, 2014
)
1.53
"Atorvastatin treatment significantly increased VEGF-induced angiogenic responsiveness and the NO-releasing properties of cECs from all of the subgroups, compared with their respective non-treated subgroups except for the late-phase diabetic rat hearts that underwent ischemia-reperfusion, and the high dose of atorvastatin treatment groups."( Effect of atorvastatin on the angiogenic responsiveness of coronary endothelial cells in normal and streptozotocin (STZ) induced diabetic rats.
Chaudagar, KK; Mehta, AA, 2014
)
1.53
"Atorvastatin treatment did not change the plasma CTSS mRNA levels, although it lowered the plasma CTSS concentrations and activity. "( Interrelated cathepsin S-lowering and LDL subclass profile improvements induced by atorvastatin in the plasma of stable angina patients.
Cerne, D; Djeric, M; Jelic-Ivanovic, Z; Kos, J; Marc, J; Milivojac, T; Mirjanic-Azaric, B; Pecar Fonovic, U; Vekic, J; Zeljkovic, A, 2014
)
2.07
"Atorvastatin treatment may eliminate SDH and improve the neural function of the rats through its anti-inflammatory effects. "( Effects of atorvastatin on the inflammation regulation and elimination of subdural hematoma in rats.
Chen, J; Cui, W; Jiang, R; Li, T; Quan, W; Tian, Y; Wang, D; Wang, Y; Yu, H; Zhang, J; Zhou, L, 2014
)
2.23
"Atorvastatin treatment exhibited significant analgesic activity in hot plate model (P = 0.022). "( Atorvastatin exerts anti-nociceptive activity and decreases serum levels of high-sensitivity C-reactive protein and tumor necrosis factor-α in a rat endometriosis model.
Gul, M; Ozerol, E; Ozerol, IH; Parlakpinar, H; Simsek, Y; Yilmaz, E, 2014
)
3.29
"Atorvastatin treatment may have a therapeutic potential in the treatment of endometriosis through its anti-inflammatory and anti-nociceptive properties."( Atorvastatin exerts anti-nociceptive activity and decreases serum levels of high-sensitivity C-reactive protein and tumor necrosis factor-α in a rat endometriosis model.
Gul, M; Ozerol, E; Ozerol, IH; Parlakpinar, H; Simsek, Y; Yilmaz, E, 2014
)
3.29
"All atorvastatin-treated groups showed higher expression of IRS-1, PI3K, Akt, GSK-3, IL-10, eNOS, VEGF, and ERK on Day 7."( Effect of atorvastatin on wound healing in rats.
Araujo, EP; Azevedo, FF; Caricilli, AM; do Amaral, ME; Lima, MH; Saad, MJ; Suzuki-Banhesse, VF, 2015
)
1.3
"Atorvastatin treatment significantly decreased circulating low-density lipoprotein cholesterol (LDL-C) and total cholesterol concentrations by 42% and 24% (p<0.0001) respectively, and reached the efficacy objective of the protocol. "( Evaluation of atorvastatin efficacy and toxicity on spermatozoa, accessory glands and gonadal hormones of healthy men: a pilot prospective clinical trial.
Brugnon, F; Drevet, J; Gouby, G; Gremeau, AS; Grizard, G; Janny, L; Maqdasy, S; Marceau, G; Pereira, B; Pons-Rejraji, H; Sion, B; Tauveron, I, 2014
)
2.21
"Atorvastatin treatment significantly increased AMD (18%) at 3 wk in group B, compared with week 0."( Evaluation of statin therapy on endothelial function in hypercholesterolemic rabbits by automatic measurement of arterial wall movement using ultrasound images.
Mokhtari-Dizaji, M; Rahmani-Cherati, T; Rostami, A; Vajhi, A, 2014
)
1.12
"Atorvastatin treatment also decreased Fn14 expression in the atherosclerotic plaques of ApoE KO mice."( [Atorvastatin inhibits the atherosclerotic lesion induced by tumor necrosis factor-like weak inducer of apoptosis in apolipoprotein E deficient mice].
Blanco-Colio, LM; Egido, J; Fernández-Laso, V; Martín-Ventura, JL; Sastre, C,
)
1.76
"Atorvastatin treatment for 48 h after the infarction did not change GLUT4 expression, and after 7 days it had an additional negative effect on GLUT4 content (~ 39%, P = 0.030)."( Atorvastatin administered before myocardial infarction in rats improves contractility irrespective of metabolic changes.
Belló-Klein, A; Lehnen, AM; Lehnen, TE; Machado, UF; Markoski, MM; Schaan, B; Tavares, AM, 2014
)
2.57
"Atorvastatin treatment efficiently reduced serum cholesterol levels. "( Chemically induced mouse liver tumors are resistant to treatment with atorvastatin.
Braeuning, A; Bucher, P; Buchmann, A; Hofmann, U; Schwarz, M, 2014
)
2.08
"Atorvastatin treatment reduced spike frequencies and amplitudes significantly throughout the experiment."( HMG-CoA reductase inhibitor rosuvastatin improves abnormal brain electrical activity via mechanisms involving eNOS.
Caglayan, AB; Caglayan, B; Demirci, S; Dogan, A; Ekimci, N; Ethemoglu, MS; Kilic, E; Kilic, U; Oztezcan, S; Sahin, F; Seker, FB; Yilmaz, B, 2015
)
1.14
"Atorvastatin treatment reduced infarct size in B6 mice by 19% (p<0.05). "( Atorvastatin at reperfusion reduces myocardial infarct size in mice by activating eNOS in bone marrow-derived cells.
French, BA; Linden, J; Tian, Y; Yang, Z, 2014
)
3.29
"Atorvastatin treatment increased the expression levels of p85αPI3K, phosphorylated Akt, phosphorylated glycogen synthase kinase-3β, phosphorylated ERK, and Bcl-2, which are proteins related to survival."( Atorvastatin Protects NSC-34 Motor Neurons Against Oxidative Stress by Activating PI3K, ERK and Free Radical Scavenging.
Choi, H; Choi, NY; Huh, YM; Koh, SH; Lee, KY; Lee, SH; Lee, YJ; Park, J; Yu, HJ, 2016
)
2.6
"Atorvastatin treatment significantly reduced overall cardiovascular (p=0.046) and coronary events (p=0.004), and coronary revascularisation (p=0.007) in these patients."( High-dose atorvastatin is superior to moderate-dose simvastatin in preventing peripheral arterial disease.
Boekholdt, SM; Fayyad, R; Hovingh, GK; Laskey, R; Pedersen, TR; Stoekenbroek, RM; Tikkanen, MJ, 2015
)
1.54
"Atorvastatin treatment of PC3 cells for 24 h increased the expression of green fluorescent protein‑LC3‑II by >25%, and expression continued for >72 h, while apoptosis was not significantly induced within this time period."( Atorvastatin induces autophagic cell death in prostate cancer cells in vitro.
He, Z; Qi, P; Wang, Z; Yuan, J; Zhang, L, 2015
)
2.58
"Atorvastatin treatment (groups III and IV) significantly reduced the level of motor dysfunction."( Neuroprotective effect of atorvastatin in spinal cord ischemia-reperfusion injury.
Alpay, MF; Cakir, O; Colak, N; Nazli, Y; Uysal, S; Uzunlar, AK, 2015
)
1.44
"Atorvastatin treatment partially restored endothelial function by increasing NO level by 98%, reducing ONOO(-) by 40% and favorably elevating [NO]/[ONOO(-)] to 1.1 ± 0.2 for diabetic SHR rats and 1.6 ± 0.3 for SHR rats."( Atorvastatin enhanced nitric oxide release and reduced blood pressure, nitroxidative stress and rantes levels in hypertensive rats with diabetes.
Corbalan, JJ; Dawoud, H; Jacob, RF; Malinski, T; Mason, RP, 2015
)
2.58
"Atorvastatin treatment produced a significant 34% reduction in sputum neutrophil count, and a 57% reduction in CD45+ cells in lung biopsies (expressed as integrated optical density -IOD; median IOD 62.51% before, 27.01% after atorvastatin treatment, P=0.008)."( Anti-inflammatory effects of atorvastatin treatment in chronic obstructive pulmonary disease. A controlled pilot study.
Bierla, J; Boros, P; Chyczewska, E; Duszewska, AM; Lisowska, A; Lisowski, P; MacNee, W; Milewski, R; Minarowski, L; Mroz, RM; Musial, WJ; Sobkowicz, B; Trzeciak, PZ; Tycinska, A, 2015
)
1.43
"Atorvastatin treatment increased the percentage and inhibitory ability of nTregs, decreased serum IFN-γ and hsCRP levels, and decreased IL-10 and TGF-β1 levels, as compared with the non-atorvastatin group.Our findings suggest that nTregs play an atheroprotective role in atherosclerosis."( Changes of naturally occurring CD4(+)CD25(+) FOXP3(+) regulatory T cells in patients with acute coronary syndrome and the beneficial effects of atorvastatin treatment.
Ding, Y; Feng, GK; Jiang, XJ; Li, XY; Wang, CQ; Wang, ZX, 2015
)
1.34
"Atorvastatin pretreatment conferred 70-90% hepatic protection in all animals."( Acute atorvastatin is hepatoprotective against ischaemia-reperfusion injury in mice by modulating eNOS and microparticle formation.
Ajamieh, H; Chu, E; Farrell, GC; Lam, W; McCuskey, RS; Teoh, NC; Wong, HJ; Yu, J, 2015
)
1.62
"Atorvastatin treatment prevented dyslipidemia, reversed hepatic steatosis, optimized composition of bone, and improved bone mechanical properties."( The effects of atorvastatin on the prevention of osteoporosis and dyslipidemia in the high-fat-fed ovariectomized rats.
Cui, L; Fu, Z; Huang, J; Lee, WY; Li, G; Liang, Y; Lin, S; Qin, L; Sun, Y; Wu, H; Wu, T; Xu, L, 2015
)
1.49
"Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs."( Atorvastatin calcium inhibits phenotypic modulation of PDGF-BB-induced VSMCs via down-regulation the Akt signaling pathway.
Chen, S; Kong, D; Li, C; Li, S; Liu, B; Sun, Y; Wang, H, 2015
)
2.58
"Atorvastatin pretreatment also prevented AβO-induced decreases in Akt and Erk1/2 kinase activity and the increases in GSK3β and Cdk5 kinase activity."( Atorvastatin prevents Aβ oligomer-induced neurotoxicity in cultured rat hippocampal neurons by inhibiting Tau cleavage.
Jin, Y; Liu, Z; Sui, HJ; Zhang, LL, 2015
)
2.58
"Atorvastatin treatment increased total bilirubin concentration (median 6.95 μmol/L vs. "( Atorvastatin treatment increases plasma bilirubin but not HMOX1 expression in stable angina patients.
Cerne, D; Hallstroem, S; Jürgens, G; Marc, J; Mirjanic-Azaric, B; Rizzo, M; Srdic, S, 2015
)
3.3
"Atorvastatin treatment could significantly suppress the increase of both IL-37 and Smad3."( Increased IL-37 in Atherosclerotic Disease could be Suppressed by Atorvastatin Therapy.
Hongcheng, F; Ming, D; Shaoyuan, C; Yulang, H, 2015
)
1.38
"Atorvastatin treatment did not affect lesion inflammation (aortic arch mRNA levels of CXCL 1, ICAM-1, MCP-1, TNF-α, VCAM, IL-6, and IL-1β) or cellular composition (smooth muscle cell, macrophage, and T-cell content)."( Imaging of Intracellular and Extracellular ROS Levels in Atherosclerotic Mouse Aortas Ex Vivo: Effects of Lipid Lowering by Diet or Atorvastatin.
Adiels, M; Borén, J; Ekstrand, M; Fogelstrand, P; Gustafsson Trajkovska, M; Johansson, M; Levin, M; Mattsson-Hultén, L; Perman-Sundelin, J, 2015
)
1.34
"Atorvastatin treatment improved cardiac function of rats with isoproterenol-induced chronic heart failure and decreased the Rac1, p47phox and p67phox mRNA expressions."( Atorvastatin improves cardiac function of rats with chronic cardiac failure via inhibiting Rac1/P47phox/P67phox-mediated ROS release.
An, LP; An, SK; Fu, SY; Wei, XH; Wu, HA, 2015
)
2.58
"Atorvastatin pretreatment provides protection against oxidative stress in a rat kidney model of ischemia-reperfusion injury, reinforcing the evidence of a beneficial effect of statins beyond their cholesterol-lowering properties."( N-Acetylcysteine and High-Dose Atorvastatin Reduce Oxidative Stress in an Ischemia-Reperfusion Model in the Rat Kidney.
Caristo, ME; Ciavarella, LP; Citterio, F; Copponi, G; Crea, F; Cusumano, G; Giubilato, S; Liuzzo, G; Manchi, M; Romagnoli, J; Severino, A; Stigliano, E; Zannoni, GF, 2015
)
2.15
"Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg."( Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes.
Aggarwal, S; Aslam, M; Galav, V; Madhu, SV; Sharma, KK, 2016
)
1.16
"Atorvastatin treatment also reduced the intensity of Oil Red O staining in pigs on high-fat diet."( A Translational Model for Diet-related Atherosclerosis: Effect of Statins on Hypercholesterolemia and Atherosclerosis in a Minipig.
Amuzie, C; Denham, S; Mais, DE; Rogers, CS; Swart, JR; Vihtelic, T, 2016
)
1.16
"Atorvastatin pre-treatment dose-dependently decreased hs-CRP and resistin levels but increased adiponectin levels in mice."( Inflammation Activation Contributes to Adipokine Imbalance in Patients with Acute Coronary Syndrome.
Chen, LZ; Huang, XS; Li, R; Zhao, SP, 2016
)
1.16
"Atorvastatin-treated group (n=50) received interferon β-1a similar to control group in addition to atorvastatin (40 mg/day) for 18-months."( Interferon β-1a and Atorvastatin in the Treatment of Multiple Sclerosis.
Faraji, F; Fazeli, M; Ghasami, K; Ghazavi, A; Mosayebi, G, 2016
)
1.48
"Atorvastatin or fluoxetine treatment was effective in protecting mice hippocampal slices from glutamate toxicity by preventing the oxidative stress and mitochondrial dysfunction."( Atorvastatin and Fluoxetine Prevent Oxidative Stress and Mitochondrial Dysfunction Evoked by Glutamate Toxicity in Hippocampal Slices.
Binder, LB; Constantino, LC; Dal-Cim, T; Ludka, FK; Massari, C; Tasca, CI, 2017
)
2.62
"Atorvastatin (10 mg/kg) treatment for 7 days prevented the QA-induced decrease in glutamate uptake, but had no effect on increased glutamate release induced by QA."( Atorvastatin Prevents Glutamate Uptake Reduction Induced by Quinolinic Acid Via MAPKs Signaling.
Bertoldo, DB; Leal, RB; Maestri, M; Martins, WC; Rieger, DK; Tasca, CI; Vandresen-Filho, S, 2016
)
2.6
"An atorvastatin treatment (2.5 mg/kg/day) was tested against controls on 34 male 3 to 12 month-old WHHL rabbits. "( A non-hypocholesterolemic atorvastatin treatment improves vessel elasticity by acting on elastin composition in WHHL rabbits.
Aubry, T; Bourgeois, N; Desfontis, JC; Didier, R; Dubreuil, M; Gilard, M; Goanvec, C; Le Grand, Y; Mallem, Y; Mansourati, J; Pichavant-Rafini, K; Plee-Gautier, E; Roquefort, P; Theron, M; Tissier, F, 2016
)
1.36
"Atorvastatin treatment resulted in a rise in both CK (2X) and myoglobin (6X) level with graded degrees of muscle necrosis."( Elucidation of the mechanism of atorvastatin-induced myopathy in a rat model.
Abdallah, D; El-Ganainy, SO; El-Khatib, AS; El-Mallah, A; Khattab, MM; Mohy El-Din, MM, 2016
)
1.44
"Atorvastatin treatment did not affect glycemia levels. "( Treatment with high dose of atorvastatin reduces vascular injury in diabetic rats.
Botelho, T; de Batista, PR; Padilha, AS; Ribeiro-Júnior, RF; Simões, FV; Vassallo, DV, 2016
)
2.17
"Atorvastatin treatment increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in casein injection mice."( Inflammatory Stress Sensitizes the Liver to Atorvastatin-Induced Injury in ApoE-/- Mice.
Chen, Y; Li, B; Moorhead, JF; Ruan, XZ; Varghese, Z; Wu, W; Yang, P; Zhao, L; Zhou, W, 2016
)
1.42
"Atorvastatin treatment strongly inhibited proliferation in estrogen receptor (ER) negative cell lines and a commensurate response was also evident on the genome-wide transcriptional scale, with ER negative cells displaying a robust deregulation of genes involved in the regulation of cell cycle progression and apoptosis."( High expression of cholesterol biosynthesis genes is associated with resistance to statin treatment and inferior survival in breast cancer.
Borgquist, S; Bosch, A; Feldt, M; Kimbung, S; Lettiero, B, 2016
)
1.16
"Atorvastatin treatment in vitro quantitatively and functionally improved BM EPCs derived from subjects with PGF through downregulation of the p38 MAPK pathway."( Atorvastatin enhances endothelial cell function in posttransplant poor graft function.
Huang, XJ; Kong, Y; Liu, KY; Shi, MM; Song, Y; Sun, YQ; Wang, Y; Xu, LP; Zhang, XH, 2016
)
2.6
"Atorvastatin treatment increased flap survival rate and capillary density. "( The Effect of Atorvastatin on the Viability of Ischemic Skin Flaps in Diabetic Rats.
Chai, YM; Chen, HH; Jia, YC; Kang, QL; Xu, J, 2017
)
2.26
"Atorvastatin treatment increases vitamin D (33%, p = 0.007) and decreases the individuals with vitamin D insufficiency. "( Effect of atorvastatin on bone mineral density in patients with acute coronary syndrome.
Abad, L; Dueñas, A; García-Porrero, M; Pérez-Castrillón, JL; Pinacho, F; Sanz-Cantalapiedra, A; Vega, G,
)
1.98
"Atorvastatin treatment was associated with elevated levels of myocardial protein oxidation and lipid peroxidation. "( Atorvastatin increases myocardial indices of oxidative stress in a porcine model of hypercholesterolemia and chronic ischemia.
Bianchi, C; Boodhwani, M; Clements, RT; Feng, J; Mieno, S; Ramlawi, B; Sellke, FW; Sodha, NR; Xu, SH,
)
3.02
"Atorvastatin treatment modified the expression of 86 genes."( Monocyte gene-expression profile in men with familial combined hyperlipidemia and its modification by atorvastatin treatment.
Alegret, M; Cofán, M; Laguna, JC; Llaverias, G; Pou, J; Ros, E; Sánchez, A; Sánchez, RM; Vázquez-Carrera, M; Zambón, D, 2008
)
1.28
"Atorvastatin treatment of human PBMC before MLR reduced their response to stimulated WT (P<0.05) and GTKO (P<0.05) pAEC."( Atorvastatin down-regulates the primate cellular response to porcine aortic endothelial cells in vitro.
Ayares, D; Cooper, DK; Ezzelarab, M; Hara, H; Long, C; Torres, C; Welchons, D; Yeh, P, 2008
)
2.51
"Atorvastatin treatment increased the superoxide dismutase level and inhibited the degree of renal tubular cell N-acetyl glucosaminidase compared with stone forming control group 3."( Atorvastatin inhibits renal crystal retention in a rat stone forming model.
Momohara, C; Nonomura, N; Okuyama, A; Tsujihata, M; Tsujimura, A; Yoshioka, I, 2008
)
2.51
"Atorvastatin treatment was equally effective in patients with ischemic and nonischemic HF."( Atorvastatin therapy is associated with reduced levels of N-terminal prohormone brain natriuretic peptide and improved cardiac function in patients with heart failure.
Assmann, G; Breithardt, G; Nofer, JR; Schubert, A; Schulte, H; Stypmann, J; Welp, H, 2008
)
2.51
"Atorvastatin treatment is associated with improved cardiac function in HF, and may represent an additional option for patients with this disease."( Atorvastatin therapy is associated with reduced levels of N-terminal prohormone brain natriuretic peptide and improved cardiac function in patients with heart failure.
Assmann, G; Breithardt, G; Nofer, JR; Schubert, A; Schulte, H; Stypmann, J; Welp, H, 2008
)
3.23
"Atorvastatin treatment, alone and in combination with pioglitazone, revealed a significant regression in IMT (0.923+/-0.013 to 0.874+/-0.012 mm and 0.921+/-0.015 to 0.882+/-0.015 mm; mean +/- SEM; p<0.05 respectively) and Aix@75 (27.3+/-1.2 to 25.9+/-1.4; and 25.6+/-1.4 to 24.8+/-1.7%; p<0.05)."( Investigation of the vascular and pleiotropic effects of atorvastatin and pioglitazone in a population at high cardiovascular risk.
Forst, T; Fuchs, W; Hanefeld, M; Konrad, T; Lehmann, U; Müller, J; Pfützner, A; Schaper, F; Weber, M; Wilhelm, B, 2008
)
1.31
"Atorvastatin treatment was similarly effective regardless of baseline lipoprotein levels."( Baseline blood pressure, low- and high-density lipoproteins, and triglycerides and the risk of vascular events in the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial.
Amarenco, P; Callahan, A; Goldstein, LB; Hennerici, MG; O'Neill, BJ; Rudolph, AE; Sillesen, H; Simunovic, L; Welch, KM; Zivin, JA, 2009
)
1.07
"Only atorvastatin treatment did not show any histological atheroprotective effect."( Anti-atherosclerotic effect of atorvastatin and clopidogrel alone and in combination in rats.
Annapurna, A; Reddy, YN; Srinivas, M, 2008
)
1.09
"Atorvastatin treatment prevented fructose-induced ChREBP translocation and the increase in ChREBP DNA-binding activity while reducing SREBP-1c DNA-binding activity."( Atorvastatin prevents carbohydrate response element binding protein activation in the fructose-fed rat by activating protein kinase A.
Barroso, E; Coll, T; Laguna, JC; Merlos, M; Palomer, X; Rodríguez-Calvo, R; Sánchez, RM; Serrano, L; Vázquez-Carrera, M, 2009
)
2.52
"Atorvastatin treatment of NaCl-infused rats had only marginal effects."( Treatment with atorvastatin partially protects the rat heart from harmful catecholamine effects.
Ehmke, H; El-Armouche, A; Eschenhagen, T; Grimm, M; Höppner, G; Schmechel, A; Schwoerer, AP, 2009
)
1.43
"Atorvastatin treatment had no effect on plasma adiponectin levels."( Role of plasma adiponectin on the HDL-cholesterol raising effect of atorvastatin in patients with type 2 diabetes.
Dallinga-Thie, GM; Jansen, H; Kastelein, JJ; Sijbrands, EJ; van Hoek, M; van Tol, A; van Vark-van der Zee, LC, 2009
)
1.31
"Atorvastatin treatment at different doses, particularly 80 mg, significantly reduced hsCRP serum concentrations. "( Effect of atorvastatin on circulating hsCRP concentrations: a sub-study of the achieve cholesterol targets fast with atorvastatin stratified titration (ACTFAST) study.
Blanco-Colio, LM; de Teresa, E; Dilaghi, B; Egido, J; Farsang, C; Gaw, A; Gensini, GF; Gori, AM; Langer, A; Leiter, LA; Martineau, P; Nozza, A; Rostagno, C, 2010
)
2.21
"Atorvastatin treatment was generally well tolerated."( Effect of very low LDL-cholesterol on cortisol synthesis.
Akbay, E; Corapcioglu, D; Emral, R; Gen, R; Sezer, K, 2008
)
1.07
"Atorvastatin treatment prevented ischemia-reperfusion-induced up-regulation of both TNF-alpha and IL-10 mRNA, and improved left ventricular function (P<0.01)."( Effect of atorvastatin on expression of IL-10 and TNF-alpha mRNA in myocardial ischemia-reperfusion injury in rats.
Li, J; Li, X; Li, ZQ; Liu, YY; Pan, W; Sun, YM; Tian, Y; Wang, LF, 2009
)
1.48
"In atorvastatin-treated SHRs, relaxation to acetylcholine was normalized, fully sensitive to N(G)-nitro-L-arginine methyl ester, and not affected by SC-560, DuP-697, SQ 29548, or antioxidants."( Atorvastatin prevents endothelial dysfunction in mesenteric arteries from spontaneously hypertensive rats: role of cyclooxygenase 2-derived contracting prostanoids.
Antonioli, L; Blandizzi, C; Colucci, R; Daghini, E; Del Tacca, M; Duranti, E; Fornai, M; Ghisu, N; Giannarelli, C; Taddei, S; Versari, D; Virdis, A, 2009
)
2.31
"Atorvastatin treatment acutely reduces JNK expression and dendritic cells, resulting in reduced inflammatory cell content and expression of MMPs in the AAA wall."( Short-term 20-mg atorvastatin therapy reduces key inflammatory factors including c-Jun N-terminal kinase and dendritic cells and matrix metalloproteinase expression in human abdominal aortic aneurysmal wall.
Amano, A; Daida, H; Kajimoto, K; Kasai, T; Kojima, Y; Miyauchi, K; Niinami, H; Shimada, A; Shimada, K, 2009
)
2.14
"Atorvastatin-treated groups had significantly lower bleeding rates (p = 0.0011) and infarct volume (p = 0.0007) compared with controls."( Early atorvastatin reduces hemorrhage after acute cerebral ischemia in diabetic rats.
El-Remessy, AB; Elewa, HF; Ergul, A; Fagan, SC; Frye, RF; Johnson, MH; Kozak, A, 2009
)
1.56
"Atorvastatin treatment with 1 mg/kg/day did not significantly prevent QA-induced seizures (13.34%)."( Atorvastatin prevents hippocampal cell death due to quinolinic acid-induced seizures in mice by increasing Akt phosphorylation and glutamate uptake.
Boeck, CR; Carqueja, CL; Dal'agnolo, D; de Araújo Herculano, B; Martins, WC; Piermartiri, TC; Stroeh, E; Tasca, CI; Vandresen-Filho, S, 2009
)
2.52
"Atorvastatin treatment was associated with a modest improvement in annual change in eGFR (net, 0.18 mL/min/1.73 m(2)/y; 95% confidence interval [CI], 0.04 to 0.32; P = 0.01) that was most apparent in those with albuminuria (net improvement, 0.38 mL/min/1.73 m(2)/y; P = 0.03)."( Effects of atorvastatin on kidney outcomes and cardiovascular disease in patients with diabetes: an analysis from the Collaborative Atorvastatin Diabetes Study (CARDS).
Betteridge, DJ; Charlton-Menys, V; Colhoun, HM; DeMicco, DA; Durrington, PN; Fuller, JH; Hitman, GA; Livingstone, SJ; Neil, HA, 2009
)
1.46
"Atorvastatin treatment is associated with less augmentation of the carotid BP waveform and less wave reflection from the body."( Atorvastatin treatment is associated with less augmentation of the carotid pressure waveform in hypertension: a substudy of the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT).
Hughes, AD; Manisty, C; Mayet, J; McG Thom, SA; Poulter, N; Sever, PS; Tapp, RJ, 2009
)
2.52
"Atorvastatin treatment lowered cholesterol, triglyceride, insulin, TNF-alpha, and IL-6 plasma levels, and restored whole-body insulin sensitivity."( Anti-inflammatory effect of atorvastatin ameliorates insulin resistance in monosodium glutamate-treated obese mice.
Favaro, RR; Furuya, DT; Machado, UF; Martins, JO; Poletto, AC; Zorn, TM, 2010
)
1.38
"Atorvastatin treatment decreased cholesterol concentrations in all LDL subfractions (P<0.001 for each dose)."( Atorvastatin treatment lowers fasting remnant-like particle cholesterol and LDL subfraction cholesterol without affecting LDL size in type 2 diabetes mellitus: Relevance for non-HDL cholesterol and apolipoprotein B guideline targets.
Dallinga-Thie, GM; Dullaart, RP; Kappelle, PJ, 2010
)
2.52
"Atorvastatin treatment resulted in significant decrease in sponge vascularization (Hb content) and in VEGF levels at both doses."( Atorvastatin inhibits inflammatory angiogenesis in mice through down regulation of VEGF, TNF-alpha and TGF-beta1.
Andrade, SP; Araújo, FA; Mendes, JB; Rocha, MA, 2010
)
2.52
"Atorvastatin treatment significantly reduced the levels of total cholesterol (24.5%), low density lipoprotein (LDL) cholesterol (25.4%), triglycerides (24.4%), CD (4.4%), MDA (15.2%), TP (13.0%) and OSI (24.0%), and significantly increased the levels of TAS (27.3%), and PON1 activity (14.0%)."( Effect of atorvastatin on paraoxonase1 (PON1) and oxidative status.
Chinwattana, K; Deakin, S; Nagila, A; Permpongpaiboon, T; Porapakkham, P; Porntadavity, S; Tantrarongroj, S,
)
1.26
"Atorvastatin treated groups showed smaller size of lipid deposits and a lower level of inflammation than non-treated groups."( Effect of atorvastatin and diet on non-alcoholic fatty liver disease activity score in hyperlipidemic chickens.
Adánez, G; Ayala, I; Castells, MT; Martín-Castillo, A; Pérez, BG; Polo, MT, 2010
)
1.48
"Atorvastatin treatment significantly decreases the concentration of IL-6, and NT-proBNP in patients with DCM after 2 months of therapy. "( The influence of atorvastatin on parameters of inflammation and function of the left ventricle in patients with dilated cardiomyopathy.
Banach, M; Bielecka-Dabrowa, A; Goch, JH; Maciejewski, M; Mikhailidis, DP; Rysz, J, 2009
)
2.14
"Atorvastatin-treated yeast cells display marked morphological deformities, have reduced cell viability and are highly vulnerable to perturbed mitochondrial function."( Atorvastatin-induced cell toxicity in yeast is linked to disruption of protein isoprenylation.
Andrews, S; Callegari, S; de Barros Lopes, MA; McKinnon, RA, 2010
)
2.52
"Atorvastatin treatment decreased expression of IL-6, TNF-alpha, nuclear factor kappaB (NF-kappaB) and I-kappa-B (IkappaB) kinase-beta, but increased the expression of IkappaB, in adipose tissue."( Atorvastatin improves insulin sensitivity in mice with obesity induced by monosodium glutamate.
Huan, Y; Huang, H; Shen, ZF; Song, GM; Sun, SJ; Zhang, N, 2010
)
2.52
"Atorvastatin treatment of PC3 cells for 40 hrs increased expression of LC3-II by more than 10 fold in a dose-dependent manner. "( Statin-induced autophagy by inhibition of geranylgeranyl biosynthesis in prostate cancer PC3 cells.
Childress, C; Deitrick, K; Lin, Q; Parikh, A; Rukstalis, D; Yang, W, 2010
)
1.8
"Atorvastatin treatment led to a significantly lower expression of CD40L, CD11b and CD54 on monocytes (p<0.05) and neutrophils (p<0.05). "( Effect of atorvastatin on cellular adhesion molecules on leukocytes in patients with normocholesterolemic coronary artery disease.
Borggrefe, M; Dempfle, CE; Hoffmeister, HM; Suselbeck, T; Swoboda, S; Walter, T,
)
1.98
"Atorvastatin treatment lowered plasma triglyceride but not cholesterol levels. "( Atorvastatin protects renal function in the rat with acute unilateral ureteral obstruction.
Chou, SY; Gulmi, FA; Kamdar, C; Kim, H; Mooppan, UM, 2010
)
3.25
"Atorvastatin treatment affords protection of renal function in acute UUO and reduces urinary microalbumin levels without lowering cholesterol levels. "( Atorvastatin protects renal function in the rat with acute unilateral ureteral obstruction.
Chou, SY; Gulmi, FA; Kamdar, C; Kim, H; Mooppan, UM, 2010
)
3.25
"On atorvastatin treatment there was a significant decrease in the LDL-C levels (p=0.021)."( Effect of genetic variant (rs11887534) in ABCG8 gene in coronary artery disease and response to atorvastatin therapy.
Garg, N; Mittal, B; Srivastava, A; Srivastava, K, 2010
)
1.09
"Atorvastatin treatment was neuroprotective against cell degeneration induced by Aβ(1-40), reducing inflammatory and oxidative responses and increasing the expression of glutamatergic transporters."( Atorvastatin prevents hippocampal cell death, neuroinflammation and oxidative stress following amyloid-β(1-40) administration in mice: evidence for dissociation between cognitive deficits and neuronal damage.
Bezerra, SC; de Bem, AF; Duarte, FS; Figueiredo, CP; Mancini, G; Piermartiri, TC; Prediger, RD; Rial, D; Tasca, CI, 2010
)
2.52
"Atorvastatin treatment alone decreased I(Ca,L) similar to rapid atrial pacing alone, currents were also further reduced by additional atrial tachypacing. "( Atorvastatin treatment affects atrial ion currents and their tachycardia-induced remodeling in rabbits.
Bentz, K; Eick, C; Kettering, K; Laszlo, R; Menzel, KA; Schreieck, J; Schreiner, B, 2010
)
3.25
"Atorvastatin treatment alone reduced low density lipoprotein (LDL) cholesterol by 1.4 mmol/l (44%, p<0.001), triglycerides by 0.3 mmol/l (20%, p<0.0001) and lanosterol by 0.36 μmol/l (72%, p<0.001)."( Impact of atorvastatin and omega-3 ethyl esters 90 on plasma plant sterol concentrations and cholesterol synthesis in type 2 diabetes: a randomised placebo controlled factorial trial.
Ceglarek, U; Farmer, A; Holman, RR; Neil, HA; Paul, S; Thiery, J, 2010
)
1.48
"Atorvastatin (Lipitor®) treatment was started at a fixed dose of 20 mg daily."( Biomarker assessment of the immunomodulator effect of atorvastatin in stable renal transplant recipients and hypercholesterolemic patients.
Brunet, M; Cofán, F; Cofán, M; Guillén, D; Millán, O; Ros, E, 2010
)
2.05
"Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD."( Atorvastatin improves tubular status in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study.
Aleksandrowicz, E; Larczyński, W; Lysiak-Szydłowska, W; Neuwelt, A; Renke, M; Rutkowski, B; Rutkowski, P; Tylicki, L; Ziętkiewicz, M, 2010
)
3.25
"Atorvastatin treatment completely abolished histological signs of necroinflammation, reducing the hepatic expression of metallothionein-1 and nuclear factor kappa B binding."( Reduction of liver fructokinase expression and improved hepatic inflammation and metabolism in liquid fructose-fed rats after atorvastatin treatment.
Alegret, M; Ađalsteisson, GS; Laguna, JC; Merlos, M; Rebollo, A; Roglans, N; Vilà, L, 2011
)
1.3
"Atorvastatin treatment did not affect diet induced body weight gain and did not lower plasma total cholesterol levels."( Atorvastatin inhibits plaque development and adventitial neovascularization in ApoE deficient mice independent of plasma cholesterol levels.
Biessen, EA; Bot, I; Jukema, JW; Lankhuizen, IM; van Berkel, TJ, 2011
)
2.53
"Atorvastatin treatment did not decrease LDLoxab;(mU/mL, median [CI 95%]: baseline: 413 [187-1,196] and 24 weeks: 349 [101-1559])."( [Atorvastatin and oxidized low density lipoprotein antibody. Relationship to age].
Cámara, C; Costo, A; Crespo, L; Fernández Pereira, L; Pereira, G; Sánchez Muñoz-Torrero, JF, 2011
)
2
"Atorvastatin treatment for 1 year significantly decreased circulating levels of total cholesterol, LDL-cholesterol, triglycerides, and AGEs, while it increased HDL-cholesterol levels."( Atorvastatin reduces proteinuria in non-diabetic chronic kidney disease patients partly via lowering serum levels of advanced glycation end products (AGEs).
Fujiwara, N; Kawagoe, Y; Maeda, S; Nakamura, T; Sato, E; Takeuchi, M; Yamagishi, S,
)
2.3
"Atorvastatin pre-treatment of EC was found to reduce the expression of adhesion molecules and P. "( Atorvastatin prevents Plasmodium falciparum cytoadherence and endothelial damage.
Arrouss, I; Assi, S; Mazier, D; N'dilimabaka, N; Pino, P; Rebollo, A; Soubrier, F; Taoufiq, Z, 2011
)
3.25
"Atorvastatin treatment increased the SOD and catalase level compared with the stone-forming control group."( Why does atorvastatin inhibit renal crystal retention?
Nonomura, N; Okuyama, A; Tsujihata, M; Tsujimura, A; Yoshioka, I, 2011
)
1.51
"Atorvastatin pretreatment, however, prevented the decrease in α(1D)-adrenoceptor mRNA expression in septic animals."( Atorvastatin prevents vascular hyporeactivity to norepinephrine in sepsis: role of nitric oxide and α₁-adrenoceptor mRNA expression.
Ahanger, AA; Choudhury, S; Kandasamy, K; Mishra, SK; More, AS; Parida, S; Prawez, S; Singh, TU, 2011
)
2.53
"Atorvastatin treatment did not significantly preserve beta cell function although there may have been a slower decline of beta-cell function which merits further study."( Residual beta cell function in newly diagnosed type 1 diabetes after treatment with atorvastatin: the Randomized DIATOR Trial.
Heinemann, L; Heise, T; Herder, C; Koenig, W; Kolb, H; Martin, S; Schloot, NC, 2011
)
2.04
"Atorvastatin treatment resulted in a significant decrease of total, VLDL and LDL cholesterol, atherosclerotic lesion size and endoglin serum levels in comparison with CHOL mice."( Endoglin as a possible marker of atorvastatin treatment benefit in atherosclerosis.
Andrys, C; Brcakova, E; Micuda, S; Mullerova, Z; Nachtigal, P; Rathouska, J; Slanarova, M; Strasky, Z; Vecerova, L, 2011
)
1.37
"In atorvastatin-treated patients, NGAL decreased (mean, -7.4 ng/mL/year; SD 128.4), whereas it increased in the placebo group [mean, 4.6 ng/mL/year; SD 56.6), the difference being statistically significant (P = 0.049)."( Effects of atorvastatin on NGAL and cystatin C in chronic kidney disease: a post hoc analysis of the LORD trial.
Ball, MJ; Cardinal, JW; Coombes, JS; Fassett, RG; Geraghty, DP; Robertson, IK, 2012
)
1.28
"Atorvastatin treatment did not affect the duration of status epilepticus or the development of epilepsy. "( Atorvastatin treatment during epileptogenesis in a rat model for temporal lobe epilepsy.
Aronica, E; Gorter, JA; Holtman, L; Schmitz, LJ; van Vliet, EA; Wadman, WJ, 2011
)
3.25
"Atorvastatin treatment significantly improved lipid profile across with increased apelin (from 0.307 ± 0.130 pg/ml to 1.537 ± 0.427 pg/ml; P < 0.001) and suppressed visfatin (from 21.54 ± 10.14 ng/ml to 15.13 ± 7.61 ng/ml; P = 0.002) serum levels in our diabetic patients."( Effects of atorvastatin on apelin, visfatin (nampt), ghrelin and early carotid atherosclerosis in patients with type 2 diabetes.
Kadoglou, NP; Kapelouzou, A; Kostakis, A; Lampropoulos, S; Liapis, CD; Sailer, N; Vitta, I, 2012
)
1.49
"Atorvastatin treatment did not alter BMD compared with the control group, even in the highest dose of atorvastatin group."( Effects of atorvastatin on bone metabolism and bone mineral density in Wistar rats.
Chang, B; Chen, L; Fang, P; Li, H; Lu, S; Yang, J, 2011
)
1.48
"Atorvastatin treatment in a certain extent inhibits bone resorption and promotes bone formation, but has no significant effects on bone mineral density in healthy rats."( Effects of atorvastatin on bone metabolism and bone mineral density in Wistar rats.
Chang, B; Chen, L; Fang, P; Li, H; Lu, S; Yang, J, 2011
)
2.2
"Atorvastatin treatment promotes functional restoration after PDT, but does not promote glioma growth in vitro and in vivo."( Atorvastatin reduces functional deficits caused by photodynamic therapy in rats.
Chopp, M; Ding, C; Jiang, F; Jiang, J; Lu, Y; Yang, H; Zhang, L; Zhao, D; Zheng, X, 2011
)
2.53
"Atorvastatin pretreatment attenuated bronchoalveolar lavage MMP-2 increases."( Sildenafil improves the beneficial hemodynamic effects exerted by atorvastatin during acute pulmonary thromboembolism.
Czaikoski, PG; Dias-Junior, CA; Neto-Neves, EM; Pereira, RP; Spiller, F; Tanus-Santos, JE; Uzuelli, JA, 2011
)
1.33
"Atorvastatin treatment do not modify APOE expression, however those individuals without LDL cholesterol goal achievement after atorvastatin treatment according to the IV Brazilian Guidelines for Dyslipidemia and Atherosclerosis Prevention had lower APOE expression than patients with desirable response after the treatment (p < 0.05)."( Apolipoprotein E mRNA expression in mononuclear cells from normolipidemic and hypercholesterolemic individuals treated with atorvastatin.
Arazi, SS; Bernik, MM; Bertolami, MC; Cerda, A; Dorea, EL; Faludi, AA; Genvigir, FD; Hirata, MH; Hirata, RD; Willrich, MA, 2011
)
1.3
"Atorvastatin treatment for 4 weeks in subjects with SCR significantly improved endothelial function and suppressed systemic inflammatory status by decreasing circulating levels of IL-1b and sVCAM-1."( Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta.
Antoniades, C; Antonopoulos, AS; Bakogiannis, C; Brili, S; Hatzis, G; Papageorgiou, N; Stefanadis, C; Tousoulis, D, 2012
)
2.21
"Atorvastatin pretreatment has been reported to reduce myocardial damage in patients undergoing percutaneous coronary intervention (PCI). "( Effects of atorvastatin pretreatment on infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.
Ahn, KJ; Choi, JH; Choi, SH; Choi, YJ; Gwon, HC; Hahn, JY; Jo, SH; Kim, HJ; Lee, KH; Lee, S; Lee, SH; Song, YB, 2011
)
2.2
"Atorvastatin treatment for 6 months caused a significant reduction in the following biomarkers compared with baseline: BNP, from median (interquartile range) 268 (190-441) pg/mL to 185 (144-344) pg/mL; high-sensitivity C-reactive protein (hs-CRP), from 5.26 (1.95 -9.29) mg/L to 3.70 (2.34-6.81) mg/L; and PIIINP, from 4.65 (1.86) to 4.09 (1.25) pg/mL (all P < 0.05 baseline vs 6 months)."( Long-term statin therapy in patients with systolic heart failure and normal cholesterol: effects on elevated serum markers of collagen turnover, inflammation, and B-type natriuretic peptide.
Abulhul, E; Baugh, J; Hennessy, M; Ledwidge, M; Martos, R; McDonald, K; O'Loughlin, C; Phelan, D; Spiers, JP; Watson, C, 2012
)
1.1
"In atorvastatin-treated patients, the decrease in LpPLA2 was associated with reduced fatal risk [HR per standard deviation 0·74 (0·62-0·90); P = 0·002], an effect not seen in the placebo group."( Lipoprotein-associated phospholipase A2 and outcome in patients with type 2 diabetes on haemodialysis.
Drechsler, C; Hoffmann, MM; Krane, V; Wanner, C; Winkler, K, 2012
)
0.89
"Atorvastatin treatment of lipemia was followed by a decrease in the total LP-C, total LDL-C (LDL(1-3)-C subfraction), and the LDL(1-3)-TG subfraction."( Influence of atorvastatin and carboxymethylated glucan on the serum lipoprotein profile and MMP activity of mice with lipemia induced by poloxamer 407.
Cherkanova, MS; Filjushina, EE; Johnston, TP; Kaledin, VI; Korolenko, TA; Loginova, VM; Tuzikov, FV; Tuzikova, NA, 2012
)
1.47
"Atorvastatin pretreatment significantly reduced the occurrence of AF after bypass grafting; nonetheless, the difference between the beneficial effects of intensive and routine atorvastatin treatments on postoperative AF was not significant."( The effect of a high dose of atorvastatin on the occurrence of atrial fibrillation after coronary artery bypass grafting.
Bidhendi, LM; Bina, P; Fathollahi, MS; Karimi, A; Molai, M; Rezvanfard, M; Sadeghian, S; Yousefi, A; Zare, E, 2012
)
2.11
"Atorvastatin treatment may be effective in slowing the decline of beta cell function in a patient subgroup defined by above median levels of CRP and other inflammation associated immune mediators."( Improved preservation of residual beta cell function by atorvastatin in patients with recent onset type 1 diabetes and high CRP levels (DIATOR trial).
Heinemann, L; Heise, T; Herder, C; Koenig, W; Kolb, H; Martin, S; Roden, M; Schloot, NC; Simon, MC; Strom, A, 2012
)
2.07
"Atorvastatin treatment significantly decreased development of new brain MRI T2 lesion activity, although it did not achieve the composite clinical and imaging PEP."( Randomized controlled trial of atorvastatin in clinically isolated syndrome: the STAyCIS study.
Bar-Or, A; Calabresi, PA; Cohen, JA; Cross, A; Ding, L; Goodman, A; Iklé, D; Kachuck, N; Kita, M; Kopetskie, H; Mass, M; Miller, A; Mokhtarani, M; Murphy, S; Pelletier, D; Preiningerova, J; Racke, M; Rosenberg, E; Schwid, S; Spencer, C; Stüve, O; Vollmer, T; Waubant, E; Weinstock-Guttman, B; Zamvil, SS, 2012
)
2.11
"Atorvastatin donor pre-treatment of brain dead organ donors combined with 24h of cold preservation has no influence on graft rejection and infiltration with ED1 or MHCII positive cells in an allogeneic rat renal transplantation model. "( Atorvastatin donor pre-treatment in a model of brain death and allogeneic kidney transplantation in rat.
Benck, U; Gottmann, U; Hoeger, S; Krämer, BK; Petrov, K; Schnuelle, P; Waldherr, R; Yard, BA,
)
3.02
"Atorvastatin treatment significantly decreased total plasma cholesterol levels at 4, 8 and 12 weeks (12 weeks: 6.7 ± 4.2 mmol/L versus control 38.7 ± 10.6 mmol/L, p<0.0002)."( Statin therapy prevents expansive remodeling in venous bypass grafts.
Butany, J; Fefer, P; Fujii, H; Leong-Poi, H; Nili, N; Osherov, AB; Qiang, B; Samuel, M; Sparkes, JD; Strauss, BH; Toma, J, 2012
)
1.1
"The atorvastatin treatment also produced a repression of microRNA 21 and genes involved in cell proliferation and neointimal formation (vascular endothelial growth factor [VEGF] A, VEGF receptor 1, VEGFC)."( Lysophosphatidic acid pretreatment prevents micromolar atorvastatin-induced endothelial cell death and ensures the beneficial effects of high-concentration statin therapy on endothelial gene expression.
Alaminos, M; Esteban, M; Garrido, JM; Roda, O; Sánchez-Montesinos, I, 2012
)
1.11
"Atorvastatin pretreatment was independently associated with a decreased risk of CIN (OR 0.084, 95% CI 0.015-0.462, p = 0.004)."( Beneficial effects of high-dose atorvastatin pretreatment on renal function in patients with acute ST-segment elevation myocardial infarction undergoing emergency percutaneous coronary intervention.
Fan, W; Fu, X; Geng, W; Gu, X; Hao, G; Jiang, Y; Li, S; Li, W; Li, X; Wang, X; Wang, Y; Wu, W; Yang, Z, 2012
)
1.38
"Atorvastatin pretreatment can accelerate both neointimal coverage and re-endothelialization after SES implantation, which may be mediated by the mobilization of EPC and enhancement of the endothelial function of the neointima."( Atorvastatin accelerates both neointimal coverage and re-endothelialization after sirolimus-eluting stent implantation in a porcine model: new findings from optical coherence tomography and pathology.
Jin, C; Mintz, GS; Tang, Y; Tian, Y; Wang, TJ; Xu, B; Yang, YJ; Zhang, Q, 2012
)
3.26
"Atorvastatin treatment inhibits proliferation, apoptosis and cytokine production of MFB in bile duct-ligated (BDL) rats in vivo."( Atorvastatin inhibits proliferation and apoptosis, but induces senescence in hepatic myofibroblasts and thereby attenuates hepatic fibrosis in rats.
Fürst, DO; Granzow, M; Huss, S; Klein, S; Klösel, J; Körner, C; Lammert, F; Mazar, IG; Nattermann, J; Pieper-Fürst, U; Sauerbruch, T; Schierwagen, R; Trebicka, J; van den Ven, PF; Weber, S, 2012
)
2.54
"Atorvastatin pretreatment inhibit cellular apoptosis induced by H₂O₂ (39.45%, 20.53% and 7.83%)."( [Atorvastatin inhibits the H₂O₂-induced apoptosis of human vascular endothelial cells through a down-regulation of cleaved caspase-9/caspase-3].
Li, SJ; Wu, WZ; Xu, ZR; Yang, YM; Yao, HP, 2012
)
2.01
"Atorvastatin treatment for 2 and 8 weeks restored BBB integrity, indicated by a substantial reduction of IgG and apo B, particularly within the hippocampus. "( Restoration of dietary-fat induced blood-brain barrier dysfunction by anti-inflammatory lipid-modulating agents.
Clark, K; Galloway, S; Lam, V; Mamo, J; Pallebage-Gamarallage, M; Takechi, R, 2012
)
1.82
"Atorvastatin treatment of HepG2 cells resulted in increased HMGCR-1b mRNA levels, but unaltered proximal promoter activity compared to untreated cells."( A novel 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) splice variant with an alternative exon 1 potentially encoding an extended N-terminus.
Berg, JP; Grimholt, RM; Kringen, MK; Piehler, AP; Stormo, C, 2012
)
1.1
"Atorvastatin treatment increased total myocardial protein oxidation and serum lipid peroxidation."( Atorvastatin increases oxidative stress and modulates angiogenesis in Ossabaw swine with the metabolic syndrome.
Chu, LM; Elmadhun, NY; Feng, J; Lassaletta, AD; Liu, Y; Sellke, FW, 2012
)
2.54
"Atorvastatin treatment was associated with increased myocardial and serum oxidative stress, which might contribute to the lack of collateral-dependent perfusion in the setting of angiogenesis."( Atorvastatin increases oxidative stress and modulates angiogenesis in Ossabaw swine with the metabolic syndrome.
Chu, LM; Elmadhun, NY; Feng, J; Lassaletta, AD; Liu, Y; Sellke, FW, 2012
)
2.54
"Atorvastatin treatment increases RANKL levels with no measurable effect on bone metabolism and mobilization of progenitor cells from BM to PB. "( Atorvastatin-induced increase in progenitor cell levels is rather caused by enhanced receptor activator of NF-kappaB ligand (RANKL) cell proliferation than by bone marrow mobilization.
Arnal, JF; Lucanus, E; Nickenig, G; Pelster, B; Steinmetz, M; Werner, N, 2013
)
3.28
"Atorvastatin treatment decreased serum low-density lipoprotein (-39%, P=0.0001), total cholesterol (-32%, P=0.0001), and triglycerides (-22%, P=0.0001), and increased high-density lipoprotein (+13%, P=0.0001) at 12 weeks compared to baseline. "( Effects of short-term atorvastatin treatment on global fibrinolytic capacity, and sL-selectin and sFas levels in hyperlipidemic patients with coronary artery disease.
Açil, T; Aksöyek, S; Atalar, E; Haznedaroglu, I; Kes, S; Ovünç, K; Ozer, N; Ozmen, F, 2002
)
2.07
"Atorvastatin treatment resulted in a significant decrease (i.e., 30-37%) in levels of total triglyceride, cholesterol, LDL-C, and apoB in all six patients."( Effect of atorvastatin on plasma apoE metabolism in patients with combined hyperlipidemia.
Barrett, PH; Batal, R; Bernier, L; Cohn, JS; Davignon, J; Dubreuil, D; Jacques, H; Mamer, O; Rodriguez, C; Roy, M; Tremblay, M; Veilleux, L, 2002
)
1.44
"Atorvastatin treatment of either APC or T cells suppressed antigen-specific T-cell activation."( The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease.
Bravo, M; Hur, EM; Mitchell, DJ; Patarroyo, JC; Radosevich, JL; Ruiz, PJ; Sobel, RA; Steinman, L; Stüve, O; Youssef, S; Zamvil, SS, 2002
)
1.32
"Atorvastatin treatment resulted in a 32% reduction in total serum cholesterol (CH), 41% reduction in low density lipoprotein (LDL) CH, 16% reduction in triglycerides and a 21% increase in high density lipoprotein CH. "( [Effect of atorvastatin on endothelial function in patients with familial hypercholesterolemia].
At'kov, OIu; Balakhonova, TV; Kobylianskiĭ, AG; Kukharchuk, VV; Kuznetsova, TV; Masenko, VP; Pogorelova, OA; Susekov, AV; Titov, VN; Tvorogova, MG, 2002
)
2.15
"Atorvastatin treatment in diabetic dyslipidemia results in a significant dose-dependent decrease in HL activity, regardless of sex or the LIPC promoter variant."( Atorvastatin dose-dependently decreases hepatic lipase activity in type 2 diabetes: effect of sex and the LIPC promoter variant.
Berk-Planken, II; Bootsma, AH; Hoogerbrugge, N; Jansen, H; Stolk, RP, 2003
)
2.48
"Atorvastatin treatment was effective with a mean percentage reduction of total cholesterol of 41 +/- 10% (p < 0.01 vs."( Atorvastatin treatment for hyperlipidemia in pediatric renal transplant recipients.
Aitken, M; Argent, E; Kainer, G; Mackie, FE; Rosenberg, AR, 2003
)
2.48
"Atorvastatin treatment significantly reduced plasma total cholesterol, LDL-cholesterol and triglyceride levels and increased plasma HDL-cholesterol."( Effects of atorvastatin on electrophoretic characteristics of LDL particles among subjects with heterozygous familial hypercholesterolemia.
Bergeron, J; Couture, P; Gagné, C; Hogue, JC; Lamarche, B; Larivière, M; Pirro, M, 2003
)
1.43
"Atorvastatin treatment significantly reduced CETP mass dose-dependently by 18% (A10) and 29% (A80; both vs."( Common cholesteryl ester transfer protein gene polymorphisms and the effect of atorvastatin therapy in type 2 diabetes.
Banga, JD; Dallinga-Thie, GM; Erkelens, DW; Sijmonsma, TP; Stolk, RP; van Tol, A; van Venrooij, FV, 2003
)
1.27
"Atorvastatin treatment significantly decreased plasma triglycerides (P < 0.05), total and LDL cholesterol (P < 0.05), apoB100 in LDL, IDL, and VLDL (P < 0.05)."( Effect of atorvastatin on apolipoprotein B100 containing lipoprotein metabolism in type-2 diabetes.
Charbonnel, B; Krempf, M; Laouenan, H; Magot, T; Marchini, JS; Ouguerram, K; Zaïr, Y, 2003
)
1.44
"With atorvastatin treatment initiated 1 day after stroke, animals exhibited significant increases in vascular endothelial growth factor, cyclic guanosine monophosphate, angiogenesis, endogenous cell proliferation and neurogenesis, and an increase in the synaptic protein, synaptophysin."( Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke.
Chen, J; Chopp, M; Feldkamp, CS; Jiang, H; Katakowski, M; Li, Y; Lu, M; Wang, L; Wang, Y; Zhang, C; Zhang, ZG, 2003
)
0.77
"Atorvastatin treatment did not produce any change in oral glucose tolerance categories or induce any change in glucose and insulin response in OGTT."( Effects of atorvastatin on glucose homeostasis, postprandial triglyceride response and C-reactive protein in subjects with impaired fasting glucose.
Alvarez, L; Casals, E; Casamitjana, R; Conget, I; Costa, A; Gomis, R; Hernández, G; Masramón, X; Morales, J, 2003
)
1.43
"Atorvastatin treatment reduced total and LDL-cholesterol by 31% and 40%, respectively."( Increased levels of pregnancy-associated plasma protein-A in patients with hypercholesterolemia: the effect of atorvastatin treatment.
Ceska, R; Fialová, L; Malbohan, I; Malík, J; Soukupová, J; Stulc, T, 2003
)
1.25
"Atorvastatin treatment significantly reduces SUA levels in patients with CHD, thus offsetting an additional factor associated with CHD risk."( Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: a subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study.
Athyros, VG; Bouloukos, VI; Elisaf, M; Mikhailidis, DP; Milionis, HJ; Papageorgiou, AA; Pehlivanidis, AN; Symeonidis, AN, 2004
)
1.24
"Atorvastatin treatment increased sFasL concentrations (111 pg/ml, p < 0.0001), reaching normal values."( Decreased circulating Fas ligand in patients with familial combined hyperlipidemia or carotid atherosclerosis: normalization by atorvastatin.
Blanco-Colio, LM; Díaz, C; Egido, J; Hernández, G; Martín-Ventura, JL; Sol, JM, 2004
)
1.25
"Atorvastatin treatment decreased the serum total cholesterol level with a mean of 38 and 28% in the elderly and the young, respectively (P < 0.001)."( Effect of atorvastatin on impaired vascular function in healthy old men.
Blauw, GJ; Meinders, AE; Weverling-Rijnsburger, AW, 2004
)
1.45
"Atorvastatin 10- and 80-mg treatment significantly decreased plasma apoC-III (atorvastatin 10 mg, 21%, and 80 mg, 27%), HDL apoC-III (atorvastatin 10 mg, 22%, and 80 mg, 28%) and LpB:C-III (atorvastatin 10 mg, 23%, and 80 mg, 28%; all P < 0.001)."( Atorvastatin decreases apolipoprotein C-III in apolipoprotein B-containing lipoprotein and HDL in type 2 diabetes: a potential mechanism to lower plasma triglycerides.
Berk-Planken, II; Bootsma, AH; Dallinga-Thie, GM; Jansen, H, 2004
)
2.49
"Atorvastatin treatment resulted in a significant dose-dependent reduction in plasma apoC-III, HDL apoC-III, and LpB:C-III levels in patients with type 2 diabetes. "( Atorvastatin decreases apolipoprotein C-III in apolipoprotein B-containing lipoprotein and HDL in type 2 diabetes: a potential mechanism to lower plasma triglycerides.
Berk-Planken, II; Bootsma, AH; Dallinga-Thie, GM; Jansen, H, 2004
)
3.21
"The atorvastatin-treated ICH group showed better performance on Rotorod and limb placing tests when compared with the vehicle-treated group (P<0.01). "( HMG-CoA reductase inhibitor, atorvastatin, promotes sensorimotor recovery, suppressing acute inflammatory reaction after experimental intracerebral hemorrhage.
Chu, K; Han, SY; Jeong, SW; Jung, KH; Kim, JY; Kim, M; Lee, ST; Roh, JK, 2004
)
1.17
"Atorvastatin treatment led to a significant down-regulation of HLA-DR and the CD38 activation marker on peripheral T cells, whereas simvastatin up-regulated both of these molecules."( Statin-induced immunomodulatory effects on human T cells in vivo.
Ammann, P; Fehr, T; Fierz, W; Joller-Jemelka, HI; Kahlert, C; Rickli, H; Riesen, WF; Wüthrich, RP, 2004
)
1.04
"Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia."( Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia.
Akin, M; Aliyev, E; Altuglu, I; Ercan, E; Ercan, HE; Sekuri, C; Tengiz, I, 2004
)
3.21
"Atorvastatin treatment resulted in a 55% reduction of low-density lipoprotein (LDL) cholesterol (from mean of 162 (SD 32) to 72 (20) mg/dl)."( Short-term effect of atorvastatin on ischaemic threshold in hypercholesterolaemic patients with stable ischaemic heart disease.
Carlier, M; Claeys, MJ; Cools, F; Cosyns, B; De Meester, A; Dewit, B; Gobin, E; Hoffer, E; Missault, L; Vermeersch, P, 2004
)
1.36
"Atorvastatin treatment resulted in a 30% reduction of total and a 45% reduction of LDL cholesterol (6.06 +/- 1.39 mmol/L versus 4.14 +/- 1.27 mmol/L and 4.11 +/- 1.13 mmol/L versus 2.27 +/- 0.89 mmol/L, both P < 0.0001)."( Atorvastatin improves diabetic dyslipidemia and increases lipoprotein lipase activity in vivo.
Dugi, KA; Hamann, A; Nawroth, PP; Parhofer, KG; Schiekofer, S; Schneider, JG; Volkmer, JE; von Eynatten, M, 2004
)
2.49
"Atorvastatin treatment had a favourable effect on lipid profile and increased the activity of HDL-associated PON."( Effect of short term treatment with simvastatin and atorvastatin on lipids and paraoxonase activity in patients with hyperlipoproteinaemia.
Balogh, Z; Harangi, M; Illyés, L; Kovács, P; Paragh, G; Seres, I; Törocsik, D, 2004
)
1.3
"Atorvastatin treatment did not affect the creatinine kinase level, and no classical adverse effects were observed during the study."( Effects of atorvastatin on triglyceride-rich lipoproteins, low-density lipoprotein subclass, and C-reactive protein in hemodialysis patients.
Adachi, M; Gushiken, N; Hirano, T; Hyodo, T; Ikejiri, A; Murayama, S; Taira, T; Yoshino, G, 2004
)
1.43
"Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015)."( Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
Florkowski, CM; Frampton, CM; George, PM; Molyneux, SL; Scott, RS; Strey, CH; Young, JM, 2005
)
1.05
"Atorvastatin treatment had no effect on Th1 and Th2 cytokine transcription. "( The effects of atorvastatin in experimental autoimmune uveitis.
Albini, T; Evans, M; Giri, RK; Rao, NA; See, RF; Thomas, PB, 2005
)
2.12
"Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C."( High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome: results from the MIRACL trial.
Ezekowitz, MD; Ganz, P; Oliver, MF; Olsson, AG; Sasiela, WJ; Schwartz, GG; Szarek, M; Waters, D; Zeiher, A, 2005
)
1.05
"Atorvastatin treatment activated peroxisome proliferator activated receptor gamma and increased LXR-mediated gene expression suggesting that atorvastatin induces cholesterol efflux through a molecular cascade involving inhibition of RhoA signaling, leading to increased peroxisome proliferator activated receptor gamma activity, enhanced LXR activation, increased ABCA1 expression, and cholesterol efflux."( Regulation of macrophage cholesterol efflux through hydroxymethylglutaryl-CoA reductase inhibition: a role for RhoA in ABCA1-mediated cholesterol efflux.
Argmann, CA; Edwards, JY; Hegele, RA; Huff, MW; O'Neil, CH; Pickering, JG; Sawyez, CG, 2005
)
1.05
"Atorvastatin treatment may be of some clinical benefit and could be established as an effective therapy for Alzheimer disease if the current findings are substantiated by a much larger multicenter trial."( Atorvastatin for the treatment of mild to moderate Alzheimer disease: preliminary results.
Browne, P; Connor, DJ; Johnson-Traver, S; Launer, LJ; Lochhead, J; Lopez, J; Sabbagh, MN; Sparks, DL; Wasser, D; Ziolwolski, C, 2005
)
3.21
"Atorvastatin treatment compared to placebo resulted in a significant decrease in serum cholesterol (5.85 +/- 1.04 mmol/l vs. "( The effect of atorvastatin on serum lipoproteins in acromegaly.
Davies, R; Durrington, P; Gibson, M; Kaushal, K; Mackness, M; Mishra, M; Ray, DW; Siddals, KW, 2005
)
2.13
"Atorvastatin treatment was safe, well tolerated and effective in improving the atherogenic lipoprotein profile in acromegaly."( The effect of atorvastatin on serum lipoproteins in acromegaly.
Davies, R; Durrington, P; Gibson, M; Kaushal, K; Mackness, M; Mishra, M; Ray, DW; Siddals, KW, 2005
)
2.13
"Atorvastatin treatment was associated with an improvement in the stiffness of leg arteries in type 2 diabetes mellitus. "( Effect of atorvastatin on regional arterial stiffness in patients with type 2 diabetes mellitus.
Emoto, M; Fujiwara, S; Fukumoto, S; Hatsuda, S; Kimoto, E; Koyama, H; Maeno, T; Nishizawa, Y; Shinohara, K; Shoji, T; Yokoyama, H, 2005
)
2.17
"In atorvastatin-treated NRCM, a second band of Ggamma3 with a lower apparent molecular weight appeared in cytosol and particulate fractions that was absent in vehicle-treated NRCM, but also seen after GGTI-298, a geranylgeranyl transferase inhibitor."( Atorvastatin desensitizes beta-adrenergic signaling in cardiac myocytes via reduced isoprenylation of G-protein gamma-subunits.
Eschenhagen, T; Mühlhäuser, U; Münzel, F; Rau, T; Wieland, T; Zolk, O, 2006
)
2.29
"Atorvastatin treatment reduced myocardial infarction which has been reflected by improvement in serum parameters, ATPase activities and histopathological lesions."( Effect of atorvastatin treatment on isoproterenol-induced myocardial infarction in rats.
Balaraman, R; Bothara, SB; Majithiya, JB; Trivedi, CJ, 2006
)
1.46
"Atorvastatin treatment decreased HDL-cholesterol levels (3.56 +/- 0.24 vs. "( Effects of atorvastatin on high-density lipoprotein apolipoprotein A-I metabolism in dogs.
Briand, F; Krempf, M; Magot, T; Nguyen, P; Ouguerram, K, 2006
)
2.17
"Atorvastatin treatment also induced a significant decrease in neointimal vascular smooth muscle cells and cellular density (respectively: 2.0 +/- 0.2 vs."( Short-term atorvastatin treatment does not modify neointimal morphology but reduces MMP-2 expression in normocholesterolemic rabbit stented arteries.
Busseuil, D; Collin, B; Cottin, Y; Duvillard, L; Korandji, C; Pitois-Merli, I; Rioufol, G; Rochette, L; Zeller, M, 2006
)
1.45
"Atorvastatin treatment resulted in decreased PLTP activity (10 mg atorvastatin: -8.3%, P < 0.05; 80 mg atorvastatin: -12.1%, P < 0.002)."( Plasma phospholipid transfer protein activity is decreased in type 2 diabetes during treatment with atorvastatin: a role for apolipoprotein E?
Dallinga-Thie, GM; Hattori, H; Rensen, PC; Sijbrands, EJ; van Tol, A, 2006
)
1.27
"Atorvastatin treatment resulted in a 1.7- to 8.0-fold increase in CEPs from baseline levels (P < 0.0001), but the numbers returned to within baseline levels at posttreatment."( Increase in circulating endothelial precursors by atorvastatin in patients with systemic sclerosis.
Ikeda, Y; Kaburaki, J; Kawakami, Y; Kuwana, M; Okazaki, Y; Yasuoka, H, 2006
)
1.31
"Atorvastatin treatment decreased plasma triglycerides, APOA5, APOC3 and APOE (all p<0.0001)."( Plasma apolipoprotein A5 and triglycerides in type 2 diabetes.
Dallinga-Thie, GM; Hattori, H; Jansen, H; Sijbrands, EJ; van Tol, A; van Vark-van der Zee, LC, 2006
)
1.06
"Atorvastatin pretreatment prevented these increases, blunted expression of membrane subunit gp91(phox), and prevented translocation of cytoplasmic subunit p47(phox) to the membrane in the penumbra 2 h after reperfusion."( Atorvastatin protects against cerebral infarction via inhibition of NADPH oxidase-derived superoxide in ischemic stroke.
Chen, AF; Hong, H; Kaufman, DI; Kreulen, DL; Zeng, JS, 2006
)
2.5
"Atorvastatin treatment was associated with increased phosphorylation of Akt (5.7-fold increase versus NORM; P=0.001), decreased vascular endothelial growth factor expression (-68+/-8%; P<0.001 versus NORM), and increased expression of the antiangiogenic protein endostatin (210+/-48%; P=0.004 versus NORM)."( High-dose atorvastatin improves hypercholesterolemic coronary endothelial dysfunction without improving the angiogenic response.
Bianchi, C; Boodhwani, M; Feng, J; Laham, R; Li, J; Mieno, S; Nakai, Y; Ramlawi, B; Sellke, FW; Voisine, P, 2006
)
1.46
"Atorvastatin pre-treatment reduced hypernociception induced by bradykinin and cytokines (TNF-alpha, IL-1beta and KC), and the release of IL-1beta and PGE(2) in paw skin, induced by lipopolysaccharide."( Atorvastatin inhibits inflammatory hypernociception.
Cunha, FQ; Cunha, TM; Ferreira, SH; Parada, CA; Poole, S; Santodomingo-Garzón, T; Valério, DA; Verri, WA, 2006
)
2.5
"In atorvastatin treatment group, the increments of these two factors were attenuated significantly at the two time points, respectively."( Tubulointerstitial macrophage accumulation is regulated by sequentially expressed osteopontin and macrophage colony-stimulating factor: implication for the role of atorvastatin.
Chu, G; Ding, G; Jia, R; Tian, S, 2006
)
1.04
"In 3 atorvastatin treated groups mice were fed the same diet as described above except atorvastatin was added to the diet at the dosage of 10 mg/kg per day for the last 8 weeks before euthanasia."( Atorvastatin has distinct effects on endothelial markers in different mouse models of atherosclerosis.
Jamborova, G; Nachtigal, P; Pospechova, K; Pospisilova, N; Semecky, V; Solichova, D; Zdansky, P, 2006
)
2.23
"Atorvastatin treatment of human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1) resulted in significant increase in ATP breakdown and adenosine formation both if analysed in intact cell studies and as enzyme activity in cell lysates."( Stimulatory effects of atorvastatin on extracellular nucleotide degradation in human endothelial cells.
Amrani, M; Isley, C; Osman, L; Smolenski, RT; Yacoub, MH, 2006
)
1.37
"Atorvastatin treatment resulted in a 38% reduction in relative risk ([95% CI -58 to -8], P = 0.017) of first major cardiovascular events in older patients and a 37% reduction ([-57 to -7], P = 0.019) in younger patients. "( Analysis of efficacy and safety in patients aged 65-75 years at randomization: Collaborative Atorvastatin Diabetes Study (CARDS).
Betteridge, DJ; Colhoun, HM; DeMicco, DA; Durrington, PN; Fuller, JH; Hitman, GA; Livingstone, SJ; Luo, D; Neil, HA, 2006
)
2
"Atorvastatin treatment, in addition to its beneficial effect on cholesterol levels, improved the inflammatory state of these patients without modifying fibrinolytic balance."( Effects of atorvastatin on inflammatory and fibrinolytic parameters in patients with chronic kidney disease.
Abad, S; Cachofeiro, V; de Vinuesa, SG; Goicoechea, M; Gómez-Campderá, F; Lahera, V; Luño, J; Vega, A, 2006
)
1.45
"Atorvastatin treatment prevented the elevation of autoantibody titers against all forms of oxidized LDL."( Short- and long-term elevation of autoantibody titers against oxidized LDL in patients with acute coronary syndromes. Role of the lipoprotein-associated phospholipase A2 and the effect of atorvastatin treatment.
Goudevenos, JA; Lourida, ES; Papathanasiou, AI; Tselepis, AD; Tsironis, LD, 2008
)
1.26
"Atorvastatin treatment reverses hypercholesterolemia-induced endothelial dysfunction without appreciable improvements in collateral-dependent myocardial perfusion in response to vascular endothelial growth factor treatment. "( High-dose atorvastatin is associated with impaired myocardial angiogenesis in response to vascular endothelial growth factor in hypercholesterolemic swine.
Boodhwani, M; Feng, J; Li, J; Mieno, S; Sellke, FW; Sodha, N; Voisine, P, 2006
)
2.18
"Atorvastatin treatment inhibited ACE induction during differentiation."( Atorvastatin inhibits angiotensin-converting enzyme induction in differentiating human macrophages.
Fyhrquist, F; Nyman, T; Saijonmaa, O, 2007
)
2.5
"Atorvastatin treatment decreased total (P < 0.001) and LDL-cholesterol (P < 0.001) but had no effect on high-density lipoprotein."( Impact of atorvastatin treatment on platelet-activating factor acetylhydrolase and 15-F(2trans)-isoprostane in hypercholesterolaemic patients.
Benndorf, R; Böger, RH; Kom, GD; Maas, R; Schneider, L; Schwedhelm, E, 2007
)
1.46
"Atorvastatin treatment decreased microalbuminuria and helped preserve filtration function in chronic unilateral ureteral obstruction without altering plasma cholesterol levels, suggesting that pleiotropic renal protection is offered by this statin."( Atorvastatin preserves renal function in chronic complete unilateral ureteral obstruction.
Chou, SY; Gulmi, FA; Kim, H; Michli, E; Mooppan, UM, 2007
)
3.23
"Atorvastatin-treated patients experienced greater low-density lipoprotein cholesterol reductions than did pravastatin-treated patients, a trend toward fewer major acute cardiovascular events (hazard ratio, 0.71; 95% confidence interval, 0.46, 1.09; P=0.114), and a significantly greater reduction in all-cause death (hazard ratio, 0.33; 95% confidence interval, 0.13, 0.83; P=0.014)."( Effects of intensive versus moderate lipid-lowering therapy on myocardial ischemia in older patients with coronary heart disease: results of the Study Assessing Goals in the Elderly (SAGE).
Bairey Merz, CN; Cosin-Aguilar, J; Deedwania, P; Koylan, N; Luo, D; Ouyang, P; Piotrowicz, R; Schenck-Gustafsson, K; Sellier, P; Stein, JH; Stone, PH; Thompson, PL; Tzivoni, D, 2007
)
1.06
"Atorvastatin treatment was associated with decreases of sICAM-1 (from 274.2+/-92.2 to 197.9+/-70.0 ng/ml; p<0.01) and hsCRP (from 0.57+/-0.45 to 0.18+/-0.15 mg/dl; p<0.01), whereas placebo treatment had no effect on these markers."( Effect of atorvastatin on peripheral endothelial function and systemic inflammatory markers in patients with stable coronary artery disease.
Alber, HF; Dichtl, W; Dörler, J; Frick, M; Pachinger, O; Stocker, EM; Süssenbacher, A; Weidinger, F, 2007
)
1.46
"Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels (41+/-19 vs 47+/-19 nmol/L, p=0.003)."( Effects of Atorvastatin on vitamin D levels in patients with acute ischemic heart disease.
Abad, L; Chaves, J; Dueñas, A; Hernandez, G; Pérez-Castrillón, JL; Sanz, A; Vega, G, 2007
)
1.45
"Atorvastatin treatment was associated with significantly greater reductions in TC, LDL-C, and TG in the majority of dose comparisons with simvastatin."( A dose-specific meta-analysis of lipid changes in randomized controlled trials of atorvastatin and simvastatin.
Clarke, PJ; Grobler, MP; Levison, DB; Liew, D; Magliano, DJ; Rogers, SL; Webb, K, 2007
)
1.29
"Atorvastatin treatment increased PAAT and reduced right ventricular pressure, right ventricular hypertrophy, and vascular remodeling over the 4-wk course."( Serotonin transporter protein in pulmonary hypertensive rats treated with atorvastatin.
Christians, U; Kaisers, U; Laudi, S; McMurtry, IF; Mutlak, H; Schmitz, V; Steudel, W; Trump, S; Weimann, J; West, J, 2007
)
1.29
"Atorvastatin treatment significantly decreased total cholesterol as well as low-density lipoprotein cholesterol plasma levels, but did not modify mean blood pressure (MBP), proteinuria, creatinine clearance, or inflammatory factors."( Atorvastatin treatment in the short term: does it induce renoprotection or vasculoprotection in renal transplantation?
Bayés, B; Blanco, S; Bonet, J; Lauzurica, R; Navarro-Muñoz, M; Romero, R, 2007
)
2.5
"Atorvastatin treatment was associated with 50% reduction in non-haemorrhagic stroke (95% confidence interval 9%-72%P = 0.024), similar to the 48% reduction (11%-69%) for all strokes combined."( Stroke prediction and stroke prevention with atorvastatin in the Collaborative Atorvastatin Diabetes Study (CARDS).
Betteridge, DJ; Colhoun, H; Durrington, PN; Fuller, J; Hitman, GA; Livingstone, S; Neil, HA; Newman, C; Szarek, M, 2007
)
1.32
"In 2 atorvastatin-treated groups, mice were fed the same diets (chow or atherogenic) as described above except atorvastatin was added at the dosage of 10 mg x kg(-1) x day(-1) for the last 8 weeks before euthanasia."( Endothelial expression of endoglin in normocholesterolemic and hypercholesterolemic C57BL/6J mice before and after atorvastatin treatment.
Andrys, C; Jamborova, G; Nachtigal, P; Pospechova, K; Pospisilova, N; Semecky, V; Solichova, D; Zdansky, P, 2007
)
1
"Atorvastatin-treated rats showed fewer neurologic deficits than control animals as measured at day 3-5."( Atorvastatin attenuates mitochondrial toxin-induced striatal degeneration, with decreasing iNOS/c-Jun levels and activating ERK/Akt pathways.
Chu, K; Han, Z; Hong, NH; Im, WS; Jung, KH; Kang, L; Kim, M; Kim, MW; Lee, ST; Park, JE, 2008
)
2.51
"Atorvastatin treatment prevented the further progression of atherosclerosis by maintaining LDL-C below 100 mg/dl in patients with CHD and hypercholesterolemia (100( Randomized evaluation of atorvastatin in patients with coronary heart disease: a serial intravascular ultrasound study.
Azuma, A; Matsubara, H; Sasaki, S; Sawada, T; Yamada, T, 2007
)
2.09
"Atorvastatin treatment may have beneficial effects on LV hypertrophy in spontaneously hypertensive rats."( Atorvastatin prevents connexin43 remodeling in hypertrophied left ventricular myocardium of spontaneously hypertensive rats.
Chen, HJ; Chen, JZ; Chen, TG; Wang, LH; Yao, L; Yu, M, 2007
)
2.5
"Atorvastatin treatment improved lipid profile and significantly reduced hsCRP (p=0.002), WBC count (p=0.041), OPN (p<0.001) and OPG levels (p<0.001)."( Intensive lipid-lowering therapy ameliorates novel calcification markers and GSM score in patients with carotid stenosis.
Bandios, S; Fotiadis, G; Gerasimidis, T; Kadoglou, NP; Kapelouzou, A; Karayannacos, PE; Katinios, A; Kougias, P; Liapis, CD; Moumtzouoglou, A; Sailer, N; Vitta, I; Voliotis, K, 2008
)
1.07
"Atorvastatin treatment led to a substantial reduction in the number and volume of CEL in two-sided multivariate analysis (p = 0.003 and p = 0.008)."( Oral high-dose atorvastatin treatment in relapsing-remitting multiple sclerosis.
Aktas, O; Bellmann-Strobl, J; Dörr, J; Haertle, M; Paul, F; Volk, HD; Waiczies, H; Waiczies, S; Wernecke, KD; Wuerfel, J; Zipp, F, 2008
)
1.42
"Atorvastatin treatment also dose-dependently reduced liver X receptor alpha (LXRalpha) expression and Rho activation."( Atorvastatin inhibits ABCA1 expression and cholesterol efflux in THP-1 macrophages by an LXR-dependent pathway.
Hill, JS; Qiu, G, 2008
)
2.51
"Atorvastatin-treated rats showed a modest reduction in SBP that remained in the hypertensive range (174 +/- 8 mmHg)."( Renoprotection by statins is linked to a decrease in renal oxidative stress, TGF-beta, and fibronectin with concomitant increase in nitric oxide bioavailability.
Jaimes, EA; Raij, L; Schuman, IH; Zhou, MS, 2008
)
1.07
"Atorvastatin treatment was significantly more effective on apolipoprotein B levels in patients with AB+BB phenotype than in the AA phenotype group."( The human paraoxonase-1 phenotype modifies the effect of statins on paraoxonase activity and lipid parameters.
Derdak, Z; Harangi, M; Mirdamadi, HZ; Paragh, G; Seres, I; Sztanek, F, 2008
)
1.07
"In atorvastatin treatment groups, total serum triglyceride levels decreased in a dose-dependent manner, reductions in the 20-mg and 80-mg groups were statistically significant (P < .05) compared with placebo. "( Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia.
Bakker-Arkema, RG; Black, DM; Brown, WV; Davidson, MH; Davignon, J; Goldstein, RJ; Isaacsohn, JL; Keilson, LM; Miller, VT; Shurzinske, LJ; Weiss, SR, 1996
)
1.16
"Atorvastatin treatment significantly reduced plasma total cholesterol, LDL cholesterol, total triglyceride, and VLDL triglyceride concentrations by 16%, 31%, 19%, and 28%, respectively (P < .01)."( Inhibition of HMG-CoA reductase by atorvastatin decreases both VLDL and LDL apolipoprotein B production in miniature pigs.
Barrett, PH; Burnett, JR; Huff, MW; Kleinstiver, SJ; Newton, RS; Telford, DE; Wilcox, LJ, 1997
)
1.3
"In atorvastatin-treated rats, the half-life of the receptor was decreased by over 60%."( Atorvastatin action involves diminished recovery of hepatic HMG-CoA reductase activity.
Chambers, CM; Lopez, D; Ness, GC, 1998
)
2.26
"Atorvastatin-treated patients required a lower median dose than other treatments."( Treating patients with documented atherosclerosis to National Cholesterol Education Program-recommended low-density-lipoprotein cholesterol goals with atorvastatin, fluvastatin, lovastatin and simvastatin.
Bakker-Arkema, RG; Black, DM; Brown, AS; Campbell, CF; Guthrie, R; Henley, RW; Koren, M; McLain, R; Woo, W; Yellen, L, 1998
)
1.22
"Atorvastatin treatment also decreased the mRNA for the microsomal triglyceride transfer protein (MTP) by 22% (P < 0.02)."( Differential regulation of apolipoprotein B secretion from HepG2 cells by two HMG-CoA reductase inhibitors, atorvastatin and simvastatin.
Barrett, PH; Huff, MW; Wilcox, LJ, 1999
)
1.24
"Atorvastatin treatment significantly reduced this prolongation to 46%."( Pharmacokinetics and pharmacodynamics of nifedipine in untreated and atorvastatin-treated hyperlipidemic rats.
Eliot, LA; Jamali, F, 1999
)
1.26
"With atorvastatin (10 mg/day) treatment for 4 weeks in 19 type IIa hyperlipidemic patients, total cholesterol level was lowered by 23%, LDL-cholesterol was lowered by 32% and triacylglycerol was lowered by 19% as compared with dietary therapy alone."( Effects of atorvastatin treatment on the oxidatively modified low density lipoprotein in hyperlipidemic patients.
Choy, PC; Dembinski, T; Hatch, G; Kroeger, EA; McMaster, J; Mymin, D; Zhu, Q, 2000
)
1.15
"The atorvastatin treatment significantly improved ACh-stimulated FBF: at highest dose the FBF increased to 14.9+/-1.5 ml.100 ml tissue(-1)."( Effects of atorvastatin and vitamin C on endothelial function of hypercholesterolemic patients.
Candigliota, M; Ceravolo, R; Chello, M; Cloro, C; Maio, R; Mastroroberto, P; Mattioli, PL; Mongiardo, A; Perticone, F; Scozzafava, A, 2000
)
1.18
"Atorvastatin treatment provided significant lowering of serum lipoprotein levels: low-density lipoprotein -53% (p = 0.0001), very low density lipoprotein -43% (p = 0.0001), and triglycerides -35% (p < 0.0001)."( Effect of atorvastatin on hemorheologic-hemostatic parameters and serum fibrinogen levels in hyperlipidemic patients.
Altman, R; Black, DM; Dujovne, CA; Harris, WS; Overhiser, RW, 2000
)
1.43
"Atorvastatin treatment only reduced plasma levels in dyslipidemic rabbits (P < 0.05), which were nevertheless higher than those of controls."( The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits.
Aragoncillo, P; Cachofeiro, V; Díaz, C; Hernández, G; Lahera, V; Maeso, R; Navarro-Cid, J; Ruilope, LM; Vázquez-Pérez, S, 2000
)
1.34
"Atorvastatin treatment reduced plasma lipid levels and lesion size in dyslipidemic animals."( Effect of atorvastatin on endothelium-dependent constrictor factors in dyslipidemic rabbits.
Aragoncillo, P; Cachofeiro, V; Diaz, C; Hernández, G; Lahera, V; Maeso, R; Navarro-Cid, J; Ruilope, LM, 2000
)
1.43
"Atorvastatin treatment prevented vascular and most glomerular changes associated with hypercholesterolaemia even in the presence of very high cholesterol levels."( Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in hypercholesterolaemic rabbits.
Aragoncillo, P; Cachofeiro, V; Cediel, E; de Las Heras, N; Díaz, C; Hernández, G; Lahera, V; Navarro-Cid, J; Ruilope, LM; Sanz-Rosa, D; Vázquez-Pérez, S, 2001
)
2.47
"Atorvastatin treatment downregulated aortic AT(1) receptor mRNA expression to 44+/-12% of control and reduced mRNA expression of the essential NAD(P)H oxidase subunit p22phox to 63+/-7% of control."( HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species.
Ahlbory, K; Bäumer, AT; Böhm, M; Itter, G; Laufs, U; Linz, W; Müller, K; Nickenig, G; Rösen, R; Wassmann, S, 2001
)
1.03
"Atorvastatin treatment increased the further functional activity of EPCs, as assessed by their migratory capacity."( Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease.
Adler, K; Aicher, A; Dimmeler, S; Fichtlscherer, S; Martin, H; Vasa, M; Zeiher, AM, 2001
)
1.03
"Atorvastatin treatment also reduced cellular CE mass, exhibiting both time- and dose-dependency."( Prolonged inhibition of cholesterol synthesis by atorvastatin inhibits apo B-100 and triglyceride secretion from HepG2 cells.
Arai, Y; Funatsu, T; Goto, M; Ida, M; Kakuta, H; Miyata, K; Nishijima, S; Suzuki, K; Tanaka, H; Yasuda, S, 2001
)
1.29
"Atorvastatin treatment generally resulted in small, non significant increases in CTx."( Effects of statins on biomarkers of bone metabolism: a randomised trial.
Farnier, M; Mercuri, M; Stein, EA; Waldstreicher, J, 2001
)
1.03
"Atorvastatin-treated patients were more likely to maintain their target levels from week 6 to week 54."( Achieving and maintaining National Cholesterol Education Program low-density lipoprotein cholesterol goals with five statins.
Andrews, TC; Ballantyne, CM; Hsia, JA; Kramer, JH, 2001
)
1.03
"Atorvastatin treatment was also associated with a greater percent decrease from baseline to week 6 in triglycerides, with a trend toward statistical significance (p = 0.0982)."( Comparison of the efficacy of atorvastatin versus cerivastatin in primary hypercholesterolemia.
Davidson, M; Hunninghake, D; Insull, W; Jones, P; Kafonek, S; Knopp, R; Lohrbauer, L, 2001
)
1.32
"Atorvastatin treatment did not produce consistent changes in the appearance of apoB degradation fragments in plasma."( Atorvastatin treatment beneficially alters the lipoprotein profile and increases low-density lipoprotein particle diameter in patients with combined dyslipidemia and impaired fasting glucose/type 2 diabetes.
Adeli, K; Cheung, RC; Parris, W; Pontrelli, L, 2002
)
2.48
"Atorvastatin treatment reduced total and low-density lipoprotein cholesterol and triglyceride levels by 36 +/- 2% (p < 0.001), 48 +/- 3% (p < 0.001) and 23 +/- 5% (p = 0.003), respectively, and increased high density lipoprotein cholesterol by 7 +/- 3% (p = 0.03). "( Intensive cholesterol reduction lowers blood pressure and large artery stiffness in isolated systolic hypertension.
Baguet, JP; Cameron, JD; Dart, AM; Ferrier, KE; Jennings, GL; Kingwell, BA; Muhlmann, MH, 2002
)
1.76
"Atorvastatin treatment reduced significantly the fasting plasma concentrations of VLDL cholesterol, LDL cholesterol and VLDL triglycerides (median% change) by 29, 44 and 27%, respectively, and increased high density lipoprotein (HDL) cholesterol by 19%, compared with baseline."( Effects of atorvastatin on postprandial plasma lipoproteins in postinfarction patients with combined hyperlipidaemia.
Boquist, S; Danell-Toverud, K; Hamsten, A; Karpe, F, 2002
)
1.43
"Atorvastatin treatment had a significant main effect of decreasing plasma hs-CRP (-0.87 mg/L; 95% confidence interval, -0.10 to -1.60 mg/L; P <0.01) and IL-6 (-70 pg/L; 10 to -140 pg/L; P <0.01), but this was not seen with fish oil."( Effect of atorvastatin and fish oil on plasma high-sensitivity C-reactive protein concentrations in individuals with visceral obesity.
Barrett, PH; Beilin, LJ; Chan, DC; Mori, TA; Watts, GF, 2002
)
1.44
"Treatment with atorvastatin possibly increases the abundance of"( Atorvastatin Inhibits High-Fat Diet-Induced Lipid Metabolism Disorders in Rats by Inhibiting
He, X; Li, H; Ma, X; Wang, S; Yu, H; Yu, W, 2022
)
2.5
"Mice treated with atorvastatin post-infection showed a remarkable decrease in their survival rate."( Atorvastatin increases the production of proinflammatory cytokines and decreases the survival of Escherichia coli-infected mice.
Abdelnoor, AM; Al-Khoury, DK; Hussein, HM; Rahal, EA, 2019
)
2.28
"Co-treatment of atorvastatin + tamoxifen could strongly enhance the expression of pro/apoptotic factors of Bax and cytochrome c in melanoma cells compared to the tamoxifen and atorvastatin groups."( Atorvastatin enhances apoptotic effects of tamoxifen on melanoma cancer cells.
Esfahani, HN; Ghasemi, A; Ghasemi, M; Javanmard, SH; Malek, M; Vaseghi, G, 2019
)
2.3
"Treatment with atorvastatin reduced the number of TUNEL-positive cells."( Atorvastatin Prevents the Neuron Loss in the Hippocampal Dentate Gyrus Region through its Anti-Oxidant and Anti-Apoptotic Activities.
Arani, HZ; Jangholi, E; Karimi, A; Movassaghi, S; Parsa, Y; Sharifi, ZN; Yadollah-Damavandi, S, 2021
)
2.4
"Treatment with Atorvastatin resulted in a reduction in 25OHD concentrations; further, its efficacy in reducing LDL-C concentrations was related to the 25OHD concentrations."( To study impact of treatment with Rosuvastatin versus Atorvastatin on 25 hydroxy Vitamin D concentrations among adult Indian men- a randomized control trial.
Chiplonkar, SA; Khadilkar, AV; Khadilkar, VV; Mughal, ZM; Padidela, R; Patwardhan, VG,
)
0.73
"Pre-treatment with atorvastatin did not protect cholestatic livers from hepatocellular damage after I/R. "( Atorvastatin does not protect against ischemia-reperfusion damage in cholestatic rat livers.
Dekker, AM; Heger, M; van Golen, RF; van Gulik, TM; Verheij, J; Wiggers, JK, 2017
)
2.23
"Treatment with atorvastatin decreased cell viability and increased the mRNA expression levels of Fads1, Fads2 and ELOVL fatty acid elongase 5 (Elovl5) in a dose‑dependent manner."( Atorvastatin increases Fads1, Fads2 and Elovl5 gene expression via the geranylgeranyl pyrophosphate-dependent Rho kinase pathway in 3T3-L1 cells.
Ishihara, N; Nagayama, D; Saiki, A; Suzuki, S; Tanaka, S; Tanaka, T; Tatsuno, I; Watanabe, Y, 2017
)
2.24
"Pretreatment with atorvastatin significantly delayed the onset of arrhythmia and asystole compared with vehicle-treated group (p < .01, p < .001, respectively). "( Involvement of IL-1β and IL-6 in antiarrhythmic properties of atorvastatin in ouabain-induced arrhythmia in rats.
Bakhtiarian, A; Hojati, V; Mousavi, Z; Najjari, M; Nikoui, V; Vaezi, G, 2018
)
1.06
"Treatment with atorvastatin significantly reduced albuminuria, and improved both urine concentrating ability and glomerular filtration rate."( Renal protection by atorvastatin in a murine model of sickle cell nephropathy.
Archer, DR; Ataga, KI; Brown, LA; Chappa, P; Yin, H; Zahr, RS, 2018
)
1.14
"Treatment with atorvastatin was performed via inhalation for 10 min once a day."( Atorvastatin dose-dependently promotes mouse lung repair after emphysema induced by elastase.
Barroso, MV; Cattani-Cavalieri, I; Gitirana, LB; Lanzetti, M; Melo, AC; Quesnot, N; Valença, SS, 2018
)
2.26
"Cotreatment with atorvastatin reduced total cholesterol, rescued LDL receptor protein levels, and normalized serum LDL-C."( FXR activation by obeticholic acid or nonsteroidal agonists induces a human-like lipoprotein cholesterol change in mice with humanized chimeric liver.
Dong, B; Lewis, RD; Liu, J; Liu, X; Papazyan, R; Plummer, EM; Roth, JD; Young, MA, 2018
)
0.81
"Treatment with atorvastatin inhibited the hypertrophy induced by the AV shunt."( Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch.
Cheng, WP; Chua, SK; Lo, HM; Shyu, KG; Wang, BW, 2019
)
1.26
"Treatment with atorvastatin (1 or 10 mg/kg/day) or fluoxetine prevented LPS-induced increase in lipid peroxidation and the reduction of glutathione levels in the hippocampus and prefrontal cortex."( Atorvastatin prevents lipopolysaccharide-induced depressive-like behaviour in mice.
Buss, ZS; Doneda, DL; Ferreira, YS; Fraga-Junior, EB; Lima, E; Lopes, L; Rios-Santos, F; Stupp, IJV; Taniguti, EH; Vandresen-Filho, S; Viola, GG, 2019
)
2.3
"Mice treated with atorvastatin showed a significant reduction in cell influx in response to zymosan, and in the expression of proinflammatory cytokines and chemokines such as interleukin-1α, monocyte chemoattractant protein-1 and prostaglandin E2."( Heme oxygenase-1-Dependent anti-inflammatory effects of atorvastatin in zymosan-injected subcutaneous air pouch in mice.
Badran, B; El-Achkar, GA; Habib, A; Hamade, E; Jaffa, AA; Motterlini, R; Mouawad, CA; Mrad, MF, 2019
)
1.08
"Treatment with atorvastatin (10 and 20 mg/kg) and fluvastatin (10 mg/kg) for 21 days significantly improved the behavioral alterations [increased number of wheel rotations and locomotor activity, and anxiety like behavior (decreased number of entries and time spent in open arm)], oxidative defence and mitochondrial complex enzyme activities in brain."( Protective effect of HMG CoA reductase inhibitors against running wheel activity induced fatigue, anxiety like behavior, oxidative stress and mitochondrial dysfunction in mice.
Kalonia, H; Kumar, A; Kumar, P; Mishra, J; Vashist, A, 2012
)
0.72
"Treatment with atorvastatin alone did not demonstrate an effect significantly different from no treatment (p = 0.0573). "( Impact of methylene blue and atorvastatin combination therapy on the apparition of cerebral malaria in a murine model.
Briolant, S; Desgrouas, C; Dormoi, J; Pradines, B, 2013
)
1.03
"Treatment with atorvastatin resulted in a mean reduction of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), and triglyceride (TG) of 8.7 %, 9.2 %, and 4.1 %, respectively, and a mean increase of high density lipoprotein cholesterol (HDL-C) of 1 %. "( Do MDR1 and SLCO1B1 polymorphisms influence the therapeutic response to atorvastatin? A study on a cohort of Egyptian patients with hypercholesterolemia.
Bakhoum, SW; Issac, MS; Mishriki, AA; Shabana, MF, 2013
)
0.98
"Treatment with atorvastatin was associated with significant decreases in total cholesterol, triglycerides, and LDL-C and an elevation of HDL-C. "( Atorvastatin therapy is not associated with slowing the progression of aortic stenosis: findings of a randomized controlled trial.
Dadjou, Y; Panahi, Y; Pishgoo, B; Rakhshankhah, AS; Sahebkar, A; Taghipour, HR, 2013
)
2.19
"Treatment with atorvastatin enhanced the activity of SOD and prevented from GSH decrement during hypertension."( Effects of atorvastatin on the hypertension-induced oxidative stress in the rat brain.
Amini, R; Jahanbakhsh, Z; Mohammadi, MT; Shekarforoush, S, 2013
)
1.12
"Treatment with atorvastatin (n = 10), but not with fluvastatin (n = 10), resulted in 3-fold higher expression of SLCO2B1 compared with placebo-treated patients (n = 9) (P < 0.05)."( Atorvastatin treatment induces uptake and efflux transporters in human liver.
Bergström, H; Björkhem-Bergman, L; Ekström, L; Eriksson, M; Johansson, M; Parini, P; Rane, A, 2013
)
2.17
"Treatment with atorvastatin increased BRS after 12 months (from 6.46 ± 2.79 ms/mmHg to 8.05 ± 4.28 ms/mmHg, p = 0.03), while no effect was seen with low-fat diet."( Effect of atorvastatin on baroreflex sensitivity in subjects with type 2 diabetes and dyslipidaemia.
Eleftheriadou, I; Grigoropoulou, P; Katsilambros, N; Makrilakis, K; Margeli, A; Papassotiriou, I; Perrea, D; Tentolouris, N; Zoupas, C, 2014
)
1.14
"Treatment with atorvastatin prevented all these changes induced by TWEAK in atherosclerotic lesions."( [Atorvastatin inhibits the atherosclerotic lesion induced by tumor necrosis factor-like weak inducer of apoptosis in apolipoprotein E deficient mice].
Blanco-Colio, LM; Egido, J; Fernández-Laso, V; Martín-Ventura, JL; Sastre, C,
)
1.38
"Treatment with atorvastatin 40 mg/d significantly increased circulating EPC (p = 0.002), FMD (p = 0.001) and reduced TNF-α (p = 0.01) compared to baseline. "( Atorvastatin treatment improves endothelial function through endothelial progenitor cells mobilization in ischemic heart failure patients.
Athanasiou, D; Chrysohoou, C; Hatzis, G; Mazaris, S; Mourouzis, K; Oikonomou, E; Papavassiliou, AG; Siasos, G; Stefanadis, C; Tourikis, P; Tousoulis, D; Zaromitidou, M; Zisimos, K, 2015
)
2.21
"Pretreatment with atorvastatin (0.5, 1, 2.5 μmol/L) dose-dependently inhibited AβO-induced activation of calpain and caspase-3/7 proteases, and effectively diminished the generation of Tau fragments, attenuated synaptic damage and increased neuronal survival."( Atorvastatin prevents Aβ oligomer-induced neurotoxicity in cultured rat hippocampal neurons by inhibiting Tau cleavage.
Jin, Y; Liu, Z; Sui, HJ; Zhang, LL, 2015
)
2.18
"Pretreatment with atorvastatin and the angiotensin-receptor antagonist valsartan significantly attenuated the increase of endoglin and β-MHC induced by infarction."( MicroRNA-208a Increases Myocardial Endoglin Expression and Myocardial Fibrosis in Acute Myocardial Infarction.
Cheng, WP; Lo, HM; Shyu, KG; Wang, BW, 2015
)
0.74
"Treatment with atorvastatin and valsartan can decrease myocardial fibrosis induced by AMI through attenuating miR-208a and endoglin expression."( MicroRNA-208a Increases Myocardial Endoglin Expression and Myocardial Fibrosis in Acute Myocardial Infarction.
Cheng, WP; Lo, HM; Shyu, KG; Wang, BW, 2015
)
0.76
"Treatment with atorvastatin decreased 4βHC and 5α,6α-epoxycholesterol concentrations by 40% and 23%, respectively. "( The effect of atorvastatin treatment on serum oxysterol concentrations and cytochrome P450 3A4 activity.
Hukkanen, J; Hyötyläinen, T; Morin-Papunen, L; Orešič, M; Piltonen, T; Puurunen, J; Ruokonen, A; Savolainen, MJ; Tapanainen, JS, 2015
)
1.13
"Treatment with atorvastatin 20 mg/day, and especially with 40 mg/day, resulted in a decrease in free fatty acid levels."( Dose-dependent effects of atorvastatin on myocardial infarction.
Barbarash, O; Belik, E; Dyleva, Y; Gruzdeva, O; Karetnikova, V; Uchasova, E, 2015
)
1.06
"Treatment with atorvastatin and/or sildenafil was associated with attenuation of 2K1C hypertension-induced increases in these pro-fibrotic factors."( Atorvastatin and sildenafil decrease vascular TGF-β levels and MMP-2 activity and ameliorate arterial remodeling in a model of renovascular hypertension.
Ceron, CS; Gerlach, RF; Guimarães, DA; Martins-Oliveira, A; Rizzi, E; Shiva, S; Tanus-Santos, JE, 2015
)
2.2
"Treatment with atorvastatin along with imipenem reduced the lung bacterial load and pro-inflammatory cytokines (IL-1β and TNFα) level in BALF."( Atorvastatin along with imipenem attenuates acute lung injury in sepsis through decrease in inflammatory mediators and bacterial load.
Addison, MP; Choudhury, S; Darzi, SA; Dash, JR; Kandasamy, K; Kasa, JK; Maruti, BS; Mishra, SK; Parida, S; Singh, TU; Singh, V, 2015
)
2.2
"Treatment with atorvastatin+L-carnitine restored BMD, BMC, and bone strength to near normal levels. "( L-Carnitine, but not coenzyme Q10, enhances the anti-osteoporotic effect of atorvastatin in ovariectomized rats.
Murad, HA, 2016
)
1.02
"Pretreatment with atorvastatin could attenuate the induction of PTEN."( Atorvastatin Inhibits Myocardial Apoptosis in a Swine Model of Coronary Microembolization by Regulating PTEN/PI3K/Akt Signaling Pathway.
Chen, H; Li, L; Liu, T; Su, Q; Wang, J; Wang, XT; Zhou, Y, 2016
)
2.2
"Treatment with atorvastatin 40 mg plus ezetimibe 10 mg achieved significantly greater reductions in LDLc (p < 0.001), total cholesterol (p < 0.001) and non-HDLc (p < 0.001)."( [Utility of treatment with atorvastatin 40 mg plus ezetimibe 10 mg versus atorvastatin 80 mg in reducing the levels of LDL cholesterol in patients with ischaemic stroke or transient ischaemic attack].
Acha-Salazar, O; Larrosa-Campo, D; Novo-Robledo, F; Oterino, A; Palacio, E; Revilla, M; Viadero-Cervera, R, 2016
)
1.07
"Treatment with atorvastatin decreased the number and size of necrotic cores, increased collagen content, and downregulated tumor necrosis factor (TNF)‑α and matrix metalloproteinase (MMP)‑9 mRNA expression, as compared with the methionine group."( Atorvastatin attenuates atherosclerotic plaque destabilization by inhibiting endoplasmic reticulum stress in hyperhomocysteinemic mice.
Chen, Z; Jia, F; Lu, G; Sun, J; Wu, C, 2016
)
2.22
"Treatment with atorvastatin prevented atrial remodeling in a rabbit model of RAP-induced AF. "( Effects of atorvastatin on atrial remodeling in a rabbit model of atrial fibrillation produced by rapid atrial pacing.
Dang, Y; Hao, X; Li, Y; Qi, X; Song, X; Yang, Q, 2016
)
1.18
"Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury."( Cardioprotective effect of atorvastatin alone or in combination with remote ischemic preconditioning on the biochemical changes induced by ischemic/reperfusion injury in a mutual prospective study with a clinical and experimental animal arm.
El Desoky, ES; Fadil, SA; Hassan, AKM; Salem, SY; Taha, AF, 2016
)
1.07
"Pretreatment with atorvastatin significantly improved the recovery of cells viability from OGD/R (p<0.05). "( Atorvastatin Protects Myocardium Against Ischemia-Reperfusion Injury Through Inhibiting miR-199a-5p.
Cui, W; Hu, H; Wang, Y; Zuo, Y, 2016
)
2.21
"Treatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia."( Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia.
Cheng, WP; Chua, SK; Lo, HM; Lu, MJ; Shyu, KG; Wang, BW, 2017
)
2.27
"Treatment with atorvastatin for 4 weeks was able to attenuate ventricular dysfunction, fibrosis, and left ventricular hypertrophy after MI in rats, perhaps in part through effects on collagen metabolism and inflammation. "( Atorvastatin Improves Ventricular Remodeling after Myocardial Infarction by Interfering with Collagen Metabolism.
Carvalho Sposito, A; da Mota Silveira-Filho, L; de Souza Vilarinho, KA; Diógenes de Carvalho, D; Galluce Torina, A; Martins de Oliveira, PP; Pereira do Carmo, HR; Petrucci, O; Reichert, K, 2016
)
2.23
"The treatment with atorvastatin and simvastatin was administered via inhalation (15 min with 1 mg/mL once a day)."( Atorvastatin and Simvastatin Promoted Mouse Lung Repair After Cigarette Smoke-Induced Emphysema.
Barroso, MV; Carvalho, GMC; Cattani-Cavalieri, I; Gitirana, LB; Graca-Reis, A; Kennedy-Feitosa, E; Lanzetti, M; Melo, AC; Pinho-Ribeiro, V; Porto, LC; Valença, SS; Zin, WA, 2017
)
2.22
"Treatment with atorvastatin was associated with increased levels of myocardial tissue protein and lipid oxidative stress biomarkers and a reduced functional endogenous angiogenic response, but improved coronary microvascular reactivity. "( Atorvastatin increases myocardial indices of oxidative stress in a porcine model of hypercholesterolemia and chronic ischemia.
Bianchi, C; Boodhwani, M; Clements, RT; Feng, J; Mieno, S; Ramlawi, B; Sellke, FW; Sodha, NR; Xu, SH,
)
1.93
"Pretreatment with atorvastatin significantly reduced the occurrence of postoperative AF after off-pump CABG."( The effects of atorvastatin on the occurrence of postoperative atrial fibrillation after off-pump coronary artery bypass grafting surgery.
Kim, JH; Kim, JS; Kim, WS; Lee, SH; Lee, YT; On, YK; Shin, DH; Song, YB; Sung, J, 2008
)
1.03
"Treatment with atorvastatin decreased cholesterol content and HMGCoA reductase expression and activity in all four tissues of SHR. "( Tissue-specific effects of atorvastatin on 3-hydroxy-3-methylglutarylcoenzyme A reductase expression and activity in spontaneously hypertensive rats.
Chen, GP; Hu, SJ; Li, L; Lu, X; Yao, L, 2008
)
1
"When treated with atorvastatin, 90% of patients achieved a LDL C<1 g/L, compared to 51% when treated with fibrate (P=0.001)."( Switching fibrate to statin in type 2 diabetic patients: consequences on lipid profile.
Giraudeaux, V; Guillausseau, PJ; Kévorkian, JP; Laloi-Michelin, M; Meas, T; Peynet, J; Virally, M, 2009
)
0.68
"Treatment with atorvastatin (80 mg) over a lifetime horizon resulted in increased costs (Can$16,542 vs. "( Cost-effectiveness of intensive lipid lowering therapy with 80 mg of atorvastatin, versus 10 mg of atorvastatin, for secondary prevention of cardiovascular disease in Canada.
Chu, P; Goetghebeur, M; Merikle, E; Pandya, A; Taylor, DC; Wagner, M, 2009
)
0.94
"Treatment with atorvastatin not only reduced the overproduction of TNF-alpha and IFN-gamma, but also enhanced the expression of Cx43 and Cx45, therefore attenuating myocardial injury and improving the survival rate of viral myocarditis."( Immunomodulation by atorvastatin upregulates expression of gap junction proteins in coxsackievirus B3 (CVB3)-induced myocarditis.
Wu, S; Zhang, A; Zhang, H, 2010
)
1.02
"Pretreatment with atorvastatin 20 mg/qn for 2 to 3 days could significantly reduce procedural inflammatory reaction, attenuate urinary protein and the effect of degrading GFR in coronary angiography patients."( [Atorvastatin attenuated contrast induced renal function damage].
Chen, GL; Su, JZ, 2009
)
1.59
"Treatment with atorvastatin has been shown to increase EPC count in patients with coronary artery disease."( Atorvastatin increases the number of endothelial progenitor cells after cardiac surgery: a randomized control study.
Alfano, G; Casacalenda, A; Chello, M; Covino, E; Genovese, J; Pollari, F; Spadaccio, C, 2010
)
2.14
"Treatment with atorvastatin did not alter the mRNA level of NOX1, a catalytic subunit of NADPH oxidase, but decreased the levels of other NOX isoforms, NOX2 and NOX4, in the ApoE-deficient mice fed a high-fat diet."( NADPH oxidase isoforms and anti-hypertensive effects of atorvastatin demonstrated in two animal models.
Cui, W; Ibi, M; Ikami, K; Iwata, K; Kakehi, T; Katsuyama, M; Matsuno, K; Sasaki, M; Yabe-Nishimura, C; Zhu, K, 2009
)
0.94
"Oral treatment with Atorvastatin dramatically reduced albuminuria and histological changes in the kidneys as compared to vehicle-treated control animals."( Atorvastatin attenuates murine anti-glomerular basement membrane glomerulonephritis.
Eller, K; Eller, P; Mayer, G; Patsch, JR; Reinstadler, SJ; Rosenkranz, AR; Tagwerker, A; Wolf, AM, 2010
)
2.12
"Oral treatment with atorvastatin decreases SNA through antioxidant effects in the RVLM of stroke-prone spontaneously hypertensive rats (SHRSP)."( Sympathoinhibition induced by centrally administered atorvastatin is associated with alteration of NAD(P)H and Mn superoxide dismutase activity in rostral ventrolateral medulla of stroke-prone spontaneously hypertensive rats.
Hirooka, Y; Kishi, T; Konno, S; Sunagawa, K, 2010
)
0.92
"Treatment with atorvastatin induces a significant reduction in fractional sodium excretion compared with placebo, and sodium clearance tends to be reduced."( Acute effects of atorvastatin on glomerular filtration rate, tubular function, blood pressure, and vasoactive hormones in patients with type 2 diabetes.
Bech, JN; Matthesen, SK; Paulsen, L; Pedersen, EB; Starklint, J, 2010
)
1.04
"Treatment with atorvastatin caused an increase in the numbers of intraislet endothelial cells at postnatal day 14 and the percentage of endothelial cells undergoing DNA synthesis, suggesting that angiogenesis had preceded the increase in beta-cell mass."( Effects of atorvastatin on the regeneration of pancreatic {beta}-cells after streptozotocin treatment in the neonatal rodent.
Arany, EJ; Hill, DJ; Marchand, KC, 2010
)
1.09
"Treatment with atorvastatin enhanced the circulating pool of EPCs with fortified migratory and adherent capacity."( Intensive statin therapy: a favorable adjunct to the improvement of small-diameter vascular grafts.
Huang, MQ; Li, XX; Liu, DY; Lu, WM; Wang, SM; Yu, JX; Zhu, YF, 2010
)
0.7
"Treatment with Atorvastatin reduced the histological damage and protected the morphological integrity of the sciatic nerve in streptozotocin induced diabetes."( Statin treatment reduces oxidative stress-associated apoptosis of sciatic nerve in diabetes mellitus.
Barut, T; Ekerbiçer, N; Gürpınar, T; Harzadın, NU; Tarakçı, F; Tuglu, MI, 2011
)
0.71
"Treatment with atorvastatin prior to induction of AMI was associated with a significant reduction of serum CRP, TNF-alpha, plasma PAI-1 and an increase of serum IL-10."( Atorvastatin restores the balance between pro-inflammatory and anti-inflammatory mediators in rats with acute myocardial infarction.
Abdel-Aziz, NA; Abo-Elmatty, DM; Ghattas, MH; Tawfik, MK, 2010
)
2.14
"Treatment with atorvastatin combined with vitamins E and C significantly reduced the odds of NAFLD at the end of follow-up, 70 vs."( Atorvastatin and antioxidants for the treatment of nonalcoholic fatty liver disease: the St Francis Heart Study randomized clinical trial.
Ahmadi, N; Budoff, MJ; Foster, T; Gordon, C; Guerci, AD; Saab, S, 2011
)
2.15
"Treatment with atorvastatin may be beneficial for brain aging by reducing BACE1 protein and omega6:omega3 ratio, however, the potential adverse cognitive outcomes reported here should be more carefully explored given their relevance to human clinical outcomes."( Changes in cognition and amyloid-β processing with long term cholesterol reduction using atorvastatin in aged dogs.
Astarita, G; Barrett, E; Beckett, TL; Dowling, AL; Head, E; Kryscio, RJ; Levine, H; Lin, Y; Morales, J; Murphy, MP; Piomelli, D; Studzinski, CM; Wang, X; Weidner, A, 2010
)
0.92
"When treated with atorvastatin plus ezetimibe, MHR and HR patients had greater attainment of LDL-C, most lipids and lipoproteins and/or hs-CRP targets compared with doubling their atorvastatin dose. "( Attainment of Canadian and European guidelines' lipid targets with atorvastatin plus ezetimibe vs. doubling the dose of atorvastatin.
Bays, H; Conard, S; Hanson, ME; Leiter, LA; Lin, J; Shah, A; Tershakovec, AM, 2010
)
0.93
"Treatment with atorvastatin in type 2 diabetes did not change median total plasma plant sterol concentrations, but LDL cholesterol was reduced most efficaciously in high cholesterol synthesisers with low intestinal cholesterol absorption."( Impact of atorvastatin and omega-3 ethyl esters 90 on plasma plant sterol concentrations and cholesterol synthesis in type 2 diabetes: a randomised placebo controlled factorial trial.
Ceglarek, U; Farmer, A; Holman, RR; Neil, HA; Paul, S; Thiery, J, 2010
)
1.12
"Treatment with atorvastatin before PCI can reduce myocardial damage during the peri-PCI period."( Effect of different loading doses of atorvastatin on percutaneous coronary intervention for acute coronary syndromes.
Gao, Y; Pang, X; Qi, G; Sun, Y; Zhang, H; Zhang, Z; Zhao, W, 2010
)
0.97
"Pretreatment with atorvastatin diminished the increase in TNF-α and IL-1β."( Effect atorvastatin on serum tumor necrosis factor alpha and interleukin-1β following acute pulmonary embolism.
Li, L; Sun, TW; Wang, LX; Zhang, JY, 2011
)
1.15
"Treatment with atorvastatin was associated with a 76% reduction in lathosterol and significant increases in sitosterol (70%)."( Atorvastatin increases intestinal expression of NPC1L1 in hyperlipidemic men.
Benjannet, S; Couture, P; Davis, HR; Hoos, L; Lamarche, B; Lemelin, V; Seidah, NG; Tremblay, AJ, 2011
)
2.15
"Treatment with atorvastatin or simvastatin inhibited AngII-induced Smad activation and related-fibrosis."( Statins inhibit angiotensin II/Smad pathway and related vascular fibrosis, by a TGF-β-independent process.
Civantos, E; Egido, J; Lavoz, C; Mezzano, S; Ortiz, A; Rayego-Mateos, S; Rodrigues Díez, R; Rodrigues-Díez, R; Rodríguez-Vita, J; Ruiz-Ortega, M, 2010
)
0.7
"Treatment with atorvastatin (ATO) or dietary control has been demonstrated to benefit patients with non-alcoholic fatty liver disease (NAFLD) and hyperlipidemia. "( Comparison of dietary control and atorvastatin on high fat diet induced hepatic steatosis and hyperlipidemia in rats.
Ji, G; Jiang, Z; Leng, L; Liu, P; Zhao, X, 2011
)
1
"Pretreatment with atorvastatin of septic animals completely restored NE-induced contractions to levels similar to those of sham-operated controls and significantly increased survival time and mean arterial pressure."( Atorvastatin prevents vascular hyporeactivity to norepinephrine in sepsis: role of nitric oxide and α₁-adrenoceptor mRNA expression.
Ahanger, AA; Choudhury, S; Kandasamy, K; Mishra, SK; More, AS; Parida, S; Prawez, S; Singh, TU, 2011
)
2.14
"The treatment of atorvastatin improved the pathologic changes in the aging rats significantly, especially in the first group."( [The effects of atorvastatin on aging kidney].
Cheng, QL; Ye, P; Zhao, JH, 2011
)
1.04
"Treatment with atorvastatin (20mg/kg qd) significantly downregulated the expression of RAGE and MCP-1."( Atorvastatin exerts its anti-atherosclerotic effects by targeting the receptor for advanced glycation end products.
Feng, B; Hu, JF; Liu, F; Wang, H; Xu, L; Xue, J; Yan, X, 2011
)
2.15
"Treatment with atorvastatin limited LDL oxidation significantly (LDL thiobarbituric acid reactive substances 2.19 nmol/mg protein, LDL-conjugated diene 222 μmol/mg protein)."( Effect of atorvastatin therapy on oxidant-antioxidant status and atherosclerotic plaque formation.
Nart, D; Onat, T; Sezer, ED; Sozmen, EY, 2011
)
1.11
"Treatment with atorvastatin or pitavastatin ameliorated the activation of MMP-9."( Progressive neurovascular disturbances in the cerebral cortex of Alzheimer's disease-model mice: protection by atorvastatin and pitavastatin.
Abe, K; Ikeda, Y; Kozuki, M; Kurata, T; Miyazaki, K; Morimoto, N; Ohta, Y, 2011
)
0.92
"Treatment with atorvastatin and irbesartan, initiated on day 3 after acute ischemic stroke, did not appear to substantially modify infarct growth."( A randomized placebo controlled trial of early treatment of acute ischemic stroke with atorvastatin and irbesartan.
Beer, C; Blacker, D; Bynevelt, M; Hankey, GJ; Puddey, IB, 2012
)
0.95
"Treatment with atorvastatin was followed by a 35.6% decline in LDL cholesterol. "( Effect of low-dose atorvastatin on plasma concentrations of adipokines in patients with metabolic syndrome.
Adamczak, M; Chudek, J; Czerwienska, B; Szotowska, M; Wiecek, A, 2012
)
1.06
"Treatment with atorvastatin and carboplatin reduced the growth of xenograft A549 tumors in nude mice and enhanced the survival rate compared with carboplatin alone."( Atorvastatin sensitizes human non-small cell lung carcinomas to carboplatin via suppression of AKT activation and upregulation of TIMP-1.
An, Y; Chen, J; Hou, J; Lan, T; Li, X; Liu, J; Pan, Y; Tie, L; Zhang, J, 2012
)
2.16
"Treatment with atorvastatin significantly restored 40.9% of the widened intima and even down-regulated the ratio of intima/media by 55.5%."( Effects of atorvastatin on expression of ICAM-1 in atherosclerotic rabbits.
Cao, H; Cui, W; Du, B; Lin, S; Liu, Y; Qin, L; Xu, G, 2013
)
1.12
"Treatment with atorvastatin reversed both PUMA expression and apoptosis induced by mechanical stress in cardiomyocytes."( Regulation of PUMA induced by mechanical stress in rat cardiomyocytes.
Cheng, WP; Shyu, KG; Wang, BW; Wu, GJ, 2012
)
0.72
"Treatment with atorvastatin was well tolerated and no serious side effects were reported."( Long term efficacy and safety of atorvastatin in the treatment of severe type III and combined dyslipidaemia.
de Beer, F; Havekes, LM; Kastelein, JJ; Lansberg, PJ; Prins, MH; Smelt, AH; Trip, MD; van Dam, M; Zwart, M, 2002
)
0.94
"Treatment with atorvastatin is well tolerated and cost-effective."( Treatment with atorvastatin to the National Cholesterol Educational Program goal versus 'usual' care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study.
Athyros, VG; Athyrou, VV; Basayannis, EO; Demitriadis, DS; Kontopoulos, AG; Mercouris, BR; Papageorgiou, AA; Symeonidis, AN, 2002
)
1.01
"Treatment with atorvastatin reduced serum total cholesterol concentration from 310+/-29 mg/dl in a basal situation to 203+/-34 mg/dl ( P<0.001) at the end of the treatment and low-density lipoprotein (LDL) cholesterol concentration from 225+/-30 mg/dl to 126+/-30 mg/dl ( P<0.001), respectively."( The effect of atorvastatin on erythrocyte membranes and serum lipids in patients with type-2 hypercholesterolemia.
Broncel, M; Chojnowska-Jezierska, J; Franiak, I; Klikczynska, K; Koter, M, 2002
)
1.01
"Treatment with atorvastatin conferred stroke protection by 40% after filamentous occlusion of the middle cerebral artery followed by reperfusion. "( Withdrawal of statin treatment abrogates stroke protection in mice.
Böhm, M; Dirnagl, U; Endres, M; Gertz, K; Laufs, U; Lindauer, U; Nickenig, G, 2003
)
0.67
"Treatment with atorvastatin for 12 months was effective and safe for pediatric subjects with known familial hypercholesterolemia or severe hypercholesterolemia."( Efficacy and safety of atorvastatin in children and adolescents with familial hypercholesterolemia or severe hyperlipidemia: a multicenter, randomized, placebo-controlled trial.
Marais, AD; McCrindle, BW; Ose, L, 2003
)
0.98
"When treated with atorvastatin, patients with peripheral arterial disease may experience improvement in symptoms to complement the anticipated reduction in cardiovascular events reported in other studies of statins."( Cholesterol reduction with atorvastatin improves walking distance in patients with peripheral arterial disease.
Creager, MA; Hiatt, WR; Mohler, ER, 2003
)
0.94
"Cotreatment with atorvastatin (0.1-10 microM) dose dependently inhibited VEGF-induced ACE upregulation."( Atorvastatin completely inhibits VEGF-induced ACE upregulation in human endothelial cells.
Fyhrquist, F; Nyman, T; Saijonmaa, O; Stewen, P, 2004
)
2.09
"Treatment with atorvastatin and fenofibrate reduced serum cholesterol by 30 % and 21 % (p = 0.046) (p-values for differences between treatment groups), triglycerides by 32 % and 45 %, LDL cholesterol by 28 % and 16 %, and increased HDL cholesterol by 3 % and 6 %, respectively. "( Qualitative effect of fenofibrate and quantitative effect of atorvastatin on LDL profile in combined hyperlipidemia with dense LDL.
Baumstark, MW; Friedrich, I; Hauck, P; Hoffmann, MM; März, W; Nickell, HH; Schmitz, H; Weltzien, P; Wieland, H; Winkler, K, 2004
)
0.92
"Pretreatment with atorvastatin 40 mg/d for 7 days significantly reduces procedural myocardial injury in elective coronary intervention. "( Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study.
Di Sciascio, G; Nusca, A; Pasceri, V; Patti, G; Pristipino, C; Richichi, G, 2004
)
0.98
"Treatment with atorvastatin may be a potential strategy to reduce oxLDL and inhibit monocyte migration to inflamed tissue, thus attenuating the inflammatory response."( Circulating monocytes and plasma inflammatory biomarkers in active Crohn's disease: elevated oxidized low-density lipoprotein and the anti-inflammatory effect of atorvastatin.
Grip, O; Janciauskiene, S; Lindgren, S, 2004
)
0.86
"Treatment with atorvastatin resulted in significant decreases of serum t-chol, TG, and LDL-chol levels but not serum HDL-chol and VLDL-chol."( Effects of atorvastatin on serum lipids, lipoproteins, and hemostasis.
Abe, Y; Kushiya, F; Nakasaki, T; Nobori, T; Noda, M; Ooi, K; Sakaguchi, A; Sakurai, Y; Shiku, H; Tsukada, T; Wada, H, 2005
)
1.06
"Treatment with atorvastatin reduced total cholesterol, triglycerides (TG), low-density lipoprotein (LDL) cholesterol, apolipoprotein B (apoB) and levels of oxidised LDL (oxLDL) with 30-43%. "( Effects of atorvastatin and vitamin E on lipoproteins and oxidative stress in dialysis patients: a randomised-controlled trial.
Bilo, HJ; Diepeveen, SH; Dikkeschei, LD; Kolsters, G; Offerman, JJ; Stalenhoef, AF; Van Der Palen, J; Van Tits, LJ; Verhoeven, GW, 2005
)
1.07
"Treatment with atorvastatin is effective in lowering plasma total cholesterol, TG, LDL, apoB and oxLDL in a population of stable dialysis patients and might therefore be an effective tool in improving the poor cardiovascular outcome in these patients. "( Effects of atorvastatin and vitamin E on lipoproteins and oxidative stress in dialysis patients: a randomised-controlled trial.
Bilo, HJ; Diepeveen, SH; Dikkeschei, LD; Kolsters, G; Offerman, JJ; Stalenhoef, AF; Van Der Palen, J; Van Tits, LJ; Verhoeven, GW, 2005
)
1.07
"Treatment with atorvastatin for one and three days significantly reduced infarct size versus controls (38.9 +/- 3.1% vs. "( Failure to protect the myocardium against ischemia/reperfusion injury after chronic atorvastatin treatment is recaptured by acute atorvastatin treatment: a potential role for phosphatase and tensin homolog deleted on chromosome ten?
Mensah, K; Mocanu, MM; Yellon, DM, 2005
)
0.91
"Treatment with atorvastatin was not associated with significant changes in lipoprotein profile as determined by nuclear magnetic resonance (NMR) spectroscopy."( Effects of atorvastatin on low-density lipoprotein cholesterol phenotype and C-reactive protein levels in patients undergoing long-term dialysis.
Chin, H; Denu-Ciocca, CJ; Dornbrook-Lavender, KA; Hogan, SL; Joy, MS; Pieper, JA, 2005
)
1.06
"Treatment with atorvastatin did not affect LDL particle size but was associated with a sizable, yet nonsignificant, reduction in CRP concentrations. "( Effects of atorvastatin on low-density lipoprotein cholesterol phenotype and C-reactive protein levels in patients undergoing long-term dialysis.
Chin, H; Denu-Ciocca, CJ; Dornbrook-Lavender, KA; Hogan, SL; Joy, MS; Pieper, JA, 2005
)
1.07
"Oral treatment with atorvastatin (1-10 mg/kg) from days 10 to 15 after arthritis induction caused inhibition of the increase in paw volume."( Anti-inflammatory and analgesic effects of atorvastatin in a rat model of adjuvant-induced arthritis.
Barsante, MM; Castro, MS; Pinho, V; Roffê, E; Souza, DG; Tafuri, WL; Teixeira, MM; Yokoro, CM, 2005
)
0.91
"Treatment with atorvastatin resulted in a dose-dependent improvement in whole body insulin sensitivity in both lean and fatty rats, with an approximately two-fold increase in glucose infusion rate and glucose disposal (Rd) in ATORVA_50 versus CONT (p<0.01)."( Atorvastatin induces insulin sensitization in Zucker lean and fatty rats.
Fantus, IG; Lewis, GF; Stavar, L; Szeto, L; Uffelman, K; Wang, CH; Wong, V, 2006
)
2.12
"Treatment with atorvastatin achieved a statistically significant decrease in lipid profile. "( Effect of low doses of atorvastatin on adiponectin, glucose homeostasis, and clinical inflammatory markers in kidney transplant recipients.
Bayés, B; Bonet, J; Granada, ML; Lauzurica, R; Llopis, MA; Navarro, M; Pastor, MC; Romero, R, 2005
)
0.99
"Treatment with atorvastatin resulted in an 80% reduction of lesion area as compared with the untreated group (P < 0.001)."( Anti-atherosclerotic effect of amlodipine, alone and in combination with atorvastatin, in APOE*3-Leiden/hCRP transgenic mice.
de Maat, M; Emeis, J; Havekes, L; Jukema, W; Maas, A; Offerman, E; Princen, H; Szalai, A; Trion, A; van der Laarse, A, 2006
)
0.91
"Treatment with atorvastatin decreased mean low-density lipoprotein cholesterol by 43% and resulted in an improvement with sildenafil in domain score of 7.8 (P = 0.036); an effect was apparent by 6 weeks."( Can atorvastatin improve the response to sildenafil in men with erectile dysfunction not initially responsive to sildenafil? Hypothesis and pilot trial results.
Bradbury, D; Herrmann, HC; Kimmel, SE; Levine, LA; Macaluso, J; Mohler, ER; Schwartz, S; Walsh, M, 2006
)
1.23
"Treatment with atorvastatin improved sexual function and the response to oral sildenafil in men who did not initially respond to treatment with sildenafil. "( Can atorvastatin improve the response to sildenafil in men with erectile dysfunction not initially responsive to sildenafil? Hypothesis and pilot trial results.
Bradbury, D; Herrmann, HC; Kimmel, SE; Levine, LA; Macaluso, J; Mohler, ER; Schwartz, S; Walsh, M, 2006
)
1.24
"Pretreatment with atorvastatin significantly reduces cytokine release and neutrophil adhesion to the venous endothelium in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass."( Effects of atorvastatin on systemic inflammatory response after coronary bypass surgery.
Agrò, F; Candura, D; Carassiti, M; Chello, M; Covino, E; Di Sciascio, G; Mastrobuoni, S; Patti, G, 2006
)
1.06
"Treatment with atorvastatin inhibited the changes above in a dose-dependent manner, but no change was found in treated with DMSO."( [Atorvastatin upregulates the expression of PPAR alpha/gamma and inhibits the hypertrophy of cardiac myocytes in vitro].
Liu, YX; Sheng, L; Ye, P, 2005
)
1.58
"Treatment with atorvastatin inhibited adipocyte maturation, SLC2A4 and C/EBPalpha expressions and insulin action in 3T3-L1 cells. "( Effects of statins on the adipocyte maturation and expression of glucose transporter 4 (SLC2A4): implications in glycaemic control.
Ishibashi, S; Kusaka, I; Matsuoka, H; Nagasaka, S; Nakata, M; Yada, T, 2006
)
0.69
"Treatment with atorvastatin 80 mg significantly reduced the rate of hospitalization for HF (2.3% vs. "( Intensive statin therapy and the risk of hospitalization for heart failure after an acute coronary syndrome in the PROVE IT-TIMI 22 study.
Braunwald, E; Cannon, CP; Jarolim, P; McCabe, CH; Morrow, DA; Ray, KK; Sabatine, MS; Scirica, BM; Shui, A, 2006
)
0.69
"Treatment with atorvastatin decreased plasma APOA5, APOC3, APOE and triglycerides."( Plasma apolipoprotein A5 and triglycerides in type 2 diabetes.
Dallinga-Thie, GM; Hattori, H; Jansen, H; Sijbrands, EJ; van Tol, A; van Vark-van der Zee, LC, 2006
)
0.67
"Treatment with atorvastatin for 4 weeks markedly decreased the slow (s)-migrating TRL subfraction and both fast- and slow-migrating low-density lipoprotein (LDL) subfractions, but did not affect the fast (f)-migrating TRL subfraction in this patient. "( Effects of atorvastatin and apoA-I/phosphatidylcholine discs on triglyceride-rich lipoprotein subfractions as characterized by capillary isotachophoresis.
Arishima, H; Katafuchi, R; Matsunaga, A; Rye, KA; Saku, K; Zhang, B, 2006
)
1.08
"Treatment with atorvastatin for 3 days dose-dependently reduced hypernociception induced by lipopolysaccharide (LPS) or that following antigen challenge in sensitized animals. "( Atorvastatin inhibits inflammatory hypernociception.
Cunha, FQ; Cunha, TM; Ferreira, SH; Parada, CA; Poole, S; Santodomingo-Garzón, T; Valério, DA; Verri, WA, 2006
)
2.13
"Treatment with atorvastatin 40 mg/d, initiated 7 days before surgery, significantly reduces the incidence of postoperative AF after elective cardiac surgery with cardiopulmonary bypass and shortens hospital stay. "( Randomized trial of atorvastatin for reduction of postoperative atrial fibrillation in patients undergoing cardiac surgery: results of the ARMYDA-3 (Atorvastatin for Reduction of MYocardial Dysrhythmia After cardiac surgery) study.
Candura, D; Chello, M; Covino, E; D'Ambrosio, A; Di Sciascio, G; Pasceri, V; Patti, G, 2006
)
1.01
"Treatment with atorvastatin significantly reduced neointimal formation at day 14 (14 days after injury) and NADPH oxidase-dependent superoxide production at day 2 in ovariectomy, but not in intact and castrated males."( Gender difference of atorvastatin's vasoprotective effect in balloon-injured rat carotid arteries.
Hayashi, T; Kimura, S; Kitaura, Y; Kurumazuka, D; Matsumoto, N; Matsumura, Y; Mori, T; Nakano, D; Shirakawa, H, 2006
)
0.99
"Pretreatment with atorvastatin was associated with 49% higher nitrite/nitrate levels compared with controls (p < .05)."( Protective effects of atorvastatin in rat models of acute pulmonary embolism: involvement of matrix metalloproteinase-9.
Alves-Filho, JC; Cunha, FQ; Figueiredo-Lopes, L; Gerlach, RF; Semprini, MC; Souza-Costa, DC; Tanus-Santos, JE, 2007
)
0.98
"Pretreatment with atorvastatin caused remarkable decrease in both oxidative stress and neutrophil accumulation."( Attenuation of contractile dysfunction by atorvastatin after intestinal ischemia reperfusion injury in rats.
Cetin, A; Igdem, AA; Ozacmak, ID; Ozacmak, VH; Sayan, H, 2007
)
0.93
"Treatment with atorvastatin leads to an improvement in endothelial function and a reduction in inflammatory markers in patients with stable CAD. "( Effect of atorvastatin on peripheral endothelial function and systemic inflammatory markers in patients with stable coronary artery disease.
Alber, HF; Dichtl, W; Dörler, J; Frick, M; Pachinger, O; Stocker, EM; Süssenbacher, A; Weidinger, F, 2007
)
1.1
"Treatment with atorvastatin in the dyslipidaemic patients to lower LDL-C, was also accompanied by a reduction of proteinuria in this group (P < 0.001)."( Dyslipidaemia as predictor of progressive renal failure and the impact of treatment with atorvastatin.
Arisz, L; Kastelein, JJ; Koopman, MG; Ozsoy, RC; van der Steeg, WA, 2007
)
0.9
"Treatment with atorvastatin led to a significant reduction in levels of PAI-1 and hs-CRP; however, the elevation of vWF level was observed."( Effect of atorvastatin on endothelial function and inflammation in long-duration type 1 diabetic patients without coronary heart disease and arterial hypertension.
Cieslik, G; Fedak, D; Galicka-Latala, D; Konduracka, E; Naskalski, J; Piwowarska, W; Rostoff, P; Sieradzki, J, 2008
)
1.09
"Treatment with atorvastatin abrogated the risk associated with elevated markers of inflammation in this study, a finding that provides a novel rationale for the use of statins in acute coronary syndromes."( Inflammation, statin therapy, and risk of stroke after an acute coronary syndrome in the MIRACL study.
Ganz, P; Kinlay, S; Libby, P; Olsson, AG; Rifai, N; Schwartz, GG; Szarek, M; Waters, DD, 2008
)
0.69
"Treatment with atorvastatin to the NCEP LDL-C goal compared with 'usual care' significantly reduced CHD morbidity and mortality in both men and women. "( Effects of statin treatment in men and women with stable coronary heart disease: a subgroup analysis of the GREACE Study.
Anagnostis, P; Athyros, VG; Kakafika, AI; Karagiannis, A; Koumaras, C; Mikhailidis, DP; Pagourelias, E; Papageorgiou, AA; Paraskevas, KI; Tziomalos, K, 2008
)
0.7
"Treatment with atorvastatin significantly improved post-MI LV function (fractional shortening, +120%; dP/dt(max), +147%; and LV end-diastolic pressure, -27%)."( Atorvastatin enhances interleukin-10 levels and improves cardiac function in rats after acute myocardial infarction.
Arnold, M; Daniel, WG; Garlichs, CD; Petzi, S; Raaz, D; Seybold, K; Stumpf, C; Wasmeier, G; Yilmaz, A, 2009
)
2.14
"Pretreatment with atorvastatin (ATV) reduces infarct size (IS) and increases myocardial expression of phosphorylated endothelial nitric oxide synthase (p-eNOS), inducible NOS (iNOS), and cyclooxygenase-2 (COX2) in the rat. "( The role of eNOS, iNOS, and NF-kappaB in upregulation and activation of cyclooxygenase-2 and infarct size reduction by atorvastatin.
Birnbaum, Y; Lin, Y; Martinez, JD; Perez-Polo, RJ; Uretsky, BF; Ye, Y, 2008
)
0.89
"Treatment with atorvastatin significantly reduced low density lipoprotein cholesterol levels, and was associated with a 36% reduction in ischemic events and a significant delay in time to first ischemic event."( Medical therapy versus revascularization: the atorvastatin versus revascularization treatment AVERT trial.
Waters, DD, 2000
)
0.9
"Treatment with atorvastatin achieved the target in 83% of patients, while simvastatin (or simvastatin plus cholestyramine) achieved the target in 66% of the patients (P<0.005)."( Achievement of target plasma cholesterol levels in hypercholesterolaemic patients being treated in general practice.
Barter, PJ; O'Brien, RC, 2000
)
0.65
"The treatment with atorvastatin induced significant reduction of microalbuminuria and fibrinogen levels (p<0.01)."( Atorvastatin for the management of Type 2 diabetic patients with dyslipidaemia. A mid-term (9 months) treatment experience.
Cernigoi, AM; Merni, M; Tortul, C; Velussi, M, 1999
)
2.07
"Treatment with atorvastatin at an early stage may have an impact on the progression of atherosclerosis in these high risk patients."( Atorvastatin but not L-arginine improves endothelial function in type I diabetes mellitus: a double-blind study.
Deanfield, JE; Donald, AE; Mullen, MJ; Thomson, H; Thorne, S; Wright, D, 2000
)
2.09
"Pretreatment with atorvastatin inhibited angiotensin II-induced ROS production."( Inhibition of geranylgeranylation reduces angiotensin II-mediated free radical production in vascular smooth muscle cells: involvement of angiotensin AT1 receptor expression and Rac1 GTPase.
Bäumer, AT; Böhm, M; Konkol, C; Laufs, U; Müller, K; Nickenig, G; Sauer, H; Wassmann, S, 2001
)
0.63
"Treatment with atorvastatin reduced red cell aggregation (P<0.01), whole blood viscosity (P<0.01), plasma viscosity (P<0.01) and platelet aggregation (P<0.05), but caused a slight increase in plasma fibrinogen (by 5%; P<0.01)."( Atorvastatin improves blood rheology in patients with familial hypercholesterolemia (FH) on long-term LDL apheresis treatment.
Alt, E; Banyai, M; Banyai, S; Derfler, K; Falger, J; Jansen, M; Koppensteiner, R, 2001
)
2.09
"Treatment with atorvastatin reduced vascular mRNA expression of p22phox and nox1 and increased aortic catalase expression."( Cellular antioxidant effects of atorvastatin in vitro and in vivo.
Ahlbory, K; Bäumer, AT; Böhm, M; Konkol, C; Laufs, U; Linz, W; Müller, K; Nickenig, G; Wassmann, S, 2002
)
0.94
"Treatment with atorvastatin resulted in a statistically significant reduction in total cholesterol (41%), LDL cholesterol (55%), triglycerides (TG) (32%), and apoB (40%)."( Atorvastatin treatment beneficially alters the lipoprotein profile and increases low-density lipoprotein particle diameter in patients with combined dyslipidemia and impaired fasting glucose/type 2 diabetes.
Adeli, K; Cheung, RC; Parris, W; Pontrelli, L, 2002
)
2.1

Toxicity

In the short-term trials, the incidence of all-causality adverse events (AEs) and serious AEs (SAEs) was similar to or lower than that observed with other statins or placebo. discontinuations due to treatment-related AEs/SAEs were infrequent. Atorvastatin use in very young children with KD is safe but should be closely monitored.

ExcerptReferenceRelevance
"To assess the lipid-lowering effect of atorvastatin (a new 3-hydroxy-3-methylglutaryl coenzyme A [HMG-CoA] reductase inhibitor) on levels of serum triglycerides and other lipoprotein fractions in patients with primary hypertriglyceridemia, determine if atorvastatin causes a redistribution of triglycerides in various lipoprotein fractions, and assess its safety by reporting adverse events and clinical laboratory measurements."( Efficacy and safety of a new HMG-CoA reductase inhibitor, atorvastatin, in patients with hypertriglyceridemia.
Bakker-Arkema, RG; Black, DM; Brown, WV; Davidson, MH; Davignon, J; Goldstein, RJ; Isaacsohn, JL; Keilson, LM; Miller, VT; Shurzinske, LJ; Weiss, SR, 1996
)
0.81
" The most common adverse events reported after atorvastatin-headache and nausea-occurred as frequently after placebo."( Multiple-dose pharmacokinetics, pharmacodynamics, and safety of atorvastatin, an inhibitor of HMG-CoA reductase, in healthy subjects.
Cilla, DD; Gibson, DM; Posvar, EL; Sedman, AJ; Whitfield, LR, 1996
)
0.79
" Safety was assessed by recording adverse events and measuring clinical laboratory parameters."( Efficacy and safety of atorvastatin compared to pravastatin in patients with hypercholesterolemia.
Bertolini, S; Bon, GB; Campbell, LM; Egros, F; Farnier, M; Fayyad, R; Langan, J; Mahla, G; Nawrocki, JW; Pauciullo, P; Sirtori, C, 1997
)
0.61
" Safety profiles as determined by change from baseline in laboratory evaluations, ophthalmologic parameters, and reporting of adverse events were similar for the 2 reductase inhibitors."( Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. Atorvastatin Study Group I.
Bakker-Arkema, R; Black, D; Davidson, M; Fayyad, R; McKenney, J; Schrott, H; Stein, E, 1997
)
0.56
" No serious adverse events were considered associated with treatment."( A multicenter, double-blind, one-year study comparing safety and efficacy of atorvastatin versus simvastatin in patients with hypercholesterolemia.
Best, J; Black, D; Bracs, P; d'Emden, M; Dart, A; Hamilton-Craig, I; Jerums, G; Nicholson, G; Sullivan, D; Tallis, G; West, M, 1997
)
0.53
"Transaminase and creatine phosphokinase levels and adverse events were recorded."( An overview of the clinical safety profile of atorvastatin (lipitor), a new HMG-CoA reductase inhibitor.
Bakker-Arkema, RG; Black, DM; Nawrocki, JW, 1998
)
0.56
"Atorvastatin was well tolerated; fewer than 2% of the atorvastatin-treated patients withdrew due to drug-attributable adverse events."( An overview of the clinical safety profile of atorvastatin (lipitor), a new HMG-CoA reductase inhibitor.
Bakker-Arkema, RG; Black, DM; Nawrocki, JW, 1998
)
2
" Atorvastatin was well-tolerated, and no serious or medically important adverse events were observed."( Efficacy and safety of a new cholesterol synthesis inhibitor, atorvastatin, in comparison with simvastatin and pravastatin, in subjects with hypercholesterolemia.
Black, DM; Mahla, G; Muller, D; Pentrup, A; Wolffenbuttel, BH, 1998
)
1.45
"We conclude that atorvastatin is a safe and very efficacious cholesterol-lowering agent, which also possesses significant triglyceride-lowering properties."( Efficacy and safety of a new cholesterol synthesis inhibitor, atorvastatin, in comparison with simvastatin and pravastatin, in subjects with hypercholesterolemia.
Black, DM; Mahla, G; Muller, D; Pentrup, A; Wolffenbuttel, BH, 1998
)
0.88
" Adverse event rates were statistically equivalent (p<0."( Safety of low-density lipoprotein cholestrol reduction with atorvastatin versus simvastatin in a coronary heart disease population (the TARGET TANGIBLE trial).
Klein, G; März, W; Neiss, A; Wehling, M; Wollschläger, H, 1999
)
0.55
" The frequency of treatment-associated adverse events (AEs) in the atorvastatin LDL-C < or =80 mg/dl (2."( Safety profile of atorvastatin-treated patients with low LDL-cholesterol levels.
Bakker-Arkema, RG; Black, DM; Nawrocki, JW, 2000
)
0.88
" Only one patient withdrew due to a possible drug-related adverse event."( Efficacy and safety of atorvastatin in hyperlipidemic, type 2 diabetic patients. A 34-week, multicenter, open-label study.
Aguilar-Salinas, CA; Alvarado Vega, A; Angélica Gómez-Díaz, R; Eduardo Romero-Nava, L; Gómez-Pérez, FJ; Guillén, LE; Gulías-Herrero, A; Meaney, E; Mendoza Pérez, E; Moguel, R; Novoa, G; Posadas-Romero, C; Salinas-Orozco, S; Vázquez-Chávez, C, 2000
)
0.62
" Fewer than 6% of patients in either treatment group experienced drug-attributable adverse events, which were mostly mild to moderate in nature."( Comparison of efficacy and safety of atorvastatin (10mg) with simvastatin (10mg) at six weeks. ASSET Investigators.
Goldner, D; Insull, W; Kafonek, S; Zieve, F, 2001
)
0.58
" Withdrawal rates related to adverse events are low (< or =3%)."( Safety of HMG-CoA reductase inhibitors: focus on atorvastatin.
Bernini, F; Paoletti, R; Poli, A, 2001
)
0.57
"Data from 185 patients were retrospectively evaluated for adverse events, duration of exposure (person-days), and the mean atorvastatin dose exposure."( Safety and efficacy of atorvastatin in heart transplant recipients.
Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002
)
0.83
"Data from 185 patients were retrospectively evaluated for adverse events, duration of exposure (person-days), and the mean atorvastatin dose exposure."( Safety and efficacy of atorvastatin in heart transplant recipients.
Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002
)
0.83
"Atorvastatin, when used at moderate doses and with close biochemical and clinical monitoring, appears to be safe and is effective in aggressively lowering LDL in heart transplant recipients when treatment with other statins has failed to achieve LDL goals."( Safety and efficacy of atorvastatin in heart transplant recipients.
Aaronson, KD; Baliga, RR; Cody, RJ; Dyke, DB; Koelling, TM; Lake, KD; Pagani, FD; Patel, DN, 2002
)
2.07
" There were no significant adverse events."( A randomized, double-blind, placebo-controlled, 8-week study to evaluate the efficacy and safety of once daily atorvastatin (10 mg) in patients with elevated LDL-cholesterol.
Ting, CT; Wang, KY, 2001
)
0.52
" Ezetimibe was safe and well tolerated."( Efficacy and safety of ezetimibe coadministered with atorvastatin or simvastatin in patients with homozygous familial hypercholesterolemia.
Bruckert, E; Gagné, C; Gaudet, D, 2002
)
0.56
"In hypercholesterolemia patients, atorvastatin 10 mg every other day is safe and effective in lowering TC, TG, with LDL-c and a slight increase in HDL-c."( Efficacy and safety of atorvastatin 10 mg every other day in hypercholesterolemia.
Chatlaong, B; Laothavorn, P; Nasawadi, C; Piamsomboon, C; Pongsiri, K; Saguanwong, S; Tanprasert, P, 2002
)
0.9
" Data obtained by monitoring lipid profiles, adverse events, and laboratory tests during the 16 weeks of study were used to assess the efficacy and safety of both treatments."( Comparing the efficacy and safety of atorvastatin and simvastatin in Asians with elevated low-density lipoprotein-cholesterol--a multinational, multicenter, double-blind study.
Hin, AT; Lee, YT; Suyono, S; Sy, R; Tanphaichitr, V; Wu, CC, 2002
)
0.59
" No deaths occurred in the study population and the incidence of treatment-emergent adverse events was the same in the two groups (28%)."( Comparing the efficacy and safety of atorvastatin and simvastatin in Asians with elevated low-density lipoprotein-cholesterol--a multinational, multicenter, double-blind study.
Hin, AT; Lee, YT; Suyono, S; Sy, R; Tanphaichitr, V; Wu, CC, 2002
)
0.59
" 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors are efficacious and safe and can lower the incidence of graft coronary artery disease after heart transplantation in adults."( Efficacy and safety of atorvastatin after pediatric heart transplantation.
Bernstein, D; Chin, C; Gamberg, P; Luikart, H; Miller, J, 2002
)
0.63
" Data included medication use, clinic visits, adverse events, LDL-C and other laboratory measures."( An economic analysis of the Atorvastatin Comparative Cholesterol Efficacy and Safety Study (ACCESS).
McBurney, CR; Smith, DG, 2003
)
0.61
"Treatment with atorvastatin for 12 months was effective and safe for pediatric subjects with known familial hypercholesterolemia or severe hypercholesterolemia."( Efficacy and safety of atorvastatin in children and adolescents with familial hypercholesterolemia or severe hyperlipidemia: a multicenter, randomized, placebo-controlled trial.
Marais, AD; McCrindle, BW; Ose, L, 2003
)
0.98
" A retrospective analysis was conducted and included treatment-associated adverse events, serious adverse events, and musculoskeletal and hepatic adverse events."( Safety of atorvastatin derived from analysis of 44 completed trials in 9,416 patients.
Newman, CB; Palmer, G; Silbershatz, H; Szarek, M, 2003
)
0.72
"The estimated likelihood of the side effect occurring."( Comparison of two methods of presenting risk information to patients about the side effects of medicines.
Berry, DC; Knapp, P; Raynor, DK, 2004
)
0.32
"The mean likelihood estimate given for the constipation side effect was 34."( Comparison of two methods of presenting risk information to patients about the side effects of medicines.
Berry, DC; Knapp, P; Raynor, DK, 2004
)
0.32
" The use of verbal descriptors to improve the level of information about side effect risk leads to overestimation of the level of harm and may lead patients to make inappropriate decisions about whether or not they take the medicine."( Comparison of two methods of presenting risk information to patients about the side effects of medicines.
Berry, DC; Knapp, P; Raynor, DK, 2004
)
0.32
" Safety evaluations included adverse event (AE) reports and laboratory test results."( Long-term safety and tolerability profile of ezetimibe and atorvastatin coadministration therapy in patients with primary hypercholesterolaemia.
Alizadeh, J; Ballantyne, CM; Lipka, LJ; Sager, PT; Strony, J; Suresh, R; Veltri, EP, 2004
)
0.57
" Therefore, both placebo- and statin-treated patients with familial hypercholesterolemia are best treated with high-dose atorvastatin, a therapeutic regimen that induces atherosclerosis regression and is safe and well tolerated over a 4-year period."( Long-term safety and efficacy of high-dose atorvastatin treatment in patients with familial hypercholesterolemia.
Kastelein, JJ; Smilde, TJ; Stalenhoef, AF; Trip, MD; van Wissen, S, 2005
)
0.8
"Atorvastatin initiated at doses of 10, 20, 40, and 80 mg is effective and safe for the treatment of patients with dyslipidemia."( Comparison of the efficacy and safety of atorvastatin initiated at different starting doses in patients with dyslipidemia.
Downey, J; Jones, PH; Karalis, DG; McKenney, JM, 2005
)
2.04
"The authors reviewed adverse events (AEs) reported to the United States Food and Drug Administration to determine the percentage of statin-associated AE reports with concurrent amiodarone use for simvastatin, atorvastatin, and pravastatin."( Adverse events with concomitant amiodarone and statin therapy.
Alsheikh-Ali, AA; Karas, RH, 2005
)
0.52
" On safety assessment, there was no adverse effect with the use of Chunghyul-dan in hepatic or renal toxicity."( Efficacy and safety of chunghyul-dan (qingwie-dan) in patients with hypercholesterolemia.
Cho, KH; Jung, WS; Kang, HS; Moon, SK; Park, SU, 2005
)
0.33
" The clinical benefits of preventing vascular events, myocardial infarction, stroke, and need for revascularization outweigh the low rates of adverse events associated with high-dose statin therapy in high- and intermediate-risk patients."( Safety of high-dose atorvastatin therapy.
Waters, DD, 2005
)
0.65
"Compared with patients treated with an accepted LDL goal (80 to 100 mg/dl), there was no adverse effect on safety with lower achieved LDL levels, and apparent improved clinical efficacy."( Can low-density lipoprotein be too low? The safety and efficacy of achieving very low low-density lipoprotein with intensive statin therapy: a PROVE IT-TIMI 22 substudy.
Braunwald, E; Cannon, CP; Morrow, DA; Pfeffer, MA; Ray, KK; Wiviott, SD, 2005
)
0.33
"Although the medication caused no severe adverse events, we recommend caution when using atorvastatin for severe CKD patients until further evidence of its safety and efficacy is verified."( Safety and efficacy of atorvastatin in patients with severe renal dysfunction.
Brännström, M; Bucht, B; Crougneau, V; Dimeny, E; Ekspong, A; Granroth, B; Gröntoft, KC; Hadimeri, H; Holmberg, B; Ingman, B; Isaksson, B; Johansson, G; Lindberger, K; Lundberg, L; Mikaelsson, L; Olausson, E; Persson, B; Stegmayr, BG; Welin, D; Wikdahl, AM, 2005
)
0.86
" The study compared the safety of atorvastatin 10 mg (n = 7,258), atorvastatin 80 mg (n = 4,798), and placebo (n = 2,180) and included analyses on treatment-associated adverse events; nonserious and serious adverse events related to the musculoskeletal, hepatic, and renal systems; the incidence of elevations of creatine kinase >10 times the upper limit of normal (ULN); and hepatic transaminases >3 times ULN."( Comparative safety of atorvastatin 80 mg versus 10 mg derived from analysis of 49 completed trials in 14,236 patients.
Gibson, E; Luo, D; Newman, C; Szarek, M; Tsai, J, 2006
)
0.93
" Adverse effects have been related to the use of certain statins, high statin dosages, comorbidities, and coadministration with cyclosporine."( Safety of statins when response is carefully monitored: a study of 336 heart recipients.
Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005
)
0.33
"Between April 1991 and December 2003, we retrospectively evaluated 336 heart transplant patients (including 55 women) with regard to the occurrence of possible adverse effects of statins (rhabdomyolysis, myalgia, hepatotoxicity, high CK without muscle symptoms, and others)."( Safety of statins when response is carefully monitored: a study of 336 heart recipients.
Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005
)
0.33
"Possible adverse events of statins were suffered by 60 patients, all of them men."( Safety of statins when response is carefully monitored: a study of 336 heart recipients.
Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005
)
0.33
"Some 10% to 20% of HT patients appear to suffer adverse side effects of initial statin therapy."( Safety of statins when response is carefully monitored: a study of 336 heart recipients.
Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005
)
0.33
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" Following coadministered treatment, the adverse events reported were similar to either agent alone."( Efficacy and safety of coadministered amlodipine and atorvastatin in patients with hypertension and dyslipidemia: results of the AVALON trial.
Bakris, GL; Ferrera, D; Flack, JM; Houston, MC; Lee, E; Messerli, FH; Neutel, JM; Petrella, RJ; Sun, W, 2006
)
0.58
" However, clinical data consistently support the view that adverse events are uncommon even when intensive therapy is used to reach aggressive low-density lipoprotein cholesterol goals."( How safe is aggressive statin therapy?
Guthrie, RM, 2006
)
0.33
" Pravastatin was not toxic up to 1 mmol/l."( Toxicity of statins on rat skeletal muscle mitochondria.
Brecht, K; Kaufmann, P; Krähenbühl, S; Török, M; Waldhauser, KM; Zahno, A, 2006
)
0.33
" The incidence of all-causality and treatment-related adverse events was similar across placebo and torcetrapib treatment groups with no evidence of a dose-related response."( Efficacy and safety of torcetrapib, a novel cholesteryl ester transfer protein inhibitor, in individuals with below-average high-density lipoprotein cholesterol levels on a background of atorvastatin.
Davidson, MH; McKenney, JM; Revkin, JH; Shear, CL, 2006
)
0.52
" The serums lipid profiles and adverse effects were assessed in all the patients before treatment, and 4 and 8 weeks after treatment."( [Efficacy and safety of extended-release niacin alone or with atorvastatin for lipid profile modification].
Duan, J; Li, XP; Tan, MY; Xu, ZM; Zhang, DQ; Zhao, SP, 2006
)
0.57
" (3) Adverse effect, such as flushing (15."( [Efficacy and safety of extended-release niacin alone or with atorvastatin for lipid profile modification].
Duan, J; Li, XP; Tan, MY; Xu, ZM; Zhang, DQ; Zhao, SP, 2006
)
0.57
" Combined statin with niacin may produce a more global and effective improvement in lipid blood levels than monotherapy and is generally safe and well tolerable."( [Efficacy and safety of extended-release niacin alone or with atorvastatin for lipid profile modification].
Duan, J; Li, XP; Tan, MY; Xu, ZM; Zhang, DQ; Zhao, SP, 2006
)
0.57
" Current drug labeling warns of an increased risk of adverse events with statin and niacin combinations."( Safety of lovastatin/extended release niacin compared with lovastatin alone, atorvastatin alone, pravastatin alone, and simvastatin alone (from the United States Food and Drug Administration adverse event reporting system).
Alsheikh-Ali, AA; Karas, RH, 2007
)
0.57
" Nineteen patients reported at least one adverse event during the study; the majority were mild in severity and considered unrelated to atorvastatin."( Efficacy and safety of atorvastatin in South Asian patients with dyslipidemia: an open label noncomparative pilot study.
Gupta, S; Hughes, EA; Lie, F; Patel, JV, 2005
)
0.84
" Clinical chemistry profiles and the incidence of adverse events were similar in both groups."( Efficacy and safety of ezetimibe co-administered with atorvastatin in untreated patients with primary hypercholesterolaemia and coronary heart disease.
Blagden, MD; Chipperfield, R, 2007
)
0.59
" There were no clinically important differences in adverse event rates across quintiles."( Safety and efficacy of Atorvastatin-induced very low-density lipoprotein cholesterol levels in Patients with coronary heart disease (a post hoc analysis of the treating to new targets [TNT] study).
Greten, H; Grundy, SM; Kastelein, JJ; Kostis, JB; LaRosa, JC, 2007
)
0.65
" Comparison of adverse events profile in both the groups shows that more number of patients from atorvastatin alone group (n = 14, 28%) had adverse reactions than the number of patients from the combination group (n = 4, 8%; p < 005)."( Randomised study to compare the efficacy and safety of isapgol plus atorvastatin versus atorvastatin alone in subjects with hypercholesterolaemia.
Jayaram, S; Langade, DG; Mane, PR; Prasad, HB; Sovani, VB, 2007
)
0.79
" Atorvastatin is generally well tolerated across the range of therapeutic dosages, with the exception of a slightly higher rate of liver enzyme elevations with atorvastatin 80 mg/day which does not appear to confer an increased risk of clinically important adverse events."( Atorvastatin: a safety and tolerability profile.
Arca, M, 2007
)
2.69
" Overall, coadministered atorvastatin and amlodipine was well tolerated and without adverse pharmacodynamic interaction; combination treatment did not affect the low-density lipoprotein cholesterol-lowering efficacy and safety of atorvastatin, or the systolic blood pressure-lowering efficacy and safety of amlodipine."( A randomized, placebo-controlled trial to evaluate the efficacy, safety, and pharmacodynamic interaction of coadministered amlodipine and atorvastatin in 1660 patients with concomitant hypertension and dyslipidemia: the respond trial.
Dykstra, G; Gillen, D; Harvey, P; Herfert, O; Jukema, JW; Preston, RA; Sun, F, 2007
)
0.85
" AC, the world's best selling drug is associated with poor oral bioavailability and serious adverse effects like rhabdomyolysis on chronic administration."( Oral nanoparticulate atorvastatin calcium is more efficient and safe in comparison to Lipicure in treating hyperlipidemia.
Ankola, DD; Chandraiah, G; Kumar, MN; Meena, AK; Rao, PR; Ratnam, DV, 2008
)
0.66
" Both drugs were well-tolerated and the incidence and type of adverse events were similar in each group."( A randomised study comparing the efficacy and safety of rosuvastatin with atorvastatin for achieving lipid goals in clinical practice in Asian patients at high risk of cardiovascular disease (DISCOVERY-Asia study).
Lee, YT; Ro, YM; Sim, KH; Sriratanasathavorn, C; Tomlinson, B; Zhu, JR, 2007
)
0.57
" The percentages of patients experiencing treatment-associated adverse events (AEs), serious AEs and discontinuations due to AEs in the atorvastatin (n=1,428) and placebo (n=1,410) groups were 23."( The safety and tolerability of atorvastatin 10 mg in the Collaborative Atorvastatin Diabetes Study (CARDS).
Auster, S; Betteridge, DJ; Colhoun, HM; Demicco, DA; Durrington, PN; Fuller, JH; Hitman, GA; Neil, HA; Newman, CB; Szarek, M, 2008
)
0.83
" Among the adverse effects observed for this lipid-lowering agent, clinical cases of cutaneous adverse reactions have been reported and associated with photosensitivity disorders."( A mechanistic study on the phototoxicity of atorvastatin: singlet oxygen generation by a phenanthrene-like photoproduct.
Iesce, MI; Lhiaubet-Vallet, V; Miranda, MA; Montanaro, S; Previtera, L, 2009
)
0.61
" CPK surveillance is recommended because of a slight continued risk of adverse effects."( The efficacy and safety of ezetimibe for treatment of dyslipidemia after heart transplantation.
Castro-Beiras, A; Crespo-Leiro, MG; Flores, X; Franco, R; Grille, Z; Marzoa, R; Mosquera, V; Naya, C; Paniagua, MJ; Rodriguez, JA, 2008
)
0.35
" The incidences of clinical and laboratory adverse experiences were generally similar between groups."( Efficacy and safety of ezetimibe added on to atorvastatin (20 mg) versus uptitration of atorvastatin (to 40 mg) in hypercholesterolemic patients at moderately high risk for coronary heart disease.
Bays, HE; Bird, SR; Conard, SE; Leiter, LA; Lowe, RS; Rubino, J; Tershakovec, AM; Tomassini, JE, 2008
)
0.61
" Safety and tolerability profiles and incidence of liver and muscle adverse experiences were generally similar between groups."( Efficacy and safety of ezetimibe added on to atorvastatin (40 mg) compared with uptitration of atorvastatin (to 80 mg) in hypercholesterolemic patients at high risk of coronary heart disease.
Bays, H; Bird, S; Conard, S; Hanson, ME; Leiter, LA; Rubino, J; Tershakovec, AM; Tomassini, JE, 2008
)
0.61
" Using data from the Rating Atherosclerotic Disease Change by Imaging with a New CETP Inhibitor [corrected] (RADIANCE) trials, which assessed the impact of torcetrapib on carotid intima-media thickness (cIMT), we sought to explore potential mechanisms underlying this adverse outcome."( Cholesteryl ester transfer protein inhibitor torcetrapib and off-target toxicity: a pooled analysis of the rating atherosclerotic disease change by imaging with a new CETP inhibitor (RADIANCE) trials.
Basart, DC; Bots, ML; Evans, GW; Grobbee, DE; Kastelein, JJ; Sijbrands, EJ; Stalenhoef, AF; Stroes, ES; van Leuven, SI; Vergeer, M; Visseren, FL, 2008
)
0.35
"These analyses support mineralocorticoid-mediated off-target toxicity in patients receiving torcetrapib as a contributing factor to an adverse outcome."( Cholesteryl ester transfer protein inhibitor torcetrapib and off-target toxicity: a pooled analysis of the rating atherosclerotic disease change by imaging with a new CETP inhibitor (RADIANCE) trials.
Basart, DC; Bots, ML; Evans, GW; Grobbee, DE; Kastelein, JJ; Sijbrands, EJ; Stalenhoef, AF; Stroes, ES; van Leuven, SI; Vergeer, M; Visseren, FL, 2008
)
0.35
" Anacetrapib was well tolerated, and the incidence of adverse events was similar for placebo and all active treatment groups."( Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib as monotherapy and coadministered with atorvastatin in dyslipidemic patients.
Bloomfield, D; Carlson, GL; Littlejohn, TW; McKenney, JM; Mitchel, Y; Pasternak, RC; Sapre, A; Sisk, CM; Tribble, D, 2009
)
0.56
" Rates of any reported serious adverse event were higher in older patients, but did not differ between the 2 statin groups."( Comparison of efficacy and safety of atorvastatin (80 mg) to simvastatin (20 to 40 mg) in patients aged <65 versus >or=65 years with coronary heart disease (from the Incremental DEcrease through Aggressive Lipid Lowering [IDEAL] study).
Cater, NB; Faergeman, O; Holme, I; Kastelein, JJ; Larsen, ML; Lindahl, C; Olsson, AG; Pedersen, TR; Szarek, M; Tikkanen, MJ, 2009
)
0.63
" No major adverse events or clinical myopathy occurred in either groups."( Efficacy and safety of combination of extended release niacin and atorvastatin in patients with low levels of high density lipoprotein cholesterol.
Ajit Kumar, VK; Harikrishnan, S; Krishnamoorthy, KM; Nair, K; Rajeev, E; Sivasankaran, S; Tharakan, JA; Titus, T,
)
0.37
" The most common adverse events were peripheral oedema (11."( International open-label studies to assess the efficacy and safety of single-pill amlodipine/atorvastatin in attaining blood pressure and lipid targets recommended by country-specific guidelines: the JEWEL programme.
Bauer, B; da Silva, PM; Feldman, RD; Genest, J; Gensini, G; Harvey, P; Jenssen, TG; John Mancini, GB; Manolis, AJ; Richard Hobbs, FD, 2009
)
0.57
" The incidence of liver, muscle, and gastrointestinal-, hepatitis- and allergic reaction/rash-related adverse events were low and generally similar to those in previous studies of ezetimibe/simvastatin and/or atorvastatin."( Lipid-altering efficacy and safety of ezetimibe/simvastatin versus atorvastatin in patients with hypercholesterolemia and the metabolic syndrome (from the VYMET study).
Adewale, AJ; Ballantyne, CM; Grundy, SM; Hsueh, WA; Parving, HH; Polis, AB; Robinson, JG; Rosen, JB; Tershakovec, AM; Tomassini, JE, 2009
)
0.78
" The results of the present study indicate that intensive statin therapy with high-dose (80 mg/day) atorvastatin is more efficacious than and as safe as 20 mg/day atorvastatin when administered to elderly patients during early hospitalization for UA."( Efficacy and safety of atorvastatin during early hospitalization in elderly patients with unstable angina.
Ge, ZM; Geng, J; Kang, WQ; Wang, W; Zhang, Y; Zhao, Z, 2009
)
0.88
" This study aimed to investigate the effects of combined application of extended-release niacin and atorvastatin on lipid profile modification and the risks of adverse events in patients with coronary artery disease."( Combined use of extended-release niacin and atorvastatin: safety and effects on lipid modification.
Chen, SY; Li, YG; Li, YH; Sang, ZC; Wang, F; Wang, HP; Zhou, Q, 2009
)
0.83
" Plasma lipid profile, glucose, and adverse events were assessed at the hospitalization, and 6 and 12 months after treatment."( Combined use of extended-release niacin and atorvastatin: safety and effects on lipid modification.
Chen, SY; Li, YG; Li, YH; Sang, ZC; Wang, F; Wang, HP; Zhou, Q, 2009
)
0.61
" Combination therapy with niacin ER and atorvastatin was well tolerated and safe in patients with coronary artery disease."( Combined use of extended-release niacin and atorvastatin: safety and effects on lipid modification.
Chen, SY; Li, YG; Li, YH; Sang, ZC; Wang, F; Wang, HP; Zhou, Q, 2009
)
0.88
"Lipid-lowering drugs have been associated with severe adverse effects on skeletal muscle, including rhabdomyolysis."( Statins and fibrate target ClC-1 - from side effects to CLC pharmacology.
Zdebik, AA, 2009
)
0.35
" We defined a composite adverse event (CAE) as discontinuation for any side effect, myalgia, or CK >3x upper limit of normal during follow-up."( The SLCO1B1*5 genetic variant is associated with statin-induced side effects.
Ali, S; Ginsburg, GS; Reed, CR; Salisbury, BA; Shah, SH; Spasojevic, I; Voora, D, 2009
)
0.35
" There were no drug-related serious adverse events."( A multicenter study in Malaysia to determine the efficacy and safety of a generic atorvastatin.
Leekha, S; Lena, YL; Ong, LM; Punithavathi, N, 2009
)
0.58
"Mean percentage changes in lipid parameters, percentages of patients achieving optimal serum lipid/apolipoprotein levels, and incidence of adverse events."( Efficacy and safety of fenofibric acid co-administered with low- or moderate-dose statin in patients with mixed dyslipidemia and type 2 diabetes mellitus: results of a pooled subgroup analysis from three randomized, controlled, double-blind trials.
Cusi, K; Davidson, MH; Jones, PH; Kelly, MT; Setze, CM; Sleep, DJ; Stolzenbach, JC; Thakker, K, 2010
)
0.36
" Incidence of adverse events was generally similar among treatments."( Efficacy and safety of fenofibric acid co-administered with low- or moderate-dose statin in patients with mixed dyslipidemia and type 2 diabetes mellitus: results of a pooled subgroup analysis from three randomized, controlled, double-blind trials.
Cusi, K; Davidson, MH; Jones, PH; Kelly, MT; Setze, CM; Sleep, DJ; Stolzenbach, JC; Thakker, K, 2010
)
0.36
" 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
)
0.6
" Most importantly, Zhibitai is safe to use."( Evaluation of the lipid lowering ability, anti-inflammatory effects and clinical safety of intensive therapy with Zhibitai, a Chinese traditional medicine.
Chen, C; Huang, QY; Liu, L; Shu, J; Wasti, B; Xu, DY; Zhao, SP, 2010
)
0.36
" We retrieved data from randomized controlled trials, meta-analyses, post-marketing studies, reports to regulatory bodies and case reports of rare adverse events."( Atorvastatin: safety and tolerability.
Athyros, VG; Karagiannis, A; Mikhailidis, DP; Tziomalos, K, 2010
)
1.8
"The reader will gain insight into the incidence, severity, prevention and management of the major adverse effects of atorvastatin (i."( Atorvastatin: safety and tolerability.
Athyros, VG; Karagiannis, A; Mikhailidis, DP; Tziomalos, K, 2010
)
2.01
" Simvastatin was more toxic than atorvastatin and the lactone form more toxic than the acid form."( Cytotoxicity of atorvastatin and simvastatin on primary rainbow trout (Oncorhynchus mykiss) hepatocytes.
Asberg, A; Ellesat, KS; Hylland, K; Thomas, KV; Tollefsen, KE, 2010
)
0.99
" Most importantly, it is safe to use Zhibitai clinically."( [A comparative study of the efficacy and safety Zhibitai and atorvastatin].
Huang, QY; Liu, L; Shu, J; Xu, DY; Zhao, SP, 2010
)
0.6
" Overall, adverse events were similar in the 2 treatment groups."( Efficacy and safety of fenofibric acid in combination with atorvastatin and ezetimibe in patients with mixed dyslipidemia.
Goldberg, AC; Jones, PH; Kelly, MT; Knapp, HR; Setze, CM; Sleep, DJ; Stolzenbach, JC, 2010
)
0.6
" It is concluded that MEGX test widens opportunities for personalization and safe pharmacotherapy."( [Individual pharmacotherapy safety in the assessment of cytochrome P-450 3A4 (CYP3A4) isoenzyme activity].
Kukes, IV; Paukov, SV; Ruvinov, IuV; Sivkov, AS, 2010
)
0.36
" We studied the toxic effects of high glucose (50 mmol/L and 83 mmol/L) and its reversal by atorvastatin (0."( Atorvastatin reduces high glucose toxicity in rat peritoneal mesothelial cells.
Carrión, B; Ceña, V; Gómez-Roldán, C; Monteagudo, S; Pérez-Carrión, MD; Pérez-Martínez, FC; Pérez-Martínez, J,
)
1.79
" These toxic effects could be reversed by atorvastatin."( Atorvastatin reduces high glucose toxicity in rat peritoneal mesothelial cells.
Carrión, B; Ceña, V; Gómez-Roldán, C; Monteagudo, S; Pérez-Carrión, MD; Pérez-Martínez, FC; Pérez-Martínez, J,
)
1.84
" 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
)
0.62
" LDL-C target was maintained in 81% and 69% of patients at week 8 and 52 respectively without drug related serious adverse events."( Long-term efficacy and safety of a generic atorvastatin in usual clinical care setting.
Leekha, S; Lena, YL; Mahanim, O; Ong, LM; Punithavathi, N, 2011
)
0.63
" Adverse experiences (AEs) typically associated with niacin (flushing, pruritus, increased glucose, increased uric acid) were more common with ERN/LRPT+SIMVA, and hepatic-related laboratory AEs were more common with ATORVA."( Lipid-altering efficacy and safety profile of co-administered extended release niacin/laropiprant and simvastatin versus atorvastatin in patients with mixed hyperlipidemia.
Blomqvist, P; Chen, E; Chen, F; Davidson, M; Maccubbin, D; McKenney, JM; Sirah, W; Sisk, CM; Yan, L, 2013
)
0.6
" The purpose of this case report is to illustrate the clinical and radiological findings of focal myositis as a side effect of statins and fibrates in 2 patients with forearm involvement."( [Focal myositis as a side effect of antilipidemics - 2 patients with involvement of the forearm].
Hohendorff, B; Mühldorfer-Fodor, M; Prommersberger, KJ; Schmitt, R; Wagner, M, 2012
)
0.38
" One patient on SAR236553 experienced a serious adverse event of leukocytoclastic vasculitis."( Safety and efficacy of a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 serine protease, SAR236553/REGN727, in patients with primary hypercholesterolemia receiving ongoing stable atorvastatin therapy.
Ferrand, AC; Hanotin, C; Kereiakes, DJ; Koren, MJ; McKenney, JM; Stein, EA, 2012
)
0.57
" Polymorphisms within these genes are increasingly being implicated in disease and may also trigger adverse drug reactions."( Polymorphisms in the mitochondrial ribosome recycling factor EF-G2mt/MEF2 compromise cell respiratory function and increase atorvastatin toxicity.
Andrews, S; Bellon, J; Callegari, S; de Barros Lopes, MA; Gregory, PA; McKinnon, RA; Sykes, MJ, 2012
)
0.59
" These adverse events (AEs) can have serious impact, and form a significant barrier to therapy adherence."( A survey of the FDA's AERS database regarding muscle and tendon adverse events linked to the statin drug class.
Dimbil, M; Golomb, BA; Hoffman, KB; Kraus, C, 2012
)
0.38
" These results indicate that muscle cells may be particularly susceptible to a statin-induced suppression of essential antioxidant selenoproteins, which provides an explanation for the disposition of these drugs to evoke adverse muscular side-effects."( Prooxidative toxicity and selenoprotein suppression by cerivastatin in muscle cells.
Fuhrmeister, J; Kromer, A; Moosmann, B; Tews, M, 2012
)
0.38
" However, its clinical uses are limited due to its dose-dependent adverse effects particularly cardiac and testicular toxicities."( Protective role of atorvastatin against doxorubicin-induced cardiotoxicity and testicular toxicity in mice.
Jena, GB; Kushwaha, S; Ramanjaneyulu, SV; Trivedi, PP; Vikram, A, 2013
)
0.72
" Hepatotoxicity is one of the serious adverse effects of statins, and the exact mechanism of hepatotoxicity is not yet clear."( Mechanisms of the statins cytotoxicity in freshly isolated rat hepatocytes.
Abdoli, N; Azarmi, Y; Eghbal, MA; Heidari, R, 2013
)
0.39
" Atorvastatin use in very young children with KD is safe but should be closely monitored."( Atorvastatin safety in Kawasaki disease patients with coronary artery aneurysms.
Chahal, N; Manlhiot, C; McCrindle, BW; Niedra, E; Yeung, RS, 2014
)
2.76
" ANA was well tolerated, and dose-dependent relationships for adverse events were not observed across treatment groups."( Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib in Japanese patients with dyslipidemia.
Kikuchi, M; McCrary Sisk, C; Nakagomi, M; Numaguchi, H; Shirakawa, M; Surks, HK; Tamura, S; Teramoto, T, 2013
)
0.39
"Statins reduce cardiovascular morbidity and mortality but their administration is associated with a broad array of potential adverse effects."( Safety and tolerability of the use of atorvastatin 40 mg in common daily practice in short-term observation in 3,227 patients.
Dabrowski, M; Wiliński, J, 2013
)
0.66
"6% of all study participants) interrupted atorvastatin therapy due to drug-related adverse effects, which comprised mainly increased liver transaminases (0."( Safety and tolerability of the use of atorvastatin 40 mg in common daily practice in short-term observation in 3,227 patients.
Dabrowski, M; Wiliński, J, 2013
)
0.93
"Atorvastatin in daily dose of 40 mg is a safe and well tolerable medication for the treatment for dyslipidemic disorders in patients of different clinic profile and cardiovascular risk groups in common medical practice."( Safety and tolerability of the use of atorvastatin 40 mg in common daily practice in short-term observation in 3,227 patients.
Dabrowski, M; Wiliński, J, 2013
)
2.1
" Reports of adverse experiences were generally similar among groups."( Efficacy and safety of ezetimibe added to atorvastatin versus atorvastatin uptitration or switching to rosuvastatin in patients with primary hypercholesterolemia.
Averna, M; Bays, HE; Brudi, P; De Pellegrin, A; Farnier, M; Giezek, H; Lee, R; Lowe, RS; Majul, C; Muller-Wieland, D; Triscari, J, 2013
)
0.65
" Saroglitazar was found to be safe and well tolerated by patients."( A multicenter, prospective, randomized, double-blind study to evaluate the safety and efficacy of Saroglitazar 2 and 4 mg compared with placebo in type 2 diabetes mellitus patients having hypertriglyceridemia not controlled with atorvastatin therapy (PRES
Bhansali, A; Jani, RH; Jariwala, G; Jha, P; Joshi, S; Mukhopadhyay, S; Pai, V, 2014
)
0.59
"Saroglitazar appeared to be an effective and safe therapeutic option for improving hypertriglyceridemia in patients with T2DM."( A multicenter, prospective, randomized, double-blind study to evaluate the safety and efficacy of Saroglitazar 2 and 4 mg compared with placebo in type 2 diabetes mellitus patients having hypertriglyceridemia not controlled with atorvastatin therapy (PRES
Bhansali, A; Jani, RH; Jariwala, G; Jha, P; Joshi, S; Mukhopadhyay, S; Pai, V, 2014
)
0.59
"The NR1I3 rs2307424 genotype distribution was different between subjects with and without adverse drug reactions."( Influence of PPARA, RXRA, NR1I2 and NR1I3 gene polymorphisms on the lipid-lowering efficacy and safety of statin therapy.
Almeida, S; Bruxel, EM; Ferreira, ME; Fiegenbaum, M; Hutz, MH; Lima, LO; Pires, RC; Van der Sand, CR; Van der Sand, LC, 2013
)
0.39
" Mean percentage change from baseline in triglycerides (TGLs), non-high-density lipoprotein cholesterol (non-HDL-C), HDL-C, low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and TC-HDL ratio, incidence of adverse effects, and cost-effectiveness were compared in both the groups."( Efficacy and safety of alternate day therapy with atorvastatin and fenofibrate combination in mixed dyslipidemia: a randomized controlled trial.
David, DC; Haribalaji, N; Harivenkatesh, N; Sudhakar, MK, 2014
)
0.66
" Incidence of adverse events was reasonably less in alternate day therapy group."( Efficacy and safety of alternate day therapy with atorvastatin and fenofibrate combination in mixed dyslipidemia: a randomized controlled trial.
David, DC; Haribalaji, N; Harivenkatesh, N; Sudhakar, MK, 2014
)
0.66
"Alternate day therapy with atorvastatin-fenofibrate combination is an effective and safe alternative to daily therapy in mixed dyslipidemia."( Efficacy and safety of alternate day therapy with atorvastatin and fenofibrate combination in mixed dyslipidemia: a randomized controlled trial.
David, DC; Haribalaji, N; Harivenkatesh, N; Sudhakar, MK, 2014
)
0.95
" The serum levels of total cholesterol (TC), TG, low-density lipoprotein cholesterol (LDL-C) and HDL-C were assessed before and after 6 and 12 weeks treatment, side effects and adverse events were recorded."( [The lipid-regulating effect and safety of combined statin and bezafibrate therapy in acute coronary syndrome patients complicating with dyslipidemia].
Gong, HR; Huang, WY; Li, XP; Zhao, SP, 2013
)
0.39
"The combined statin and bezafibrate treatment is safe and could increase the ratios of reaching target lipid levels in ACS patients complicating with increased TG and (or) decreased HDL-C."( [The lipid-regulating effect and safety of combined statin and bezafibrate therapy in acute coronary syndrome patients complicating with dyslipidemia].
Gong, HR; Huang, WY; Li, XP; Zhao, SP, 2013
)
0.39
"Statins are potent cholesterol-lowering drugs that can have serious adverse effects on the muscles and liver."( Efficiency of hepatocyte pretreatment with coenzyme Q10 against statin toxicity.
Abdoli, N; Azarmi, Y; Eghbal, MA, 2014
)
0.4
" The proportion of patients experiencing any adverse event was similar among the three treatment groups."( Efficacy and safety of intensive statin therapy in Chinese patients with atherosclerotic intracranial arterial stenosis: a single-center, randomized, single-blind, parallel-group study with one-year follow-up.
Cao, Z; Feng, Y; Gao, P; Lu, Z; Wang, P; Wang, S; Zhang, G; Zhou, P, 2014
)
0.4
"In conclusion, long-term use of IAT appears to be a safe and effective treatment at least for Chinese patients with AICAS."( Efficacy and safety of intensive statin therapy in Chinese patients with atherosclerotic intracranial arterial stenosis: a single-center, randomized, single-blind, parallel-group study with one-year follow-up.
Cao, Z; Feng, Y; Gao, P; Lu, Z; Wang, P; Wang, S; Zhang, G; Zhou, P, 2014
)
0.4
" Evacetrapib monotherapy or in combination with atorvastatin was not likely to be associated with any significant change in blood pressure and did not have any adverse effects on mineralocorticoid or glucocorticoid measures."( Efficacy, safety, tolerability, and pharmacokinetic profile of evacetrapib administered as monotherapy or in combination with atorvastatin in Japanese patients with dyslipidemia.
Krueger, KA; Morisaki, Y; Ruotolo, G; Takeuchi, M; Teramoto, T, 2014
)
0.86
" We evaluated the risk of renal-associated serious adverse events (SAEs) using statins versus placebo trials and the high-dose versus low-dose statin trials that were available to us."( Statin and the risk of renal-related serious adverse events: Analysis from the IDEAL, TNT, CARDS, ASPEN, SPARCL, and other placebo-controlled trials.
Bangalore, S; DeMicco, DA; Fayyad, R; Hovingh, GK; Laskey, R; Vogt, L; Waters, DD, 2014
)
0.4
" However, the primary adverse effect limiting their use is myopathy."( Red yeast rice and coenzyme Q10 as safe alternatives to surmount atorvastatin-induced myopathy in hyperlipidemic rats.
Abdelbaset, M; Agha, AM; Mahmoud, SS; Negm, SA; Safar, MM, 2014
)
0.64
" Intolerance was defined as inability to take at least 2 different statins because of muscle-related adverse events (AEs), 1 at the lowest approved starting dose."( Efficacy and safety of alirocumab, a monoclonal antibody to PCSK9, in statin-intolerant patients: design and rationale of ODYSSEY ALTERNATIVE, a randomized phase 3 trial.
Baccara-Dinet, MT; Bruckert, E; Gipe, D; Guyton, JR; Jacobson, TA; Moriarty, PM; Thompson, PD,
)
0.13
"The aim of this study was to evaluate the effect of atorvastatin on lipid lowering, cardiovascular (CV) events, and adverse events in women compared with men in 6 clinical trials."( Impact of female sex on lipid lowering, clinical outcomes, and adverse effects in atorvastatin trials.
Betteridge, J; Bittner, VA; Fayyad, R; Hsue, PY; Laskey, R; Waters, DD; Wenger, NK, 2015
)
0.89
" Study medications were generally safe and well tolerated."( Efficacy and safety of fixed dose combination of atorvastatin and hydroxychloroquine: a randomized, double-blind comparison with atorvastatin alone among Indian patients with dyslipidemia.
Agarwal, M; Agrawal, N; Chandurkar, N; Dhruv, U; Khyalappa, R; Legha, R; Mathur, SL; Pai, V; Pareek, A; Parmar, M; Pednekar, S; Salkar, HR; Saxena, S; Sriram, U; Thulaseedharan, NK, 2015
)
0.67
" Statin therapy significantly lowers plasma TC and LDL levels in HIV-positive patients and is associated with low rates of adverse events."( Comparative safety and efficacy of statins for primary prevention in human immunodeficiency virus-positive patients: a systematic review and meta-analysis.
Ballocca, F; Barbero, U; Biondi-Zoccai, G; Bonora, S; Calcagno, A; Cannillo, M; Cerrato, E; D'Ascenzo, F; DiNicolantonio, JJ; Gaita, F; Gasparini, M; Gili, S; Grosso Marra, W; Lavie, CJ; Lonni, E; Mancone, M; Montefusco, A; Moretti, C; Omedè, P; Pianelli, M, 2016
)
0.43
" To our knowledge, no meta-analysis focusing on assessing the safety profile of atorvastatin 80 mg/day has been performed; therefore, our aim was to evaluate the tolerability and adverse event (AE) patterns of this drug/dose."( Safety Profile of Atorvastatin 80 mg: A Meta-Analysis of 17 Randomized Controlled Trials in 21,910 Participants.
Cheng, G; Li, H; Li, R; Sun, S; Wang, C; Zhang, S; Zou, M, 2016
)
1
" Nephrotoxicity, a serious side-effect of gentamicin, is related to an increase in reactive oxygen species in the kidney."( Atorvastatin improves renal organic anion transporter 3 and renal function in gentamicin-induced nephrotoxicity in rats.
Arjinajarn, P; Chatsudthipong, V; Chattipakorn, N; Jaikumkao, K; Lungkaphin, A; Pongchaidecha, A; Promsan, S, 2016
)
1.88
" We aimed to quantify co-administration of MQAB with interacting drugs and associated adverse drug reactions."( Drug safety of macrolide and quinolone antibiotics in a tertiary care hospital: administration of interacting co-medication and QT prolongation.
Corti, N; Hoppe, L; Kovari, H; Maechler, S; Niedrig, D; Russmann, S, 2016
)
0.43
" Electrocardiographic (ECG) monitoring and associated adverse events were validated in medical records."( Drug safety of macrolide and quinolone antibiotics in a tertiary care hospital: administration of interacting co-medication and QT prolongation.
Corti, N; Hoppe, L; Kovari, H; Maechler, S; Niedrig, D; Russmann, S, 2016
)
0.43
" Forty-four MQAB users had contraindicated co-administrations of simvastatin, atorvastatin, or tizanidine and three of those related adverse drug reactions."( Drug safety of macrolide and quinolone antibiotics in a tertiary care hospital: administration of interacting co-medication and QT prolongation.
Corti, N; Hoppe, L; Kovari, H; Maechler, S; Niedrig, D; Russmann, S, 2016
)
0.66
" However, adverse drug reactions were rarely found, and costs vs."( Drug safety of macrolide and quinolone antibiotics in a tertiary care hospital: administration of interacting co-medication and QT prolongation.
Corti, N; Hoppe, L; Kovari, H; Maechler, S; Niedrig, D; Russmann, S, 2016
)
0.43
" However, there is no comprehensive study on the role of NOXs in high glucose (HG)-induced toxic effect in neural tissues."( Studying neuroprotective effect of Atorvastatin as a small molecule drug on high glucose-induced neurotoxicity in undifferentiated PC12 cells: role of NADPH oxidase.
Dehpour, AR; Rayegan, S; Sharifi, AM, 2017
)
0.73
" Curcumin is one of the safe spices that have chemoprotection and cytoprotection effects against endogenous and exogenous noxious stimuli."( Curcumin improves atorvastatin-induced myotoxicity in rats: Histopathological and biochemical evidence.
El-Kenawy, AE; Elshama, SS; Osman, HH, 2016
)
0.77
" In the short-term trials, the incidence of all-causality adverse events (AEs) and serious AEs (SAEs) in Asian patients treated with atorvastatin was similar to or lower than that observed with other statins or placebo, and discontinuations due to treatment-related AEs/SAEs were infrequent (2."( Safety of atorvastatin in Asian patients within clinical trials.
Bao, W; Chan, JC; Fayyad, R; Kong, AP; Laskey, R, 2016
)
1.04
"Statins (including atorvastatin) are a widely used class of drugs, and like all medications, they have a potential for adverse effects."( Toxicity of Atorvastatin on Pancreas Mitochondria: A Justification for Increased Risk of Diabetes Mellitus.
Amirsheardost, Z; Hajhashemi, V; Minaiyan, M; Naserzadeh, P; Pourahmad, J; Sadighara, M; Salimi, A; Seydi, E, 2017
)
1.16
"Liver injury is a common adverse effect of atorvastatin."( The enhanced atorvastatin hepatotoxicity in diabetic rats was partly attributed to the upregulated hepatic Cyp3a and SLCO1B1.
Hu, M; Li, F; Ling, Z; Liu, L; Liu, P; Liu, X; Shu, N; Sun, B; Wang, F; Xie, Q; Xu, P; Zhang, M; Zhong, Z, 2016
)
1.07
" 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
"Myopathy is the most commonly reported adverse effect of statins."( Rosuvastatin safety: An experimental study of myotoxic effects and mitochondrial alterations in rats.
Abdallah, D; El-Ganainy, SO; El-Khatib, AS; El-Mallah, A; Khattab, MM; Mohy El-Din, MM, 2017
)
0.46
"Statins are generally well tolerated and adverse effects are relatively rare."( Hepatotoxicity of statins and other lipid-lowering agents.
Björnsson, ES, 2017
)
0.46
" ATOR showed similar cytotoxic effect as TMZ to glioma cells, and it may be a safer drug, regarding side effect induction, than chemotherapic agents."( Atorvastatin Promotes Cytotoxicity and Reduces Migration and Proliferation of Human A172 Glioma Cells.
Dal-Cim, T; Lopes, FG; Ludka, FK; Nedel, CB; Oliveira, KA; Tasca, CI, 2018
)
1.92
"In blinded randomised controlled trials, statin therapy has been associated with few adverse events (AEs)."( Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid-Lowering Arm (ASCOT-LLA): a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension p
Collier, T; Collins, R; Dahlof, B; Gupta, A; Poulter, N; Sever, P; Thompson, D; Whitehouse, A, 2017
)
0.46
" These results will help assure both physicians and patients that most AEs associated with statins are not causally related to use of the drug and should help counter the adverse effect on public health of exaggerated claims about statin-related side-effects."( Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid-Lowering Arm (ASCOT-LLA): a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension p
Collier, T; Collins, R; Dahlof, B; Gupta, A; Poulter, N; Sever, P; Thompson, D; Whitehouse, A, 2017
)
0.46
"9 million clinical reports submitted to FDA Adverse Event Reporting System (FAERS) from 2004 to 2015."( Effect of statins on blood pressure: Analysis on adverse events released by FDA.
Ding, F; Hou, XD; Liu, XG; Wang, XK; Xie, HH; Xie, XD; Yi, K; You, T; Zhang, P, 2017
)
0.46
"To our knowledge, this is the first pooled analysis on large-scale data of adverse events to identify the BP-lowering effect of statins."( Effect of statins on blood pressure: Analysis on adverse events released by FDA.
Ding, F; Hou, XD; Liu, XG; Wang, XK; Xie, HH; Xie, XD; Yi, K; You, T; Zhang, P, 2017
)
0.46
" No serious adverse events (AEs) related to bococizumab treatment occurred and all treatment-emergent AEs were mild or moderate in severity."( Efficacy and Safety of Bococizumab (RN316/PF-04950615), a Monoclonal Antibody Against Proprotein Convertase Subtilisin/Kexin Type 9, in Hypercholesterolemic Japanese Subjects Receiving a Stable Dose of Atorvastatin or Treatment-Naive - Results From a Rand
Chaudhuri, S; Imai, K; Kanada, S; Matsuoka, N; Matsuoka, O; Sekino, H; Tabira, J; Teramoto, T; Yokote, K, 2017
)
0.64
"Statins are generally well-tolerated and serious side effects are infrequent, but some patients experience adverse events and reduce their statin dose or discontinue treatment altogether."( Efficacy and safety of alirocumab in patients with hypercholesterolemia not adequately controlled with non-statin lipid-lowering therapy or the lowest strength of statin: ODYSSEY NIPPON study design and rationale.
Baccara-Dinet, MT; Harada-Shiba, M; Ishigaki, Y; Kawabata, Y; Kiyosue, A; Kondo, A; Ozaki, A; Sata, M; Teramoto, T; Tobita, K, 2017
)
0.46
" No deaths or serious adverse events were reported."( Efficacy and Safety of the Cholesteryl Ester Transfer Protein Inhibitor Evacetrapib in Combination With Atorvastatin in Japanese Patients With Primary Hypercholesterolemia.
Iimura, T; Kiyosue, A; Murakami, M; Riesmeyer, JS; Takita, Y; Teramoto, T, 2017
)
0.67
" The rate of ≥1 adverse event was similar with rosuvastatin 5 mg (12."( Efficacy and safety of rosuvastatin versus atorvastatin in high-risk Chinese patients with hypercholesterolemia: a randomized, double-blind, active-controlled study.
Peng, D; Zhao, S, 2018
)
0.74
"Despite being a potent hypolipidemic drug, atorvastatin (AS) possesses certain adverse effects."( Evaluating Efficacy and Safety of Combination Medication of Atorvastatin and a Herbal Formula Containing Salvia miltiorrhiza and Pueraria lobata on Hyperlipidemia.
Chan, JY; Cheung, DW; Fung, KP; Hung, AS; Ko, CH; Koon, CM; Lau, KM; Wang, YP; Wat, E; Waye, MM; Wong, PH; Yau, KC, 2017
)
0.96
" Safety outcomes included adverse events and events of interest identified in the FOURIER trial."( Clinical Efficacy and Safety of Evolocumab in High-Risk Patients Receiving a Statin: Secondary Analysis of Patients With Low LDL Cholesterol Levels and in Those Already Receiving a Maximal-Potency Statin in a Randomized Clinical Trial.
Ferreira, J; Giugliano, RP; Huber, K; Keech, A; Lewis, BS; Murphy, SA; Pedersen, TR; Pineda, AL; Sabatine, MS; Sever, PS; Somaratne, R; Tokgozoglu, SL, 2017
)
0.46
" Uncertainty persists about whether they cause symptomatic muscle adverse effects, such as pain and weakness, in the absence of statin myopathy."( Study protocol for statin web-based investigation of side effects (StatinWISE): a series of randomised controlled N-of-1 trials comparing atorvastatin and placebo in UK primary care.
Armitage, J; Beaumont, D; Brack, K; Goldacre, B; Herrett, E; MacDonald, T; Prowse, D; Roberts, I; Shakur-Still, H; Smeeth, L; Staa, TV; Williamson, E; Youssouf, N, 2017
)
0.66
" Moreover, the AC-NPs treatments were associated with significant adverse effects observed biochemically and histologically."( Efficacy and Safety Profiles of Oral Atorvastatin-Loaded Nanoparticles: Effect of Size Modulation on Biodistribution.
Abd-Rabo, MM; Ahmed, IS; El Hosary, R; Haider, M; Hassan, MA, 2018
)
0.75
"Lawyer-submitted reports may have unintended consequences on safety signal detection in spontaneous adverse event reporting systems."( Effect of Lawyer-Submitted Reports on Signals of Disproportional Reporting in the Food and Drug Administration's Adverse Event Reporting System.
Bohn, JM; Connolly, JG; Desai, RJ; Fischer, MA; Gagne, JJ; Kesselheim, AS; Khan, NF; Rogers, JR; Sarpatwari, A, 2019
)
0.51
"Our objective was to assess the impact of lawyer-submitted reports primarily for one adverse event (AE) on the ability to detect a signal of disproportional reporting for another AE for the same drug in the US FDA Adverse Event Reporting System (FAERS)."( Effect of Lawyer-Submitted Reports on Signals of Disproportional Reporting in the Food and Drug Administration's Adverse Event Reporting System.
Bohn, JM; Connolly, JG; Desai, RJ; Fischer, MA; Gagne, JJ; Kesselheim, AS; Khan, NF; Rogers, JR; Sarpatwari, A, 2019
)
0.51
" No significant adverse events were reported."( Safety and Efficacy of Atorvastatin for Chronic Subdural Hematoma in Chinese Patients: A Randomized ClinicalTrial.
Dong, JF; Fei, Z; Feng, H; Gao, G; Hao, J; Hu, J; Hu, R; Jiang, R; Jiao, B; Kang, D; Lei, P; Li, J; Li, X; Liu, N; Liu, X; Lu, Y; Mao, Y; Poon, WS; Su, N; Sun, T; Tian, Y; Wang, D; Wang, R; Wei, H; Wei, J; Yin, G; Yu, R; Yu, X; Yuan, X; Zhang, J; Zhao, S; Zhao, Y; Zhu, X, 2018
)
0.79
"Atorvastatin may be a safe and efficacious nonsurgical alternative for treating patients with CSDH."( Safety and Efficacy of Atorvastatin for Chronic Subdural Hematoma in Chinese Patients: A Randomized ClinicalTrial.
Dong, JF; Fei, Z; Feng, H; Gao, G; Hao, J; Hu, J; Hu, R; Jiang, R; Jiao, B; Kang, D; Lei, P; Li, J; Li, X; Liu, N; Liu, X; Lu, Y; Mao, Y; Poon, WS; Su, N; Sun, T; Tian, Y; Wang, D; Wang, R; Wei, H; Wei, J; Yin, G; Yu, R; Yu, X; Yuan, X; Zhang, J; Zhao, S; Zhao, Y; Zhu, X, 2018
)
2.23
" Therefore, all reported cases of IMNM in VigiBase, the WHO global database of individual case safety reports (ICSRs) including the underlying reporting patterns, were analysed to characterize more detailed this adverse drug reaction."( Statin-associated immune-mediated necrotizing myopathy: a retrospective analysis of individual case safety reports from VigiBase.
Essers, D; Kullak-Ublick, GA; Schäublin, M; Weiler, S, 2019
)
0.51
"To evaluate the onset timing of musculoskeletal adverse events (MAEs) that develop during statin monotherapy and to determine whether concomitant drugs used concurrently with statin therapy shifts the onset timing of MAEs."( Onset timing of statin-induced musculoskeletal adverse events and concomitant drug-associated shift in onset timing of MAEs.
Akimoto, H; Inoue, N; Kobayashi, D; Negishi, A; Numajiri, S; Ohshima, S; Okita, M; Oshima, S, 2018
)
0.48
" Both rosuvastatin and atorvastatin were well tolerated, with similar incidences of adverse events."( Efficacy and safety of rosuvastatin vs. atorvastatin in lowering LDL cholesterol : A meta-analysis of trials with East Asian populations.
Ge, J; Jiang, H; Yu, Y; Zhang, L; Zhang, S, 2020
)
1.14
" However, some patients have to reduce drug doses or discontinue atorvastatin therapy mainly due to adverse drug reactions (ADRs)."( Association of SLCO1B1 Polymorphisms and Atorvastatin Safety and Efficacy: A Meta-analysis.
Chen, Z; Du, Y; Li, X; Sun, S; Wang, S; Zhao, Z, 2018
)
0.98
" The primary endpoints included the incidence of adverse cardiovascular events and changed in blood lipids and high-sensitivity C-reactive protein (hs-CRP)."( Efficacy and Safety of Ezetimibe in Combination with Atorvastatin for Acute Coronary Syndrome Patients Accompanied with Type 2 Diabetes: A Single-Center, Non-randomized Cohort Study.
Huang, Z; Li, Q; Li, X; Ye, W; Zhang, Q, 2019
)
0.76
" Moreover, using C+P did not lead to any serious adverse effects when compared to the treatment group."( Low dose concomitant treatment with chlorpromazine and promethazine is safe in acute ischemic stroke.
Chandra, A; Cheng, Z; Ding, Y; Du, H; Geng, X; Tong, Y; Zhu, H, 2019
)
0.51
"While the addition of low dose chlorpromazine and promethazine to standard of care for acute ischemic stroke did not have any significant improvement in functional outcomes, there were no serious adverse effects."( Low dose concomitant treatment with chlorpromazine and promethazine is safe in acute ischemic stroke.
Chandra, A; Cheng, Z; Ding, Y; Du, H; Geng, X; Tong, Y; Zhu, H, 2019
)
0.51
"BACKGROUND Patients with diabetes mellitus (DM) commonly receive statins to suppress vulnerability to adverse cardiovascular events."( Atorvastatin Induces Hepatotoxicity in Diabetic Rats via Oxidative Stress, Inflammation, and Anti-Apoptotic Pathway.
Liu, Z; Zeng, H, 2019
)
1.96
" In conclusion, atorvastatin nanocrystals are safe and efficacious drug delivery system confirming potent competence in treatment of hyperlipidemic conditions with ease of scalability for commercialization."( Surface stabilized atorvastatin nanocrystals with improved bioavailability, safety and antihyperlipidemic potential.
Mehta, I; Sharma, M, 2019
)
1.19
" Our objective was to evaluate the possible benefits on endothelial function and vascular stiffness, as well as adverse effects of atorvastatin in SAMs."( Safety of Atorvastatin in Patients With Stable Systemic Autoimmune Myopathies: A Pilot Longitudinal Study.
Bortolotto, LA; de Oliveira, DS; Dos Santos, AM; Hong, VAC; Misse, RG; Pires Borges, IB; Shinjo, SK, 2021
)
1.23
" Myotoxicity of statins in certain individuals is often a severe side effect leading to withdrawal."( Resveratrol for protection against statin toxicity in C2C12 and H9c2 cells.
Attalah Nee Rezkallah, C; Chen, QM; Thongkum, A; Zhu, C, 2020
)
0.56
"Paclitaxel-induced peripheral neuropathy (PIPN) is a common and dose-limiting adverse event."( P-Glycoprotein Inhibition Exacerbates Paclitaxel Neurotoxicity in Neurons and Patients With Cancer.
Hammer, HS; Khalaf, S; Kroetz, DL; Mortensen, C; Nielsen, F; Poetz, O; Rodriguez-Antona, C; Stage, TB; Steffensen, V; Svenningsen, ÅF; Xiong, C, 2020
)
0.56
" Demographics, burn total body surface area, atorvastatin doses, creatinine phosphokinase, aspartate aminotransferase levels and adverse events were analyzed."( Safety profile of atorvastatin in the role of burn wound injury conversion.
Boyko, T; Flynn, W; Furnari, G; Lukan, JK; Marin, C, 2020
)
1.15
" No adverse events associated with atorvastatin were identified."( Safety profile of atorvastatin in the role of burn wound injury conversion.
Boyko, T; Flynn, W; Furnari, G; Lukan, JK; Marin, C, 2020
)
1.17
"Atorvastatin administered to patients with burn injuries was not associated with any adverse events or attributable lab abnormalities."( Safety profile of atorvastatin in the role of burn wound injury conversion.
Boyko, T; Flynn, W; Furnari, G; Lukan, JK; Marin, C, 2020
)
2.33
"This study aimed to evaluate whether the high frequency of reported statin adverse effects (AEs) may be associated with the nocebo effect."( Examining the Nocebo Effect of Statins Through Statin Adverse Events Reported in the Food and Drug Administration Adverse Event Reporting System.
Cohen Sedgh, R; Jackevicius, CA; Moon, J, 2021
)
0.62
"A retrospective cohort study was conducted using the Food and Drug Administration Adverse Event Reporting System between January 2010 and December 2019 for statins, including, atorvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin."( Examining the Nocebo Effect of Statins Through Statin Adverse Events Reported in the Food and Drug Administration Adverse Event Reporting System.
Cohen Sedgh, R; Jackevicius, CA; Moon, J, 2021
)
0.81
" The obtained results suggested a promising, easy-to-manufacture and effective ATC proniosomal gel for safe treatment of hyperlipidemia."( Optimization of transdermal atorvastatin calcium - Loaded proniosomes: Restoring lipid profile and alleviating hepatotoxicity in poloxamer 407-induced hyperlipidemia.
Abdel-Rahman, RF; El-Kayal, M; Eltellawy, YA; Salah, S; Shaker, DS, 2021
)
0.92
" For validation of this cell model, alirocumab, a human antibody against proprotein convertase subtilisin kexin type 9 (PCSK9), was selected as an emerging safe lipid-lowering drug; atorvastatin, a common statin (the most effective type of lipid-lowering drug), was used as a drug with reported side effects at high concentrations, while doxorubicin was chosen as a positive cardiotoxic drug."( Establishment of an in vitro safety assessment model for lipid-lowering drugs using same-origin human pluripotent stem cell-derived cardiomyocytes and endothelial cells.
Ding, FY; Ding, N; Han, XL; Hu, SJ; Lei, W; Ni, X; Wu, HC; Xu, GY; Yang, ZZ; Ye, LQ; Yu, M; Zhao, DD; Zhao, ZA, 2022
)
0.91
" The primary efficacy end points were the percentage change from baseline in non-high density lipoprotein cholesterol (non-HDL-C) level at the end of treatment and the adverse events recorded during treatment."( Comparison of the Efficacy and Safety of Atorvastatin 40 mg/ω-3 Fatty Acids 4 g Fixed-dose Combination and Atorvastatin 40 mg Monotherapy in Hypertriglyceridemic Patients who Poorly Respond to Atorvastatin 40 mg Monotherapy: An 8-week, Multicenter, Random
Cha, DH; Cho, EJ; Chung, WJ; Hong, SJ; Hong, TJ; Jeon, DS; Jeon, DW; Jeong, JC; Jeong, JO; Jeong, MH; Kim, CJ; Kim, KS; Kim, MH; Kim, SK; Kwan, J; Lee, HY; Lee, JH; Lee, JW; Park, CG; Shin, J; Woo, JS; Youn, HJ, 2021
)
0.89
"In patients with residual hypertriglyceridemia despite receiving statin treatment, a combination of high-dose atorvastatin/Ω-3 fatty acid was associated with a greater reduction of triglyceride and non-HDL-C compared with atorvastatin + placebo, without significant adverse events."( Comparison of the Efficacy and Safety of Atorvastatin 40 mg/ω-3 Fatty Acids 4 g Fixed-dose Combination and Atorvastatin 40 mg Monotherapy in Hypertriglyceridemic Patients who Poorly Respond to Atorvastatin 40 mg Monotherapy: An 8-week, Multicenter, Random
Cha, DH; Cho, EJ; Chung, WJ; Hong, SJ; Hong, TJ; Jeon, DS; Jeon, DW; Jeong, JC; Jeong, JO; Jeong, MH; Kim, CJ; Kim, KS; Kim, MH; Kim, SK; Kwan, J; Lee, HY; Lee, JH; Lee, JW; Park, CG; Shin, J; Woo, JS; Youn, HJ, 2021
)
1.1
" The aim of this study is to compare the risk of statin-associated adverse events among potent statins."( Real-World Analyses of the Safety Outcome among a General Population Treated with Statins: An Asian Population-Based Study.
Chen, PS; Li, YH; Lin, HW; Lin, JL; Lin, SH; Tsai, LM, 2022
)
0.72
" There were no significant effects on non-vascular mortality, site-specific cancer, or other serious adverse events."( Long-term safety and efficacy of anacetrapib in patients with atherosclerotic vascular disease.
Angermann, C; Armitage, J; Baigent, C; Barter, P; Baxter, A; Blaustein, R; Bowman, L; Braunwald, E; Brenner, S; Cannon, C; Chen, F; Chen, Y; Chen, Z; Collins, R; Dayanandan, R; DeLucca, P; Ertl, G; Fabbri, G; Fajardo-Moser, M; Goodenough, R; Goto, S; Gray, A; Hao, D; Haynes, R; Herrington, W; Hill, M; Hopewell, JC; Knott, C; Landray, M; Lay, M; Liu, J; Lucci, D; Macdonnell, S; Maggioni, A; Mihaylova, B; Mitchel, Y; Mosegaard, S; Murphy, K; Sammons, E; Stevens, W; Tobert, J; Valdes-Marquez, E; Wallendszus, K; Wanner, C; Wincott, E; Wiviott, S; Wuhan, B; Zhang, H, 2022
)
0.72
"The beneficial effects of anacetrapib on major coronary events increased with longer follow-up, and no adverse effects emerged on non-vascular mortality or morbidity."( Long-term safety and efficacy of anacetrapib in patients with atherosclerotic vascular disease.
Angermann, C; Armitage, J; Baigent, C; Barter, P; Baxter, A; Blaustein, R; Bowman, L; Braunwald, E; Brenner, S; Cannon, C; Chen, F; Chen, Y; Chen, Z; Collins, R; Dayanandan, R; DeLucca, P; Ertl, G; Fabbri, G; Fajardo-Moser, M; Goodenough, R; Goto, S; Gray, A; Hao, D; Haynes, R; Herrington, W; Hill, M; Hopewell, JC; Knott, C; Landray, M; Lay, M; Liu, J; Lucci, D; Macdonnell, S; Maggioni, A; Mihaylova, B; Mitchel, Y; Mosegaard, S; Murphy, K; Sammons, E; Stevens, W; Tobert, J; Valdes-Marquez, E; Wallendszus, K; Wanner, C; Wincott, E; Wiviott, S; Wuhan, B; Zhang, H, 2022
)
0.72
" They were tolerated well by all participants and found safe during the course of treatment."( Evaluating the safety and efficacy of a polyherbal Unani formulation in dyslipidaemia-a prospective randomized controlled trial.
Ahmad, T; Ain, Q; Kazmi, MH; Naikodi, MAR; Nawab, M, 2022
)
0.72
" Among the data extracted in this meta-analysis, bone mineral density (BMD) was the primary outcome measurement, while total effective rate, VAS, osteoprotegerin (OPG), bone Gla protein (BGP), bone alkaline phosphatase (BAP), blood P and Ca, and adverse effects were secondary outcome measurements."( Meta-Analysis of the Efficacy and Safety of Alendronate Combined with Atorvastatin in the Treatment of Osteoporosis in Diabetes Mellitus.
Shu, L; Tang, X; Xiong, Z; Yi, P; Zhang, C, 2022
)
0.96
"The results of this meta-analysis indicate that alendronate combined with atorvastatin is a better treatment for osteoporosis in diabetes mellitus, showing more effective and higher BMD and fewer adverse events than alendronate alone."( Meta-Analysis of the Efficacy and Safety of Alendronate Combined with Atorvastatin in the Treatment of Osteoporosis in Diabetes Mellitus.
Shu, L; Tang, X; Xiong, Z; Yi, P; Zhang, C, 2022
)
1.19
"There is a growing concern about the association between the combined use of daptomycin (DAP) and statins and the occurrence of musculoskeletal adverse events (MAEs), but this remains controversial."( Association Between Statin Use and Daptomycin-related Musculoskeletal Adverse Events: A Mixed Approach Combining a Meta-analysis and a Disproportionality Analysis.
Asada, M; Bando, T; Chuma, M; Goda, M; Hamano, H; Ishizawa, K; Izawa-Ishizawa, Y; Kondo, Y; Miyata, K; Nakamoto, A; Niimura, T; Okada, N; Takechi, K; Tasaki, Y; Yagi, K; Yanagawa, H; Yoshioka, T; Zamami, Y, 2022
)
0.72
" Second, we conducted a disproportionality analysis using the US Food and Drug Administration Adverse Events Reporting System (FAERS) to further confirm the results of the meta-analysis and to examine the effect of each type of statin on DAP-related MAEs in a large population."( Association Between Statin Use and Daptomycin-related Musculoskeletal Adverse Events: A Mixed Approach Combining a Meta-analysis and a Disproportionality Analysis.
Asada, M; Bando, T; Chuma, M; Goda, M; Hamano, H; Ishizawa, K; Izawa-Ishizawa, Y; Kondo, Y; Miyata, K; Nakamoto, A; Niimura, T; Okada, N; Takechi, K; Tasaki, Y; Yagi, K; Yanagawa, H; Yoshioka, T; Zamami, Y, 2022
)
0.72
" 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
" Proportion of patients achieving target lipid levels (LDL-C ≤ 100 mg/dL and non-HDL-C ≤ 120 mg/dL) and adverse events were assessed at 24 weeks."( Short-term safety and efficacy of escalating doses of atorvastatin for dyslipidemia in children with predialysis chronic kidney disease stage 2-5.
Bagga, A; Hari, P; Khandelwal, P; Lakshmy, R; Ramesh, PL; Sinha, A, 2023
)
1.16
" No differences were noted in adverse events due to atorvastatin 10 or 20 mg/day."( Short-term safety and efficacy of escalating doses of atorvastatin for dyslipidemia in children with predialysis chronic kidney disease stage 2-5.
Bagga, A; Hari, P; Khandelwal, P; Lakshmy, R; Ramesh, PL; Sinha, A, 2023
)
1.41
"Atorvastatin (10-20 mg/day) administered for 24 weeks was safe and effectively reduced LDL-C and non-HDL-C in children with CKD stages 2-5."( Short-term safety and efficacy of escalating doses of atorvastatin for dyslipidemia in children with predialysis chronic kidney disease stage 2-5.
Bagga, A; Hari, P; Khandelwal, P; Lakshmy, R; Ramesh, PL; Sinha, A, 2023
)
2.6
" Atorvastatin pretreatment prevented kidney damage following exposure to toxic doses of cadmium."( Atorvastatin prevents cadmium-induced renal toxicity in a rat model.
Bandegi, AR; Dehdashti, A; Ghanbari, A; Goodarzi, Z; Karami, E; Yosefi, S, 2023
)
3.26
" However, the clinical application of DOX is limited mainly by dose-related adverse drug reactions."( Therapeutic effects of atorvastatin on doxorubicin-induced hepatotoxicity in rats via antioxidative damage, anti-inflammatory, and anti-lipotoxicity.
Chen, NN; Li, JX; Ma, XD; Su, SW; Wang, CC; Wang, KX; Wu, YZ; Xiong, C, 2023
)
1.22
" No toxicities or adverse effects were observed in any cohort receiving inclisiran, either alone or in combination."( The N-Acetylgalactosamine-conjugated small interfering RNA inclisiran can be coadministered safely with atorvastatin in cynomolgus monkeys resulting in additive low-density lipoprotein cholesterol reductions.
Brown, AP; Kallend, D; Lehoux, D; Wijngaard, PLJ; Zerler, B, 2023
)
1.12
" There was no difference in adverse events."( Statins to prevent early cardiac dysfunction in cancer patients at increased cardiotoxicity risk receiving anthracyclines.
Abdel-Qadir, H; Amir, E; Billia, F; Brezden-Masley, C; Chan, J; Connelly, KA; Hanneman, K; Houbois, C; Huang, F; Kei, T; Marwick, TH; Maze, D; Pezo, RC; Power, C; Prica, A; Runeckles, K; Saha, S; Shalmon, T; Thavendiranathan, P; Thorpe, KE; Wintersperger, BJ, 2023
)
0.91
" However, CyA greatly increases the plasma concentration of AT; therefore, concomitant use might increase the frequency of statin-induced adverse effects."( Safety Profile of the Concomitant Use of Atorvastatin and Cyclosporine in Renal Transplant Recipients.
Harabayashi, R; Nagayama, K; Nakamura, Y; Sugimoto, T; Takahashi, K; Takahashi, M; Uchida, J, 2023
)
1.18
" There was no significant difference in the adverse events rates between RSV 10 mg/AML 5 mg, RSV 20 mg/AML 5 mg, and ATV 20 mg/AML 5 mg."( Randomized, multicenter, parallel, open, phase 4 study to compare the efficacy and safety of rosuvastatin/amlodipine polypill versus atorvastatin/amlodipine polypill in hypertension patient with dyslipidemia.
Bae, HJ; Cho, EJ; Choi, JY; Han, KR; Hong, BK; Hong, SP; Hyon, MS; Jin, HY; Jung, HW; Kim, CY; Kim, KS; Kim, SY; Kim, U; Lee, JB; Lee, KH; Lee, KJ; Lee, SR; Lee, SY; Nam, CW; Park, CG; Park, SJ; Park, TH; Rhee, MY; Ryu, JK; Seol, SH; Shin, JH; Yang, DH; Yu, GW, 2023
)
1.11
"To evaluate the impact of high-dose atorvastatin on secondary prevention of MACE and adverse events."( [Efficacy and safety of atorvastatin in major cardiovascular events: Meta-analysis].
García-Rivero, AA; González-Tovar, NB; Rivas-Ruíz, R; Rivera-Lara, P; Villegas-Quintero, VE, 2023
)
1.49
" The drug has adverse events that should be taken into account in secondary prevention."( [Efficacy and safety of atorvastatin in major cardiovascular events: Meta-analysis].
García-Rivero, AA; González-Tovar, NB; Rivas-Ruíz, R; Rivera-Lara, P; Villegas-Quintero, VE, 2023
)
1.22

Pharmacokinetics

This study shows that the SLCO1B1*15 allele may be associated with the individual difference in the AUC0-infinity of atorvastatin. The ABCB1 TT-TT diplotype may affect the elimination half-life of the drug in the Korean population.

ExcerptReferenceRelevance
" In addition, mean area under the concentration-time curve (AUC0-infinity) and half-life (t1/2) were 27."( Effect of age and gender on pharmacokinetics of atorvastatin in humans.
Bron, NJ; Gibson, DM; Hounslow, NJ; Richens, A; Sedman, AJ; Whitfield, LR, 1996
)
0.55
"The pharmacodynamic effects and pharmacokinetics of atorvastatin, a potent investigational inhibitor of HMG-CoA reductase, were studied in 16 normolipidemic subjects after administration of 40 mg daily for 15 days in the morning or evening."( Pharmacodynamic effects and pharmacokinetics of atorvastatin after administration to normocholesterolemic subjects in the morning and evening.
Cilla, DD; Gibson, DM; Sedman, AJ; Whitfield, LR, 1996
)
0.8
" Plasma elimination half-life (t1/2) ranged from 14."( Tolerance and pharmacokinetics of single-dose atorvastatin, a potent inhibitor of HMG-CoA reductase, in healthy subjects.
Cilla, DD; Posvar, EL; Radulovic, LL; Sedman, AJ; Whitfield, LR, 1996
)
0.55
" Atorvastatin peak concentration and area under the plasma concentration-time curve (AUC) values increased more than proportionally with atorvastatin dose after both single and multiple drug doses."( Multiple-dose pharmacokinetics, pharmacodynamics, and safety of atorvastatin, an inhibitor of HMG-CoA reductase, in healthy subjects.
Cilla, DD; Gibson, DM; Posvar, EL; Sedman, AJ; Whitfield, LR, 1996
)
1.44
" Pharmacokinetic parameters and lipid responses were analyzed by regression on calculated creatinine clearance."( Renal dysfunction does not alter the pharmacokinetics or LDL-cholesterol reduction of atorvastatin.
Abel, RB; Horton, M; Moore, S; Olson, SC; Stern, RH; Yang, BB, 1997
)
0.52
" Steady-state pharmacokinetic parameters (based on an enzyme inhibition assay) and lipid responses were compared."( Cimetidine does not alter atorvastatin pharmacokinetics or LDL-cholesterol reduction.
Gibson, DM; Stern, RH; Whitfield, LR, 1998
)
0.6
" For terfenadine, atorvastatin coadministration produced an 8% decrease in maximum concentration (Cmax), a 35% increase in area under the concentration-time curve extrapolated to infinity (AUC0-infinity), and a 2% decrease in elimination half-life (t1/2)."( Atorvastatin does not produce a clinically significant effect on the pharmacokinetics of terfenadine.
Olson, SC; Smithers, JA; Stern, RH, 1998
)
2.08
" In general, the pharmacokinetic consequences of hyperlipidemia include increased total drug concentrations and decreased unbound fraction in plasma."( Pharmacokinetics and pharmacodynamics of nifedipine in untreated and atorvastatin-treated hyperlipidemic rats.
Eliot, LA; Jamali, F, 1999
)
0.54
" Indeed, pharmacokinetic interactions (e."( New insights into the pharmacodynamic and pharmacokinetic properties of statins.
Baetta, R; Bellosta, S; Bernini, F; Corsini, A; Fumagalli, R; Paoletti, R, 1999
)
0.3
" Steady-state atorvastatin pharmacokinetic parameters were estimated on the last day of each dosing period."( Pharmacodynamics and pharmacokinetic-pharmacodynamic relationships of atorvastatin, an HMG-CoA reductase inhibitor.
Abel, RB; Hounslow, NJ; MacMahon, M; Olson, SC; Stern, RH; Yang, BB, 2000
)
0.9
" Pharmacokinetic parameters [AUC(0-infinity), AUC(0-tn), peak concentration (Cmax), time to reach Cmax (tmax), and half-life (t1/2)] were determined for parent statins and major metabolites."( Itraconazole alters the pharmacokinetics of atorvastatin to a greater extent than either cerivastatin or pravastatin.
Agarwal, V; Lasseter, KC; Lettieri, J; Mazzu, AL; Shamblen, EC; Sundaresen, P, 2000
)
0.57
" However, itraconazole dramatically increased atorvastatin AUC (150%), Cmax (38%), and t1/2 (30%) (P < ."( Itraconazole alters the pharmacokinetics of atorvastatin to a greater extent than either cerivastatin or pravastatin.
Agarwal, V; Lasseter, KC; Lettieri, J; Mazzu, AL; Shamblen, EC; Sundaresen, P, 2000
)
0.83
"2% lower mean Cmax and 29."( Effect of food on the pharmacodynamics and pharmacokinetics of atorvastatin, an inhibitor of HMG-CoA reductase.
Abel, R; Gibson, DM; Sedman, AJ; Stern, RH; Whitfield, LR,
)
0.37
" Pharmacokinetic assessment was performed on days 14 and 28."( Pharmacokinetic interactions between nelfinavir and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors atorvastatin and simvastatin.
Hsyu, PH; Kerr, BM; Lewis, RH; Lillibridge, JH; Schultz-Smith, MD, 2001
)
0.52
"The authors assessed the mutual influence of the immunosuppressant everolimus (Certican) and the HMG-CoA reductase inhibitors atorvastatin and pravastatin when coadministered based on pharmacokinetic and pharmacodynamic measures."( Pharmacokinetic and pharmacodynamic assessments of HMG-CoA reductase inhibitors when coadministered with everolimus.
Berthier, S; Hartmann, S; Hubert, M; Kovarik, JM; Rordorf, C; Rosenkranz, B; Schneider, W, 2002
)
0.52
"Fifty-six subjects completed both pharmacokinetic study days."( Pharmacokinetic interactions between protease inhibitors and statins in HIV seronegative volunteers: ACTG Study A5047.
Aberg, JA; Alston, B; Aweeka, F; Blaschke, T; Fang, F; Fichtenbaum, CJ; Gerber, JG; Kosel, B; Rosenkranz, SL; Segal, Y, 2002
)
0.31
"The goal of this study was to develop a preliminary pharmacodynamic model for dosing of the hydroxymethylglutaryl coenzyme A (HMG-CoA)-reductase inhibitors simvastatin and atorvastatin using neural network analysis."( A preliminary evaluation of neural network analysis for pharmacodynamic modeling of the dosing of the hydroxymethylglutaryl coenzyme A-reductase inhibitors simvastatin and atorvastatin.
Moon, A; Smith, T, 2002
)
0.7
" However, the potential bilateral pharmacokinetic interaction between atorvastatin and CsA in renal transplant recipients has not previously been examined."( Bilateral pharmacokinetic interaction between cyclosporine A and atorvastatin in renal transplant recipients.
Asberg, A; Bergan, S; Fjeldså, E; Hartmann, A; Holdaas, H, 2001
)
0.78
" Atorvastatin has been shown to reduce efficiently the levels of atherogenic lipoproteins also in patients with renal failure, but pharmacokinetic data in haemodialysis patients are lacking."( Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients.
Dratwa, M; Lameire, NH; Lins, RL; Matthys, KE; Peeters, PC; Stolear, JC; Verpooten, GA, 2003
)
1.55
" Plasma levels of atorvastatin and its active and inactive metabolites were measured by LC/MS/MS, and pharmacokinetic parameters (C(max), t(max), AUC, t(1/2)) compared between single and multiple dosing, and between the different doses."( Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients.
Dratwa, M; Lameire, NH; Lins, RL; Matthys, KE; Peeters, PC; Stolear, JC; Verpooten, GA, 2003
)
0.98
"The pharmacokinetic parameters of the parent drug atorvastatin acid were not significantly different after single and 2-week multiple dosing; they showed dose-proportionality between the 40 and 80 mg dose, and were comparable to findings in healthy volunteers."( Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients.
Dratwa, M; Lameire, NH; Lins, RL; Matthys, KE; Peeters, PC; Stolear, JC; Verpooten, GA, 2003
)
0.9
" The total plasma clearance of atorvastatin acid is 625 mL/min and the half-life is about 7 hours."( Clinical pharmacokinetics of atorvastatin.
Lennernäs, H, 2003
)
0.9
" A 10-point pharmacokinetic profile was performed prior to and on day 14 after commencement of atorvastatin therapy."( Effect of atorvastatin on cyclosporine pharmacokinetics in liver transplant recipients.
Allen, J; Butler, M; Kubler, PA; Lynch, SV; Pillans, PI; Taylor, PJ, 2004
)
0.94
" No significant change was evident for other cyclosporine pharmacokinetic parameters."( Effect of atorvastatin on cyclosporine pharmacokinetics in liver transplant recipients.
Allen, J; Butler, M; Kubler, PA; Lynch, SV; Pillans, PI; Taylor, PJ, 2004
)
0.73
" No significant changes were detected in any pravastatin pharmacokinetic parameter examined when pravastatin was taken with GFJ."( Effects of grapefruit juice on pharmacokinetics of atorvastatin and pravastatin in Japanese.
Fukazawa, I; Uchida, E; Uchida, N; Yasuhara, H, 2004
)
0.58
" In the 15 subjects completing the study, no pharmacokinetic interaction was detected between atorvastatin and ximelagatran for all parameters investigated, including melagatran (the active form of ximelagatran) area under the plasma concentration versus time curve (AUC) and maximum plasma concentration, atorvastatin acid AUC, and AUC of active 3-hydroxy-3-methyl-glutaryl-coenzyme-A (HMG-CoA) reductase inhibitors."( No pharmacokinetic or pharmacodynamic interaction between atorvastatin and the oral direct thrombin inhibitor ximelagatran.
Dorani, H; Eriksson, UG; Kalies, I; Ohlsson, L; Sarich, TC; Schützer, KM; Wall, U, 2004
)
0.79
" Studies compared the multiple-dose pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with 4 inhibitors of cytochrome P450-3A4 isoenzymes in healthy subjects."( Comparative pharmacokinetic interaction profiles of pravastatin, simvastatin, and atorvastatin when coadministered with cytochrome P450 inhibitors.
Jacobson, TA, 2004
)
0.76
"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
" No statistically significant changes in any of the calculated pharmacokinetic variables [AUC(0-12), maximum whole blood concentration (C(max)), whole blood concentration 12 h post dose (C(12)), time to C(max) (t(max)), terminal half-life (t(1/2))] for cyclosporine or the two metabolites, AM1 and AM9, upon atorvastatin treatment were observed."( Atorvastatin does not affect the pharmacokinetics of cyclosporine in renal transplant recipients.
Asberg, A; Christensen, H; Hartmann, A; Hermann, M; Holdaas, H; Reubsaet, JL, 2005
)
1.95
" The present validated method was successfully used for pharmacokinetic studies of atorvastatin in human subjects."( A simple and rapid HPLC method for the determination of atorvastatin in human plasma with UV detection and its application to pharmacokinetic studies.
Foroutan, SM; Khoddam, A; Shafaati, A; Zarghi, A, 2005
)
0.8
" Blood samples for pharmacokinetic analysis were obtained immediately before and up to 72 hours after administration during each of the 4 treatment periods."( An open-label, crossover study of the pharmacokinetics of Insoluble Drug Delivery-MicroParticle fenofibrate in combination with atorvastatin, simvastatin, and extended-release niacin in healthy volunteers.
Braun, SL; Guha-Ray, DK; Penn, R; Rains, KT; Sawyers, WG; Williams, RX, 2006
)
0.54
" ATV was administered orally (10 mg/kg) and intravenously (2 mg/kg) to rats in the absence and presence of a single intravenous dose of RIF (20 mg/kg), and pharmacokinetic parameters were compared between control and RIF-treatment groups."( Pharmacokinetics of atorvastatin and its hydroxy metabolites in rats and the effects of concomitant rifampicin single doses: relevance of first-pass effect from hepatic uptake transporters, and intestinal and hepatic metabolism.
Benet, LZ; Huang, Y; Lau, YY; Okochi, H, 2006
)
0.66
" The method was used for pharmacokinetic study of ATV and HATV."( Validated HPLC-MS-MS method for simultaneous determination of atorvastatin and 2-hydroxyatorvastatin in human plasma-pharmacokinetic study.
Barrett, B; Borek-Dohalský, V; Huclová, J; Jelínek, I; Nemec, B; Ulc, I, 2006
)
0.57
" Pharmacokinetic parameters of diltiazem and desacetyldiltiazem were determined in rats after oral administration of diltiazem (15 mg x kg(-1)) to rats pretreated with atorvastatin (0."( Effect of atorvastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats.
Chang, KS; Choi, DH; Choi, JS; Hong, SP, 2007
)
0.94
" The pharmacokinetic parameters of verapamil were measured after an oral (9 mg/kg) or intravenous (3 mg/kg) administration of verapamil to rats in the presence and absence of atorvastatin."( Effect of atorvastatin on the intravenous and oral pharmacokinetics of verapamil in rats.
Chang, KS; Choi, DH; Choi, JS; Han, HK; Hong, SP, 2008
)
0.94
" Potential pharmacodynamic interaction between drugs should be investigated as part of developing single-pill combinations."( A randomized, placebo-controlled trial to evaluate the efficacy, safety, and pharmacodynamic interaction of coadministered amlodipine and atorvastatin in 1660 patients with concomitant hypertension and dyslipidemia: the respond trial.
Dykstra, G; Gillen, D; Harvey, P; Herfert, O; Jukema, JW; Preston, RA; Sun, F, 2007
)
0.54
"The pharmacokinetic parameters of verapamil and one of its metabolites, norverapamil, were compared after oral administration of verapamil (60 mg) in the presence or absence of oral atorvastatin (40 mg) in 12 healthy volunteers."( Drug interaction between oral atorvastatin and verapamil in healthy subjects: effects of atorvastatin on the pharmacokinetics of verapamil and norverapamil.
Choi, DH; Choi, JS; Shin, WG, 2008
)
0.83
" Furthermore, the terminal half-life predictions for all three compounds were within 2-fold of the observed values."( Prediction of the pharmacokinetics of atorvastatin, cerivastatin, and indomethacin using kinetic models applied to isolated rat hepatocytes.
Gardiner, P; Paine, SW; Parker, AJ; Riley, RJ; Webborn, PJ, 2008
)
0.62
"This study investigated the potential pharmacokinetic interaction between the direct renin inhibitor aliskiren and modulators of P-glycoprotein and cytochrome P450 3A4 (CYP3A4)."( Pharmacokinetics of the oral direct renin inhibitor aliskiren in combination with digoxin, atorvastatin, and ketoconazole in healthy subjects: the role of P-glycoprotein in the disposition of aliskiren.
Bizot, MN; Camenisch, G; Dieterich, HA; Dole, WP; Howard, D; Reynolds, C; Schuetz, H; Vaidyanathan, S; Yeh, CM, 2008
)
0.57
"The pharmacokinetic parameters of atorvastatin were measured after intravenous (2 mg/kg) and intragastric (10 mg/kg) administration of atorvastatin in rats, which were pretreated with cyclosporin A (5, 10, and 20 mg/kg) or itraconazole (5, 10, and 20 mg/kg)."( Effects of cyclosporin A and itraconazole on the pharmacokinetics of atorvastatin in rats.
Chen, XJ; Dong, J; Sun, YB; Wang, GJ; Wang, L; Yu, X, 2008
)
0.86
" The lack of a clinically meaningful effect of high-dose atorvastatin on the pharmacodynamic response to prasugrel after the loading or maintenance dose indicates that no dosage adjustment should be necessary in patients receiving these drugs concomitantly."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.99
"ABCB1 haplotypes were determined in 534 healthy Finnish volunteers, of whom 24 participated in a pharmacokinetic study on simvastatin and atorvastatin."( ABCB1 haplotypes differentially affect the pharmacokinetics of the acid and lactone forms of simvastatin and atorvastatin.
Keskitalo, JE; Kurkinen, KJ; Neuvoneni, PJ; Niemi, M, 2008
)
0.76
"421C>A single-nucleotide polymorphism (SNP) was determined in 660 healthy Finnish volunteers, of whom 32 participated in a pharmacokinetic crossover study involving the administration of 20 mg atorvastatin and rosuvastatin."( ABCG2 polymorphism markedly affects the pharmacokinetics of atorvastatin and rosuvastatin.
Fromm, MF; Keskitalo, JE; Kurkinen, KJ; Neuvonen, PJ; Niemi, M; Zolk, O, 2009
)
0.78
"To identify pharmacokinetic (PK) drug-drug interactions between tipranavir-ritonavir (TPV/r) and rosuvastatin and atorvastatin, we conducted two prospective, open-label, single-arm, two-period studies."( Differential effects of tipranavir plus ritonavir on atorvastatin or rosuvastatin pharmacokinetics in healthy volunteers.
Barditch-Crovo, P; Cameron, DW; Elgadi, MM; Flexner, C; Fuchs, E; la Porte, CJ; Lee, LS; Pham, PA; Piliero, PJ; Sabo, JP; van Heeswijk, R, 2009
)
0.81
"290 Koreans were genotyped for SLCO1B1, ABCB1 and CYP3A5, and 28 subjects were selected for the pharmacokinetic study."( Effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of atorvastatin and 2-hydroxyatorvastatin in healthy Korean subjects.
Chung, JY; Jang, SB; Lee, MG; Lee, YJ; Lim, LA, 2010
)
0.6
" In lactone forms, no significant pharmacokinetic difference was found among the genotypes."( Effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of atorvastatin and 2-hydroxyatorvastatin in healthy Korean subjects.
Chung, JY; Jang, SB; Lee, MG; Lee, YJ; Lim, LA, 2010
)
0.6
"This study shows that the SLCO1B1*15 allele may be associated with the individual difference in the AUC0-infinity of atorvastatin whereas the ABCB1 TT-TT diplotype may affect the elimination half-life of the drug in the Korean population."( Effects of SLCO1B1 and ABCB1 genotypes on the pharmacokinetics of atorvastatin and 2-hydroxyatorvastatin in healthy Korean subjects.
Chung, JY; Jang, SB; Lee, MG; Lee, YJ; Lim, LA, 2010
)
0.81
" The absence of a significant pharmacokinetic interaction between fenofibrate and atorvastatin is consistent with recent results showing no difference in safety profile between atorvastatin as monotherapy or in combination with fenofibric acid."( Effect of gemfibrozil and fenofibrate on the pharmacokinetics of atorvastatin.
Abel, R; Alvey, C; Bullen, W; Hartman, D; Porcari, AR; Whitfield, LR, 2011
)
0.83
" The developed assay method was successfully applied to a pharmacokinetic study in human male volunteers."( Simultaneous determination of atorvastatin, amlodipine, ramipril and benazepril in human plasma by LC-MS/MS and its application to a human pharmacokinetic study.
Inamadugu, JK; Karra, VK; Mullangi, R; Pilli, NR; Rao, JV; Vaidya, JR, 2011
)
0.66
" Pharmacokinetic parameters, including C(max), T(max), t((1/2)), AUC(0-t), and AUC(0-infinity)), were calculated."( Pharmacokinetics and bioequivalence evaluation of two different atorvastatin calcium 10-mg tablets: A single-dose, randomized-sequence, open-label, two-period crossover study in healthy fasted Chinese adult males.
Jia, JY; Li, GX; Liu, GY; Liu, YM; Lu, C; Pu, HH; Wang, W; Weng, LP; Xu, RJ; Yu, C; Zhang, MQ, 2010
)
0.6
"7] kg/m(2)) were included in the pharmacokinetic and bioequivalence analyses; 1 subject was excluded from these analyses because he mistakenly received the same formulation in both periods."( Pharmacokinetics and bioequivalence evaluation of two different atorvastatin calcium 10-mg tablets: A single-dose, randomized-sequence, open-label, two-period crossover study in healthy fasted Chinese adult males.
Jia, JY; Li, GX; Liu, GY; Liu, YM; Lu, C; Pu, HH; Wang, W; Weng, LP; Xu, RJ; Yu, C; Zhang, MQ, 2010
)
0.6
" Our objectives were to develop a population pharmacokinetic model for atorvastatin acid and its lactone metabolite and to identify patient characteristics that are predictive of variability in the pharmacokinetic parameters of the parent drug and its lactone metabolite."( Development of a population pharmacokinetic model for atorvastatin acid and its lactone metabolite.
Akhlaghi, F; Asberg, A; Hermann, M; Narwal, R; Rosenbaum, SE, 2010
)
0.84
" The main pharmacokinetic parameters of atorvastatin acid (mean [relative standard error {RSE}]) for a subject with mean covariate values were the first-order absorption rate constant (3."( Development of a population pharmacokinetic model for atorvastatin acid and its lactone metabolite.
Akhlaghi, F; Asberg, A; Hermann, M; Narwal, R; Rosenbaum, SE, 2010
)
0.88
"To investigate the pharmacokinetic effects of co-administration of atorvastatin or rosuvastatin with aleglitazar."( Aleglitazar, a balanced PPARα/γ agonist, has no clinically relevant pharmacokinetic interaction with high-dose atorvastatin or rosuvastatin.
Foley-Comer, AJ; Jordan, P; Russell-Yarde, F; Young, AM, 2011
)
0.82
" Plasma concentrations of each drug were measured and pharmacokinetic parameters determined on day 7 in each period."( Aleglitazar, a balanced PPARα/γ agonist, has no clinically relevant pharmacokinetic interaction with high-dose atorvastatin or rosuvastatin.
Foley-Comer, AJ; Jordan, P; Russell-Yarde, F; Young, AM, 2011
)
0.58
"Co-administration of aleglitazar with a statin does not alter the pharmacokinetic profile of either drug."( Aleglitazar, a balanced PPARα/γ agonist, has no clinically relevant pharmacokinetic interaction with high-dose atorvastatin or rosuvastatin.
Foley-Comer, AJ; Jordan, P; Russell-Yarde, F; Young, AM, 2011
)
0.58
" In co-treated group, the pharmacokinetic parameters like clearance (27."( Influence of atorvastatin on the pharmacokinetics and pharmacodynamics of glyburide in normal and diabetic rats.
Gade, J; Neerati, P, 2011
)
0.74
" Serial pharmacokinetic sampling of atorvastatin was conducted on day 7 of atorvastatin dosing and day 70 of lamotrigine + atorvastatin dosing or day 28 of phenytoin + atorvastatin dosing."( Effects of lamotrigine and phenytoin on the pharmacokinetics of atorvastatin in healthy volunteers.
Alexander, S; Bullman, J; Fleck, R; Messenheimer, J; Miller, J; Nicholls, A; Van Landingham, K; Vuong, A, 2011
)
0.88
" Blood samples were collected pre-dose and up to 72 hours post-dose in each period for determination of plasma atorvastatin/metformin concentrations and calculation of the respective pharmacokinetic parameters."( Pharmacokinetics of a fixed-dose combination of atorvastatin and metformin extended release versus concurrent administration of individual formulations: a randomized, open-label, two-treatment, two-period, two-sequence, single-dose, crossover, bioequivale
Arora, R; Dey, S; Kandhwal, K; Monif, T; Nazarudheen, S; Rao, S; Reyar, S; Singh, MK; Thudi, NR, 2011
)
0.84
" Prospective, two-phase, randomized-sequence, open-label pharmacokinetic study."( Effect of cytochrome P450 3A5 genotype on atorvastatin pharmacokinetics and its interaction with clarithromycin.
Frye, RF; Johnson, JA; Langaee, T; Pacanowski, MA; Pauly, DF; Shin, J, 2011
)
0.63
" This phase I trial evaluated the pharmacokinetic (PK) and drug-drug interactions of bexarotene with chemotherapy and a lipid-lowering agent (atorvastatin or fenofibrate)."( The effect of bexarotene on atorvastatin pharmacokinetics: results from a phase I trial of bexarotene plus chemotherapy in patients with advanced non-small cell lung cancer.
Chu, Q; Dunlop, D; Hao, D; Jacobs, CD; Leighl, N; Lopez-Anaya, A; Middleton, G; Ramlau, R; Rodon, J; Rowinsky, EK; Takimoto, CH; Wakelee, HA; Zatloukal, P, 2012
)
0.87
" The developed assay method was successfully applied to a pharmacokinetic study in humans."( Simultaneous determination of atorvastatin and niacin in human plasma by LC-MS/MS and its application to a human pharmacokinetic study.
Gajula, R; Inamadugu, JK; Mullangi, R; Pilli, NR; Ponneri, V; Ravi, VB, 2012
)
0.67
" Nonlinear mixed-effects modelling was employed to determine the population pharmacokinetic estimates for atorvastatin acid and atorvastatin lactone."( Diabetes mellitus reduces the clearance of atorvastatin lactone: results of a population pharmacokinetic analysis in renal transplant recipients and in vitro studies using human liver microsomes.
Akhlaghi, F; Dostalek, M; Gohh, RY; Macwan, JS; Paryani, KR; Sam, WJ, 2012
)
0.86
" The optimal population pharmacokinetic model for atorvastatin acid and atorvastatin lactone consisted of a two- and one-compartment model, respectively, with interconversion between atorvastatin acid and atorvastatin lactone."( Diabetes mellitus reduces the clearance of atorvastatin lactone: results of a population pharmacokinetic analysis in renal transplant recipients and in vitro studies using human liver microsomes.
Akhlaghi, F; Dostalek, M; Gohh, RY; Macwan, JS; Paryani, KR; Sam, WJ, 2012
)
0.89
"The main pharmacokinetic parameters of test and reference formulations were as follows: the values of C(max) for AT were (10."( [Pharmacokinetics and bioequivalence of atorvastatin calcium tablets in healthy male Chinese volunteers].
Chen, XY; Guo, LX; Shen, Y; Zhang, YF; Zhong, DF, 2012
)
0.65
" The pharmacokinetic parameters of CLZ (6 mg/kg, twice daily) were determined in male Wistar rats after 7 days co-administration with ATV (5 mg/kg, once daily) in order to assess the interaction potential between CLZ and ATV on chronic treatment."( Drug-drug interaction study to assess the effects of atorvastatin co-administration on pharmacokinetics and anti-thrombotic properties of cilostazol in male Wistar rats.
Arla, R; Rajak, S; Varanasi, KV; Vats, R; Veeraraghvan, S, 2012
)
0.63
"The pharmacokinetic parameters of ATV were determined in Wistar rats after per-oral pre-treatment with CLZ for 7 days in order to assess the interaction potential between ATV and CLZ."( Effect of multidose cilostazol on pharmacokinetic and lipid profile of atorvastatin in male Wistar rats.
Arla, R; Murthy, AN; Rajak, S; Varanasi, KV; Vats, R; Veeraraghavan, S, 2012
)
0.61
" In conclusion, this study suggests that OATP1B1 phenotype is more important than CYP3A4 and MDR1 phenotypes for the individual pharmacokinetic variability of atorvastatin."( Impact of OATP1B1, MDR1, and CYP3A4 expression in liver and intestine on interpatient pharmacokinetic variability of atorvastatin in obese subjects.
Andersson, TB; Asberg, A; Bremer, S; Christensen, H; Hjelmesæth, J; Jakobsen, GS; Molden, E; Sandbu, R; Skottheim, IB; Ulvestad, M, 2013
)
0.8
"The objectives of this study were to determine if ABCB1 polymorphisms are associated with interindividual variability in sitagliptin pharmacokinetics and if atorvastatin alters the pharmacokinetic disposition of sitagliptin in healthy volunteers."( Effect of ABCB1 polymorphisms and atorvastatin on sitagliptin pharmacokinetics in healthy volunteers.
Aquilante, CL; Kosmiski, LA; Predhomme, JA; Sidhom, MS; Wempe, MF, 2013
)
0.87
" A 24-h pharmacokinetic study followed each sitagliptin dose, and the study phases were separated by a 14-day washout period."( Effect of ABCB1 polymorphisms and atorvastatin on sitagliptin pharmacokinetics in healthy volunteers.
Aquilante, CL; Kosmiski, LA; Predhomme, JA; Sidhom, MS; Wempe, MF, 2013
)
0.67
"Sitagliptin pharmacokinetic parameters did not differ significantly between ABCB1 CGC/CGC, CGC/TTT, and TTT/TTT diplotype groups during the monotherapy phase."( Effect of ABCB1 polymorphisms and atorvastatin on sitagliptin pharmacokinetics in healthy volunteers.
Aquilante, CL; Kosmiski, LA; Predhomme, JA; Sidhom, MS; Wempe, MF, 2013
)
0.67
"The goal of this study was to investigate the impact of high-dose atorvastatin on the pharmacodynamic (PD) effects of double-dose clopidogrel in statin-naive patients with stable coronary artery disease (CAD) and high-on-treatment platelet reactivity (HTPR) while on standard-dose clopidogrel before percutaneous coronary intervention (PCI)."( High-dose atorvastatin on the pharmacodynamic effects of double-dose clopidogrel in patients undergoing percutaneous coronary interventions: The ACHIDO (Atorvastatin and Clopidogrel HIgh DOse in stable patients with residual high platelet activity) study.
Abbate, R; Angiolillo, DJ; Bellandi, F; Giusti, B; Leoncini, M; Maioli, M; Marcucci, R; Toso, A, 2013
)
1.03
" In patients with high on-treatment platelet reactivity (HTPR) while on standard-dose clopidogrel, high-dose atorvastatin enhances the pharmacodynamic (PD) effects of double-dose clopidogrel."( Pharmacodynamic effects of adjunctive high dose atorvastatin on double dose clopidogrel in patients with high on-treatment platelet reactivity depending on diabetes mellitus status.
Abbate, R; Angiolillo, DJ; Bellandi, F; Giusti, B; Leoncini, M; Maioli, M; Marcucci, R; Toso, A, 2014
)
0.87
"The object of this study is to investigate the pharmacokinetic interaction of pioglitazone hydrochloride and atorvastatin calcium in healthy adult Beagle dogs following single and multiple oral dose administration."( [Pharmacokinetic interaction of pioglitazone hydrochloride and atorvastatin calcium in Beagle dogs].
Chen, HL; Dang, HW; Wang, XY; Yang, FY; Yang, WC; Zhang, WP, 2013
)
0.84
"Although organic anion transporting polypeptide (OATP)-mediated hepatic uptake is generally conserved between rodents and humans at a gross pharmacokinetic level, the presence of three major hepatic OATPs with broad overlap in substrate and inhibitor affinity, and absence of rodent-human orthologs preclude clinical translation of single-gene knockout/knockin findings."( Utility of Oatp1a/1b-knockout and OATP1B1/3-humanized mice in the study of OATP-mediated pharmacokinetics and tissue distribution: case studies with pravastatin, atorvastatin, simvastatin, and carboxydichlorofluorescein.
Bao, JQ; Fallon, JK; Higgins, JW; Ke, AB; Manro, JR; Smith, PC; Zamek-Gliszczynski, MJ, 2014
)
0.6
"Coamorphous ATC-NIC has improved physicochemical and pharmacokinetic properties as compared to ATC."( Coamorphous atorvastatin calcium to improve its physicochemical and pharmacokinetic properties.
Ghavimi, H; Hamishekar, H; Jouyban, A; Shayanfar, A, 2013
)
0.77
" The peak plasma concentration, Tmax and apparent clearance of 2-hydroxyatorvastatin (CL/Fm) were significantly different between subjects with the CYP3A4*1G/*1G genotype and the wild-type."( The effect of CYP3A4*1G allele on the pharmacokinetics of atorvastatin in Chinese Han patients with coronary heart disease.
He, BX; Qiu, J; Shi, L; Zeng, XH; Zhao, SJ, 2014
)
0.88
" Pharmacokinetic parameters were calculated using non-compartmental model."( Effects of silymarin on the pharmacokinetics of atorvastatin in diabetic rats.
Alizadeh-Fanalou, S; Amniattalab, A; Hassani-Dizaj, S; Malekinejad, H; Rezabakhsh, A; Rokhsartalab-Azar, S, 2014
)
0.66
" 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
)
0.89
" Aim of this study was to verify if atorvastatin and rosuvastatin have different pharmacodynamic effects also when platelet reactivity while on dual antiplatelet therapy (DAPT) is normal at baseline."( Pharmacodynamic effects of atorvastatin versus rosuvastatin in coronary artery disease patients with normal platelet reactivity while on dual antiplatelet therapy--the PEARL randomized cross-over study.
Franzoni, F; Gaudio, C; Greco, C; Marazzi, G; Pelliccia, F; Polacco, M; Rosano, G; Speziale, G; Spoletini, I; Vitale, C, 2014
)
0.97
" No difference of EVL Cmax or Tmax was found after atorvastatin coadministration."( Effects of atorvastatin on the pharmacokinetics of everolimus among kidney transplant recipients.
Avihingsanon, Y; Chancharoenthana, W; Praditpornsilpa, K; Somparn, P; Townamchai, N; Vadcharavivad, S; Wanitchanont, A, 2014
)
1.04
" Notably, plasma evacetrapib concentrations were mostly undetectable, and all pharmacodynamic biomarkers (HDL-C and LDL-C levels and CETP mass and activity) returned to baseline after a 4- to 6-week washout."( Efficacy, safety, tolerability, and pharmacokinetic profile of evacetrapib administered as monotherapy or in combination with atorvastatin in Japanese patients with dyslipidemia.
Krueger, KA; Morisaki, Y; Ruotolo, G; Takeuchi, M; Teramoto, T, 2014
)
0.61
" The method was applicable for the quality control of the mentioned drugs in raw material, bulk drug and pharmaceutical formulations as well as in pharmacokinetic studies."( Liquid Chromatographic Method for Simultaneous Quantitation of Clopidogrel, Aspirin and Atorvastatin in Rat Plasma and Its Application to the Pharmacokinetic Study.
Akhalaque Ahmad, RA; Chatpalliwar, VA; Chhajed, SS; Porwal, PK, 2015
)
0.64
"Volume of distribution is one of the most important pharmacokinetic properties of a drug candidate."( Volume of Distribution in Drug Design.
Beaumont, K; Di, L; Maurer, TS; Smith, DA, 2015
)
0.42
" Intensive steady-state 12- and 24-hour pharmacokinetic blood sampling was performed."( Pharmacokinetic Drug-Drug Interaction Study Between Raltegravir and Atorvastatin 20 mg in Healthy Volunteers.
Blonk, M; Burger, D; Colbers, A; Schouwenberg, B; van Beek, M, 2015
)
0.65
" The purpose of the present study is to develop a physiologically based pharmacokinetic (PBPK) model for atorvastatin and its two primary metabolites, 2-hydroxy-atorvastatin acid and atorvastatin lactone, using in vitro and in vivo data."( Physiologically based pharmacokinetic modeling of disposition and drug-drug interactions for atorvastatin and its metabolites.
Zhang, T, 2015
)
0.85
" Blood samples for pharmacokinetic analysis were taken until 168 hours postdose."( Evaluation of the effects of the weak CYP3A inhibitors atorvastatin and ethinyl estradiol/norgestimate on lomitapide pharmacokinetics in healthy subjects.
Dutta, S; Foulds, P; King, A; Korb, S; Patel, G; Sumeray, M; Wade, JR, 2016
)
0.68
" With the endogenous molecules, which showed a good correlation with pharmacokinetic parameters, a refined partial least-squares model was calculated based on predose data from a training set of 36 individuals and exhibited good predictive capability for the other 12 individuals in the prediction set."( A Pharmacometabonomic Approach To Predicting Metabolic Phenotypes and Pharmacokinetic Parameters of Atorvastatin in Healthy Volunteers.
Aa, J; Cao, B; Huang, Q; Jia, H; Liu, L; Shi, J; Song, Q; Tao, C; Wang, G; Xin, X; Yong, Y; Zhou, G; Zou, B, 2015
)
0.63
" The plasma concentrations of atorvastatin were measured for 48 h using Tandem Liquid Chromatography-Mass Spectrometry, LC-MS-MS, and the peak plasma concentration (C(max)), time to peak plasma concentration (T(max)), elimination half-life (t1/2), constant rate of elimination (k(el)), mean residence time (MRT, expo), volume of distribution (Vd/kg), clearance (CL/kg), area under curve AUC(0."( Effects of single nucleotide polymorphisms and haplotypes of the SLCO1B1 gene on the pharmacokinetic profile of atorvastatin in healthy Macedonian volunteers.
Daka, A; Dimovski, A; Eftimov, A; Geshkovska, MN; Jakjovski, K; Kapedanovska, A; Labachevski, N; Mladenovska, K; Nebija, D; Vavlukis, M, 2015
)
0.92
" A new model was developed for the prediction of AUC of statins that utilized the slopes of the above 2 models, with pharmacokinetic (Cmax) and a pharmacodynamic (IC50 value) components for the statins."( Dual Incorporation of the in vitro Data (IC50) and in vivo (Cmax) Data for the Prediction of Area Under the Curve (AUC) for Statins using Regression Models Developed for Either Pravastatin or Simvastatin.
Srinivas, NR, 2016
)
0.43
" Other pharmacokinetic parameters of both products were also determined."( Single dose pharmacokinetics of atorvastatin oral formulations using a simple HPLC-UV method.
Ahmad, M; Minhas, MU; Sohail, M, 2016
)
0.72
" 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
)
0.69
"No clinically significant pharmacokinetic or pharmacodynamic interactions were identified and no new safety issues observed with combined treatment with semaglutide."( Effect of Semaglutide on the Pharmacokinetics of Metformin, Warfarin, Atorvastatin and Digoxin in Healthy Subjects.
Anderson, TW; Derving Karsbøl, J; Golor, G; Hausner, H; Holst, AG; Jacobsen, JB; Wagner, FD, 2017
)
0.69
" 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
)
0.68
" We aimed to develop a semiphysiologically based pharmacokinetic (semi-PBPK) model involving both enzyme and transporters for predicting the contributions of altered function and expression of CYP3a and transporters to atorvastatin transport in diabetic rats by combining high-fat diet feeding and low-dose streptozotocin injection."( Prediction of Atorvastatin Pharmacokinetics in High-Fat Diet and Low-Dose Streptozotocin-Induced Diabetic Rats Using a Semiphysiologically Based Pharmacokinetic Model Involving Both Enzymes and Transporters.
Chen, N; Chen, Y; Geng, D; Li, P; Liang, L; Liu, L; Liu, X; Wang, Z; Xu, J; Yang, H; Zhang, X; Zhao, K, 2019
)
1.06
" The method was applied in a pharmacokinetic study following administration of a single oral 20, 40 or 80 mg ATV dose in healthy volunteers (n = 15)."( Simultaneous analysis of the total plasma concentration of atorvastatin and its five metabolites and the unbound plasma concentration of atorvastatin: Application in a clinical pharmacokinetic study of single oral dose.
Cestari, RN; de Oliveira, RDR; Lanchote, VL; Marques, MP; Rocha, A, 2019
)
0.76
" Though the statin-induced rhabdomyolysis is not common during statin therapy, its incidence will significantly increase due to pharmacokinetic drug-drug interactions (DDIs) with inhibitor drugs which inhibit atorvastatin's and its lactone's metabolism and hepatic uptake."( Prediction of pharmacokinetic drug-drug interactions causing atorvastatin-induced rhabdomyolysis using physiologically based pharmacokinetic modelling.
Cai, W; Dai, Y; Han, B; Jiao, Z; Jin, Z; Li, S; Lin, H; Ma, G; Xiang, X; Yu, Y, 2019
)
0.94
" In this work, we aim to employ the physiologically based pharmacokinetic (PBPK) model with the drug-target residence time model to predict and characterize both the pharmacokinetics (PK) and pharmacodynamics (PD) of topiroxostat in humans."( Prediction of the pharmacokinetics and pharmacodynamics of topiroxostat in humans by integrating the physiologically based pharmacokinetic model with the drug-target residence time model.
Han, X; Huang, H; Ji, Y; Liu, Y; Luo, Z; Sun, W; Wang, G; Yang, T; Yu, G, 2020
)
0.56
"There were significant differences in the pharmacokinetic parameters of the H4 active metabolite of CLP in the atorvastatin and rosuvastatin group divided according to their CYP2C19 genotype."( Impact of genetic variants of selected cytochrome P450 isoenzymes on pharmacokinetics and pharmacodynamics of clopidogrel in patients co-treated with atorvastatin or rosuvastatin.
Burchardt, P; Danielak, D; Główka, F; Karaźniewicz-Łada, M; Krzyżańska, D; Rzeźniczak, J; Słomczyński, M, 2020
)
0.97
"This study aimed to describe the pharmacokinetic profile of atorvastatin and its major metabolite, and to evaluate drug-drug interactions (DDIs) with antiretrovirals (ARVs)."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.04
"The atorvastatin pharmacokinetic profile was best described by a two-compartment model with first-order absorption and elimination."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.36
"Full pharmacokinetic profiles (98 atorvastatin + 62 o-OH-atorvastatin concentrations) and sparse concentrations (78 and 53 for atorvastatin and o-OH-atorvastatin, respectively) were collected in 59 PLWH."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.08
" We aimed to establish a whole-body physiologically-based pharmacokinetic (PBPK) model which predicts disposition of CsA and nine victim drugs including atorvastatin, cerivastatin, pravastatin, rosuvastatin, fluvastatin, simvastatin, lovastatin, repaglinide and bosentan, as well as drug-drug interactions (DDIs) of CsA with nine victim drugs to investigate the integrated effect of enzymes and transporters in liver, intestinal and kidney on drug disposition."( Prediction of Cyclosporin-Mediated Drug Interaction Using Physiologically Based Pharmacokinetic Model Characterizing Interplay of Drug Transporters and Enzymes.
Li, P; Liu, L; Liu, X; Wang, Z; Yang, Y; Zhang, Z, 2020
)
0.76
" The pharmacokinetic (PK) interactions studies on co-administration of ATR (8."( Pharmacokinetics and Pharmacodynamic Herb-Drug Interaction of Piperine with Atorvastatin in Rats.
Choudhary, DC; Nagrik, SS; Raje, A; Thomas, AB, 2021
)
0.85
" This study aimed to evaluate the pharmacokinetic interaction of atorvastatin and fixed-dose combination of sofosbuvir/ledipasvir "FDCSL" with rationalization to the underlying mechanism."( Pharmacokinetic interaction between atorvastatin and fixed-dose combination of sofosbuvir/ledipasvir in healthy male Egyptian volunteers.
Abdelaziz, AE; Abdelkawy, KS; Ali, AA; Belal, F; Elbarbry, F; Elmekawy, HA, 2021
)
1.13
"This phase 1, 2-part, 2-period, open-label, drug-drug interaction study evaluated the potential for pharmacokinetic interactions between upadacitinib and rosuvastatin, an organic anion transporting polypeptide (OATP) 1B1 and breast cancer resistance protein substrate, or atorvastatin, a cytochrome P450 3A, OATP1B1, and OATP1B3 substrate, in 36 healthy volunteers."( Effect of Upadacitinib on the Pharmacokinetics of Rosuvastatin or Atorvastatin in Healthy Subjects.
Camp, HS; Coppola, S; Feng, T; Kim, E; Mohamed, MF; Othman, AA, 2021
)
1.04
" Because pharmacodynamic interaction between statins and bempedoic acid is complex, a dose-response model was developed to predict LDL-C pharmacodynamics following administration of statins combined with bempedoic acid."( Pharmacodynamic effect of bempedoic acid and statin combinations: predictions from a dose-response model.
Amore, BM; Barrett, PHR; Catapano, AL; Chapel, S; Crass, RL; Emery, MG; Jadhav, SB; Kerschnitzki, M; Sasiela, WJ; Watts, GF, 2022
)
0.72
"This method was successfully applied to a pharmacokinetic interaction study in Wistar rats."( High-throughput LC-MS/MS Method for Simultaneous Determination of Pantoprazole and Atorvastatin in Rat Plasma: Application to a Pharmacokinetic Interaction Study.
Chen, X; Hong, Z; Le, J; Li, S; Liao, Y, 2021
)
0.85
" Serial pharmacokinetic blood samples were collected, and safety was assessed."( Assessment of the Effect of Filgotinib on the Pharmacokinetics of Atorvastatin, Pravastatin, and Rosuvastatin in Healthy Adult Participants.
Alani, M; Anderson, K; Gong, Q; Nelson, CH; Othman, AA; Tarnowski, T, 2022
)
0.96
" Our aim was to develop a flexible approach based on therapeutic drug monitoring (TDM), nonparametric population pharmacokinetic modeling, and Monte Carlo simulation to differentiate adherent patients from partially and nonadherent individuals in a nonrandomized, unicentric, observational study."( A pharmacokinetics-based approach to the monitoring of patient adherence to atorvastatin therapy.
Imreh, É; Karádi, I; Karvaly, GB; Neely, MN; Prohászka, Z; Trojnár, E; Vásárhelyi, B; Vincze, I; Zsáry, A, 2021
)
0.85
"The pharmacokinetic parameters of AC combined with GQD were significantly affected (P < 0."( Influence of Gegenqinlian Decoction on Pharmacokinetics and Pharmacodynamics of Atorvastatin Calcium in Hyperlipidemic Rats.
Chen, T; Cui, M; Sui, Y; Yan, X; Yin, Y; Zhu, F, 2022
)
0.95
" To assess the pharmacokinetic profile of daclatasvir in vivo, rats were divided into three groups receiving either saline, standard P-gp inhibitor verapamil (25 mg/kg), or atorvastatin (10 mg/kg), 2 hrs prior to a single dose of daclatasvir (7 mg/kg)."( Effect of Atorvastatin on Single Oral Pharmacokinetics and Safety of Daclatasvir in Rats: Emphasis on P-glycoprotein and Cytochrome P450.
El-Demerdash, E; Elbadawy, HA; Wahdan, SA, 2022
)
1.32
" In vivo, Cmax (peak plasma concentration) and area under the curve (AUC (0-t)) of daclatasvir after atorvastatin treatment increased compared to the vehicle group but not in a significant manner."( Effect of Atorvastatin on Single Oral Pharmacokinetics and Safety of Daclatasvir in Rats: Emphasis on P-glycoprotein and Cytochrome P450.
El-Demerdash, E; Elbadawy, HA; Wahdan, SA, 2022
)
1.34
"Co-intake of ATR with Acai berry resulted in slight decrease in Cmax from 41."( Investigation of the effect of Acai berry on the pharmacokinetics of Atorvastatin, Alogliptin and Empagliflozin: a herb-drug interaction study.
Nanjappan, SK; Ravichandiran, V; Somabattini, RA, 2022
)
0.96
"There was a significant change in the AUC0-t and Cmax of ATR, ALO and EMPA after co-administration with Acai berry."( Investigation of the effect of Acai berry on the pharmacokinetics of Atorvastatin, Alogliptin and Empagliflozin: a herb-drug interaction study.
Nanjappan, SK; Ravichandiran, V; Somabattini, RA, 2022
)
0.96
" Further studies using physiologically based pharmacokinetic modelling are required to investigate the drug-drug interactions between these drugs."( Simvastatin, but Not Atorvastatin, Is Associated with Higher Peak Rivaroxaban Serum Levels and Bleeding: an Asian Cohort Study from Singapore.
Chan, ECY; Soh, XQ; Tan, DS, 2023
)
1.23
" The objective of the current analysis was to evaluate the effects on the gastric emptying rate caused by semaglutide on pharmacokinetic model parameters of paracetamol and atorvastatin in healthy subjects."( Population pharmacokinetic of paracetamol and atorvastatin with co-administration of semaglutide.
Kristensen, K; Langeskov, EK, 2022
)
1.17
" This study aimed to investigate the pharmacokinetic interactions among atorvastatin, its active metabolite 2-hydroxy atorvastatin, and tangeretin after oral administration of atorvastatin with tangeretin in rats."( Ultra-high performance supercritical fluid chromatography-tandem mass spectrometry method for simultaneous determination of atorvastatin, 2-hydroxy atorvastatin, and tangeretin in rat plasma and its application to the pharmacokinetic study.
Gong, L; Jiang, Q; Li, W; Li, Y; Ni, D; Wang, S; Wang, W; Wu, W; Xu, X; Zhang, J; Zhang, T; Zhang, Y, 2022
)
1.16
" To investigate whether there are pharmacokinetic interactions among ATV, its metabolite 2-hydroxy atorvastatin (2-ATV), and NG, in the current study, we developed and validated a simple, rapid, and specific UPLC-MS/MS method to simultaneously determine the concentrations of these analytes in the rat plasma."( Development of a UPLC-MS/MS method for the simultaneous determination of atorvastatin, 2-hydroxy atorvastatin, and naringenin in rat plasma and its application to pharmacokinetic interaction studies.
Li, W; Li, Y; Wang, S; Xu, X; Zhang, T; Zhang, Y, 2023
)
1.36
" Several physiologically based pharmacokinetic (PBPK) models have been developed to assess its non-straightforward pharmacokinetics (PK) as well as that of its metabolites and have been only applied to assess drug-drug interactions (DDI)."( A physiologically based pharmacokinetic model for open acid and lactone forms of atorvastatin and metabolites to assess the drug-gene interaction with SLCO1B1 polymorphisms.
García-Arieta, A; Mangas-Sanjuán, V; Merino-Sanjuan, M; Reig-López, J, 2022
)
0.95
" Physiologically-based pharmacokinetic (PBPK) modeling, in lieu of a clinical trial, is a promising tool for evaluating these complex DDDIs in patients."( Understanding Statin-Roxadustat Drug-Drug-Disease Interaction Using Physiologically-Based Pharmacokinetic Modeling.
Ahlström, C; Dong, J; Elebring, M; Huang, Y; Lundahl, A; Någård, M; Prieto Garcia, L; Sjögren, E; Tang, W; Vildhede, A, 2023
)
0.91
" The objective of this study was to develop physiologically-based pharmacokinetic (PBPK) models that could describe drug-drug interactions (DDIs) of simeprevir with concomitant drugs via CYP3A4 and OATP1B inhibition, and also to capture the effects on coproporphyrin-I (CP-I), an endogenous biomarker of OATP1B."( Physiologically-based pharmacokinetic modeling for investigating the effect of simeprevir on concomitant drugs and an endogenous biomarker of OATP1B.
Nakayama, S; Snoeys, J; Sugiyama, Y; Toshimoto, K; Yamazaki, S, 2023
)
0.91

Compound-Compound Interactions

The aim of this study was to test the efficacy and possible drug-drug interactions of the new HMG-CoA reductase inhibitors (statins) atorvastatin and cerivastatin in cyclosporin A (CsA)-treated renal transplant patients.

ExcerptReferenceRelevance
" The aim of this study was to test the efficacy and possible drug-drug interactions of the new HMG-CoA reductase inhibitors (statins) atorvastatin and cerivastatin in cyclosporin A (CsA)-treated renal transplant patients."( Efficacy and drug interactions of the new HMG-CoA reductase inhibitors cerivastatin and atorvastatin in CsA-treated renal transplant recipients.
Burkhardt, K; Hauser, IA; Koch, C; Mayer-Kadner, I; Renders, L; Schärffe, S; Schmieder, RE; Veelken, R, 2001
)
0.74
"This study evaluated the effects of rosiglitazone therapy on lipids and the efficacy and safety of rosiglitazone in combination with atorvastatin in patients with type 2 diabetes mellitus."( Effects of rosiglitazone alone and in combination with atorvastatin on the metabolic abnormalities in type 2 diabetes mellitus.
Biswas, N; Brunzell, JD; Cohen, BR; Freed, MI; Kreider, MM; Marcovina, SM; Ratner, R, 2002
)
0.77
" Pravastatin does not appear to interact with warfarin but has caused an increased INR when combined with the anticoagulant fluindione."( Oral anticoagulant drug interactions with statins: case report of fluvastatin and review of the literature.
Andrus, MR, 2004
)
0.32
" Since DDIs are associated with adverse reactions, we performed a cross-sectional study to assess the prevalence of potentially critical drug-drug and drug-statin interactions in an outpatient adult population with dyslipidaemia."( Prevalence of potentially severe drug-drug interactions in ambulatory patients with dyslipidaemia receiving HMG-CoA reductase inhibitor therapy.
Hess, L; Krähenbühl, S; Krähenbühl-Melcher, A; Rätz Bravo, AE; Schlienger, RG; Tchambaz, L, 2005
)
0.33
"To report the case of a patient who underwent orthotopic heart transplant (OHT) and demonstrated a supratherapeutic response to ezetimibe when administered with cyclosporine."( Supratherapeutic response to ezetimibe administered with cyclosporine.
Burton, I; Koshman, SL; Lalonde, LD; Pearson, GJ; Tymchak, WJ, 2005
)
0.33
"The objective of the study was to demonstrate the effect of pioglitazone and pioglitazone in combination with statin on East Indian patients with hyperinsulinemia and hyperlipidemia."( Effect of pioglitazone and its combination with statins in coronary artery disease patients with hyperinsulinemia.
Baxi, H; Chag, M; Chandarana, A; Goyal, R; Mehta, A; Naik, A; Parikh, K; Shah, K; Shah, U, 2007
)
0.34
"This study was undertaken to investigate the effect of ezetimibe (10 mg/day) alone or in combination with atorvastatin (10 mg twice a week) on hypercholesterolemia in 56 high-risk patients intolerant to daily statin use."( Effectiveness of ezetimibe alone or in combination with twice a week Atorvastatin (10 mg) for statin intolerant high-risk patients.
Athyros, VG; Kakafika, AI; Karagiannis, A; Koumaras, H; Mikhailidis, DP; Tziomalos, K, 2008
)
0.79
" We studied the effects of a statin (atorvastatin) and its combination with an acyl-CoA:cholesterol O-acyltransferase (ACAT) inhibitor (avasimibe) on atherosclerotic regression and plaque stability as measured by matrix metalloproteinase 1 and 3 (MMP-1 and MMP-3) levels."( Statin therapy alone and in combination with an acyl-CoA:cholesterol O-acyltransferase inhibitor on experimental atherosclerosis.
Badimon, JJ; Chew, DP; Corti, R; Fallon, JT; Fayad, ZA; Fuster, V; Helft, G; Worthley, MI; Worthley, SG; Zaman, AG, 2007
)
0.61
"Ezetimibe did not alter serum visfatin concentrations, either when administered as monotherapy or combined with a statin."( Effects of ezetimibe, either alone or in combination with atorvastatin, on serum visfatin levels: a pilot study.
Derdemezis, C; Elisaf, M; Filippatos, T; Mikhailidis, D; Tselepis, A, 2008
)
0.59
" A comprehensive, controlled clinical trial programme was thus designed to evaluate three separate statins in combination with ABT-335, a new formulation of fenofibric acid."( Evaluation of a new formulation of fenofibric acid, ABT-335, co-administered with statins : study design and rationale of a phase III clinical programme.
Bays, HE; Buttler, SM; Davidson, MH; Jones, PH; Kelly, MT; Setze, CM; Sleep, DJ; Stolzenbach, JC, 2008
)
0.35
" The current review focuses distinctly on three aspects: (a) an in-depth coverage on the bioanalytical methods for the quantification of clopidogrel and its inactive carboxylic acid metabolite as well as the active metabolite in pre-clinical and clinical samples; (b) an overview of the pharmacokinetic/pharmacodynamic aspects of clopidogrel; and (c) enumerating the key findings from drug-drug interaction studies of clopidogrel with various co-substrates such as lanzoprazole, fluvastatin, atorvastatin, pravastatin, digoxin, ketoconazole, donezepil and theophylline."( Clopidogrel: review of bioanalytical methods, pharmacokinetics/pharmacodynamics, and update on recent trends in drug-drug interaction studies.
Mullangi, R; Srinivas, NR, 2009
)
0.51
" As statins are the standard of clinical care, any new therapies must have adjunctive activity, when given in combination with statins."( Thyroid hormone beta receptor activation has additive cholesterol lowering activity in combination with atorvastatin in rabbits, dogs and monkeys.
Cable, EE; Chi, B; Erion, MD; Fujitaki, JM; Ito, BR; Linemeyer, DL; MacKenna, DA; Song, X; van Poelje, PD; Wilker, CE; Zhang, BH, 2009
)
0.57
"We evaluated the activity of a liver-targeted prodrug, MB07811, of a novel TH receptor beta agonist, MB07344, as monotherapy and in combination with atorvastatin in rabbits, dogs and monkeys."( Thyroid hormone beta receptor activation has additive cholesterol lowering activity in combination with atorvastatin in rabbits, dogs and monkeys.
Cable, EE; Chi, B; Erion, MD; Fujitaki, JM; Ito, BR; Linemeyer, DL; MacKenna, DA; Song, X; van Poelje, PD; Wilker, CE; Zhang, BH, 2009
)
0.77
" This multicenter, double-blind, active-controlled study evaluated ABT-335 (fenofibric acid) in combination with 2 doses of atorvastatin in patients with mixed dyslipidemia."( Efficacy and safety of ABT-335 (fenofibric acid) in combination with atorvastatin in patients with mixed dyslipidemia.
Ballantyne, CM; Bays, HE; Buttler, SM; Goldberg, AC; Kelly, MT; Setze, CM; Sleep, DJ; Stolzenbach, JC, 2009
)
0.79
"We hypothesized that atorvastatin combined with amlodipine has additive beneficial vascular and metabolic effects that are superior to monotherapy in patients with hypertension."( Additive beneficial effects of atorvastatin combined with amlodipine in patients with mild-to-moderate hypertension.
Han, SH; Kim, SJ; Koh, KK; Koh, Y; Lee, Y; Park, JB; Quon, MJ; Shin, EK, 2011
)
0.97
"Atorvastatin combined with amlodipine therapy improves endothelial function and increases adiponectin levels and insulin sensitivity to a greater extent than monotherapy with either drug in hypertensive patients."( Additive beneficial effects of atorvastatin combined with amlodipine in patients with mild-to-moderate hypertension.
Han, SH; Kim, SJ; Koh, KK; Koh, Y; Lee, Y; Park, JB; Quon, MJ; Shin, EK, 2011
)
2.1
"To evaluate the long-term therapeutic effects of atorvastatin via cytochrome P450 (CYP)3A4 pathway or a non-CYP 3A4 pathway statin, pravastatin, combined with clopidogrel for the patients undergoing coronary stenting."( [Comparison on long-term effects of atorvastatin or pravastatin combined with clopidogrel for patients undergoing coronary stenting: a randomized controlled trial].
Han, YL; Jing, QM; Li, Y; Wang, DM; Wang, SL; Wang, ZL; Zhang, ZL, 2009
)
0.88
"The 12 month clinical outcomes were similar between patients receiving atorvastatin 20 mg/d or pravastatin 20 mg/d combined with clopidogrel after coronary stenting."( [Comparison on long-term effects of atorvastatin or pravastatin combined with clopidogrel for patients undergoing coronary stenting: a randomized controlled trial].
Han, YL; Jing, QM; Li, Y; Wang, DM; Wang, SL; Wang, ZL; Zhang, ZL, 2009
)
0.86
" We compared the effects of two statins (rosuvastatin and atorvastatin) combined with exercise on coenzyme Q10 and HDL-C levels in CAD patients."( Rosuvastatin combined with regular exercise preserves coenzyme Q10 levels associated with a significant increase in high-density lipoprotein cholesterol in patients with coronary artery disease.
Iwasaki, Y; Jinnouchi, H; Matsui, K; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2011
)
0.61
"Compared to atorvastatin, rosuvastatin combined with exercise significantly preserved ubiquinol levels associated with an increase in HDL-C."( Rosuvastatin combined with regular exercise preserves coenzyme Q10 levels associated with a significant increase in high-density lipoprotein cholesterol in patients with coronary artery disease.
Iwasaki, Y; Jinnouchi, H; Matsui, K; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2011
)
0.75
"To establish in vitro and in silico models that predict clinical drug-drug interactions (DDIs) with the OATP1B1 (SLCO1B1) transporter."( In vitro and in silico strategies to identify OATP1B1 inhibitors and predict clinical drug-drug interactions.
Ahlin, G; Artursson, P; Bergström, CA; Karlgren, M; Palm, J; Svensson, R, 2012
)
0.38
" Few studies have documented the efficacy and safety of CETP inhibitors in combination with commonly used statins."( Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol: a randomized controlled trial.
Brewer, HB; Hu, B; Kastelein, JJ; Krueger, KA; McErlean, E; Nicholls, SJ; Nissen, SE; Shao, M; Wang, MD, 2011
)
0.37
"To examine the biochemical effects, safety, and tolerability of evacetrapib, as monotherapy and in combination with statins, in patients with dyslipidemia."( Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol: a randomized controlled trial.
Brewer, HB; Hu, B; Kastelein, JJ; Krueger, KA; McErlean, E; Nicholls, SJ; Nissen, SE; Shao, M; Wang, MD, 2011
)
0.37
" In combination with statin therapy, evacetrapib, 100 mg/d, produced increases in HDL-C of 42."( Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol: a randomized controlled trial.
Brewer, HB; Hu, B; Kastelein, JJ; Krueger, KA; McErlean, E; Nicholls, SJ; Nissen, SE; Shao, M; Wang, MD, 2011
)
0.37
"Compared with placebo or statin monotherapy, evacetrapib as monotherapy or in combination with statins increased HDL-C levels and decreased LDL-C levels."( Effects of the CETP inhibitor evacetrapib administered as monotherapy or in combination with statins on HDL and LDL cholesterol: a randomized controlled trial.
Brewer, HB; Hu, B; Kastelein, JJ; Krueger, KA; McErlean, E; Nicholls, SJ; Nissen, SE; Shao, M; Wang, MD, 2011
)
0.37
" There were differences in the incidence, time to cerebral malaria and the level of parasitaemia when the drug combination was administered to mice."( Atorvastatin treatment is effective when used in combination with mefloquine in an experimental cerebral malaria murine model.
Amalvict, R; Baret, E; Briolant, S; Dormoi, J; Mosnier, J; Pradines, B; Rogier, C; Savini, H; Soulard, R; Souraud, JB, 2012
)
1.82
" Mean plasma concentration-time profiles for atazanavir, tenofovir disoproxil fumarate/emtricitabine (TDF/FTC), darunavir (DRV, administered with ritonavir [RTV]), and drospirenone/ethinylestradiol were similar following co-administration of GSK2248761."( Drug interaction profile for GSK2248761, a next generation non-nucleoside reverse transcriptase inhibitor.
de Serres, M; Gould, E; Johnson, M; Kim, J; Lou, Y; Mayers, D; Pietropaolo, K; Piscitelli, S; White, S; Zhou, XJ, 2012
)
0.38
"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
" In the present study, the drug-drug interaction potential of multi-dose ATV co-administration with CLZ on both pharmacokinetics and the anti-thrombotic property of CLZ is demonstrated."( Drug-drug interaction study to assess the effects of atorvastatin co-administration on pharmacokinetics and anti-thrombotic properties of cilostazol in male Wistar rats.
Arla, R; Rajak, S; Varanasi, KV; Vats, R; Veeraraghvan, S, 2012
)
0.63
"SilverHawk Plaque Excision combined with aggressive pharmacotherapy in this presented high-risk population is associated with promising long-term outcomes that compare favorably with accepted standards of care."( Long-term results of plaque excision combined with aggressive pharmacotherapy in high-risk patients with advanced peripheral artery disease (SAVE a LEG registry).
Buszman, PE; Buszman, PP; Kiesz, RS; Konkolewska, MD; Martin, JL; Radvany, MG; Szymanski, R; Wiernek, BK; Wiernek, SL, 2013
)
0.39
" The objective of this study was to evaluate the prevalence and clinical consequences of potential drug-drug interactions of clopidogrel with drugs affecting CYP3A4 activity."( Epidemiology of CYP3A4-mediated clopidogrel drug-drug interactions and their clinical consequences.
Heikkilä, P; Huupponen, R; Laine, K; Tirkkonen, T; Vahlberg, T, 2013
)
0.39
" The aim of this study was to determine the effects of statins combined with exercise on the renal function of CAD patients."( Statins combined with exercise are associated with the increased renal function mediated by high-molecular-weight adiponectin in coronary artery disease patients.
Iwasaki, Y; Jinnouchi, H; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2014
)
0.4
"We performed a sub-analysis of a clinical trial that determined the 20-week-effects of two statins (rosuvastatin, n=14; atorvastatin, n=14) combined with regular exercise on renal function, as assessed by the estimated glomerular filtration rates (eGFRs) of CAD patients."( Statins combined with exercise are associated with the increased renal function mediated by high-molecular-weight adiponectin in coronary artery disease patients.
Iwasaki, Y; Jinnouchi, H; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2014
)
0.61
" Both atorvastatin and rosuvastatin combined with regular exercise produced increases in eGFR."( Statins combined with exercise are associated with the increased renal function mediated by high-molecular-weight adiponectin in coronary artery disease patients.
Iwasaki, Y; Jinnouchi, H; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2014
)
0.88
"Statins combined with exercise significantly increased eGFR in CAD patients, and these improvements in renal function were correlated with increases in HMW-adiponectin levels."( Statins combined with exercise are associated with the increased renal function mediated by high-molecular-weight adiponectin in coronary artery disease patients.
Iwasaki, Y; Jinnouchi, H; Ogawa, H; Oka, H; Sugiyama, S; Sumida, H; Tanaka, T; Tayama, S; Toyama, K, 2014
)
0.4
"The aim of this study was to observe the effects of atorvastatin combined with ezetimibe on carotid atherosclerosis in elderly patients with hypercholesterolemia."( Effects of atorvastatin in combination with ezetimibe on carotid atherosclerosis in elderly patients with hypercholesterolemia.
Du, S; Han, YG; Li, L; Luo, P; Wang, GG; Wang, LX; Wu, SL; Zhu, HH, 2014
)
1.04
" Colchicine is a potent anti-inflammatory agent and whether colchicine combined with atorvastatin has synergistic effects on inflammation amelioration and endothelial function improvement is unknown."( Synergistic effects of colchicine combined with atorvastatin in rats with hyperlipidemia.
Cen, C; Ding, X; Huang, C; Wang, C; Zhan, H, 2014
)
0.88
"5 mg/kg body weight/day), or atorvastatin combined with colchicines (same dosages) were prescribed for 2 weeks."( Synergistic effects of colchicine combined with atorvastatin in rats with hyperlipidemia.
Cen, C; Ding, X; Huang, C; Wang, C; Zhan, H, 2014
)
0.95
"Colchicine combined with atorvastatin may have stronger protective effects on improving endothelial function and ameliorating inflammation in rats with hyperlipidemia."( Synergistic effects of colchicine combined with atorvastatin in rats with hyperlipidemia.
Cen, C; Ding, X; Huang, C; Wang, C; Zhan, H, 2014
)
0.96
" In the present study, we aimed to investigate the effect of berberine combined with atorvastatin on LOX‑1 and explore the underlying molecular mechanism involved."( Berberine combined with atorvastatin downregulates LOX‑1 expression through the ET‑1 receptor in monocyte/macrophages.
Chi, L; Hu, X; Pan, N; Peng, L; Zhang, Y, 2014
)
0.93
"The cholesteryl ester transfer protein (CETP) inhibitor evacetrapib has been previously shown to increase high-density lipoprotein cholesterol (HDL-C) and decrease low-density lipoprotein cholesterol (LDL-C) levels, as monotherapy or in combination with statins."( Efficacy, safety, tolerability, and pharmacokinetic profile of evacetrapib administered as monotherapy or in combination with atorvastatin in Japanese patients with dyslipidemia.
Krueger, KA; Morisaki, Y; Ruotolo, G; Takeuchi, M; Teramoto, T, 2014
)
0.61
" The interindividual differences in transporter expression and CLupt resulted in marked differences in drug-drug interactions due to isoform-specific inhibition."( Hepatic uptake of atorvastatin: influence of variability in transporter expression on uptake clearance and drug-drug interactions.
Artursson, P; Karlgren, M; Lai, Y; Norén, A; Svedberg, EK; Vildhede, A; Wisniewski, JR, 2014
)
0.74
"In a comparative aspect, the dynamics of indices of lipidogram, functional state of liver and level of C-reactive of protein have been analyzed in 79 patients with myocardial infarction in combination with non-alcoholic steatohepatitis, who received a 9-months treatment by rosuvastatin of 20 mg, atorvastatin of 80 mg, as well as rosuvastatin of 10 mg, atorvastatin of 40 mg in combination with ursodeoxycholic acid (UDCA)."( [Optimization of long-term hypolipidemia treatment of patients with myocardial infarction in combination with non-alcoholic steatohepatitis].
, 2014
)
0.58
"Compound danshen dripping pills combined with atorvastatin produces better effects than the drugs used alone in inhibiting vascular smooth muscle cell proliferation in rabbits after abdominal aorta angioplasty possibly due to a decreased expression of MCP-1 as a result of NF-κB inhibition."( [Effect of compound Danshen dripping pills combined with atorvastatin on restenosis after angioplasty in rabbits].
Chen, C; Li, P; Song, J; Zeng, J; Zhang, L; Zhang, Y, 2014
)
0.91
" However, the effects on platelet activation of high levels of LDL-C combined with low levels of HDL-C (HLC) have not yet been reported."( High levels of LDL-C combined with low levels of HDL-C further increase platelet activation in hypercholesterolemic patients.
Chan, LW; Gu, XY; Li, J; Liu, L; Luo, XP; Ni, HC; Qiao, J; Shi, HM; Wen, ZC, 2015
)
0.42
"To determine the effects of atorvastatin alone and in combination with inhaled corticosteroid on a range of sputum cytokines, chemokines and growth factors implicated in the pathogenesis of asthma, and their association with asthma control questionnaire (ACQ) and/or asthma quality of life questionnaire (AQLQ) scores."( Atorvastatin in combination with inhaled beclometasone modulates inflammatory sputum mediators in smokers with asthma.
Charron, CE; Chaudhuri, R; Ito, K; McSharry, C; Spears, M; Thomson, NC, 2015
)
2.15
" Atorvastatin significantly reduced sputum concentrations of CCL7, IL-12p70, sCD40L, FGF-2, CCL4, TGF-α and MMP-8 compared with placebo and, when combined with inhaled beclometasone, reduced sputum concentrations of MMP-8, IL-1β, IL-10, MMP-9, sCD40L, FGF-2, IL-7, G-CSF and CCL7 compared to ICS alone."( Atorvastatin in combination with inhaled beclometasone modulates inflammatory sputum mediators in smokers with asthma.
Charron, CE; Chaudhuri, R; Ito, K; McSharry, C; Spears, M; Thomson, NC, 2015
)
2.77
"Short-term treatment with atorvastatin alone or in combination with inhaled beclometasone reduces several sputum cytokines, chemokines and growth factors concentrations unresponsive to inhaled corticosteroids alone, in smokers with asthma."( Atorvastatin in combination with inhaled beclometasone modulates inflammatory sputum mediators in smokers with asthma.
Charron, CE; Chaudhuri, R; Ito, K; McSharry, C; Spears, M; Thomson, NC, 2015
)
2.16
"Ion mobility was performed on stored plasma samples collected from patients before and after treatment with anacetrapib alone (150 and 300 mg/d) or in combination with atorvastatin (20 mg/d) in a previously conducted 8-week phase IIb study."( Changes in LDL particle concentrations after treatment with the cholesteryl ester transfer protein inhibitor anacetrapib alone or in combination with atorvastatin.
Dansky, HM; Johnson-Levonas, AO; Krauss, RM; Liu, Y; Pinto, CA,
)
0.53
"The results of investigations had showed the high efficiency of the combination of atorvastatin with telmisartan in patients with arterial hypertension combined with obesity and NAFLD."( Combined effect of appointment telmisartan and atorvastatin on hemodynamic indicators and the indicators of lipid profile in patients with arterial hypertension combined with obesity and steatohepatitis.
Bochar, OM, 2014
)
0.88
"To study the protective effects of valsartan (Val) and benazepril, (Ben) combined with atorvastatin (Ato), on cardiorenal syndrome (CRS) in rats."( Protective effects of valsartan and benazepril combined with atorvastatin on cardiorenal syndrome in rats.
Chen, J; Hu, YJ; Peng, DF; Tang, SY, 2015
)
0.88
"Valsartan and benazepril, combined with atorvastatin, can have significant protective effects on cardiorenal functions of rats with CRS, with no significant difference between these two drugs."( Protective effects of valsartan and benazepril combined with atorvastatin on cardiorenal syndrome in rats.
Chen, J; Hu, YJ; Peng, DF; Tang, SY, 2015
)
0.93
"To observe the clinical effect of acupuncture therapy combined with Lipitor in the treatment of primary hyperlipidemia (spleen deficiency and food stagnation type)."( [Clinical trials for treatment of primary hyperlipidemia by using acupuncture in combination with Lipitor].
Song, J; Sun, YZ, 2015
)
0.42
"Acupuncture combined with administration of Lipitor is effective in improving primary hyperlipidemia in patients, which is superior to administration of simple Lipitor."( [Clinical trials for treatment of primary hyperlipidemia by using acupuncture in combination with Lipitor].
Song, J; Sun, YZ, 2015
)
0.42
"The aims to investigate the different protective effects of valsartan and benazepril when combined with atorvastatin in the cardio-renal functions of cardio-renal syndrome (CRS) patients."( Comparison of valsartan and benazepril when combined with atorvastatin in protecting patients with early cardio-renal syndrome (CRS).
Chen, J; Hu, YJ; Huang, Q; Peng, DF; Peng, X; Tang, SY, 2015
)
0.88
"When combined with atorvastatin, both valsartan and benazepril effectively improved the cardio-renal functions of early CRS patients."( Comparison of valsartan and benazepril when combined with atorvastatin in protecting patients with early cardio-renal syndrome (CRS).
Chen, J; Hu, YJ; Huang, Q; Peng, DF; Peng, X; Tang, SY, 2015
)
0.99
" The model was used to predict the pharmacokinetic profiles and drug-drug interaction (DDI) effect for atorvastatin and its metabolites in different DDI scenarios."( Physiologically based pharmacokinetic modeling of disposition and drug-drug interactions for atorvastatin and its metabolites.
Zhang, T, 2015
)
0.85
"To investigate the effects of atorvastatin combined with trimetazidine on periprocedural myocardial injury and serum inflammatory mediators in unstable angina pectoris (UAP) patients following percutaneous coronary intervention (PCI) treatment."( Effects of atorvastatin combined with trimetazidine on myocardial injury and inflammatory mediator in unstable angina patients during perioperative of percutaneous coronary intervention.
Cui, W; Du, H; Hao, J; Li, WW; Liu, F; Lu, JC; Yang, XC; Zhao, ZF, 2015
)
1.1
" The control group had 42 patients were treated with atorvastatin alone, while the experimental group had 48 cases treated with atorvastatin combined with trimetazidine."( Effects of atorvastatin combined with trimetazidine on myocardial injury and inflammatory mediator in unstable angina patients during perioperative of percutaneous coronary intervention.
Cui, W; Du, H; Hao, J; Li, WW; Liu, F; Lu, JC; Yang, XC; Zhao, ZF, 2015
)
1.06
"No unexpected symptom was found in patients with large dose atorvastatin combined with large dose trimetazidine."( Effects of atorvastatin combined with trimetazidine on myocardial injury and inflammatory mediator in unstable angina patients during perioperative of percutaneous coronary intervention.
Cui, W; Du, H; Hao, J; Li, WW; Liu, F; Lu, JC; Yang, XC; Zhao, ZF, 2015
)
1.05
" EPA inhibition was enhanced when combined with atorvastatin metabolite at low equimolar concentrations."( Eicosapentaenoic Acid Inhibits Oxidation of ApoB-containing Lipoprotein Particles of Different Size In Vitro When Administered Alone or in Combination With Atorvastatin Active Metabolite Compared With Other Triglyceride-lowering Agents.
Jacob, RF; Mason, RP; Sherratt, SC, 2016
)
0.89
" As several HF patients are likely to use statins as co-medications, the potential for a pharmacokinetic drug-drug interaction between atorvastatin and LCZ696 was evaluated."( Assessment of Drug-Drug Interaction Potential Between Atorvastatin and LCZ696, A Novel Angiotensin Receptor Neprilysin Inhibitor, in Healthy Chinese Male Subjects.
Ayalasomayajula, S; Han, Y; Langenickel, T; Pal, P; Pan, W; Rajman, I; Sunkara, G; Yang, F; Yuan, Y; Zhou, W, 2017
)
0.91
" The aim of the study was to investigate possible effect of this drug alone and in combination with RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm."( Cardioprotective effect of atorvastatin alone or in combination with remote ischemic preconditioning on the biochemical changes induced by ischemic/reperfusion injury in a mutual prospective study with a clinical and experimental animal arm.
El Desoky, ES; Fadil, SA; Hassan, AKM; Salem, SY; Taha, AF, 2016
)
0.73
"Clinical and experimental parts showed that groups with RIPC combined with atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P<0."( Cardioprotective effect of atorvastatin alone or in combination with remote ischemic preconditioning on the biochemical changes induced by ischemic/reperfusion injury in a mutual prospective study with a clinical and experimental animal arm.
El Desoky, ES; Fadil, SA; Hassan, AKM; Salem, SY; Taha, AF, 2016
)
0.96
"Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury."( Cardioprotective effect of atorvastatin alone or in combination with remote ischemic preconditioning on the biochemical changes induced by ischemic/reperfusion injury in a mutual prospective study with a clinical and experimental animal arm.
El Desoky, ES; Fadil, SA; Hassan, AKM; Salem, SY; Taha, AF, 2016
)
1.07
"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
)
0.69
" In vitro and clinical data suggest that doravirine is unlikely to cause significant drug-drug interactions via major drug-metabolizing enzymes or transporters."( Results of a Doravirine-Atorvastatin Drug-Drug Interaction Study.
Fan, L; Iwamoto, M; Jordan, H; Khalilieh, S; Maklad, N; Martell, M; Sanchez, RI; Triantafyllou, I; Yee, KL, 2017
)
0.76
"This study aims to investigate the drug-drug interactions (DDIs) between orally administered atorvastatin (ATV) and rifampicin (RIF) in rats."( Quantitative Analysis of the Transporter-Mediated Drug-Drug Interaction Between Atorvastatin and Rifampicin Using a Stable Isotope-IV Method.
Hasegawa, T; Higashino, H; Kataoka, M; Minami, K; Mutaguchi, K; Tachihara, M; Togashi, K; Yamashita, S, 2017
)
0.9
"The aim of this study was to evaluate the efficacy of ezetimibe combined with atorvastatin in treatment of carotid artery plaque in patients with type 2 diabetes mellitus complicated with coronary heart disease (CHD)."( Efficacy of ezetimibe combined with atorvastatin in the treatment of carotid artery plaque in patients with type 2 diabetes mellitus complicated with coronary heart disease.
Ai, XB; Li, L; Wang, F; Wang, J; Yi, XL; Zou, YW, 2017
)
0.96
"Evacetrapib daily in combination with atorvastatin was superior to placebo in lowering LDL-C after 12 weeks, and resulted in a statistically significant increase of HDL-C compared with placebo."( Efficacy and Safety of the Cholesteryl Ester Transfer Protein Inhibitor Evacetrapib in Combination With Atorvastatin in Japanese Patients With Primary Hypercholesterolemia.
Iimura, T; Kiyosue, A; Murakami, M; Riesmeyer, JS; Takita, Y; Teramoto, T, 2017
)
0.94
" They were often used in combination with antibiotics, blood-activating and stasis-dissolving prescription, and adrenal cortical hormone drugs."( [Real world analysis to explore clinical features of Shenxiong glucose injection combined with other medications].
Jia, PP; Liu, H; Wang, GQ; Xie, YM; Zhang, Y; Zhuang, Y, 2017
)
0.46
" Three months later, he was noted to have elevated creatine kinase (CK), thought to be related to a potential drug-drug interaction between ticagrelor and atorvastatin."( Elevated Creatine Kinase due to Potential Drug Interaction With Ticagrelor and Atorvastatin.
Beavers, JC, 2019
)
0.94
"A probable drug-drug interaction occurred with concomitant ticagrelor and atorvastatin."( Elevated Creatine Kinase due to Potential Drug Interaction With Ticagrelor and Atorvastatin.
Beavers, JC, 2019
)
0.97
"56%) was the most common triple Western medicine therapy, often combined with antibiotics and blood stasis drugs in use."( [Drug combination characteristics of Shenxiong glucose injection in treating ischemic cerebrovascular disease in real world].
Jia, PP; Liu, H; Wang, GQ; Xie, YM; Zhang, Y; Zhuang, Y, 2017
)
0.46
" We studied the effect of high-dose atorvastatin combined with ticagrelor loading on endothelial dysfunction in a model of forearm vascular ischemia-reperfusion (IR) injury."( Atorvastatin combined with ticagrelor prevent ischemia-reperfusion induced vascular endothelial dysfunction in healthy young males - A randomized, placebo-controlled, double-blinded study.
Kerbel, T; Litschauer, B; Weisshaar, S; Wolzt, M, 2018
)
2.2
"Chronic atorvastatin treatment combined with ticagrelor loading prevents against endothelial dysfunction after acute forearm ischemia."( Atorvastatin combined with ticagrelor prevent ischemia-reperfusion induced vascular endothelial dysfunction in healthy young males - A randomized, placebo-controlled, double-blinded study.
Kerbel, T; Litschauer, B; Weisshaar, S; Wolzt, M, 2018
)
2.36
" Due to drug-drug interactions caused by the inhibition or induction of cytochrome P450 enzymes, changes in drug metabolism are the major causes of drug toxicity, CYP3A4 is one of the key isozymes, and involved in the metabolism of over 60% of clinical drugs."( The enhancement of cardiotoxicity that results from inhibiton of CYP 3A4 activity and hERG channel by berberine in combination with statins.
Fang, L; Fang, Q; Feng, P; Guo, F; Li, B; Liang, Z; Xu, X; Zhan, G; Zhang, B; Zhao, L, 2018
)
0.48
" To explore the efficacy and safety of ezetimibe in combination with atorvastatin for the treatment of patients with T2DM and acute coronary syndrome (ACS)."( Efficacy and Safety of Ezetimibe in Combination with Atorvastatin for Acute Coronary Syndrome Patients Accompanied with Type 2 Diabetes: A Single-Center, Non-randomized Cohort Study.
Huang, Z; Li, Q; Li, X; Ye, W; Zhang, Q, 2019
)
1
" This study was designed to find out whether there is an augmentation of the therapeutic effectiveness of the antiinflammatory drugs like diclofenac sodium (NSAID), prednisolone (steroid) and atorvastatin (statin) when used in combination with ascorbic acid (antioxidant)."( Evaluation of the Anti-Inflammatory Activities of Diclofenac Sodium, Prednisolone and Atorvastatin in Combination with Ascorbic Acid.
Ahmed, T; Ahsan, CR; Al Shoyaib, A; Archie, SR; Chowdhury, FA; Faruk, A, 2020
)
0.97
" The inhibitions of such responses were measured after administering a drug alone and in combination with ascorbic acid."( Evaluation of the Anti-Inflammatory Activities of Diclofenac Sodium, Prednisolone and Atorvastatin in Combination with Ascorbic Acid.
Ahmed, T; Ahsan, CR; Al Shoyaib, A; Archie, SR; Chowdhury, FA; Faruk, A, 2020
)
0.78
" As the management of drug-drug interactions (DDIs) constitutes a key aspect of the care of PLWH, the magnitude of pharmacokinetic DDIs between cardiovascular and anti-HIV drugs needs to be more thoroughly characterized."( UHPLC-MS/MS assay for simultaneous determination of amlodipine, metoprolol, pravastatin, rosuvastatin, atorvastatin with its active metabolites in human plasma, for population-scale drug-drug interactions studies in people living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Desfontaine, V; Marzolini, C; Spaggiari, D, 2019
)
0.73
" Though the statin-induced rhabdomyolysis is not common during statin therapy, its incidence will significantly increase due to pharmacokinetic drug-drug interactions (DDIs) with inhibitor drugs which inhibit atorvastatin's and its lactone's metabolism and hepatic uptake."( Prediction of pharmacokinetic drug-drug interactions causing atorvastatin-induced rhabdomyolysis using physiologically based pharmacokinetic modelling.
Cai, W; Dai, Y; Han, B; Jiao, Z; Jin, Z; Li, S; Lin, H; Ma, G; Xiang, X; Yu, Y, 2019
)
0.94
": The risk of drug-drug interactions (DDIs) is elevated in aging people living with HIV (PLWH) because of highly prevalent age-related comorbidities leading to more comedications."( Aging does not impact drug--drug interaction magnitudes with antiretrovirals.
Battegay, M; Cavassini, M; Courlet, P; Decosterd, L; Marzolini, C; Saldanha, SA; Stader, F; Stoeckle, M, 2020
)
0.56
"In this study, we aimed to determine the drug-drug interaction potential between atorvastatin (ATOR), and talinolol (TAL)."( Effects of atorvastatin on talinolol absorption: A potential drug-drug interaction.
Baktir, G; Kara, ZP; Okyar, A; Orman, MN; Ozturk, D; Ozturk, N, 2020
)
1.17
"This study aimed to describe the pharmacokinetic profile of atorvastatin and its major metabolite, and to evaluate drug-drug interactions (DDIs) with antiretrovirals (ARVs)."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.04
" Here, we aim to explore the effects of atorvastatin combined with bivalirudin on coagulation function, cardiac function, and inflammatory factors in elderly patients with AMI who underwent PCI."( Effects of atorvastatin combined with bivalirudin on coagulation function, cardiac function, and inflammatory factors of percutaneous coronary intervention in elderly patients with acute myocardial infarction.
Chen, X; Ding, S; Wu, S; Xu, S, 2020
)
1.22
"Atorvastatin combined with bivalirudin can improve the efficiency of clinical treatment in elderly AMI patients who undergo PCI, while simultaneously improving blood coagulation function and reducing the occurrence of bleeding, compared with bivalrudin alone."( Effects of atorvastatin combined with bivalirudin on coagulation function, cardiac function, and inflammatory factors of percutaneous coronary intervention in elderly patients with acute myocardial infarction.
Chen, X; Ding, S; Wu, S; Xu, S, 2020
)
2.39
" This study evaluated the efficacy of atorvastatin in combination with standard therapy in patients with glioblastoma."( Atorvastatin in combination with radiotherapy and temozolomide for glioblastoma: a prospective phase II study.
Aldanan, S; Alghareeb, WA; Alhussain, H; AlNajjar, FH; Alsaeed, E; Alsharm, AA; Altwairgi, AK; Balbaid, AAO; Orz, Y, 2021
)
2.34
"This study evaluated the cardioprotective effects of NXT alone and in combination with ticagrelor (TIC) and atorvastatin (ATO)."( Protective effects of Naoxintong capsule alone and in combination with ticagrelor and atorvastatin in rats with Qi deficiency and blood stasis syndrome.
He, Y; Li, PB; Lin, QW; Liu, H; Su, WW; Wang, YG; Wu, H; Yan, ZH; Yao, HL; Zhang, WJ, 2020
)
0.99
" Drug-drug interaction (DDI) of CsA with victim drugs occurs via disordering interplay of transporters and enzymes."( Prediction of Cyclosporin-Mediated Drug Interaction Using Physiologically Based Pharmacokinetic Model Characterizing Interplay of Drug Transporters and Enzymes.
Li, P; Liu, L; Liu, X; Wang, Z; Yang, Y; Zhang, Z, 2020
)
0.56
"Self-controlled designs, specifically the case-crossover (CCO) and the self-controlled case series (SCCS), are increasingly utilized to generate real-world evidence (RWE) on drug-drug interactions (DDIs)."( Drug-Drug Interaction Surveillance Study: Comparing Self-Controlled Designs in Five Empirical Examples in Real-World Data.
Bykov, K; Gagne, JJ; Kim, S; Li, H; Lo Re, V; Vine, SM, 2021
)
0.62
" Compared to vehicle controls, the most effective drug combination consisted of low doses of levetiracetam, atorvastatin and ceftriaxone, which markedly reduced the incidence of electrographic seizures (by 60%; p<0."( Systematic evaluation of rationally chosen multitargeted drug combinations: a combination of low doses of levetiracetam, atorvastatin and ceftriaxone exerts antiepileptogenic effects in a mouse model of acquired epilepsy.
Bergin, DH; Johne, M; Klein, P; Löscher, W; Schidlitzki, A; Twele, F; Welzel, L, 2021
)
1.04
" Combined atorvastatin with celecoxib and tipifarnib synergistically decreased the sphere forming ability of Panc-1 cells and the drug combination also strongly inhibited cell proliferation and promoted apoptosis in the sphere-forming cells."( Effects of atorvastatin in combination with celecoxib and tipifarnib on proliferation and apoptosis in pancreatic cancer sphere-forming cells.
Chen, J; Goodin, S; Li, DL; Ma, YR; Ma, YY; Ren, X; Wang, X; Xu, XT; Zhang, K; Zhao, DG; Zheng, X; Zhou, RP, 2021
)
1.41
" In this study, we evaluated the drug-drug interaction potential of the hepatitis C virus inhibitors elbasvir (EBR) and grazoprevir (GZR) with statins."( Evaluation of Pharmacokinetic Drug Interactions of the Direct-Acting Antiviral Agents Elbasvir and Grazoprevir with Pitavastatin, Rosuvastatin, Pravastatin, and Atorvastatin in Healthy Adults.
Butterton, JR; Caro, L; Fandozzi, CM; Feng, HP; Fraser, IP; Guo, Z; Iwamoto, M; Levine, V; Panebianco, D; Prueksaritanont, T; Swearingen, D; Wolford, D; Yeh, WW, 2021
)
0.82
" This study assessed the potential protective effects of coenzyme Q10 (CoQ10) alone or combined with N-acetyl cysteine (NAC) or atorvastatin against CIN in diabetic rats."( Evaluation of coenzyme Q10 combined with or without N-acetyl cysteine or atorvastatin for preventing contrast-induced kidney injury in diabetic rats.
Alshogran, OY; Alzoubi, KH; El-Elimat, T; Nusair, SD; Obeidat, A; Sweidan, M, 2021
)
1.06
"This open-label, repeat-dose, fixed-sequence study in healthy subjects examined pharmacokinetic drug-drug interactions between the components of a novel fixed-dose combination product containing ramipril, amlodipine, and atorvastatin."( Mechanistic Considerations About an Unexpected Ramipril Drug-Drug Interaction in the Development of a Triple Fixed-Dose Combination Product Containing Ramipril, Amlodipine, and Atorvastatin.
Gundlach, K; Hermann, R; Seiler, D, 2021
)
1
" Our study aimed to determine whether pioglitazone combined with atorvastatin can restrain the progression of atherosclerosis and promote plaque stabilization in a rabbit model."( Pioglitazone combined with atorvastatin promotes plaque stabilization in a rabbit model.
Chen, X; Liang, Z; Nie, M; Yan, Y; Zhang, X; Zhao, Q, 2022
)
1.26
" Pioglitazone combined with atorvastatin can further restrain the progression of atherosclerosis and promote plaque stabilization in a rabbit model."( Pioglitazone combined with atorvastatin promotes plaque stabilization in a rabbit model.
Chen, X; Liang, Z; Nie, M; Yan, Y; Zhang, X; Zhao, Q, 2022
)
1.31
"This study aimed to investigate the effect of the therapy of amiodarone combined with atorvastatin on cardiac function of patients with acute myocardial infarction after percutaneous coronary intervention (PCI)."( Effect of the therapy of amiodarone combined with atorvastatin on cardiac function of patients with acute myocardial infarction after percutaneous coronary intervention (PCI).
Li, Z; Tu, Y; Zhang, J; Zhang, M; Zhou, Q; Zong, W, 2021
)
1.1
" We wish to extend this evidence in a study that aims to determine the efficacy and safety of atorvastatin combined with low-dose dexamethasone in patients with CSDH."( Atorvastatin combined with dexamethasone in chronic subdural haematoma (ATOCH II): study protocol for a randomized controlled trial.
Anderson, CS; De Zhu, X; Gao, C; Huang, Y; Ji, HM; Jiang, RC; Jiang, XC; Kang, Z; Lei, P; Li, X; Liu, JF; Qu, Y; Quan, W; Song, LL; Sun, XC; Tian, Y; Wang, D; Wang, JJ; Wang, RZ; Wei, HJ; Wei, JJ; Yue, SY; Zhang, JN; Zhang, S; Zhao, SG; Zhao, ZM; Zhu, XG, 2021
)
2.28
"The second ATorvastatin On Chronic subdural Hematoma (ATOCH-II) study is a multi-centre, randomized, placebo-controlled, double-blind trial which aims to enrol 240 adult patients with a conservative therapeutic indication for CSDH, randomly allocated to standard treatment with atorvastatin 20 mg combined with low-dose dexamethasone (or matching placebos) daily for 28 days, and with 152 days of follow-up."( Atorvastatin combined with dexamethasone in chronic subdural haematoma (ATOCH II): study protocol for a randomized controlled trial.
Anderson, CS; De Zhu, X; Gao, C; Huang, Y; Ji, HM; Jiang, RC; Jiang, XC; Kang, Z; Lei, P; Li, X; Liu, JF; Qu, Y; Quan, W; Song, LL; Sun, XC; Tian, Y; Wang, D; Wang, JJ; Wang, RZ; Wei, HJ; Wei, JJ; Yue, SY; Zhang, JN; Zhang, S; Zhao, SG; Zhao, ZM; Zhu, XG, 2021
)
2.45
" The aim of this study was to perform a meta-analysis of the effects of alendronate combined with atorvastatin compared with alendronate alone in the treatment of osteoporosis in diabetes mellitus."( Meta-Analysis of the Efficacy and Safety of Alendronate Combined with Atorvastatin in the Treatment of Osteoporosis in Diabetes Mellitus.
Shu, L; Tang, X; Xiong, Z; Yi, P; Zhang, C, 2022
)
1.17
" Our results showed that alendronate combined with atorvastatin is more effective than alendronate alone, with higher BMD, OPG, BGP, and BAP, more significant pain relief, and fewer adverse events."( Meta-Analysis of the Efficacy and Safety of Alendronate Combined with Atorvastatin in the Treatment of Osteoporosis in Diabetes Mellitus.
Shu, L; Tang, X; Xiong, Z; Yi, P; Zhang, C, 2022
)
1.21
"The results of this meta-analysis indicate that alendronate combined with atorvastatin is a better treatment for osteoporosis in diabetes mellitus, showing more effective and higher BMD and fewer adverse events than alendronate alone."( Meta-Analysis of the Efficacy and Safety of Alendronate Combined with Atorvastatin in the Treatment of Osteoporosis in Diabetes Mellitus.
Shu, L; Tang, X; Xiong, Z; Yi, P; Zhang, C, 2022
)
1.19
"This research aimed to study the optimization effects of the low-rank matrix denoising (LRMD) algorithm based on the Gaussian mixture model (GMM) on MRI images of stroke patients, aiming to evaluate the effects of atorvastatin combined with folic acid on poststroke cognitive impairment (PSCI) in patients with ischemic stroke."( Evaluation of the Effects of Folic Acid Combined with Atorvastatin on the Poststroke Cognitive Impairment by Low-Rank Matrix Denoising Algorithm-Based MRI Imaging.
Fang, F; Fang, Z; Li, J; Li, X; Li, Y; Wang, J; Wang, X, 2022
)
1.16
" First three groups were treated with Acai berry (PO; 250 mg/kg); fourth, fifth and sixth groups received sodium CMC (vehicle) for 10 days and on eleventh day, first and fourth groups were administered with ATR (PO; 10 mg/kg); second and fifth groups with ALO (PO; 25 mg/kg) and third and sixth groups received EMPA (PO; 25 mg/kg)."( Investigation of the effect of Acai berry on the pharmacokinetics of Atorvastatin, Alogliptin and Empagliflozin: a herb-drug interaction study.
Nanjappan, SK; Ravichandiran, V; Somabattini, RA, 2022
)
0.96
"To analyze the significance of ezetimibe in combination with low- to moderate-intensity atorvastatin adjuvant aspirin therapy for cerebrovascular disease."( Implications of Ezetimibe in Combination with Low- to Moderate-Intensity Atorvastatin Adjuvant Aspirin Therapy for Cerebrovascular Disease.
Tang, X; Wang, L, 2022
)
1.18
"Ezetimibe combined with medium- and low-intensity atorvastatin with aspirin in the treatment of cerebrovascular diseases can effectively improve the coagulation function of patients, reduce the level of inflammatory factors in patients, and improve the level of blood lipids in patients, with high safety and worthy of clinical application."( Implications of Ezetimibe in Combination with Low- to Moderate-Intensity Atorvastatin Adjuvant Aspirin Therapy for Cerebrovascular Disease.
Tang, X; Wang, L, 2022
)
1.21
"Our previous studies have confirmed that aspirin combined with Lipitor inhibited the development of prostate cancer (PCa), but the mechanisms need to be comprehensively expounded."( Identification of target and pathway of aspirin combined with Lipitor treatment in prostate cancer through integrated bioinformatics analysis.
Chen, M; Li, D; Liu, J; Liu, W; Ma, Y; Sheng, Z; Wang, X; Wu, Y; Xu, X; Zhao, D; Zheng, X, 2022
)
0.72
" The effects of silent DNA replication and sister chromatid cohesion 1 (siDSCC1) combined with Lipitor and aspirin on DSCC1 expression, viability, invasion and migration of PCa cells were detected by qRT-PCR, Wound healing and transwell assays."( Identification of target and pathway of aspirin combined with Lipitor treatment in prostate cancer through integrated bioinformatics analysis.
Chen, M; Li, D; Liu, J; Liu, W; Ma, Y; Sheng, Z; Wang, X; Wu, Y; Xu, X; Zhao, D; Zheng, X, 2022
)
0.72
"The enrichment pathways and targets of Lipitor combined with aspirin in PCa are discovered, and DSCC1 silencing can potentiate the effect of Lipitor combined with aspirin in the treatment of PCa."( Identification of target and pathway of aspirin combined with Lipitor treatment in prostate cancer through integrated bioinformatics analysis.
Chen, M; Li, D; Liu, J; Liu, W; Ma, Y; Sheng, Z; Wang, X; Wu, Y; Xu, X; Zhao, D; Zheng, X, 2022
)
0.72
"To explore the related factors of cerebral hemorrhage transformation after cerebral infarction and the value of atorvastatin calcium tablets combined with early intensive care measures."( Related Factors of Cerebral Hemorrhage after Cerebral Infarction and the Effect of Atorvastatin Combined with Intensive Nursing Care.
Li, X; Yang, Q; Yang, Y, 2022
)
1.16
" For patients with bleeding transformation, atorvastatin calcium tablets combined with early intensive nursing intervention has a certain value for improving the prognosis of patients."( Related Factors of Cerebral Hemorrhage after Cerebral Infarction and the Effect of Atorvastatin Combined with Intensive Nursing Care.
Li, X; Yang, Q; Yang, Y, 2022
)
1.21
" The symptoms were presumably caused by a drug-drug interaction between an antiretroviral drug combination and atorvastatin."( [Rhabdomyolysis due to drug-drug interaction of atorvastatin and cobicistat].
Hennersdorf, F; Intert, E; Knop, K; Krause, M; Rosenkranz, T, 2022
)
1.19
"Epidemiological and clinical evidence suggests that high-dose intake of omega 3 fatty acids (n-3 FA) have a favorable role in altering serum triglycerides (TG) and non-high density lipoprotein cholesterol (non-HDL-C) when combined with statins in hyperlipidemic patients."( N-3 fatty acid supplementation mediates lipid profile, including small dense LDL, when combined with statins: a randomized double blind placebo controlled trial.
Dogay Us, G; Mushtaq, S, 2022
)
0.72
" In addition, this case used amiodarone (AMD), and it has been reported that the RDV concentration increases when used in combination with AMD."( [Significant Prolongation of the International Normalized Ratio Associated with COVID-19 Treatment: Possible Drug Interaction with Remdesivir].
Bando, Y; Ishii, H; Otori, K; Yokota, N, 2022
)
0.72
" In this light, we investigated whether inhibition of IL-1β combined with cholesterol-lowering therapies can reduce OA development in dyslipidemic APOE∗3Leiden mice under pro-inflammatory dietary conditions."( IL-1β inhibition combined with cholesterol-lowering therapies decreases synovial lining thickness and spontaneous cartilage degeneration in a humanized dyslipidemia mouse model.
Blom, AB; Kruisbergen, NNL; Pieterman, EJ; Princen, HMG; van den Bosch, MHJ; van der Kraan, PM; van Gemert, Y; van Lent, PLEM, 2023
)
0.91
" Treatments included atorvastatin alone or with an anti-IL1β antibody, and atorvastatin combined with proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitor alirocumab without or with the anti-IL1β antibody."( IL-1β inhibition combined with cholesterol-lowering therapies decreases synovial lining thickness and spontaneous cartilage degeneration in a humanized dyslipidemia mouse model.
Blom, AB; Kruisbergen, NNL; Pieterman, EJ; Princen, HMG; van den Bosch, MHJ; van der Kraan, PM; van Gemert, Y; van Lent, PLEM, 2023
)
1.23
" Synovial thickening and cartilage degeneration were significantly decreased in mice that received cholesterol-lowering treatment combined with inhibition of IL-1β (P < 0."( IL-1β inhibition combined with cholesterol-lowering therapies decreases synovial lining thickness and spontaneous cartilage degeneration in a humanized dyslipidemia mouse model.
Blom, AB; Kruisbergen, NNL; Pieterman, EJ; Princen, HMG; van den Bosch, MHJ; van der Kraan, PM; van Gemert, Y; van Lent, PLEM, 2023
)
0.91
"These results indicate that inhibition of IL-1β combined with cholesterol-lowering therapy diminishes synovial thickening and cartilage degeneration in mice and may imply that this combination therapy could be beneficial in patients with metabolic inflammation."( IL-1β inhibition combined with cholesterol-lowering therapies decreases synovial lining thickness and spontaneous cartilage degeneration in a humanized dyslipidemia mouse model.
Blom, AB; Kruisbergen, NNL; Pieterman, EJ; Princen, HMG; van den Bosch, MHJ; van der Kraan, PM; van Gemert, Y; van Lent, PLEM, 2023
)
0.91
" However, there are few studies on the regulation and efficacy of atorvastatin combined with amlodipine on Th17/Treg balance in hypertension combined with carotid atherosclerosis."( Effects of amlodipine combined with atorvastatin on Th17/Treg imbalance and vascular microcirculation in hypertensive patients with atherosclerosis: A double-blind, single-center randomized controlled trial.
Qiu, Y; Yang, G, 2023
)
1.42
"These data indicate that amlodipine combined with atorvastatin can improve Th17/Treg imbalance, vascular endothelial function and efficacy in patients with hypertension and atherosclerosis."( Effects of amlodipine combined with atorvastatin on Th17/Treg imbalance and vascular microcirculation in hypertensive patients with atherosclerosis: A double-blind, single-center randomized controlled trial.
Qiu, Y; Yang, G, 2023
)
1.44
" Our objective was to evaluate potential drug-drug interactions of cilofexor as a victim and as a perpetrator."( Evaluation of the Potential for Cytochrome P450 and Transporter-Mediated Drug-Drug Interactions for Cilofexor, a Selective Nonsteroidal Farnesoid X Receptor (FXR) Agonist.
Kirby, BJ; Nelson, C; Othman, AA; Shen, G; Watkins, TR; Weber, E; Xiao, D; Younis, I, 2023
)
0.91
"In this Phase 1 study, healthy adult participants (n = 18-24 per each of the 6 cohorts) were administered cilofexor in combination with either perpetrators or substrates of cytochrome P-450 (CYP) enzymes and drug transporters."( Evaluation of the Potential for Cytochrome P450 and Transporter-Mediated Drug-Drug Interactions for Cilofexor, a Selective Nonsteroidal Farnesoid X Receptor (FXR) Agonist.
Kirby, BJ; Nelson, C; Othman, AA; Shen, G; Watkins, TR; Weber, E; Xiao, D; Younis, I, 2023
)
0.91
" Linear discriminant analysis effect size (LEfSe) analysis combined with receiver operating characteristic (ROC) curves revealed the marker bacteria associated with taking medication were g_Parabacteroides(AUC = 0."( Effects of long-term regular oral aspirin combined with atorvastatin to prevent ischemic stroke on human gut microbiota.
Chen, C; Chen, G; Cui, J; Liao, Y; Ming, J; Song, W; Wang, X; Wang, Z; Xu, K, 2023
)
1.16
"A different drug-drug interaction (DDI) scenario may exist in patients with chronic kidney disease (CKD) compared with healthy volunteers (HVs), depending on the interplay between drug-drug and disease (drug-drug-disease interaction (DDDI))."( Understanding Statin-Roxadustat Drug-Drug-Disease Interaction Using Physiologically-Based Pharmacokinetic Modeling.
Ahlström, C; Dong, J; Elebring, M; Huang, Y; Lundahl, A; Någård, M; Prieto Garcia, L; Sjögren, E; Tang, W; Vildhede, A, 2023
)
0.91
" This study aimed to investigate the effects of evolocumab, alone or in combination with atorvastatin, on the progression of atherosclerosis."( The effect of evolocumab alone and in combination with atorvastatin on atherosclerosis progression and TLRs expression.
Ali, N; Gali, F; Hadi, NR; Qassam, H; Saud, A, 2023
)
1.38
"To investigate the application of atorvastatin (AT) combined with ezetimibe (EZ) in elderly patients with hypertension (HY) combined with type 2 diabetes mellitus (T2DM) and the significance analysis of changes in serum bilirubin levels during treatment."( Application of Atorvastatin Combined with Ezetimibe in Elderly Patients with Hypertension Combined with T2DM and Analysis of Significance of Changes in Serum Bilirubin Levels During Treatment.
Du, M; Wang, Q; Wang, T; Zhu, S, 2023
)
1.54
"One hundred and twelve elderly patients with HY combined with T2DM admitted to our hospital from September 2019 to March 2022 were selected and divided into a control group (AT) and a combined group (AT + EZ) according to the random number table method, with 56 cases in each group."( Application of Atorvastatin Combined with Ezetimibe in Elderly Patients with Hypertension Combined with T2DM and Analysis of Significance of Changes in Serum Bilirubin Levels During Treatment.
Du, M; Wang, Q; Wang, T; Zhu, S, 2023
)
1.26
"AT combined with EZ can effectively improve glucose, lipids, inflammation and upregulate serum bilirubin in patients with HY combined with T2DM."( Application of Atorvastatin Combined with Ezetimibe in Elderly Patients with Hypertension Combined with T2DM and Analysis of Significance of Changes in Serum Bilirubin Levels During Treatment.
Du, M; Wang, Q; Wang, T; Zhu, S, 2023
)
1.26

Bioavailability

Atorvastatin directly improves vascular NO bioavailability and reduces vascular O(2)(·-) through tetrahydrobiopterin-mediated endothelial NO synthase coupling. Quercetin does not alter the oral bioavailability of AtorVastatin Calcium in rats.

ExcerptReferenceRelevance
" The bioavailability of atorvastatin capsules was similar to that of solution."( Tolerance and pharmacokinetics of single-dose atorvastatin, a potent inhibitor of HMG-CoA reductase, in healthy subjects.
Cilla, DD; Posvar, EL; Radulovic, LL; Sedman, AJ; Whitfield, LR, 1996
)
0.86
"Grapefruit juice greatly increases the bioavailability of lovastatin and simvastatin."( Grapefruit juice increases serum concentrations of atorvastatin and has no effect on pravastatin.
Kivistö, KT; Lilja, JJ; Neuvonen, PJ, 1999
)
0.56
" Lovastatin, Atorvastatin, Pravastatin and Simvastatin demonstrate variable potency to enhance the NO/O2- concentration ratio after stimulation of NOS, resulting in an increase of NO bioavailability in endothelial cells."( Statin-stimulated nitric oxide release from endothelium.
Dobrucki, IT; Dobrucki, LW; Kalinowski, L; Malinski, T,
)
0.5
" Nevertheless, an increase in pravastatin bioavailability has been reported in the presence of cyclosporine A, possibly because of an interaction at the level of biliary excretion."( Pharmacological interactions of statins.
Bellosta, S; Corsini, A; Paoletti, R, 2002
)
0.31
" However, atorvastatin acid is subject to extensive first-pass metabolism in the gut wall as well as in the liver, as oral bioavailability is 14%."( Clinical pharmacokinetics of atorvastatin.
Lennernäs, H, 2003
)
1.01
" Hypertensive Dahl salt-sensitive (DS) rats have endothelial dysfunction and cardiorenal injury associated with decreased NO bioavailability and increased superoxide (O2-) production linked to a functional upregulation of angiotensin II."( Atorvastatin prevents end-organ injury in salt-sensitive hypertension: role of eNOS and oxidant stress.
Jaimes, EA; Raij, L; Zhou, MS, 2004
)
1.77
"Endothelial nitric oxide (eNO) bioavailability is severely reduced after myocardial infarction (MI) and in heart failure."( Statin-induced improvement of endothelial progenitor cell mobilization, myocardial neovascularization, left ventricular function, and survival after experimental myocardial infarction requires endothelial nitric oxide synthase.
Bahlmann, FH; Drexler, H; Engberding, N; Fuchs, M; Haller, H; Heineke, A; Hilfiker-Kleiner, D; Hornig, B; Kotlarz, D; Landmesser, U; Mueller, M; Schaefer, A; Spiekermann, S; Templin, C; Wiencke, A, 2004
)
0.32
" eNO bioavailability after MI likely represents an important therapeutic target in heart failure after MI and mediates beneficial effects of statin treatment after MI."( Statin-induced improvement of endothelial progenitor cell mobilization, myocardial neovascularization, left ventricular function, and survival after experimental myocardial infarction requires endothelial nitric oxide synthase.
Bahlmann, FH; Drexler, H; Engberding, N; Fuchs, M; Haller, H; Heineke, A; Hilfiker-Kleiner, D; Hornig, B; Kotlarz, D; Landmesser, U; Mueller, M; Schaefer, A; Spiekermann, S; Templin, C; Wiencke, A, 2004
)
0.32
"The study was designed to evaluate the relative bioavailability of two formulations of atorvastatin (CAS 134523-03-8)."( Bioequivalence study of atorvastatin tablets.
Alpan, RS; Erenmemisoglu, A; Koytchev, R; Ozalp, Y; van der Meer, MJ, 2004
)
0.85
" Damage to the endothelium leads to reduced NO bioavailability and facilitates vessel wall permeability to low-density lipoprotein."( A rationale for combination therapy in risk factor management: a mechanistic perspective.
Mason, RP, 2005
)
0.33
" 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
" The validated method has been successfully used to analyze human plasma samples for application in pharmacokinetic, bioavailability or bioequivalence studies."( Simultaneous quantification of atorvastatin and active metabolites in human plasma by liquid chromatography-tandem mass spectrometry using rosuvastatin as internal standard.
Anjaneyulu, Y; Boosi, R; Kandikere, VN; Maurya, S; Mudigonda, K; Nirogi, RV; Shukla, M, 2006
)
0.62
" Oral bioavailability was studied on prepared SMEDDS hard capsules and compared with that of the conventional tablet in Beagle dogs in vivo."( [Preparation and evaluation of self-microemulsifying drug delivery systems containing atorvastatin].
Li, ZD; Shen, HR; Zhong, MK, 2005
)
0.55
" Oral bioavailability of atorvastatin SMEDDS was greater than that of the conventional tablet."( [Preparation and evaluation of self-microemulsifying drug delivery systems containing atorvastatin].
Li, ZD; Shen, HR; Zhong, MK, 2005
)
0.86
" Both hepatic and intestinal metabolism contribute to the low oral bioavailability of ATV in rats."( Pharmacokinetics of atorvastatin and its hydroxy metabolites in rats and the effects of concomitant rifampicin single doses: relevance of first-pass effect from hepatic uptake transporters, and intestinal and hepatic metabolism.
Benet, LZ; Huang, Y; Lau, YY; Okochi, H, 2006
)
0.66
" This might be because concomitant administration of P-glycoprotein substrates, such as statins, and colchicine, which is a P-glycoprotein inhibitor, modifies pharmacokinetics by increasing bioavailability and organ uptake of the substrates, leading to more adverse reactions and toxicities."( Rhabdomyolysis in a patient treated with colchicine and atorvastatin.
Altintas, ND; Cavus, S; Dede, DS; Iskit, AB; Topeli, A; Tufan, A,
)
0.38
"Atorvastatin is insoluble in aqueous solution and the bioavailability after oral administration is low."( Preparation and evaluation of self-microemulsifying drug delivery systems (SMEDDS) containing atorvastatin.
Shen, H; Zhong, M, 2006
)
2
" These findings suggest that the T-786C polymorphism modulates the effects of atorvastatin on NO bioavailability and oxidative stress."( eNOS gene T-786C polymorphism modulates atorvastatin-induced increase in blood nitrite.
Bem, AF; Metzger, IF; Nagassaki, S; Rocha, JB; Sertório, JT; Tanus-Santos, JE, 2006
)
0.83
"The aim of this study was to compare the bioavailability of two atorvastatin formulations (Divator Drogsan Pharmaceuticals, Ankara, Turkey, as the test formulation, and Lipitor, Pfizer Ireland Pharmaceuticals, Dublin, Ireland, as the reference formulation) in 52 healthy volunteers."( Pharmacokinetic and bioequivalence testing of atorvastatin formulations in healthy male volunteers.
Emritte, N; Hajdúch, M; Mendoza, L; Platílová, V; Plausinaitis, R; Svoboda, M, 2006
)
0.83
" Consequently, absolute bioavailability values of diltiazem pretreated with atorvastatin (8."( Effect of atorvastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats.
Chang, KS; Choi, DH; Choi, JS; Hong, SP, 2007
)
0.97
" Human oral bioavailability is an important pharmacokinetic property, which is directly related to the amount of drug available in the systemic circulation to exert pharmacological and therapeutic effects."( Hologram QSAR model for the prediction of human oral bioavailability.
Andricopulo, AD; Moda, TL; Montanari, CA, 2007
)
0.34
"05) increased the bioavailability of verapamil in rats."( Effect of atorvastatin on the intravenous and oral pharmacokinetics of verapamil in rats.
Chang, KS; Choi, DH; Choi, JS; Han, HK; Hong, SP, 2008
)
0.75
" Thus, the relative bioavailability increased by the same magnitude with atorvastatin."( Drug interaction between oral atorvastatin and verapamil in healthy subjects: effects of atorvastatin on the pharmacokinetics of verapamil and norverapamil.
Choi, DH; Choi, JS; Shin, WG, 2008
)
0.87
" AC, the world's best selling drug is associated with poor oral bioavailability and serious adverse effects like rhabdomyolysis on chronic administration."( Oral nanoparticulate atorvastatin calcium is more efficient and safe in comparison to Lipicure in treating hyperlipidemia.
Ankola, DD; Chandraiah, G; Kumar, MN; Meena, AK; Rao, PR; Ratnam, DV, 2008
)
0.66
" In particular, reduced bioavailability of endothelial-dependent nitric oxide production as a result of enhanced oxidative stress represents a common pathological mechanism of cardiovascular risk factors."( Scientific rationale for combination of a calcium channel antagonist and an HMG-CoA reductase inhibitor: a new approach to risk factor management.
Mason, RP, 2008
)
0.35
"05) compared with crystalline atorvastatin, suggesting that the enhanced bioavailability was attributed to amorphous nature and particle size reduction."( Physicochemical properties and oral bioavailability of amorphous atorvastatin hemi-calcium using spray-drying and SAS process.
Hwang, SJ; Jin, SJ; Kim, JS; Kim, MS; Lee, S; Park, HJ, 2008
)
0.87
" One possible mechanism for this effect is reduced bioavailability of nitric oxide, a key mediator of angiogenesis, secondary to increased oxygen free radicals."( Atorvastatin increases myocardial indices of oxidative stress in a porcine model of hypercholesterolemia and chronic ischemia.
Bianchi, C; Boodhwani, M; Clements, RT; Feng, J; Mieno, S; Ramlawi, B; Sellke, FW; Sodha, NR; Xu, SH,
)
1.57
"After 14 days of dosing, the rate and extent of exposure (AUCtau, C(max,ss)) to atorvastatin and its active metabolites were similar with both treatments, indicating that administration of P-OM3 did not affect the steady-state bioavailability of orally administered atorvastatin."( Effect of omega-3-acid ethyl esters on steady-state plasma pharmacokinetics of atorvastatin in healthy adults.
Di Spirito, M; Doyle, RT; Johnson, J; McKenney, J; Morelli, G, 2008
)
0.8
" Our results indicate that AMPK phosphorylation of eNOS Ser633 is a functional signaling event for NO bioavailability in ECs."( AMP-activated protein kinase functionally phosphorylates endothelial nitric oxide synthase Ser633.
Chen, Z; DeFea, K; Fu, Y; Hsu, PH; Pan, S; Peng, IC; Shyy, JY; Su, MI; Sun, W; Tsai, MD; Zhu, Y, 2009
)
0.35
" Our data support the effects of statins in vivo that have been demonstrated on the endothelium ex vivo, suggesting a beneficial effect by acting on the initial processes that trigger the disease, reducing oxidative stress (increase in the bioavailability of nitric oxide as peroxynitrite levels decrease) and curtailing the inflammatory processes which perpetuate the disease."( In vivo confirmation of the role of statins in reducing nitric oxide and C-reactive protein levels in peripheral arterial disease.
Aguilar, EM; Casariego, CV; García, FA; González, AF; Miralles, Jde H; Moreno, SB, 2009
)
0.35
"Maternal protein restriction in rats leads to endothelial dysfunction and decreased NO bioavailability in the offspring."( Atorvastatin restores endothelial function in offspring of protein-restricted rats in a cholesterol-independent manner.
Anthony, FW; Curzen, NP; Hanson, MA; Hopkins, LA; Kelsall, CJ; Torrens, C, 2009
)
1.8
" Previous results suggest that vascular dysfunction in OZR is associated with chronic reduction in vascular nitric-oxide (NO) bioavailability and chronic inflammation, both frequently associated with hypercholesterolemia."( Impact of chronic anticholesterol therapy on development of microvascular rarefaction in the metabolic syndrome.
Frisbee, JC; Frisbee, SJ; Goodwill, AG; James, ME; Stapleton, PA, 2009
)
0.35
"While the positive impact of chronic statin treatment on vascular outcomes in the metabolic syndrome are independent of changes to total cholesterol, and are more strongly associated with improvements to vascular NO bioavailability and attenuated inflammation, these results provide both a spatial and temporal framework for targeted investigation into mechanistic determinants of vasculopathy in the metabolic syndrome."( Impact of chronic anticholesterol therapy on development of microvascular rarefaction in the metabolic syndrome.
Frisbee, JC; Frisbee, SJ; Goodwill, AG; James, ME; Stapleton, PA, 2009
)
0.35
"Induced endothelin-1 (ET-1) production and decreased nitric oxide synthase (NOS) bioavailability have been found in aneurysmal subarachnoid hemorrhage (SAH)."( Atorvastatin preconditioning attenuates the production of endothelin-1 and prevents experimental vasospasm in rats.
Chang, CZ; Howng, SL; Hwang, SL; Kwan, AL; Lin, CL; Wu, SC, 2010
)
1.8
" The main pharmacokinetic parameters of atorvastatin acid (mean [relative standard error {RSE}]) for a subject with mean covariate values were the first-order absorption rate constant (3."( Development of a population pharmacokinetic model for atorvastatin acid and its lactone metabolite.
Akhlaghi, F; Asberg, A; Hermann, M; Narwal, R; Rosenbaum, SE, 2010
)
0.88
" The in-vitro study showed that solid dispersions increased the solubility and dissolution rate of ATR, and thus may improve its bioavailability compared with plain ATR."( Microwave induced solubility enhancement of poorly water soluble atorvastatin calcium.
Belgamwar, V; Maurya, D; Tekade, A, 2010
)
0.6
" In this study, we examined the effect of AMPK phosphorylation on Hcy-induced NO bioavailability impairment and NADPH oxidase 4 (Nox4) derived reactive oxygen species (ROS) accumulation in EPCs."( AMP-activated protein kinase inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells.
Chen, Z; Jia, F; Lu, G; Wu, C, 2011
)
0.37
" The population pharmacokinetic model described differences between the liquid-filled capsule used in phase I and phase IIb and the hot-melt extruded (HME) tablet formulation introduced in phase III, allowing for bridging of the two formulations, and quantified the complex relationship of apparent anacetrapib bioavailability with subject meal intake."( Model-based development of anacetrapib, a novel cholesteryl ester transfer protein inhibitor.
Bergman, AJ; Dockendorf, MF; Dykstra, K; Green, M; Krishna, R; Wagner, JA, 2011
)
0.37
" NO bioavailability was assessed using cyclic guanosine monophosphate quantification."( Atorvastatin worsens left ventricular diastolic dysfunction and endothelial dysfunction of epicardial coronary arteries in normocholesterolemic porcine with left ventricular hypertrophy.
Aubin, MC; Carrier, M; Forcillo, J; Maltais, S; Perrault, LP; Shi, YF; Tardif, JC, 2011
)
1.81
"We first examined the association of statin treatment with vascular NO bioavailability and arterial superoxide (O(2)(·-)) in 492 patients undergoing coronary artery bypass graft surgery."( Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin-mediated endothelial nitric oxide synthase coupling.
Antoniades, C; Antonopoulos, AS; Bakogiannis, C; Bendall, J; Casadei, B; Channon, KM; Demosthenous, M; Guzik, TJ; Hale, A; Leeson, P; Marinou, K; Paschalis, A; Psarros, C; Stefanadis, C; Tousoulis, D; Triantafyllou, C; Zhang, MH, 2011
)
0.37
" Atorvastatin directly improves vascular NO bioavailability and reduces vascular O(2)(·-) through tetrahydrobiopterin-mediated endothelial NO synthase coupling."( Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin-mediated endothelial nitric oxide synthase coupling.
Antoniades, C; Antonopoulos, AS; Bakogiannis, C; Bendall, J; Casadei, B; Channon, KM; Demosthenous, M; Guzik, TJ; Hale, A; Leeson, P; Marinou, K; Paschalis, A; Psarros, C; Stefanadis, C; Tousoulis, D; Triantafyllou, C; Zhang, MH, 2011
)
1.28
" Since tetrahydrobiopterin (BH(4)) is an essential cofactor for endothelial nitric oxide synthase (NOS3), decreased bioavailability of the substrate l-arginine and/or BH(4) may contribute to decreased NO production with hypercholesterolaemia."( Acute localized administration of tetrahydrobiopterin and chronic systemic atorvastatin treatment restore cutaneous microvascular function in hypercholesterolaemic humans.
Holowatz, LA; Kenney, WL, 2011
)
0.6
"The bioavailability of clopidogrel bisulfate (CAS 135046-48-9) form I was compared with that of clopidogrel bisulfate form II in 12 male Sprague-Dawley rats."( Study on bioavailability difference between clopidogrel bisulfate form I and form II using liquid chromatography/tandem mass spectrometry.
Che, WJ; Ou-Yang, PK; Tan, XH; Wei, P; Zhang, ZJ; Zou, QG, 2011
)
0.37
"A novel approach to improve the bioavailability and stability of atorvastatin (AT) was developed by constructing a nano-sized polymer-atorvastatin conjugate."( Enhanced bioavailability of nano-sized chitosan-atorvastatin conjugate after oral administration to rats.
Ahmad, FJ; Akhter, S; Anwar, M; Gahoi, S; Jain, GK; Khar, RK; Mallick, N; Talegaonkar, S; Warsi, MH, 2011
)
0.86
"Oral bioavailability of atorvastatin calcium (ATC) is very low (only 14%) due to instability and incomplete intestinal absorption and/or extensive gut wall extraction."( Enhanced bioavailability of atorvastatin calcium from stabilized gastric resident formulation.
Dehghan, MH; Khan, FN, 2011
)
0.97
"Atorvastatin/metformin ER 10 mg/500 mg FDC has similar bioavailability to the co-administration of separate atorvastatin 10 mg and metformin 500 mg tablets."( Pharmacokinetics of a fixed-dose combination of atorvastatin and metformin extended release versus concurrent administration of individual formulations: a randomized, open-label, two-treatment, two-period, two-sequence, single-dose, crossover, bioequivale
Arora, R; Dey, S; Kandhwal, K; Monif, T; Nazarudheen, S; Rao, S; Reyar, S; Singh, MK; Thudi, NR, 2011
)
2.07
"Statins, which improve the bioavailability of endogenous nitric oxide and upregulate endothelial nitric oxide synthase, have been used to prevent cerebral vasospasm after aneurysmal subarachnoid hemorrhage."( Atorvastatin decreases computed tomography and S100-assessed brain ischemia after subarachnoid aneurysmal hemorrhage: a comparative study.
Aout, M; Clarençon, F; Colonne, C; Fonfrede, M; Jean, B; Le Jean, L; Nouet, A; Puybasset, L; Sanchez-Peña, P; Vicaut, E, 2012
)
1.82
" 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
"The main aim of the present investigation is to develop and characterize the self-nanoemulsifying drug delivery systems (SNEDDS) of atorvastatin calcium (ATV) for improving the dissolution thereby oral bioavailability and to minimize the gastric degradation."( Development and characterization of self-nanoemulsifying drug delivery systems (SNEDDS) of atorvastatin calcium.
Mantri, SK; Murthy, KV; Pashikanti, S, 2012
)
0.8
"The aim of this study was to improve the solubility, stability and bioavailability of amorphous atorvastatin calcium (AT) by complexing it with hydroxypropyl-beta-cyclodextrin."( Preparation, physicochemical characteristics and bioavailability studies of an atorvastatin hydroxypropyl-beta-cyclodextrin complex.
Lv, HX; Waddad, AY; Zhang, ZH; Zhou, JP, 2012
)
0.82
" The relative bioavailability of AT and o-OAT in test formulation were (105."( [Pharmacokinetics and bioequivalence of atorvastatin calcium tablets in healthy male Chinese volunteers].
Chen, XY; Guo, LX; Shen, Y; Zhang, YF; Zhong, DF, 2012
)
0.65
"The solubility, absorption and distribution of a drug are involved in the basic aspects of oral bioavailability Solubility is an essential characteristic and influences the efficiency of the drug."( Preparation of candesartan and atorvastatin nanoparticles by solvent evaporation.
Dohnal, J; Grunwaldova, V; Jampilek, J; Kral, V; Vaculikova, E, 2012
)
0.66
" Atorvastatin has pleiotropic actions, including increasing nitric oxide (NO) bioavailability and reducing inflammation and oxidative damage."( Atorvastatin protects against deleterious cardiovascular consequences induced by chronic intermittent hypoxia.
Baldazza, M; Cachot, S; Faury, G; Fhayli, W; Joyeux-Faure, M; Korichneva, I; Lévy, P; Pépin, JL; Ribuot, C; Totoson, P, 2013
)
2.74
"The present study evaluated the bioavailability and bioequivalence of fixed dose combination test formulation (atorvastatin 10 mg and aspirin 150 mg capsule) against marketed reference formulations (Lipitor® tablets 10 mg and Nu-Seals tablets 75 mg)."( Bioequivalence of fixed dose combination of atorvastatin 10 mg and aspirin 150 mg capsules: a randomized, open-label, single-dose, two-way crossover study in healthy human subjects.
Battula, R; Betha, MR; Cheerla, R; Gadiko, C; Khan, SM; Nakkawar, M; Thota, S; Tippabhotla, SK; Vobalaboina, V; Yergude, S, 2013
)
0.86
" Knockin of OATP1B1 or OATP1B3 partially restored control clearance, volume, and bioavailability values (24%-142% increase, ≤47% increase, and ≤77% decrease vs."( Utility of Oatp1a/1b-knockout and OATP1B1/3-humanized mice in the study of OATP-mediated pharmacokinetics and tissue distribution: case studies with pravastatin, atorvastatin, simvastatin, and carboxydichlorofluorescein.
Bao, JQ; Fallon, JK; Higgins, JW; Ke, AB; Manro, JR; Smith, PC; Zamek-Gliszczynski, MJ, 2014
)
0.6
" The amorphous form of ATC possesses higher solubility, dissolution rate, and bioavailability than its crystalline form."( Coamorphous atorvastatin calcium to improve its physicochemical and pharmacokinetic properties.
Ghavimi, H; Hamishekar, H; Jouyban, A; Shayanfar, A, 2013
)
0.77
"Vascular aging is characterized by vascular cell senescence, increased oxidative stress, and endothelial and inducible nitric oxide (NO) synthase (eNOS/iNOS) imbalance, which reduces NO bioavailability and causes endothelial dysfunction."( Long-term atorvastatin improves age-related endothelial dysfunction by ameliorating oxidative stress and normalizing eNOS/iNOS imbalance in rat aorta.
Fu, G; Gong, X; Ma, Y; Ruan, Y; Wu, S, 2014
)
0.8
"Serious efforts have been made to overcome the bioavailability problems of ever increasing number of poorly soluble drugs, including atorvastatin (ATO); however, enhancing its gastric solubility has not received much attention."( Amorphous solid dispersion with increased gastric solubility in tandem with oral disintegrating tablets: a successful approach to improve the bioavailability of atorvastatin.
Asghar, S; Lv, H; Salmani, JM; Zhou, J, 2015
)
0.82
"To improve the bioavailability of ATO by increasing its gastric solubility in a stable oral disintegration tablet (ODT) formulation."( Amorphous solid dispersion with increased gastric solubility in tandem with oral disintegrating tablets: a successful approach to improve the bioavailability of atorvastatin.
Asghar, S; Lv, H; Salmani, JM; Zhou, J, 2015
)
0.61
" In vivo results showed an overall enhancement in the apparent bioavailability (83% and 434% more than Lipitor® and plain amorphous ATO tablets, respectively)."( Amorphous solid dispersion with increased gastric solubility in tandem with oral disintegrating tablets: a successful approach to improve the bioavailability of atorvastatin.
Asghar, S; Lv, H; Salmani, JM; Zhou, J, 2015
)
0.61
" The pharmacokinetic study illustrated that the fast absorption and increased oral bioavailability of atorvastatin as well as therapeutic concentration of atenolol in blood were made available through adoption of formulation strategy of bilayer tablets."( Formulation and evaluation of fixed-dose combination of bilayer gastroretentive matrix tablet containing atorvastatin as fast-release and atenolol as sustained-release.
Chattopadhyay, S; Dey, S; Mazumder, B, 2014
)
0.83
"The aim of the present study was to investigate the effect of Soluplus® on the solubility of atorvastatin calcium and to develop a solid dispersion formulation that can improve the oral bioavailability of atorvastatin calcium."( Preparation and evaluation of solid dispersion of atorvastatin calcium with Soluplus® by spray drying technique.
Baek, IH; Cho, W; Ha, ES; Hwang, SJ; Kim, MS, 2014
)
0.88
" The in vitro drug release and in vivo and ex vivo studies clearly demonstrated the potential of hydrophilic NG in enhancing the solubility, dissolution rate, and bioavailability of ATR."( Solubility and bioavailability enhancement of poorly aqueous soluble atorvastatin: in vitro, ex vivo, and in vivo studies.
Devkar, TB; Divase, GT; Rodde, MS; Tekade, AR, 2014
)
0.64
"Oxidative stress [increased bioavailability of reactive oxygen species (ROS)] plays a role in the endothelial dysfunction and vascular inflammation, which underlie vascular damage in diabetes."( Vascular injury in diabetic db/db mice is ameliorated by atorvastatin: role of Rac1/2-sensitive Nox-dependent pathways.
Antunes, TT; Bruder-Nascimento, T; Callera, GE; He, Y; Montezano, AC; Nguyen Dinh Cat, A; Tostes, RC; Touyz, RM, 2015
)
0.66
"The objective of this study was to investigate the impact of a novel spray-dried ternary solid dispersion (TSD) on the dissolution rate and bioavailability of a biopharmaceutics classification system (BCS) class II model drug, atorvastatin calcium trihydrate (ATC), and evaluate its in-vitro and in-vivo performance."( Preparation, in-vitro and in-vivo evaluation of spray-dried ternary solid dispersion of biopharmaceutics classification system class II model drug.
Ahuja, BK; Devasari, N; Jena, SK; Paidi, SK; Suresh, S, 2015
)
0.6
" It exhibited a fourfold increase in dissolution rate in comparison to ATC, with a considerable enhancement in oral bioavailability (relative bioavailability of 134."( Preparation, in-vitro and in-vivo evaluation of spray-dried ternary solid dispersion of biopharmaceutics classification system class II model drug.
Ahuja, BK; Devasari, N; Jena, SK; Paidi, SK; Suresh, S, 2015
)
0.42
"The TSD exhibits a significant increase in dissolution rate, and for this reason should be useful as an efficacious tool to enhance the bioavailability of BCS class II drug molecule, ATC."( Preparation, in-vitro and in-vivo evaluation of spray-dried ternary solid dispersion of biopharmaceutics classification system class II model drug.
Ahuja, BK; Devasari, N; Jena, SK; Paidi, SK; Suresh, S, 2015
)
0.42
"7 ng/mL), low endothelial NO bioavailability and high ONOO(-)."( Atorvastatin enhanced nitric oxide release and reduced blood pressure, nitroxidative stress and rantes levels in hypertensive rats with diabetes.
Corbalan, JJ; Dawoud, H; Jacob, RF; Malinski, T; Mason, RP, 2015
)
1.86
"The present work was aimed at developing an optimized oral nanostructured lipid carrier (NLC) formulation of poorly soluble atorvastatin Ca (AT Ca) and assessing its in vitro release, oral bioavailability and pharmacodynamic activity."( Chlorogenic acid stabilized nanostructured lipid carriers (NLC) of atorvastatin: formulation, design and in vivo evaluation.
Ali, J; Baboota, S; Khan, S; Narang, JK; Narang, RS, 2016
)
0.88
"This study sought to investigate whether the individual cholesterol absorption rate affects atorvastatin's effectiveness to reduce cardiovascular risk in hemodialysis patients."( Intestinal cholesterol absorption, treatment with atorvastatin, and cardiovascular risk in hemodialysis patients.
Baumgartner, I; Drechsler, C; Fauler, G; Genser, B; Grammer, TB; Krane, V; März, W; Ritz, E; Scharnagl, H; Silbernagel, G; Wanner, C, 2015
)
0.89
"The concentrations of crospovidone (CP), maltodextrin and microcrystalline cellulose (MCC) have been optimized in the development of self-microemulsified tablets (SMET) to improve the oral bioavailability of an anti-hyperlipidemic drug, atorvastatin, and the in-vivo pharmacokinetic parameters of the optimized SMET were compared with those of a commercial tablet in rabbits."( Effects of carbohydrate polymers in self-microemulsified tablets on the bioavailability of atorvastatin: In vitro-in vivo study.
Biswal, PK; Dixit, PK; Pani, NR, 2015
)
0.82
"The present results indicate that the bioavailability of the SMET of atorvastatin is better than the commercial formulation."( Effects of carbohydrate polymers in self-microemulsified tablets on the bioavailability of atorvastatin: In vitro-in vivo study.
Biswal, PK; Dixit, PK; Pani, NR, 2015
)
0.87
"Poor water solubility of a drug is a major challenge in drug delivery research and a main cause for limited bioavailability and pharmacokinetic parameters."( Custom fractional factorial designs to develop atorvastatin self-nanoemulsifying and nanosuspension delivery systems--enhancement of oral bioavailability.
Ahmed, OA; Al-Sawahli, MM; Hashem, FM; Nasr, M, 2015
)
0.67
"This work focuses on the development of atorvastatin utilizing zein, a natural, safe, and biocompatible polymer, as a nanosized formulation in order to overcome the poor oral bioavailability (12%) of the drug."( Optimized zein nanospheres for improved oral bioavailability of atorvastatin.
Ahmed, OA; Al-Sawahli, MM; Hashem, FM; Nasr, M, 2015
)
0.92
" In Wistar albino rats, the bioavailability of atorvastatin from the optimized atorvastatin-zein formulation was 3-fold greater than that from the atorvastatin suspension and the commercially available tablet."( Optimized zein nanospheres for improved oral bioavailability of atorvastatin.
Ahmed, OA; Al-Sawahli, MM; Hashem, FM; Nasr, M, 2015
)
0.91
" Quercetin does not alter the oral bioavailability of Atorvastatin Calcium in rats."( Quercetin does not alter the oral bioavailability of Atorvastatin in rats.
Babu, N; Challa, SR; Devi, R; Geddam, LB; Koritala, R; Ragam, SK; Sattenapalli, S; Venkatesh Reddy Challa, VR, 2015
)
0.92
" As a result of this, a significant decrease in the intestinal uptake and peroral bioavailability of the P-glycoprotein substrates (verapamil and atorvastatin) was observed along with the progression of diabetes as compared to normal animals."( Increased intestinal P-glycoprotein expression and activity with progression of diabetes and its modulation by epigallocatechin-3-gallate: Evidence from pharmacokinetic studies.
Agarwal, M; Dash, RP; Ellendula, B; Nivsarkar, M, 2015
)
0.62
" Pharmacokinetic study in Charles Foster rats showed significant enhancement in oral bioavailability as compared to pure drug suspension."( Atorvastatin calcium encapsulated eudragit nanoparticles with enhanced oral bioavailability, safety and efficacy profile.
Chaurasia, S; Khan, G; Kumar, N; Kumar, V; Mishra, B; Patel, RR, 2017
)
1.9
" SEDDS, with their unique solubilization properties, provide the opportunity to deliver lipophilic drugs to the gastrointestinal tract in a solubilized state, avoiding dissolution-a restricting factor in absorption rate of BCS Class 2 drugs, including atorvastatin."( Development and Evaluation of Liquid and Solid Self-Emulsifying Drug Delivery Systems for Atorvastatin.
Amelian, A; Czajkowska-Kośnik, A; Szekalska, M; Szymańska, E; Winnicka, K, 2015
)
0.82
"We believed that our findings can help the use of mesoporous silica materials in improving bioavailability of poorly water-soluble drugs."( Dissolution enhancement of a model poorly water-soluble drug, atorvastatin, with ordered mesoporous silica: comparison of MSF with SBA-15 as drug carriers.
Hamidi, M; Maleki, A, 2016
)
0.67
"Atorvastatin calcium (AC) is a BCS class II drug which shows poor bioavailability due to inadequate dissolution."( Dissolution enhancement of atorvastatin calcium by co-grinding technique.
Patravale, V; Prabhu, P, 2016
)
2.17
" PK results, on the other hand, revealed that the two freeze-dried AC-NPs formulations were of significantly lower bioavailability compared to Lipitor(®)."( PD-PK evaluation of freeze-dried atorvastatin calcium-loaded poly-ε-caprolactone nanoparticles.
Abd-Rabo, MM; Ahmed, IS; El-Hosary, R; Elkhateeb, DG; Nour, S; Shalaby, S, 2016
)
0.72
"To improve the dissolution and oral bioavailability (BA) of atorvastatin calcium (ATV), we previously introduced an optimized self-microemulsifying drug delivery system (SMEDDS) using Capmul(®) MCM (oil), Tween(®) 20 (surfactant), and tetraglycol (cosurfactant)."( Development of a solidified self-microemulsifying drug delivery system (S-SMEDDS) for atorvastatin calcium with improved dissolution and bioavailability.
Chae, BR; Choi, YW; Kim, JH; Kim, SR; Lee, SG; Son, HY; Song, SH; Yeom, DW, 2016
)
0.9
" Our analysis suggested that patients carrying one variant allele for the rs2622604 polymorphism (ABCG2) show a 55% (95% confidence interval: 16-131%) increase in atorvastatin oral bioavailability relative to the value in individuals without the variant allele."( Modelling of atorvastatin pharmacokinetics and the identification of the effect of a BCRP polymorphism in the Japanese population.
Aarons, L; Galetin, A; Guo, Y; Hall, S; Tsamandouras, N; Wendling, T, 2017
)
1.02
"The goal of the present investigation was to improve ATV bioavailability and overcome complications attendant with peroral administration by developing a new nanovesicular system encapsulating ATV for its delivery via the transdermal route."( Transdermal delivery of atorvastatin calcium from novel nanovesicular systems using polyethylene glycol fatty acid esters: Ameliorated effect without liver toxicity in poloxamer 407-induced hyperlipidemic rats.
Aboud, HM; Ali, AA; Hassan, AH; Johnston, TP; Mahmoud, MO, 2017
)
0.76
" However, the poor aqueous solubility and low bioavailability hinders the therapeutic potential of it when administrated orally."( Preparation and characterisation of atorvastatin and curcumin-loaded chitosan nanoformulations for oral delivery in atherosclerosis.
J B, VK; Madhusudhan, B; Ramakrishna, S, 2017
)
0.73
"This article presents the development of lyophilized orally disintegrating tablets prepared with the dry emulsion technique to enhance the in-vitro dissolution and in-vivo performance of the poorly bioavailable drug atorvastatin calcium (ATV)."( Experimentally designed lyophilized dry emulsion tablets for enhancing the antihyperlipidemic activity of atorvastatin calcium: Preparation, in-vitro evaluation and in-vivo assessment.
Basha, M; El Awdan, S; Salama, AH, 2018
)
0.88
" The results revealed that the oral bioavailability of two selected AC-NPs formulations was 235% and 169% relative to Lipitor."( Efficacy and Safety Profiles of Oral Atorvastatin-Loaded Nanoparticles: Effect of Size Modulation on Biodistribution.
Abd-Rabo, MM; Ahmed, IS; El Hosary, R; Haider, M; Hassan, MA, 2018
)
0.75
"13-folds increase in the bioavailability as compared to AC suspension."( In vitro and in vivo evaluation of cyclodextrin-based nanosponges for enhancing oral bioavailability of atorvastatin calcium.
Afouna, MI; Ibrahim, EA; Ibrahim, HM; Zidan, MF, 2018
)
0.7
" Endothelial dysfunction represents an early but reversible step in atherosclerosis and is characterized by a reduction in the bioavailability of NO."( Eicosapentaenoic acid improves endothelial function and nitric oxide bioavailability in a manner that is enhanced in combination with a statin.
Dawoud, H; Jacob, RF; Malinski, T; Mason, RP; Sherratt, SCR, 2018
)
0.48
"1 mg/mL) and poor oral bioavailability has limited therapeutic application of atorvastatin."( Atorvastatin-loaded lipid nanoparticles: antitumor activity studies on MCF-7 breast cancer cells.
Gambhire, MS; Gambhire, VM; Salunkhe, SM, 2018
)
2.15
"Atorvastatin is a lipid lowering agent with poor oral bioavailability (12%) because of poor solubility and extensive first pass hepatic metabolism."( Systematic approach for the formulation and optimization of atorvastatin loaded solid lipid NANOAPARTICLES using response surface methodology.
Jana, U; Manna, PK; Mohanta, GP; Sahoo, J; Sarangi, B, 2018
)
2.17
" Augmented bioavailability and reduced lipoprotein levels were key observations."( Investigation of different types of nano drug delivery systems of atorvastatin for the treatment of hyperlipidemia.
Devi Vemula, K; Mathur, M, 2018
)
0.72
" However, the low bioavailability of Ato limits its widespread use and clinical effectiveness."( Synergistic effects of liposomes encapsulating atorvastatin calcium and curcumin and targeting dysfunctional endothelial cells in reducing atherosclerosis.
Chen, B; Chen, X; Cheng, D; Li, X; Lin, C; Sun, W; Wang, J; Wu, T; Xiao, H, 2019
)
0.77
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
"Atorvastatin, a favored option for hyperlipidemia exhibits the problem of poor gastric solubility and low absolute bioavailability (12%) along with higher pre-systemic clearance (>80%)."( Surface stabilized atorvastatin nanocrystals with improved bioavailability, safety and antihyperlipidemic potential.
Mehta, I; Sharma, M, 2019
)
2.29
"A nanoemulsion system was designed for Atorvastatin calcium (ATOR) transdermal delivery to overcome its poor bioavailability of (30%) resulting from the extensive first-pass effect and dissolution rate-limited in vivo absorption."( Boosting transdermal delivery of atorvastatin calcium via o/w nanoemulsifying system: Two-step optimization, ex vivo and in vivo evaluation.
Elhuoni, MA; Ghoneim, AM; Ishak, RAH; Shaker, DS, 2020
)
1.11
"Atorvastatin calcium (AT) is an ocular anti-inflammatory with limited bioavailability when taken orally due to its low solubility in low pH and extensive first-pass effect."( Chitosan-Coated PLGA Nanoparticles for Enhanced Ocular Anti-Inflammatory Efficacy of Atorvastatin Calcium.
Arafa, MG; El-Dahan, MS; Girgis, GNS, 2020
)
2.22
" Poor bioavailability and blood-aqueous barrier may however limit significant ocular concentration of statins following oral administration."( Atorvastatin-loaded solid lipid nanoparticles as eye drops: proposed treatment option for age-related macular degeneration (AMD).
Giansanti, F; Guzman-Aranguez, A; Kaur, IP; Papucci, L; Perez de Lara, MJ; Schiavone, N; Singh, M; Yadav, M, 2020
)
2
"Despite the fact that atrovastatin (At) is being one of the bestselling statins used to prevent complicated cardiovascular diseases, its low oral bioavailability decreases its clinical relevance."( Enhancement of atorvastatin oral bioavailability via encapsulation in polymeric nanoparticles.
Al Thagfan, SS; Elbadawy, HM; Shaker, MA, 2021
)
0.97
"Atorvastatin has a significant effect on P-gp mediated intestinal transport of daclatasvir; however, it did not affect the systemic bioavailability of a single oral dose of daclatasvir."( Effect of Atorvastatin on Single Oral Pharmacokinetics and Safety of Daclatasvir in Rats: Emphasis on P-glycoprotein and Cytochrome P450.
El-Demerdash, E; Elbadawy, HA; Wahdan, SA, 2022
)
2.57
" Assessment of the individual cholesterol absorption rate to guide initiation of statin treatment is not supported by the findings in the AURORA study."( High cholesterol absorption is associated with increased cardiovascular risk in haemodialysis patients: insights from the AURORA study.
Duarte, K; Fauler, G; Fellström, B; Girerd, N; Jardine, AG; März, W; Massy, ZA; Rossignol, P; Sadiku, S; Scharnagl, H; Schmieder, RE; Silbernagel, G; Zannad, F, 2022
)
0.72
" Our study aimed to explore the effect of IBS and IBD on atorvastatin (ATV) pharmacokinetics, enhance ATV oral bioavailability (BCS II drug) using SFT, and analyze drug-disease-formulation interaction using a whole-body physiologically based pharmacokinetic (wbPBPK) model in rat and human."( Enhancing Atorvastatin In Vivo Oral Bioavailability in the Presence of Inflammatory Bowel Disease and Irritable Bowel Syndrome Using Supercritical Fluid Technology Guided by wbPBPK Modeling in Rat and Human.
Abu-Farsakh, NA; Al-Daoud, NM; Alsmadi, MM; Obaidat, RM, 2022
)
1.37
" The increase in sofosbuvir bioavailability was more pronounced after atorvastatin intake."( Statins Increase the Bioavailability of Fixed-Dose Combination of Sofosbuvir/Ledipasvir by Inhibition of P-glycoprotein.
Abdelaziz, A; Abdelgaied, MY; Abdelkawy, KS; Belal, F; El-Khodary, NM; Elmekawy, HA, 2022
)
0.96
" Like other long-acting GLP-1 analogues, semaglutide reduces gastric emptying and, potentially, alters the rate of absorption of orally co-administered drugs."( Population pharmacokinetic of paracetamol and atorvastatin with co-administration of semaglutide.
Kristensen, K; Langeskov, EK, 2022
)
0.98
" Upon successful application of the method to a pharmacokinetic interaction study, the results indicated that NG significantly enhanced the bioavailability of ATV and 2-ATV."( Development of a UPLC-MS/MS method for the simultaneous determination of atorvastatin, 2-hydroxy atorvastatin, and naringenin in rat plasma and its application to pharmacokinetic interaction studies.
Li, W; Li, Y; Wang, S; Xu, X; Zhang, T; Zhang, Y, 2023
)
1.14
" In this study, we constructed ATV-loaded nanoemulsions (ATV-NEs) containing multivalent intestinal transporter-targeting lipids to improve the oral bioavailability of ATV."( Enhancement of the anticancer effect of atorvastatin-loaded nanoemulsions by improving oral absorption via multivalent intestinal transporter-targeting lipids.
Byun, Y; Cho, SS; Khadka, B; Kim, KT; Kweon, S; Pandey, P; Park, JW; Shim, JH; Subedi, L, 2022
)
0.99
" Although statin therapy can reduce the chances of atherosclerotic plaque formation, they need to be administered in high doses due to low systemic bioavailability and encountered with side effects."( Enhancing the biopharmaceutical attributes of atorvastatin calcium using polymeric and lipid-polymer hybrid nanoparticles: An approach for atherosclerosis treatment.
Gao, T; Jiang, L; Li, F; Li, S; Liu, M; Shi, B, 2023
)
1.17
" Co-administration of linagliptin with either carvedilol or atorvastatin can modulate the oral bioavailability of linagliptin."( Investigation of the effect of concurrently administered carvedilol, atorvastatin and bile salts on intestinal absorption of linagliptin.
El Maghraby, GM; Embaby, MA; Osman, MA; Sultan, AA, 2023
)
1.39
"Atorvastatin calcium (AC), a cholesterol-lowering medication, has limited oral bioavailability (14 %) and adverse impacts on the gastrointestinal tract (GIT), liver, and muscle."( Formulation, and optimization of transdermal Atorvastatin Calcium-Loaded Ultra-flexible vesicles; ameliorates poloxamer 407-caused dyslipidemia.
Akl, MA; Ibrahim, MF; Kassem, AA; Ryad, S, 2023
)
2.61
"Despite significant advances in oral drug delivery technologies, many drugs are prone to limited oral bioavailability due to biological barriers that hinder drug absorption."( Atorvastatin-loaded pro-nanolipospheres with ameliorated oral bioavailability and antidyslipidemic activity.
Gardouh, AR; Ghorab, MM; Khafagy, ES; Motawee, AO, 2023
)
2.35

Dosage Studied

Amlodipine besylate (Norvasc) with atorvastatin calcium (Lipitor) marketed as Caduet (Pfizer Ltd) First dual-therapy compound designed to treat hypertension and/or angina and dyslipidemia concurrently with a single daily pill.

ExcerptRelevanceReference
" In 4 studies [2-wk rising dose (daily increasing doses for 1 wk; maintenance for 1 wk), 12-wk rising dose (daily dosing with weekly increases in dose), 2-wk toxicity (daily dosing for 2 wk; 3 dose levels), 13-wk toxicity (daily dosing for 13 wk; 3 dose levels)], dogs received up to 400 mg/kg orally."( Subchronic toxicity of atorvastatin, a hydroxymethylglutaryl-coenzyme A reductase inhibitor, in beagle dogs.
Albassam, MA; Clarke, DE; Walsh, KM,
)
0.44
"52 mmol/L (400 mg/dl) received once-daily dosing with atorvastatin (Lipitor) 10 mg or simvastatin (Zocor) 10 mg."( A multicenter, double-blind, one-year study comparing safety and efficacy of atorvastatin versus simvastatin in patients with hypercholesterolemia.
Best, J; Black, D; Bracs, P; d'Emden, M; Dart, A; Hamilton-Craig, I; Jerums, G; Nicholson, G; Sullivan, D; Tallis, G; West, M, 1997
)
0.77
" The two dosage groups were well matched and had no difference in lipoprotein responses."( Atorvastatin: an effective lipid-modifying agent in familial hypercholesterolemia.
Bateman, ME; Byrnes, P; Firth, JC; Marais, AD; Martens, C; Mountney, J, 1997
)
1.74
" A 52-week interim sacrifice and a reversal group in which dosing was terminated at week 52 and the dogs sacrificed at week 64, was included in the 104-week study."( Atorvastatin is not cataractogenic in beagle dogs.
Robertson, DG; Rothwell, CE; Urda, ER; Walsh, KM, 1997
)
1.74
" Thus atorvastatin had no consistent effect on the anticoagulant activity of warfarin and adjustment in warfarin dosing should not be necessary."( Atorvastatin does not alter the anticoagulant activity of warfarin.
Abel, R; Besserer, J; Gibson, GL; Stern, R, 1997
)
2.22
" The two drugs exhibited similar IC50's for inhibition of either rat or human reductase, and single oral dosing in rats showed the compounds to be nearly equipotent at inhibiting hepatic cholesterol synthesis."( Hepatic responses to inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase: a comparison of atorvastatin and simvastatin.
Bergstrom, JD; Bostedor, RG; Chao, YS; Geissler, WM; Rew, DJ; Wright, SD, 1998
)
0.52
" In accordance with manufacturers' recommendations, maximum dosage was atorvastatin 80 mg daily or simvastatin 40 mg daily (+cholestyramine 4 g daily in 84% of cases)."( Comparison of atorvastatin alone versus simvastatin +/- cholestyramine in the management of severe primary hypercholesterolaemia (the six cities study).
Simons, LA, 1998
)
0.89
" Twenty-seven (N = 27) patients with primary hypertriglyceridemia (TG > 350 mg/dL) were studied before and after 4 weeks on atorvastatin treatment at a dosage of either 20 (n = 16) or 80 (n = 11) mg/d."( Lipid and apolipoprotein levels and distribution in patients with hypertriglyceridemia: effect of triglyceride reductions with atorvastatin.
Bakker-Arkema, R; Black, D; Brown, WV; Innis-Whitehouse, W; Le, NA; Li, X, 2000
)
0.72
" LDL cholesterol levels were reduced by 17% at the 40 mg/day and by 28% at the 80 mg/day dosage (P<0."( Inhibition of cholesterol synthesis by atorvastatin in homozygous familial hypercholesterolaemia.
Black, DM; Firth, JC; Heinonen, TM; Illingworth, DR; Kotze, MJ; Marais, AD; Pappu, AS; Pilcher, GJ; Raal, FJ, 2000
)
0.58
" Steady-state atorvastatin pharmacokinetic parameters were estimated on the last day of each dosing period."( Pharmacodynamics and pharmacokinetic-pharmacodynamic relationships of atorvastatin, an HMG-CoA reductase inhibitor.
Abel, RB; Hounslow, NJ; MacMahon, M; Olson, SC; Stern, RH; Yang, BB, 2000
)
0.9
"6 mmol/l (100 mg/dl) maintained the same dosage regimen until they had completed 16 weeks of treatment."( Efficacy and safety of atorvastatin in hyperlipidemic, type 2 diabetic patients. A 34-week, multicenter, open-label study.
Aguilar-Salinas, CA; Alvarado Vega, A; Angélica Gómez-Díaz, R; Eduardo Romero-Nava, L; Gómez-Pérez, FJ; Guillén, LE; Gulías-Herrero, A; Meaney, E; Mendoza Pérez, E; Moguel, R; Novoa, G; Posadas-Romero, C; Salinas-Orozco, S; Vázquez-Chávez, C, 2000
)
0.62
" The calculated average annual maintenance cost was based on the distribution of the final daily dosing regimens and the public drug prices for each regimen."( Cost-minimization analysis of simvastatin versus atorvastatin for maintenance therapy in patients with coronary or peripheral vascular disease.
Allen, SE; Attanasio, E; Russo, P, 2001
)
0.57
" Dose-response curves to acetylcholine (10(-9)-10(-4) mol/l) and sodium nitroprusside (10(-9)-10(-4) mol/l) were studied in segmental arteries in the presence or absence of the thromboxane A2/PGH2 receptor antagonist ifetroban (10(-5) mol/l)."( Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in hypercholesterolaemic rabbits.
Aragoncillo, P; Cachofeiro, V; Cediel, E; de Las Heras, N; Díaz, C; Hernández, G; Lahera, V; Navarro-Cid, J; Ruilope, LM; Sanz-Rosa, D; Vázquez-Pérez, S, 2001
)
1.75
" Dose-response curves of simvastatin for bone formation and resorption differed."( Effect of statins on bone mineral density and bone histomorphometry in rodents.
Conradie, MM; Gopal, R; Hough, S; Hulley, PA; Maritz, FJ, 2001
)
0.31
" Six product brands encompassing 20 dosage strengths have been available during the past two years."( Managed care trends in statin usage.
Bazalo, GR, 2001
)
0.31
" Trends in market share, mean daily dose, and dosage distribution of the six current statin brands were examined."( Managed care trends in statin usage.
Bazalo, GR, 2001
)
0.31
" Nelfinavir increased the steady-state area under the plasma concentration-time curve during one dosing period (AUC(tau)) of atorvastatin 74% and the maximum concentration (C(max)) of atorvastatin 122% and increased the AUC(tau) of simvastatin 505% and the C(max) of simvastatin 517%."( Pharmacokinetic interactions between nelfinavir and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors atorvastatin and simvastatin.
Hsyu, PH; Kerr, BM; Lewis, RH; Lillibridge, JH; Schultz-Smith, MD, 2001
)
0.73
" After 5 years of failed therapy with other antihyperlipidemic agents, the patient finally agreed to undergo test dosing to a similar statin agent atorvastatin."( Using test dose challenges to restore essential therapy in patients with idiopathic anaphylaxis and pharmacophobia: report of a patient with idiopathic anaphylaxis and statin phobia.
Davison, R; Harris, KE; Mastrovich, JD; Patterson, R,
)
0.33
"The investigation showed that half-tablet dosing was as effective as whole-tablet dosing."( Effect of tablet splitting on serum cholesterol concentrations.
Castle, SS; Duncan, MC; Streetman, DS, 2002
)
0.31
"Neural networks have been used in diagnosing and treating many diseases, including the diagnosis of myocardial infarction and insulin dosing in diabetes mellitus."( A preliminary evaluation of neural network analysis for pharmacodynamic modeling of the dosing of the hydroxymethylglutaryl coenzyme A-reductase inhibitors simvastatin and atorvastatin.
Moon, A; Smith, T, 2002
)
0.51
"The goal of this study was to develop a preliminary pharmacodynamic model for dosing of the hydroxymethylglutaryl coenzyme A (HMG-CoA)-reductase inhibitors simvastatin and atorvastatin using neural network analysis."( A preliminary evaluation of neural network analysis for pharmacodynamic modeling of the dosing of the hydroxymethylglutaryl coenzyme A-reductase inhibitors simvastatin and atorvastatin.
Moon, A; Smith, T, 2002
)
0.7
"A neural network model for the dosing of the HMG-CoA-reductase inhibitors simvastatin and atorvastatin demonstrated an ability to predict appropriate dosing, but inclusion of other factors (eg, age, body weight, sex) and a larger sample size may be necessary for development of a more accurate model."( A preliminary evaluation of neural network analysis for pharmacodynamic modeling of the dosing of the hydroxymethylglutaryl coenzyme A-reductase inhibitors simvastatin and atorvastatin.
Moon, A; Smith, T, 2002
)
0.73
" However, atorvastatin had a different dose-response effect from simvastatin on both lipid parameters."( Dose-response effects of atorvastatin and simvastatin on high-density lipoprotein cholesterol in hypercholesterolaemic patients: a review of five comparative studies.
Mikhailidis, DP; Wierzbicki, AS, 2002
)
1.02
"The mean dosage of atorvastatin was 24 mg/day."( Treatment with atorvastatin to the National Cholesterol Educational Program goal versus 'usual' care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study.
Athyros, VG; Athyrou, VV; Basayannis, EO; Demitriadis, DS; Kontopoulos, AG; Mercouris, BR; Papageorgiou, AA; Symeonidis, AN, 2002
)
1
"The objective of this pilot study was to evaluate the comparative efficacy of alternate-day dosing of atorvastatin compared with the standard once-daily dose based on mean low-density lipoprotein (LDL) reduction from baseline at 6 and 12 weeks of treatment."( Is alternate daily dose of atorvastatin effective in treating patients with hyperlipidemia? The Alternate Day Versus Daily Dosing of Atorvastatin Study (ADDAS).
Deedwania, PC; Matalka, MS; Ravnan, MC, 2002
)
0.83
" Overall, more patients in the initial rosuvastatin 10-mg group achieved their ATP-II LDL-C goal than those in the initial atorvastatin 10-mg group (98% vs 87%), with 82% of patients treated with rosuvastatin achieving their goal at the 10-mg starting dosage without the need for titration, compared with 59% of patients treated with atorvastatin."( Effects of rosuvastatin and atorvastatin compared over 52 weeks of treatment in patients with hypercholesterolemia.
Istad, H; Luurila, O; Olsson, AG; Ose, L; Pears, J; Southworth, H; Stender, S; Tuomilehto, J; Wiklund, O; Wilpshaar, JW, 2002
)
0.82
" Policosanol is a cholesterol-lowering drug purified from sugar cane wax with a therapeutic dosage range from 5-20 mg/day."( Comparison of the efficacy and tolerability of policosanol with atorvastatin in elderly patients with type II hypercholesterolaemia.
Alvarez, E; Castaño, G; Fernández, L; Illnait, J; Lezcay, M; Mas, R; Mesa, M, 2003
)
0.56
" The accumulation of NO2/NO3 in HMEC exposed to increasing concentrations of more intensively oxidized-LDLs showed a nonlinear dose-response curve."( The effect of lipoproteins on endothelial nitric oxide synthase is modulated by lipoperoxides.
Baldi, S; Blandizzi, C; Del Tacca, M; L'Abbate, A; Lubrano, V; Natali, A; Palombo, C; Vassalle, C, 2003
)
0.32
" Moreover, the reduction in the cholesterol content of LDL <255 A was directly correlated with the daily dosage of atorvastatin (P=0."( Effects of atorvastatin on electrophoretic characteristics of LDL particles among subjects with heterozygous familial hypercholesterolemia.
Bergeron, J; Couture, P; Gagné, C; Hogue, JC; Lamarche, B; Larivière, M; Pirro, M, 2003
)
0.92
" Therefore there is no need to adapt atorvastatin dosage in this particular patient population."( Pharmacokinetics of atorvastatin and its metabolites after single and multiple dosing in hypercholesterolaemic haemodialysis patients.
Dratwa, M; Lameire, NH; Lins, RL; Matthys, KE; Peeters, PC; Stolear, JC; Verpooten, GA, 2003
)
0.92
"Comparing the dose-response of a new drug to that of a previously studied drug can aid in understanding their relative potencies."( Comparison of the dose-response relationships of 2 lipid-lowering agents: a Bayesian meta-analysis.
Berry, DA; Berry, SM; McKellar, J; Pearson, TA, 2003
)
0.32
"Combining this study and literature results substantially increased the power to compare the dose-response relationships of rosuvastatin and atorvastatin."( Comparison of the dose-response relationships of 2 lipid-lowering agents: a Bayesian meta-analysis.
Berry, DA; Berry, SM; McKellar, J; Pearson, TA, 2003
)
0.52
"Bayesian meta-analysis of results from related studies allows the comparison of the dose-response relationships of 2 drugs, better estimates of a particular dose-response relationship within an individual study, and the expression of relative benefits (of dose and drug) in terms of probabilities."( Comparison of the dose-response relationships of 2 lipid-lowering agents: a Bayesian meta-analysis.
Berry, DA; Berry, SM; McKellar, J; Pearson, TA, 2003
)
0.32
"Alternate-day dosing of atorvastatin is an efficacious and safe alternative to daily dosing."( Efficacy of alternate-day dosing versus daily dosing of atorvastatin.
Ahmadi-Kashani, M; Balian, H; Bashir, M; Ebrahimi, R; Jafari, M, 2003
)
0.87
" Dosage was increased to 20 mg if LDL cholesterol (LDL-C) levels remained >3."( Efficacy and safety of atorvastatin in children and adolescents with familial hypercholesterolemia or severe hyperlipidemia: a multicenter, randomized, placebo-controlled trial.
Marais, AD; McCrindle, BW; Ose, L, 2003
)
0.63
" The mean dose-response relationship has been shown to be log-linear for atorvastatin, but plasma concentrations of atorvastatin acid and its metabolites do not correlate with LDL-cholesterol reduction at a given dose."( Clinical pharmacokinetics of atorvastatin.
Lennernäs, H, 2003
)
0.84
" All these parameters were evaluated in patients after 6 and 12 months of treatment with atorvastatin at a dosage of 20 mg/day."( Long-term hemostatic effects of cholesterol-lowering therapy with atorvastatin.
Frisina, N; Gaudio, A; La Rocca, R; Lasco, A; Morini, E; Pizzoleo, MA; Scamardi, R; Trifiletti, A,
)
0.59
" Indeed, an interim analysis demonstrated the efficacy of atorvastatin, at a daily dosage of 10 mg as compared to placebo, in the prevention of major cardiovascular events, so that it appeared unethical to continue the study until the end."( [Clinical study of the month. Premature interruption of ASCOT and CARDS clinical trials of cardiovascular prevention with atorvastatin in patients with arterial hypertension or diabetes mellitus: compromise between ethics and statistics in evidence-based
Scheen, AJ, 2003
)
0.77
" These results were achieved with atorvastatin 10 mg/day (80 mg/day used in MIRACL), lovastatin 20 to 40 mg/day (caused by dosage titration), pravastatin 40 mg/day, simvastatin 20 to 80 mg/day (caused by dosage titration) or fluvastatin 80 mg/day."( Atorvastatin: gold standard for prophylaxis of myocardial ischemia and stroke - comparison of the clinical benefit of statins on the basis of randomized controlled endpoint studies.
Gathof, BS; Gresser, U, 2004
)
2.05
"A 67-year-old man receiving a stable maintenance dosage of warfarin experienced an increased international normalized ratio (INR) without bleeding when his atorvastatin therapy was switched to fluvastatin."( Oral anticoagulant drug interactions with statins: case report of fluvastatin and review of the literature.
Andrus, MR, 2004
)
0.52
" Combination therapy of amlodipine besylate (Norvasc, Pfizer Ltd) with atorvastatin calcium (Lipitor, Pfizer Ltd), marketed as Caduet (Pfizer Ltd) is the first dual-therapy compound designed to treat hypertension and/or angina and dyslipidemia concurrently with a single daily pill in the full range of dosing combinations."( Amlodipine/atorvastatin: the first cross risk factor polypill for the prevention and treatment of cardiovascular disease.
Frishman, WH; Zuckerman, AL, 2004
)
0.95
"5) After a 4-week wash-out period, they were randomized to amlodipine (5 mg) or atorvastatin (20 mg) or their combination at the same oral dosage for 12 weeks in three cross-over periods each separated by a 4-week placebo period (3 by 3 latin square design)."( Effect of amlodipine-atorvastatin combination on fibrinolysis in hypertensive hypercholesterolemic patients with insulin resistance.
Derosa, G; Fogari, E; Fogari, R; Lazzari, P; Mugellini, A; Rinaldi, A; Zoppi, A, 2004
)
0.87
" 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
"On average, AUC(0-12) [area under the whole blood concentration versus time curve in the dosing interval (0-12 h)] of cyclosporine was 5% (-16, 5) (90% confidence interval) lower upon co-administration with atorvastatin."( Atorvastatin does not affect the pharmacokinetics of cyclosporine in renal transplant recipients.
Asberg, A; Christensen, H; Hartmann, A; Hermann, M; Holdaas, H; Reubsaet, JL, 2005
)
1.96
" In addition to recommending lifestyle modifications, eight dosage strengths of amlodipine/atorvastatin single pill (5/10, 5/20, 5/40, 5/80, 10/10, 10/20, 10/40, and 10/80 mg) were electively titrated to improve blood pressure and lipid control."( Single-pill therapy in the treatment of concomitant hypertension and dyslipidemia (the amlodipine/atorvastatin gemini study).
Blank, R; LaSalle, J; Maroni, J; Reeves, R; Sun, F; Tarasenko, L, 2005
)
0.77
" The type and dosage of antihypertensive medications were not altered during statin therapy."( Statin therapy helps to control blood pressure levels in hypertensive dyslipidemic patients.
Akcay, A; Bilgi, M; Bozbas, H; Kanbay, M; Muderrisoglu, H; Ozdemir, FN; Ulus, T; Yildirir, A, 2005
)
0.33
" It is advisable to increase the dosage of atorvastatin and preferable to administer it in the evening to guarantee adequate concentrations during the nighttime rapid cholesterol synthesis when rifampin or other potent inducers of cytochrome P450 3A4 are coadministered."( Rifampin markedly decreases and gemfibrozil increases the plasma concentrations of atorvastatin and its metabolites.
Backman, JT; Luurila, H; Neuvonen, M; Neuvonen, PJ, 2005
)
0.82
" Moreover, it is unclear if the cardiovascular disease history length was similar in the two treatment groups as well as the length and dosage of statin treatment of the about 25% of patients taking statins before the enrollment."( REVERSAL and PROVE-IT: are clinically oriented trials really better than "pure" scientific studies?
Cicero, AF; Gaddi, A, 2005
)
0.33
" These changes were dependent upon dosage and were directly proportional to dosage rate."( Histological and ultrastructural changes in cross-striation muscle cells, under the influence of atorvastatin-reductase HMG-CoA inhibitor.
Czerny, K; Jedrych, B; Lańcut, M; Lis-Sochocka, M, 2004
)
0.54
" Heart weight/body weight ratio and the degree of inflammation were significantly lower in the two dosage statin-treated groups than that in the untreated one."( Effects of atorvastatin on the Th1/Th2 polarization of ongoing experimental autoimmune myocarditis in Lewis rats.
Gao, C; Li, WM; Liu, W; Sun, NL, 2005
)
0.72
" Group I-treated with pravastatin, group II--with simvastatin--both drugs in a dosage of 40 mg/kg daily, 5 days/week for a total of 3 weeks."( Effect of pravastatin, simvastatin and atorvastatin on the phagocytic activity of mouse peritoneal macrophages.
Bergman, M; Bessler, H; Djaldetti, M; Salman, H, 2006
)
0.6
" Low-density lipoprotein cholesterol is the first priority for treatment, with a statin in adequate dosage as the first choice for pharmacological therapy."( Reducing cardiovascular risk in diabetes: beyond glycemic and blood pressure control.
Hobbs, FD, 2006
)
0.33
"Correct execution of prescribed dosing regimen(s) is essential for patients to benefit from lipid lowering treatments."( Effect of intervention through a pharmaceutical care program on patient adherence with prescribed once-daily atorvastatin.
Belmans, A; de Klerk, E; Lesaffre, E; Matthys, K; Vrijens, B, 2006
)
0.55
"A supportive pharmaceutical care program consisting of review by patient and pharmacist of each patient's electronically compiled dosing history, plus educational reminders, improves patient adherence to the once-daily atorvastatin dosing regimen, mainly by extending persistence."( Effect of intervention through a pharmaceutical care program on patient adherence with prescribed once-daily atorvastatin.
Belmans, A; de Klerk, E; Lesaffre, E; Matthys, K; Vrijens, B, 2006
)
0.73
" Resolution on reduction of dosage or discontinuance and/or change of statin were deemed to constitute confirmation of cause."( Safety of statins when response is carefully monitored: a study of 336 heart recipients.
Aldama-López, G; Campo-Pérez, R; Castro-Beiras, A; Crespo-Leiro, MG; Llinares-García, D; Marzoa-Rivas, R; Muñiz-Garcia, J; Paniagua-Marin, MJ; Piñón-Esteban, P, 2005
)
0.33
"We searched Medline, the international medical database, to conduct a systematic review of the literature on the efficacy and tolerability of statins in CKD and renal transplant patients and on specific recommendations for dosage adjustments in this population."( [Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant].
Deray, G; Isnard-Bagnis, C; Karie, S; Launay-Vacher, V, 2006
)
0.33
" Although most statins are not excreted by the kidneys, the dosage of some must be adapted in CKD patients because of pharmacokinetic modifications induced by renal impairment."( [Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant].
Deray, G; Isnard-Bagnis, C; Karie, S; Launay-Vacher, V, 2006
)
0.33
"Statins have been known to reduce progression of atherosclerosis when used in high dosage in patients with elevated cholesterol."( Prevention of atherosclerosis progression using atorvastatin in normolipidemic coronary artery disease patients--a controlled randomized trial.
Goel, PK; Jain, A; Sharma, MK; Shukla, A,
)
0.39
" When the dosage of torcetrapib was doubled (at maximum tolerated dose), HDL increased by over 100%."( Torcetrapib and atorvastatin: a novel combination therapy for dyslipidemia.
Zareba, G, 2006
)
0.68
" The area under the plasma concentration-time curve (AUC(0-infinity)) for ATV also increased significantly after intravenous dosing of ATV with RIF, but the extent was much less than that observed for oral ATV dosing."( Pharmacokinetics of atorvastatin and its hydroxy metabolites in rats and the effects of concomitant rifampicin single doses: relevance of first-pass effect from hepatic uptake transporters, and intestinal and hepatic metabolism.
Benet, LZ; Huang, Y; Lau, YY; Okochi, H, 2006
)
0.66
"Ezetimibe added to atorvastatin therapy compared with treatment with the most common fixed atorvastatin daily dosage (10 mg) or with common atorvastatin titration strategies (up to 20 mg daily; up to 40 mg daily) resulted in cost per QALY estimates ranging from 25,344 to 44,332 Canadian dollars."( Cost effectiveness of adding ezetimibe to atorvastatin therapy in patients not at cholesterol treatment goal in Canada.
Alemao, E; Attard, C; Bourgault, C; Cook, J; Huse, D; Kohli, M; Lam, A; Marentette, M; Yin, D, 2006
)
0.93
" In 3 atorvastatin treated groups mice were fed the same diet as described above except atorvastatin was added to the diet at the dosage of 10 mg/kg per day for the last 8 weeks before euthanasia."( Atorvastatin has distinct effects on endothelial markers in different mouse models of atherosclerosis.
Jamborova, G; Nachtigal, P; Pospechova, K; Pospisilova, N; Semecky, V; Solichova, D; Zdansky, P, 2006
)
2.26
"An analysis is made of the effect of alternateday dosing of atorvastatin and standard once-daily dosing, based on mean low-density lipoprotein (LDL) reduction from baseline in type 2 diabetics."( Alternate-day dosing of atorvastatin: effects in treating type 2 diabetic patients with dyslipidaemia.
Ferrer-García, JC; Herrera-Ballester, A; Martínez-Mir, I; Pérez-Silvestre, J, 2006
)
0.88
"We sought to test the platelet inhibitory and anti-inflammatory effects of a higher statin dosage compared with combined treatment with ezetimibe plus a low statin dose."( Treatment with ezetimibe plus low-dose atorvastatin compared with higher-dose atorvastatin alone: is sufficient cholesterol-lowering enough to inhibit platelets?
Fischer, S; Jaster, M; Martus, P; Morguet, AJ; Piorkowski, M; Rauch, U; Schultheiss, HP; Stellbaum, C, 2007
)
0.61
" Statins were replaced with an equal dosage of fluvastatin."( Fluvastatin as co-medication in heart transplant recipients with elevated creatine-kinase.
Delgado, O; Kaczmarek, I; Meiser, B; Reichart, B; Sadoni, S; Schmöckel, M, 2007
)
0.34
"A rapid high performance liquid chromatographic method was developed and validated for determination of atorvastatin in pharmaceutical dosage forms, and for evaluation of its stability in the solid phase."( Validation of HPLC method for determination of atorvastatin in tablets and for monitoring stability in solid phase.
Kania, L; Stanisz, B,
)
0.6
" Treatment was started with 40 mg, followed by a dosage increase to 80 mg after 4 weeks."( Effects of short term atorvastatin treatment on cerebral hemodynamics in CADASIL.
Dichgans, M; Freilinger, T; Opherk, C; Peters, N; Pfefferkorn, T, 2007
)
0.65
" Canadian data on statin dosing were combined with efficacy data from a published meta-analysis to determine the proportion of patients who would be expected to achieve LDL-C targets after treatment with atorvastatin or generic simvastatin."( A model for assessing the cost-effectiveness of atorvastatin and simvastatin in achieving Canadian low-density lipoprotein cholesterol targets.
Lachaine, J; Merikle, E; Montpetit, M; Rinfret, S; Tarride, JE, 2007
)
0.78
"Two simple and accurate methods to determine atorvastatin calcium (ATO) and fenofibrate (FEN) in combined dosage forms were developed using second-derivative spectrophotometry and reversed-phase liquid chromatography (LC)."( Estimation of atorvastatin calcium and fenofibrate in tablets by derivative spectrophotometry and liquid chromatography.
Bhatt, HS; Bhatt, KK; Nakarani, NV; Patel, RD,
)
0.75
" Application of this flexible first dosing strategy in general practice will, based on available evidence, increase adherence to atorvastatin treatment in patients with high CHD risk."( Efficacy of atorvastatin after LDL-cholesterol-based dose selection in high risk dyslipidaemic patients: results of the target dose study.
Claeys, M; Commers, K; Deforce, J; Ducobu, J; Nachtergaele, H; Van Mieghem, W; Vandenbroucke, M, 2007
)
0.92
"To investigate the effects of two different dosage of atorvastatin on endothelium protection in spontaneously hypertensive rats (SHR)."( [Effects of atorvastatin on endothelium protection in spontaneously hypertensive rats].
Hu, SJ; Sun, J; Zhang, ZJ, 2007
)
0.97
" The results suggest that the effect of hydrophobic statins on the engulfing capacity of human peripheral blood phagocytes and apoptosis is dependent on their dosage and physiochemical properties."( Hydrophobic but not hydrophilic statins enhance phagocytosis and decrease apoptosis of human peripheral blood cells in vitro.
Bergman, M; Bessler, H; Djaldetti, M; Salman, H, 2008
)
0.35
" The study was performed in a group of stable coronary patients treated for two years with a moderate dosage of atorvastatin (20mg/day)."( E-selectin and TFPI are associated with carotid intima-media thickness in stable IHD patients: the baseline findings of the MIAMI study.
Amato, M; Arquati, M; Baldassarre, D; Brusoni, B; Camera, M; Cortellaro, M; Fiorentini, C; Montorsi, P; Porta, B; Romano, S; Tremoli, E, 2008
)
0.56
" In 2 atorvastatin-treated groups, mice were fed the same diets (chow or atherogenic) as described above except atorvastatin was added at the dosage of 10 mg x kg(-1) x day(-1) for the last 8 weeks before euthanasia."( Endothelial expression of endoglin in normocholesterolemic and hypercholesterolemic C57BL/6J mice before and after atorvastatin treatment.
Andrys, C; Jamborova, G; Nachtigal, P; Pospechova, K; Pospisilova, N; Semecky, V; Solichova, D; Zdansky, P, 2007
)
1.03
" It is not associated with neurological, cognitive or renal adverse effects and does not require dosage adjustment in patients with renal dysfunction, due to its favourable pharmacokinetic profile, which is unique among the statins."( Atorvastatin: a safety and tolerability profile.
Arca, M, 2007
)
1.78
" Estimated GFR improved in both treatment groups but was significantly greater with 80 mg than with 10 mg, suggesting this benefit may be dosage related."( Effect of intensive lipid lowering with atorvastatin on renal function in patients with coronary heart disease: the Treating to New Targets (TNT) study.
Bittner, V; Breazna, A; Deedwania, P; Dobson, S; Kastelein, JJ; Shepherd, J; Wenger, NK; Wilson, DJ; Zuckerman, A, 2007
)
0.61
" Fifty-six patients were randomized to receive optimal dosage of atorvastatin (n = 27) or 200 mg/d micronized fenofibrate (n = 29) for 24 weeks."( Comparison of atorvastatin versus fenofibrate in reaching lipid targets and influencing biomarkers of endothelial damage in patients with familial combined hyperlipidemia.
Antonini, R; Antonini, TM; Arca, M; Fraioli, A; Letizia, C; Luigi, P; Maddaloni, M; Mastrantoni, M; Montali, A; Pigna, G, 2007
)
0.94
" Our objective was to explore how differences in prevalences of use, dosing characteristics, choice of statin and continuity of therapy in individual patients adds new information to previous results."( Aspects of statin prescribing in Norwegian counties with high, average and low statin consumption - an individual-level prescription database study.
Eggen, AE; Engeland, A; Furu, K; Hartz, I; Njølstad, I; Sakshaug, S; Skurtveit, S, 2007
)
0.34
" Forty one patients remained throughout the study and had their weekly dosage reduced."( Efficacy of atorvastatin when not administered daily.
Ghattas, AE; Pimenta, J, 2007
)
0.72
" If the target cholesterol levels has not been achieved 6 weeks after the treatment, then the daily atorvastatin dosage has been increased."( The effects of atorvastatin therapy on endothelial function in patients with coronary artery disease.
Baskurt, M; Cakar, MA; Coskun, U; Guzelsoy, D; Okcun, B; Yildiz, A, 2007
)
0.91
" Eight dosage strengths of single-pill amlodipine/atorvastatin were flexibly titrated."( Improved attainment of blood pressure and cholesterol goals using single-pill amlodipine/atorvastatin in African Americans: the CAPABLE trial.
Bruschi, P; Ferdinand, KC; Flack, JM; Jamieson, MJ; Saunders, E; Shi, H; Tarasenko, L; Victor, R; Watson, K, 2008
)
0.82
" The proposed method can be useful in the quality control of bulk manufacturing and pharmaceutical dosage forms."( Stability-indicating reversed-phase liquid chromatographic method for simultaneous determination of atorvastatin and ezetimibe from their combination drug products.
Chaudhari, BG; Patel, LJ; Patel, NM; Patel, VP; Shah, PB,
)
0.35
" The control group of animals (n=8) was fed with the western type diet (atherogenic diet) and in other two groups atorvastatin was added to the atherogenic diet at the dosage of either 10 mg/kg or 100 mg/kg per day for a period of 2 months."( Atorvastatin has hypolipidemic and anti-inflammatory effects in apoE/LDL receptor-double-knockout mice.
Andrys, C; Jamborova, G; Micuda, S; Nachtigal, P; Pospechova, K; Pospisilova, N; Semecky, V; Solichova, D; Zdansky, P, 2008
)
2
"Flexible initial dosing and early aggressive titration of atorvastatin according to LDL-C levels is an efficient and safe strategy for achieving the target level and for improving endothelial dysfunction in hyperlipidemic patients with type 2 diabetes."( Flexible initial dosing of atorvastatin based upon initial low-density lipoprotein cholesterol levels in type 2 diabetic patients.
, 2008
)
0.89
" There was also evidence of a dose-response relationship between CRP reductions from baseline and rosuvastatin."( Models for the analysis of C-reactive protein in statin trials.
Dane, A; Southworth, H,
)
0.13
"A number of analytical methods were reported for the estimation of atorvastatin and ramipril from their individual dosage forms or in combination with other drugs (Valiyare, 2004; Vachareau and Neirinck, 2000)."( Simultaneous estimation of atorvastatin and ramipril by RP-HPLC and spectroscopy.
George, M; Joseph, L; Rao B, VR, 2008
)
0.88
" They were assigned to receive a daily dosage of atorvastatin based on their initial LDL-C levels."( Efficacy of atorvastatin for achieving cholesterol targets after LDL-cholesterol based dose selection in patients with type 2 diabetes.
Albalat-Galera, R; Berzosa-Sanchez, M; Ferrer-García, JC; Herrera-Ballester, A; Sanchez-Ballester, E, 2008
)
0.98
" The dose-response effect of atorvastatin on biomarkers of inflammation and oxidative stress has not been investigated in subjects with MS."( Comparison effect of atorvastatin (10 versus 80 mg) on biomarkers of inflammation and oxidative stress in subjects with metabolic syndrome.
Devaraj, S; Jialal, I; Siegel, D; Singh, U, 2008
)
0.96
"Eligible patients had a 6-month period of no statin use prior to the initial statin prescription, an initial statin dosage of either 20 or 40 mg of simvastatin or 10 or 20 mg of atorvastatin (the most commonly used doses of both drugs), a 0 to 3-month 'qualifying period' after the first prescription to allow for varying minimum lengths of statin use, and no statin switches."( Differences in cardiovascular event rates between atorvastatin and simvastatin among new users: managed-care experience.
Vogel, RA; Willke, RJ; Zhou, S, 2008
)
0.79
" Eight dosage strengths of single-pill amlodipine/atorvastatin (5/10, 10/10, 5/20, 10/20, 5/40, 10/40, 5/80 and 10/80 mg) were titrated to improve blood pressure and lipid control."( Single-pill amlodipine/atorvastatin helps patients of diverse ethnicity attain recommended goals for blood pressure and lipids (the Gemini-AALA study).
Aguilar-Salinas, CA; Chaves, H; Chopra, P; Erdine, S; Guindy, R; Howes, LG; Moller, RA; Ro, YM; Schou, IM; Tse, HF, 2009
)
0.92
" The results indicated that the bilayer tablets could be a potential dosage form for delivering AT and NA."( Bilayer tablets of atorvastatin calcium and nicotinic acid: formulation and evaluation.
Godwinkumar, S; Muralidharan, S; Nagarajan, M; Nirmal, J; Peddanna, C; Saisivam, S, 2008
)
0.67
" To position the PMRP database for large-scale pharmacogenetic association studies in the context of lipid-lowering therapy, we constructed an electronic phenotyping algorithm to quantify exposure and dose-response for atorvastatin, the most commonly prescribed lipid-lowering agent within this population."( Characterization of low-density lipoprotein cholesterol-lowering efficacy for atorvastatin in a population-based DNA biorepository.
Berg, RL; Krauss, RM; Linneman, JG; McCarty, CA; Wilke, RA; Zhao, C, 2008
)
0.76
"The impact of the 2 ezetimibe dosing strategies on percent lowering of low-density lipoprotein cholesterol (LDL-C) and achievement of National Cholesterol Education Program Adult Treatment Panel III (ATP III) goals was assessed in all patients prescribed ezetimibe 5 or 10 mg."( Ezetimibe 5 and 10 mg for lowering LDL-C: potential billion-dollar savings with improved tolerability.
Agarwal, S; Baruch, L; Eng, C; Gupta, B; Lieberman-Blum, SS, 2008
)
0.35
" Patients were excluded if the dosage of their antidiabetic drugs was changed, if their drug therapy was altered within 3 months before starting statin therapy, or if events occurred that could affect glycemic control such as hospitalization."( Influence of pitavastatin on glucose tolerance in patients with type 2 diabetes mellitus.
Kadonosono, K; Takano, T; Tanaka, S; Terauchi, Y; Yamakawa, T, 2008
)
0.35
"The primary determinants of drug interaction were the ln-transformed area under the plasma concentration versus time curve (AUCtau) and maximum measured steady-state plasma concentration (C(max,ss)) over the final 24 h dosing interval (day 14) for atorvastatin and 2-hydroxyatorvastatin."( Effect of omega-3-acid ethyl esters on steady-state plasma pharmacokinetics of atorvastatin in healthy adults.
Di Spirito, M; Doyle, RT; Johnson, J; McKenney, J; Morelli, G, 2008
)
0.75
" The drug was given as monotherapy for 10 days, and after a 6-day run-in period with atorvastatin 80 mg/day, the same dosage of atorvastatin was continued with the respective thienopyridine for 10 days."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.97
"Blood samples were collected before and at various time points after dosing on days 1 and 11 for determination of plasma concentrations of metabolites and for measurement of platelet aggregation induced by adenosine 5'-diphosphate 20 microM and vasodilator-stimulated phosphoprotein (VASP)."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.75
" The lack of a clinically meaningful effect of high-dose atorvastatin on the pharmacodynamic response to prasugrel after the loading or maintenance dose indicates that no dosage adjustment should be necessary in patients receiving these drugs concomitantly."( Effect of atorvastatin on the pharmacokinetics and pharmacodynamics of prasugrel and clopidogrel in healthy subjects.
Brandt, JT; Ernest, CS; Farid, NA; Jakubowski, JA; Konkoy, CS; Li, YG; Payne, CD; Salazar, DE; Small, DS; Winters, KJ, 2008
)
0.99
"Alternate-day dosing of atorvastatin causes a significant lipid-lowering and antiinflammatory effects similar to that of daily administration and yet may provide some cost savings."( The comparison of the effects of standard 20 mg atorvastatin daily and 20 mg atorvastatin every other day on serum LDL-cholesterol and high sensitive C-reactive protein levels.
Akar Bayram, N; Aydoğdu, S; Canbay, A; Diker, E; Durmaz, T; Kayhan, T; Keleş, T; Ozdemir, O; Sahin, D, 2008
)
0.91
"022) compared with no treatment, and there was an apparent dose-response effect with the lowest levels of total testosterone seen in men treated with >or=20 mg atorvastatin (9."( Statin therapy is associated with lower total but not bioavailable or free testosterone in men with type 2 diabetes.
Channer, KS; Jones, TH; Kapoor, D; Stanworth, RD, 2009
)
0.55
" Twenty-two patients (15 without nephropathy and seven with nephropathy) received atorvastatin in individually adjusted oral dosage (range 10-20 mg) once per day for 12 weeks."( Modulating effect of atorvastatin on paraoxonase 1 activity in type 2 diabetic Egyptian patients with or without nephropathy.
Abdin, AA; El-Noeman, Sel-D; Hassanien, MA; Ibrahim, EA,
)
0.68
"The effects of demographic and clinical covariates on the apparent clearance (CL/F) of orally administered atorvastatin, with chronic dosing in a patient population that included the elderly, were studied in 143 patients (atorvastatin: 34 +/- 26 mg/day, mean +/- SD; men (n = 64), age 64."( Population analyses of atorvastatin clearance in patients living in the community and in nursing homes.
Schwartz, JB; Verotta, D, 2009
)
0.88
" A dose of 10 mg of atorvastatin daily to target LDL-C goal was taken as the standard dosage targeting goal (SDTG)."( [The statin dosage for achieving goal of cholesterol-lowering based on risk stratification in patients with ischemic cerebrovascular diseases].
Fu, YG; Guo, YD; Tan, ZF; Wang, TG; Xu, AD; Yang, WY, 2009
)
0.68
" The amplitude of LDL-C lowering was 32% - 35%, 46% - 49%, 51% - 52% and 60% - 65% with corresponding to daily dosage of 10 mg, 20 mg, 40 mg and 80 mg atorvastatin."( [The statin dosage for achieving goal of cholesterol-lowering based on risk stratification in patients with ischemic cerebrovascular diseases].
Fu, YG; Guo, YD; Tan, ZF; Wang, TG; Xu, AD; Yang, WY, 2009
)
0.55
" The dose-response relationship for atorvastatin in elderly patients with unstable angina (UA) during early hospitalization in terms of lowering inflammatory factors, improving vascular endothelium function and safety is unclear."( Efficacy and safety of atorvastatin during early hospitalization in elderly patients with unstable angina.
Ge, ZM; Geng, J; Kang, WQ; Wang, W; Zhang, Y; Zhao, Z, 2009
)
0.94
" Moreover, nonsignificant interactions between dosage and duration of therapy were found."( Pleiotropic effects of atorvastatin on monocytes in atherosclerotic patients.
Deng, JT; Hu, XY; Li, L; Liu, XL; Shang, YY; Wang, ZH; Zhang, LP; Zhang, W; Zhang, Y; Zhong, M, 2010
)
0.67
" ATN Ca unit dosage form was developed and evaluated for physico-chemical properties, stability, and dissolution rate."( Solubility and stability enhancement of atorvastatin by cyclodextrin complexation.
Palem, CR; Patel, S; Pokharkar, VB,
)
0.4
"The CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titration (CanACTFAST) trial tested whether an algorithm-based statin dosing approach would enable patients to achieve LDL-C and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio targets quickly."( Achieving cholesterol targets by individualizing starting doses of statin according to baseline low-density lipoprotein cholesterol and coronary artery disease risk category: the CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titr
Calciu, CD; Langer, A; Leiter, LA; Rabkin, SW; Ur, E, 2010
)
0.8
"Algorithm-based statin dosing enables patients to achieve LDL-C and TC/HDL-C ratio targets quickly, with either no titration or a single titration."( Achieving cholesterol targets by individualizing starting doses of statin according to baseline low-density lipoprotein cholesterol and coronary artery disease risk category: the CANadians Achieve Cholesterol Targets Fast with Atorvastatin Stratified Titr
Calciu, CD; Langer, A; Leiter, LA; Rabkin, SW; Ur, E, 2010
)
0.54
" Patients switched to an equivalent simvastatin dose had lower LDL-C levels and were more likely to achieve LDL-C targets than patients switched to a non-equivalent dose, suggesting physicians must consider dosage equivalence when switching statins, and should measure LDL-C and titrate statins as necessary to achieve LDL-C control."( LDL-C goal attainment in patients who remain on atorvastatin or switch to equivalent or non-equivalent doses of simvastatin: a retrospective matched cohort study in clinical practice.
Burke, JP; Rublee, DA, 2010
)
0.62
" In conclusion, commercial ATC samples exhibited diverse solid state behavior that can impact the performance and stability of the dosage forms."( Solid state characterization of commercial crystalline and amorphous atorvastatin calcium samples.
Bansal, AK; Kumar, L; Puri, V; Shete, G, 2010
)
0.6
"Fifty-four patients with CAD who had received atorvastatin treatment for at least 8 weeks (mean dosage 30 mg/day) and 54 patients with CAD who had not received atorvastatin therapy were selected from a larger prospective, randomized, double-blind study for inclusion in this post hoc analysis."( Effect of atorvastatin on haemostasis, fibrinolysis and inflammation in normocholesterolaemic patients with coronary artery disease: a post hoc analysis of data from a prospective, randomized, double-blind study.
Borggrefe, M; Dempfle, CE; Hoffmeister, HM; Lang, S; Suselbeck, T; Swoboda, S; Szabo, S; Walter, T, 2010
)
1.02
" CsA inhibition ranged from 28 to 77% within a dosing interval, whereas it was less than 1% for Tac, considering free concentrations and assuming competitive inhibition."( Cyclosporine A, but not tacrolimus, shows relevant inhibition of organic anion-transporting protein 1B1-mediated transport of atorvastatin.
Amundsen, R; Asberg, A; Christensen, H; Zabihyan, B, 2010
)
0.57
"The existing data suggest that atorvastatin is generally well tolerated across the range of its therapeutic dosage (10 - 80 mg/day)."( Atorvastatin: safety and tolerability.
Athyros, VG; Karagiannis, A; Mikhailidis, DP; Tziomalos, K, 2010
)
2.09
" Furthermore, the following trends of interest were calculated for each calendar year: the percentage of statin users prescribed simvastatin or atorvastatin, the median dose of simvastatin and atorvastatin prescribed, and the percentage of simvastatin users prescribed a dosage of 40 mg/day (which is recommended by the Dutch multidisciplinary guideline)."( Statin prescribing in the elderly in the Netherlands: a pharmacy database time trend study.
Geleedst-De Vooght, M; Jansen, P; Maitland-van der Zee, AH; Mantel-Teeuwisse, A; Schalekamp, T, 2010
)
0.56
"Two crossover studies were performed in healthy subjects: a two-period study of dalcetrapib 900 mg concurrently with atorvastatin (concurrent dosing study) and a three-period study of dalcetrapib 600 mg (dose chosen for Phase III) with atorvastatin concurrently or serially 4 h after dalcetrapib (interval dosing study)."( No clinically relevant drug-drug interactions when dalcetrapib is co-administered with atorvastatin.
Abt, M; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Young, AM, 2010
)
0.79
" In the interval study (n = 52), serial and concurrent co-administration of atorvastatin resulted in similar reductions in dalcetrapib exposure that were comparable to those observed in the concurrent dosing study."( No clinically relevant drug-drug interactions when dalcetrapib is co-administered with atorvastatin.
Abt, M; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Young, AM, 2010
)
0.81
"Two spectrophotometric methods are presented for the simultaneous determination of ezetimibe/simvastatin and ezetimibe/atorvastatin binary mixtures in combined pharmaceutical dosage forms without prior separation."( Enhanced spectrophotometric determination of two antihyperlipidemic mixtures containing ezetimibe in pharmaceutical preparations.
Barary, MA; El-Kimary, EI; Hassan, EM; Maher, HM; Youssef, RM, 2011
)
0.58
" These data therefore demonstrate that dosing considerations in the current labels for atorvastatin are similar for Asian compared with Caucasian subjects."( Systemic exposure to atorvastatin between Asian and Caucasian subjects: a combined analysis of 22 studies.
Fung, GL; Gandelman, K; Laskey, R; Messig, M, 2012
)
0.92
"In this work the effects of Atorvastatin (liptonorm) in a dosage of 10 mg/24h during 12 months concerning the basic indicators of a lipid spectrum of blood in the patients with a metabolic syndrome are estimated."( [Effect of atorvastatin (liptonorm) on indicators of the lipid spectrum of blood in patients with the metabolic syndrome].
Lakhin, DI; Vasil'eva, LV, 2010
)
1.04
"Microwave energy was used to prepare an enhanced release dosage form of the poorly water soluble drug ATR with PEG 6000 as a hydrophilic carrier."( Microwave induced solubility enhancement of poorly water soluble atorvastatin calcium.
Belgamwar, V; Maurya, D; Tekade, A, 2010
)
0.6
" The decrease can be prevented by the suggested dosage scheme."( Use of ultra high performance liquid chromatography-tandem mass spectrometry to demonstrate decreased serum statin levels after extracorporeal LDL-cholesterol elimination.
Bláha, M; Bláha, V; Lánská, M; Malý, J; Nováková, L; Solich, P; Solichová, D; Vlcková, H, 2011
)
0.37
"To compare the safety and myocardial effects of different atorvastatin loading doses and dosing frequency before PCI in non-ST segment elevation acute coronary syndrome (NSTE-ACS) patients."( Effect of different loading doses of atorvastatin on percutaneous coronary intervention for acute coronary syndromes.
Gao, Y; Pang, X; Qi, G; Sun, Y; Zhang, H; Zhang, Z; Zhao, W, 2010
)
0.88
" The reduced liver TG mass induced by a high dosage of atorvastatin may be important for the treatment of patients with fatty liver."( Effects of high-dose statin on the human hepatic expression of genes involved in carbohydrate and triglyceride metabolism.
Eriksson, M; Gustafsson, U; Parini, P; Pramfalk, C; Sahlin, S, 2011
)
0.62
"This study was designed to compare the efficacy and tolerability of a generic formulation of atorvastatin 20 mg/d versus a branded formulation at the same dosage in hypercholesterolemic Korean adults at high risk for cardiovascular events."( Efficacy and tolerability of a generic and a branded formulation of atorvastatin 20 mg/d in hypercholesterolemic Korean adults at high risk for cardiovascular disease: a multicenter, prospective, randomized, double-blind, double-dummy clinical trial.
Cho, YS; Hong, SJ; Hyon, MS; Kim, DW; Kim, HS; Kim, SH; Lee, MY; Moon, GW; Park, K; Sung, JD; Yoon, MH, 2010
)
0.82
"Two simple and accurate methods to determine atorvastatin calcium and ramipril in capsule dosage forms were developed and validated using HPLC and HPTLC."( Simultaneous determination of atorvastatin calcium and ramipril in capsule dosage forms by high-performance liquid chromatography and high-performance thin layer chromatography.
Panchal, HJ; Suhagia, BN,
)
0.68
" As there is neither any consensus nor any guidelines regarding this issue, we aimed to define the optimal statin type and dosage for these patients."( Optimal statin type and dosage for vascular patients.
Mikhailidis, DP; Paraskevas, KI; Veith, FJ, 2011
)
0.37
" Atorvastatin and rosuvastatin at the maximum dosage both significantly (p <0."( Effects of maximal atorvastatin and rosuvastatin treatment on markers of glucose homeostasis and inflammation.
Ai, M; Asztalos, BF; Himbergen, TV; Jones, PH; Nakajima, K; Otokozawa, S; Schaefer, EJ; Stein, E; Thongtang, N, 2011
)
1.61
" A linear mixed-effects model was applied to account for the inherent correlation of multiple-plaque measurements from the same patient and to assess dose-response differences to statin therapy."( In vivo carotid plaque MRI using quantitative T2* measurements with ultrasmall superparamagnetic iron oxide particles: a dose-response study to statin therapy.
Gillard, JH; Graves, MJ; Müller, KH; Patterson, AJ; Tang, TY, 2011
)
0.37
" At 40 mg dosage from 3rd month to 6th month versus 1st month to 3rd month it was significant decrease, at the end of 1st month and 3rd month it was not significant."( Short-term therapy with high dose atorvastatin in patients with coronary artery disease can reduce inflammatory process.
Abdollahian, F; Nesar Hossein, V; Yosef Nejad, K,
)
0.41
"Despite recent advances in solid-state NMR spectroscopy, the structural characterization of amorphous active pharmaceutical ingredients (APIs) in solid dosage forms continues to be a monumental challenge."( New perspectives of 19F MAS NMR in the characterization of amorphous forms of atorvastatin in dosage formulations.
Brus, J; Brusova, H; Sedenkova, I; Urbanova, M, 2011
)
0.6
" Serum levels of LDL-C, high-density lipoprotein cholesterol, total cholesterol, triglycerides, and creatinine kinase (CK) were measured before (day 1) and 7, 13, 14, 15, 16, 21, and 28 days after dosing initiation."( Effect of HMGCR variant alleles on low-density lipoprotein cholesterol-lowering response to atorvastatin in healthy Korean subjects.
Cho, SK; Chung, JY; Jang, SB; Lee, DH; Lee, YJ; Lim, LA; Oh, ES; Park, K; Park, MS, 2012
)
0.6
"The results of our adverse drug analysis suggest a dose-response relationship."( Statin-associated rhabdomyolysis: is there a dose-response relationship?
Baker, S; Holbrook, A; Ribic, C; Sung, M; Wright, M,
)
0.13
" Reduction of atorvastatin dosage when moderate amounts of GFJ are co-ingested does not appear to be necessary."( Serum concentrations and clinical effects of atorvastatin in patients taking grapefruit juice daily.
Browne, K; Derendorf, H; Ellington, D; Greenblatt, DJ; Harmatz, JS; Parent, SJ; Reddy, P; Zdrojewski, I; Zhu, Y, 2011
)
0.99
" Serial pharmacokinetic sampling of atorvastatin was conducted on day 7 of atorvastatin dosing and day 70 of lamotrigine + atorvastatin dosing or day 28 of phenytoin + atorvastatin dosing."( Effects of lamotrigine and phenytoin on the pharmacokinetics of atorvastatin in healthy volunteers.
Alexander, S; Bullman, J; Fleck, R; Messenheimer, J; Miller, J; Nicholls, A; Van Landingham, K; Vuong, A, 2011
)
0.88
" Blood samples were collected scheduled intervals for 24 hours after the last dosing to determine plasma concentrations of atorvastatin acid, atorvastatin lactone, 2-hydroxy atorvastatin acid, and 2-hydroxy atorvastatin lactone."( The effect of the newly developed angiotensin receptor II antagonist fimasartan on the pharmacokinetics of atorvastatin in relation to OATP1B1 in healthy male volunteers.
Cho, JY; Jang, IJ; Kim, SE; Kim, TE; Lee, MG; Shin, KH; Shin, SG; Song, IS; Yoon, SH; Yu, KS, 2011
)
0.79
" The primary objective of the study was to determine the effect of once-daily dosing of a combination therapy for blood pressure (BP) and dyslipidemia using home BP monitoring on reaching clinical BP and the effect of daily dosing of combination therapy on reaching lipid goals."( Improving adherence with amlodipine/atorvastatin therapy: IMPACT study.
Crabbe, A; Delkhah, Y; Jones, J; Leonard, D; Nesbitt, S; Oliver, S, 2011
)
0.64
" The selected excipients such as docusate sodium enhanced the stability and solubility of ATC in gastric media and tablet dosage form."( Enhanced bioavailability of atorvastatin calcium from stabilized gastric resident formulation.
Dehghan, MH; Khan, FN, 2011
)
0.66
"Three simple, specific, accurate and precise spectrophotometric methods manipulating ratio spectra are developed for the simultaneous determination of Amlodipine besylate (AM) and Atorvastatin calcium (AT) in tablet dosage forms."( Three different spectrophotometric methods manipulating ratio spectra for determination of binary mixture of Amlodipine and Atorvastatin.
Darwish, HW; El-Zeiny, BA; Hassan, SA; Salem, MY, 2011
)
0.77
" However, for a better interpretation of the experimental data as well as to possibly predict cholesterol levels given a certain dosing regimen of statins and phytosterols/-stanols a more theoretically based approach is helpful."( Modelling approach to simulate reductions in LDL cholesterol levels after combined intake of statins and phytosterols/-stanols in humans.
Eussen, SR; Klungel, OH; Rompelberg, CJ; van Eijkeren, JC, 2011
)
0.37
" A daily oral dose of atorvastatin calcium treatment for 70 days weakened the long bones of methylprednisolone acetate treated rabbits irrespective of the dosage (2, 10, or 20 mg)."( Effect of atorvastatin on the cortical bones of corticosteroid treated rabbits.
Braitman, LE; Goldstein, DT; Handal, JA; John, TK; Khurana, JS; Saing, M; Samuel, SP, 2012
)
1.1
" According to the dosage of preprocedural atorvastatin, the high hs-CRP group was further divided into 10 mg group (n = 49), 20 mg group (n = 66) and 40 mg group (n = 61)."( [Association between high sensitivity C-reactive protein and contrast induced acute kidney injury in patients with acute coronary syndrome undergoing percutaneous coronary intervention: impact of atorvastatin].
Cai, WQ; Chai, DJ; Chen, GL; Chen, XP; Huang, QY; Su, JZ; Wang, FB; Xue, Y; Zhang, DS, 2011
)
0.82
"8) who underwent a primary PCI for a first ST-elevated AMI were randomized for pretreatment with atorvastatin 80 mg (n = 20) or placebo (n = 22) and continued with the same dosage daily for 1 week."( Early statin treatment prior to primary PCI for acute myocardial infarction: REPERATOR, a randomized placebo-controlled pilot trial.
Doevendans, PA; Eefting, FD; Goumans, MJ; Post, MC; Post, S; Rensing, BJ; Stella, PR; van den Branden, BJ; van Es, HW; Wildbergh, TX, 2012
)
0.6
"The primary objective of this study was to evaluate the low-density lipoprotein cholesterol (LDL-C)-lowering efficacy of 5 SAR236553/REGN727 (SAR236553) dosing regimens versus placebo at week 12 in patients with LDL-C ≥100 mg/dl on stable atorvastatin therapy."( Safety and efficacy of a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 serine protease, SAR236553/REGN727, in patients with primary hypercholesterolemia receiving ongoing stable atorvastatin therapy.
Ferrand, AC; Hanotin, C; Kereiakes, DJ; Koren, MJ; McKenney, JM; Stein, EA, 2012
)
0.75
"SAR236553 demonstrated a clear dose-response relationship with respect to percentage LDL-C lowering for both Q2W and Q4W administration: 40%, 64%, and 72% with 50, 100, and 150 mg Q2W, respectively, and 43% and 48% with 200 and 300 mg Q4W."( Safety and efficacy of a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 serine protease, SAR236553/REGN727, in patients with primary hypercholesterolemia receiving ongoing stable atorvastatin therapy.
Ferrand, AC; Hanotin, C; Kereiakes, DJ; Koren, MJ; McKenney, JM; Stein, EA, 2012
)
0.57
" These additional reductions are both dose- and dosing frequency-dependent."( Safety and efficacy of a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 serine protease, SAR236553/REGN727, in patients with primary hypercholesterolemia receiving ongoing stable atorvastatin therapy.
Ferrand, AC; Hanotin, C; Kereiakes, DJ; Koren, MJ; McKenney, JM; Stein, EA, 2012
)
0.57
"Evidence suggests that statins reduce cardiovascular complications in patients undergoing noncardiac surgery, although questions remain regarding the mechanism of benefit and the preferred dosing strategy."( STAR VaS--Short Term Atorvastatin Regime for Vasculopathic Subjects: a randomized placebo-controlled trial evaluating perioperative atorvastatin therapy in noncardiac surgery.
Bryson, GL; Neilipovitz, DT; Taljaard, M, 2012
)
0.7
"2%, usually atorvastatin), or increasing atorvastatin dosage (59."( Effectiveness of lipid-lowering therapy with statins for secondary prevention of atherosclerosis--guidelines vs. reality.
Bożentowicz-Wikarek, M; Chudek, J; Kocełak, P; Olszanecka-Glinianowicz, M; Smertka, M, 2012
)
0.76
"Muscular symptoms associated with average dosage statin therapy are more frequent than in clinical trials and have a greater impact on patients' life than usually thought."( Discontinuation of statin therapy due to muscular side effects: a survey in real life.
Bruckert, E; Dallongeville, J; Rosenbaum, D; Sabouret, P, 2013
)
0.39
"The aim of the present study was to combine vibrational spectroscopy and chemometrics for investigating excipient-induced disproportionation of the calcium salt of atorvastatin into the corresponding free acid form in environments relevant to manufacturing and storage of solid dosage formulations."( Disproportionation of the calcium salt of atorvastatin in the presence of acidic excipients.
Christensen, NP; Cornett, C; Rantanen, J; Taylor, LS, 2012
)
0.84
"Alternative dosing is often used clinically to address common barriers with statin therapy, such as intolerance and cost."( The high-dose rosuvastatin once weekly study (the HD-ROWS).
Backes, JM; Gibson, CA; Moriarty, PM; Ruisinger, JF,
)
0.13
" The type and dosage of concomitant drugs were not changed during the study periods."( Association of cholesteryl ester transfer protein mass with peripheral leukocyte count following statin therapy: a pilot study.
Hirayama, A; Nagao, K; Tani, S, 2012
)
0.38
"To compare the therapeutic effects of intensive versus moderate dosage of atorvastatin regimens in new-onset unstable angina with borderline lesions, 100 patients were randomized to receive either 80 mg/d or 20 mg/d atorvastatin for 9 months."( Intensive-dose atorvastatin regimen halts progression of atherosclerotic plaques in new-onset unstable angina with borderline vulnerable plaque lesions.
Gong, P; Lin, J; Liu, S; Lu, J; Lu, X; Qiu, J; Wang, H; Zhang, X, 2013
)
0.97
" Log dose-response data revealed linear dose-related effects on blood total cholesterol, low-density lipoprotein (LDL)-cholesterol and triglycerides."( Lipid lowering efficacy of atorvastatin.
Adams, SP; Tsang, M; Wright, JM, 2012
)
0.68
" Log dose-response data was linear over the commonly prescribed dose range."( Lipid lowering efficacy of atorvastatin.
Adams, SP; Tsang, M; Wright, JM, 2012
)
0.68
"Three simple, specific, accurate and precise spectrophotometric methods depending on the proper selection of two wavelengths are developed for the simultaneous determination of Amlodipine besylate (AML) and Atorvastatin calcium (ATV) in tablet dosage forms."( Three different methods for determination of binary mixture of Amlodipine and Atorvastatin using dual wavelength spectrophotometry.
Darwish, HW; El-Zeany, BA; Hassan, SA; Salem, MY, 2013
)
0.81
" Statistically significant increases in the systemic exposure of ortho- and para-hydroxyatorvastatin were also observed upon concomitant dosing with CP-778875."( Elucidation of the biochemical basis for a clinical drug-drug interaction between atorvastatin and 5-(N-(4-((4-ethylbenzyl)thio)phenyl)sulfamoyl)-2-methyl benzoic acid (CP-778875), a subtype selective agonist of the peroxisome proliferator-activated recep
Chen, D; Feng, B; Francone, OL; Frederick, KS; Goosen, TC; Gosset, JR; Kalgutkar, AS; Rotter, CJ; Scialis, RJ; Terra, SG; Varma, MV; Walsky, RL; West, MA, 2013
)
0.84
" Subsequently, dogs with CHF (n = 12) were treated with atorvastatin at a dosage of 2 mg/kg q24 h for 8 weeks."( Short-term effects of atorvastatin in normal dogs and dogs with congestive heart failure due to myxomatous mitral valve disease.
Cunningham, SM; Freeman, LM; Rush, JE,
)
0.69
" In this cohort, genotypes associated with statin concentration were not differently distributed among dosing groups, implying providers had not yet optimized each patient's risk-benefit ratio."( Clinical and pharmacogenetic predictors of circulating atorvastatin and rosuvastatin concentrations in routine clinical care.
Choi, YH; DeGorter, MK; Dresser, GK; Hegele, RA; Iwuchukwu, O; Kim, RB; Myers, K; Schwarz, UI; Suskin, N; Tirona, RG; Wei, WQ; Wilke, RA; Zou, G, 2013
)
0.64
" Most of the patients on more potent statins were not advised by their cardiologists to change the type or dosage of statin, which was more common in patients on less potent statins."( Prevalence and types of persistent dyslipidemia in patients treated with statins.
Reiner, Ž; Tedeschi-Reiner, E, 2013
)
0.39
" The results were better in patients treated with more potent statins and cardiologists advised them much less frequently to change the type and dosage of statin."( Prevalence and types of persistent dyslipidemia in patients treated with statins.
Reiner, Ž; Tedeschi-Reiner, E, 2013
)
0.39
"The Biopharmaceutics Drug Disposition Classification System (BDDCS) predicts intestinal transporter effects to be clinically insignificant following oral dosing for highly soluble and highly permeable/metabolized drugs (class 1 drugs)."( Effect of P-glycoprotein on the rat intestinal permeability and metabolism of the BDDCS class 1 drug verapamil.
Benet, LZ; Estudante, M; Maya, M; Morais, JG; Soveral, G, 2013
)
0.39
" We leveraged electronic medical records (EMRs) to extract potency (ED50) and efficacy (Emax) of statin dose-response curves and tested them for association with 144 preselected variants."( Characterization of statin dose response in electronic medical records.
Berg, RL; Davis, RL; Denny, JC; Feng, Q; Iwuchukwu, OF; Jiang, L; Jiang, M; Krauss, RM; McCarty, CA; Nickerson, DA; Peissig, PL; Roden, DM; Rotter, JI; Waitara, MS; Wei, WQ; Wilke, RA; Xu, H, 2014
)
0.4
" The proposed method can be used for simultaneous estimation of these drugs in marketed dosage forms."( RP-HPLC method development and validation for simultaneous estimation of atorvastatin calcium and pioglitazone hydrochloride in pharmaceutical dosage form.
Ammineni, P; Kondreddy, Vk; Mallikarjuna, S; Peraman, R, 2014
)
0.63
" The intrinsic dissolution rate and solubility of ATC-NIC were determined along with plasma concentrations of ATC using HPLC after oral dosing in rats."( Coamorphous atorvastatin calcium to improve its physicochemical and pharmacokinetic properties.
Ghavimi, H; Hamishekar, H; Jouyban, A; Shayanfar, A, 2013
)
0.77
" Patients were monitored for 5 years, during which time they received regular visits with the opportunity to increase their dosage if they were above their LDL-C goal."( Impact of switching treatment from rosuvastatin to atorvastatin on rates of cardiovascular events.
Andy Schuetz, C; Folse, H; Gandhi, S; Rengarajan, B; Sternhufvud, C, 2014
)
0.65
" Additional studies with multiple dosing of both drugs are needed to further determine the clinical implications of these results."( Effect of steady-state atorvastatin on the pharmacokinetics of a single dose of colchicine in healthy adults under fasted conditions.
Davis, MW; Wason, S, 2014
)
0.71
" These data suggest that modeling of dose-response relationships may be useful in predicting clinical equivalence, lowering cost/timelines through effective powering of studies, and predicting the effectiveness of new dosage formulations without the need for additional clinical efficacy trials in regulatory settings."( Prediction of clinical irrelevance of PK differences in atorvastatin using PK/PD models derived from literature-based meta-analyses.
Adewale, A; Behm, MO; Kerbusch, T; Mandema, J; Vargo, R, 2014
)
0.65
" The developed methods were applied for simultaneous analysis of aspirin, atorvastatin and clopedogrel in capsule dosage forms and results were in good concordance with alternative liquid chromatography."( Comparative study of three modified numerical spectrophotometric methods: an application on pharmaceutical ternary mixture of aspirin, atorvastatin and clopedogrel.
Hegazy, ND; Issa, MM; Nejem, RM; Shanab, AA; Stefan-van Staden, RI, 2014
)
0.84
" The only pharmacologically mediated changes observed during the dosing period were the anticipated changes in circulating cholesterol."( Combined administration of RG7652, a recombinant human monoclonal antibody against PCSK9, and atorvastatin does not result in reduction of immune function.
Baruch, A; Chilton, J; Erwin, R; Forrest, AS; Gelzleichter, TR; Halpern, W; Leabman, M; Peng, K; Satterwhite, CM; Stevens, D, 2014
)
0.62
"Atorvastatin has a limited advantage to formulate oral dosage forms."( Solid self microemulsification of Atorvastatin using hydrophilic carriers: a design.
Nanda Kishore, R; Rasheed, A; Sushma, M; Vadlamudi, HC; Vandana, KR; Yalavarthi, PR, 2015
)
2.14
" Periodic dosing was negotiated following several patients' refusal of statin therapy because of muscle aches or cost."( Periodic rosuvastatin or atorvastatin dosing arrays (PRADA): patient-centered practice.
Christou, T; Dimitrov, R; Omar, HR, 2014
)
0.71
" The primary endpoint was to assess the concentration of low-density lipoprotein cholesterol (LDL-C) and the total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C) ratio with patient-directed dosing intervals."( Periodic rosuvastatin or atorvastatin dosing arrays (PRADA): patient-centered practice.
Christou, T; Dimitrov, R; Omar, HR, 2014
)
0.71
"Periodic dosing of rosuvastatin or atorvastatin using a gradual, patient-directed, stepwise approach guided by cholesterol levels is an effective method of lipid lowering and carried a favorable 95."( Periodic rosuvastatin or atorvastatin dosing arrays (PRADA): patient-centered practice.
Christou, T; Dimitrov, R; Omar, HR, 2014
)
0.98
" Cultures were treated with a therapeutic dosage of 5 commonly used statins: CEL, ATV + CEL, PGE2, and a selective antagonist of PGE2 receptor 4 (EP4)."( Statins enhance rotator cuff healing by stimulating the COX2/PGE2/EP4 pathway: an in vivo and in vitro study.
Brosh, T; Chechik, O; Dolkart, O; Gabet, Y; Liron, T; Maman, E; Somjen, D, 2014
)
0.4
" The flexibility of the alirocumab dosing regimen allows for individualized therapy based on the degree of LDL-C reduction required to achieve the desired LDL-C level."( Efficacy and safety of alirocumab as add-on therapy in high-cardiovascular-risk patients with hypercholesterolemia not adequately controlled with atorvastatin (20 or 40 mg) or rosuvastatin (10 or 20 mg): design and rationale of the ODYSSEY OPTIONS Studies
Bays, HE; Colhoun, HM; Donahue, S; Du, Y; Hanotin, C; Jones, PH; Robinson, JG, 2014
)
0.6
"Opportunity to increase simvastatin dosing through education, prescribing targets and incentives."( Quality and efficiency of statin prescribing across countries with a special focus on South Africa: findings and future implications.
Bishop, I; Campbell, SM; Godman, B; Malmström, RE; Truter, I, 2015
)
0.42
"To conduct a cost-effectiveness analysis of three statin dosing schemes in the Brazilian Unified National Health System (SUS) perspective."( Cost-effectiveness of high, moderate and low-dose statins in the prevention of vascular events in the Brazilian public health system.
Duncan, BB; Polanczyk, CA; Restelatto, LM; Ribeiro, RA; Stella, SF; Vieira, JL; Ziegelmann, PK, 2015
)
0.42
" Expected differences between FDC and the corresponding co-administered doses were predicted from a dose-response relationship model; sample size was estimated given the expected difference and equivalence margins (±4%)."( Fixed-dose combination ezetimibe+atorvastatin lowers LDL-C equivalent to co-administered components in randomized trials: use of a dose-response model.
Bays, HE; Chen, E; McPeters, G; Polis, AB; Tomassini, JE; Triscari, J, 2015
)
0.7
" After the dosage of cyclosporine was increased to 300 mg every day for 8 months, the patient developed body pain and leg weakness, with a serum creatine kinase increase and evidence on magnetic resonance imaging of muscle oedema."( Increased dosage of cyclosporine induces myopathy with increased seru creatine kinase in an elderly patient on chronic statin therapy.
Dong, B; He, J; Huang, X; Mo, L; Yue, Q, 2015
)
0.42
" We hypothesized that the pharmacological and pharmacokinetic properties of atorvastatin-induced myopathy are the result of its interaction with high dosage of cyclosporine."( Increased dosage of cyclosporine induces myopathy with increased seru creatine kinase in an elderly patient on chronic statin therapy.
Dong, B; He, J; Huang, X; Mo, L; Yue, Q, 2015
)
0.65
" The injection is administered intravenously,with most patients receiving a dosage of 15-20 mL per dose for between 1 and 14 days."( [Analysis of clinical use of shuxuening injection in treatment of cerebral infarction based on real world].
Luo, YH; Wang, YY; Xie, YM; Yang, W; You, L; Zhuang, Y, 2014
)
0.4
"This paper describes a new RP-HPLC method for simultaneous quantification of these compounds in the bulk sample drug as well as in tablet dosage forms."( New Validated RP-HPLC Analytical Method for Simultaneous Estimation of Atorvastatin and Ezetimibe in Bulk Samples as Well in Tablet Dosage Forms by Using PDA Detector.
Debnath, M; Kumar, SA; Seshagiri Rao, JV, 2014
)
0.64
" The dosage of atorvastatin will be increased by titration within the usual dose range with a treatment goal of lowering LDL-C below 70 mg/dL based on consecutive measures of LDL-C at follow-up visits."( Plaque REgression with Cholesterol absorption Inhibitor or Synthesis inhibitor Evaluated by IntraVascular UltraSound (PRECISE-IVUS Trial): Study protocol for a randomized controlled trial.
Fujimoto, K; Hokimoto, S; Ishihara, M; Kaikita, K; Koide, S; Komura, N; Matsui, K; Matsumura, T; Matsuyama, K; Morikami, Y; Nakamura, N; Nakamura, S; Nakao, K; Ogawa, H; Oka, H; Ono, T; Oshima, S; Sakaino, N; Sakamoto, K; Shimomura, H; Sugiyama, S; Sumida, H; Tsujita, K; Tsunoda, R; Yamamoto, N; Yamanaga, K; Yamashita, T, 2015
)
0.77
" Log dose-response data from both trial designs revealed linear dose-related effects on blood total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides."( Lipid-lowering efficacy of atorvastatin.
Adams, SP; Tsang, M; Wright, JM, 2015
)
0.71
" It is a major determinant of half-life and dosing frequency of a drug."( Volume of Distribution in Drug Design.
Beaumont, K; Di, L; Maurer, TS; Smith, DA, 2015
)
0.42
"The average daily dosage of atorvastatin was 10, 27, and 40 mg in patients with PHC, FCHL, and FH, respectively; after 12 months of atorvastatin treatment, LDL cholesterol (LDL-C) plasma levels decreased by 44%, 50%, and 53%, respectively (all, P < ."( Changes in ultracentrifugally separated plasma lipoprotein subfractions in patients with polygenic hypercholesterolemia, familial combined hyperlipoproteinemia, and familial hypercholesterolemia after treatment with atorvastatin.
Hayashi, K; Homma, K; Homma, Y; Hori, S; Itoh, H; Ozawa, H; Shiina, Y; Wakino, S; Yoshida, T,
)
0.61
" The proposed methods were successfully applied for the determination of the investigated drugs in pure form, dosage form and in synthetic mixtures with good recovery and the results obtained were favorably compared to those obtained with a reference method."( Application of new spectrofluorometric techniques for determination of atorvastatin and ezetimibe in combined tablet dosage form.
Ayad, MF; Magdy, N, 2015
)
0.65
"A number of clinical trials have shown that patients with overt atherovascular disease may benefit from more aggressive dosage of statins."( [In what extend we can reach the current LDL-cholesterol treatment goals in secondary prevention].
Bruthans, J; Mayer, O, 2015
)
0.42
"Although the majority of CHD patients are currently being treated with statin, the usual dosage regimen and adherence to the recommended target values were not consistent with current therapeutic standards for secondary prevention of CHD."( [In what extend we can reach the current LDL-cholesterol treatment goals in secondary prevention].
Bruthans, J; Mayer, O, 2015
)
0.42
"25 mg once daily, n = 32) dosing was initiated on days 11 or 8, respectively, with evening (arm 1) or morning (arm 2) dosing; at steady state (days 15 or 22), a single lomitapide dose was administered; CYP3A inhibitor dosing continued for 6 days."( Evaluation of the effects of the weak CYP3A inhibitors atorvastatin and ethinyl estradiol/norgestimate on lomitapide pharmacokinetics in healthy subjects.
Dutta, S; Foulds, P; King, A; Korb, S; Patel, G; Sumeray, M; Wade, JR, 2016
)
0.68
" Selection criteria comprised 28 subcriteria under the following main criteria: clinical efficacy, best publish evidence and experience, adverse effects, drug interaction, dosing time, and fixed dose combination availability."( Statin Selection in Qatar Based on Multi-indication Pharmacotherapeutic Multi-criteria Scoring Model, and Clinician Preference.
Al-Badriyeh, D; Al-Khal, A; Alabbadi, I; Fahey, M; Zaidan, M, 2015
)
0.42
" Pigs in the CME group received a total dosage of 100,000 microspheres (42 μm) suspended in 10 ml normal saline within 40 min, while animals in the sham group received the same dosage of normal saline."( Effects of atorvastatin on PDCD4/NF-κB/TNF-α signaling pathway during coronary microembolization of miniature pigs.
Li, L; Liu, T; Liu, Y; Su, Q; Wang, J; Zhou, Y, 2015
)
0.81
"Two advanced, accurate and precise chemometric methods are developed for the simultaneous determination of amlodipine besylate (AML) and atorvastatin calcium (ATV) in the presence of their acidic degradation products in tablet dosage forms."( Advanced stability indicating chemometric methods for quantitation of amlodipine and atorvastatin in their quinary mixture with acidic degradation products.
Darwish, HW; El-Zeany, BA; Hassan, SA; Salem, MY, 2016
)
0.86
" Due to the disadvantages of liquid SEDDS (few choices for dosage forms, low stability and portability during the manufacturing process), attempts were also made to obtain solid SEDDS."( Development and Evaluation of Liquid and Solid Self-Emulsifying Drug Delivery Systems for Atorvastatin.
Amelian, A; Czajkowska-Kośnik, A; Szekalska, M; Szymańska, E; Winnicka, K, 2015
)
0.64
" These two mixtures were, therefore, subjected to studies for the evaluation of precompression parameters in order to find their amenability to satisfactory compression into tablet dosage form."( Stable amorphous binary systems of glipizide and atorvastatin powders with enhanced dissolution profiles: formulation and characterization.
Gulati, M; Narang, R; Singh, SK, 2017
)
0.71
" Duration and dosage of statin use were obtained from pharmaceutical claims."( Statin use associated with a reduced risk of pneumonia requiring hospitalization in patients with myocardial infarction: a nested case-control study.
Chang, YH; Chien, LN; Chuang, MT; Lin, CF; Liu, JC, 2016
)
0.43
" Due to an observational study design, atorvastatin dosage was not intentionally modified for other reasons."( Effects of Atorvastatin Dose and Concomitant Use of Angiotensin-Converting Enzyme Inhibitors on Renal Function Changes over Time in Patients with Stable Coronary Artery Disease: A Prospective Observational Study.
Surdacki, A; Świerszcz, J; Wieczorek-Surdacka, E, 2016
)
1.09
" A similar dose-response relationship was observed."( Atorvastatin and fluvastatin are associated with dose-dependent reductions in cirrhosis and hepatocellular carcinoma, among patients with hepatitis C virus: Results from ERCHIVES.
Bonilla, H; Butt, AA; Chung, RT; Simon, TG; Yan, P, 2016
)
1.88
" Atorvastatin was administered orally to the statin group according to a dosage schedule (80 mg single dose on the evening prior to surgery; 40 mg on the morning of surgery; three further doses of 40 mg on the evenings of postoperative days 0, 1, and 2)."( Effect of atorvastatin on the incidence of acute kidney injury following valvular heart surgery: a randomized, placebo-controlled trial.
Kwak, YL; Park, JH; Shim, JK; Soh, S; Song, JW, 2016
)
1.75
" These results suggest that S(M)-SEMDDS offers great potential for the development of solid dosage forms with improved oral absorption of drugs with poor water solubility."( Development of a solidified self-microemulsifying drug delivery system (S-SMEDDS) for atorvastatin calcium with improved dissolution and bioavailability.
Chae, BR; Choi, YW; Kim, JH; Kim, SR; Lee, SG; Son, HY; Song, SH; Yeom, DW, 2016
)
0.66
" The dosage of atorvastatin was uptitrated with a treatment goal of lowering low-density lipoprotein cholesterol to below 70 mg/dl in both groups."( Synergistic effect of ezetimibe addition on coronary atheroma regression in patients with prior statin therapy: Subanalysis of PRECISE-IVUS trial.
Fujimoto, K; Hokimoto, S; Ishihara, M; Kaikita, K; Koide, S; Komura, N; Matsui, K; Matsumura, T; Matsuyama, K; Morikami, Y; Nakamura, N; Nakamura, S; Nakao, K; Ogawa, H; Oka, H; Oshima, S; Sakaino, N; Sakamoto, K; Shimomura, H; Sugiyama, S; Sumida, H; Tsujita, K; Tsunoda, R; Yamamoto, N; Yamanaga, K; Yamashita, T, 2016
)
0.79
"Accurate prediction of drug target activity and rational dosing regimen design require knowledge of drug concentrations at the target."( Intracellular Unbound Atorvastatin Concentrations in the Presence of Metabolism and Transport.
Korzekwa, K; Kulkarni, P; Nagar, S, 2016
)
0.75
"BACKGROUND Is the timing of dosing for amlodipine and atorvastatin important with regard to therapeutic efficacy? To answer this question, we designed an outpatient, practice-based, case-control study lasting 8 weeks."( Is Time an Important Problem in Management of Hypertension and Hypercholesterolemia by Using an Amlodipine-Atorvastatin Single Pill Combination?
Wang, M; Zeng, R; Zhang, L, 2016
)
0.9
" However, regulatory authorities permit the use of in vitro data in establishing similarity between immediate release oral dosage forms containing biopharmaceutical classification system class I and III drugs only."( PHARMACEUTICAL QUALITY OF GENERIC ATORVASTATIN PRODUCTS COMPARED WITH THE INNOVATOR PRODUCT: A NEED FOR REVISING PRICING POLICY IN PALESTINE.
Abed, E; Al-Saghir, R; Hroub, AK; Jibali, S; Shawahna, R; Zaid, AN,
)
0.41
" To address this in experimental rats, in the present work, atorvastatin was orally dosed for 1 month to evaluate the outcomes of the subsequent occlusive stroke induced by middle cerebral artery occlusion (MCAO)."( Association of Long-Term Atorvastatin with Escalated Stroke-Induced Neuroinflammation in Rats.
Khodagholi, F; Mehrpour, M; Naderi, N; Nasoohi, S; Simani, L, 2017
)
1
" This study is the first to indicate that low doses of atorvastatin and rosuvastatin, the dosing regimen for which has been controversial, could significantly improve diabetes-related metabolic disorders, and could modulate pro-inflammatory cytokines, alleviating inflammation and simultaneously restoring overall humoral and cell-mediated immunity."( Atorvastatin and rosuvastatin improve physiological parameters and alleviate immune dysfunction in metabolic disorders.
An, J; Kim, J; Kim, K; Kong, H; Lee, H; Lee, S; Lee, Y; Song, Y, 2016
)
2.12
" The aim of this article was to characterize the relevant classification of drug impurities and to review the methods of impurities determination for atorvastatin (ATV) and duloxetine (DLX) (both in active pharmaceutical ingredients and in different dosage forms)."( Impurities in Drug Products and Active Pharmaceutical Ingredients.
Frankowski, M; Kątny, M, 2017
)
0.65
" The model developed may be of clinical importance to guide dosing recommendations tailored specifically for the Japanese."( Modelling of atorvastatin pharmacokinetics and the identification of the effect of a BCRP polymorphism in the Japanese population.
Aarons, L; Galetin, A; Guo, Y; Hall, S; Tsamandouras, N; Wendling, T, 2017
)
0.82
" Electronic pharmacy records were used to abstract information on the type, length, and dosage of statin exposures starting in the year prior to diagnosis."( Influence of Statins and Cholesterol on Mortality Among Patients With Pancreatic Cancer.
Chang, JI; Huang, BZ; Li, E; Wu, BU; Xiang, AH, 2017
)
0.46
" Vitamin D (25-OHD) dosing was performed by chemiluminescence method through the LIAISON® Vitamin D assay (Diasorin Inc)."( Impact of high-dose statins on vitamin D levels and platelet function in patients with coronary artery disease.
Barbieri, L; Bellomo, G; Daffara, V; De Luca, G; Marino, P; Nardin, M; Pergolini, P; Rolla, R; Schaffer, A; Suryapranata, H; Verdoia, M, 2017
)
0.46
"To assess whether the protective effect of statins on the risk of glaucoma varies depending on the daily dosage or type of statin taken."( Association of Daily Dosage and Type of Statin Agent With Risk of Open-Angle Glaucoma.
Musch, DC; Stein, JD; Talwar, N, 2017
)
0.46
" Using multivariable regression modeling, we assessed the hazard of developing OAG and how it varied by the daily dosage or type of statin and whether any protective effect persists after accounting for baseline low-density lipoprotein level."( Association of Daily Dosage and Type of Statin Agent With Risk of Open-Angle Glaucoma.
Musch, DC; Stein, JD; Talwar, N, 2017
)
0.46
" Our study helps inform researchers of a reasonable daily dosage and type of statin to use when designing randomized clinical trials to assess the association between statin use and glaucoma."( Association of Daily Dosage and Type of Statin Agent With Risk of Open-Angle Glaucoma.
Musch, DC; Stein, JD; Talwar, N, 2017
)
0.46
" The case for fixed-dose combination (FDC) oral dosage forms and orally disintegrating tablet (ODT) technology to enhance outcomes and compliance is strong."( Fixed-dose combination orally disintegrating tablets to treat cardiovascular disease: formulation, in vitro characterization and physiologically based pharmacokinetic modeling to assess bioavailability.
Badhan, RK; Dennison, TJ; Mohammed, AR; Smith, JC, 2017
)
0.46
" Unfortunately, the high dosage used poses side-effects relatively in comparison to other statins."( Preparation and characterisation of atorvastatin and curcumin-loaded chitosan nanoformulations for oral delivery in atherosclerosis.
J B, VK; Madhusudhan, B; Ramakrishna, S, 2017
)
0.73
" Patients were randomly assigned to receive daily 20mg atorvastatin for 10days (n=21) or placebo in the same dosage (n=23)."( Effects of atorvastatin on brain contusion volume and functional outcome of patients with moderate and severe traumatic brain injury; a randomized double-blind placebo-controlled clinical trial.
Derakhshan, N; Farzanegan, GR; Ghaffarpasand, F; Khalili, H; Paydar, S, 2017
)
1.09
"The relative benefit of higher statin dosing in patients with peripheral artery disease has not been reported previously."( High-Intensity Statin Therapy Is Associated With Improved Survival in Patients With Peripheral Artery Disease.
Amsterdam, EA; Armstrong, EJ; Choy, HK; Foley, TR; Kokkinidis, DG; Laird, JR; Pham, T; Rutledge, JC; Singh, GD; Waldo, SW, 2017
)
0.46
"This study explored the impact of intensive daily dosing of atorvastatin on in-hospital N-terminal pro-B-type natriuretic peptide level, left ventricular systolic function and incidence of major adverse cardiac events in non-ST-segment elevation myocardial infarction patients."( Prognostic impact of intensive statin therapy on N-terminal pro-BNP level in non-ST-segment elevation acute myocardial infarction patients.
Dardiri, M; Samir, A; Shehata, M, 2017
)
0.7
"Animals dosed with 10 mg/kg presented the worst neurological function and brain damage in the acute phase of stroke injury."( Coenzyme Q10 supplementation improves acute outcomes of stroke in rats pretreated with atorvastatin.
Faizi, M; Khodagholi, F; Naderi, N; Nasoohi, S; Nikseresht, S; Simani, L, 2019
)
0.74
"The dosing schedules for hypercholesterolemic subjects randomized in the four phase I studies were (1) ascending, single, intravenous (IV) bococizumab (0."( The effects of single- and multiple-dose administration of bococizumab (RN316/PF-04950615), a humanized IgG2Δa monoclonal antibody binding proprotein convertase subtilisin/kexin type 9, in hypercholesterolemic subjects treated with and without atorvastati
Baum, CM; Billotte, S; Forgues, P; Garzone, PD; Gumbiner, B; Joh, T; Levisetti, M; Liang, H; Pons, J; Shelton, DL; Vana, AM; Wan, H, 2018
)
0.48
" The obtained results suggest a promising, easy-to-manufacture and effective dosage form for the treatment of hyperlipidemia."( Experimentally designed lyophilized dry emulsion tablets for enhancing the antihyperlipidemic activity of atorvastatin calcium: Preparation, in-vitro evaluation and in-vivo assessment.
Basha, M; El Awdan, S; Salama, AH, 2018
)
0.69
" Their in vivo PK as well as PD measures following oral administration in different dosage regimens in hyperlipidemic rats were evaluated."( Efficacy and Safety Profiles of Oral Atorvastatin-Loaded Nanoparticles: Effect of Size Modulation on Biodistribution.
Abd-Rabo, MM; Ahmed, IS; El Hosary, R; Haider, M; Hassan, MA, 2018
)
0.75
"4 years) who received a single oral dose of atorvastatin 20 mg on day 1 (period 1), multiple daily dosing of bazedoxifene 40 mg on days 4-11 (period 2), and coadministration of atorvastatin 20 mg + bazedoxifene 40 mg on day 12 (period 3)."( A Study of the Potential Interaction Between Bazedoxifene and Atorvastatin in Healthy Postmenopausal Women.
Baird-Bellaire, S; Ermer, J; McKeand, W; Patat, A, 2018
)
0.98
" In subanalyses, a trend of a dose-response relationship was observed."( Statin use associated with lower risk of epilepsy after intracranial haemorrhage: A population-based cohort study.
Ho, YF; Lin, FJ; Lin, HW, 2018
)
0.48
"We determined the proportion of Medicare beneficiaries 66 to 75 years of age taking a low/moderate-intensity statin with (n = 6718) and without (n = 6414) DM who titrated to a high-intensity statin dosage (i."( Titration to High-Intensity Statin Therapy Following Acute Myocardial Infarction in Patients With and Without Diabetes Mellitus.
Brown, TM; Carson, AP; Colantonio, LD; Dai, Y; Farkouh, ME; Giustino, G; Monda, KL; Muntner, P; Rosenson, RS, 2018
)
0.48
"The first statin fill following hospital discharge was for a high-intensity dosage among 37."( Titration to High-Intensity Statin Therapy Following Acute Myocardial Infarction in Patients With and Without Diabetes Mellitus.
Brown, TM; Carson, AP; Colantonio, LD; Dai, Y; Farkouh, ME; Giustino, G; Monda, KL; Muntner, P; Rosenson, RS, 2018
)
0.48
"Most patients taking a low/moderate-intensity statin were not titrated to a high-intensity dosage following AMI irrespective of their diabetes status, potentially leaving substantial residual risk for recurrent CVD events."( Titration to High-Intensity Statin Therapy Following Acute Myocardial Infarction in Patients With and Without Diabetes Mellitus.
Brown, TM; Carson, AP; Colantonio, LD; Dai, Y; Farkouh, ME; Giustino, G; Monda, KL; Muntner, P; Rosenson, RS, 2018
)
0.48
"All patients with age ≤75 years undergoing PCI between January 2011 and May 2016 at an urban, tertiary care center and discharged with available statin dosage data were included."( Temporal trends, determinants, and impact of high-intensity statin prescriptions after percutaneous coronary intervention: Results from a large single-center prospective registry.
Aquino, M; Baber, U; Barman, N; Camaj, A; Chandrasekhar, J; Claessen, B; Dangas, G; Faggioni, M; Farhan, S; Guedeney, P; Kalkman, DN; Kini, A; Kovacic, JC; Mehran, R; Moreno, P; Shah, S; Sharma, S; Sorrentino, S; Sweeny, J; Vijay, P; Vogel, B, 2019
)
0.51
"Four new, simple, and reproducible spectrophotometric methods were developed and validated for the simultaneous determination of Amlodipine (AML) and Atorvastatin (AT) in bulk powder and pharmaceutical dosage form."( Determination of amlodipine and atorvastatin mixture by different spectrophotometric methods with or without regression equations.
Fares, NV; Farouk, M; Hemdan, A; Magdy, R, 2019
)
1
" Dosing shall continue for 24-mo or until reaching a safety endpoint."( Atorvastatin Treatment of Cavernous Angiomas with Symptomatic Hemorrhage Exploratory Proof of Concept (AT CASH EPOC) Trial.
Akers, AL; Awad, IA; Cao, Y; Christoforidis, GA; Fam, MD; Flemming, KD; Girard, R; Hanley, DF; Hobson, N; Koenig, JI; Koskimäki, J; Lane, K; Lee, C; Liao, JK; Lyne, SB; McBee, N; Morrison, L; Piedad, K; Polster, SP; Shenkar, R; Sorrentino, M; Stadnik, A; Thompson, RE; Whitehead, KJ; Zeineddine, HA, 2019
)
1.96
" RESULTS Ato prevented myocardial fibrosis in spontaneous hypertension rats, especially at the dosage of 50 mg/kg/d."( Atorvastatin Prevents Myocardial Fibrosis in Spontaneous Hypertension via Interleukin-6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Endothelin-1 (ET-1) Pathway.
Fang, T; Guo, B; Wang, L; Xue, L, 2019
)
1.96
"5-5 mg atorvastatin daily combined with dexamethasone with stepwise-decreasing dosing for a total of 4 weeks."( Treatment of Relapsed Chronic Subdural Hematoma in Four Young Children with Atorvastatin and Low-dose Dexamethasone.
Dong, J; Gao, C; Huang, J; Jiang, R; Li, L; Quan, W; Sun, J; Tian, Q; Tian, Y; Wang, D; Zhang, J, 2019
)
1.2
" Atorvastatin and metabolites' steady-state levels were analyzed before first dosing with bempedoic acid and after 2 weeks of treatment."( Complementary low-density lipoprotein-cholesterol lowering and pharmacokinetics of adding bempedoic acid (ETC-1002) to high-dose atorvastatin background therapy in hypercholesterolemic patients: A randomized placebo-controlled trial.
Cramer, CT; Hanselman, JC; Lalwani, ND; MacDougall, DE; Sterling, LR,
)
1.25
"The aim of this study was to develop a new dosage form as an alternative to the classical tablet forms of atorvastatin calcium (AtrCa)."( Formulation and In Vitro Evaluation of Self Microemulsifying Drug Delivery System Containing Atorvastatin Calcium.
Diril, M; Karasulu, HY; Türkyılmaz, GY, 2019
)
0.95
"5%) were adherent to the therapy (PDC ≥ 80%); among them, a small percentage required dosage modification."( Treatment with Free Triple Combination Therapy of Atorvastatin, Perindopril, Amlodipine in Hypertensive Patients: A Real-World Population Study in Italy.
Degli Esposti, L; Gambera, M; Nati, G; Perone, F; Perrone, V; Tagliabue, PF; Veronesi, C; Volpe, M, 2019
)
0.77
" More evidence is needed to evaluated of dose-response effects of these drugs before to study in clinical trials."( Comparison of four pharmacological strategies aimed to prevent the lung inflammation and paraquat-induced alveolar damage.
Buendía, JA; Justinico Castro, JA; Sánchez Villamil, JP; Sinisterra, D; Vela, LJT; Zuluaga Salazar, AF, 2019
)
0.51
"Increased bococizumab dosage resulted in increased exposure."( Pharmacokinetics and exploratory efficacy biomarkers of bococizumab, an anti-PCSK9 monoclonal antibody, in hypercholesterolemic Japanese subjects
.
Li, Y; Matsuoka, N; Suzuki, A; Teramoto, T; Yokote, K, 2019
)
0.51
" Furthermore, most preclinical antiepileptogenic studies lack information needed for translation, such as dose-blood level relationship, brain target engagement, and dose-response, and many use treatment parameters that cannot be applied clinically, for example, treatment initiation before or at the time of injury and dosing higher than tolerated human equivalent dosing."( Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy?
Bar-Klein, G; Friedman, A; Hameed, MQ; Jozwiak, S; Kaminski, RM; Klein, P; Klitgaard, H; Koepp, M; Löscher, W; Prince, DA; Rotenberg, A; Twyman, R; Vezzani, A; Wong, M, 2020
)
0.56
" Since boosted ARVs double atorvastatin exposure, the initial dosage might be reduced by half, and titrated based on individual clinical targets."( Influence of Drug-Drug Interactions on the Pharmacokinetics of Atorvastatin and Its Major Active Metabolite ortho-OH-Atorvastatin in Aging People Living with HIV.
Alves Saldanha, S; Buclin, T; Cavassini, M; Courlet, P; Csajka, C; Decosterd, LA; Guidi, M; Marzolini, C; Stader, F; Stoeckle, M, 2020
)
1.09
" Low-density lipoprotein cholesterol (LDL-C) levels and intensity of statin therapy (based on dosage and type of statin) were assessed from all available hospital records."( Treatment Patterns of Lipid-Lowering Therapy in Patients with Coronary Artery Disease Aged Above and Below 75 Years: A Retrospective Cross-Sectional Study of 1500 Patients in a Tertiary Care Referral Center in Germany.
Al-Rashid, F; Dykun, I; Hendricks, S; Jánosi, RA; Mahabadi, AA; Rassaf, T; Totzeck, M; Wiefhoff, D, 2020
)
0.56
"This study aimed to investigate whether the drug-specific and dosage effects of statin use were associated with a lower risk of cancer in adults in South Korea."( Drug-specific and dosage effects of statins and the risk of cancer: a population-based cohort study in South Korea.
Oh, TK; Song, IA, 2021
)
0.62
" 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
" Cox proportional hazard regression analysis was used to determine the association between the 2 high-intensity atorvastatin dosing regimens and the primary outcome at 1 month and 12 months postdischarge."( Clinical outcomes of high-intensity doses of atorvastatin in patients with acute coronary syndrome: A retrospective cohort study using real-world data.
Al-Shekh, I; Al-Yafei, S; AlAhmad, Y; Aljundi, AH; Alzaeem, H; Arabi, AR; Awaisu, A; Habra, M; Khir, F; Mahfouz, A; Rahhal, A, 2021
)
1.09
" It also reduced the dosage of levetiracetam and achieved better control of epilepsy compared to levetiracetam mono-treatment."( Effects of atorvastatin and aspirin on post-stroke epilepsy and usage of levetiracetam.
Ding, Y; Feng, X; Lin, W; Zhao, T; Zhou, C, 2020
)
0.95
"Atorvastatin and aspirin co-treatment with levetiracetam can reduce epilepsy in PSE patients and reduce the dosage of levetiracetam required for effective control of PSE."( Effects of atorvastatin and aspirin on post-stroke epilepsy and usage of levetiracetam.
Ding, Y; Feng, X; Lin, W; Zhao, T; Zhou, C, 2020
)
2.39
" Doses and dosing intervals were based on previous pharmacokinetic and tolerability studies in mice."( Systematic evaluation of rationally chosen multitargeted drug combinations: a combination of low doses of levetiracetam, atorvastatin and ceftriaxone exerts antiepileptogenic effects in a mouse model of acquired epilepsy.
Bergin, DH; Johne, M; Klein, P; Löscher, W; Schidlitzki, A; Twele, F; Welzel, L, 2021
)
0.83
" No consistent differences in plasma exposure of atorvastatin or M1 were observed in mice after single or repeat dosing of atorvastatin with or without mineral oil."( Effects of mineral oil administration on the pharmacokinetics, metabolism and pharmacodynamics of atorvastatin and pravastatin in mice and dogs.
Abrahamsson, B; Agrawal, R; Bergenholm, L; Björkbom, A; Bright, J; Cavallin, A; Gopaul, VS; Hammarberg, M; Hawthorne, G; Hurt-Camejo, E; Jansson-Löfmark, R; Jarke, A; Johansson, MJ; Li, X; Lundborg, E; Pieterman, EJ; Princen, HMG; Svensson, L, 2021
)
1.09
" Only rosuvastatin was assessed in a repeated dosing PK study."( A systematic review on pharmacokinetics, cardiovascular outcomes and safety profiles of statins in cirrhosis.
Abraldes, JG; Al-Karaghouli, M; Cabrera Garcia, L; Kalainy, S; Sung, S, 2021
)
0.62
" Blood samples were taken over the dosing intervals and drug concentrations quantified by high-performance liquid chromatography-mass spectrometry."( Mechanistic Considerations About an Unexpected Ramipril Drug-Drug Interaction in the Development of a Triple Fixed-Dose Combination Product Containing Ramipril, Amlodipine, and Atorvastatin.
Gundlach, K; Hermann, R; Seiler, D, 2021
)
0.81
" Because pharmacodynamic interaction between statins and bempedoic acid is complex, a dose-response model was developed to predict LDL-C pharmacodynamics following administration of statins combined with bempedoic acid."( Pharmacodynamic effect of bempedoic acid and statin combinations: predictions from a dose-response model.
Amore, BM; Barrett, PHR; Catapano, AL; Chapel, S; Crass, RL; Emery, MG; Jadhav, SB; Kerschnitzki, M; Sasiela, WJ; Watts, GF, 2022
)
0.72
"Bempedoic acid and statin dosing and LDL-C data were pooled from 14 phase 1-3 clinical studies."( Pharmacodynamic effect of bempedoic acid and statin combinations: predictions from a dose-response model.
Amore, BM; Barrett, PHR; Catapano, AL; Chapel, S; Crass, RL; Emery, MG; Jadhav, SB; Kerschnitzki, M; Sasiela, WJ; Watts, GF, 2022
)
0.72
"The study was able to progress through all 4 dosing levels of sorafenib by the accrual of 40 patients."( Phase I Study Evaluating Dose De-escalation of Sorafenib with Metformin and Atorvastatin in Hepatocellular Carcinoma (SMASH).
Ankathi, SK; Banavali, SD; Bhargava, PG; Daddi, A; Goel, M; Gota, V; Jadhav, S; Mandavkar, S; Nashikkar, C; Naughane, D; Ostwal, V; Patkar, S; Ramaswamy, A; Shetty, N; Shriyan, B; Srinivas, S, 2022
)
0.95
" We performed an open-label study comparing pharmacokinetics of atorvastatin (OATP1B probe) dosed alone (20 mg single dose) and coadministered with two dose strengths of KHKi (50 and 280 mg once daily) in 12 healthy participants."( Effect of a Ketohexokinase Inhibitor (PF-06835919) on In Vivo OATP1B Activity: Integrative Risk Assessment Using Endogenous Biomarker and a Probe Drug.
Bergman, A; Fonseca, KR; Kimoto, E; King-Ahmad, A; Litchfield, J; Qui, R; Rodrigues, AD; Somayaji, V; Tess, DA; Varma, MVS; Vourvahis, M; Weng, Y, 2022
)
0.96
" Peak and trough drug plasma concentrations were collected based on the dosing interval and pharmacokinetics of the drugs and quantified using high performance liquid chromatography."( Simvastatin, but Not Atorvastatin, Is Associated with Higher Peak Rivaroxaban Serum Levels and Bleeding: an Asian Cohort Study from Singapore.
Chan, ECY; Soh, XQ; Tan, DS, 2023
)
1.23
" Finally, the established wbPBPK model could describe ATV ADME in the presence of IBS and IBD after oral administration of raw ATV and using the novel SFT formula and can help scale the optimized ATV dosing regimens in the presence of IBS and IBD from rats to humans."( Enhancing Atorvastatin In Vivo Oral Bioavailability in the Presence of Inflammatory Bowel Disease and Irritable Bowel Syndrome Using Supercritical Fluid Technology Guided by wbPBPK Modeling in Rat and Human.
Abu-Farsakh, NA; Al-Daoud, NM; Alsmadi, MM; Obaidat, RM, 2022
)
1.12
"After establishing an orthodontic tooth movement model, the left teeth of the retention-stage rats were the maintained side, and the right teeth were the nonmaintained side, which were given physiological saline or atorvastatin dosing at 7d, 14d, and 21d, respectively, by tube feeding, in order to keep the rats as a control group at the beginning of the retention stage."( The Impact of Atorvastatin on RANKL Expression in Rats during the Retention Stage after Orthodontic Tooth Movement.
Gao, Y; Wang, T; Zhao, Y, 2022
)
1.27
" In addition, PGx-guided dosing guidelines are now available for multiple CVD drugs, including clopidogrel, warfarin, and statins."( Pharmacogenomics implementation in cardiovascular disease in a highly diverse population: initial findings and lessons learned from a pilot study in United Arab Emirates.
Al-Mahayri, ZN; Al-Maskari, F; Ali, BR; AlKaabi, J; Alqasrawi, MN; Altoum, SM; AlZaabi, A; Badawi, S; George, L; Hamza, D; Jamil, G; Khasawneh, LQ; Ouda, H; Patrinos, GP, 2022
)
0.72
" Regarding warfarin, only 20% of the participants exhibited reference alleles at VKORC1-1639G > A, CYP2C9*2, and CYP2C9*3, leaving 80% with alternative genotypes at any of the two genes that can be integrated into the warfarin dosing algorithms and can be used whenever the patient receives a warfarin prescription."( Pharmacogenomics implementation in cardiovascular disease in a highly diverse population: initial findings and lessons learned from a pilot study in United Arab Emirates.
Al-Mahayri, ZN; Al-Maskari, F; Ali, BR; AlKaabi, J; Alqasrawi, MN; Altoum, SM; AlZaabi, A; Badawi, S; George, L; Hamza, D; Jamil, G; Khasawneh, LQ; Ouda, H; Patrinos, GP, 2022
)
0.72
" After a 5-week run-in period of treatment with atorvastatin 10 or 20 mg/d (cohorts A and B, respectively), or a bioequivalent dosage of another statin, patients were randomized in a 1:1 ratio within each cohort to receive EZ/AS 10/10 mg FDC (EZ10/AS10) or atorvastatin 20 mg (AS20), once daily (cohort A); or EZ/AS 10/20 mg FDC (EZ10/AS20) or atorvastatin 40 mg (AS40), once daily (cohort B)."( Efficacy and Tolerability of Ezetimibe/Atorvastatin Fixed-dose Combination Versus Atorvastatin Monotherapy in Hypercholesterolemia: A Phase III, Randomized, Active-controlled Study in Chinese Patients.
Chen, J; Ding, C; Ge, J; Li, Z; Liu, Y; Qian, J; Ren, X; Shi, M; Yang, P; Zhang, X, 2022
)
1.25
" Logistic regression showed that d, L, different therapeutic agents, and dosage groups were independent risk factors of ISR."( Treatment effect of metformin combined with atorvastatin in reducing in-stent restenosis after percutaneous coronary intervention in coronary artery disease patients with type 2 diabetic patients.
Chen, M; Li, M; Liu, S; Ma, F; Su, B; Wang, C; Yuan, L; Zhang, S; Zhang, Y; Zheng, Q, 2022
)
0.98
" Here we present a full PBPK model for atorvastatin and its metabolites able to predict within a 2-fold error their PK after the administration of a solid oral dosage form containing the calcium salt of atorvastatin in single and multiple dosing schedules at 20, 40, and 80 mg and 10 mg dose levels, respectively."( A physiologically based pharmacokinetic model for open acid and lactone forms of atorvastatin and metabolites to assess the drug-gene interaction with SLCO1B1 polymorphisms.
García-Arieta, A; Mangas-Sanjuán, V; Merino-Sanjuan, M; Reig-López, J, 2022
)
1.22
" Through a simple and direct technique based on deconvolution and synchronous of the spectrofluorometric spectra, the innovative method enables simultaneous quantification of bisoprolol and atorvastatin as single or co-formulated dosage forms in bulk and plasma."( Novel Deconvoluted Synchronous Spectrofluorimetric Method For Simultaneous Determination Of Bisoprolol and Atorvastatin As Single or Co-administrated Drugs in Bulk and Plasma; Green Assessment.
Abdel-Monem, AH; Abdel-Raoof, AM; Attia, KAM; Eissa, AS, 2023
)
1.31
" Furthermore, proCPU concentration and the dosage of atorvastatin were inversely correlated."( Atorvastatin downregulates plasma procarboxypeptidase U concentrations and improves fibrinolytic potential dose-dependently in hyperlipidemic individuals.
Basir, S; Bosmans, J; Bringmans, T; Claesen, K; De Belder, S; De Keulenaer, GW; De Meester, I; Hendriks, D; Sim, Y; Stoffelen, H; van den Keybus, T; Van Edom, G, 2023
)
2.6
" In the treat-to-target group (n = 2200), which had 6449 person-years of follow-up, moderate-intensity and high-intensity dosing were used in 43% and 54%, respectively."( Treat-to-Target or High-Intensity Statin in Patients With Coronary Artery Disease: A Randomized Clinical Trial.
Ahn, CM; Choi, D; Hong, BK; Hong, MK; Hong, SJ; Jang, Y; Kang, WC; Kim, BK; Kim, JS; Ko, YG; Lee, JB; Lee, JY; Lee, SJ; Lee, YJ; Yang, TH; Yoon, J, 2023
)
0.91
"The results revealed the protective effects of specific types of statins on DLC risk in patients with T2DM and indicated a dose-response relationship."( Protective effects of statins on the incidence of NAFLD-related decompensated cirrhosis in T2DM.
Chen, WM; Chiang, MF; Lee, MC; Lo, HC; Soong, RS; Wu, MS; Wu, SY, 2023
)
0.91
"This study aimed to develop atorvastatin-loaded emulgel and nano-emulgel dosage forms and investigate their efficiency on surgical wound healing and reducing post-operative pain."( Efficacy of topical atorvastatin-loaded emulgel and nano-emulgel 1% on post-laparotomy pain and wound healing: A randomized double-blind placebo-controlled clinical trial.
Jafari-Nedooshan, J; Kargar, S; Ramezani, V; Saghafi, F; Sahebnasagh, A; Tabatabaei, SM; Zarekamali, J, 2023
)
1.53
" Log dose-response data over the doses of 5 mg to 160 mg revealed strong linear dose-related effects on blood total cholesterol and LDL cholesterol, and a weak linear dose-related effect on blood triglycerides."( Pravastatin for lowering lipids.
Adams, SP; Alaeiilkhchi, N; Tasnim, S; Wright, JM, 2023
)
0.91
" There are limited data on effect of dosage of statins and functional outcome in stroke patients."( Effects of Serum Cholesterol on Severity of Stroke and Dosage of Statins on Functional Outcome in Acute Ischemic Stroke.
Chatterjee, A; Gorthi, SP; Nair, R; Prakashini, K; Shridharan, P,
)
0.13
" On comparing the mRS values at baseline and on day 90 with the dose of statins, patients who received a higher dosage had a statistically significant fall in mRS (p-0."( Effects of Serum Cholesterol on Severity of Stroke and Dosage of Statins on Functional Outcome in Acute Ischemic Stroke.
Chatterjee, A; Gorthi, SP; Nair, R; Prakashini, K; Shridharan, P,
)
0.13
" At the visits, the general condition of patients was evaluated; electrocardiography and echocardiography were performed at rest and during dosed physical exercise (PE); anthropometry was analyzed; and office blood pressure (BP), heart rate (HR) and parameters of systolic and diastolic LV function were recorded."( [Can a lipophilic statin improve the treatment of heart failure with preserved ejection fraction in patients with hypertension and obesity?]
Namazova, GA; Shupenina, EY; Vasyuk, YA; Zavyalova, AI, 2023
)
0.91
"Long-term use of the lipophilic statin (atorvastatin) in addition to a standard therapy was associated with regression of clinical manifestations of HFpEF, provided preservation of the systolic function, and some improvement in the LV diastolic function both at rest and during dosed PE."( [Can a lipophilic statin improve the treatment of heart failure with preserved ejection fraction in patients with hypertension and obesity?]
Namazova, GA; Shupenina, EY; Vasyuk, YA; Zavyalova, AI, 2023
)
1.18
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (2)

RoleDescription
environmental contaminantAny minor or unwanted substance introduced into the environment that can have undesired effects.
xenobioticA xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
[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
dihydroxy monocarboxylic acidAny hydroxy monocarboxylic acid carrying at least two hydroxy groups.
pyrrolesAn azole that includes only one N atom and no other heteroatom as a part of the aromatic skeleton.
aromatic amideAn amide in which the amide linkage is bonded directly to an aromatic system.
monofluorobenzenesAny member of the class of fluorobenzenes containing a mono- or poly-substituted benzene ring carrying a single fluorine substitutent.
statin (synthetic)A statin which does not occur naturally and which is not obtained by chemical transformation of a naturally occurring statin.
[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]

Pathways (1)

PathwayProteinsCompounds
Atorvastatin Action Pathway2143

Protein Targets (43)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, CruzipainTrypanosoma cruziPotency7.07950.002014.677939.8107AID1476
RAR-related orphan receptor gammaMus musculus (house mouse)Potency6.75060.006038.004119,952.5996AID1159521; AID1159523
SMAD family member 2Homo sapiens (human)Potency51.33810.173734.304761.8120AID1346859; AID1346924
SMAD family member 3Homo sapiens (human)Potency51.33810.173734.304761.8120AID1346859; AID1346924
GLI family zinc finger 3Homo sapiens (human)Potency44.79610.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency15.72830.000221.22318,912.5098AID1259243; AID743035; AID743036; AID743054; AID743063
caspase 7, apoptosis-related cysteine proteaseHomo sapiens (human)Potency57.11230.013326.981070.7614AID1346978
estrogen receptor 2 (ER beta)Homo sapiens (human)Potency36.03540.000657.913322,387.1992AID1259377
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency22.30880.001022.650876.6163AID1224838; AID1224893
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency6.11160.000214.376460.0339AID720691; AID720692
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency53.87530.003041.611522,387.1992AID1159552; AID1159553; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency40.05500.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency37.56610.001530.607315,848.9004AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
pregnane X nuclear receptorHomo sapiens (human)Potency32.11660.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency37.72020.000229.305416,493.5996AID1259244; AID1259248; AID743069; AID743075; AID743078; AID743091
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency51.33810.001024.504861.6448AID743212
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency31.68760.001019.414170.9645AID743094; AID743140; AID743191
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency36.34460.023723.228263.5986AID743223
caspase-3Homo sapiens (human)Potency57.11230.013326.981070.7614AID1346978
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency5.71120.001723.839378.1014AID743083
Caspase-7Cricetulus griseus (Chinese hamster)Potency36.03540.006723.496068.5896AID1346980
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency25.11890.354828.065989.1251AID504847
thyroid hormone receptor beta isoform aHomo sapiens (human)Potency112.20200.010039.53711,122.0200AID1479
caspase-3Cricetulus griseus (Chinese hamster)Potency36.03540.006723.496068.5896AID1346980
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency57.11230.000323.4451159.6830AID743065; AID743067
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency28.62400.000627.21521,122.0200AID743202
gemininHomo sapiens (human)Potency33.49830.004611.374133.4983AID624297
Voltage-dependent calcium channel gamma-2 subunitMus musculus (house mouse)Potency57.11230.001557.789015,848.9004AID1259244
Cellular tumor antigen p53Homo sapiens (human)Potency5.71120.002319.595674.0614AID651631
Glutamate receptor 2Rattus norvegicus (Norway rat)Potency57.11230.001551.739315,848.9004AID1259244
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)IC50 (µMol)0.00640.00000.79498.9000AID241793; AID625271; AID737918
3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)Ki0.00620.00090.00830.0235AID1525544
ATP-dependent translocase ABCB1Homo sapiens (human)IC50 (µMol)289.00000.00022.318510.0000AID679461; AID679464
Insulin receptor Rattus norvegicus (Norway rat)IC50 (µMol)0.00020.00010.78463.3700AID625271
Dipeptidyl peptidase 4Sus scrofa (pig)IC50 (µMol)175.10000.43001.14002.5000AID313844
Prostaglandin G/H synthase 2Homo sapiens (human)IC50 (µMol)0.00020.00010.995010.0000AID625271
3-hydroxy-3-methylglutaryl-coenzyme A reductase Rattus norvegicus (Norway rat)IC50 (µMol)0.00540.00090.20949.0300AID1798163; AID313910; AID384740
Histone deacetylase 1Homo sapiens (human)IC50 (µMol)11.61900.00010.55439.9000AID737917
Histone deacetylase 2Homo sapiens (human)IC50 (µMol)22.54700.00010.72219.9700AID737916
Histone deacetylase 6Homo sapiens (human)IC50 (µMol)14.46600.00000.53769.9000AID737915
Broad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)IC50 (µMol)4.30000.00401.966610.0000AID1873192
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)IC50 (µMol)1.00000.05002.37979.7000AID1218863; AID1218864; AID1218865
[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 2B1 Homo sapiens (human)Km2.84000.70005.00608.0900AID699532
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)Km0.73000.03912.93886.4000AID699531
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)Km6.58500.00763.201810.0000AID678959; AID699530
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (331)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
prostaglandin transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transport across blood-brain barrierSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
cholesterol biosynthetic process3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
visual learning3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
coenzyme A metabolic process3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
negative regulation of protein catabolic process3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
negative regulation of protein secretion3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
long-term synaptic potentiation3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
regulation of ERK1 and ERK2 cascade3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
negative regulation of amyloid-beta clearance3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
isoprenoid biosynthetic process3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
sterol biosynthetic process3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
G2/M transition of mitotic cell cycleATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic metabolic processATP-dependent translocase ABCB1Homo sapiens (human)
response to xenobiotic stimulusATP-dependent translocase ABCB1Homo sapiens (human)
phospholipid translocationATP-dependent translocase ABCB1Homo sapiens (human)
terpenoid transportATP-dependent translocase ABCB1Homo sapiens (human)
regulation of response to osmotic stressATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
transepithelial transportATP-dependent translocase ABCB1Homo sapiens (human)
stem cell proliferationATP-dependent translocase ABCB1Homo sapiens (human)
ceramide translocationATP-dependent translocase ABCB1Homo sapiens (human)
export across plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
positive regulation of anion channel activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
regulation of chloride transportATP-dependent translocase ABCB1Homo sapiens (human)
prostaglandin biosynthetic processProstaglandin G/H synthase 2Homo sapiens (human)
angiogenesisProstaglandin G/H synthase 2Homo sapiens (human)
response to oxidative stressProstaglandin G/H synthase 2Homo sapiens (human)
embryo implantationProstaglandin G/H synthase 2Homo sapiens (human)
learningProstaglandin G/H synthase 2Homo sapiens (human)
memoryProstaglandin G/H synthase 2Homo sapiens (human)
regulation of blood pressureProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of cell population proliferationProstaglandin G/H synthase 2Homo sapiens (human)
response to xenobiotic stimulusProstaglandin G/H synthase 2Homo sapiens (human)
response to nematodeProstaglandin G/H synthase 2Homo sapiens (human)
response to fructoseProstaglandin G/H synthase 2Homo sapiens (human)
response to manganese ionProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of vascular endothelial growth factor productionProstaglandin G/H synthase 2Homo sapiens (human)
cyclooxygenase pathwayProstaglandin G/H synthase 2Homo sapiens (human)
bone mineralizationProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of prostaglandin biosynthetic processProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of fever generationProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of synaptic plasticityProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of synaptic transmission, dopaminergicProstaglandin G/H synthase 2Homo sapiens (human)
prostaglandin secretionProstaglandin G/H synthase 2Homo sapiens (human)
response to estradiolProstaglandin G/H synthase 2Homo sapiens (human)
response to lipopolysaccharideProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylationProstaglandin G/H synthase 2Homo sapiens (human)
response to vitamin DProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to heatProstaglandin G/H synthase 2Homo sapiens (human)
response to tumor necrosis factorProstaglandin G/H synthase 2Homo sapiens (human)
maintenance of blood-brain barrierProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of protein import into nucleusProstaglandin G/H synthase 2Homo sapiens (human)
hair cycleProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of apoptotic processProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of nitric oxide biosynthetic processProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of cell cycleProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of vasoconstrictionProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of smooth muscle contractionProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of smooth muscle contractionProstaglandin G/H synthase 2Homo sapiens (human)
decidualizationProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of smooth muscle cell proliferationProstaglandin G/H synthase 2Homo sapiens (human)
regulation of inflammatory responseProstaglandin G/H synthase 2Homo sapiens (human)
brown fat cell differentiationProstaglandin G/H synthase 2Homo sapiens (human)
response to glucocorticoidProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of calcium ion transportProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of synaptic transmission, glutamatergicProstaglandin G/H synthase 2Homo sapiens (human)
response to fatty acidProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to mechanical stimulusProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to lead ionProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to ATPProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to hypoxiaProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to non-ionic osmotic stressProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to fluid shear stressProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of transforming growth factor beta productionProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of cell migration involved in sprouting angiogenesisProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of fibroblast growth factor productionProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of brown fat cell differentiationProstaglandin G/H synthase 2Homo sapiens (human)
positive regulation of platelet-derived growth factor productionProstaglandin G/H synthase 2Homo sapiens (human)
cellular oxidant detoxificationProstaglandin G/H synthase 2Homo sapiens (human)
regulation of neuroinflammatory responseProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to osmotic stressProstaglandin G/H synthase 2Homo sapiens (human)
cellular response to homocysteineProstaglandin G/H synthase 2Homo sapiens (human)
response to angiotensinProstaglandin G/H synthase 2Homo sapiens (human)
negative regulation of myotube differentiationHistone deacetylase 1Homo sapiens (human)
negative regulation of apoptotic processHistone deacetylase 1Homo sapiens (human)
positive regulation of signaling receptor activityHistone deacetylase 1Homo sapiens (human)
negative regulation of transcription by RNA polymerase IIHistone deacetylase 1Homo sapiens (human)
chromatin organizationHistone deacetylase 1Homo sapiens (human)
chromatin remodelingHistone deacetylase 1Homo sapiens (human)
DNA methylation-dependent heterochromatin formationHistone deacetylase 1Homo sapiens (human)
regulation of transcription by RNA polymerase IIHistone deacetylase 1Homo sapiens (human)
protein deacetylationHistone deacetylase 1Homo sapiens (human)
endoderm developmentHistone deacetylase 1Homo sapiens (human)
positive regulation of cell population proliferationHistone deacetylase 1Homo sapiens (human)
epidermal cell differentiationHistone deacetylase 1Homo sapiens (human)
positive regulation of gene expressionHistone deacetylase 1Homo sapiens (human)
negative regulation of gene expressionHistone deacetylase 1Homo sapiens (human)
hippocampus developmentHistone deacetylase 1Homo sapiens (human)
neuron differentiationHistone deacetylase 1Homo sapiens (human)
negative regulation of cell migrationHistone deacetylase 1Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayHistone deacetylase 1Homo sapiens (human)
circadian regulation of gene expressionHistone deacetylase 1Homo sapiens (human)
cellular response to platelet-derived growth factor stimulusHistone deacetylase 1Homo sapiens (human)
odontogenesis of dentin-containing toothHistone deacetylase 1Homo sapiens (human)
regulation of cell fate specificationHistone deacetylase 1Homo sapiens (human)
embryonic digit morphogenesisHistone deacetylase 1Homo sapiens (human)
negative regulation of apoptotic processHistone deacetylase 1Homo sapiens (human)
negative regulation of canonical NF-kappaB signal transductionHistone deacetylase 1Homo sapiens (human)
negative regulation by host of viral transcriptionHistone deacetylase 1Homo sapiens (human)
negative regulation of gene expression, epigeneticHistone deacetylase 1Homo sapiens (human)
negative regulation of DNA-templated transcriptionHistone deacetylase 1Homo sapiens (human)
positive regulation of DNA-templated transcriptionHistone deacetylase 1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIHistone deacetylase 1Homo sapiens (human)
positive regulation of smooth muscle cell proliferationHistone deacetylase 1Homo sapiens (human)
oligodendrocyte differentiationHistone deacetylase 1Homo sapiens (human)
positive regulation of oligodendrocyte differentiationHistone deacetylase 1Homo sapiens (human)
negative regulation of androgen receptor signaling pathwayHistone deacetylase 1Homo sapiens (human)
hair follicle placode formationHistone deacetylase 1Homo sapiens (human)
eyelid development in camera-type eyeHistone deacetylase 1Homo sapiens (human)
fungiform papilla formationHistone deacetylase 1Homo sapiens (human)
negative regulation of canonical Wnt signaling pathwayHistone deacetylase 1Homo sapiens (human)
negative regulation of stem cell population maintenanceHistone deacetylase 1Homo sapiens (human)
positive regulation of stem cell population maintenanceHistone deacetylase 1Homo sapiens (human)
regulation of stem cell differentiationHistone deacetylase 1Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathwayHistone deacetylase 1Homo sapiens (human)
heterochromatin formationHistone deacetylase 1Homo sapiens (human)
positive regulation of signaling receptor activityHistone deacetylase 2Homo sapiens (human)
negative regulation of transcription by RNA polymerase IIHistone deacetylase 2Homo sapiens (human)
response to amphetamineHistone deacetylase 2Homo sapiens (human)
cardiac muscle hypertrophyHistone deacetylase 2Homo sapiens (human)
chromatin remodelingHistone deacetylase 2Homo sapiens (human)
positive regulation of cell population proliferationHistone deacetylase 2Homo sapiens (human)
response to xenobiotic stimulusHistone deacetylase 2Homo sapiens (human)
epidermal cell differentiationHistone deacetylase 2Homo sapiens (human)
positive regulation of epithelial to mesenchymal transitionHistone deacetylase 2Homo sapiens (human)
negative regulation of transcription by competitive promoter bindingHistone deacetylase 2Homo sapiens (human)
negative regulation of neuron projection developmentHistone deacetylase 2Homo sapiens (human)
dendrite developmentHistone deacetylase 2Homo sapiens (human)
negative regulation of cell migrationHistone deacetylase 2Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayHistone deacetylase 2Homo sapiens (human)
response to caffeineHistone deacetylase 2Homo sapiens (human)
heterochromatin formationHistone deacetylase 2Homo sapiens (human)
response to lipopolysaccharideHistone deacetylase 2Homo sapiens (human)
positive regulation of interleukin-1 productionHistone deacetylase 2Homo sapiens (human)
positive regulation of tumor necrosis factor productionHistone deacetylase 2Homo sapiens (human)
circadian regulation of gene expressionHistone deacetylase 2Homo sapiens (human)
positive regulation of collagen biosynthetic processHistone deacetylase 2Homo sapiens (human)
cellular response to heatHistone deacetylase 2Homo sapiens (human)
response to nicotineHistone deacetylase 2Homo sapiens (human)
protein modification processHistone deacetylase 2Homo sapiens (human)
response to cocaineHistone deacetylase 2Homo sapiens (human)
odontogenesis of dentin-containing toothHistone deacetylase 2Homo sapiens (human)
positive regulation of tyrosine phosphorylation of STAT proteinHistone deacetylase 2Homo sapiens (human)
regulation of cell fate specificationHistone deacetylase 2Homo sapiens (human)
embryonic digit morphogenesisHistone deacetylase 2Homo sapiens (human)
negative regulation of apoptotic processHistone deacetylase 2Homo sapiens (human)
negative regulation of DNA-binding transcription factor activityHistone deacetylase 2Homo sapiens (human)
negative regulation of MHC class II biosynthetic processHistone deacetylase 2Homo sapiens (human)
positive regulation of proteolysisHistone deacetylase 2Homo sapiens (human)
negative regulation of DNA-templated transcriptionHistone deacetylase 2Homo sapiens (human)
positive regulation of DNA-templated transcriptionHistone deacetylase 2Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIHistone deacetylase 2Homo sapiens (human)
behavioral response to ethanolHistone deacetylase 2Homo sapiens (human)
positive regulation of oligodendrocyte differentiationHistone deacetylase 2Homo sapiens (human)
response to hyperoxiaHistone deacetylase 2Homo sapiens (human)
hair follicle placode formationHistone deacetylase 2Homo sapiens (human)
negative regulation of dendritic spine developmentHistone deacetylase 2Homo sapiens (human)
eyelid development in camera-type eyeHistone deacetylase 2Homo sapiens (human)
fungiform papilla formationHistone deacetylase 2Homo sapiens (human)
cellular response to hydrogen peroxideHistone deacetylase 2Homo sapiens (human)
cellular response to retinoic acidHistone deacetylase 2Homo sapiens (human)
cellular response to transforming growth factor beta stimulusHistone deacetylase 2Homo sapiens (human)
positive regulation of male mating behaviorHistone deacetylase 2Homo sapiens (human)
negative regulation of stem cell population maintenanceHistone deacetylase 2Homo sapiens (human)
positive regulation of stem cell population maintenanceHistone deacetylase 2Homo sapiens (human)
cellular response to dopamineHistone deacetylase 2Homo sapiens (human)
response to amyloid-betaHistone deacetylase 2Homo sapiens (human)
regulation of stem cell differentiationHistone deacetylase 2Homo sapiens (human)
negative regulation of peptidyl-lysine acetylationHistone deacetylase 2Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
polyamine deacetylationHistone deacetylase 6Homo sapiens (human)
spermidine deacetylationHistone deacetylase 6Homo sapiens (human)
positive regulation of signaling receptor activityHistone deacetylase 6Homo sapiens (human)
protein polyubiquitinationHistone deacetylase 6Homo sapiens (human)
response to amphetamineHistone deacetylase 6Homo sapiens (human)
protein deacetylationHistone deacetylase 6Homo sapiens (human)
protein quality control for misfolded or incompletely synthesized proteinsHistone deacetylase 6Homo sapiens (human)
intracellular protein transportHistone deacetylase 6Homo sapiens (human)
autophagyHistone deacetylase 6Homo sapiens (human)
actin filament organizationHistone deacetylase 6Homo sapiens (human)
negative regulation of microtubule depolymerizationHistone deacetylase 6Homo sapiens (human)
regulation of autophagyHistone deacetylase 6Homo sapiens (human)
positive regulation of epithelial cell migrationHistone deacetylase 6Homo sapiens (human)
negative regulation of hydrogen peroxide metabolic processHistone deacetylase 6Homo sapiens (human)
regulation of macroautophagyHistone deacetylase 6Homo sapiens (human)
axonal transport of mitochondrionHistone deacetylase 6Homo sapiens (human)
negative regulation of protein-containing complex assemblyHistone deacetylase 6Homo sapiens (human)
regulation of protein stabilityHistone deacetylase 6Homo sapiens (human)
protein destabilizationHistone deacetylase 6Homo sapiens (human)
lysosome localizationHistone deacetylase 6Homo sapiens (human)
protein-containing complex disassemblyHistone deacetylase 6Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylationHistone deacetylase 6Homo sapiens (human)
cellular response to heatHistone deacetylase 6Homo sapiens (human)
peptidyl-lysine deacetylationHistone deacetylase 6Homo sapiens (human)
response to immobilization stressHistone deacetylase 6Homo sapiens (human)
cellular response to topologically incorrect proteinHistone deacetylase 6Homo sapiens (human)
erythrocyte enucleationHistone deacetylase 6Homo sapiens (human)
ubiquitin-dependent protein catabolic process via the multivesicular body sorting pathwayHistone deacetylase 6Homo sapiens (human)
negative regulation of protein-containing complex disassemblyHistone deacetylase 6Homo sapiens (human)
regulation of fat cell differentiationHistone deacetylase 6Homo sapiens (human)
negative regulation of gene expression, epigeneticHistone deacetylase 6Homo sapiens (human)
negative regulation of proteolysisHistone deacetylase 6Homo sapiens (human)
negative regulation of DNA-templated transcriptionHistone deacetylase 6Homo sapiens (human)
collateral sproutingHistone deacetylase 6Homo sapiens (human)
negative regulation of axon extension involved in axon guidanceHistone deacetylase 6Homo sapiens (human)
positive regulation of dendrite morphogenesisHistone deacetylase 6Homo sapiens (human)
negative regulation of oxidoreductase activityHistone deacetylase 6Homo sapiens (human)
response to corticosteroneHistone deacetylase 6Homo sapiens (human)
response to misfolded proteinHistone deacetylase 6Homo sapiens (human)
positive regulation of synaptic transmission, glutamatergicHistone deacetylase 6Homo sapiens (human)
cilium assemblyHistone deacetylase 6Homo sapiens (human)
regulation of microtubule-based movementHistone deacetylase 6Homo sapiens (human)
regulation of androgen receptor signaling pathwayHistone deacetylase 6Homo sapiens (human)
dendritic spine morphogenesisHistone deacetylase 6Homo sapiens (human)
cilium disassemblyHistone deacetylase 6Homo sapiens (human)
parkin-mediated stimulation of mitophagy in response to mitochondrial depolarizationHistone deacetylase 6Homo sapiens (human)
regulation of establishment of protein localizationHistone deacetylase 6Homo sapiens (human)
cellular response to hydrogen peroxideHistone deacetylase 6Homo sapiens (human)
aggresome assemblyHistone deacetylase 6Homo sapiens (human)
polyubiquitinated misfolded protein transportHistone deacetylase 6Homo sapiens (human)
response to growth factorHistone deacetylase 6Homo sapiens (human)
cellular response to misfolded proteinHistone deacetylase 6Homo sapiens (human)
cellular response to parathyroid hormone stimulusHistone deacetylase 6Homo sapiens (human)
response to dexamethasoneHistone deacetylase 6Homo sapiens (human)
tubulin deacetylationHistone deacetylase 6Homo sapiens (human)
positive regulation of tubulin deacetylationHistone deacetylase 6Homo sapiens (human)
positive regulation of cellular response to oxidative stressHistone deacetylase 6Homo sapiens (human)
negative regulation of protein acetylationHistone deacetylase 6Homo sapiens (human)
regulation of autophagy of mitochondrionHistone deacetylase 6Homo sapiens (human)
positive regulation of cholangiocyte proliferationHistone deacetylase 6Homo sapiens (human)
negative regulation of aggrephagyHistone deacetylase 6Homo sapiens (human)
epigenetic regulation of gene expressionHistone deacetylase 6Homo sapiens (human)
lipid transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid biosynthetic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate metabolic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transmembrane transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transepithelial transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
renal urate salt excretionBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
export across plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
cellular detoxificationBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo 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 (95)

Processvia Protein(s)Taxonomy
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
hydroxymethylglutaryl-CoA reductase (NADPH) activity3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
protein binding3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
GTPase regulator activity3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
NADPH binding3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
coenzyme A binding3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATP bindingATP-dependent translocase ABCB1Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
efflux transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ATP hydrolysis activityATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ubiquitin protein ligase bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylcholine floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylethanolamine flippase activityATP-dependent translocase ABCB1Homo sapiens (human)
ceramide floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
peroxidase activityProstaglandin G/H synthase 2Homo sapiens (human)
prostaglandin-endoperoxide synthase activityProstaglandin G/H synthase 2Homo sapiens (human)
protein bindingProstaglandin G/H synthase 2Homo sapiens (human)
enzyme bindingProstaglandin G/H synthase 2Homo sapiens (human)
heme bindingProstaglandin G/H synthase 2Homo sapiens (human)
protein homodimerization activityProstaglandin G/H synthase 2Homo sapiens (human)
metal ion bindingProstaglandin G/H synthase 2Homo sapiens (human)
oxidoreductase activity, acting on single donors with incorporation of molecular oxygen, incorporation of two atoms of oxygenProstaglandin G/H synthase 2Homo sapiens (human)
nucleosomal DNA bindingHistone deacetylase 1Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingHistone deacetylase 1Homo sapiens (human)
RNA polymerase II core promoter sequence-specific DNA bindingHistone deacetylase 1Homo sapiens (human)
core promoter sequence-specific DNA bindingHistone deacetylase 1Homo sapiens (human)
transcription corepressor bindingHistone deacetylase 1Homo sapiens (human)
p53 bindingHistone deacetylase 1Homo sapiens (human)
transcription corepressor activityHistone deacetylase 1Homo sapiens (human)
histone deacetylase activityHistone deacetylase 1Homo sapiens (human)
protein bindingHistone deacetylase 1Homo sapiens (human)
enzyme bindingHistone deacetylase 1Homo sapiens (human)
protein lysine deacetylase activityHistone deacetylase 1Homo sapiens (human)
Krueppel-associated box domain bindingHistone deacetylase 1Homo sapiens (human)
histone deacetylase bindingHistone deacetylase 1Homo sapiens (human)
NF-kappaB bindingHistone deacetylase 1Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingHistone deacetylase 1Homo sapiens (human)
E-box bindingHistone deacetylase 1Homo sapiens (human)
DNA-binding transcription factor bindingHistone deacetylase 1Homo sapiens (human)
histone decrotonylase activityHistone deacetylase 1Homo sapiens (human)
promoter-specific chromatin bindingHistone deacetylase 1Homo sapiens (human)
nucleosomal DNA bindingHistone deacetylase 2Homo sapiens (human)
chromatin bindingHistone deacetylase 2Homo sapiens (human)
RNA bindingHistone deacetylase 2Homo sapiens (human)
histone deacetylase activityHistone deacetylase 2Homo sapiens (human)
protein bindingHistone deacetylase 2Homo sapiens (human)
enzyme bindingHistone deacetylase 2Homo sapiens (human)
heat shock protein bindingHistone deacetylase 2Homo sapiens (human)
protein lysine deacetylase activityHistone deacetylase 2Homo sapiens (human)
histone bindingHistone deacetylase 2Homo sapiens (human)
histone deacetylase bindingHistone deacetylase 2Homo sapiens (human)
NF-kappaB bindingHistone deacetylase 2Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingHistone deacetylase 2Homo sapiens (human)
histone decrotonylase activityHistone deacetylase 2Homo sapiens (human)
protein de-2-hydroxyisobutyrylase activityHistone deacetylase 2Homo sapiens (human)
promoter-specific chromatin bindingHistone deacetylase 2Homo sapiens (human)
serine-type endopeptidase inhibitor activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
acetylspermidine deacetylase activityHistone deacetylase 6Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingHistone deacetylase 6Homo sapiens (human)
transcription corepressor bindingHistone deacetylase 6Homo sapiens (human)
actin bindingHistone deacetylase 6Homo sapiens (human)
histone deacetylase activityHistone deacetylase 6Homo sapiens (human)
protein bindingHistone deacetylase 6Homo sapiens (human)
beta-catenin bindingHistone deacetylase 6Homo sapiens (human)
microtubule bindingHistone deacetylase 6Homo sapiens (human)
zinc ion bindingHistone deacetylase 6Homo sapiens (human)
enzyme bindingHistone deacetylase 6Homo sapiens (human)
polyubiquitin modification-dependent protein bindingHistone deacetylase 6Homo sapiens (human)
ubiquitin protein ligase bindingHistone deacetylase 6Homo sapiens (human)
protein lysine deacetylase activityHistone deacetylase 6Homo sapiens (human)
histone deacetylase bindingHistone deacetylase 6Homo sapiens (human)
tubulin deacetylase activityHistone deacetylase 6Homo sapiens (human)
alpha-tubulin bindingHistone deacetylase 6Homo sapiens (human)
ubiquitin bindingHistone deacetylase 6Homo sapiens (human)
tau protein bindingHistone deacetylase 6Homo sapiens (human)
beta-tubulin bindingHistone deacetylase 6Homo sapiens (human)
misfolded protein bindingHistone deacetylase 6Homo sapiens (human)
Hsp90 protein bindingHistone deacetylase 6Homo sapiens (human)
dynein complex bindingHistone deacetylase 6Homo sapiens (human)
transcription factor bindingHistone deacetylase 6Homo sapiens (human)
protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ABC-type xenobiotic transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
efflux transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP hydrolysis activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATPase-coupled transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
identical protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
protein homodimerization activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo 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 (56)

Processvia Protein(s)Taxonomy
plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
apical plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
apical plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
peroxisomal membrane3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
endoplasmic reticulum3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
endoplasmic reticulum membrane3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
endoplasmic reticulum membrane3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
peroxisomal membrane3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
cytoplasmATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
cell surfaceATP-dependent translocase ABCB1Homo sapiens (human)
membraneATP-dependent translocase ABCB1Homo sapiens (human)
apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
extracellular exosomeATP-dependent translocase ABCB1Homo sapiens (human)
external side of apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneGlutamate receptor 2Rattus norvegicus (Norway rat)
nuclear inner membraneProstaglandin G/H synthase 2Homo sapiens (human)
nuclear outer membraneProstaglandin G/H synthase 2Homo sapiens (human)
cytoplasmProstaglandin G/H synthase 2Homo sapiens (human)
endoplasmic reticulumProstaglandin G/H synthase 2Homo sapiens (human)
endoplasmic reticulum lumenProstaglandin G/H synthase 2Homo sapiens (human)
endoplasmic reticulum membraneProstaglandin G/H synthase 2Homo sapiens (human)
caveolaProstaglandin G/H synthase 2Homo sapiens (human)
neuron projectionProstaglandin G/H synthase 2Homo sapiens (human)
protein-containing complexProstaglandin G/H synthase 2Homo sapiens (human)
neuron projectionProstaglandin G/H synthase 2Homo sapiens (human)
cytoplasmProstaglandin G/H synthase 2Homo sapiens (human)
nucleusHistone deacetylase 1Homo sapiens (human)
nucleoplasmHistone deacetylase 1Homo sapiens (human)
cytoplasmHistone deacetylase 1Homo sapiens (human)
cytosolHistone deacetylase 1Homo sapiens (human)
NuRD complexHistone deacetylase 1Homo sapiens (human)
neuronal cell bodyHistone deacetylase 1Homo sapiens (human)
Sin3-type complexHistone deacetylase 1Homo sapiens (human)
histone deacetylase complexHistone deacetylase 1Homo sapiens (human)
chromatinHistone deacetylase 1Homo sapiens (human)
heterochromatinHistone deacetylase 1Homo sapiens (human)
transcription repressor complexHistone deacetylase 1Homo sapiens (human)
protein-containing complexHistone deacetylase 1Homo sapiens (human)
nucleusHistone deacetylase 1Homo sapiens (human)
chromosome, telomeric regionHistone deacetylase 2Homo sapiens (human)
nucleusHistone deacetylase 2Homo sapiens (human)
nucleoplasmHistone deacetylase 2Homo sapiens (human)
cytoplasmHistone deacetylase 2Homo sapiens (human)
NuRD complexHistone deacetylase 2Homo sapiens (human)
Sin3-type complexHistone deacetylase 2Homo sapiens (human)
histone deacetylase complexHistone deacetylase 2Homo sapiens (human)
chromatinHistone deacetylase 2Homo sapiens (human)
protein-containing complexHistone deacetylase 2Homo sapiens (human)
ESC/E(Z) complexHistone deacetylase 2Homo sapiens (human)
nucleusHistone deacetylase 2Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
nucleusHistone deacetylase 6Homo sapiens (human)
nucleoplasmHistone deacetylase 6Homo sapiens (human)
cytoplasmHistone deacetylase 6Homo sapiens (human)
multivesicular bodyHistone deacetylase 6Homo sapiens (human)
centrosomeHistone deacetylase 6Homo sapiens (human)
cytosolHistone deacetylase 6Homo sapiens (human)
microtubuleHistone deacetylase 6Homo sapiens (human)
caveolaHistone deacetylase 6Homo sapiens (human)
inclusion bodyHistone deacetylase 6Homo sapiens (human)
aggresomeHistone deacetylase 6Homo sapiens (human)
axonHistone deacetylase 6Homo sapiens (human)
dendriteHistone deacetylase 6Homo sapiens (human)
cell leading edgeHistone deacetylase 6Homo sapiens (human)
ciliary basal bodyHistone deacetylase 6Homo sapiens (human)
perikaryonHistone deacetylase 6Homo sapiens (human)
perinuclear region of cytoplasmHistone deacetylase 6Homo sapiens (human)
axon cytoplasmHistone deacetylase 6Homo sapiens (human)
histone deacetylase complexHistone deacetylase 6Homo sapiens (human)
microtubule associated complexHistone deacetylase 6Homo sapiens (human)
nucleoplasmBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
brush border membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
mitochondrial membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
membrane raftBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
external side of apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo 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 (273)

Assay IDTitleYearJournalArticle
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.
AID678715Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1698011Fraction unbound in human plasma
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID503308Antiproliferative activity against human PC3 cells at 30 uM after 120 hrs by MTT assay relative to DMSO2006Nature chemical biology, Jun, Volume: 2, Issue:6
Identifying off-target effects and hidden phenotypes of drugs in human cells.
AID1212337Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of dextromethorphan2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID1217708Time dependent inhibition of CYP2D6 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID680431TP_TRANSPORTER: inhibition of Pravastatin uptake (Pravastatin: 0.5 uM, Atorvastatin: 50 uM) in Oatp1-expressing 293c18 cells1999The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52
A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
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.
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
AID385211Myotoxicity in guinea pig assessed as drug dose causing >10 fold increase in plasma creatine kinase activity relative to control2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1232319Volume of distribution at steady state in wild type mouse2015Journal of medicinal chemistry, Aug-13, Volume: 58, Issue:15
Volume of Distribution in Drug Design.
AID1192795Ratio of drug uptake in liver to plasma in rat2015Bioorganic & medicinal chemistry letters, Mar-01, Volume: 25, Issue:5
Transporter-mediated tissue targeting of therapeutic molecules in drug discovery.
AID385202Metabolic stability in human assessed as hepatic extraction2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1212312Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of propranolol2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID558840Antimalarial activity against Plasmodium falciparum IMT 10336 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID631050Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as increase in serum HDL level at 10 mg/kg, po administered once daily for 7 days relative to vehicle treated control2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID558059Antimalarial activity against chloroquine-resistant Plasmodium falciparum Dd2 assessed as Plasmodium lactate dehydrogenase release after 48 hrs by colorimetry2009Antimicrobial agents and chemotherapy, May, Volume: 53, Issue:5
Statins as potential antimalarial drugs: low relative potency and lack of synergy with conventional antimalarial drugs.
AID1649238Activation of TXNDC11 (unknown origin)2020Journal of medicinal chemistry, 05-14, Volume: 63, Issue:9
Degradation versus Inhibition: Development of Proteolysis-Targeting Chimeras for Overcoming Statin-Induced Compensatory Upregulation of 3-Hydroxy-3-methylglutaryl Coenzyme A Reductase.
AID1192793Unbound fraction in Sprague-Dawley rat plasma at 10 uM measured over 18 hrs by equilibrium dialysis method2015Bioorganic & medicinal chemistry letters, Mar-01, Volume: 25, Issue:5
Transporter-mediated tissue targeting of therapeutic molecules in drug discovery.
AID1884871Upregulation of Cpt1b gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1390358Reduction in plasma total cholesterol level in C57BL/6 mouse at 4 mg/kg, sc administered once daily for 2 weeks with high fat diet by enzymatic method relative to untreated control2018Bioorganic & medicinal chemistry letters, 04-15, Volume: 28, Issue:7
Small molecule modulators of PCSK9 - A literature and patent overview.
AID1221856Activity of CYP3A4 in human hepatocytes assessed as increase in nifedipine oxidation activity using nifedipine as substrate at 10 uM relative to control2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID678949TP_TRANSPORTER: transepithelial transport of vinblastine in the presence of Atrovastatin at 50uM in KBV1 cells2004Pharmaceutical research, Sep, Volume: 21, Issue:9
Interactions of human P-glycoprotein with simvastatin, simvastatin acid, and atorvastatin.
AID1884868Upregulation of Cyp4a10 gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
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]
AID313910Inhibition of rat microsomal HMGCoA reductase2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID1212314Drug uptake in lysosomes of human Fa2N-4 cells assessed as inhibition of LysoTracker Red fluorescence after 30 mins2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID699531Activity at human liver OATP1B3 expressed in HEK293 Flp-In cells2012Journal 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.
AID737916Inhibition of recombinant HDAC2 (unknown origin) after 10 mins by fluorimetric analysis2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID384740Inhibition of HMGR in rat hepatic microsomes assessed as conversion of [14C]HMG-CoA to [14C]mevalonic acid2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558850Antimalarial activity against Plasmodium falciparum D6 harboring Ppcrt I371R mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID699537Ratio of Vmax to Km for human liver OATP1B3 expressed in HEK293 Flp-In cells assessed per mg protein2012Journal 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.
AID1218863Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using pitavastatin substrate2012Drug 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.
AID311524Oral bioavailability in human2007Bioorganic & medicinal chemistry, Dec-15, Volume: 15, Issue:24
Hologram QSAR model for the prediction of human oral bioavailability.
AID737915Inhibition of recombinant HDAC6 (unknown origin) after 10 mins by fluorimetric analysis2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1884862Upregulation of Acaa1a gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID406855Toxicity against rat L6 cells assessed as induction of cell death at 100 uM2007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID1525544Inhibition of HMG-CoA Reductase (unknown origin)2019Journal of medicinal chemistry, 11-27, Volume: 62, Issue:22
Why Some Targets Benefit from beyond Rule of Five Drugs.
AID699532Activity at human liver OATP2B1 expressed in HEK293 Flp-In cells2012Journal 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.
AID1218865Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estrone-3-sulfate substrate2012Drug 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.
AID313843Inhibition of pig DPP4 at 500 uM2008Bioorganic & medicinal chemistry letters, Jan-15, Volume: 18, Issue:2
Inhibition of dipeptidyl peptidase-IV (DPP-IV) by atorvastatin.
AID1212341Cytotoxicity against human Fa2N-4 cells by lactate dehydrogenase assay2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1884867Upregulation of peroxisomal bifunctional enzyme gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID539467Lipophilicity, log D of compound at pH 72010Bioorganic & medicinal chemistry letters, Dec-15, Volume: 20, Issue:24
Experimental solubility profiling of marketed CNS drugs, exploring solubility limit of CNS discovery candidate.
AID777267Inhibition of cholesterol synthesis in Wistar rat at 3 mg/kg, po in presence of [14C]acetic acid2013ACS medicinal chemistry letters, Oct-10, Volume: 4, Issue:10
Discovery of DF-461, a Potent Squalene Synthase Inhibitor.
AID558856Antimalarial activity against Plasmodium falciparum IMT Bres harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 h2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1212340Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of diclofenac2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID1221849Inhibition of HMGCR activity in human hepatocytes assessed as increase in lathosterol level per gram of protein by GC-MS analysis (Rvb = 47.7 ug)2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID558843Antimalarial activity against Plasmodium falciparum IMT K14 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID737911Cytotoxicity against human A549 cells after 72 hrs by MTT assay2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID680572TP_TRANSPORTER: inhibition of Taurocholate uptake (Taurocholate: 0.5 uM, Atorvastatin: 50 uM) in OATP-C-expressing 293c18 cells1999The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52
A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID384747Inhibition of hepatic cholesterol synthesis in po dosed Sprague-Dawley rat assessed as incorporation of [14C]acetate into hepatic sterols2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558839Antimalarial activity against Plasmodium falciparum IMT 9881 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884892In vivo activation of PPARalpha/PGC1alpha pathway in HFD-induced C57BL/6J mouse model of NAFL assessed as effect on PPARgamma expression in liver at 15 mg/kg/day, ip administered from week 7 to week 12 by immunoblotting analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID384760Hepatotoxicity in guinea pig assessed as hepatocellular degeneration at >50 mg/kg2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID313844Inhibition of pig DPP42008Bioorganic & medicinal chemistry letters, Jan-15, Volume: 18, Issue:2
Inhibition of dipeptidyl peptidase-IV (DPP-IV) by atorvastatin.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID558832Antimalarial activity against Plasmodium falciparum HB3 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1593968Drug level assessed as esterase (unknown origin)-mediated compound release in pH 4.5 PBS buffer incubated for 3 to 24 hrs by mass spectrometry2019Bioorganic & medicinal chemistry, 06-01, Volume: 27, Issue:11
Targeted delivery of atorvastatin via asialoglycoprotein receptor (ASGPR).
AID1217707Time dependent inhibition of CYP2C19 in human liver microsomes at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID737909Cytotoxicity against human HS68 cells after 72 hrs by MTT assay2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID558859Antimalarial activity against Plasmodium falciparum IMT 31 harboring Ppcrt I371R mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID678716Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1812683Induction of Cholesterol accumulation in human HepG2 cells assessed as fold increase in LDL-cholesterol level at 10 uM after 48 hrs2021Journal of medicinal chemistry, 07-22, Volume: 64, Issue:14
LXR-Mediated Regulation of Marine-Derived Piericidins Aggravates High-Cholesterol Diet-Induced Cholesterol Metabolism Disorder in Mice.
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.
AID1212338Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of chloroquine2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID527840Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in total cholesterol level at 10 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID1217711Metabolic activation in human liver microsomes assessed as [3H]GSH adduct formation rate measured per mg of protein at 100 uM by [3H]GSH trapping assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID571001Antimalarial activity against Plasmodium falciparum infected in mouse assessed as mouse survival at 20 mg/kg, ip, qd administered 4 days post infection for 3 days measured after 6 days relative to control2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1212316Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
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.
AID1217712Time dependent inhibition of CYP2C8 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1884866Upregulation of Acox2 gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID313912Inhibition of cholesterol synthesis in rat L6 myocyte2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID678722Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID385183Hepatotoxicity in guinea pig assessed as alanine aminotransferase level at 150 mg/kg coadministered with mevalonate after 10 days2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
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.
AID680728TP_TRANSPORTER: inhibition of Pravastatin uptake (Pravastatin: 0.5 uM, Atorvastatin: 50 uM) in OATP-C-expressing 293c18 cells1999The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52
A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
AID384748Reduction in plasma total cholesterol level in guinea pig after 10 days2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1212313Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of imipramine2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID384745Partition coefficient, log P by octanol-water partitioning method2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558833Antimalarial activity against Plasmodium falciparum 106/1 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID781329pKa (acid-base dissociation constant) as determined by other workers2014Pharmaceutical research, Apr, Volume: 31, Issue:4
Comparison of the accuracy of experimental and predicted pKa values of basic and acidic compounds.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID558834Antimalarial activity against Plasmodium falciparum IMT Bres assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID558868Antimalarial activity against Plasmodium falciparum IMT L1 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID558835Antimalarial activity against Plasmodium falciparum IMT Guy assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884872Upregulation of Cpt1c gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID1291842Cytotoxicity against African green monkey BGM cells assessed as cell viability after 24 hrs by neutral red assay2016Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8
New pentasubstituted pyrrole hybrid atorvastatin-quinoline derivatives with antiplasmodial activity.
AID558865Antimalarial activity against Plasmodium falciparum IMT K14 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S mutant gene, Pmdr1 Y184F, S1034C, N1042D, D1246Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanth2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID699536Ratio of Vmax to Km for human liver OATP1B1 expressed in HEK293 Flp-In cells assessed per mg protein2012Journal 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.
AID384751Myotoxicity in guinea pig assessed as drug dose causing >2.5 fold increase in plasma creatine kinase activity relative to control2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1884893In vivo activation of PPARalpha/PGC1alpha pathway in HFD-induced C57BL/6J mouse model of NAFL assessed as effect on PPARdelta expression in liver at 15 mg/kg/day, ip administered from week 7 to week 12 by immunoblotting analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID1369326Inhibition of pig liver microsomal HMG-CoA reductase by colorimetric method2018Journal of medicinal chemistry, 04-26, Volume: 61, Issue:8
Structural Modification of Natural Product Ganomycin I Leading to Discovery of a α-Glucosidase and HMG-CoA Reductase Dual Inhibitor Improving Obesity and Metabolic Dysfunction in Vivo.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID558841Antimalarial activity against Plasmodium falciparum IMT 10500 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
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.
AID678717Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1698007Ratio of drug level in human blood to plasma administered through iv dosing by LC-MS/MS analysis
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1212339Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of rifampin2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID1884891In vivo activation of PPARalpha/PGC1alpha pathway in HFD-induced C57BL/6J mouse model of NAFL assessed as effect on PPARbeta expression in liver at 15 mg/kg/day, ip administered from week 7 to week 12 by immunoblotting analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID558058Antimalarial activity against chloroquine-sensitive Plasmodium falciparum 3D7 assessed as Plasmodium lactate dehydrogenase release after 48 hrs by colorimetry2009Antimicrobial agents and chemotherapy, May, Volume: 53, Issue:5
Statins as potential antimalarial drugs: low relative potency and lack of synergy with conventional antimalarial drugs.
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.
AID385189Myotoxicity in po dosed weanling Sprague-Dawley rat assessed as drug dose causing >2.5 fold increase in plasma creatine kinase activity relative to control2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558862Antimalarial activity against Plasmodium falciparum IMT 10336 harboring Pfcrt Q271E mutant gene and Ppcrt I371R mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884864Upregulation of Medium-chain specific acyl-CoA dehydrogenase gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID558854Antimalarial activity against Plasmodium falciparum HB3 harboring Ppcrt I371R mutant gene and Pfmdr1 Y184F mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID241793Inhibitory concentration against 3-hydroxy-3-methylglutaryl-CoA reductase2005Bioorganic & medicinal chemistry letters, Feb-15, Volume: 15, Issue:4
Three-dimensional quantitative structure (3-D QSAR) activity relationship studies on imidazolyl and N-pyrrolyl heptenoates as 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) inhibitors by comparative molecular similarity indices analysis (CoMSIA).
AID385201Absorption in human gut2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558826Antimalarial activity against Plasmodium falciparum 3D7 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID558828Antimalarial activity against Plasmodium falciparum D6 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID527841Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in HDL level at 10 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID558845Antimalarial activity against Plasmodium falciparum IMT K4 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID527839Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in triglyceride level at 10 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID558842Antimalarial activity against Plasmodium falciparum IMT 16332 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1289612Induction of SREBP2 maturation in human HepG2 cells at 10 uM after overnight incubation by immunoblot analysis2016Journal of medicinal chemistry, Feb-11, Volume: 59, Issue:3
Synthesis and Characterization of Fatty Acid Conjugates of Niacin and Salicylic Acid.
AID699538Ratio of Vmax to Km for human liver OATP2B1 expressed in HEK293 Flp-In cells assessed per mg protein2012Journal 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]
AID699530Activity at human liver OATP1B1 expressed in HEK293 Flp-In cells2012Journal 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.
AID1221857Induction of CYP3A4 mRNA expression in human hepatocytes at 10 uM after 12 to 48 hrs by RT-PCR analysis2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID679464TP_TRANSPORTER: inhibition of Daunorubicin transport in 3T3-G185 cells2001Pharmaceutical research, Jun, Volume: 18, Issue:6
HMG-CoA reductase inhibitors (statins) characterized as direct inhibitors of P-glycoprotein.
AID558844Antimalarial activity against Plasmodium falciparum IMT K2 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID527842Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in HDL to total cholesterol ratio at 10 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID1073308Inhibition of HIV1 integrase/LEDGF-75 (unknown origin) interaction2014Journal of medicinal chemistry, Feb-13, Volume: 57, Issue:3
Inhibiting the HIV integration process: past, present, and the future.
AID384744Partition coefficient, log P by reverse phase HPLC method2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
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]
AID737910Cytotoxicity against mouse MEF cells after 72 hrs by MTT assay2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID1222793Dissociation constant, pKa of the compound2013Drug metabolism and disposition: the biological fate of chemicals, May, Volume: 41, Issue:5
Which metabolites circulate?
AID558855Antimalarial activity against Plasmodium falciparum 106/1 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs 2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID631053Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as increase in serum ratio of serum HDL/total cholesterol level at 10 mg/kg, po administered once daily for 7 days relative to vehicle treated control2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID558863Antimalarial activity against Plasmodium falciparum IMT 10500 harboring Pfcrt Q271E mutant gene and Ppcrt I371R mutant gene and Pfnhe-1 ms4760 microsatellite mutant assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1221851Inhibition of HMGCR activity in human hepatocytes assessed as increase in 7-dehydrocholesterol level per gram of protein by GC-MS analysis (Rvb = 16.3 ug)2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID558853Antimalarial activity against Plasmodium falciparum PA harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by 2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884869Upregulation of Cyp4a14 gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID384742Inhibition of cholesterol synthesis in rat L6 cells assessed as incorporation of [14C]acetate into cholesterol2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1192794Unbound fraction in Sprague-Dawley rat liver at 1 uM measured over 18 hrs by equilibrium dialysis method2015Bioorganic & medicinal chemistry letters, Mar-01, Volume: 25, Issue:5
Transporter-mediated tissue targeting of therapeutic molecules in drug discovery.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID558860Antimalarial activity against Plasmodium falciparum IMT 8425 harboring Ppcrt I371R mutant gene and Pfnhe-1 ms4760 microsatellite mutant assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1593965Inhibition of HMG CoA reductase in human Hep3G cells assessed as increase in LDL receptor expression at 25 uM incubated for 48 hrs by immunofluorescence method2019Bioorganic & medicinal chemistry, 06-01, Volume: 27, Issue:11
Targeted delivery of atorvastatin via asialoglycoprotein receptor (ASGPR).
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1221861Inhibition of HMGCR activity in human hepatocytes assessed as increase in FF-MAS level per gram of protein by GC-MS analysis (Rvb = 0.7 ug)2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID1217727Intrinsic clearance for reactive metabolites formation per mg of protein in human liver microsomes based on [3H]GSH adduct formation rate at 100 uM by [3H]GSH trapping assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID737908Selectivity index, ratio of IC50 for mouse MEF cells to IC50 for human A549 cells2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID558867Antimalarial activity against Plasmodium falciparum IMT K4 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S mutant gene, Pmdr1 S1034C, N1042D mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID699533Activity at human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as rate of compound transport per mg of protein2012Journal 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.
AID678714Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID558838Antimalarial activity against Plasmodium falciparum IMT 8425 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID558829Antimalarial activity against Plasmodium falciparum FCM29 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1698008Hepatic clearance in Wistar Hannover rat at 1 mg/kg, iv
AID1291841Antiplasmodial activity against chloroquine-resistant Plasmodium falciparum W2 infected in human red blood cells after 48 hrs by SYBR test2016Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8
New pentasubstituted pyrrole hybrid atorvastatin-quinoline derivatives with antiplasmodial activity.
AID1698001Lipophilicity, log D of the compound at pH 7.4 by by shake flask method
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]
AID558858Antimalarial activity against Plasmodium falciparum IMT A4 harboring Ppcrt M74I, N75E, K76T, A220H, Q271E, N326S and I356T mutant gene, Pmdr1 Y184F, N1042D, D1246Y mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation cou2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID679345TP_TRANSPORTER: transepithelial transport in L-MDR1 cells2004Pharmaceutical research, Sep, Volume: 21, Issue:9
Interactions of human P-glycoprotein with simvastatin, simvastatin acid, and atorvastatin.
AID570999Antimalarial activity against Plasmodium falciparum infected in mouse assessed as parasitemia at 20 mg/kg, ip, qd administered 4 days post infection for 3 days measured after 6 days (Rvb =8.7+/-1.4 %)2008Antimicrobial agents and chemotherapy, Nov, Volume: 52, Issue:11
Statins alone are ineffective in cerebral malaria but potentiate artesunate.
AID385190Safety index, ratio of ED50 for inhibition of hepatic cholesterol synthesis in Sprague-Dawley rat to drug dose not causing >2.5 fold increase in plasma creatine kinase level in weanling Sprague-Dawley rat2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1212317Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of ammonium chloride2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID631052Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum LDL level at 10 mg/kg, po administered once daily for 7 days relative to vehicle treated control2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID679461TP_TRANSPORTER: inhibition of Rhodamine 123 transport in 3T3-G185 cells2001Pharmaceutical research, Jun, Volume: 18, Issue:6
HMG-CoA reductase inhibitors (statins) characterized as direct inhibitors of P-glycoprotein.
AID1698010Hepatic clearance in human administered through iv dosing
AID737907Selectivity index, ratio of IC50 for human HS68 cells to IC50 for human A549 cells2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID1593962Inhibition of HMG CoA reductase (unknown origin) in pH 4.5 PBS in presence of NADPH incubated for 10 mins2019Bioorganic & medicinal chemistry, 06-01, Volume: 27, Issue:11
Targeted delivery of atorvastatin via asialoglycoprotein receptor (ASGPR).
AID558846Antimalarial activity against Plasmodium falciparum IMT L1 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1217728Intrinsic clearance for reactive metabolites formation per mg of protein based on cytochrome P450 (unknown origin) inactivation rate by TDI assay2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID558848Antimalarial activity against Plasmodium falciparum 3D7 harboring Ppcrt I371R mutant gene and Pfnhe-1 ms4760 microsatellite mutant assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1873192Inhibition of ABCG2 (unknown origin) expressed in human HEK293-A cells membrane vesicles assessed inhibition of ABCG2-mediated urate transport activity by rapid filtration technique2022European journal of medicinal chemistry, Jul-05, Volume: 237Targeting breast cancer resistance protein (BCRP/ABCG2): Functional inhibitors and expression modulators.
AID737917Inhibition of recombinant HDAC1 (unknown origin) after 10 mins by fluorimetric analysis2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID1217709Time dependent inhibition of CYP3A4 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID678959TP_TRANSPORTER: uptake in OATP1B1-expressing HEK293 cells2005Pharmacogenetics and genomics, Jul, Volume: 15, Issue:7
Functional characterization of SLCO1B1 (OATP-C) variants, SLCO1B1*5, SLCO1B1*15 and SLCO1B1*15+C1007G, by using transient expression systems of HeLa and HEK293 cells.
AID384752Safety index, ratio of ED50 for reduction in plasma total cholesterol level to drug dose not causing >2.5 fold increase in plasma creatine kinase in guinea pig2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1217706Time dependent inhibition of CYP2C9 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID558060Antimalarial activity against chloroquine-resistant Plasmodium falciparum E8B assessed as Plasmodium lactate dehydrogenase release after 48 hrs by colorimetry2009Antimicrobial agents and chemotherapy, May, Volume: 53, Issue:5
Statins as potential antimalarial drugs: low relative potency and lack of synergy with conventional antimalarial drugs.
AID1698000Apparent permeability in dog MDCKII-LE cells at pH 7.4
AID1217705Time dependent inhibition of CYP2B6 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1440496Cmax in human at 10 mg, po administered as single dose capsule2017Journal of medicinal chemistry, 03-09, Volume: 60, Issue:5
The Essential Medicinal Chemistry of Curcumin.
AID1192796Ratio of drug uptake in liver to muscle in rat2015Bioorganic & medicinal chemistry letters, Mar-01, Volume: 25, Issue:5
Transporter-mediated tissue targeting of therapeutic molecules in drug discovery.
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.
AID1210300Drug metabolism 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.
AID737918Inhibition of recombinant HMG-CoA reductase (unknown origin) after 10 mins by spectrophotometric analysis2013Journal of medicinal chemistry, May-09, Volume: 56, Issue:9
Design and synthesis of dual-action inhibitors targeting histone deacetylases and 3-hydroxy-3-methylglutaryl coenzyme A reductase for cancer treatment.
AID1884870Upregulation of Cpt1a gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID1698003Fraction unbound in rat plasma
AID558827Antimalarial activity against Plasmodium falciparum W2 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID558869Antimalarial activity against Plasmodium falciparum IMT Vol harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H] hypoxanthine after 48 hrs by scin2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID631049Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum total cholesterol level at 10 mg/kg, po administered once daily for 7 days relative to vehicle treated control2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
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.
AID1235929Inhibition of pig liver microsomes HMG-CoA reductase incubated for 5 mins in using HMG-CoA and NADPH by colorimetric method2015Journal of natural products, Aug-28, Volume: 78, Issue:8
Lanostane Triterpenes from the Tibetan Medicinal Mushroom Ganoderma leucocontextum and Their Inhibitory Effects on HMG-CoA Reductase and α-Glucosidase.
AID577579Inhibition of CYP3A4 in human liver microsome2011Bioorganic & medicinal chemistry letters, Feb-15, Volume: 21, Issue:4
Conformationally constrained farnesoid X receptor (FXR) agonists: heteroaryl replacements of the naphthalene.
AID313914Inhibition of acute cholesterol synthesis in mouse at 1 mg/kg2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID558849Antimalarial activity against Plasmodium falciparum W2 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [[3H]hypoxanthine after 48 hrs by2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884865Upregulation of Acox1 gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID558837Antimalarial activity against Plasmodium falciparum IMT 31 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID558861Antimalarial activity against Plasmodium falciparum IMT 9881 harboring Ppcrt I371R mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1884863Upregulation of long-chain specific acyl-CoA dehydrogenase gene transcriptional level in HFD-induced C57BL/6J mouse model of NAFL at 15 mg/kg/day, ip administered from week 7 to week 12 by qRT-PCR analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID1221847Inhibition of HMGCR activity in human hepatocytes assessed as increase in desmosterol level per gram of protein by GC-MS analysis (Rvb = 5.5 ug)2011Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 39, Issue:1
Inhibition of human sterol Δ7-reductase and other postlanosterol enzymes by LK-980, a novel inhibitor of cholesterol synthesis.
AID678712Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID558857Antimalarial activity against Plasmodium falciparum IMT Guy harboring Ppcrt K76T, A220S, N326D and I371R mutant gene, Pmdr1 T184FN, 1042D and D1246Y, mutant gene and Pfmrp H191Y and S437A mutant gene and Pfnhe-1 ms4760 microsatellite mutant assessed as in2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1218864Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estradiol-17beta-glucuronide substrate2012Drug 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.
AID312172Inhibition of HMG-CoA reductase in Sprague-Dawley rat liver microsomes2008Journal of medicinal chemistry, Jan-10, Volume: 51, Issue:1
Substituted pyrazoles as hepatoselective HMG-CoA reductase inhibitors: discovery of (3R,5R)-7-[2-(4-fluoro-phenyl)-4-isopropyl-5-(4-methyl-benzylcarbamoyl)-2H-pyrazol-3-yl]-3,5-dihydroxyheptanoic acid (PF-3052334) as a candidate for the treatment of hyper
AID1212336Drug uptake in lysosomes of human Fa2N-4 cells assessed as cellular partitioning measured per 10'6 cells at 1 uM after 5 mins by LC-MS analysis in presence of astemizole2013Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 41, Issue:4
Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells).
AID313911Inhibition of cholesterol synthesis in rat hepatocyte2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID1427928Inhibition of HMG-CoA reductase in pig liver microsomes using HMG-CoA as substrate preincubated for 5 mins followed by NADPH addition measured after 15 mins by colorimetric method2017European journal of medicinal chemistry, Feb-15, Volume: 127A novel class of α-glucosidase and HMG-CoA reductase inhibitors from Ganoderma leucocontextum and the anti-diabetic properties of ganomycin I in KK-A
AID313913Selectivity, ratio of IC50 for rat hepatocyte to IC50 for rat L6 myocyte2008Bioorganic & medicinal chemistry letters, Feb-01, Volume: 18, Issue:3
Hepatoselectivity of statins: design and synthesis of 4-sulfamoyl pyrroles as HMG-CoA reductase inhibitors.
AID699535Activity at human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as rate of compound transport per mg of protein2012Journal 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.
AID558866Antimalarial activity against Plasmodium falciparum IMT K2 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S mutant gene, Pmdr1 S1034C, N1042D mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID472694Upregulation of LDL receptor expression in human HepG2 cells at 1 uM in presence of ARH-specific siRNA2010Journal of medicinal chemistry, Apr-22, Volume: 53, Issue:8
A novel class of antihyperlipidemic agents with low density lipoprotein receptor up-regulation via the adaptor protein autosomal recessive hypercholesterolemia.
AID558830Antimalarial activity against Plasmodium falciparum FCR3 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1593969Drug level assessed as esterase (unknown origin)-mediated compound release in pH 7.4 PBS buffer incubated for 3 to 24 hrs by mass spectrometry2019Bioorganic & medicinal chemistry, 06-01, Volume: 27, Issue:11
Targeted delivery of atorvastatin via asialoglycoprotein receptor (ASGPR).
AID384741Inhibition of cholesterol synthesis in rat hepatocytes assessed as incorporation of [14C]acetate into cholesterol2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1649241Inhibition of cholesterol biosynthesis in human HuH7 cells preincubated for 14 hrs and followed by addition of 14C-acetate and measured after 2 hrs by TL method2020Journal of medicinal chemistry, 05-14, Volume: 63, Issue:9
Degradation versus Inhibition: Development of Proteolysis-Targeting Chimeras for Overcoming Statin-Induced Compensatory Upregulation of 3-Hydroxy-3-methylglutaryl Coenzyme A Reductase.
AID1217710Covalent binding in human liver microsomes measured per mg of protein using radiolabelled compound at 10 uM after 1 hr incubation by liquid scintillation counting2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID558864Antimalarial activity against Plasmodium falciparum IMT 16332 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E mutant gene, Pmdr1 N86Y mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID385187Hepatotoxicity in guinea pig assessed as effect on liver histology at 150 mg/kg coadministered with mevalonate after 10 days2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID558847Antimalarial activity against Plasmodium falciparum IMT Vol assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID1291843Selectivity index, ratio of MLD50 for African green monkey BGM cells to IC50 for chloroquine-resistant Plasmodium falciparum W2 infected in human red blood cells2016Bioorganic & medicinal chemistry letters, Apr-15, Volume: 26, Issue:8
New pentasubstituted pyrrole hybrid atorvastatin-quinoline derivatives with antiplasmodial activity.
AID385185Hepatotoxicity in guinea pig assessed as aspartate aminotransferase level at 150 mg/kg coadministered with mevalonate after 10 days2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1698005Ratio of drug level in Wistar Hannover rat blood to plasma administered through iv dosing by LC-MS/MS analysis
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]
AID699534Activity at human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as rate of compound transport per mg of protein2012Journal 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.
AID558831Antimalarial activity against Plasmodium falciparum PA assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID680263TP_TRANSPORTER: inhibition of Taurocholate uptake (Taurocholate: 0.5 uM, Atorvastatin: 50 uM) in Oatp1-expressing 293c18 cells1999The Journal of biological chemistry, Dec-24, Volume: 274, Issue:52
A novel human hepatic organic anion transporting polypeptide (OATP2). Identification of a liver-specific human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor transporters.
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.
AID781330pKa (acid-base dissociation constant) as determined by potentiometric titration2014Pharmaceutical research, Apr, Volume: 31, Issue:4
Comparison of the accuracy of experimental and predicted pKa values of basic and acidic compounds.
AID558836Antimalarial activity against Plasmodium falciparum IMT A4 assessed as incorporation of [3H]hypoxanthine after 48 hrs by scintillation counter2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID496781Induction of cell differentiation in mouse C2C12 cells assessed as myosin heavy chain expression at 1 uM2010Nature chemical biology, Mar, Volume: 6, Issue:3
Carbon metabolism-mediated myogenic differentiation.
AID1761630Hypolipidemic activity in human HepG2 cells assessed as reduction in FFA-induced intracellular fat deposition at 10 uM after 24 hrs by Oil Red O staining based assay2021Journal of natural products, 02-26, Volume: 84, Issue:2
Natural Piperine Improves Lipid Metabolic Profile of High-Fat Diet-Fed Mice by Upregulating SR-B1 and ABCG8 Transporters.
AID558851Antimalarial activity against Plasmodium falciparum FCM29 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs 2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
AID406854Plasma concentration at steady state in human at 2.5 to 80 mg2007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
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.
AID678713Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1217729Intrinsic clearance for reactive metabolites formation assessed as summation of [3H]GSH adduct formation rate-based reactive metabolites formation and cytochrome P450 (unknown origin) inactivation rate-based reactive metabolites formation2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID384743Selectivity index, ratio of IC50 for cholesterol synthesis in rat L6 cells to IC50 for cholesterol synthesis in rat hepatocytes2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID558852Antimalarial activity against Plasmodium falciparum FCR3 harboring Ppcrt M74I, N75E, K76T, A220S, Q271E, N326S and I356T mutant gene, Pmdr1 N86Y mutant gene and Pfmrp H191Y and S437A mutant gene assessed as incorporation of [3H]hypoxanthine after 48 hrs b2009Antimicrobial agents and chemotherapy, Jun, Volume: 53, Issue:6
Atorvastatin is a promising partner for antimalarial drugs in treatment of Plasmodium falciparum malaria.
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]
AID1217704Time dependent inhibition of CYP1A2 (unknown origin) at 100 uM by LC/MS system2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Combination of GSH trapping and time-dependent inhibition assays as a predictive method of drugs generating highly reactive metabolites.
AID1884890In vivo activation of PPARalpha/PGC1alpha pathway in HFD-induced C57BL/6J mouse model of NAFL assessed as effect on PPARalpha expression in liver at 15 mg/kg/day, ip administered from week 7 to week 12 by immunoblotting analysis2022Journal of natural products, 07-22, Volume: 85, Issue:7
Xyloketal B Reverses Nutritional Hepatic Steatosis, Steatohepatitis, and Liver Fibrosis through Activation of the PPARα/PGC1α Signaling Pathway.
AID631048Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum triglyceride level at 10 mg/kg, po administered once daily for 7 days relative to vehicle treated control2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1798163HMG-CoA Reductase Enzyme Assay and Inhibition of Cellular Cholesterol Synthesis Assay from Article 10.1021/jm800001n: \\(3R,5S,E)-7-(4-(4-Fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1H-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic Aci2008Journal of medicinal chemistry, May-08, Volume: 51, Issue:9
(3R,5S,E)-7-(4-(4-fluorophenyl)-6-isopropyl-2-(methyl(1-methyl-1h-1,2,4-triazol-5-yl)amino)pyrimidin-5-yl)-3,5-dihydroxyhept-6-enoic acid (BMS-644950): a rationally designed orally efficacious 3-hydroxy-3-methylglutaryl coenzyme-a reductase inhibitor with
AID1346822Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)2001Science (New York, N.Y.), May-11, Volume: 292, Issue:5519
Structural mechanism for statin inhibition of HMG-CoA reductase.
AID1346822Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)2005Biochemistry, Sep-06, Volume: 44, Issue:35
Binding thermodynamics of statins to HMG-CoA reductase.
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)2001The American journal of cardiology, Mar-08, Volume: 87, Issue:5A
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (7,093)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's177 (2.50)18.2507
2000's2773 (39.09)29.6817
2010's3299 (46.51)24.3611
2020's844 (11.90)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 153.49

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index153.49 (24.57)
Research Supply Index9.16 (2.92)
Research Growth Index5.53 (4.65)
Search Engine Demand Index293.41 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (153.49)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials2,058 (27.74%)5.53%
Reviews467 (6.29%)6.00%
Case Studies390 (5.26%)4.05%
Observational75 (1.01%)0.25%
Other4,430 (59.70%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (874)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Effect of a Fibrate (Fenofibrate) and a Statin (Atorvastatin) and on Endothelial Dysfunction in Diabetes Mellitus and the Metabolic Syndrome [NCT00491400]28 participants (Actual)Interventional2005-09-30Terminated(stopped due to Insufficient enrollment)
Efficacy and Safety of Co-administration of Omacor Plus Atorvastatin Compared With Atorvastatin Monotherapy in Patients With Type Ⅱb Dyslipidemia: a Multicenter, Double-blind, Randomized, Active-controlled, Parallel, Phase Ⅲ Study [NCT02035215]Phase 380 participants (Anticipated)Interventional2014-01-31Recruiting
A Study of STAtins for Reducing Events in the Elderly (STAREE) [NCT02099123]Phase 49,971 participants (Actual)Interventional2015-07-31Active, not recruiting
Systemic Immunomodulatory Effects and Pharmacogenetics of Atorvastatin in Early Atherosclerosis [NCT00361283]Phase 4108 participants (Actual)Interventional2004-06-30Completed
The Multicenter Atorvastatin Plaque Stabilization (MAPS) Study [NCT01053065]60 participants (Actual)InterventionalCompleted
Atorvastatin Pre-Treatment Influences the Risk of Percutaneous Coronary Intervention Study 2 [NCT01058057]Phase 3200 participants (Anticipated)Interventional2008-02-29Recruiting
A Single- and Multiple-Ascending Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of LY3502970 in Healthy Subjects [NCT03929744]Phase 1133 participants (Actual)Interventional2019-06-12Completed
An 8-Week, Double-Blind, Randomized, Placebo-Controlled, Dose-Ranging Study of the Efficacy and Safety of Gemcabene Administered as Monotherapy or in Combination With Atorvastatin in the Treatment of Hypercholesterolemic Patients [NCT02591836]Phase 2277 participants (Actual)Interventional2003-01-31Completed
Assessment of the Efficacy and Tolerability of Two Formulations of Atorvastatin In Korean Adult With Hypercholesterolemia : A Multicenter, Prospective, Open-Label, Randomized, Trial [NCT01285544]Phase 4289 participants (Actual)Interventional2008-09-30Completed
A Single Center, Open Label, Randomized Study to Compare the Effect of Vytorin (Simvastatin/Ezetimibe) 10/20mg Versus Atorvastatin 20mg on ApoB/ApoA1 Ratio in Subjects With Diabetes [NCT01185236]Phase 4132 participants (Anticipated)Interventional2010-09-30Not yet recruiting
A Prospective, Double-blinded, Randomised Study to Evaluate the Effects of Different Doses of Statin Treatment on Plaque Volume and Composition in Coronary Disease Determined by Virtual Histology Using Intravascular Ultrasound [NCT01200056]Phase 440 participants (Actual)Interventional2007-08-31Completed
A Randomised Controlled Trial of Atorvastatin as an Anti-Inflammatory Agent in Non-Cystic Fibrosis Bronchiectasis in Patients With Pseudomonas Aeruginosa [NCT01299194]Phase 432 participants (Actual)Interventional2010-11-30Completed
A Multicenter, Randomized, Open-label Study to Evaluate the Lipid-Altering Efficacy and Safety of Ezetimibe (+) Simvastatin Versus Atorvastatin in Patients With Primary Hypercholesterolemia [NCT00166504]Phase 4203 participants (Actual)Interventional2005-10-31Completed
"SWiss Atorvastatin and Interferon-Beta 1b Trial In Multiple Sclerosis - Follow up Study (SWABIMS Follow Up-study)" [NCT01111656]Phase 228 participants (Actual)Interventional2007-03-31Completed
Statin Therapeutic Interchange by Pharmacist Collaborative Practice Process [NCT01222182]260 participants (Actual)Observational2009-09-30Completed
The Effect of Atorvastatin on Androgen Synthesis, Glucose Metabolism and Inflammation in Women With Polycystic Ovary Syndrome (PCOS). A Placebo Controlled Trial [NCT01072097]30 participants (Anticipated)Interventional2006-09-30Completed
A Randomized, Double-Blind, Placebo-Controlled Study Followed by an Open Label Treatment Period to Evaluate the Efficacy and Safety of Alirocumab in Children and Adolescents With Heterozygous Familial Hypercholesterolemia [NCT03510884]Phase 3153 participants (Actual)Interventional2018-05-31Completed
Pharmacodynamic Effects of Atorvastatin vs. Rosuvastatin on pLatelet Reactivity in Stable Patients With Coronary Artery Disease Treated With Dual Antiplatelet Therapy [NCT01567774]Phase 4100 participants (Anticipated)Interventional2012-04-30Recruiting
Study of Potential for Drug Interactions Mediated by CYP3A4 Inhibition With Aramchol in Healthy Volunteers [NCT03760848]Phase 115 participants (Actual)Interventional2018-11-12Completed
Phase II, Dose-ranging Study to Evaluate the Efficacy Dose Response and Pharmacokinetics of Intravenous Atorvastatin in Hypercholesterolemic Patients Previously Controlled With Oral Atorvastatin [NCT03611010]Phase 240 participants (Actual)Interventional2018-08-07Completed
A Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study to Evaluate the Efficacy and Safety of Triplet Therapy With Bempedoic Acid (ETC 1002) 180 mg, Ezetimibe 10 mg, and Atorvastatin 20 mg in Patients With Elevated LDL C [NCT03051100]Phase 263 participants (Actual)Interventional2017-01-19Completed
Estudio clínico Fase III Para Evaluar la Eficacia terapéutica en Pacientes Mexicanos Con Dislipidemia Mediante el Uso vía Oral de L-Carnitina + Atorvastatina Comparado Con Atorvastatina [NCT03696940]Phase 3120 participants (Actual)Interventional2018-05-28Active, not recruiting
A Double-blind, Randomized, Multi-center Phase 3 Clinical Trial to Evaluate the Safety and Efficacy of CJ-30061 Compared With Amlodipine/Valsartan Combination Therapy and Valsartan/Atorvastatin Combination Therapy in Hypertensive Patients With Hyperlipide [NCT03639480]Phase 3180 participants (Anticipated)Interventional2017-10-13Enrolling by invitation
A Multicenter, Randomized, Open-label, Parallel-group Usability Study of the Commercial 1 mL Alirocumab Auto-injector Device (AI) and the New 2 mL Auto-injector Device (SYDNEY) in High or Very High Cardiovascular Risk Patients With Hypercholesterolemia No [NCT03415178]Phase 369 participants (Actual)Interventional2018-03-29Completed
An Open-label, Randomized, Single-dose, 3-period Replicated Crossover Study to Compare the Pharmacokinetics and Safety Following Administration of CJ-30061 Alone and Co-administration of Amlodipine/Valsartan and Atorvastatin in Healthy Adult Volunteers [NCT03657472]Phase 142 participants (Actual)Interventional2016-09-19Completed
Double Blind, Prospective Randomized, Crossover Study of Patients With Muscle Complaints on Statin Therapy [NCT00127335]Phase 40 participants (Actual)Interventional2005-08-31Withdrawn(stopped due to Lack of funding)
ASP1585 Pharmacokinetic Interaction Study - Pharmacokinetic Interaction With Atorvastatin - [NCT01115985]Phase 124 participants (Actual)Interventional2010-03-31Completed
A Multicenter, Eight Weeks Treatment, Single Step Titration, Open Label Study Assessing the Percentage of Korean Diabetic Dyslipidemic Patients Achieving LDL Cholesterol Target With Atorvastatin Starting Dose 10mg, 20mg, 40mg [NCT01239849]Phase 4500 participants (Anticipated)Interventional2009-02-28Recruiting
Atorvastatin Reduces Sympathetic Activity in Patients With Chronic Kidney Disease [NCT01257009]Phase 410 participants Interventional2009-08-31Completed
A Phase 1 Feasibility Study of Cholesterol Metabolism Reprogramming (Evolocumab, Atorvastatin and Ezetimibe) in Combination With the Standard of Care in Patients With Advanced or Metastatic Pancreatic Adenocarcinoma [NCT04862260]Early Phase 112 participants (Anticipated)Interventional2021-10-04Recruiting
A Single-centre Open Label Study to Investigate the Effect of Repeat Doses of SB-649868 on the Pharmacokinetics of Simvastatin and Atorvastatin in Healthy Male Volunteers. [NCT01299597]Phase 130 participants (Actual)Interventional2010-01-18Completed
Clinical Study on Hyperlipidemia and Comparative Evaluation of Efficacy of a Compound Unani Formulation (Safoof e Muhazzil) and Compressed Tablet of Safoof e Muhazzil in Its Management [NCT01332747]Phase 2128 participants (Actual)Interventional2010-05-31Completed
Effects of Long-term Vitamin C+E and Statin Therapy on Vasospasm Improvement and Regression of Atheroma in Patients With Variant Angina [NCT03228238]Phase 4300 participants (Anticipated)Interventional2014-09-01Recruiting
A Phase 1, Open-Label, Drug-Drug Interaction, Study to Evaluate the Effect of ASC42 on the Pharmacokinetics of Atorvastatin Tablets in Healthy Volunteers (HVs) [NCT05464628]Phase 112 participants (Anticipated)Interventional2022-08-08Recruiting
A Randomized, Open-label, Multiple Dosing, 3-way Crossover Study to Evaluate the Drug-drug Interaction Between Atorvastatin and Fenofibric Acid in Healthy Male Volunteers [NCT02422030]Phase 130 participants (Actual)Interventional2015-03-17Completed
Statin Therapy Operates to Prevent (STOP) Heart Disease in Breast Cancer Survivors Trial [NCT02674204]Phase 22 participants (Actual)Interventional2016-05-05Terminated(stopped due to Closed due to low accrual)
A Phase IV, 6-week, Randomised, Double-blind, Multicentre, Parallel Group, Comparative Study to Evaluate the Efficacy of Rosuvastatin 5mg and Atorvastatin 10mg in UK Asian Subjects With Primary Hypercholesterolaemia [NCT00427960]Phase 455 participants (Actual)Interventional2006-12-31Terminated(stopped due to Due to inadequate recruitment)
The Role of Statins in the Prevention of Contrast-induced Acute Kidney Injury in Patients With Cardiovascular Diseases [NCT04666389]150 participants (Actual)Interventional2020-10-15Completed
The Safety and Efficacy of Intensive Statin Therapy in PCI Patient With Acute Coronary Syndrome [NCT01372839]Phase 4300 participants (Anticipated)Interventional2010-07-31Recruiting
A Randomized Double Blind, Placebo-controlled Study Determining the Role of Adjuvant Statin Therapy in Patients Who Underwent Radical Prostatectomy for Locally Advanced Prostate Cancer [NCT01759836]Phase 2364 participants (Actual)Interventional2012-10-31Completed
A Single-center Prospective Randomized Study of Atorvastatin in the Treatment of Newly Diagnosed Primary Immune Thrombocytopenia (ITP) [NCT03692754]Phase 2/Phase 330 participants (Anticipated)Interventional2021-11-01Not yet recruiting
Could Early Atorvastatin Offer Anti Inflammatory Effects Upon Brain in Traumatic Head Injury? a Randomized Double-blind Clinical Trial [NCT04718155]30 participants (Actual)Interventional2021-03-01Completed
A Randomized, Open-label, Blinded Intravascular Ultrasound Analysis, Parallel Group, Multicenter Study to Evaluate the Effect of Praluent® (Alirocumab) on Coronary Atheroma Volume in Japanese Patients Hospitalized for Acute Coronary Syndrome With Hypercho [NCT02984982]Phase 4206 participants (Actual)Interventional2016-11-15Completed
The Clinical Effect of Intensive Statin Therapy in STEMI(ST-elevated Myocardial Infarction) Patients Before Emergency PCI(Percutaneous Coronary Intervention) [NCT01334671]Phase 3150 participants (Anticipated)Interventional2011-02-28Recruiting
DescripTion of the Effectiveness, Safety, Tolerability and Adherence to Amlodipine/atoRvastatin/Perindopril sinGle Pill Combination trEatmenT in Patients With Arterial Hypertension and Dyslipidemia in the Daily Clinical Practice. (TARGET) [NCT05764317]400 participants (Anticipated)Observational2023-04-30Not yet recruiting
COMPARATIVE EVALUATION OF CLINICAL EFFICACY OF SUBGINGIVALLY DELIVERED 1.2% ATORVASTATIN AND 1.2% SIMVASTATIN IN TREATMENT OF CHRONIC PERIODONTITIS: A RANDOMIZED CONTROLLED TRIAL [NCT02060032]Phase 2/Phase 396 participants (Actual)Interventional2013-02-28Completed
A Randomized, Double-Blind, Active-Controlled, Multicenter, Crossover Study to Evaluate the Efficacy and Safety of Ezetimibe/Atorvastatin 10 mg/20 mg Fixed-Dose Combination Tablet Compared to Co-administration of Marketed Ezetimibe 10 mg and Atorvastatin [NCT01370590]Phase 3406 participants (Actual)Interventional2011-09-30Completed
Atorvastatin and Prevention of Contrast Induced Nephropathy Following Coronary Angiography [NCT02113540]Phase 30 participants Interventional2012-01-31Recruiting
An International, Investigator Initiated and Conducted, Pragmatic Clinical Trial to Determine Whether 40mg Atorvastatin Daily Can Improve Neurocognitive Function in Adults With Long COVID Neurological Symptoms [NCT04904536]Phase 3400 participants (Anticipated)Interventional2022-03-10Recruiting
Ezetimibe Phase IV Clinical Study in Patients With Hypercholesterolemia [NCT00871351]Phase 4125 participants (Actual)Interventional2009-02-01Completed
Evaluate The Lipid-Lowering Efficacy and Safety of Vytorin in Comparison With Atorvastatin in Hypercholesterolaemic Patients With Coronary Artery Disease [NCT00442897]Phase 4229 participants (Actual)Interventional2006-09-30Completed
A Phase I, Single-center, Drug Interaction Study Between Simvastatin, Atorvastatin, Rosuvastatin, and GSK2248761 in Healthy Subjects. [NCT01138072]Phase 114 participants (Actual)Interventional2010-06-30Completed
[NCT02098460]Phase 4250 participants (Anticipated)Interventional2013-10-31Recruiting
[NCT02119520]Phase 296 participants (Actual)Interventional2013-02-28Completed
Atorvastatin Action on Oxidative Stress and Inflammation in Type II Diabetes: The HDL Particle Protection Study [NCT02125682]Phase 416 participants (Actual)Interventional2012-01-31Completed
the Impact of Statin on Quality of Life in Cirrhotic Patients [NCT05563389]Phase 2/Phase 3100 participants (Anticipated)Interventional2022-06-15Recruiting
The Potential Role of Allopurinol Versus Atorvastatin to Prevent Complications of Liver Cirrhosis: A Quadruple Blind Clinical Study [NCT05511766]Phase 2/Phase 3150 participants (Anticipated)Interventional2022-11-15Recruiting
A Randomized, Double-Blind, Multiple-Ascending Dose, Placebo-Controlled Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of LY3549492 in Patients With Type 2 Diabetes Mellitus [NCT05327595]Phase 196 participants (Anticipated)Interventional2022-05-09Recruiting
PRagmatic EValuation of evENTs And Benefits of Lipid-lowering in oldEr Adults (PREVENTABLE) [NCT04262206]Phase 420,000 participants (Anticipated)Interventional2020-09-01Recruiting
The Effects of Human Umbilical Cord Mesenchymal Stem Cell Therapy on Neurological Function for Cerebral Infarction Patients in Convalescent Period. [NCT03176498]Phase 1/Phase 240 participants (Anticipated)Interventional2023-12-31Suspended(stopped due to Others)
A Phase II, Open-labeled, Ophthalmological External Investigator-blinded, Single-center, Randomized, Superiority, Non Profit, Pilot Clinical Trial to Evaluate the Effects of Atorvastatin on Graves' Orbitopathy (GO) in Hypercholesterolemic Patients With Mo [NCT03110848]Phase 288 participants (Actual)Interventional2020-06-01Completed
The Impact of Nurse-led Programme With and Without Carotid Ultrasound on Addressing Cardiovascular Risk in Patients With Arthritis: a Prospective, Multicentre, Randomised, Controlled Trial [NCT03625089]0 participants (Actual)Interventional2018-09-01Withdrawn(stopped due to Limited funding support)
Pharmacodynamic Comparison of Rosuvastatin Versus Atorvastatin on Platelet Reactivity in Patients With Coronary Artery Disease on Dual Antiplatelet Therapy With New P2Y12 Inhibitors [NCT02030054]Phase 4150 participants (Anticipated)Interventional2015-01-31Not yet recruiting
Phase 4 of Atorvastatin for Preventing Occlusion and Restenosis After Intracranial Artery Stenting [NCT01255852]Phase 4100 participants (Actual)Interventional2011-01-31Completed
MUscle Side-Effects of Atorvastatin in Coronary Patients (MUSE) -a Randomized Controlled Trial [NCT03874156]Phase 477 participants (Actual)Interventional2019-03-05Completed
Comparison of Carvedilol and Atorvastatin for Prevention of Contrast-Induced Nephropathy After Cardiac Catheterization [NCT03867994]Phase 2144 participants (Actual)Interventional2016-02-01Completed
Full-dose Atorvastatin Versus Conventional Medical Therapy After Non-ST-elevation Acute Myocardial Infarction in Patients With Advanced Non-revascularisable Coronary Artery Disease [NCT01187992]Phase 3290 participants (Actual)Interventional2003-09-30Terminated(stopped due to Interim analysis showed significant effect in favour of full-dose atorvastatin.)
Cross-over Analysis of the Control of Coronary Risk Factors and Level of Platelet Inhibition With a Polypill [NCT05030818]Phase 488 participants (Anticipated)Interventional2022-10-14Recruiting
Assessment of Immediate Postoperative Delirium (IPD) in Adult Patients: Incidence, Implication of Type of Anesthesia and Identification of Other Etiological Factors [NCT03967496]402 participants (Actual)Observational [Patient Registry]2019-01-01Completed
A Randomized, Open-label, Cross-over, Multiple Dosing Study to Evaluate Drug-drug Interaction Between Teneligliptin and Atorvastatin in Healthy Male Adults [NCT03769870]Phase 130 participants (Actual)Interventional2019-01-11Completed
A Multi-center, Randomized, Open-labeled Clinical Trial to Evaluate Efficacy and Safety of Lipinon® 20mg Versus Lipitor® 20mg in Korean Patients With Hypercholesterolemia [NCT01081548]Phase 417 participants (Actual)Interventional2008-08-31Completed
Early Alirocumab to Reduce LDL-C in Myocardial Infarction [NCT03750760]Phase 40 participants (Actual)Interventional2020-01-31Withdrawn(stopped due to Changes in funding decision)
Comparative Evaluation Of 1.2% Atorvastatin and 1.2% Simvastatin Gel Local Drug Delivery And Redelivery In Chronic Periodontitis Subjects With Diabetes Mellitus: A Randomized Controlled Clinical Trial. [NCT03745300]Phase 2/Phase 3120 participants (Actual)Interventional2017-03-03Completed
A Randomized, Double-Blind, Placebo-Controlled, Multi-Center Study to Evaluate the Efficacy and Safety of Atorvastatin in Patients With Clinically Isolated Syndrome and High Risk of Conversion to Multiple Sclerosis (ITN020AI) [NCT00094172]Phase 282 participants (Actual)Interventional2005-05-31Completed
A Cluster Randomized Trial On Cardiovascular Risk Factor Management: Caduet Versus Usual Care In Subjects With Hypertension And Additional Cardiovascular Risk Factors In Clinical Practice [NCT00407537]Phase 41,531 participants (Actual)Interventional2007-03-31Completed
Same Lipid Lowering by Atorvastatin Versus Atorvastatin Plus Ezetimibe on Coronary Plaque Progression [NCT01086020]Phase 4400 participants (Anticipated)Interventional2010-01-31Recruiting
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
High Loading ROsuvastatin Pretreatment in Patients Undergoing Elective PCI to Reduce the Incidence of MyocArdial Periprocedural Necrosis : Comparison With Atorvastatin High Dose Reloading. [NCT01228227]Phase 3310 participants (Anticipated)Interventional2010-10-31Completed
A Randomized, Double-blind, Multicenter, Phase III Study to Evaluate the Efficacy and Safety of Combination Treatment of Fimasartan/Atorvastatin in Patients With Essential Hypertension and Dyslipidemia [NCT03338426]Phase 3133 participants (Actual)Interventional2018-01-15Completed
Protective Effect of Statin on Arrhythmia and Heart Rate Variability in Healthy People With 48 Hours of Sleep Deprivation [NCT02496962]72 participants (Anticipated)Interventional2015-07-31Recruiting
FRANCIS-ACS Trial: A Study of the Safety and Efficacy of A 002 in Subjects With Acute Coronary Syndromes [NCT00743925]Phase 2625 participants (Actual)Interventional2008-07-31Completed
Impact of Lipophilic Versus Hydrophilic Statin Administration on The Clinical Outcome and Cardiac Markers of Patients With Heart Failure [NCT03255044]Phase 485 participants (Actual)Interventional2017-06-15Completed
Intermediate-dose Versus Standard Prophylactic Anticoagulation In cRitically-ill pATIents With COVID-19: An opeN Label Randomized Controlled Trial---A Randomized Trial of Atorvastatin vs. Placebo In Critically-ill Patients With COVID-19 [NCT04486508]Phase 3600 participants (Actual)Interventional2020-07-30Completed
The Evaluation of Vitiligous Lesions Repigmentation After the Administration of Atorvastatin Calcium Salt and Simvastatin-acid Sodium Salt in Patients With Active Vitiligo (EVRAAS) [NCT03247400]Phase 1/Phase 224 participants (Actual)Interventional2016-12-01Completed
Open-Label Pharmacokinetics Study to Evaluate Drug-Drug Interactions and Safety of ELPIDA® in Co-Administration With Other Drugs in Healthy Volunteers [NCT03709355]Phase 156 participants (Actual)Interventional2018-11-14Completed
The Safety and Efficacy Study of High Dose Atorvastatin After Thrombolytic Treatment in Acute Ischemic Stroke [NCT02452502]254 participants (Actual)Interventional2015-09-02Completed
A Multicenter, Randomized, Double-blind, Active-controlled, Parallel Group, Factorial Design, Phase III Clinical Trial To Evaluate the Efficacy and Safety of Atorvastatin+Ezetimibe Combination Therapy and Atorvastatin Monotherapy in Patients With Primary [NCT02451098]Phase 3385 participants (Actual)Interventional2015-03-31Completed
A Double-Blind, Randomized Study to Evaluate the Efficacy and Safety of Lapaquistat Acetate 50 mg or Placebo When Co-administered With Statins in Subjects With Hypercholesterolemia, With an Optional Open-Label Extension [NCT00532311]Phase 3411 participants (Actual)Interventional2007-07-31Terminated(stopped due to Overall profile of the compound does not offer significant clinical advantage to patients over currently available lipid lowering agents)
Phase 3, Multi-Center, Double-Blind, Randomized, Crossover Study Of The Efficacy, Safety, And Tolerability Of Fixed Combination Torcetrapib (Cp-529,414)/Atorvastatin, Compared With Atorvastatin Therapy Alone, And Fenofibrate Alone, In Subjects With Fredri [NCT00145431]Phase 341 participants (Actual)Interventional2005-03-31Terminated
Combination Therapies to Reduce the Nasopharyngeal Carriage of SARS-CoV-2 and Improve the Outcome of COVID-19 Infection in Ivory Coast (INTENSE-COV): a Phase IIb Randomized Clinical Trial [NCT04466241]Phase 2/Phase 3294 participants (Anticipated)Interventional2020-11-27Recruiting
Atorvastatin in Active Vitiligo: a Bicentric Prospective Randomized Trial [NCT02432534]Phase 228 participants (Actual)Interventional2015-05-31Completed
High-intensity Atorvastatin for Arteriovenous Fistula Failure (HAFF): A Feasibility Pilot Study [NCT03188978]Phase 1/Phase 20 participants (Actual)Interventional2018-11-01Withdrawn(stopped due to Unable to recruit)
Open Label, Randomized, Two-treatment, Two-period, Two-sequence, Oral Bioequivalence Study of Amlodipine Besylate/Atorvastatin Calcium Tablets 10mg/80mg Under Fed Condition [NCT02292069]Phase 190 participants (Actual)Interventional2011-09-30Completed
A Randomized, Open-label, Six-sequence, Three-period, Multiple Dosing Study to Evaluate the Pharmacokinetic Interaction Between Fimasartan and Atorvastatin in Healthy Male Volunteers [NCT02397590]Phase 136 participants (Actual)Interventional2015-03-31Completed
Prediction and Prevention of Asymptomatic Cardiovascular Insult in Type 1 Diabetic Children: Comparative Effectiveness of Cardio-protective Drugs [NCT03660293]150 participants (Actual)Interventional2017-04-01Completed
Anti-inflammatory Effect of Atorvastatin on Graft Donor Kidney Transplantation in Vivo [NCT02355704]Phase 348 participants (Actual)Interventional2012-01-31Completed
A Multi-country, Multicenter, Single-arm, Open-label Study to Document the Safety, Tolerability and Effect of Alirocumab on Atherogenic Lipoproteins in High Cardio-vascular Risk Patients With Severe Hypercholesterolemia Not Adequately Controlled With Conv [NCT02476006]Phase 3998 participants (Actual)Interventional2015-06-23Completed
A Randomized, Double-Blind, Active-Controlled Study of Patients With Cardiovascular Disease and Diabetes Mellitus Not Adequately Controlled With Simvastatin or Atorvastatin: Comparison of Switching to Combination Tablet Ezetimibe/Simvastatin Versus Switch [NCT00862251]Phase 3808 participants (Actual)Interventional2009-04-30Completed
A Multicenter, Randomized, Double-Blind, Parallel Arm, 6-Week Study to Evaluate the Efficacy and Safety of Ezetimibe/Simvastatin Versus Atorvastatin in Patients With Metabolic Syndrome and Hypercholesterolemia at High Risk for Coronary Heart Disease [NCT00409773]Phase 31,143 participants (Actual)Interventional2007-01-31Completed
Lipid-lowering Therapy Individualization [NCT03604471]Phase 475 participants (Actual)Interventional2017-08-08Completed
Comparison of Effects of Atorvastatin Versus Rosuvastatin Treatment on Cardiac Function and Inflammation in Patients With Chronic Heart Failure With Reduced Ejection Fraction: A Randomised, Double Blind Clinical Study [NCT05072054]Phase 480 participants (Anticipated)Interventional2019-10-16Recruiting
Effects of Early Atorvastatin Treatment During the Acute Phase of Stroke on Immunoinflammatory Markers and Outcome in Patients With Acute Ischemic Stroke Classified as LAAS According TOAST Classification [NCT02225834]Phase 450 participants (Actual)Interventional2011-11-30Completed
Atorvastatin in Hospitalized COVID-19 Patients: A Randomized, Double-blinded, Placebo-Controlled, Clinical Trial [NCT04952350]Phase 3220 participants (Actual)Interventional2021-08-14Active, not recruiting
Phase I/II Safety and Efficacy Investigation of Atorvastatin for Treatment of PI-Associated Increased LDL Cholesterol in HIV-Infected Children and Adolescents [NCT00663234]Phase 1/Phase 228 participants (Actual)Interventional2009-08-31Terminated(stopped due to The study was prematurely discontinued due to administrative reasons.)
A Non Randomised, Non Blinded Real World Trial of the Safety, Tolerability and Effectiveness of Metabolic Medicines for the Treatment of Cancer Compared Against Matched Controls [NCT02201381]Phase 30 participants (Actual)Interventional2022-05-23Withdrawn(stopped due to Prospective recruitment not possible)
A 12-Week, Randomized, Semi Double-Blinded Study Evaluating the Effects of Daily Oral High-Dose Atorvastatin or BMS-582949 on Atherosclerotic Plaque Inflammation as Determined by FDG-PET in High Risk Atherosclerotic Patients [NCT00570752]Phase 272 participants (Actual)Interventional2008-12-31Completed
Evaluating the Effect of High Dose Atorvastatin (80 mg/d) Comparing With Placebo in Preventing Contrast-induced Nephropathy in Patients Undergoing Computed Tomography Coronary Angiography [NCT02114346]Phase 2/Phase 3250 participants (Actual)Interventional2013-07-31Completed
A Randomised, Double-blind, Placebo-controlled Trial on the Efficacy of Atorvastatin in Chronic Subdural Haematoma (The REACH Study) [NCT03956368]Phase 3690 participants (Anticipated)Interventional2020-01-09Recruiting
Phase 3 Multi Center, Double Blind, Randomized, Parallel Group Evaluation Of The Fixed Combination Torcetrapib/Atorvastatin, Administered Orally, Once Daily (Qd), Compared With Atorvastatin Alone, On The Occurrence Of Major Cardiovascular Events In Subjec [NCT00134264]Phase 315,067 participants (Actual)Interventional2004-07-31Terminated
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
A Phase III Efficacy And Safety Study of Ezetimibe (SCH58235) 10 mg in Addition to Atorvastatin or Simvastatin in the Therapy of Homozygous Familial Hypercholesterolemia [NCT03884452]Phase 350 participants (Actual)Interventional2000-05-03Completed
Therapeutic Metabolic Intervention in Patients With Spastic Paraplegia SPG5 [NCT02314208]Phase 212 participants (Actual)Interventional2015-01-31Completed
[NCT02155530]30 participants (Actual)Interventional2014-06-30Completed
Effects and Underlying Mechanism of Lipid Lowering Intervention on Vascular Protection in Hypertensive Patients (EMINENT Study) [NCT02254824]Phase 4300 participants (Anticipated)Interventional2013-10-31Recruiting
"Study of the Therapeutic Effect of Atorvastatin on the Clinical Outcomes in HER2 Negative Breast Cancer Patients" [NCT05103644]Phase 2/Phase 360 participants (Anticipated)Interventional2021-10-30Recruiting
Study of Curative Effect Evaluation of DanLou Tablet on Coronary Artery Disease Not Amenable to Revascularization on the Basis of Western Medicine Therapy [NCT03072082]Phase 4440 participants (Anticipated)Interventional2017-06-30Not yet recruiting
Randomized Study of Atorvastatin Prophylaxis as a Supplement to Standard of Care Prophylaxis to Prevent Chronic Graft Versus Host Disease Allogeneic Stem Cell Transplantation From Matched Unrelated Donors [NCT03066466]Phase 30 participants (Actual)Interventional2019-12-10Withdrawn(stopped due to No participants were enrolled)
A Multi-Center, Randomized, Double-Blind, Parallel Phase III Study to Evaluate the Efficacy and Safety of KI1106 in Patients Whose TG Level is Not Adequately Controlled With Atorvastatin Calcium Monotherapy While LDL-C is Properly Controlled [NCT03482180]Phase 3215 participants (Actual)Interventional2016-05-04Completed
The Program to Assess the Influence of Routing and In-depth Consultation of Patients With Cardiovascular Risk Factors on the Choice of Medicine and Treatment Compliance [NCT04863274]2,912 participants (Actual)Observational2018-06-21Completed
Statin Adjunct Therapy Among HAART-treated Adults in Sub-Saharan Africa: Equivalence of Atorvastatin and Rosuvastatin [NCT03037372]Phase 3320 participants (Anticipated)Interventional2017-06-01Not yet recruiting
The Combination of Atorvastatin, Acetylcysteine and Danazol as the Treatment of Steroid-resistant/Relapse Immune Thrombocytopenia [NCT03460808]Phase 1/Phase 2200 participants (Anticipated)Interventional2018-03-10Not yet recruiting
Randomized,Double Blind,Double Dummy, Multi-center Study of Efficacy and Safety of HS-25 Combination With Atorvastatin in Subjects With Hypercholesterolemia in Coronary Heart Diseases [NCT03433196]Phase 3255 participants (Actual)Interventional2016-06-07Completed
A Prospective Randomized, Open-Label, Parallel-Group Comparative Study: Atorvastatin Pre-Treatment Versus Usual Care In Asian Patients With Acute Coronary Syndromes Undergoing Early Percutaneous Coronary Intervention [NCT00728988]Phase 4499 participants (Actual)Interventional2008-09-30Completed
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 Phase 3, Double Blind, Placebo-Controlled, Randomized, Parallel Group, Multicenter Study of the Efficacy, Safety and Tolerability of Fixed Combination Torcetrapib/Atorvastatin Administered Orally Once Daily for 6 Months, Compared to Atorvastatin Alone o [NCT00138762]Phase 33,800 participants Interventional2004-07-31Completed
Evaluation of the Effect in Platelet Count of Atorvastatin and N-acetyl Cysteine in Patients With Primary Immune Thrombocytopenia Resistant to Steroid Treatment or in Relapse: An Exploratory Clinical Trial [NCT05551624]Early Phase 115 participants (Actual)Interventional2018-07-04Completed
Phase 3 Multi-Center, Double-Blind, Randomized, Parallel Group, Carotid B-mode Ultrasound Evaluation of the Anti-Atherosclerotic Efficacy, Safety, and Tolerability of Fixed Combination CP-529,414/Atorvastatin, Administered Orally, Once Daily (QD) for 24 M [NCT00134238]Phase 3755 participants (Actual)Interventional2003-11-30Terminated
A Randomized, Double-blind, Placebo-controlled, Parallel Group Study to Evaluate the Efficacy and Safety of Alirocumab in Patients With Hypercholesterolemia Not Adequately Controlled With Non-statin Lipid Modifying Therapy or the Lowest Strength of Statin [NCT02584504]Phase 3163 participants (Actual)Interventional2015-11-30Completed
A Multicenter, Randomized, Open Label Study to Evaluate the Lipid Lowering Efficacy and Safety of Vytorin® 10/20 vs. Atorvastatin 10mg in Hypercholesterolemia Patients With Metabolic Syndrome in Korea [NCT00496730]Phase 3256 participants (Actual)Interventional2007-07-31Completed
A Randomized, Double-blind, Multi-center, Phase III Trial to Evaluate the Efficacy and Safety of BR1017A and BR1017B Combination Therapy in Essential Hypertension Patients With Primary Hypercholesterolemia [NCT05930028]Phase 3156 participants (Anticipated)Interventional2023-07-13Recruiting
The Effects of Atorvastatin on the Nitric Oxide-system in Patients With Non-diabetic Nephropathy [NCT01213498]Phase 225 participants (Actual)Interventional2010-05-31Completed
The Effects of Atorvastatin on the Nitric Oxide-system in Healthy Young Man [NCT01214746]Phase 226 participants (Actual)Interventional2010-05-31Completed
EFFECTS OF ATORVASTATIN ON BLOOD PRESSURE AND URINARY ALBUMIN EXCRETION IN PATIENTS WITH ESSENTIAL HYPERTENSION [NCT01126684]50 participants (Actual)Interventional2008-06-30Completed
A Double-blind, Randomized, Placebo and Ezetimibe Controlled, Multicenter Study to Evaluate Safety, Tolerability and Efficacy of AMG 145 on LDL-C in Combination With Statin Therapy in Subjects With Primary Hypercholesterolemia and Mixed Dyslipidemia [NCT01763866]Phase 32,067 participants (Actual)Interventional2013-01-15Completed
[NCT02185066]Phase 142 participants (Actual)Interventional2014-07-31Completed
The Clinical Study of Atorvastatin and Dexamethasone on Treatment for Chronic Subdural Hematoma in the Patients With Coagulation Disorders [NCT02192320]Phase 260 participants (Anticipated)Interventional2014-07-31Not yet recruiting
Effects of Oxygen Treatment on Mechanisms Involved in Ischemia-reperfusion Injury: A Single Center, Randomized, Controlled Pilot Study in Healthy Volunteers [NCT02286544]Phase 136 participants (Actual)Interventional2014-10-31Completed
A Multicenter, Double-Blind, Randomized, Parallel Group, 6-Week Study to Evaluate the Efficacy and Safety of Ezetimibe/Simvastatin Combination Tablet Versus Atorvastatin in Patients With Hypercholesterolemia [NCT00092690]Phase 31,902 participants (Actual)Interventional2003-06-30Completed
Serum Concentration and Gene Expression of Sirtuin-1 and Advanced Glycation End-products in Postmenopausal Women With Atherosclerotic Coronary Disease After Administration of Atorvastatin and Supplementation With Quercetin: Randomized Trial [NCT03943459]Phase 360 participants (Anticipated)Interventional2019-08-02Recruiting
CKD-391 in Healthy Volunteers to Investigate the Pharmacokinetic Drug Interaction Between Atorvastatin an Ezetimibe After Oral Administration [NCT02288338]Phase 136 participants (Actual)Interventional2014-11-30Completed
A Phase 3, Open-Label, Multisite, Randomized, Parallel Group Study of the Efficacy and Safety of Fixed Combination Torcetrapib/Atorvastatin Administered Once Daily (QD) Compared to Simvastatin for 6 Weeks in Subjects With Hypercholesterolemia (A5091031) [NCT00267280]Phase 3640 participants Interventional2006-01-31Terminated
The Effect of Atorvastatin on the NO-system in Patients With Type 2 Diabetes and Nephropathy [NCT01208701]Phase 225 participants (Actual)Interventional2010-05-31Completed
Pilot Study of Atorvastatin and Anakinra in Children With Coronary Artery Abnormalities Secondary to Kawasaki Disease [NCT04747847]Early Phase 110 participants (Anticipated)Interventional2017-10-09Recruiting
Multicenter, Randomized, Phase II Study of Neoadjuvant Chemotherapy Associated or Not With Zoledronate and Atorvastatin in Triple Negative Breast Cancers - YAPPETIZER Study [NCT03358017]Phase 254 participants (Actual)Interventional2018-03-05Completed
Open Label, Randomized, Two-treatment, Two-period, Two-sequence,Crossover, Single Dose, Oral Bioequivalence Study of Amlodipine Besylate/Atorvastatin Calcium Tablets 10mg/80mg Under Fasting Condition [NCT02295046]Phase 180 participants (Actual)Interventional2011-10-31Completed
On-admission Low-dose Colchicine in Addition to Atorvastatin to Reduce Inflammation in Acute Coronary Syndrome [NCT05250596]Phase 2175 participants (Anticipated)Interventional2022-02-24Recruiting
Intensive Statin Treatment in Chinese Coronary Artery Disease Patients Undergoing Percutaneous Coronary Intervention(PCI) [NCT01293097]Phase 42,884 participants (Actual)Interventional2010-06-30Completed
Atorvastatin Effects On Arterial Stiffness In Hemodialysis Patients [NCT04472637]Phase 250 participants (Actual)Interventional2020-11-01Completed
A Randomised Controlled Trial of Atorvastatin as an Anti-Inflammatory Agent in Non-Cystic Fibrosis Bronchiectasis [NCT01299181]Phase 460 participants (Actual)Interventional2010-11-30Completed
Efficacy of Atorvastatin vs Colchicine in Decrease of Troponin I of High Sensitivity as a Biomarker of Myocardial Damage in Patients With Rheumatoid Arthritis With Severe Activity. [NCT04056039]Phase 260 participants (Actual)Interventional2018-08-14Completed
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
Managing Endothelial Dysfunction in COVID-19 : A Randomized Controlled Trial at the Lebanese American University Medical Center- Rizk Hospital [NCT04631536]Phase 342 participants (Actual)Interventional2021-01-10Active, not recruiting
Preventing Anthracycline Cardiovascular Toxicity With Statins (PREVENT) [NCT01988571]Phase 2279 participants (Actual)Interventional2014-02-01Completed
A MC, DB, Rand, Study to Evaluate Efficacy, Safety and Tolerability of Eze/Simva 10/40 mg, Atorva 40 mg, Rosuva 10 mg in Achieving LDL-C <2 mmol/l in Pts With CVD...on Simva 40 mg With LDL-C ³2 mmol/l [NCT00462748]Phase 3786 participants (Actual)Interventional2007-03-31Completed
A Multicenter, Randomized, Double-Blind, Parallel Arm, 12-Week Study to Evaluate the Efficacy and Safety of Ezetimibe 10 mg When Added to Atorvastatin 10 mg Versus Titration to Atorvastatin 20 mg and to 40 mg in Elderly Patients With Hypercholesterolemia [NCT00418834]Phase 31,053 participants (Actual)Interventional2007-01-31Completed
A Cross-over, Randomized and Open-label Clinical Trial to Evaluate the Effects of Food on the Bioavailability of CKD-337 After a Single Oral Dose in Healthy Male Subjects [NCT03382756]Phase 116 participants (Actual)Interventional2017-10-12Completed
Statin Therapy To Limit Cognitive Dysfunction After Cardiac Surgery [NCT01186289]0 participants (Actual)Interventional2010-10-31Withdrawn(stopped due to Principal Investigator decided not to pursue enrollment due to changes in standard of care.)
Use of High Potency Statins and Rates of Admission for Acute Kidney Injury: Multicenter, Retrospective Observational Analysis of Administrative Databases [NCT02518516]2,067,639 participants (Actual)Observational2011-01-31Completed
A Phase III Trial of Acetylsalicylic Acid and Atorvastatin in Patients With Castrate-resistant Prostate Cancer [NCT03819101]Phase 31,210 participants (Anticipated)Interventional2019-06-06Recruiting
An Open-Label Study to Evaluate the Efficacy and Safety of Alirocumab in Children and Adolescents With Homozygous Familial Hypercholesterolemia [NCT03510715]Phase 318 participants (Actual)Interventional2018-08-31Completed
Study of Statins' Effect on Serum IgG, IgA Ang IgM Level in Chronic Hemodialysis Patients [NCT01305317]74 participants (Actual)Interventional2007-01-31Completed
Comparison Between Effect of High Dose and Low Dose of Atorvastatin in Reduction Level of CRP in Patients With Unstable Angina and NSTEMI (Non ST Elevation MI) [NCT01306565]100 participants (Actual)Interventional2009-01-31Completed
Atorvastatin and Clopidogrel HIgh DOse in Stable Patients With Residual High Platelet Activity [NCT01335048]Phase 450 participants (Anticipated)Interventional2011-04-30Completed
A Multicenter Study to Assess the Cholesterol Lowering Level of Switching to an Investigational Drug Compared to Doubling the Dose of an Investigational Drug in Patients With Hypercholesterolemia and Atherosclerotic or Coronary Vascular Disease [NCT00090168]Phase 3435 participants (Actual)Interventional2004-01-27Completed
Efficacy of Atorvastatin Versus Rosuvastatin on LV Function and Inflammatory Biomarkers in Type 2 Diabetic Patients With Dyslipidemia [NCT03784703]Phase 4160 participants (Actual)Interventional2018-01-01Completed
Effects on Oxidative Stress, Coagulation, Platelet Activation and Inflammatory Indexes of Atorvastatin and/or Aspirin Treatment in Patients at High Risk of Vascular Events [NCT01322711]Phase 460 participants (Anticipated)Interventional2011-03-31Active, not recruiting
The Effect of Seven-Day Atorvastatin Administration on Emotional Processing, Reward Processing, and Inflammation in Healthy Volunteers [NCT03966859]50 participants (Actual)Interventional2019-06-19Completed
"A Open-Label, Randomized, 2-sequence, 4-period, Fasting Condition, Singledose, Per Oral, Cross-over Study to Evaluate the Bioequivalence Between Dong-A Atorvastatin 80mg Tab and Lipitor 80mg Tab in Healthy Volunteers" [NCT04325009]Phase 156 participants (Anticipated)Interventional2020-03-30Recruiting
A Randomized, Double-blind, Parallel-group, Placebo-controlled, Multicenter Study Evaluating the Efficacy and Safety of Five Doses and Two Dose Regimens of SAR236553 Over 12 Weeks in Patients With Primary Hypercholesterolemia and LDL-cholesterol ≥ 100 mg/ [NCT01288443]Phase 2183 participants (Actual)Interventional2011-01-31Completed
Systems Biological Assessment of Statin Effect on Vaccine Responses [NCT06024096]Phase 460 participants (Anticipated)Interventional2023-09-20Recruiting
An Open-label, Two-cohort Study to Assess the Effect of Lamotrigine and Phenytoin on the Pharmacokinetics of Atorvastatin in Healthy Subjects [NCT00627575]Phase 1119 participants (Actual)Interventional2008-02-04Completed
Carotid Plaque Composition by Magnetic Resonance Imaging During Lipid Lowering Therapy [NCT00715273]Phase 4217 participants (Actual)Interventional2001-05-01Completed
Does Atorvastatin Prevent Post Operative Atrial Fibrillation After Pulmonary Resection: A Randomized Clinical Study [NCT00756886]73 participants (Actual)Interventional2008-09-30Completed
Evaluating the Effectiveness of Atorvastatin on the Progression of Aortic Dilatation and Valvular Degeneration in Patients With Bicuspid Aortic Valve (BICATOR) [NCT02679261]Phase 3220 participants (Actual)Interventional2016-06-30Completed
A Multicenter, Open-Label Extension Study Of High-Risk Hyperlipidemic Patients Treated With An Atorvastatin Starting Dose Adapted To Their Baseline LDL-C Level [NCT00644709]Phase 4196 participants (Actual)Interventional2003-09-30Completed
An Open-Label, Multicenter Study to Assess the Efficacy of Switching to a Combination Tablet Ezetimibe/Simvastatin 10mg/40mg, Compared to Doubling the Dose of Statin in Patients Hospitalized With a Coronary Event [NCT00132717]Phase 3450 participants (Actual)Interventional2005-01-01Completed
A 6-Week, Randomized,Open-Label, Comparative Study to Evaluate the Efficacy and Safety of Rosuvastatin and Atorvastatin in the Treatment of Hypercholesterolaemia in South Asian Subjects. [NCT00654225]Phase 32,340 participants (Anticipated)Interventional2002-10-31Completed
A 6 Week Open Label, Dose Comparison Study to Evaluate the Safety and Efficacy of Rosuvastatin Versus Atorvastatin, Pravastatin, and Simvastatin in Subjects With Hypercholesterolemia. [NCT00654537]Phase 35,625 participants (Anticipated)Interventional2001-04-30Completed
A Multicenter, Randomized, Double-Blind, Placebo- and Active-Controlled Study to Assess the Efficacy, and Tolerability of MK-6213 Co-Administered With Atorvastatin in Patients With Primary Hypercholesterolemia [NCT00687271]Phase 2334 participants (Actual)Interventional2008-06-14Completed
Efficacy of WelChol as an Add-on to Atorvastatin Therapy [NCT00754507]Phase 465 participants (Actual)Interventional2002-11-30Completed
Double Blinded Study of the Effects of Pioglitazone in Combination With Atorvastatin in Comparison to Atorvastatin Treatment Alone on Intima-Media Thickness in Patients at Risk for Vascular Complications [NCT00770575]Phase 2148 participants (Actual)Interventional2005-06-30Completed
An Open Label, Randomized, Single Dose, Two-Way Crossover Bioequivalence Study Comparing A Pediatric Appropriate Formulation To A 10 Mg Commercial Atorvastatin Calcium Tablet Formulation In Healthy Subjects [NCT00777517]Phase 176 participants (Actual)Interventional2008-11-30Completed
The Effect of Atorvastatin on The Prevention of 5-fluorouracil-induced Mucositis in Colorectal Cancer Patients [NCT04151355]100 participants (Anticipated)Interventional2019-10-01Recruiting
A Multicenter, Randomized, Open-labeled, Parallel Group Comparison Study to Evaluate the Efficacy, Safety and Tolerability of Ezetimibe Added to Ongoing Statin Therapy Versus Doubling the Dose of Ongoing Statin in the Treatment of Hypercholesterolemia. [NCT00652327]Phase 483 participants (Actual)Interventional2005-12-31Completed
Efficacy of High Dose Atorvastatin Loading in ST Elevation Myocardial Infarction [NCT00808717]Phase 4170 participants (Anticipated)Interventional2007-07-31Completed
A Pilot Trial of Atorvastatin in p53-Mutant and p53 Wild-Type Malignancies [NCT03560882]Phase 150 participants (Anticipated)Interventional2018-07-19Recruiting
Regulation of Lipoprotein Kinetics by Atorvastatin and Fenofibrate With the Metabolic Syndrome [NCT00632840]Phase 411 participants (Actual)Interventional2001-06-30Completed
A One-Directional, Open-Label Drug Interaction Study to Investigate the Effects of Multiple-Dose Atorvastatin on the Single-Dose Pharmacokinetics of Colchicine in Healthy Volunteers [NCT00960323]Phase 124 participants (Actual)Interventional2009-02-28Completed
Comparative Evaluation of Locally Delivered 1.2% Atorvastatin and 1.2% Rosuvastatin Gel in Treatment of Mandibular Degree ii Furcation Defects in Chronic Periodontitis Subjects: A Randomized Controlled Clinical Trial [NCT02800902]Phase 2/Phase 390 participants (Actual)Interventional2015-05-31Completed
Assessment of Endothelial Function in Patients With Non Alcoholic Fatty Liver Disease and the Impact of Statin Treatment [NCT01987310]0 participants (Actual)Interventional2015-12-31Withdrawn(stopped due to the study was stopped because of lack of interest)
A Double-Blind, Randomized Study to Evaluate the Efficacy and Safety of TAK-475 (100 mg) Vs Placebo When Coadministered With Atorvastatin (10 or 20 mg) in Subjects With Primary Hypercholesterolemia [NCT00864643]Phase 2172 participants (Actual)Interventional2004-09-30Completed
A Multicenter, Randomized, Double-Blind, Parallel-Group, Placebo-Controlled Study of Statin Therapy In Patients With Vasospastic Angina [NCT02790528]Phase 40 participants (Actual)Interventional2017-07-31Withdrawn(stopped due to Funding issue)
Cognitive Decline and Underlying Mechanisms in Asymptomatic Intracranial Artery Stenosis Patients: A Cohort Study [NCT05504330]100 participants (Anticipated)Observational2022-08-15Recruiting
Rosuvastatin for Reduction of Myocardial Damage and Systemic Inflammation During Coronary Angioplasty - The REMEDY Study [NCT02205775]Phase 3280 participants (Actual)Interventional2010-05-31Terminated(stopped due to difficult recruitment)
Atorvastatin Use and Portal Hypertension in Patients With Hepatitis B Virus-related Liver Cirrhosis: A Randomized Controlled Trial [NCT05483894]Phase 236 participants (Anticipated)Interventional2022-08-01Not yet recruiting
[NCT02160743]Phase 128 participants (Actual)Interventional2014-05-31Completed
A Study to Evaluate the Efficacy and Safety of Pravastatin/Fenofibrate Complex in Patients With Combined Dyslipidemia With Adequately Controlled LDL-C But Inadequately Controlled Triglyceride Level by Atorvastatin Monotherapy [NCT02166593]Phase 3302 participants (Actual)Interventional2014-05-31Completed
Relative Bioavailability of Dabigatran and Atorvastatin After 150 mg BID Dabigatran Etexilate and Atorvastatin at 80 mg QD Alone or Following Concomitant Multiple Oral Administrations in Healthy Male and Female Volunteers (an Open-label, Randomised, Multi [NCT02171039]Phase 124 participants (Actual)Interventional2006-06-30Completed
"A Multicenter, Randomized, Placebo-controlled, Factorial Design, 12-month Study to Evaluate the Efficacy and Safety of AVE5530 25 mg/Day and 50 mg/Day Co-administered With All Registered Atorvastatin Strengths Ranging From 10 mg to 80 mg in Patients With [NCT00741715]Phase 31,736 participants (Actual)Interventional2008-08-31Terminated(stopped due to AVE5530 in hypercholesterolemia was stopped due to insufficient efficacy)
A Double-blind, Randomized, Placebo-controlled, Multicenter Study to Evaluate Safety and Efficacy of Evolocumab (AMG 145) in Combination With Statin Therapy in Diabetic Subjects With Hyperlipidemia or Mixed Dyslipidemia (BERSON) [NCT02662569]Phase 3986 participants (Actual)Interventional2016-04-14Completed
Effect of Statins (Atorvastatin) on Inflammation and Cardiac Function in Patients With Chronic Chagas Disease: Pathophysiological Studies in a Multicenter Proof-of-concept [NCT04984616]Phase 2300 participants (Anticipated)Interventional2021-10-12Recruiting
Higher Potency Statins and the Risk of New Diabetes: Multicentre, Observational Study of Administrative Databases [NCT02518503]136,966 participants (Actual)Observational2012-07-31Completed
Randomized Double Blind Placebo Controlled Trial of Statins for the Primary pREvention of Heart Failure in Patients With Cancer Receiving Anthracycline Based Chemotherapy [NCT03186404]Phase 2112 participants (Actual)Interventional2018-05-10Active, not recruiting
Atorvastatin and Alkali Therapy in Patients With Autosomal Dominant Polycystic Kidney Disease, A Pilot Trial for Safety and Feasibility [NCT05870007]Phase 230 participants (Anticipated)Interventional2023-05-31Enrolling by invitation
A Phase 1 Study to Evaluate OATP Transporter-Mediated Drug-Drug Interactions Between Filgotinib and Statins as Probe Drugs in Healthy Participants [NCT04608344]Phase 127 participants (Actual)Interventional2020-11-04Completed
Effect of Atorvastatin on Glycemic Control in Prediabetic Patients [NCT02470455]75 participants (Actual)Observational2011-07-31Completed
A Phase 3, Double-Blind Efficacy and Safety Study of Ezetimibe (SCH 58235) 10 mg in Addition to Atorvastatin Compared to Placebo in Subjects With Primary Hypercholesterolemia (Protocol P00692) [NCT03867110]Phase 3628 participants (Actual)Interventional2000-03-06Completed
A Study to Evaluate the Drug-drug Interactions (DDIs) of IBI362 With Metformin, Warfarin, Atorvastatin, Digoxin in Overweight or Obese Subjects [NCT05815680]Phase 148 participants (Actual)Interventional2023-04-06Completed
Effects of Decrease in Cholesterol Levels Induced by a Statin on Sperm Quality [NCT02094313]Phase 117 participants (Actual)Interventional2008-01-31Completed
The Effect of Short-term Atorvastatin Treatment on Immune Responses to Pneumovax 23 [NCT02097589]Phase 133 participants (Actual)Interventional2014-06-30Completed
Relationship Between Insulin Resistance and Statin Induced Type 2 Diabetes, and Integrative Personal Omics Profiling [NCT02437084]Phase 4115 participants (Actual)Interventional2015-05-31Completed
Intensive Statin Treatment in Acute Ischemic Stroke Patients With INtracranial Atherosclerosis - High-Resolution Magnetic Resonance Imaging Study (STAMINA-MRI Study) [NCT02458755]Phase 480 participants (Anticipated)Interventional2012-02-29Recruiting
Comparative Evaluation of Subgingivally Delivered 1% Alendronate Versus 1.2% Atorvastatin Gel in Treatment of Chronic Periodontitis: a Randomized Placebo Controlled Clinical Trial [NCT02455869]Phase 2/Phase 3104 participants (Actual)Interventional2014-07-31Completed
A Phase 3, Double-blind, Double-dummy, Randomized, Placebo And Active Controlled, Parallel-group Study To Assess The Efficacy, Safety And Tolerability Of Pf-04950615 In Subjects With Dyslipidemia Who Are Intolerant To Statins [NCT02135029]Phase 3184 participants (Actual)Interventional2014-06-30Completed
Continuous Atorvastatin Therapy Compared With Intermittent Atorvastatin Therapy for the Effect of LDL-c Level Variability and the Regulation of Trained Immunity [NCT05790499]12 participants (Anticipated)Interventional2023-03-20Recruiting
A Randomized, Double-Blind, Active-Controlled, Multicenter, Crossover Study to Evaluate the Efficacy of Ezetimibe/Atorvastatin 10 mg/40 mg Fixed-Dose Combination Tablet Compared to Co-Administration of Marketed Ezetimibe 10 mg and Atorvastatin 40 mg in Pa [NCT01370603]Phase 3328 participants (Actual)Interventional2011-09-30Completed
A Study to Assess the Pharmacokinetics, Pharmacodynamics and Safety of Adding ETC-1002 180 mg to Atorvastatin 80 mg Background Therapy in Statin-Treated Patients [NCT02659397]Phase 268 participants (Actual)Interventional2015-12-31Completed
Open-label, Randomized, Multiple-dose, Crossover Study to Evaluate the Pharmacokinetic Interaction Between Fenofibrate and Atorvastatin in Healthy Male Volunteers [NCT02066207]Phase 130 participants (Actual)Interventional2014-03-18Completed
Socket Augmentation Using Atorvastatin With Or Without PRGF Derived Fibrin Scaffold (Clinical and Histomorphometric Study) [NCT03228771]Phase 430 participants (Actual)Interventional2016-03-31Completed
Effect of Allopurinol on Mono and Co-administration With Statins on Platelets Reactivity on Diabetic Patiets Treated With Aspirin and Insulin [NCT03195153]Phase 4200 participants (Anticipated)Interventional2017-03-28Recruiting
The Effect of Atorvastatin on Prevention of Postoperative Acute Kidney Injury in Patients Undergoing Aortic Surgery [NCT02157337]Phase 423 participants (Actual)Interventional2014-03-12Completed
A Phase 1 Open-label, Single-sequence Study to Evaluate the Effect of Coadministration of BMS-919373 on the Single-dose Pharmacokinetics of Rosuvastatin and Atorvastatin in Healthy Subjects [NCT02089061]Phase 126 participants (Actual)Interventional2014-03-31Completed
The Effect of Atorvastatin on Microvascular Endothelial Function and Raynaud in Early Diffuse Systemic Sclerosis [NCT02370784]Phase 224 participants (Actual)Interventional2015-02-28Completed
An Open Label, Non-comparative Phase II Trial to Evaluate the Effects of Atorvastatin on the Persistent Coronary Arterial Aneurysm in Children With Kawasaki Disease: Safety and Efficacy [NCT02114099]Phase 220 participants (Anticipated)Interventional2007-06-30Recruiting
HElping Alleviate the Longer-term Consequences of COVID-19 (HEAL-COVID): a National Platform Trial [NCT04801940]Phase 32,631 participants (Anticipated)Interventional2021-05-19Recruiting
Statin InTensity to Prevent Coronary Artery Vasculopathy After Heart Transplantation - SToP-CAV [NCT05251129]70 participants (Anticipated)Interventional2025-01-31Not yet recruiting
The Role of DLBS1033 in the Management of Acute Ischemic Stroke Patients: Study Protocol for a Randomized Controlled Study [NCT04425590]Phase 2/Phase 3180 participants (Anticipated)Interventional2020-04-01Recruiting
"Multicenter Randomized Double-Blind Placebo and Active Comparator Controlled Parallel-group, Multicenter Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Efficacy of MBX-8025 in Moderately Obese Hyperlipidemic Patients With/Out Concomitan [NCT00701883]Phase 2183 participants (Actual)Interventional2007-08-31Completed
Efficacy and Safety of Atorvastatin + Perindopril Fixed-Dose Combination S05167 in Adult Patients With Arterial Hypertension and Dyslipidemia, 8 Weeks, Phase 3, Randomized, Double-blind, Active-control, Multinational, Multi-center, Parallel Study [NCT04591808]Phase 3146 participants (Actual)Interventional2021-09-09Terminated(stopped due to for strategic reasons)
Vascular Endothelial Activation in Obstructive Sleep Apnea [NCT03122639]Early Phase 1106 participants (Actual)Interventional2017-09-01Completed
A Phase II Study of Atorvastatin in Patients With Low Grade or Refractory Non-Hodgkin's Lymphoma [NCT00185731]Phase 225 participants (Actual)Interventional2005-04-30Completed
The Effect of InTensive Statin in Ischemic Stroke With inTracranial Atherosclerotic Plaques: a Prospective, Random, Single-center Study Based on High Resolution Magnetic Resonance Imaging [NCT03753555]Phase 4100 participants (Anticipated)Interventional2018-12-01Recruiting
Statins for Prevention of Disease Progression and Hospitalization in Liver Cirrhosis: A Multi-center, Randomized, Double Blind, Placebo-controlled Trial. The STATLiver Trial [NCT04072601]Phase 478 participants (Actual)Interventional2019-11-08Terminated(stopped due to Study part one completed)
Effects of Atorvastatin on Endothelial Function, Vascular and Myocardial Redox State in High Cardiovascular Risk Patients [NCT01013103]Phase 472 participants (Actual)Interventional2007-10-31Completed
Early Detection of Atherosclerosis in the Primary Care Setting: a Randomized Trial to Assess the Efficacy of a Novel Strategy in the Primary Prevention of Cardiovascular Diseases. [NCT00734123]Phase 42,948 participants (Anticipated)Interventional2008-04-30Recruiting
Effects of High Dose Simvastatin vs. Atorvastatin on Baseline Lipoprotein Profiles, Apo-A-1 and C Reactive Protein [NCT00736463]Phase 480 participants (Anticipated)Interventional2005-01-31Recruiting
Effect of Atorvastatin on Vascular Inflammation in Type 2 Diabetes: Analysis With 18F-Fluorodeoxyglucose Positron Emission Tomography [NCT00932048]0 participants (Actual)Interventional2011-08-31Withdrawn
[NCT02566187]Phase 199 participants (Actual)Interventional2015-08-31Completed
A Randomized, Double Blind Comparator-controlled, Parallel-group Study to Evaluate the Safety and Efficacy of the Combination of AEGR-733 and Atorvastatin 20 mg vs Atorvastatin Monotherapy in Subjects With Moderate Hypercholesterolemia [NCT00690443]Phase 244 participants (Actual)Interventional2008-05-31Completed
Statin for Preventing Hepatocellular Carcinoma Recurrence After Curative Treatment: a Double-blind Randomized Placebo-controlled Trial [NCT03024684]Phase 4240 participants (Anticipated)Interventional2017-01-03Recruiting
Study the Effect of CYP3A Genetic Polymorphisms on the Pharmacokinetics of Atorvastatin in Chinese Subjects With Coronary Heart Disease [NCT00973986]Phase 120 participants (Actual)Interventional2009-06-30Completed
Strengthening Transplantation Effects of Bone Marrow Mononuclear Cells With Atorvastatin in Myocardial Infarction [NCT00979758]Phase 2100 participants (Actual)Interventional2009-01-31Completed
Short Term Atorvastatin Regime for Vasculopathic Surgical (STAR-VaS) Patients Study [NCT00967434]60 participants (Actual)Interventional2007-12-31Completed
Impact of Atorvastatin on Cerebral Perfusion and Endothelial Function [NCT00751907]Phase 216 participants (Actual)Interventional2006-06-30Completed
A Phase IIb, Multicenter, Randomized, Placebo-Controlled, Double-Blind, Dose-Ranging Study to Assess the Efficacy and Safety of MK0859 in Japanese Patients With Dyslipidemia [NCT00977288]Phase 2408 participants (Actual)Interventional2009-09-30Completed
Short Term Statin Treatment and Endothelial Dysfunction Due to Ischemia and Reperfusion Injury [NCT00987974]Phase 448 participants (Anticipated)Interventional2009-09-30Completed
Impact of Atorvastatin on Prostate Cancer Progression After Initiation of Androgen Deprivation Therapy - Lipid Metabolism as a Novel Biomarker to Predict Prostate Cancer Progression [NCT04026230]Phase 3400 participants (Anticipated)Interventional2019-08-15Recruiting
A Pilot Study Evaluating the Effect of Atorvastatin on Biomarkers of Inflammation, Coagulopathy, Angiogenesis, and T-lymphocyte Activation in HIV-1 Infected Individuals With Suppressed HIV-1 RNA and LDL Cholesterol < 130 mg/dL [NCT01351025]Phase 298 participants (Actual)Interventional2011-04-14Completed
A 12-Month, Open-Label, Extension Study of the Safety and Efficacy of LCP-AtorFen in Subjects With Dyslipidemia [NCT00664859]Phase 2/Phase 3140 participants (Actual)Interventional2007-10-31Completed
Plaque REgression With Cholesterol Absorption Inhibitor or Synthesis Inhibitor Evaluated by IntraVascular UltraSound [NCT01043380]Phase 4245 participants (Actual)Interventional2010-01-31Completed
Open-label, Long-term Study of Coadministration of Ezetimibe and Atorvastatin in Patients With Primary Hypercholesterolemia Who Have Not Reached LDL-cholesterol Target With HMG-CoA Reductase Inhibitors [NCT00654095]Phase 3146 participants (Actual)Interventional2007-12-01Completed
A Multi-Center, Randomized Study To Evaluate Efficacy And Safety Of A Fixed Combination Therapy Of Amlodipine And Atorvastatin In The Treatment Of Concurrent Hypertension And Hyper-LDL-Cholesterolemia [NCT00530946]Phase 3165 participants (Actual)Interventional2007-09-30Completed
Role of Statins In Slowing Rheumatic Heart Disease (RHD) Progression: A Feasibility Study For A Randomized Controlled Trial [NCT04575857]100 participants (Actual)Observational2022-02-08Active, not recruiting
A Double-blind Randomized, Placebo-Controlled, Single-Center Study to Assess the Impact of Statins on the Autonomic Nervous System and Cardiac Structure/Function in Non-Ischemic Heart Failure [NCT00233480]Phase 427 participants (Actual)Interventional2005-08-31Completed
[NCT02374047]Phase 1118 participants (Actual)Interventional2015-01-31Completed
Study on Left Atrial Function of Atrial Fibrillation After Radiofrequency Ablation With Statin Therapy [NCT02776956]180 participants (Actual)Interventional2016-04-30Completed
Evaluating the Anti-Proliferative Effects of Atorvastatin on the Endometrium of Endometrial Cancer Patients: A Pre-Operative Window Study [NCT02767362]Early Phase 124 participants (Actual)Interventional2015-11-30Completed
Investigations on Differences in Atorvastatin Metabolites Ratios as a Diagnostic Tool in Detecting Atorvastatin Induced Myotoxicity [NCT00414531]Phase 453 participants (Actual)Interventional2005-05-31Completed
A Single Center, Open-label, Drug Interaction Study of MGL-3196 With Atorvastatin in Healthy Subjects [NCT02749578]Phase 114 participants (Actual)Interventional2016-04-30Completed
Open Label, Comparative, Multiple-dose, Fixed-sequence Steady State Trial in Healthy Volunteers to Assess the Pharmacokinetic Interaction of Ramipril, Atorvastatin and Amlodipine After a Multiple Oral Dose Administration [NCT04262765]Phase 118 participants (Actual)Interventional2019-02-23Completed
A Phase I Study to Evaluate the Drug-Drug Interaction of Chiglitazar With Empagliflozin,Atorvastatin and Valsartan in Healthy Subjects. [NCT05681273]Phase 148 participants (Actual)Interventional2023-02-17Completed
Effects of Statins on Lower Extremity Arterial Function Assessed by Magnetic Resonance Imaging [NCT00770679]16 participants (Actual)Interventional2008-06-30Terminated(stopped due to Delayed recruitment, funding exhausted)
Pharmacodynamic Equivalence Study of Ramipril 10 mg and Atorvastatin 40 mg Administered as a Cardiovascular Fixed Dose Combination Pill AAR as Compared to Monotherapy With the Reference Products Altace® 10 mg and Lipitor® 40 mg [NCT02791958]Phase 2528 participants (Anticipated)Interventional2016-03-31Active, not recruiting
A Phase II Randomised, Double-blind, Placebo-controlled Study of the Effect of Atorvastatin on Postoperative Renal Function in Patients Undergoing Elective Cardiopulmonary Bypass. [NCT00910221]Phase 2/Phase 3100 participants (Actual)Interventional2008-03-31Completed
An Open Label, Randomized, Single Dose, Two-Way Crossover Bioequivalence Study Comparing A New 10 Mg Atorvastatin Tablet To A 10 Mg Atorvastatin Commercial Tablet In Healthy Subjects [NCT00917579]Phase 476 participants (Actual)Interventional2008-07-31Completed
Atorvastatin Reduces Chronic Inflammation and aVerage Epogen Dose (ARChIVED) [NCT02764736]0 participants (Actual)Interventional2016-03-04Withdrawn(stopped due to Enrollment did not progress as anticipated. No participants enrolled.)
A Multicenter., Rand., Double-Blind, Titration Study to Evaluate & Compare the Efficacy & Safety of Ezetimibe Plus Atorvastatin Vs Atorvastatin in Hypercholesterolemic Pts. at Moderately High Risk for CHD Not Adequately Controlled on Atorvastatin 20 Mg [NCT00276458]Phase 3196 participants (Actual)Interventional2006-02-28Completed
A Phase 1, Fixed-Sequence, Open-label Study in Healthy Subjects to Estimate the Effects of ITCA 650 on Gastric Emptying and on the Absorption Pharmacokinetics of Each of 4 Commonly Studied Drug/Drug Interaction (DDI) Probe Compounds [NCT02641899]Phase 133 participants (Actual)Interventional2015-12-31Completed
[NCT02706860]Phase 494 participants (Actual)Interventional2013-06-30Completed
High Dose Atorvastatin Raises Threshold of Contrast Induced Nephropathy in Diabetic Patients Undergoing Elective Coronary Intervention [NCT04375787]Phase 4200 participants (Actual)Interventional2020-03-15Completed
A Multicenter, Randomized, Double-blind, Parallel Group, 6-Week Study to Evaluate the Efficacy and Safety of Ezetimibe/Simvastatin Combination Tablet Versus Atorvastatin in Patients With Type 2 Diabetes Mellitus (T2DM) and Hypercholesterolemia [NCT00110435]Phase 31,229 participants (Actual)Interventional2005-05-31Completed
A Phase 1 Open-Label Study in Healthy Adult Subjects to Assess the Effect of Cenicriviroc Mesylate (CVC) on the Pharmacokinetics (PK) of HMG-CoA Reductase Inhibitors (Rosuvastatin, Atorvastatin and Simvastatin), Caffeine and Digoxin [NCT02685462]Phase 136 participants (Actual)Interventional2016-01-31Completed
A Multicenter, Twelve-Week Treatment, Single-Step Titration, Open-Label Study Assessing The Percentage Of Dyslipidemic High-Risk Patients Achieving LDL Cholesterol Targets With Atorvastatin Starting Doses Of 10 Mg, 20 Mg And 40 Mg. [NCT00644670]Phase 4232 participants (Actual)Interventional2003-06-30Completed
Efficacy Study of Atorvastatin to Treat Variant Angina [NCT00620204]Phase 4136 participants (Anticipated)Interventional2008-01-31Recruiting
Statins and 90-day Functional Efficiency and Survival in Patients With Spontaneous Intracerebral Hemorrhage [NCT06094244]153 participants (Actual)Interventional2017-03-17Completed
Atorvastatin in Triple-Negative Breast Cancer (TNBC) Patients Who Did Not Achieve a Pathologic Complete Response (pCR) After Receiving Neoadjuvant Chemotherapy, a Multicenter Pilot Study [NCT03872388]Phase 26 participants (Actual)Interventional2019-01-14Completed
[NCT00681525]Phase 118 participants (Actual)Interventional2008-04-30Completed
Self-Assessment Method for Statin Side-effects Or Nocebo [NCT02668016]Phase 460 participants (Actual)Interventional2016-03-31Active, not recruiting
A Randomized, Open-label, Multiple-dose, Crossover Study to Evaluate the Drug-drug Interaction Between Telmisartan and Atorvastatin in Healthy Male Volunteers [NCT02579356]Phase 148 participants (Actual)Interventional2014-05-31Completed
The Acute Effect of Atorvastatin on Renal Sodium Excretion, Glomerular Filtration Rate, Tubular Function and Vasoactive Hormones in Patients With Non-Insulin Dependent Type II Diabetes. [NCT00678522]Phase 425 participants (Anticipated)Interventional2007-09-30Completed
An Open-label, Two-treatment, Two-period, Two-sequence, Crossover Study to Evaluate the Effect of Atorvastatin on the Pharmacokinetics of Fimasartan in Healthy Male Volunteers [NCT00991705]Phase 128 participants (Actual)Interventional2009-07-31Completed
A Randomized, Double-Blind, Placebo-Controlled, Forced Titration Study to Assess the Efficacy and Safety of Omacor, Co-Administered With Open-Label Atorvastatin Therapy, in Hypertriglyceridemic Subjects [NCT00435045]Phase 3245 participants (Actual)Interventional2007-02-28Completed
A Six-week Double Blinded, Randomized Trial of Atorvastatin for the Treatment of PCOS Women With Elevated LDL Cholesterol [NCT00529542]Phase 220 participants (Actual)Interventional2004-12-31Completed
A Study to Evaluate the Effect of Daily Doses of Obicetrapib Tablets on the Pharmacokinetics of Atorvastatin Calcium Tablets or Rosuvastatin Calcium Tablets in Healthy Adult Subjects [NCT06081166]Phase 174 participants (Anticipated)Interventional2023-10-31Not yet recruiting
Bone-Targeted Therapy Combining Zoledronate With Atorvastatin in Renal Cell Carcinoma: A Phase II Study [NCT00490698]Phase 211 participants (Actual)Interventional2006-10-31Completed
Phase IV Study of Statins for Assess the Long-term Pleiotropic Effect Upon Nitric Oxide and C-Reactive Protein Levels in Patients With Peripheral Arterial Disease [NCT01041729]Phase 460 participants (Actual)Interventional2008-01-31Completed
A 6-Week, Prospective, Randomized, Double-Blind, Double-Dummy Phase IV Clinical Trial Designed to Evaluate the Efficacy of an Aggressive Multi-Risk Factor Management Strategy With Caduet (A3841045) Versus a Guideline-Based Approach in Achieving Blood Pres [NCT00412113]Phase 4245 participants (Actual)Interventional2007-01-31Completed
Randomised Controlled Trial of Effect of Pre-operative Statin Use on Matrix Metalloproteinases (MMP) & Tissue Inhibitors of Matrix Metalloproteinases (TIMP) in Abdominal Aortic Aneurysm (AAA). [NCT01062802]Phase 440 participants (Actual)Interventional2005-01-31Completed
Randomised, Double-blind, 52-wk, Parallel-grp, Multicentre, PIIb Study to Evaluate Effects of Rosuvastatin 10mg, Rosuvastatin 40mg and Atorvastatin 80mg on Urinary Protein Excretion in Hypercholesterolaemic Diabetic Patients With Moderate Proteinuria [NCT00296374]Phase 2353 participants (Actual)Interventional2006-02-28Completed
Reload of High Dose Atorvastatin for Preventing Deep Vein Thrombosis in Statin Users Undergoing Total Knee Replacement Arthroplasty: RE-STOP-DVT Study- A Prospective Randomized Controlled Trial [NCT01063426]Phase 4180 participants (Anticipated)Interventional2009-11-30Recruiting
A Multi-Center, Randomized, Double-Blind, Placebo- and Active-Controlled Study Assessing the Efficacy, Safety and Tolerability of Diazoxide Choline Controlled-Release Tablet (DCCR) in Subjects Without Diabetes Mellitus Having Very High Fasting Triglycerid [NCT00973271]Phase 30 participants (Actual)Interventional2011-03-31Withdrawn(stopped due to Did not continue with development of DCCR in Very High Triglycerides)
A Multicenter, Randomized, Double-Blind, Parallel Group, 12 Week Study to Evaluate the Efficacy and Safety of MK0524B Versus Atorvastatin in Patients With Mixed Hyperlipidemia [NCT00289900]Phase 32,340 participants (Actual)Interventional2006-01-24Completed
A Multi-center, Randomized, Double-blinded Equivalence Clinical Trial to Evaluate Efficacy and Safety of LipiLou 20 mg Versus Lipitor 20 mg in Hypercholesterolemic Patients With Higher Risk Cardiovascular Disease in Korea [NCT01029522]Phase 4244 participants (Actual)Interventional2008-08-31Completed
A Multicenter, Eight-Week Treatment, Single-Step Titration Open-Label Study Assessing The Percentage Of Korean Dyslipidemic Patients Achieving LDL Cholesterol Target With Atorvastatin Starting Doses Of 10 MG, 20 MG, And 40 MG. [NCT00540293]Phase 4425 participants (Actual)Interventional2007-10-31Completed
Effects of Single-Dose Atorvastatin on Peri-Procedural Myonecrosis During Percutaneous Coronary Intervention in Patients With Acute Coronary Syndromes - The NO-MI Study [NCT00344019]Phase 497 participants (Actual)Interventional2006-05-31Terminated(stopped due to slow recruitment)
[NCT02614352]Phase 160 participants (Anticipated)InterventionalNot yet recruiting
Treatment Study for Severe High-Density Lipoprotein Deficiency [NCT00458055]19 participants (Actual)Interventional2006-11-30Completed
A Multicenter, Eight-Week Treatment, Single-Step Titration, Open-Label Study Assessing The Percentage Of Dyslipidemic Patients Achieving LDL Cholesterol Target With Atorvastatin Starting Doses Of 10 Mg, 20 Mg, And 40 Mg [NCT00647543]Phase 4242 participants (Actual)Interventional2003-08-31Completed
A Randomized, Open-label, Single Oral Dose, 2-way Crossover Clinical Trial to Compare Safety and Pharmacokinetic Characteristics of CKD-337 in Healthy Male Volunteers. [NCT02651753]Phase 148 participants (Actual)Interventional2016-01-31Completed
A 12-Week, Randomized, Open-Label, 3 Arm Parallel Group, Multicenter, Phase IIIb Study Comparing the Efficacy and Safety of Rosuvastatin With Atorvastatin and Simvastatin Achieving NCEP ATP III LDL-C Goals in High Risk Subjects With Hypercholesterolaemia [NCT00654173]Phase 34,444 participants (Actual)Interventional2002-06-30Completed
An Open Label, Randomized, Multi-Center, Phase IIIB, Parallel Group Switching Study to Compare the Efficacy and Safety of Lipid Lowering Agents Atorvastatin and Simvastatin With Rosuvastatin in High Risk Subjects With Type IIa and IIb Hypercholesterolemia [NCT00654407]Phase 34,875 participants (Anticipated)Interventional2001-11-30Completed
A 12 Week Randomized, Double-Blind, Force-Titration, Parallel Group, Multi Centre, Phase IIIb Study to Compare the Efficacy of Rosuvastatin With Atorvastatin and Placebo in the Treatment of Non-Diabetic, Non-Atheroscleric, Metabolic Syndrome Subjects With [NCT00654485]Phase 3940 participants (Anticipated)Interventional2002-05-31Completed
Mobilization of Endothelial Progenitor Cells Induced by Atorvastatin in Patients With Stable Coronary Artery Disease Treated With Anti-CD 34 Antibodies Coated Stents [NCT00911339]Phase 313 participants (Actual)Interventional2009-01-31Terminated(stopped due to prematurely interrupted because of difficulty in enrolment of patients.)
Systemic Inflammation and Obstructive Sleep Apnea Syndrome: Effect of Atorvastatin [NCT00669695]Phase 254 participants (Actual)Interventional2008-05-31Terminated(stopped due to Interim analysis performed without efficient results)
INdians Followed for INtensive Lipid Lowering Treatment and Its safetY: To Assess The Safety And Effectiveness Of Ezetimibe Co-Administered With Any Statin Compared To Doubling Of Current Statin Daily Dose In South Asian Canadians [NCT00664469]Phase 364 participants (Actual)Interventional2007-08-31Terminated(stopped due to Poor enrollment)
A Randomized and Placebo-Controlled Phase II Trial Targeting Dominant-Negative Missense Mutant P53 by Atorvastatin for Reducing the Risk of Longstanding Ulcerative Colitis-Associated Cancer [NCT04767984]Phase 270 participants (Anticipated)Interventional2021-09-24Recruiting
A Randomized Clinical Trial to Evaluate the Effects of High Dose Statin and Niacin Therapy on Excised Plaque Biomarkers in Patients Undergoing Carotid Endarterectomy (CEA) [NCT00804843]Phase 2100 participants (Actual)Interventional2009-04-30Completed
[NCT02609711]Phase 190 participants (Anticipated)Interventional2015-11-30Active, not recruiting
The Use of Statins for Myocardial Death Prevention: From Cell to Bedside [NCT00772564]Phase 425 participants (Actual)Interventional2008-08-31Completed
A Relative Bioavailability Study of Three LY900020 Tablet Formulations in Healthy Chinese Subjects [NCT04047940]Phase 132 participants (Actual)Interventional2019-11-29Completed
Comparison of Pain Relief and Inflammatory Status in Women With Surgically Confirmed Endometriosis Treated With Atorvastatin, Oral Contraceptive or Combined Oral Contraceptives and Atorvastatin: Open Randomized Controlled Trial [NCT00675779]44 participants (Anticipated)Interventional2008-04-30Active, not recruiting
The Effect of Statin Therapy (Atorvastatin) on the Progression of Calcific Valvular Aortic Stenosis [NCT00590135]Phase 459 participants (Actual)Interventional2000-08-31Terminated(stopped due to Poor Reducibility - primary endpoint measure not obtainable)
Assessment of the Effects of Aggressive Atorvastatin Therapy on Myocardial Deformation Characteristics, Vascular Rigidity, 24 Hour ECG Monitoring Parameters and Quality of Life in Patients With STEMI [NCT02590653]Phase 4200 participants (Actual)Interventional2014-10-31Completed
Evaluation of Statin-induced Lipid-rich Plaque Progression by Optical Coherence Tomography (OCT)Combined With Intravascular Ultrasound (IVUS) [NCT01023607]Phase 4120 participants (Actual)Interventional2009-12-31Completed
Quality of Life and Metabolic Alterations in Patients With Statin-Associated Myopathy [NCT00850460]Phase 414 participants (Actual)Interventional2009-02-28Terminated(stopped due to Investigator left institution and no PI has been found to continue the study)
A Three Year, Prospective, Open-label, Study To Evaluate Clinical Efficacy, Safety And Tolerability Of Atorvastatin In Children And Adolescents With Heterozygous Familial Hypercholesterolemia [NCT00827606]Phase 3272 participants (Actual)Interventional2009-03-31Completed
An Open Label, Single Dose, Randomized 2-Way Crossover Study To Estimate The Relative Bioavailability Of Atorvastatin Commercial Tablet, And An Extemporaneous Preparation (EP) Suspension Formulation, In Healthy Subjects [NCT00844376]Phase 412 participants (Actual)Interventional2008-02-29Completed
A Study of the Effect of Oral, Multiple-Dose 300 mg and 900 mg Gemcabene (CI-1027) Administration on the Steady-State Pharmacokinetics of Atorvastatin 80 mg [NCT02587416]Phase 120 participants (Actual)Interventional2002-11-30Completed
China Intensive Lipid Lowering With Statins in Acute Coronary Syndrome [NCT00728013]1,600 participants (Anticipated)Interventional2006-12-31Recruiting
Interest of Statin in Surgical Aortic Stenosis: From Myocardial Preconditioning to Ventricular Reverse Remodeling. [NCT00811330]Phase 360 participants (Anticipated)Interventional2008-12-31Recruiting
Effect of Atorvastatin Therapy on Fibrous Cap Thickness in Coronary Atherosclerotic Plaque as Assessed by Optical Coherence Tomography [NCT00700037]Phase 470 participants (Actual)Interventional2009-08-31Completed
A Phase II Study of Neo-Adjuvant Statin Therapy in Postmenopausal Primary Breast Cancer: A Window-of-Opportunity Study [NCT00816244]Phase 250 participants (Actual)Interventional2009-01-31Completed
Impact of Atorvastatin on the Distribution, Composition, and Metabolism of LDL and HDL Subfractions: A Double-blind Placebo-controlled Phase IV Study With Patients Suffering From Combined Hyperlipidemia and Diabetes. Atorvastatin and LDL Profile in NIDDM [NCT00640549]Phase 441 participants (Actual)Interventional2003-03-31Terminated(stopped due to See termination reason in detailed description.)
Prospective Randomized Study to Assess Impact of Statins in Septic Shock [NCT02681653]40 participants (Actual)Interventional2012-01-31Completed
Effect of Atorvastatin Administration Before Primary Percutaneous Coronary Intervention in Patients With ST-segment Elevation Myocardial Infarction [NCT00610870]173 participants (Actual)Interventional2007-07-31Completed
STACIE: Statins for Reduction of Cardiac Toxicity in Patients Receiving HER2 Targeted Therapy [NCT05559164]Phase 260 participants (Anticipated)Interventional2022-09-19Recruiting
Real Life Experience With Caduet Evaluating Effectiveness, Safety and Tolerability in the Management of Cardiovascular Risk Factors (EXCEL Study) [NCT00579254]112 participants (Actual)Observational2007-12-31Terminated(stopped due to See the termination reason in detailed description.)
Effect of Pitavastatin on Erythrocyte Membrane Fatty Acid Contents in Patients With Chronic Kidney Disease [NCT02863185]Phase 445 participants (Actual)Interventional2016-05-01Completed
Atorvastatin for Prevention of Atrial Fibrillation Recurrence Following Pulmonary Veins Isolation: A Double-Blind, Placebo-Controlled, Randomized Pilot Trial [NCT00579098]Phase 4125 participants (Actual)Interventional2007-12-31Completed
An Open Label, Randomized, Single Dose, Two-Way Crossover Bioequivalence Study Comparing A New 80 Mg Atorvastatin Tablet To A 80 Mg Atorvastatin Commercial Tablet In Healthy Subjects [NCT00917644]Phase 476 participants (Actual)Interventional2008-07-31Completed
A 6-Week, Randomized, Open-Label, Comparative Study to Evaluate the Efficacy and Safety of Rosuvastatin and Atorvastatin in the Treatment of Hypercholesterolaemia in Hispanic Subjects. [NCT00653965]Phase 33,000 participants (Anticipated)Interventional2003-05-31Completed
Safety and Efficacy of Long-Term Treatment With Atorvastatin in Patients With Primary Biliary Cirrhosis [NCT00844402]Phase 340 participants (Actual)Interventional2006-01-31Completed
Effects of Three Statins, Simvastatin, Atorvastatin, and Pitavastatin, on the Pharmacokinetics for Midazolam in Healthy Volunteers [NCT00716846]11 participants (Actual)Interventional2006-06-30Completed
Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) [NCT00620542]Phase 32,333 participants (Actual)Interventional2008-01-31Completed
Evaluation of Long-term Lipid-lowering Therapy on Myocardial Electrical Heterogeneity, Myocardial Deformation, Arterial Stiffness and Quality of Life in Patients With Primary STEMI/NSTEMI With Coronavirus Infection COVID-19 [NCT04900155]45 participants (Actual)Interventional2020-11-20Active, not recruiting
Assessment of the Effects of Long-term Lipid-lowering Therapy on Parameters of Electrical Myocardial Heterogeneity, Myocardial Deformation Characteristics, Vascular Rigidity, and Quality of Life in Patients With Primary STEMI or NSTEMI [NCT04347434]Phase 4300 participants (Anticipated)Interventional2020-02-12Recruiting
Open Label, Comparative, Multiple-dose, Fixed-sequence Steady State Trial in Healthy Volunteers to Assess the Pharmacokinetic Interaction of Candesartan, Atorvastatin and Amlodipine After a Multiple Oral Dose Administration [NCT04245046]Phase 118 participants (Actual)Interventional2019-01-18Completed
Characteristic Study on Chinese Patients With Multiple Sclerosis [NCT00818103]600 participants (Anticipated)Interventional2006-01-31Recruiting
A Series of Randomised Controlled N-of 1 Trials in Patients Who Have Discontinued or Are Considering Discontinuing Statin Use Due to Muscle-related Symptoms to Assess if Atorvastatin Treatment Causes More Muscle Symptoms Than Placebo [NCT02781064]Phase 4200 participants (Actual)Interventional2016-09-01Completed
48 Week Pilot Trial Assessing the Efficacy of Pioglitazone, Atorvastatin, Pegasys and Weight Based Ribavirin in Chronic Hepatitis C, Genotype 1 Patients Who Have Previously Relapsed or Did Not Respond to PegInterferon /Ribavirin Therapy [NCT00926614]Phase 420 participants (Actual)Interventional2008-09-30Completed
A Phase I Prevention Study of Atorvastatin in Women at Increased Risk for Breast Cancer [NCT00637481]Phase 166 participants (Actual)Interventional2008-03-31Completed
Atherosclerotic Plaque Texture-Experimental and Clinical Study on the Diagnostic and Therapeutic Strategies of Atherosclerotic Plaque Vulnerability [NCT00636766]300 participants (Actual)Interventional2005-09-30Completed
Evaluation of the Influence of Statins and Proton Pump Inhibitors on Clopidogrel Antiplatelet Effects [NCT00930670]Phase 4320 participants (Actual)Interventional2009-06-30Completed
The Effect of Statins on Skeletal Muscle Function [NCT00609063]420 participants (Actual)Interventional2008-01-31Completed
Atorvastatin 80mg Versus Atorvastatin 20mg in Perioperative Vascular Surgery to Evaluate Cardiovascular Outcomes [NCT00610545]Phase 4100 participants (Anticipated)Interventional2007-07-31Completed
Plaque Regression and Progenitor Cell Mobilization With Intensive Lipid Elimination Regimen (PREMIER) [NCT01004406]Phase 359 participants (Actual)Interventional2011-09-30Completed
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
The Effect of Acute HMG-CoA-Reductase Inhibition (Atorvastatin) on Renal Sodium Excretion, Renal Hemodynamics, Tubular Function and Vasoactive Hormones in Healthy Subjects During Normal and High Sodium Intake [NCT00678184]Phase 423 participants (Actual)Interventional2007-01-31Completed
The Evaluation of Atorvastatin on Wall Shear Stress, Atherosclerosis Composition, and Microvascular Function in Patients With Moderate Coronary Disease [NCT00576576]27 participants (Actual)Interventional2007-07-31Completed
An Open Label, Randomized, Single Dose, Two-Way Crossover Bioequivalence Study Comparing A New 80 Mg (2x40 mg) Pediatric Appropriate Formulation To A 80 Mg Commercial Atorvastatin Calcium Tablet Formulation In Healthy Subjects [NCT00758004]Phase 176 participants (Actual)Interventional2008-10-31Completed
European Society of Hypertension and Chinese Hypertension League Stroke in Hypertension Optimal Treatment Trial [NCT01563731]Phase 4200 participants (Actual)Interventional2013-04-30Completed
A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Clinical Trial to Evaluate the Safety and Efficacy of Statins in Adult Patients With Non-Alcoholic Steatohepatitis (NASH) [NCT04679376]Phase 270 participants (Anticipated)Interventional2023-01-25Recruiting
EndothelIal progeNitor Cell Capture steNt With 1-mOnth Dual Antiplatelet Therapy Versus eVerolimus-eluting Stent With stAndard 12-month Dual anTIplatelet Therapy in Elderly (≥ 70 Year) With Stable corONary Artery Disease - INNOVATION Trial [NCT01394848]Phase 41 participants (Actual)Interventional2011-10-31Terminated(stopped due to Previous other study including EPC capture stent raised the issue of safety (significant high incidence of instent restenosis))
DIATOR - Diabetes Intervention With Atorvastatin. A Randomized, Double-blind, Placebo-controlled, Parallel Group Study to Investigate the Effect of Atorvastatin on Residual Beta-cell Function and Glycemic Control in Patients With Newly Diagnosed Type 1 Di [NCT00974740]Phase 163 participants (Actual)Interventional2004-03-31Terminated(stopped due to for lack of recruitment)
Usefulness of Atorvastatin (80 mg) in Prevention of Contrast-Induced Nephropathy in Patients With Chronic Renal Disease [NCT00770796]Phase 4304 participants (Actual)Interventional2006-04-30Completed
An Observational Trial of Perioperative Atorvastatin on Inflammatory and Endothelial Function in Patients Undergoing Vascular Surgery (STAR-VaS 2) [NCT00967252]50 participants (Anticipated)Observational2008-11-30Completed
A Year 2, Long-Term, Open-Label, Safety Extension Study of the Combination of ABT-335 and Statin Therapy for Subjects With Mixed Dyslipidemia [NCT00491530]Phase 3310 participants (Actual)Interventional2007-06-30Completed
Yokohama Assessment of Fluvastatin, Pravastatin, Pitavastatin and Atorvastatin in Acute Coronary Syndrome (Yokohama-ACS) [NCT00549926]Phase 4200 participants (Anticipated)Interventional2007-10-31Completed
A Phase II, Fixed-sequenced, Open- Label, Research Study to Assess Pharmacokinetic Drug Interactions of AEGR-733 on Lipid-lowering Therapies in Healthy Volunteers [NCT00359281]Phase 2125 participants (Actual)Interventional2006-03-31Completed
Effects of High-dose Statin Treatments on Patients With Aspirin Mono Antiplatelet Therapy 12-months After Drug-eluting Stents Implantation: a Randomized Controlled Study [NCT01557075]Phase 42,000 participants (Anticipated)Interventional2010-07-31Recruiting
A Randomised, Double-blind Trial to Compare the Efficacy of Rosuvastatin 5 and 10 mg to Atorvastatin 10 mg in the Treatment of High Risk Patients With Hypercholesterolemia Followed by an Open Label Treatment Period With Rosuvastatin Up-titrated to the Max [NCT00683618]Phase 3934 participants (Actual)Interventional2008-05-31Completed
A Study Of The Usage Of Statins In A Community Heart Failure Population: The Impact of HMG Co-Enzyme A Reductase Inhibitors on Heart Structural Parameters, Brain Naturetic Peptide, Markers of Inflammation and Fibrosis [NCT00795912]Phase 456 participants (Actual)Interventional2003-05-31Completed
A Multiple Dose Study to Investigate the Effect of MK0859 on Lipoprotein Metabolism When Added to Ongoing Statin Therapy in Dyslipidemic Patients [NCT00990808]Phase 146 participants (Actual)Interventional2009-11-30Completed
A Phase 4, Multicenter, Randomized, Open-label, Active-controlled Study to Evaluate the Effectiveness and Safety of Early add-on of Ezetimibe With Atorvastatin in Very High-risk Patients [NCT05761444]Phase 4126 participants (Anticipated)Interventional2023-07-26Recruiting
"An Open-Label, Randomized, Parallel-Group, Multicenter Study to Compare the Efficacy and Safety of Switching to Rosuvastatin 10 mg Daily Versus Atorvastatin 10 mg Daily With Ezetimibe 10 mg Daily Versus Doubling the Dose of Atorvastatin to 20 mg Daily in [NCT00651378]Phase 487 participants (Actual)Interventional2004-09-01Terminated(stopped due to Slow enrollment [HIGH SCREEN FAILURE RATE])
The Success of Opening Single CTO Lesions to Improve Myocardial Viability Study (SOS-comedy) [NCT02767401]Phase 4200 participants (Actual)Interventional2015-09-15Completed
Randomized Placebo-controlled Crossover Trial of Endothelial Function Improvement in Subjects With History of Premature Coronary Artery Disease [NCT00917527]Phase 477 participants (Anticipated)Interventional2009-06-30Recruiting
Intracranial Hemorrhage Risk of Intensive Statin Therapy in Patients With Acute Ischemic Stroke Combined With Cerebral Microbleeds [NCT05589454]Phase 4344 participants (Anticipated)Interventional2023-01-31Not yet recruiting
An Open-label, Randomized, Multiple-dose, Replicated Crossover Study to Evaluate Drug-drug Interaction Following Co-administration of Tegoprazan or RAPA114 With Atorvastatin in Healthy Adults [NCT04221321]Phase 132 participants (Actual)Interventional2020-01-07Completed
Efficacy, Safety and Tolerability of Atorvastatin 40 mg in Patients With Relapsing-remitting Multiple Sclerosis Treated With Interferon-beta-1b.SWiss Atorvastatin and Interferon-Beta 1b Trial In Multiple Sclerosis. [NCT00942591]Phase 277 participants (Actual)Interventional2005-05-31Completed
The Renal Protective Effects of Low-dose and High-dose Atorvastatin in Patients With Glomerular Disease and Proteinuria: a Randomized Controlled Double Blinded Study [NCT00768638]Phase 423 participants (Actual)Interventional2008-10-31Completed
The Mission Connect Mild TBI Translational Research Consortium's Integrated Clinical Protocol [NCT01013870]Phase 252 participants (Actual)Interventional2010-02-28Terminated(stopped due to inability to recruit adequate numbers of subjects)
Effect of Atorvastatin on Inflammatory Atherosclerotic Plaques Assessed by FDG-PET Imaging [NCT00920101]Phase 430 participants (Anticipated)Interventional2009-06-30Recruiting
Impact of Early High-dose Atorvastatin Versus Rosuvastatin on Contrast Induced Acute Kidney Injury in Unselected Patients With Non- ST Elevation Acute Coronary Syndromes Scheduled for Early Invasive Strategy. [NCT01870804]Phase 4760 participants (Actual)Interventional2013-05-31Completed
Aspirin Statins Or Both For The Reduction Of Thrombin Generation In Diabetic People [NCT00793754]Phase 430 participants (Actual)Interventional2009-03-31Completed
Pharmaco-metabolomic Effects of Statins: METASTATINE [NCT03837925]Phase 3120 participants (Actual)Interventional2019-06-13Completed
The Effect of Efavirenz and Nelfinavir on the Pharmacokinetics of Hydroxymethylglutaryl Coenzyme A Reductase Inhibitors [NCT00017758]Phase 156 participants InterventionalCompleted
A Multi-Center, Randomized, Open-Label Study To Evaluate Efficacy And Safety Of Dual Therapy With Atorvastatin Plus Amlodipine When Compared Amlodipine Therapy Alone In The Treatment Of Subjects With Concurrent Hyperlipidemia And Hypertension. [NCT00174330]Phase 4330 participants Interventional2005-05-31Completed
[NCT02942602]58 participants (Actual)Interventional2014-04-03Completed
A Double-Blind, Randomized, Placebo- Controlled Study Of Atorvastatin As Prevention Of Cerebrovascular Events In Patients With A Previous Transient Ischemic Attack (TIA) Or Stroke [NCT00147602]Phase 44,732 participants Interventional1998-11-30Completed
A Multicenter, 12 Week Treatment Single Step Titration Open-Label Study Assessing The % Of Patients Achieving Ldl-C Target With Atorvastatin Starting Doses Of 10mg, 20mg, 40mg and 80mg. [NCT00150371]Phase 31,100 participants Interventional2004-06-30Completed
A Randomized, Double-blind, Placebo-controlled, Parallel Group Study to Assess the Effect of Atorvastatin Treatment for 14 Days in Combination With an Acute Dose of Ticagrelor on Ischemia Reperfusion Induced Endothelial Dysfunction of the Forearm Vasculat [NCT02910778]Phase 432 participants (Actual)Interventional2016-10-31Completed
Statin-Induced Vulnerable Plaque Regression After Atorvastatin Treatment: Serial Evaluation by 18F-Fluorodeoxyglucose Positron Emission Tomography Study [NCT00172419]43 participants (Actual)Interventional2007-03-31Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-way Crossover Oral BE Study of Atorvastatin Ca 80 mg Tablets of Dr. Reddy's and Lipitor 80 mg Tablets of Pfizer in Healthy Adult, Human Subjects Under Fed Conditions [NCT01645423]Phase 177 participants (Actual)Interventional2009-08-31Completed
Phase 4 Study of Atorvastatin 10mg vs. 40mg in Follow-up CFR in AMI Patients [NCT00536887]Phase 4100 participants (Anticipated)Interventional2005-07-31Completed
A Single Center, Randomized, Parallel Groups, Placebo-Controlled Study Comparing The Efficacy, Safety, And Tolerability Of The Daily Co-administration Of Ezetimibe 10 Mg Or Ezetimibe Placebo To Ongoing Treatment With Atorvastatin 10 Mg In Subjects With Pr [NCT00319449]Phase 422 participants (Actual)Interventional2005-09-30Completed
A Multicenter, Rand., Double-Blind, Titration Study to Evaluate & Compare the Efficacy & Safety of Ezetimibe Plus Atorvastatin Vs Atorvastatin in Hypercholesterolemic Pts. at High Risk for CHD Not Adequately Controlled on Atorvastatin 40 Mg [NCT00276484]Phase 3579 participants (Actual)Interventional2006-02-28Completed
Using AtorVASTatin to Prevent VAscular Inflammatory OccLUSion in the Critically Ill [NCT01073800]Phase 2/Phase 3100 participants (Anticipated)Interventional2009-04-30Completed
Effect of Intensive Statin Treatment on 90-day Prognosis of STEMI Patients Undergoing Emergency Primary PCI Compared With Usual Care [NCT01033058]Phase 4500 participants (Anticipated)Interventional2009-12-31Not yet recruiting
Intensive Lipid Lowering Treatment in Patients With Non-ST-elevation ACS Undergoing Percutaneous Coronary Intervention [NCT01040936]Phase 4300 participants (Anticipated)Interventional2010-05-31Recruiting
A 6-week, Randomised, Open-label, Parallel Group, Multi-centre Study to Compare the Efficacy of Rosuvastatin 10mg With Atorvastatin 10mg in the Treatment of Metabolic Syndrome Subjects With Raised LDL-C [NCT00395486]Phase 4258 participants (Actual)Interventional2006-09-30Completed
Double-Blind Study of Atorvastatin Versus Placebo to Reduce Cardiopulmonary Complications After Thoracic Surgery [NCT00375518]162 participants (Actual)Interventional2006-07-31Completed
A Double Blinded Randomized Placebo Controlled Study: To Investigate the Role of Upstream High Dose Statin Treatment in Patients With ST Segment Elevation Myocardial Infarction [NCT01050348]Phase 4120 participants (Actual)Interventional2009-06-30Completed
A Randomized Placebo Controlled Trial of Atorvastatin in HIV Positive Patients Not on Antiretroviral Medications With the Specific Aims of Studying the Effects of Atorvastatin on HIV Viral Load and Immune Activation Markers [NCT00367458]Phase 224 participants (Actual)Interventional2006-10-18Completed
Survival Benefits of Statins in Breast Cancer Patients With Abnormal Lipid Metabolism [NCT03971019]Phase 3314 participants (Anticipated)Interventional2019-03-28Recruiting
Targeting Cerebrovascular Reactivity for Precision Medicine: Pilot Trial of Atorvastatin [NCT04765137]Phase 220 participants (Anticipated)Interventional2021-05-21Recruiting
Randomised, Double-blind, 52-wk, Parallel-grp Multicentre, PIIb Study to Evaluate Effects of Rosuvastatin 10mg, Rosuvastatin 40mg and Atorvastatin 80mg on Urinary Protein Excretion in Hypercholesterolaemic Non-diabetic Patients With Moderate Proteinuria [NCT00296400]Phase 2237 participants (Actual)Interventional2006-02-28Completed
Atorvastatin as a Disease Modifying Agent in Stage II and III Pulmonary Sarcoidosis: A Randomized, Double-Blind, Placebo-Controlled Trial [NCT00279708]Phase 255 participants (Actual)Interventional2006-01-31Completed
Caduet® Drug Use Investigation (Regulatory Post Marketing Commitment Plan) [NCT01107743]1,291 participants (Actual)Observational2010-06-30Completed
Effects of Intensive Statin Therapy on Left Ventricular Function for Patients With the First Acute Anterior Myocardial Infarction After Directly to Percutaneous Coronary Intervention. [NCT01936103]Phase 4120 participants (Anticipated)Interventional2012-04-30Recruiting
Early Therapeutic Effects of Statins and Fibrates on Unstable Atherosclerotic Plaques: a Randomised Microarray-Study on Endarterectomy Specimens of Human Carotid Arteries [NCT00243672]Phase 4100 participants (Anticipated)Interventional2005-10-31Withdrawn(stopped due to The study chair changed his employment, the realization of the study was not possible)
Short Term Effects of HMG-CoA Reductase Inhibition (Atorvastatin)on Renal Hemodynamics, Tubular Function and Vasoactive Hormones on Healthy Subjects. [NCT00345202]Phase 420 participants Interventional2004-09-30Completed
Efficacy and Safety of Fenofibrate Added on to Atorvastatin Compared With Atorvastatin in Mixed Hypercholesterolemic Patient: Multi Center, Randomized, Double-blind, Parallel-group, Therapeutic Confirmatory Study. [NCT01956201]Phase 3476 participants (Anticipated)Interventional2013-12-31Recruiting
A Multi-center, Randomized, Double-blind, Active-controlled, Phase 3 Clinical Trial to Evaluate the Safety and Efficacy of Metformin/Atorvastatin Combination Therapy in Subjects With Type II Diabetes and Dyslipidemia [NCT02947620]Phase 3185 participants (Actual)Interventional2015-08-31Completed
A Multi-Centre, Randomised, Double-Blind, Placebo-Controlled, Parallel-Group Study of TA-8995 in Patients With Mild Dyslipidaemia, Alone and In Combination With Statin Therapy [NCT01970215]Phase 2364 participants (Actual)Interventional2013-08-31Completed
Comparison of the Efficacy and AtorVastatin 20mg mOnotherapy Versus Combination Atorvastatin/Fenofibric Acid 10/135mg in the Mixed hyperlipiDemia Who Were Not at Lipid gOals With Atorvastatin 10mg Monotherapy. [NCT01974297]194 participants (Anticipated)Interventional2013-07-31Recruiting
Sequential Therapy of Atorvastatin Improving Tissue Reperfusion and Clinical Outcomes of ST-elevated Acute Myocardial Infarction Study(The STRAIT Study) [NCT01997294]1,200 participants (Actual)Interventional2013-01-31Active, not recruiting
Randomized Trial of the Association Between Low-Dose Statins and Nutraceuticals in High-intEnsity Statin-intoleRant patiENts With Very High Risk Coronary Artery diseasE [NCT02001883]Phase 4100 participants (Anticipated)Interventional2013-11-30Recruiting
A Randomized, Double Blind, Parallel, Multi-center, Phase 3 Clinical Trial to Evaluate the Efficacy and Safety of DW1125 and DW1125A in Patient With Primary Hypercholesterolemia or Mixed Dyslipidemia [NCT05970679]Phase 3252 participants (Actual)Interventional2022-08-17Completed
Statin Therapy to Improve Inflammation and Atherosclerosis in HIV Patients [NCT00965185]40 participants (Actual)Interventional2009-09-30Completed
A Randomized, Double-blind, Parallel-group, Placebo-controlled, Fixed Dose/Dose Regimen, Multicenter Study Evaluating the Efficacy and Safety of SAR236553 When Co-administered With 80 mg of Atorvastatin Over 8 Weeks in Patients With Primary Hypercholester [NCT01288469]Phase 292 participants (Actual)Interventional2011-01-31Completed
Atorvastatin in Preventing Nasopharyngeal Carcinoma Patients Receiving Radiotherapy From Carotid Stenosis: A Multicenter, Double-blind, Placebo-Controlled, Randomized Trial [NCT02022293]Phase 2324 participants (Anticipated)Interventional2017-01-31Suspended(stopped due to Enrollment target could not be achieved.)
The Effect of Single Dose of Atorvastatin on Change of Circulating Endothelial Microparticles [NCT02023892]Phase 430 participants (Anticipated)Interventional2014-06-30Not yet recruiting
Multi-Center, Randomized, Placebo-Controlled, Double Blind Study of the Atorvastatin: Effect on Patients With Chronic Subdural Hematoma [NCT02024373]Phase 2200 participants (Actual)Interventional2013-12-31Completed
Effect of Acupoint Application With Herbal Medicine in Patients With Stable Angina Pectoris: Randomized, Controlled,Double Blind Clinical Study [NCT02029118]Early Phase 1200 participants (Actual)Interventional2012-10-31Completed
Intensive Statin Therapy Effect on Incidence of Post-Operative Atrial Fibrillation [NCT02029534]Phase 4200 participants (Anticipated)Interventional2013-08-31Recruiting
Phase II Study of Atorvastatin in Combination With Radiotherapy and Temozolomide in Glioblastoma [NCT02029573]Phase 236 participants (Actual)Interventional2014-01-01Completed
Phase III Interventional Study Using Atorvastatin to Reduce Cisplatin-Induced Hearing Loss Among Individuals With Head and Neck Cancer [NCT04915183]Phase 3186 participants (Anticipated)Interventional2024-01-03Not yet recruiting
Influence of Adding Atorvastatin to Dual Renin-Angiotensin-Aldosterone System Blockade on Proteinuria [NCT00572312]0 participants Interventional2005-02-28Completed
The Effect of Chronic Statin Therapy on Peripheral Arterial Tone Response to Sildenafil Citrate (Viagra), and on Erectile Function in Men With Coronary Artery Endothelial Cell Dysfunction [NCT00587379]0 participants (Actual)Interventional2004-06-30Withdrawn(stopped due to Study closed per the request of PI due to lack of participant accrual)
Effectiveness and Safety of Low Intracranial Pressure Treatment Strategies for Patients With Chronic Subdural Hematoma - A Randomized, Controlled, Multi-center Clinical Study [NCT04607447]160 participants (Anticipated)Interventional2020-08-04Recruiting
A Randomized, Double-blind, Placebo-controlled, Parallel Group Study to Evaluate the Safety and Efficacy of the Combination of AEGR-733 (Formerly BMS201038) and Atorvastatin 20 mg vs. Monotherapy in Subjects With Moderate Hypercholesterolemia [NCT00474240]Phase 2157 participants (Actual)Interventional2007-04-30Completed
A Multicenter, Randomized, Double-Blind, Parallel Group, 12 Week Study to Evaluate the Efficacy and Safety of Extended-release (ER) Niacin/Laropiprant in Patients With Primary Hypercholesterolemia or Mixed Dyslipidemia. [NCT00479388]Phase 31,216 participants (Actual)Interventional2007-07-31Completed
Open-label, Balanced, Randomized, Two-treatment, Two-sequence, Two-period, Single Oral Dose, Crossover BE Study of Atorvastatin Ca 40mg Tablets of Dr.Reddy's With Lipitor® 40 mg Tablets of Pfizer in Healthy Subjects Under Fed Conditions [NCT01645410]Phase 171 participants (Actual)Interventional2009-03-31Completed
An Open Label, Balanced, Randomized, Two-treatment, Two-period, Two-way Crossover Oral BE Study of Atorvastatin Ca 80 mg Tablets of Dr. Reddy's and Lipitor 80 mg Tablets of Pfizer in Healthy Adult, Human Subjects Under Fasting Conditions [NCT01645449]Phase 177 participants (Actual)Interventional2010-06-30Completed
Effect of Atorvastatin Versus Rosuvastatin Intensive Statin Regimens on Chinese Elderly Patients Undergoing Percutaneous Coronary Intervention [NCT01646307]Phase 41,000 participants (Anticipated)Interventional2012-01-31Recruiting
The Role of Androgen Deprivation Therapy In Cardiovascular Disease - A Longitudinal Prostate Cancer Study (RADICAL PC1) & A RAndomizeD Intervention for Cardiovascular and Lifestyle Risk Factors in Prostate Cancer Patients (RADICAL PC2) [NCT03127631]6,000 participants (Anticipated)Interventional2015-10-21Recruiting
Extra Alirocumab in Addition to Statin Therapy in Asymptomatic Intracranial Atherosclerotic Stenosis (EAST-aICAS)----a Pilot Study [NCT06080256]Phase 380 participants (Anticipated)Interventional2023-12-30Not yet recruiting
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 Phase I, 2-Panel, Open-Label Study in Healthy Subjects to Investigate the Pharmacokinetic Interaction Between TMC435 and the HMG-CoA Reductase Inhibitors Atorvastatin and Simvastatin [NCT01689623]Phase 136 participants (Actual)Interventional2012-06-30Completed
A Prospective, Randomized, Crossover Evaluation of the Effect of Atorvastatin on the Pharmacokinetics of Irinotecan in Colorectal Cancer Patients Receiving FOLFIRI [NCT01605344]Phase 10 participants (Actual)Interventional2012-04-30Withdrawn(stopped due to Study was withdrawn due to lack of patient enrollment.)
An Open-label Study of the Effect of ALT-801 on the Pharmacokinetics of Metformin, Warfarin, Atorvastatin, Digoxin, and the Combined Oral Contraceptive Ethinylestradiol/Levonorgestrel in Healthy Volunteers [NCT04972396]Phase 140 participants (Actual)Interventional2021-10-05Completed
Evaluation of Carotid Intima Media Thickness by Treatment of Vascular and Metabolic Factors With Combined Antihypertensive and Hypolipidemic Therapy [NCT04306627]Phase 4200 participants (Anticipated)Interventional2020-04-15Not yet recruiting
Short-term Atorvastatin's Effect on Acute Kidney Injury Following Cardiac Surgery [NCT00791648]653 participants (Actual)Interventional2009-07-31Completed
Impact of Combined Ezetimibe and Atorvastatin Therapy on Coronary Thin-cap Fibroatheroma As Assessed by Optical Coherence Tomography [NCT02588235]Phase 4100 participants (Anticipated)Interventional2015-10-31Recruiting
Naturopathic Treatment for the Prevention of Cardiovascular Disease: a Pragmatic Randomized Controlled Trial [NCT00718796]Phase 3300 participants (Anticipated)Interventional2008-04-30Completed
Phase 3 Study of Effect of ATorvastatin on Fractional Flow Reserve in Coronary Artery Disease [NCT01946815]Phase 3119 participants (Actual)Interventional2013-09-30Completed
Platelet Rich Fibrin Combined With 1.2% Atorvastatin Gel in Treatment of Mandibular Degree II Furcation Defects: a Randomized Controlled Clinical Trial [NCT02612792]Phase 2/Phase 382 participants (Actual)Interventional2014-12-31Completed
Effect of Atorvastatin and Lifestyle Intervention on Progression of Carotid Intima-Media Thickness in Chinese People Without Manifest Atherosclerotic Disease [NCT00723320]1,200 participants (Anticipated)Interventional2008-02-29Recruiting
Carotid Endarterectomy Versus Optimal Medical Treatment of Asymptomatic High Grade Carotid Artery Stenosis [NCT00805311]Phase 4400 participants (Actual)Interventional2009-04-30Terminated(stopped due to Due to the clear advantage of carotid endarterectomy)
A Randomized Double Blind Study Of The Evaluation Of The Potential Analgesic And Anti-Inflammatory Effects Of Atorvastatin In Patients Undergoing Abdominal Surgery [NCT00902967]Phase 340 participants (Anticipated)Interventional2009-07-31Not yet recruiting
Phase 3 Multi-Center, Double-Blind, Randomized, Parallel Group, Forced Titration Study Of The Efficacy, Safety, And Tolerability Of Torcetrapib/Atorvastatin Compared To Fenofibrate In Subjects With Fredrickson Type IIB Dyslipidemia (Mixed Hyperlipidemia [NCT00139061]Phase 3128 participants Interventional2005-03-31Completed
Efficacy Evaluation of Metabolic, Anti-inflammatory, and Antioxidative Factors of Irbesartan/Atorvastatin Fixed-dose Combination in Type 2 Diabetic Patients Diagnosed With Hyperlipidemia and Hypertension, With Adequately Controlled Blood Glucose Levels [NCT02842359]Phase 411 participants (Actual)Interventional2016-08-23Completed
Randomized Controlled Trial of Early Versus Late Statin Therapy in Patients With Ischemic Stroke [NCT02549846]Phase 4270 participants (Actual)Interventional2015-09-30Completed
A Phase I, Single Centre, Open-label Study to Assess the Pharmacokinetics of Both AZD5672 (Steady-state) and Atorvastatin (Single Dose) When Co Administered in Healthy Volunteers [NCT00722956]Phase 112 participants (Anticipated)Interventional2008-07-31Completed
A 26-Week, Double Blind, Randomised, Multi-Centre, Phase IIIb, Parallel Group Study to Compare the Efficacy and Safety of Rosuvastatin (40 mg) With Atorvastatin (80 mg) in Subjects With Hypercholesterolaemia and Coronary Heart Disease or CHD Risk Equivale [NCT00653588]Phase 30 participants Interventional2003-04-30Completed
Comparison Between Combined Therapy With Red Yeast Rice and Low-dose Statin and Standardized Statin: a Single-center, Non-inferiority, Randomized Clinical Trial [NCT02726555]Phase 3240 participants (Anticipated)Interventional2015-11-30Recruiting
A 6-Week, Randomized, Open-Label, Comparative Study to Evaluate the Efficacy and Safety of Rosuvastatin Versus Atorvastatin in the Treatment of Hypercholesterolaemia in African American Subjects. (ARIES) [NCT00653744]Phase 31,700 participants (Anticipated)Interventional2002-03-31Completed
A 4-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study Evaluating the Safety and Efficacy of JTT-705 600 mg Versus Placebo Administered Once Daily in Combination With Atorvastatin 20 mg in Patients With Low HDL Levels [NCT00689442]Phase 2105 participants (Actual)Interventional2004-01-31Completed
Comparison of the Effects Noted in The ApoB/ApoA-I Ratio Using Rosuvastatin and Atorvastatin in Patients With acUte Coronary Syndrome - CENTAURUS [NCT00296387]Phase 31,160 participants (Anticipated)Interventional2006-01-31Completed
Comparison of the Effect Noted in The Apo/Apo-1 Ratio Using Rosuvastatin and Atorvastatin in Patients With acUte Coronary Syndrome CENTAURUS Study [NCT00665834]Phase 418 participants (Actual)Interventional2006-04-30Completed
Oral High-Dose Atorvastatin Treatment in Relapsing-Remitting Multiple Sclerosis [NCT00616187]Phase 241 participants (Actual)Interventional2003-10-31Completed
A 12-Week, Multi-Center, Double-Blind, Randomized, Parallel-Group Study, Followed by a 12 Month Extension Study, of the Efficacy and Safety of LCP-AtorFen in Subjects With Dyslipidemia [NCT00504829]Phase 2220 participants (Actual)Interventional2007-07-31Completed
A Decentralized Phase II Randomized Controlled Trial of Atorvastatin in Resected High-Risk Melanoma [NCT06157099]Phase 2150 participants (Anticipated)Interventional2024-01-01Not yet recruiting
The Effects of Atorvastatin on the Occurrence of Postoperative Atrial Fibrillation After Off-Pump Coronary Artery Bypass Grafting Surgery [NCT00611143]124 participants (Actual)Interventional2006-05-31Completed
Clinical Effect and Tolerability of Atorvastatin Versus Placebo in Patients With Pulmonary Hypertension: Double-blinded, Randomised, Prospective Phase II Study for 6 Months With Adjusted Doses of Atorvastatin [NCT00615823]Phase 2220 participants (Actual)Interventional2007-02-28Completed
Non Interventional (NI) Open Label Prospective Study On Liprimar (Atorvastatin) In Patients With Coronary Heart Disease (CHD) And High Risk Of Cardiovascular Complications [NCT00993915]687 participants (Actual)Observational2010-04-30Completed
A Multicenter, Eight-Week Treatment, Single Step Titration, Open-Label Study Assessing The Percentage Of Subjects Achieving Low Density Lipoprotein Cholesterol Target With Atorvastatin Starting Doses Of 10 Mg, 20 Mg, 40 Mg, And 80 Mg (Latin American Atorv [NCT00645151]Phase 4512 participants (Actual)Interventional2004-04-30Completed
Acetazolamide and Statins for the Treatment of Chronic Mountain Sickness in Highlanders: A Randomized Controlled Trial [NCT04251364]60 participants (Anticipated)Interventional2020-02-15Recruiting
A Study to Evaluate the Definitive Bioequivalence of SCH 900068 With Marketed Products (Protocol No. P07551) [NCT01236430]Phase 1200 participants (Actual)Interventional2011-02-28Completed
A Multicenter, Randomized, Open-label Study to Evaluate the Lipid-Altering Efficacy and Safety of Ezetimibe (+) Simvastatin Versus Atorvastatin in Hypercholesterolemic Patients With Diabetes Mellitus or Metabolic Syndrome [NCT00157924]Phase 4190 participants (Actual)Interventional2005-11-30Completed
Phase 2 Study Of The Effects Of Open-Label CP-690,550 And Double-Blind Atorvastatin On Lipids In Patients With Active Rheumatoid Arthritis [NCT01059864]Phase 2111 participants (Actual)Interventional2010-02-28Completed
Phase 3 Study of Atorvastatin Effects on Carotid Atherosclerosis [NCT00640744]Phase 412 participants (Anticipated)Interventional2006-02-28Recruiting
A Randomized, 12-Week, Open Labeled Study To Evaluate The Efficacy And Safety Of Once Daily Atorvastatin In Diabetes Mellitus Type 2 With Hyperlipidemia [NCT00645424]Phase 4155 participants (Actual)Interventional2003-12-31Completed
A Randomized, Double-Blind, Active-Controlled, Multicenter Study of Patients With Primary Hypercholesterolemia and High Cardiovascular Risk Who Are Not Adequately Controlled With Atorvastatin 10 mg: A Comparison of the Efficacy and Safety of Switching to [NCT01154036]Phase 31,547 participants (Actual)Interventional2010-07-31Completed
Repurposing Atorvastatin in Patients With Ulcerative Colitis Treated With Mesalamine by Modulation of mTOR/NLRP3 Pathway. [NCT05567068]Phase 244 participants (Anticipated)Interventional2023-02-01Recruiting
Combination of Atorvastatin and Mesalazine to Enhance Anti-inflammatory Effects and Attenuates Progression of Ulcerative Colitis [NCT05561062]Phase 250 participants (Anticipated)Interventional2022-12-01Recruiting
Statins in Children With Type 1 Diabetes: Effects on Metabolism, Inflammation and Endothelial Function [NCT01236365]Phase 342 participants (Actual)Interventional2010-10-31Completed
Standard Medical Management in Secondary Prevention of Ischemic Stroke in China. [NCT00664846]4,000 participants (Anticipated)Interventional2008-04-30Completed
Statins and Breast Cancer Biomarkers [NCT00914017]Phase 2100 participants (Anticipated)Interventional2005-01-31Recruiting
[NCT00120055]Phase 40 participants Interventional2005-02-28Completed
Efficacy and Safety of Chinese Herbal Medicine Wen Xin Granules for the Treatment of Unstable Angina Pectoris With Yang Deficiency and Blood Stasis Syndrome: Study Protocol for a Randomized Controlled Trial [NCT04661709]Phase 4502 participants (Anticipated)Interventional2021-03-01Not yet recruiting
Vascular Endothelial Receptor Activity in Patients With Coronary Artery Disease on Medication With Statins [NCT00329069]50 participants Interventional2002-05-31Completed
[NCT00432354]Phase 2/Phase 340 participants Interventional2007-03-31Recruiting
The Effect of Statins on D-dimer Levels in Patients With a Previous Venous Thromboembolic Event [NCT00437892]Phase 210 participants (Actual)Interventional2007-05-31Terminated(stopped due to Competitive trials and slow recruitment rate)
Effects of Atorvastatin Versus Probucol on Low-Density Lipoprotein Subtype Distribution and Renal Function in Hyperlipidemic Patients With Non-Diabetic Nephropathy [NCT00276133]Phase 424 participants (Actual)Interventional2004-01-31Completed
Comparison of the Treatment Efficacy of Rosuvastatin Versus Atorvastatin Loading Prior to Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction [NCT04974814]99 participants (Anticipated)Interventional2021-05-26Recruiting
Confirmatory Study of the Efficacy and Safety of the Fixed-dose Combination Atorvastatin / Fenofibrate Versus Atorvastatin on the Lipid Profile of Patients With Type 2 Diabetes (T2D) and Dyslipidaemia (DLP). [NCT04882293]Phase 378 participants (Anticipated)Interventional2022-02-15Recruiting
A Clinical Observational Trail on Atorvastatin Regulates Intestinal Flora and Metabolomics. [NCT04215237]30 participants (Anticipated)Interventional2017-11-13Recruiting
Effect of Atorvastatin on Subclinical Atherosclerosis in Virally-suppressed HIV-infected Patients With CMV Seropositivity: a Randomized Double-blind Placebo-controlled Trial [NCT04101136]80 participants (Anticipated)Interventional2019-09-30Enrolling by invitation
Effect of Virgin Coconut Oil (VCO) on Cardiometabolic Parameters in Patients With Dyslipidemia: A Randomized, add-on, Placebo-controlled Clinical Trial [NCT03906539]Phase 4150 participants (Actual)Interventional2019-05-22Completed
The Effect of Statin Use on Vascular Function in Hypertensive Subjects [NCT00181181]Phase 424 participants (Actual)Interventional2003-05-31Terminated(stopped due to Coronary flow by echo Doppler was obtainable in about 50% of subjects. The study was stopped early because of insufficient sample size to achieve adequate power)
Clinical Utility Of Caduet In Simultaneously Achieving Blood Pressure And Lipid Endpoints In A Specific Patient Population (CAPABLE) [NCT00150384]Phase 4500 participants Interventional2004-07-31Completed
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
Medroxyprogesterone Acetate Plus Atorvastatin in Young Women With Atypical Endometrial Hyperplasia and Early Endometrial Carcinoma [NCT05675787]Phase 282 participants (Anticipated)Interventional2023-01-06Recruiting
[NCT01856374]Phase 460 participants (Actual)Interventional2011-08-31Completed
[NCT01857921]290 participants (Actual)Interventional2010-12-31Completed
A Randomized, Double-blind, Placebo-controlled, Single Dose, Parallel Group Study to Assess the Safety, Tolerability, Bioavailability, Pharmacokinetics, and Pharmacodynamics of Subcutaneous LGT209 in Hypercholesterolemic Patients on Stable Doses of Atorva [NCT01859455]Phase 125 participants (Actual)Interventional2011-07-31Completed
A Phase 2 Multiple-Dose Study to Characterize the Pharmacokinetics of RVX000222 Capsule Formulation in Combination With Either Atorvastatin or Rosuvastatin in Patients With Dyslipidemia [NCT01863225]Phase 213 participants (Actual)Interventional2013-05-31Terminated
Anti-inflmmation Treatment in Mood Disorder and Deep Learning Prediction Model [NCT04685642]Phase 4180 participants (Anticipated)Interventional2020-08-24Recruiting
A Double Blinded, Randomized Study Comparing the Effectiveness of Fish Oil Supplements, Oral Statins, and Placebo in Reducing the Incidence of Atrial Fibrillation Following a Lung Resection in Patients With Lung Cancer [NCT01259284]Phase 2/Phase 32 participants (Actual)Interventional2011-01-31Terminated(stopped due to Terminated due to low accrual.)
Mechanisms and Interventions to Address Cardiovascular Risk of Gender-affirming Hormone Therapy in Trans Men [NCT04922424]Phase 10 participants (Actual)Interventional2022-09-30Withdrawn(stopped due to not funded)
A Placebo-Controlled, Randomized, Double-Blind, Parallel Group, Drug Interaction Study to Evaluate the Safety, Tolerability and Effect on Atorvastatin Pharmacokinetics of ETC-1002 Added to Atorvastatin 10 mg/Day in Subjects With Hypercholesterolemia [NCT01779453]Phase 258 participants (Actual)Interventional2012-12-31Completed
Double-blind, Randomized, Placebo-controlled Trial to Evaluate the Safety and Efficacy of Atorvastatin to Reduce Inflammation After Tuberculosis Treatment Completion in HIV-infected and HIV-uninfected Adults Measured by FDG-PET/CT [NCT04147286]Phase 2/Phase 3220 participants (Anticipated)Interventional2020-07-14Recruiting
Long-Term, Open-Label, Safety and Tolerability Study of Ezetimibe (SCH 58235) in Addition to Atorvastatin in Subjects With Coronary Heart Disease or Multiple Risk Factors and With Primary Hypercholesterolemia Not Controlled by a Starting Dose (10 mg) of A [NCT03882996]Phase 3432 participants (Actual)Interventional2000-10-06Completed
A Phase 1, Randomized, Double-blind, Placebo-controlled Study To Assess Safety, Tolerability, And Pharmacokinetics Of Multiple Oral Doses Of Pf-06835919 In Healthy Adult Subjects (Part A); And An Open-label Study To Assess Multiple Oral Doses Of Pf-068359 [NCT03031119]Phase 162 participants (Actual)Interventional2017-01-31Completed
[NCT02084069]Phase 358 participants (Actual)Interventional2013-01-31Completed
The Effect of Atorvastatin on Endothelial Cell Dysfunction in Chronic Kidney Disease [NCT02133534]Phase 41 participants (Actual)Interventional2008-02-29Terminated(stopped due to failure to enroll)
A Randomized, Double-blind, Placebo-controlled, Parallel-group Study to Evaluate Low Doses of the MTP-Inhibitor AEGR-733 on Hepatic Fat Accumulation as Measured by Magnetic Resonance Spectroscopy [NCT00559962]Phase 2260 participants (Actual)Interventional2007-10-31Completed
Randomized Comparison Multicenter Trial of High Dose Atorvastatin Pre-treatment on Microcirculatory Dysfunction After Drug-ElutIng Stent Implantation in Patients With Acute Coronary Syndrome [NCT01491256]100 participants (Anticipated)Interventional2010-02-28Recruiting
Statin Combination Therapy in Patients Receiving Sorafenib for Advanced Hepatocellular Carcinoma: A Randomized Controlled Study [NCT03275376]Phase 234 participants (Actual)Interventional2017-12-21Terminated(stopped due to Slow in patient enrollment)
Dose Finding Trial of Rosuvastatin and Atorvastatin Versus Hepatitis C [NCT00446940]Phase 216 participants (Anticipated)Interventional2006-12-31Completed
A Randomized Clinical Trial Of Atorvastatin 10 Mg And 80 Mg In The Reversal Of Or Stabilization Of Carotid Atheroma Lipid Pool [NCT00343655]Phase 3160 participants Interventional2007-01-31Terminated(stopped due to The study was terminated on June 22, 2007 for inability to enroll patients within an appropriate timeframe. There were no efficacy/safety concerns.)
[NCT00454545]Phase 212 participants (Anticipated)Interventional2006-10-31Completed
Atorvastatin Pre-Treatment Influences the Risk of Percutaneous Coronary Intervention Study [NCT00469326]Phase 3200 participants (Actual)Interventional2005-04-30Completed
Effect of Statins on Asthma Control and Airway Inflammation in Smokers With Asthma: a Randomised Controlled Double-blind Parallel Group Study [NCT00463827]Phase 271 participants (Actual)Interventional2007-08-31Completed
A Multicenter, Open Labeled, Cross-Over Designed Prospective Study Evaluating the Effects of Lipid Lowering Treatment on Steroid Synthesis [NCT00433823]Phase 40 participants Interventional2007-01-31Recruiting
"The Effect on Endothelial Progenitor Cells (EPCs) by Statin Loading in All Comers With an Acute Coronary Syndrome (ACS)" [NCT02957162]Phase 440 participants (Actual)Interventional2016-03-31Completed
ACTFAST (2): Achieve Cholesterol Targets Fast With Atorvastatin Stratified Titration: A Multicenter, Twelve-Week Treatment, Single-Step Titration, Open-Label Study Assessing The Percentage Of Dyslipidemic High-Risk Patients Achieving Low Density Lipoprote [NCT00442325]Phase 4595 participants Interventional2003-01-31Completed
Does Atorvastatin Reduce Ischemia-Reperfusion Injury in Humans in-Vivo? [NCT00441597]Phase 430 participants (Anticipated)Interventional2007-02-28Completed
Cholesterol Lowering and Arrhythmia Recurrences After Internal Defibrillator Implantation (CLARIDI) [NCT00457340]Phase 4220 participants Interventional2000-02-29Completed
Does Statin Therapy Reduce Sympathoexcitation in Hypertension? [NCT00497016]13 participants (Anticipated)Interventional2007-05-31Completed
"Randomized Crossover Four Period Single Dose Full Replicative Bioequivalence Study of Two Formulations Atorvastatin Film-coated Tablets 40 mg (Pharmtechnology LLC, Republic of Belarus) and Liprimar® Film-coated Tablets 40 mg (Manufacturer: Pfizer Pharmac [NCT05642845]Phase 150 participants (Anticipated)Interventional2022-11-11Recruiting
A Phase 1, Open-Label Study to Evaluate the Effect of Multiple Doses of Isavuconazole on the Pharmacokinetics of a Single Dose of Atorvastatin [NCT01635946]Phase 124 participants (Actual)Interventional2012-08-31Completed
Phase I-II Randomized, Placebo-Controlled, Single-Blinded, Single-Site Clinical Trial of Atorvastatin in the Treatment of Cavernous Angiomas With Symptomatic Hemorrhage Exploratory Proof of Concept (AT CASH EPOC) [NCT02603328]Phase 1/Phase 280 participants (Actual)Interventional2018-07-17Active, not recruiting
A Randomized, Open-label, Parallel, Multi-Center Phase IV Study to Compare of the Efficacy and Safety of Lipilou 20 mg and Lipilou 10 mg in High-risk Patients With Hypercholesterolemia(PEARL Study) [NCT04511000]Phase 4250 participants (Actual)Interventional2017-10-11Completed
Atorvastatin Toronto Retinal Vein Occlusion Study (ATORVO) [NCT00517257]Phase 3180 participants (Anticipated)Interventional2007-08-31Recruiting
Statins and Lupus: Effects of Statins on Clinical Lupus Parameters, Serological Markers and Toll-like Receptors. [NCT00519363]Phase 1/Phase 215 participants (Anticipated)Interventional2007-09-30Completed
Early Intensive Medical Therapy for the Prevention of Early Neurological Deterioration in Branch Atheromatous Disease [NCT04824911]Phase 2424 participants (Anticipated)Interventional2021-03-23Recruiting
Multi-center,Randomized,Double Blind, Double Dummy,Placebo Controlled, Efficacy and Safety Study of HS-25 in Combination With Atovastatin in Adults With Primary Hypercholesterolemia [NCT03464682]Phase 3720 participants (Anticipated)Interventional2015-02-28Active, not recruiting
A Randomized, Double-blind, Active-controlled, Multicenter Phase 3 Trial to Evaluate the Efficacy and Safety of Administrated AD-221 and AD-221A in Patients With Primary Hypercholesterolemia [NCT05131997]Phase 3290 participants (Actual)Interventional2021-11-16Completed
Statin Recapture Therapy Before Coronary Artery Bypass Grafting [NCT01715714]Phase 42,630 participants (Actual)Interventional2012-11-07Completed
A PHASE 1, OPEN-LABEL, TWO-PART STUDY TO EVALUATE THE EFFECT OF TWO STEADY-STATE DOSE LEVELS OF PF-06882961 ON THE PHARMACOKINETICS OF SINGLE ORAL DOSES OF ATORVASTATIN AND MIDAZOLAM IN HEALTHY ADULTS AND AN ORAL CONTRACEPTIVE IN HEALTHY POST-MENOPAUSAL F [NCT05093205]Phase 135 participants (Actual)Interventional2021-10-25Completed
Comparison Between Atorvastatin and Rosuvastatin in Reduction of Inflammatory Biomarkers in Patients With Acute Coronary Syndrome [NCT06053983]Phase 4126 participants (Actual)Interventional2023-01-01Completed
The Safety and Efficacy of Atorvastatin on Xanthoma in Alagille Syndrome [NCT05488067]Phase 410 participants (Anticipated)Interventional2022-03-22Recruiting
Pentoxifylline, Atorvastatin, and Vitamin E (PAVE) as Treatment for Radiation-Induced Erectile Dysfunction [NCT03830164]Phase 214 participants (Actual)Interventional2019-11-20Completed
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
A Phase III Double-Blind Efficacy and Safety of Ezetimibe (SCH 58235) 10 MG in Addition to Atorvastatin in Subjects With Coronary Heart Disease or Multiple Cardiovascular Risk Factors and With Primary Hypercholesterolemia Not Controlled by a Starting Dose [NCT03867318]Phase 3621 participants (Actual)Interventional2000-04-24Completed
SCH 58235: A Multicentre, Randomised, Parallel Group, Placebo-Controlled Study Comparing the Efficacy, Safety, And Tolerability of the Daily Co-Administration of Ezetimibe 10 mg With Atorvastatin 10 mg vs. Ezetimibe Placebo With Atorvastatin 10 mg in Untr [NCT00653796]Phase 4148 participants (Actual)Interventional2003-09-01Completed
A Two-way Pharmacokinetic Interaction Study of Single-Dose Atorvastatin (LIPITOR®) With Tipranavir/Ritonavir (500mg/200mg) at Steady-State and the Effect of Antacid (MAALOX®) on the Pharmacokinetics of Single-Dose Tipranavir/Ritonavir (500mg/200mg) in Hea [NCT02245269]Phase 123 participants (Actual)Interventional2003-07-31Completed
A Multicenter, Double-Blind, Randomized, Forced-Titration Study to Compare the Efficacy and Safety of the Combination of 145 mg Fenofibrate and 20 or 40 mg Simvastatin With Atorvastatin Monotherapy in Patients With Mixed Dyslipidemia at Risk of Cardiovasc [NCT00362934]Phase 3516 participants (Actual)Interventional2006-10-31Completed
A Double-blind, Randomized, Placebo-controlled and Active-comparator-controlled Phase 2b Study to Evaluate Statin-associated Myalgia Incidence, Lipid Profile Effect, and Safety and Tolerability Associated With PPD10558 Versus Atorvastatin in Patients With [NCT01279590]Phase 2282 participants (Actual)Interventional2011-03-31Completed
Paricalcitol Action on Parameters of Inflammation and Oxidative Stress in Patients With Chronic Kidney Disease Stage Vd Carriers Tunneled Hemodialysis Catheters [NCT01820767]Phase 331 participants (Actual)Interventional2012-08-31Completed
Atorvastatin for the Treatment of Lithium-Induced Nephrogenic Diabetes Insipidus: A Randomized Controlled Trial [NCT02967653]Phase 260 participants (Actual)Interventional2017-07-13Completed
Assessment of Change in Atherosclerotic Plaque by Serial CCTA [NCT03414840]400 participants (Anticipated)Observational2018-04-01Recruiting
A 12 Week, Randomised, Double Blind Study Evaluating the Effects of Low Dose (10mg) and High Dose (80mg) Atorvastatin on Macrophage Activity and Carotid Plaque Inflammation as Determined by Ultra Small Super-Paramagnetic Iron Oxide (USPIO) Enhanced Caroti [NCT00368589]47 participants (Actual)Observational2006-07-31Completed
A Placebo-Controlled, Double-Blind, Randomized Study to Evaluate the Efficacy and Safety of Lapaquistat Acetate 100 mg in Subjects With Type 2 Diabetes Currently Treated With Lipid-Lowering Therapy [NCT00251680]Phase 3400 participants (Actual)Interventional2005-10-31Completed
Prevention of Reperfusion Damage and Late Left Ventricular Remodelling With Atorvastatin Administered Before Reperfusion Therapy. The REPERATOR Study [NCT00286312]Phase 450 participants (Anticipated)Interventional2006-02-28Completed
The Comparison of the Efficacy of Ezetimibe and Fenofibrate Versus Atorvastatin Alone in the Lowering of LDL Cholesterol [NCT00299884]45 participants (Actual)Observational2005-01-31Completed
Pilot Study of Statin Treatment in Patients With Stable Moderate to Severe Asthma [NCT00292201]Phase 210 participants (Actual)Interventional2006-02-28Terminated(stopped due to Lack of funding to complete subject recruitment and testing)
The Effect Of LDL-Cholesterol, Lowering Beyond Currently Recommended Minimum Targets On Coronary Heart Disesse (CHD) Recurrence In Patients With Pre-Existing CHD [NCT00327691]Phase 48,600 participants Interventional1998-04-30Completed
A 6-Week Open-Label, Randomised, Multicentre, Phase IIIb, Parallel-Group Study to Compare the Efficacy and Safety of Rosuvastatin (10 mg) With Atorvastatin (20 mg) in Subjects With Hypercholesterolaemia and Either a History of CHD or Clinical Evidence of [NCT00329173]Phase 31,000 participants Interventional2003-11-30Completed
A Double Blind Placebo Controlled Study of Atorvastatin as Prevention of CHD in High Risk Patients With Non-Insulin Dependent Diabetes Mellitus (Collaborative Atorvastatin Study - CARDS) [NCT00327418]Phase 42,800 participants Interventional1997-01-31Completed
Randomised Controlled Trial to Evaluate the Effect of Statins on Asthma Control of Patients With Chronic Asthma [NCT00126048]Phase 2/Phase 354 participants (Actual)Interventional2005-07-31Completed
Assessment of the Antiviral Effect of Atorvastatin on Hepatitis C Virus [NCT00403533]Phase 210 participants Interventional2006-02-28Completed
PPAR Alpha (LY518674): A Phase 2 Study of the Combinatorial Effect of LY518674 and Atorvastatin in Subjects With Hypercholesterolemia [NCT00133380]Phase 2300 participants Interventional2005-07-31Completed
Phase 3 Multi-Center, Open Label, Forced Titration Study To Evaluate The Efficacy, Safety, And Tolerability Of Torcetrapib/Atorvastatin Combination Administered Orally, Once Daily (Qd) In Patients With Homozygous Familial Hypercholesterolaemia [NCT00134511]Phase 330 participants Interventional2005-03-31Completed
Improving Diabetic Foot Ulcers With Atorvastatin [NCT00134550]Phase 213 participants (Actual)Interventional2005-02-28Completed
Use of Statins in Modulation of Inflammatory Answer in Septic Patients [NCT00452608]Phase 280 participants (Anticipated)Interventional2006-12-31Recruiting
A Double-blind, Randomized Placebo-controlled Study to Evaluate the Efficacy and Safety of TAK-475 50 mg, 100 mg, or Placebo When Co-administered With Atorvastatin (10 mg to 40 mg) in Subjects With Primary Hypercholesterolemia [NCT00143676]Phase 3448 participants (Actual)Interventional2005-08-31Completed
Eliminate Coronary Artery Disease [NCT02245087]Phase 228 participants (Actual)Interventional2014-08-31Terminated(stopped due to Lack of Funding)
Silent Cerebrovascular Lesion and Cognitive Decline Prevention in Atrial Fibrillation by Intensive Cholesterol Lowering in Elderly Patients [NCT00449410]Phase 435 participants Interventional2005-05-31Completed
Rho Kinase in Patients With Atherosclerosis: Effects of Statins - A Double Blind, Randomized Clinical Trial Comparing Rosuvastatin and Atorvastatin [NCT00115830]Phase 340 participants Interventional2004-12-31Completed
The Effects of Atorvastatin on the Rho/Rho Kinase Pathway in Patients With Atherosclerosis [NCT00115817]Phase 336 participants Interventional2005-06-30Completed
Lupus Atherosclerosis Prevention Study [NCT00120887]Phase 4200 participants Interventional2002-04-30Completed
Effects of Atorvastatin Versus Pravastatin on Platelet Inhibition by Clopidogrel in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention [NCT00405717]Phase 41,300 participants (Anticipated)Interventional2006-02-28Completed
Pediatric Atorvastatin in Diabetes Intervention Trial (PADIT) [NCT00130481]100 participants Interventional2005-04-30Completed
A Phase IV, Multicenter, Randomized, Open Label Study To Evaluate The Efficacy And Safety Of Atorvastatin Versus Simvastatin In Type 2 Diabetic Subjects With Hypercholesterolemia [NCT00141141]Phase 4383 participants (Actual)Interventional2004-01-31Completed
Phase 3, Multi-Site, Double-Blind, Randomized, Forced Titration, Parallel Group Evaluation Of The Efficacy, Safety, And Tolerability Of Fixed Combination Torcetrapib (CP 529,414)/Atorvastatin Administered Orally, Once Daily (Qd) For Eighteen Weeks, Compar [NCT00134498]Phase 3160 participants Interventional2005-02-28Completed
Peri-vascular Adipose Tissue Inflammation Evaluated Using Coronary CT [NCT04181749]Phase 2200 participants (Anticipated)Interventional2020-11-18Recruiting
A Phase 3, Double-Blind, Randomized, Multisite Trial Of The Efficacy, Safety, And Tolerability Of The Fixed Combination Torcetrapib/Atorvastatin Administered Orally, Once Daily For 12 Months, Compared To Atorvastatin Alone, Titrated Based On NCEP ATP-III [NCT00137462]Phase 3900 participants Interventional2004-11-30Completed
The Effect of Eplerenone and Atorvastatin on Markers of Collagen Turnover in Diastolic Heart Failure [NCT00505336]43 participants (Actual)Interventional2006-04-30Completed
Clinical Utility of Amlodipine/Atorvastatin to Improve Concomitant Cardiovascular Risk Factors of Hypertension and Dyslipidemia [NCT00143234]Phase 31,825 participants Interventional2004-05-31Completed
Use of Atorvastatin (Lipitor) to Decrease Panel Reactive Antibody Titers [NCT00143741]Phase 120 participants (Actual)Interventional2005-05-31Completed
A Phase 2 Efficacy and Safety Study of LY2484595 Alone and in Combination With Atorvastatin, Simvastatin, and Rosuvastatin in Patients With Hypercholesterolemia or Low HDL-C [NCT01105975]Phase 2398 participants (Actual)Interventional2010-04-30Completed
Prospective Randomized Open-label Trial of Atorvastatin as Adjunctive Treatment of COVID-19 [NCT04380402]Phase 2300 participants (Anticipated)Interventional2020-06-25Recruiting
The Effect of HMG-CoA Reductase Inhibition on Postprandial GLP-1 Secretion [NCT03018444]15 participants (Actual)Interventional2016-10-31Completed
A Clinical Trial to Compare Efficacy and Tolerability of Atorvastatin in Addition to Endocrine Treatment With Focus on Mechanisms of Resistance to Endocrine Treatment (Fulvestrant/Aromatase Inhibitors) in Patients With Advanced Breast Cancer [NCT02958852]Phase 2126 participants (Anticipated)Interventional2016-11-30Recruiting
A Prospective Randomized Open Label Blinded Endpoint Multicenter Study in Patients With Coronary Artery Disease to Assess the LDL Lowering Effect of Switching to Ezetimibe (+) Simvastatin for Cholesterol Lowering, Compared the Dose of the Statin Used. [NCT00166530]Phase 4367 participants (Actual)Interventional2005-11-30Completed
Combined Effects of Non-statin Treatments on Apolipoprotein A-I Up-Regulation (CENTAUR): A Feasibility Study [NCT00728910]Phase 225 participants (Actual)Interventional2008-06-30Completed
The Role of P-glycoprotein in Sitagliptin Clinical Pharmacology [NCT01112670]Phase 433 participants (Actual)Interventional2009-11-30Completed
Phase II Study Evaluating the Safety and Efficacy of Atorvastatin for the Prophylaxis of Acute Graft-versus-host Disease in Patients Undergoing Matched Sibling Hematopoietic Stem Cell Transplantation [NCT01175148]Phase 260 participants (Actual)Interventional2010-07-31Completed
Study of Influence of Atorvastatin on the Repolarisation Phase of Cardiomyocytes [NCT00520585]0 participants Interventional2007-08-31Not yet recruiting
HDL Modulation and Endothelial Function [NCT00150722]Phase 375 participants (Actual)Interventional2005-09-30Completed
An 80-Week, Randomized, Multi-Center, Parallel-Group, Double-Blind Study of the Efficacy and Safety of Atorvastatin 80 MG Plus an Acetylcholinesterase Inhibitor Versus an Acetylcholinesterase Inhibitor Alone in the Treatment of Mild to Moderate Alzheimer' [NCT00151502]Phase 3600 participants Interventional2002-11-30Completed
A Multicenter, Randomized Double-Blind Study Comparing The Pleiotropic Effects Of Atorvastatin 10 Mg And 80 Mg Over A 26-Week Period In Subjects With Coronary Atherosclerosis [NCT00163202]Phase 4330 participants Interventional2002-06-30Completed
Effect of 80-mg Atorvastatin on Myocardial Edema Following Coronary Artery Bypass Surgery in Relation With Follistatin-Like Protein-1 [NCT02901379]Phase 340 participants (Actual)Interventional2016-10-31Completed
Effect of High Dose Statin Therapy on Endothelial Function in Patients With Type 2 Diabetes Mellitus Without CAD [NCT00124397]Phase 4186 participants Interventional2001-07-31Completed
SLIM: Combined Effects of Slo-Niacin and Atorvastatin on Lipoproteins and Inflammatory Markers [NCT00194402]Phase 464 participants (Actual)Interventional2003-08-31Completed
A Randomized, Multicenter, Double-blind, Placebo-controlled Comparison of Standard (Neo)Adjuvant Therapy Plus Placebo Versus Standard (Neo)Adjuvant Therapy Plus Atorvastatin in Patients With Early Breast Cancer [NCT04601116]Phase 33,360 participants (Anticipated)Interventional2021-01-04Recruiting
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
A Study to Investigate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of Administering Multiple Oral Doses of GSK1292263 Alone and With Atorvastatin [NCT01218204]Phase 2287 participants (Actual)Interventional2010-09-14Completed
An International, Multicentre, Open Label Study To Assess The Effectiveness Of Amlodipine -Atorvastatin Combination In Subjects With Hypertension and Dyslipidaemia. (The JEWEL Study) [NCT00330785]Phase 31,250 participants Interventional2004-10-31Completed
ACTFAST: Achieve Cholesterol Targets Fast With Atorvastatin Stratified Titration. A Multicenter, Twelve-Week Treatment, Single Step Titration, Open-Label Study Assessing The Percentage Of Dyslipidemic High-Risk Patients Achieving Low Density Lipoprotein C [NCT00442845]Phase 42,080 participants Interventional2003-01-31Completed
Atorvastatin Treatment to Attenuate the Progression of Cardiovascular Disease: Prospective, Randomized, Controlled Study [NCT00481364]Phase 3446 participants (Actual)Interventional2006-11-30Completed
A Double-Blind, Randomized, Parallel Group Study to Evaluate the Safety, Tolerability and Efficacy of Lapaquistat Acetate Alone or Coadministered With Atorvastatin in Subjects With Primary Dyslipidemia [NCT00487994]Phase 32,130 participants (Actual)Interventional2004-11-30Completed
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
[NCT00522158]Phase 40 participants InterventionalCompleted
Syöpäpotilaan Ennusteen Parantaminen Muuttamalla syövän mikroympäristöä ja Metaboliaa Liikunnalla ja lääkkeellisesti - Measuring Oncological Value of Exercise and Statin [NCT05796973]Phase 3240 participants (Anticipated)Interventional2023-03-31Recruiting
A Two-way Cross-over, Placebo-controlled Interaction Trial in Two Parts (in Healthy Subjects), Studying Liraglutide's Potential Influence on the Absorption Pharmacokinetics of Lisinopril, Atorvastatin, Griseofulvin and Digoxin, and Liraglutide's Potential [NCT01518166]Phase 170 participants (Actual)Interventional2006-05-31Completed
Phase 1 Study of Autologous Peripheral Hematopoietic Stem Cell Transplantation in Ischemic Stroke [NCT01518231]Phase 140 participants (Anticipated)Interventional2012-01-31Recruiting
The Randomized Double-blind Placebo-Controlled Multi-center Clinical Trial of Transplantation Efficacy of Autologous Bone Marrow Mesenchymal Stem Cells With Intensive Atorvastatin in Acute Myocardial Infarction Patients [NCT03047772]Phase 2124 participants (Anticipated)Interventional2018-03-06Not yet recruiting
Phase II Trial Evaluating the Safety and Efficacy of Atorvastatin for the Prophylaxis of Acute Graft Versus Host Disease(GVHD) in Patients With Hematological Malignancies Undergoing HLA-Matched Related Donor Hematopoietic Stem Cell Transplantation (HSCT) [NCT01491958]Phase 240 participants (Actual)Interventional2011-12-10Completed
Prospective, Randomized, Single Center, Open Label Study Designed to Evaluate the Effect on Platelet Reactivity in Response to High Doses of Atorvastatin or Rosuvastatin Administered Before Percutaneous Coronary Intervention (PCI) [NCT01526460]Phase 2146 participants (Actual)Interventional2011-08-31Completed
A Phase 3, Randomized, Double- Blind, Multi-center, Double Dummy, Clinical Trial Comparing HL-040XC With Single Component Therapies(Atorvastatin, Losartan) to Assess the Efficacy and Safety of HL-040XC in Patients With Essential Hypertension and Hyperlipi [NCT01541943]Phase 3356 participants (Actual)Interventional2012-03-31Completed
Multicenter Randomized Controlled Trial of Loading Dose Statins for the Prevention of Cardiovascular Complications in High-Risk Non-Cardiac Surgery [NCT01543555]Phase 3648 participants (Actual)Interventional2012-11-30Completed
Metformin Versus Atorvastatin in Nonalcoholic Hepatic Steatosis: a Randomized Study [NCT01544751]150 participants (Anticipated)Interventional2011-09-30Recruiting
Anti-inflammatory and Renoprotective Effect of Pretreatment Loading Dose Atorvastatin in CABG [NCT01547455]96 participants (Actual)Interventional2012-04-30Completed
Effects of Short-term Atorvastatin Treatment on Vaccination Efficacy in Nonresponder Persons to Hepatitis B Vaccine [NCT01548326]Phase 452 participants (Anticipated)Interventional2011-09-30Enrolling by invitation
Effect of Atorvastatin on the Frequency of Ventilator-associated Pneumonia in Patients With Ischemic Stroke [NCT01550419]Early Phase 1100 participants (Anticipated)Interventional2012-03-31Recruiting
COVID-19 Vaccination Detoxication in Low Density Lipoprotein Cholesterol [NCT05839236]Phase 11 participants (Actual)Interventional2023-05-01Active, not recruiting
Application of Atorvastatin in the TREATment of Patients With Intracranial Unruptured Vertebrobasilar Dissecting Aneurysms [NCT04943783]40 participants (Anticipated)Interventional2021-07-01Recruiting
Use of Atorvastatin (Lipitor) to Prevent Bone Pain Following Infusion of Pamidronate or Zoledronic Acid [NCT00120133]12 participants (Actual)Interventional2004-12-31Completed
Evaluation of Potential Pharmacokinetic Interactions Between Protease Inhibitors and Lipid Lowering Agents [NCT00000941]Phase 156 participants InterventionalCompleted
Atorvastatin to Reduce Psoriasis Severity and Improve Endothelial Function in Patients With Severe Psoriasis and Non-Elevated LDL Levels: A Randomized, Double Blind, Placebo-Controlled Study. [NCT01527097]Phase 30 participants (Actual)Interventional2012-08-31Withdrawn(stopped due to We strongly feel that the ability to recruit the required number of patients is very low and thus decided to stop the study.)
"Pre-Surgical Window of Opportunity Trial of the Combination of Metformin and Atorvastatin in Newly Diagnosed Operable Breast Cancer" [NCT01980823]Early Phase 123 participants (Actual)Interventional2013-10-31Completed
Randomized, Multicenter, Parallel, Open, Phase 4 Study to Compare the Efficacy and Safety of Rosuvastatin/Amlodipine Combination Therapy Versus Atorvastatin/Amlodipine Combination Therapy in Hypertension Patient With Dyslipidemia [NCT03951207]Phase 4259 participants (Actual)Interventional2019-05-30Completed
CHORD1 - CHOlesterol Lowering and Residual Risk in Diabetes, Type 1 [NCT05641753]Phase 4125 participants (Anticipated)Interventional2022-12-06Recruiting
A Multicenter, 6-Week-Treatment, Open-Label Study Assessing The Percentage Of Hyperlipidemic Patients Achieving Low Density Lipoprotein Cholesterol Target With Atorvastatin [NCT00136942]Phase 3370 participants Interventional2005-04-30Completed
Phase 3 Multi-Center, Double-Blind, Randomized, Parallel Group, Carotid B-Mode Ultrasound Evaluation of the Anti-Atherosclerotic Efficacy, Safety and Tolerability of Fixed Combination CP-529,414/Atorvastatin, Administered Orally, Once Daily (QD) for 24 Mo [NCT00136981]Phase 3800 participants Interventional2003-12-31Completed
A Multicentre, Randomised, Double Blind Placebo Controlled Trial Evaluating Atorvastatin in Factorial With Omega-3 Fatty Acids Cardiovascular Risk Reduction in Patients With Type 2 Diabetes [NCT00141232]Phase 4810 participants (Actual)Interventional2004-11-30Completed
[NCT01806324]Phase 130 participants (Actual)Interventional2012-04-30Completed
Effect of the HMG-CoA Reductase Inhibitor Atorvastatin Calcium, Lipitor, in the Treatment of Alzheimer's Disease [NCT00024531]Phase 298 participants Interventional2000-10-31Completed
Effect of Atorvastatin and Fish Oils on Lipoprotein Metabolism in Visceral Obesity [NCT00392717]Phase 348 participants Interventional1998-02-28Completed
Phase III, Double-blinded, Multicenter, Randomized Clinical Trial to Evaluate the Effects of Atorvastatin on Moderate-to-severe and Active Graves' Orbitopathy (GO) Treated With Intravenous Glucocorticoids: the STAGO-2 Study [NCT05049603]Phase 3102 participants (Anticipated)Interventional2024-01-01Not yet recruiting
Statins and CPAP in Adipose Tissue: A Randomized Clinical Trial in Obstructive Sleep Apnea [NCT03308578]Phase 1/Phase 290 participants (Anticipated)Interventional2018-01-08Enrolling by invitation
Calcineurin Inhibitor Sparing Protocol in Living Donor Pediatric Kidney Transplantation [NCT00023231]35 participants (Actual)Interventional2001-02-28Completed
A Study to Evaluate the Potential for Pharmacokinetic Interaction Between SB 462795 and SSRIs in Healthy Subjects [3A] [NCT00411190]Phase 132 participants (Actual)Interventional2006-10-19Completed
CARE-2 (Calcium Acetate (PhosLo®)/Sevelamer(Renagel®) Evaluation Study 2) [NCT00211939]Phase 4203 participants (Actual)Interventional2005-01-31Completed
A 12-week Randomized, Open-label 3-arm, Parallel Group, Multicenter Phase IIIb Study Comparing Efficacy and Safety of Rosuvastatin 20mg and 40mg With That of Atorvastatin 80 mg in Subjects With Acute Coronary Syndromes [NCT00214630]Phase 3825 participants (Actual)Interventional2003-12-31Completed
Comparative Efficacy Evaluation of Lipid Levels When Treated With Niaspan and Statin or Other Lipid-Modifying Therapies [NCT00079638]Phase 4300 participants Interventional2004-04-30Completed
Phase 3, Multi-Center, Double-Blind, Randomized, Parallel Group, Coronary Artery Intravascular Ultrasound Evaluation of the Anti-Atherosclerotic Efficacy, Safety, and Tolerability of Fixed Combination CP-529,414/Atorvastatin, Administered Orally, Once Dai [NCT00134173]Phase 31,100 participants Interventional2003-10-31Completed
Phase 3, Multi-Center, Double-Blind, Randomized, Parallel Group, Study of the Efficacy, Safety, and Tolerability of Fixed Combination Torcetrapib (CP-529,414) / Atorvastatin Administered Orally, Once Daily (QD) for Six Months, Compared With Maximally Tole [NCT00134485]Phase 3400 participants Interventional2005-03-31Completed
Characterization of Local Vascular Effects of Angiotensin II and Histamine After Treatment With Irbesartan and Atorvastatin. [NCT00154024]0 participants Interventional2003-03-31Completed
Double Blind Atorvastatin Amlodipine Study (DUAAL) Effect Of Amlodipine, Atorvastatin And The Combination On Transient Myocardia Ischemia In Coronary Artery Disease. [NCT00159718]Phase 4360 participants Interventional2001-07-31Completed
Atorvastatin Compared With Simvastatin In The Prevention of CHD Morbidity And Mortality In Patients With CHD [NCT00159835]Phase 48,600 participants Interventional1999-02-28Completed
Lacunar-Brain Infarction Cerebral Hyperactivity And Atorvastatin Trial. A Placebo-Controlled Trial Of High-Dose Atorvastatin In Patients With Cerebral Small Vessel Disease. [NCT00163150]Phase 4128 participants Interventional2003-06-30Completed
[NCT00164086]Phase 10 participants InterventionalNot yet recruiting
An International, Multicentre, Open Label Study To Assess The Effectiveness Of Amlodipine/Atorvastatin Combination In Subjects With Hypertension And Dyslipidaemia. (The JEWEL II Study) [NCT00174304]Phase 41,120 participants Interventional2004-10-31Completed
[NCT00408382]Phase 450 participants InterventionalCompleted
A Multicenter, Randomized, Double-Blind, Prospective, Parallel Study to Compare the Safety and Efficacy of Fenofibrate or Ezetimibe as Add-On Therapy to Atorvastatin in Subjects With Combined Hyperlipidemia, Typical of the Metabolic Syndrome [NCT00195793]Phase 3174 participants (Actual)Interventional2004-08-31Completed
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
Multi-center Double Blind, Placebo-controlled Study to Evaluate the Safety and Efficacy of Long-term Atorvastatin (20 mg/Day) v. Placebo on HCC Risk in Individuals With Advanced Liver Fibrosis [NCT05028829]Phase 260 participants (Anticipated)Interventional2023-05-10Recruiting
AVN Prevention With Lipitor in Lupus Erythematosus APLLE Trial [NCT00412841]Phase 243 participants (Actual)Interventional2002-11-30Terminated
Randomized. Open Label Trial of Comparison Between Rosuvastatin and Atorvastatin on Oxidative Stress, Inflammatory and Thrombogenic Biomarkers in Patients With Hyperlipidemia [NCT02979704]Phase 2/Phase 390 participants (Anticipated)Interventional2016-09-30Recruiting
A Prospective, Single-center, Randomized Study to Evaluate the Effect of Sarpogrelate, a Selective Serotonin Receptor Antagonist, and High Dose Statin on the Reduction of Coronary Spasm in the Patients With Variant Angina [NCT01674686]Phase 4200 participants (Anticipated)Interventional2012-08-01Recruiting
A Randomized, Open-label, Single Dose, 3x3 Partial Replicated Crossover Study to Evaluate the Pharmacokinetics and Safety/Tolerability Between a Fixed Dose Combination of Fimasartan 120mg/Atorvastatin 40mg and Co-administration of Fimasartan 120mg and Ato [NCT02994745]Phase 160 participants (Actual)Interventional2016-12-23Completed
A Randomized, Double-Blind, Parallel Group Study to Evaluate the Effects of High Dose Statin Therapy on 18Fluorine Fluorodeoxyglucose (18FDG) Uptake in Arteries of Patients With Atherosclerotic Vascular Disease [NCT00703261]Phase 183 participants (Actual)Interventional2008-08-31Completed
A Double-Blind, Multicenter Study to Assess the LDL-C Lowering of Combination Tablets Ezetimibe/Simvastatin (10mg/20mg) and Ezetimibe/Simvastatin (10mg/40mg) Compared to Atorvastatin 20mg in Patients With Type II Diabetes. [NCT00541697]Phase 3648 participants (Actual)Interventional2005-01-19Completed
Compare Ezetimibe 10mg and Simvastatin 40mg vs Atorvastatin 80mg Daily in Subjects With Cardiovascular Heart Disease and/or Diabetes Mellitus With Uncontrolled Lipids on Statin Therapy [NCT00395603]Phase 3550 participants (Anticipated)Interventional2006-09-30Terminated(stopped due to This study was terminated early due to poor recruitment.)
Implications for Treatment of the Metabolic Syndrome [NCT00666029]Phase 240 participants (Actual)Interventional2006-02-28Completed
A Phase 1, Three-Part, Open-label Study in Healthy Adult Volunteers to Assess Vadadustat as a Perpetrator in Drug-Drug Interactions With Rosuvastatin, Sulfasalazine, Pravastatin, Atorvastatin and Simvastatin [NCT03801733]Phase 1134 participants (Actual)Interventional2018-06-17Completed
Novel Therapies for Resistant Focal Segmental Glomerulosclerosis [NCT00814255]Phase 232 participants (Actual)Interventional2008-12-31Completed
Study of the Influence of Atorvastatin in Plasma Viral Replication Given Prior to Antiretroviral Treatment Interruption in Patients With HIV-1 Infection and Viral Suppression. [NCT00355251]Phase 45 participants (Actual)Interventional2006-07-31Terminated(stopped due to On the basis of published results of SMART study, it has been observed that the results are worse in patients who have interrupted their treatments.)
A Phase 2, Randomized, Double Blind, Placebo Controlled Clinical Study Investigating the Effects of Obeticholic Acid and Atorvastatin Treatment on Lipoprotein Metabolism in Subjects With Nonalcoholic Steatohepatitis [NCT02633956]Phase 284 participants (Actual)Interventional2015-12-04Completed
Statin Modulation of Monocyte/Macrophage Activation for HAND Treatment [NCT01600170]Phase 411 participants (Actual)Interventional2013-01-31Completed
Use of Atorvastatin as Adjuvant Therapy Among Suboptimal Responders to Antiretroviral Therapy in an African Cohort of HAART-treated Adults: A Randomised Controlled Trial [NCT01766076]Phase 330 participants (Actual)Interventional2013-01-31Completed
"Study of the Effect of Atorvastatin for Reducing Inflaming (Aging-related Complication) in HIV-infected Patients Older Than 45 Years Receiving a Protease Inhibitor-based Regimen Versus a Raltegravir-based Regimen" [NCT02577042]Phase 442 participants (Actual)Interventional2015-10-15Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Test the Safety and Efficacy of Lipitor (Atorvastatin) in Reducing the Progression of Carotid IMT in Early Childhood SLE [NCT00065806]Phase 3221 participants (Actual)Interventional2003-09-30Completed
Effects of High Intensity Statin Therapy on Steroid Hormones and Vitamin D in Type 2 Diabetic Men [NCT05806723]Phase 4104 participants (Actual)Interventional2021-03-01Completed
A Multicentre Study Comparing the Efficacy of Rosuvastatin With Atorvastatin When Given for a Period of 16 Wks to Subjects With Coronary Heart Disease & a Previously Performed Percutaneous Coronary Intervention [NCT00235950]Phase 4255 participants Interventional2004-01-31Completed
Investigations on Differences in Atorvastatin Metabolite Ratios as a Diagnostic Tool in Detecting Atorvastatin Induced Myotoxicity [NCT00199745]Phase 453 participants (Anticipated)Interventional2005-10-31Completed
High-dose Statin Therapy in the Perioperative Period and DVT Prevention. [NCT00259662]29 participants (Actual)Interventional2005-11-30Completed
Phase 3, Open-Label, Multi-Center, Double-Blind, Randomized, Parallel Group Study Efficacy and Safety of Fixed Combination Torcetrapib/Atorvastatin, Administered Once Daily (QD) Compared to Fixed Combination Ezetimibe/Simvastatin for 6 Weeks in Subjects W [NCT00267267]Phase 31,784 participants Interventional2006-01-31Terminated
An Open-label, Randomised, Multi-centre, Phase IIIb, Parallel Group Study to Compare the Efficacy and Safety of Rosuvastatin and Atorvastatin in Subjects With Type IIa and IIb Hypercholesterolaemia [NCT00239330]Phase 3824 participants Interventional2003-06-30Completed
An Open-label, Randomized, Single Oral Dose, Two Way Crossover Bioequivalence Study of Atorvastatin Ca 40 mg Tablets of Dr.Reddy's With Lipitor® 40 mg Tablets of Pfizer in 74 Healthy, Adult, Human Subjects Under Fasting Conditions [NCT01645384]Phase 169 participants (Actual)Interventional2009-05-31Completed
The Effect of Puerarin Tablets in Treating Metabolism Syndrome in Patients With Chronic Rheumatic Diseases [NCT02219191]150 participants (Anticipated)Interventional2014-08-31Active, not recruiting
A Double-Blind, Randomized Study to Evaluate the Efficacy and Safety of Lapaquistat or Placebo When Co-Administered With High Dose Statin Therapy in Subjects With Primary Hypercholesterolemia [NCT00249899]Phase 3649 participants (Actual)Interventional2005-11-30Terminated(stopped due to Overall profile of the compound does not offer significant clinical advantage to patients over currently available lipid lowering agents)
A 8-Week, Open-Label, Phase 1 Study To Evaluate Pharmacokinetics, Pharmacodynamics, Safety And Tolerability Of Atorvastatin In Children And Adolescents With Heterozygous Familial Hypercholesterolemia [NCT00739999]Phase 139 participants (Actual)Interventional2008-12-31Completed
A Phase 2 Efficacy and Safety Dose-Ranging Study of LY3015014 in Patients With Primary Hypercholesterolemia [NCT01890967]Phase 2527 participants (Actual)Interventional2013-06-30Completed
A Phase 1, Open-Label, Randomized, 2-Arm Study to Evaluate the Effect of Atorvastatin, a Weak CYP3A4 Inhibitor, on the Pharmacokinetics of Lomitapide in Healthy Subjects [NCT02080455]Phase 132 participants (Actual)Interventional2014-01-27Completed
A Phase 3, Open-Label, Multisite, Randomized, Parallel Group Study of the Efficacy and Safety of Fixed Combination Torcetrapib/Atorvastatin Administered Once Daily (QD) Compared to Simvastatin for 6 Weeks in Subjects With Hypercholesterolemia (A5091030) [NCT00267254]Phase 3640 participants Interventional2006-01-31Completed
Statin Induced Regression of Cardiomyopathy Trial - SirCat [NCT00317967]Phase 322 participants (Actual)Interventional2007-04-30Completed
Studies to Gain Insight How the Drugs PCSK9-inhibitors and Statins Affect Cholesterol and Bile Acid Metabolism [NCT06140095]Early Phase 18 participants (Anticipated)Interventional2024-02-29Not yet recruiting
Assessment of the Effect of Atorvastatin and N-acetyl Cysteine on Prevention of Contrast Induced Nephropathy in Patients Undergoing Coronary Angiography CIN [NCT06139952]Phase 4120 participants (Anticipated)Interventional2023-12-01Not yet recruiting
Multi-Arm Multi-Stage Adaptive Platform Trial (APT) for the Acute Treatment of Traumatic Brain Injury [NCT05826912]Phase 2672 participants (Anticipated)Interventional2024-03-29Not yet recruiting
[NCT01497912]Phase 420 participants (Actual)Interventional2005-01-31Completed
A Bioequivalence Study Of 80 Mg Atorvastatin Calcium Tablets Versus 80 Mg Lipitor® Tablets Under Fasting Conditions. [NCT01499758]Phase 180 participants (Actual)Interventional2009-10-31Completed
A Bioequivalence Study Of 80 Mg Atorvastatin Calcium Tablets Versus 80 Mg Lipitor® Tablets Under Fed Conditions. [NCT01499771]Phase 180 participants (Actual)Interventional2009-10-31Completed
Studies of Traditional Chinese Medicine Clinical Efficacy Evaluation Index With Stable Angina Pectoris of Coronary Heart Disease as an Example [NCT01502943]Phase 4480 participants (Actual)Interventional2011-05-31Completed
Effects of Atorvastatin Treatment on Left Ventricular Diastolic Function in Peritoneal Dialysis Patients (ALEVENT) [NCT01503671]Phase 436 participants (Anticipated)Interventional2011-11-30Recruiting
Impact of Statin Therapy on Adaptations to Aerobic Exercise [NCT03360916]Phase 4119 participants (Actual)Interventional2018-02-01Active, not recruiting
A Multi-center, Randomized, Open-labeled Clinical Trial to Evaluate Efficacy and Safety of Atorva® 20mg Versus Lipitor® 20mg in Korean Patients With Hypercholesterolemia [NCT01624207]Phase 4376 participants (Actual)Interventional2010-03-31Completed
The Randomly Controlled Clinical Trial of the Association Between Very Small Embryonic-like Stem Cells and the Prognosis of Coronary Artery Disease Patients [NCT01633359]Phase 4300 participants (Anticipated)Interventional2012-07-31Not yet recruiting
Erythrocyte-bound Apolipoprotein B After Withdrawal of Statin Therapy [NCT01634906]55 participants (Actual)Interventional2012-07-31Completed
Effects of Short Term, High Dose Atorvastatin Therapy on Periprocedural Myonecrosis and Platelet Inhibition After PCI [NCT00979940]60 participants (Actual)Interventional2008-11-30Terminated(stopped due to Slower than anticipated enrollment for pilot study.)
CHOlesterol Lowering and Residual Risk in Type 2 Diabetes [NCT04369664]Phase 4151 participants (Actual)Interventional2020-08-12Completed
The Correlation Study Between Blood Pressure Variability and the Prognosis of Ischemic Stroke With Intracranial Artery Stenosis [NCT01665235]200 participants (Anticipated)Interventional2012-08-31Recruiting
[NCT00004466]Phase 25 participants (Actual)Interventional1998-10-31Terminated(stopped due to Very poor enrollment)
Role of Statin Therapy in Prevention of Anthracycline-Induced Cardiotoxicity [NCT05792293]Phase 2/Phase 3100 participants (Anticipated)Interventional2021-06-01Recruiting
The Therapeutic Effects of Combination of Statins With Berberine on the Patients With Hyperlipemia:a Single-center, Open Clinical Trial [NCT01697735]Phase 424 participants (Actual)Interventional2012-09-30Terminated(stopped due to Because of lack of participants and funds)
An Randomized Open Label Trial on the Impact of 24 Weeks of Atorvastatin Therapy on Liver Fat Content and Abdominal Fat Content in Patients With Type 2 Diabetes Combined With High LDL-C and Non-alcoholic Fatty Liver Disease [NCT01720719]Phase 4120 participants (Anticipated)Interventional2013-05-31Recruiting
The Effects of Atorvastatin Treatment in COPD Patients [NCT01748279]Phase 418 participants (Actual)Interventional2012-12-31Completed
Clinical Study to Evaluate the Possible Efficacy of Dapagliflozin and Atorvastatin in Patients With Major Depressive Disorders [NCT05792540]Phase 275 participants (Anticipated)Interventional2023-06-06Recruiting
Pilot Study of Statins in Patients With Clonal Cytopenia of Undetermined Significance (CCUS) and Myelodysplastic Syndromes (MDS) [NCT05483010]Phase 216 participants (Anticipated)Interventional2024-01-03Not yet recruiting
Effect of Statin on the Post-interventional Coronary Microcirculation Dysfunction [NCT01751295]84 participants (Anticipated)Interventional2012-12-31Active, not recruiting
Atorvastatin for Reduction of Myocardial Damage During Angiography and Its Mechanism Associated With IMR [NCT01761656]Phase 2180 participants (Anticipated)Interventional2012-12-31Recruiting
An Open-label, Fixed-sequence Study to Evaluate Pharmacokinetic Interactions Between Atorvastatin and Metformin in Healthy Male Subjects [NCT01765023]Phase 180 participants (Actual)Interventional2012-10-31Completed
Intervention précoce Sur Les Indices d'athérogénèse Des Adolescents à Risque [NCT01768481]Phase 316 participants (Actual)Interventional2004-01-31Completed
A Multicenter, Open-label, 30-week Observational Clinical Study to Examine the Progress of Patients After Leaving the Cardiology Clinic or Unit Due to Acute Cardiovascular Event. [NCT01770210]670 participants (Actual)Observational2013-02-28Completed
Pharmacokinetic Drug Interaction Study Between Raltegravir and Atorvastatin (AVIATOR). [NCT01779687]Phase 124 participants (Actual)Interventional2013-03-31Completed
Prevention of Atrial Oxidative Stress and Electrical Remodelling in Patients Undergoing Cardiac Surgery: Randomised Placebo-controlled Trial of Perioperative High-dose Atorvastatin [NCT01780740]Phase 480 participants (Actual)Interventional2012-01-31Completed
Drug Interaction and Pharmacokinetic Assessment of Everolimus When Coadministered With Atorvastatin in Renal Transplantation Recipient [NCT01780948]18 participants (Actual)Interventional2012-09-30Completed
A Double-Blind Efficacy and Safety Study of Evacetrapib in Combination With Atorvastatin in Japanese Patients With Primary Hypercholesterolemia [NCT02260648]Phase 3149 participants (Actual)Interventional2015-01-31Terminated(stopped due to Study termination due to insufficient efficacy.)
A Randomized, Double-Blind, Placebo-Controlled, Single and Multiple Oral Ascending Dose Study to Evaluate the Safety, Tolerability and Pharmacokinetics of LY3202328 [NCT02714569]Phase 160 participants (Actual)Interventional2016-03-31Completed
The Impact of Atorvastatin on Prostate Cancer - a Randomized, Pre-surgical Clinical Trial [NCT01821404]Phase 2160 participants (Actual)Interventional2012-08-31Completed
A Randomized, Open-label, Single Dose, Two-treatment, Two-period, Two-sequence Crossover Study to Investigate the Effect of Atorvastatin on the Pharmacokinetic Properties of Telmisartan/S-amlodipine After Oral Administration in Healthy Volunteers [NCT01842230]Phase 124 participants (Actual)Interventional2013-04-30Completed
A Randomized, Open-label, Single Dose, Two-treatment, Two-period, Two-sequence Crossover Study to Investigate the Effect of Telmisartan/S-amlodipine on the Pharmacokinetic Properties of Atorvastatin After Oral Administration in Healthy Volunteers [NCT01842256]Phase 124 participants (Actual)Interventional2013-04-30Completed
Study on Effect of Highly Potent Statins on Lipid Lowering Effect and Glucose Metabolism in Hypercholesterolemia Patients With Diabetes Mellitus [NCT01544309]1,049 participants (Actual)Interventional2012-03-31Completed
Efficacy and Safety of Atorvastatin 40mg Versus Rosuvastatin 20mg in Type II Diabetic Patients With Previous Acute Coronary Syndrome : Randomized Clinical Trial [NCT05306990]108 participants (Actual)Interventional2017-04-20Completed
Atorvastatin as Adjunctive Therapy for Chronic Plaque Type Psoriasis Versus Betamethasone Valerate Alone:A Randomized, Double-Blind, Placebo-Controlled Trial [NCT02432040]Phase 228 participants (Actual)Interventional2013-02-28Completed
Reduction in YEllow Plaque by Aggressive Lipid LOWering Therapy. (YELLOW Trial) [NCT01567826]Phase 487 participants (Actual)Interventional2010-05-31Completed
Phase II Study of Atorvastatin, Micro-dose Methotrexate and Tacrolimus Administered Only to Transplant Recipients for the Prophylaxis of Acute Graft-versus-host Disease Following Allogeneic Hematopoietic Cell Transplantation [NCT01665677]Phase 269 participants (Actual)Interventional2014-01-20Completed
Impact of Atorvastatin ± Aspirin on Colorectal Biomarkers in Patients With Lynch Syndrome: a Pilot Study [NCT04379999]Early Phase 146 participants (Anticipated)Interventional2018-09-10Recruiting
Effect of LY2189265 on the Pharmacokinetics of Atorvastatin in Healthy Subjects [NCT01250834]Phase 127 participants (Actual)Interventional2010-12-31Completed
Pilot Study to Evaluate Effects of Atorvastatin on Monocyte Activation in HAART-treated HIV Infected Individuals [NCT01263938]Phase 45 participants (Actual)Interventional2011-09-30Completed
Plaque Regression and Progenitor Cell Mobilization With Intensive Lipid Elimination Regimen (PREMIER), Phase II [NCT02347098]Phase 3270 participants (Actual)Interventional2015-03-30Completed
A Pilot Study of Using Statins in Patients With Acute Venous Thromboembolism (VTE) [NCT02331095]Early Phase 121 participants (Actual)Interventional2015-01-31Terminated(stopped due to Low recruitment)
Effect of Atorvastatin on OPG/RANK/RANKL Expression in Immune Cells and Circulating Levels of Osteoprogenitor Cells [NCT02342015]Phase 420 participants (Actual)Interventional2012-11-30Completed
The Effect of Atorvastatin on Endothelial Dysfunction and Albuminuria in Sickle Cell Disease (in the Grant Entitled: Endothelial Dysfunction in the Pathogenesis of Sickle Cell Nephropathy) [NCT01732718]Phase 213 participants (Actual)Interventional2013-09-30Completed
A Randomized, Double-Blind Study of the Efficacy and Safety of Alirocumab Added on to Atorvastatin Versus Ezetimibe Added on to Atorvastatin Versus Atorvastatin Dose Increase Versus Switch to Rosuvastatin in Patients Who Are Not Controlled on Atorvastatin [NCT01730040]Phase 3355 participants (Actual)Interventional2012-10-31Completed
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 Statins In The Prevention of Contrast-Induced Nephropathy in Patients With Chronic Renal Insufficiency (SCIN Trial): A Double-Blind, Placebo-Controlled Trial [NCT01071993]21 participants (Actual)Interventional2010-03-31Terminated(stopped due to Sponsor can not supply drugs anymore.)
Atorvastatin vs. Atorvastatin/Ezetimibe in Patients With Hypo-response to Initial Dose Statin Therapy [NCT00965055]Phase 32 participants (Actual)Interventional2009-09-30Terminated(stopped due to The study was terminated due to inability to recruit subjects. A total of 2/100 anticipated were radomized.)
Clinical Assessment Of Association Pharmacokinetics Atorvastatin + Losartana + Hydrochlorothiazide Produced By Lab Hypermarcas S/A In Healthy Subjects [NCT01692717]Phase 190 participants (Actual)Interventional2013-02-28Completed
Hydroxychloroquine/Atorvastatin in the Treatment of OA of the Knee [NCT01645176]Phase 221 participants (Actual)Interventional2012-05-31Completed
STOP-CA (Statins TO Prevent the Cardiotoxicity From Anthracyclines) [NCT02943590]Phase 2300 participants (Actual)Interventional2017-01-13Completed
One Versus Twice Daily Administration of Multiple Cardiovascular Agents in Patients With Ischemic Heart Disease: An Open Label, Randomized, Multicenter Study [NCT04148820]Phase 4100 participants (Anticipated)Interventional2019-11-01Not yet recruiting
Efficacy of Two Different Doses of Atorvastatin for Prevention of Periprocedural Ischemic Brain Damage in Chinese Patients Undergoing Carotid Artery Stenting (CAS) [NCT03079115]Phase 4130 participants (Anticipated)Interventional2017-08-21Recruiting
Randomized Controlled Trial for Corticosteroids Versus NSAIDs With or Without Adjunctive Atorvastatin for the Treatment for Paradoxical Tuberculosis Immune Reconstitution Inflammatory Syndrome [NCT01442428]Phase 2/Phase 30 participants (Actual)Interventional2014-01-31Withdrawn(stopped due to 2011 Thailand flooding led to loss of GMP pharmacy, project delays, and further regulatory challenges.)
Efficacy and Safety of Coadministered Irbesartan and Atorvastatin in Patients With Hypertension and Hyperlipidemia [NCT01442987]Phase 3230 participants (Actual)Interventional2011-05-31Completed
Special Drug Use-Results Survey of Lipitor Tablets [NCT01446679]24,050 participants (Actual)Observational2010-09-30Completed
Single Dose Open-label Comparative Pharmacokinetic Study to Assess the Pharmacokinetic Characteristics of Irbesartan and Atorvastatin Between Irbesartan/Atorvastatin Combination Tablet and Coadministration of Irbesartan and Atorvastatin Tablets in Healthy [NCT01447797]Phase 152 participants (Actual)Interventional2011-09-30Completed
Salusin-alpha - a New Factor in the Pathogenesis of Lipid Abnormalities in Hemodialysis Patients [NCT01448174]Phase 4310 participants (Actual)Interventional2011-10-31Completed
A Randomized, Multicenter Clinical Trial to Assess the Effect of Atorvastatin in Patients With Acute Coronary Syndrome and Intended Percutaneous Coronary Intervention [NCT01448642]Phase 44,191 participants (Actual)Interventional2012-04-30Completed
Multicenter, Parallel-group, Double-blind, Randomized, Active-controlled, Dose-ranging Study to Assess the Safety, Efficacy, and Tolerability of CKD-519, Administered With HMG-CoA Reductase Inhibitors, in Subjects With Dyslipidemia [NCT02977065]Phase 262 participants (Actual)Interventional2017-03-23Completed
Investigator-initiated, Placebo-controlled, Randomized Trial to Assess the Efficacy and Safety of Platelet Inhibition and/ or Lipid Lowering in Non-ACS-patients With Elevated High-sensitivity Troponin Values [NCT03820466]Phase 368 participants (Actual)Interventional2020-02-21Terminated(stopped due to insufficient recruitment due to the pandemic situation)
Dark Adaptation as an Early Indicator of Response to Statin Therapy for Intermediate AMD [NCT04735263]Phase 221 participants (Anticipated)Interventional2021-02-04Recruiting
Comparative Clinical Study Evaluating the Anti-tumor Effect of Metformin Versus Atorvastatin as an Adjuvant Therapy With Chemotherapy in Patients With Non-metastatic Breast Cancer [NCT05507398]Phase 4100 participants (Anticipated)Interventional2022-10-31Not yet recruiting
A Phase III, Randomized, Active Comparator-controlled Clinical Trial to Study the Efficacy and Safety of MK-0653C in Japanese Patients With Hypercholesterolemia [NCT02550288]Phase 3309 participants (Actual)Interventional2015-09-29Completed
[NCT00004564]0 participants InterventionalRecruiting
Comparison Of Cardiovascular Event Rates In Elderly Patients With Newly Initiated Atorvastatin Or Simvastatin [NCT01304641]31,603 participants (Actual)Observational2009-11-30Completed
A Single-center, Randomized, Open-label, Four Treatments, Four Periods, Four Sequence, Four-way Crossover Study to Explore the Pharmacokinetic Performance of Dalcetrapib and Atorvastatin Fixed Dose Combination Prototype Formulations in Healthy Volunteers [NCT01363999]Phase 124 participants (Actual)Interventional2011-06-30Completed
"Comparative Evaluation Of The Efficacy Of Atorvastatin Gel As An Adjunct To Allografts In The Treatment Of Intrabony Defects - A Clinico Radiological Study" [NCT03009097]Phase 426 participants (Actual)Interventional2013-04-30Completed
Assessment of the Effects of Atorvastatin on Endothelial Progenitor Cells After Coronary ByPass Surgery; A Randomized Controlled Trial [NCT01096875]Phase 460 participants (Actual)Interventional2010-02-28Completed
Phase II Trial of Atorvastatin and Celecoxib in Patients With Hormone-Dependent Prostate-Specific Antigen Progression After Local Therapy for Prostate Cancer. [NCT01220973]Phase 227 participants (Actual)Interventional2009-02-28Completed
Evaluation of the Efficacy and Safety of Rosuvastatin 5 mg Versus Pravastatin 40 mg and Atorvastatin 10 mg in Subjects With Type IIa and IIb Hypercholesterolaemia [NCT00631189]Phase 4668 participants (Actual)Interventional2007-10-31Completed
Impact of LILRB5 Genotype on Immune Response to Atorvastatin [NCT02984293]Phase 418 participants (Actual)Interventional2017-04-17Completed
Amlodipine Plus/Minus Atorvastatin for Protection of Arteries [NCT01922687]Phase 4109 participants (Anticipated)Interventional2011-04-30Recruiting
The Post-Operative Statin for Thromboprophylaxis & Cardiovascular Outcomes Protection (POST-OP) Pilot Trial [NCT02197065]Phase 220 participants (Actual)Interventional2014-09-30Completed
Syringeable Atorvastatin Loaded Eugenol Enriched PEGylated Cubosomes In-situ Gel for the Intra-pocket Treatment of Periodontitis: Statistical Optimization and Clinical Assessment [NCT05583643]Phase 124 participants (Actual)Interventional2021-12-07Completed
Effect of PCSK9-Antibody (Alirocumab) on Dyslipidemia Secondary to Nephrotic Syndrome [NCT03004001]Phase 23 participants (Actual)Interventional2017-01-31Terminated(stopped due to Difficult recruitment)
Fixed Combination for Lipid and Blood Pressure Control. Randomized Cross-over Study [NCT03047538]Phase 40 participants (Actual)Interventional2017-09-01Withdrawn(stopped due to Insufficient funds)
Phase I/IIa Study of Pharmacokinetics and Safety of Atorvastatin in Children With Coronary Artery Abnormalities Secondary to Kawasaki Disease [NCT01431105]Phase 1/Phase 234 participants (Actual)Interventional2012-07-31Completed
Effect of Upstream Treatment With High Intensity Statin on the Outcomes of ST Segment Elevation Myocardial Infarction Patients Treated With Primary Percutaneous Coronary Intervention [NCT04754789]Phase 3160 participants (Anticipated)Interventional2021-02-20Not yet recruiting
Donor Statin Treatment for Prevention of Severe Acute GVHD After Nonmyeloablative Hematopoietic Cell Transplantation [NCT01527045]Phase 247 participants (Actual)Interventional2012-09-25Completed
A Study Comparing the Effects of Pitavastatin, Atorvastatin, and Rosuvastatin on Plasma Levels of CoQ10 (SPARQ) [NCT01660191]Phase 4134 participants (Actual)Interventional2011-12-31Completed
Atorvastatin Therapy for the Prevention of Atrial Fibrillation (SToP-AF) [NCT00252967]Phase 364 participants (Actual)Interventional2005-10-31Terminated(stopped due to Insufficient power to show therapy difference at interim analysis.)
Effect of Atorvastatin in the Management of Hypertension [NCT05679102]120 participants (Actual)Interventional2022-12-20Completed
The Effect of Statin Treatment on Arterial Wall Inflammation in Patients With Diabetes Mellitus as Assessed With 68Ga-DOTATATE PET-CT [NCT05730634]24 participants (Actual)Interventional2019-06-01Completed
A Multicenter, Randomized, Double-Blind, Prospective Study Comparing the Safety and Efficacy of Fenofibric Acid and Atorvastatin Calcium Combination Therapy to Fenofibric Acid and Atorvastatin Calcium Monotherapy in Subjects With Mixed Dyslipidemia [NCT00300469]Phase 3613 participants (Actual)Interventional2006-03-31Completed
Intensive Statin and Antiplatelet Therapy for High-risk Intracranial or Extracranial Atherosclerosis (INSPIRES) [NCT03635749]Phase 36,100 participants (Actual)Interventional2018-09-17Active, not recruiting
Statin Induced Augmentation of Circulating Endothelial Progenitor Cells and Myocardial Viability in Patients With Ischemic and Nonischemic Cardiomyopathy [NCT00701220]Phase 49 participants (Actual)Interventional2007-04-30Completed
Blood Pressure and Lipids Reduction in High Risk Elderly Patients With Isolated Systolic Hypertension [NCT05165251]Phase 4480 participants (Anticipated)Interventional2022-01-04Recruiting
A Phase III Multi-Center, Double-Blind, Randomized, Parallel Group, Placebo-Controlled Clinical Trial in High-Risk Type 2 Diabetes Mellitus (T2DM) Subjects With Coronary Artery Disease (CAD) to Determine Whether Bromodomain Extraterminal Domain (BET) Inhi [NCT02586155]Phase 32,425 participants (Actual)Interventional2015-11-30Completed
Managing Endothelial Dysfunction in Critically Ill COVID-19 Patients at the Lebanese American University Medical Center- Rizk Hospital [NCT04813471]Phase 370 participants (Anticipated)Interventional2021-01-20Recruiting
Effect of Atorvastatin as a Renal Protection in Patients With Systemic Inflammatory Response Syndrome Using Renal Arterial Resistive Index [NCT05946122]Phase 1106 participants (Anticipated)Interventional2023-05-30Recruiting
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
Comparative Study of the Antiarrhythmic and Cardioprotective Effects of Atorvastatin Versus Magnesium Sulfate in Cardiac Valve Replacement Surgery [NCT03289429]Phase 496 participants (Anticipated)Interventional2017-09-24Recruiting
Efficacy of Two Different Pre-Intervention Therapeutic Strategies With Clopidogrel and Atorvastatin for the Prevention of Cerebral Damage During Carotid Artery Stenting. Armyda-Caro Randomized Trial. [NCT01572623]Phase 4150 participants (Anticipated)Interventional2011-07-31Recruiting
Randomised, Double Blind, Placebo Controlled Trial of Angiotensin Converting Enzyme Inhibitors and Statins in the Prevention of Long Term Complications in Young People With Type 1 Diabetes [NCT01581476]Phase 3443 participants (Actual)Interventional2009-01-31Completed
Application of Contrast Enhance Ultrasound to Evaluate Hemodynamics Change in MCA With Moderate to Severe Stenosis After 24-week Atorvastatin Treatment [NCT01617538]Phase 1/Phase 230 participants (Anticipated)Interventional2012-01-31Recruiting
Clinical Trial to Determine the Effects of Statins on Brain Health - STAREE-Mind Imaging Substudy [NCT05586750]Phase 4341 participants (Actual)Interventional2019-09-19Active, not recruiting
HDL Increased Plaque Stabilization in the Elderly [NCT00127218]Phase 3145 participants (Actual)Interventional2003-09-30Completed
Acute Effect of HMG-CoA Reductase Inhibition (Atorvastatin)on Renal Hemodynamics, Tubular Function and Vasoactive Hormones on Healthy Subjects [NCT00344955]Phase 420 participants Interventional2003-01-31Completed
Comparison the Effectiveness of L-Carnitine With Atorvastatin in Non-Alcoholic Steatohepatitis (NASH) [NCT01617772]Phase 2440 participants (Anticipated)Interventional2016-01-01Recruiting
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
Effects Of Combination Therapy Of Statin And Ascorbic Acid For Prevention Of Contrast-Induced Nephropathy. Randomised Controlled Study [NCT03391830]250 participants (Actual)Interventional2018-01-15Completed
A 24-week, Multi-center, Randomized, Open-Label Clinical Trial to Compare the Impact of Xuezhikang and Atorvastatin on Glucose Metabolism in Dyslipidemia Patients With Prediabetes (XTREME Study) [NCT05238012]Phase 4392 participants (Anticipated)Interventional2022-07-01Not yet recruiting
Short-term Effect of 2% Atorvastatin Dentifrice as an Adjunct to Periodontal Therapy: A Randomized Double-blind Clinical Trial. [NCT01929135]Phase 238 participants (Actual)Interventional2013-05-31Completed
A Pharmacokinetic, Pharmacodynamic, and Drug-Drug Interaction Study of Evacetrapib With Selected Statins in Healthy Chinese Subjects [NCT02156492]Phase 162 participants (Actual)Interventional2014-06-30Completed
Effects of Statin Therapy on Vascular Properties and Outcomes in Diastolic Heart Failure Patients [NCT00585611]1 participants (Actual)Interventional2005-12-31Terminated(stopped due to Unable to recruit into the study)
A Prospective, Randomized, Double-Blind, Multi-Center Study Comparing the Effects of Atorvastatin Versus Pravastatin on the Progression and Quantification of Coronary Atherosclerotic Lesions as Measured by Intravascular Ultrasound (REVERSAL) [NCT00380939]Phase 4600 participants Interventional1999-04-30Completed
Evaluation of the Effect of Atorvastatin and Pioglitazone in Carotid Atherosclerosis With the Use of 18Fluoride-Fludeoxyglucose(FDG) Positron Emission Tomography-computed Tomography (PET-CT)Imaging [NCT01341730]Phase 441 participants (Actual)Interventional2011-06-30Terminated
[NCT01925937]30 participants (Anticipated)Interventional2013-06-30Recruiting
A Phase 3 Randomized, Active-comparator-controlled Clinical Study to Evaluate the Efficacy and Safety of Ezetimibe/Atorvastatin Combination Tablet (MK-0653C) as Second Line Lipid Lowering Treatment in Chinese Participants [NCT03768427]Phase 3454 participants (Actual)Interventional2019-05-27Completed
CT COMPARE: CT Coronary Angiography to Measure Plaque Reduction [NCT02740699]Phase 4108 participants (Actual)Interventional2016-04-11Terminated(stopped due to Principal Investigator resigned and closed program)
Pilot Study of Statin Therapy in Young Adult Survivors of Childhood Cancer [NCT01733953]Phase 227 participants (Actual)Interventional2012-11-30Completed
Safety and Efficacy of Drug-Coated Balloon Angioplasty for the Treatment of Chronic Total Occlusions [NCT04744571]200 participants (Anticipated)Interventional2021-02-28Enrolling by invitation
Optimization of Pre-surgical Testing With an Intensive Multifactorial Intervention to MinimiZe Cardiovascular Events in Orthopedic Surgery [NCT01837069]Phase 4198 participants (Actual)Interventional2014-02-28Terminated(stopped due to Low recruitment / DSMB approval to halt recruitment)
Subclinical Cardiovascular Disease in Psoriatic Disease [NCT03228017]Phase 463 participants (Actual)Interventional2017-08-01Completed
Effects of Atorvastatin on Disease Activity and HDL Cholesterol Anti-inflammatory Properties in Patients With Rheumatoid Arthritis [NCT00356473]Phase 420 participants (Actual)Interventional2003-03-31Completed
Aggressive Cholesterol Therapy to Inhibit Vein Graft Events (ACTIVE Trial): Does High-Dose Postoperative Statin Therapy Improve Graft Patency After Coronary Bypass? [NCT01528709]Phase 3173 participants (Actual)Interventional2012-03-31Completed
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
Pharmacokinetics of Rosuvastatin and Atorvastatin in Pediatric Dyslipidemia Patients: Clinical Impact of Genetic Variation in Statin Disposition [NCT02364258]Phase 128 participants (Actual)Interventional2014-07-31Completed
Progesterone Therapeutic Regimen Plus Statins in Young Women With Early Endometrial Carcinoma and Atypical Endometrial Hyperplasia [NCT06102863]Phase 238 participants (Anticipated)Interventional2023-04-01Recruiting
A Double-Blind, Randomized, Placebo-controlled, Multicenter Study to Evaluate Long-Term Tolerability and Durable Efficacy of AMG 145 (Evolocumab) on LDL-C in Hyperlipidemic Subjects [NCT01516879]Phase 3905 participants (Actual)Interventional2012-01-05Completed
A Phase III Randomized Clinical Trial to Study the Efficacy and Safety of the Co-administration of Sitagliptin and Atorvastatin in Patients With Type 2 Diabetes Mellitus With Inadequate Glycemic Control on Metformin Monotherapy [NCT01477853]Phase 3166 participants (Actual)Interventional2011-10-24Terminated(stopped due to The study was terminated early by the Sponsor for business reasons.)
Phase II, Double Blind, Randomized, Placebo-controlled Trial to Evaluate the Safety and Efficacy of Atorvastatin in Subjects With Newly Diagnosed Type 1 Diabetes Mellitus. [NCT00529191]Phase 240 participants (Actual)Interventional2007-07-31Completed
Statin Neuroprotection and Carotid Endarterectomy: Safety, Feasibility and Outcomes [NCT02850081]Phase 331 participants (Actual)Interventional2017-06-01Completed
Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome [NCT00242944]Phase 4307 participants (Actual)Interventional2005-11-30Completed
A Phase 2 Dose Response Study of LY2484595 in Japanese Subjects [NCT01375075]Phase 2165 participants (Actual)Interventional2011-06-30Completed
A Randomized, Double-Blind, Active-Controlled Study of Patients With Primary Hypercholesterolemia and High Cardiovascular Risk and Not Adequately Controlled With Atorvastatin: A Comparison of Switching to a Combination Tablet Ezetimibe/Simvastatin Versus [NCT00782184]Phase 3250 participants (Actual)Interventional2008-11-30Completed
Statin Intensity, Achieved LDL Cholesterol, and Cardiovascular Outcome in Statin Therapy in Patients With Coronary Artery Disease (Post-hoc Study of TNT Trial) [NCT03073863]Phase 410,001 participants (Actual)Interventional1998-04-03Completed
Intensive Management of Blood Pressure and Cholesterol in Elderly Chinese With Hypertension and Atrial Fibrillation (IMPRESSION) [NCT04111419]Phase 41,200 participants (Anticipated)Interventional2020-07-01Recruiting
Investigating the Changes of the Cognition in Asymptomatic Intracranial Stenosis Patients After 1-Year Standard Medical Treatment Without Stenting [NCT04850001]40 participants (Anticipated)Observational2020-09-10Recruiting
Non-commercial Clinical Trial of Statins CAncer Preventive and Pleiotropic TherApy IN Smokers With Chronic Obstructive Pulmonary Disease (COPD) [NCT04789057]Phase 4460 participants (Anticipated)Interventional2022-02-11Recruiting
A Phase II, Randomized, Non-comparative, Pre-surgical Study of Atorvastatin or Observation in Ki-67 Positive, TAZ-expressing Early Breast Cancer Patients (TRINACRIA Trial) [NCT02416427]Phase 278 participants (Anticipated)Interventional2015-05-31Not yet recruiting
[NCT02411903]Phase 4160 participants (Anticipated)Interventional2015-03-31Enrolling by invitation
An Adaptive Randomized Trial Comparing Multiple Treatments for Ebola Virus (EBOV) Infected Children and Adults [NCT02380625]Phase 1/Phase 2150 participants (Anticipated)Interventional2015-04-30Not yet recruiting
A Randomized, Open-labeled, Single-dose, Crossover Design Clinical Trial to Evaluate Pharmacokinetics and Safety of CJ-30056 20/750mg and Co-administration of Lipitor® 20mg and Glucophage SR 750mg in Fed Healthy Male Subjects [NCT02378441]Phase 142 participants (Actual)Interventional2015-02-28Completed
A Multicenter, Actual Use Trial In A Simulated Over-the-counter Environment Of Atorvastatin Calcium 10 Mg [NCT01964326]Phase 31,311 participants (Actual)Interventional2013-10-31Completed
Comparative Study Between the Effects of High Doses Rosuvastatin and Atorvastatin on Ventricular Remodeling in Patients With ST-Segment Elevation Myocardial Infarction [NCT05895123]Phase 280 participants (Actual)Interventional2022-10-01Completed
Clinical Efficacy of Subgingivally Delivered Atorvastatin in the Treatment of Mandibular Degree II Furcation Defects: A Randomized Controlled Clinical Trial . [NCT02386033]Phase 2/Phase 360 participants (Actual)Interventional2013-11-30Completed
A Double-blind, Randomized, Placebo-controlled, Multicenter Study to Evaluate Safety, Tolerability and Efficacy of Evolocumab (AMG 145) on LDL-C in Combination With Statin Therapy in Japanese Subjects With High Cardiovascular Risk and With Hyperlipidemia [NCT01953328]Phase 3409 participants (Actual)Interventional2013-10-31Completed
The Study of Berberine Affecting Metabolism, Inflammation Status, Endothelial Function and Thrombotic Events in Patients With Coronary Artery Disease by Remodeling Gut Microbiota [NCT04434365]Phase 1/Phase 224 participants (Actual)Interventional2019-06-21Active, not recruiting
A Pilot Study of Atorvastatin on Prevention of Metabolic Syndrome in Subjects With Prostate Cancer on Long Term Androgen-deprivation Therapy [NCT01555632]0 participants (Actual)Interventional2012-03-31Withdrawn(stopped due to Other more favorable treatments are now available.)
High Dose of Atorvastatin for Preventing Cerebral Vascular Wall Damage in Patients Undergoing Mechanical Thrombectomy [NCT05912686]Phase 4162 participants (Anticipated)Interventional2023-07-01Not yet recruiting
Clinical Utility of Endothelial Dysfunction in PAD [NCT00491751]Phase 1108 participants (Actual)Interventional2004-05-31Terminated(stopped due to Insufficient enrollment)
Randomized, Phase II Trial of Atorvastatin, RAFTILOSE Synergy 1, and Sulindac Among Patients at Increased Risk for Sporadic Colorectal Neoplasia [NCT00335504]Phase 285 participants (Actual)Interventional2006-03-31Completed
Elite Controller and ART-Treated HIV+ Statin Versus ASA Treatment Intervention Study [NCT02081638]Phase 253 participants (Actual)Interventional2014-04-18Completed
A Prospective Observational Cohort Study of Predictive Factors Related to Prognosis of In-hosiptal Patients With Ischemic Stroke Due to Large-artery Atherosclerosis [NCT04847752]1,000 participants (Anticipated)Observational2021-03-01Recruiting
The Contribution of Inflammation and Insulin Resistance to Intermittent Claudication [NCT00153166]Phase 2/Phase 376 participants (Actual)Interventional2004-01-31Completed
Effect of Statins on Oxidative Stress and Endothelial Progenitor Cells: Comparison of Atorvastatin With Pravastatin [NCT00166036]Phase 236 participants (Actual)Interventional2004-09-30Completed
Donor Statin Treatment for Prevention of Severe Acute GVHD After Myeloablative Hematopoietic Cell Transplantation [NCT01525407]Phase 283 participants (Actual)Interventional2012-05-31Completed
Statin Therapy With Atorvastatin in Surgical Aortic Valve Replacement - a Randomized Controlled Trial [NCT05076019]266 participants (Anticipated)Interventional2022-02-01Recruiting
Effectiveness of Atorvastatin on IL2, IL6, TNFalpha and HLA Levels in the Recipient's Kidney Graft From a Living Donor [NCT02522117]Phase 348 participants (Actual)Interventional2015-08-31Completed
A Long-Term, Open-Label, Safety Extension Study of the Combination of Fenofibric Acid and Statin Therapy for Subjects With Mixed Dyslipidemia [NCT00300430]Phase 31,911 participants (Actual)Interventional2006-09-30Completed
SUPREME: A 12-Week, Open-Label, Multicenter Study to Compare the Lipid Effects of Niacin ER and Simvastatin (NS) to Atorvastatin in Subjects With Hyperlipidemia or Mixed Dyslipidemia [NCT00465088]Phase 3199 participants (Actual)Interventional2007-04-30Completed
Extra Alirocumab in Addition to Statin Therapy in Symptomatic IntraCranial Atherosclerotic Stenosis ----a Pilot Study [NCT06052020]50 participants (Anticipated)Observational2023-09-15Recruiting
A Multicenter, Double-Blind, Randomized, Parallel Group, 28-Week Study to Evaluate the Efficacy and Safety of Ezetimibe and Simvastatin Co-administration Versus Atorvastatin in Patients With Hypercholesteremia [NCT00092716]Phase 3655 participants (Actual)Interventional2002-05-31Completed
Application of Atorvastatin in the Treatment of Patients With Intracranial Unruptured Aneurysms [NCT04149483]Phase 260 participants (Anticipated)Interventional2019-11-07Recruiting
Effects of Statins on Endothelial Function in Patients With Coarctation of the Aorta [NCT00767572]Phase 412 participants (Actual)Interventional2008-08-31Terminated(stopped due to low enrollment)
Evaluation of Ubiquinol on the Association of Statins and Mitochondrial Oxidative Capacity Using 31P Magnetic Resonance Imaging [NCT01702987]22 participants (Actual)Interventional2012-10-31Completed
An Open-label, One-sequence Cross Over, Single Centre Trial, Investigating the Influence of Semaglutide on the Pharmacokinetics of Single Doses of Atorvastatin and Digoxin in Healthy Subjects [NCT02243098]Phase 131 participants (Actual)Interventional2014-09-16Completed
Vascular Endothelial Dysfunction in Sleep Apnea [NCT05289063]Phase 1110 participants (Anticipated)Interventional2022-10-03Recruiting
Preventing Cardiac Complication of COVID-19 Disease With Early Acute Coronary Syndrome Therapy: A Randomised Controlled Trial. [NCT04333407]320 participants (Actual)Interventional2020-04-03Terminated(stopped due to Difficulty in recruiting eligible participants)
A Multicenter, Randomized, Parallel Groups, Placebo-controlled Study Comparing the Efficacy, Safety, and Tolerability of the Daily Coadministration of Ezetimibe 10 mg With Atorvastatin 10 mg in Untreated Subjects With Primary Hypercholesterolemia and Coro [NCT00650689]Phase 3122 participants (Actual)Interventional2003-05-31Completed
Repurposing a Lipid Lowering Drug to Treat Tuberculosis: Effectiveness of Statins as Adjuvant to Treatment of Pulmonary Tuberculosis in Nigeria [NCT04721795]Phase 2/Phase 3150 participants (Actual)Interventional2021-01-19Completed
Impact of Statin Therapy on Muscle Mitochondrial Function and Aerobic Capacity [NCT03351998]Phase 468 participants (Actual)Interventional2018-02-22Completed
Study of Curative Effect Evaluation of Shexiang Baoxin Pill on Coronary Artery Disease Not Amenable to Revascularization on the Basis of Western Medicine Therapy [NCT03072121]Phase 4440 participants (Anticipated)Interventional2017-06-30Not yet recruiting
Statins and prOgression of Coronary atheRosclerosis in melanomA Patients Treated With chEckpoint inhibitorS [NCT05180942]Phase 2180 participants (Anticipated)Interventional2022-11-07Recruiting
Evaluation of Choline Fenofibrate (ABT-335) on Carotid Intima-Media Thickness (cIMT) in Subjects With Type IIb Dyslipidemia With Residual Risk in Addition to Atorvastatin Therapy (FIRST) Trial [NCT00616772]Phase 3682 participants (Actual)Interventional2008-02-29Completed
A Multicenter, Randomized, Double-Blind, Prospective Study Comparing the Safety and Efficacy of ABT-335 in Combination With Atorvastatin and Ezetimibe to Atorvastatin in Combination With Ezetimibe in Subjects With Combined (Atherogenic) Dyslipidemia [NCT00639158]Phase 3543 participants (Actual)Interventional2008-02-29Completed
A Safety, Tolerability, Pharmacokinetic, and Pharmacodynamic Study of Single-and Multiple Ascending Doses of LY3478045in Healthy Subjects [NCT04270370]Phase 172 participants (Actual)Interventional2020-03-16Completed
Interactions of Thrombogenic, Lipogenic, and Inflammatory Markers in Women With the Metabolic Syndrome - Effect of Atorvastatin [NCT01785615]Phase 1/Phase 2116 participants (Actual)Interventional2004-11-30Completed
Dapagliflozin Effect in Cognitive Impairment in Stroke Trial [NCT05565976]Phase 2/Phase 3270 participants (Anticipated)Interventional2020-08-01Recruiting
Effect of Atorvastatin and Omega 3 Combination Therapy on Carotid Atherosclerosis Estimated by 3D Ultrasound in Patients With Type 2 Diabetes and Combined Dyslipidemia [NCT05365438]Phase 4105 participants (Anticipated)Interventional2022-10-01Recruiting
Investigation of Interactions Between Faldaprevir, Itraconazole, Atorvastatin and Rosuvastatin in Healthy Male and Female Subjects (Open-label, Fixed-sequence) [NCT01795937]Phase 151 participants (Actual)Interventional2013-02-28Completed
A Multicenter, Randomized, Double-blind, Parallel-group, Placebo-controlled Study Evaluating the Efficacy and Safety of Three Doses of SAR236553 (REGN727) Over 12 Weeks in Patients With Primary Hypercholesterolemia and LDL-cholesterol ≥100 mg/dL (≥2.59 mm [NCT01812707]Phase 2100 participants (Actual)Interventional2013-03-31Completed
A Randomized, Double Blind, Trial of Metformin and Atorvastatin in Delaying Androgen Deprivation Therapy Among Men With Rising PSA Following Radical Prostatectomy or Radiotherapy: The LIGAND (LIpitor and biGuanide to Androgen Delay) Trial [NCT02497638]Phase 20 participants (Actual)Interventional2021-12-31Withdrawn(stopped due to Drug intervention no longer relevant for the proposed population)
A Randomized, Double-blind, Parallel Group Study to Evaluate the Efficacy and Safety of Alirocumab (SAR236553/REGN727) Versus Ezetimibe in Asia in High Cardiovascular Risk Patients With Hypercholesterolemia Not Adequately Controlled With Their Statin Ther [NCT02715726]Phase 3615 participants (Actual)Interventional2016-07-27Completed
MicroRNA Activation of LOX-1 Mechanisms in Endometriosis [NCT05331053]Phase 410 participants (Anticipated)Interventional2018-05-01Suspended(stopped due to COVID halting human subjects research and preliminary data from this proposal were used to submit an NIH grant. The NIH grant was funded and 3 other protocols were launched.)
Evaluation of Adverse Plaque Characteristics in Coronary Computed Tomography Angiography Using Combined Near Infrared Spectroscopy With Intravascular Ultrasound [CITRUS Study] [NCT02350959]Phase 4100 participants (Anticipated)Interventional2015-01-31Recruiting
A Randomized, Double-Blind, Placebo-Controlled Study to Assess the Safety and Efficacy of CAT-2054 in Combination With Atorvastatin in Patients With Hypercholesterolemia [NCT02608697]Phase 2153 participants (Actual)Interventional2015-10-31Completed
Study ATG115317, a Comparison of Atorvastatin and Glimepiride Fixed Dose Combination and Atorvastatin and Glimepiride Loose Combination in the Treatment of Patients With Type 2 Diabetes Mellitus [NCT01495013]Phase 3427 participants (Actual)Interventional2011-12-31Completed
Efficacy and Safety of Prescription Omega-3 Fatty Acid Added to Stable Statin Therapy in Patients With Type 2 Diabetes and Hypertriglyceridemia [NCT02305355]Phase 468 participants (Actual)Interventional2009-02-28Completed
An Experimental Study on the Effect of Tenofovir Amibufenamide on Blood Lipid During Anti-HBV Treatment [NCT05398393]150 participants (Anticipated)Interventional2022-01-01Enrolling by invitation
MUscle Side-Effects of Atorvastatin in Coronary Patients (MUSE) -Follow-up Study [NCT04453735]Phase 427 participants (Actual)Interventional2020-08-19Completed
A Single-center, Open-label, Randomized, Three-way Cross-over Study Evaluating Drug Drug Interaction Between JNJ-70033093 and Atorvastatin in Healthy Participants [NCT04388501]Phase 123 participants (Actual)Interventional2021-06-07Completed
An Open-label, Randomized, Two-sequence, Multiple-dose, Crossover Study to Evaluate Drug-drug Interaction Following Oral Administration of Telmisartan/Amlodipine and Atorvastatin in Healthy Adult Volunteers [NCT03461081]Phase 132 participants (Actual)Interventional2017-05-07Completed
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
Evaluation Of Human Urinary Kallidinogenase in Acute Stroke Patients: Magnetic Resonance Spectrum and CT Perfusion [NCT03431909]Phase 480 participants (Actual)Interventional2014-01-01Completed
A Multicenter, Randomized, Double-Blind, Parallel, 12-Week Study to Evaluate the Efficacy and Safety of Ezetimibe/Simvastatin Combination Tablet Versus Atorvastatin in Elderly Patients With Hypercholesterolemia at High or Moderately High Risk for Coronary [NCT00535405]Phase 31,289 participants (Actual)Interventional2007-11-30Completed
A Multicentric Open-label Randomized Controlled Study for Evaluating the Improvement of Endothelial Function in Stage II Peripheral Arterial Obstructive Disease Patients Treated With Sulodexide + Conventional Treatment {CT] Vs CT Alone [NCT03370705]Phase 3156 participants (Anticipated)Interventional2019-01-31Active, not recruiting
INvestigating the Lowest Threshold of Vascular bENefits From LDL Cholesterol Lowering With a PCSK9 mAb InhibiTor (Alirocumab) in Patients With Stable Cardiovascular Disease (INTENSITY-HIGH) [NCT03355027]60 participants (Actual)Interventional2017-11-30Active, not recruiting
A Pilot Study of Atorvastatin as a Potential Adjunct to Misoprostol for Termination of Pregnancy [NCT05342974]Early Phase 130 participants (Anticipated)Interventional2022-04-19Recruiting
Can Atorvastatin Improve Vascular Function in Women With a History of Preeclampsia? A Randomised, Double-blinded, Placebo-controlled Crossover Trial of Atorvastatin in Women With a History of Preeclampsia. [NCT01278459]Phase 311 participants (Actual)Interventional2011-10-31Completed
A Phase 1, Open-Label, Drug-Drug Interaction Study to Evaluate the Effects of Multiple Oral Doses of Fluconazole and Atorvastatin on the Pharmacokinetics of a Single Oral Dose of TAK-385 in Healthy Subjects [NCT02093390]Phase 140 participants (Actual)Interventional2014-03-31Completed
Double-blind, Randomized, Placebo-controlled, Single Site Study to Evaluate the Effects of Evolocumab (AMG 145) Treatment, Alone and in Combination With Atorvastatin, on Lipoprotein Kinetics [NCT02189837]Phase 389 participants (Actual)Interventional2014-07-08Completed
Statin Therapy in Acute Influenza [NCT02056340]Phase 2116 participants (Actual)Interventional2013-10-31Completed
Evolocumab Added to Statin Therapy in Patients With Symptomatic Intracranial Atherosclerotic Stenosis (EAST-ICAS)---a Pilot Study [NCT05741086]Phase 380 participants (Anticipated)Interventional2023-04-15Recruiting
A Double-blind, Randomized, Multicenter Study to Evaluate the Safety and Efficacy of Evolocumab, Compared With Ezetimibe, in Hypercholesterolemic Subjects Unable to Tolerate an Effective Dose of a HMG-CoA Reductase Inhibitor Due to Muscle Related Side Eff [NCT01984424]Phase 3511 participants (Actual)Interventional2013-12-10Completed
Long-Term, Open-Label, Safety and Tolerability Study of SCH 58235 in Addition to Atorvastatin or Simvastatin in the Therapy of Homozygous Familial Hypercholesterolemia [NCT03885921]Phase 344 participants (Actual)Interventional2000-10-25Completed
The Success of Opening Concurrent Chronic Total Occlusion leSion to Improve Cardiac Function Trial in Patients With Multi-vessel Disease (SOS-moral): Study Protocol of a Prospective Multicenter Study [NCT03372785]240 participants (Anticipated)Observational [Patient Registry]2018-04-10Enrolling by invitation
A Randomized, Open-label, Single Oral Dose, 2-way Crossover Clinical Trial to Compare Safety and Pharmacokinetic Characteristics of CKD-337 in Healthy Male Volunteers [NCT03346187]Phase 160 participants (Actual)Interventional2017-05-19Completed
"An Open Label, One-sequence, 3-period Study to Evaluate Drug-drug Interactions and Safety Between BR1017-1 and BR1017-2 in Healthy Volunteers" [NCT05372380]Phase 132 participants (Actual)Interventional2022-05-09Completed
A Randomized, Double-Blind, Double-Dummy, Active-Controlled Study to Evaluate the Efficacy and Safety of REGN727/SAR236553 in Patients With Primary Hypercholesterolemia Who Are Intolerant to Statins [NCT01709513]Phase 3314 participants (Actual)Interventional2012-09-30Completed
Women's IschemiA TRial to Reduce Events In Non-ObstRuctive CAD [NCT03417388]Phase 44,422 participants (Anticipated)Interventional2018-02-09Recruiting
Phase 1-2 Study of Development of Rational Ways of Medical and Non-medical Treatment Methods for Metabolic Syndrome [NCT02503865]Phase 1/Phase 2351 participants (Actual)Interventional2003-01-31Completed
The SCCS Polypill Pilot Trial [NCT02278471]Phase 2303 participants (Actual)Interventional2015-12-31Completed
A Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study to Evaluate the Efficacy and Safety of REGN727/SAR236553 in Patients With Heterozygous Familial Hypercholesterolemia Not Adequately Controlled With Their Lipid-Modifying Therapy [NCT01709500]Phase 3249 participants (Actual)Interventional2012-12-31Completed
The Addition of Evacetrapib to Atorvastatin Compared to Placebo, High Intensity Atorvastatin, and Atorvastatin With Ezetimibe to Evaluate LDL-C Lowering in Patients With Primary Hyperlipidemia - The ACCENTUATE Study [NCT02227784]Phase 3366 participants (Actual)Interventional2014-10-31Terminated(stopped due to Study termination due to program termination.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00065806 (19) [back to overview]Change in Mean-Max Bifurcation CIMT
NCT00065806 (19) [back to overview]Change in Triglycerides
NCT00065806 (19) [back to overview]Change in Total Cholesterol
NCT00065806 (19) [back to overview]Change in Natural Log of mg/L for hsCRP
NCT00065806 (19) [back to overview]Change in Mean-Mean Near Wall CIMT
NCT00065806 (19) [back to overview]Change in Mean-Mean Internal CIMT
NCT00065806 (19) [back to overview]Change in Mean-Mean Far Wall CIMT
NCT00065806 (19) [back to overview]Change in Mean-Max Common CIMT
NCT00065806 (19) [back to overview]Change in Mean-Max Far Wall CIMT
NCT00065806 (19) [back to overview]Change in Mean-Max Internal CIMT
NCT00065806 (19) [back to overview]Change in Mean-Max Near Wall CIMT
NCT00065806 (19) [back to overview]Change in Mean-Max CIMT
NCT00065806 (19) [back to overview]Change in Lipoprotein A
NCT00065806 (19) [back to overview]Change in LDL Cholesterol
NCT00065806 (19) [back to overview]Change in Homocysteine
NCT00065806 (19) [back to overview]Change in HDL Cholesterol
NCT00065806 (19) [back to overview]Change in Mean-Mean Common Carotid IMT (CIMT)
NCT00065806 (19) [back to overview]Change in Mean-Mean Bifurcation CIMT
NCT00065806 (19) [back to overview]Change in Mean-Mean CIMT
NCT00094172 (3) [back to overview]The Occurrence of ≥ 3 New T2 Lesions With or Without Gd+ Enhancement or Clinical Exacerbation Through 12 Months.
NCT00094172 (3) [back to overview]Proportion of Participants Who Are Diagnosed With Multiple Sclerosis According to the McDonald Criteria
NCT00094172 (3) [back to overview]Proportion of Participants Diagnosed With Multiple Sclerosis According to the McDonald Criteria
NCT00127218 (2) [back to overview]Changes in Plaque Architecture and Composition Directly Measured by Magnetic Resonance Imaging (MRI) in the Aorta and Carotid Arteries
NCT00127218 (2) [back to overview]Multiple Combined Events ( Cardiovascular and Cerebrovascular Events as Well as Myocardial Revascularization)
NCT00153166 (2) [back to overview]Lower Extremity Skeletal Muscle Glucose Uptake
NCT00153166 (2) [back to overview]'M' = Whole Body Insulin Sensitivity
NCT00166036 (2) [back to overview]Change in Plasma Thiobarbituric Acid Reactive Substance (TBARS) Levels
NCT00166036 (2) [back to overview]Change in Flow-mediated Dilatation (FMD)
NCT00166504 (1) [back to overview]LDL-C Lowering Efficacy
NCT00185731 (3) [back to overview]Correlation of Tumor Apoptosis to Clinical Response
NCT00185731 (3) [back to overview]Atorvastatin Toxicity
NCT00185731 (3) [back to overview]Tumor Apoptosis
NCT00233480 (6) [back to overview]High-sensitivity C-reactive Protein (hsCRP) as a Cardiac Biomarker
NCT00233480 (6) [back to overview]Cardiac Biomarker Level BNP
NCT00233480 (6) [back to overview]Cardiac Troponin I (cTnI)
NCT00233480 (6) [back to overview]Left Ventricular End-diastolic Dimension (LVEDD)
NCT00233480 (6) [back to overview]LVEF (Left Ventricular Ejection Fraction)
NCT00233480 (6) [back to overview]Muscle Sympathetic Nerve Activity (by Sympathetic Microneurography)
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 High Density Lipoprotein Cholesterol (HDL-C)
NCT00249249 (12) [back to overview]Oxidized LDL at 12 Weeks
NCT00249249 (12) [back to overview]Apolipoprotein-A1 (Apo-A1)
NCT00249249 (12) [back to overview]Non-HDL:HDL Ratio
NCT00249249 (12) [back to overview]High Sensitivity C-reactive Protein (Hs-CRP) at 12 Weeks
NCT00249249 (12) [back to overview]National Cholesterol Education Program [NCEP]LDL-C Target Attainment
NCT00249249 (12) [back to overview]Apo-B:Apo-A1 Ratio
NCT00249249 (12) [back to overview]Apolipoprotein B (Apo B)
NCT00249249 (12) [back to overview]Percent Change From Baseline in Total Cholesterol (TC)
NCT00252967 (9) [back to overview]Comparison of Derivatives of Reactive Oxygen Metabolites Values
NCT00252967 (9) [back to overview]Comparison of Interleukin-1 Values
NCT00252967 (9) [back to overview]Comparison of High Sensitivity C-reactive Protein
NCT00252967 (9) [back to overview]Comparison of Interleukin-6 Values
NCT00252967 (9) [back to overview]Comparison of Isoprostanes Values
NCT00252967 (9) [back to overview]Comparison of Redox Potential for Cysteine Values
NCT00252967 (9) [back to overview]Comparison of Redox Potential for Glutathione Values
NCT00252967 (9) [back to overview]Comparison of Tumor Necrosis Factor Alpha Values
NCT00252967 (9) [back to overview]Time of Atrial Fibrillation Recurrence
NCT00276458 (14) [back to overview]Percent Change From Baseline in Total-Cholesterol:High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (HDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Total-Cholesterol at Week 6
NCT00276458 (14) [back to overview]Number of Participants Who Attained Target LDL-C <100 mg/dL at Week 6
NCT00276458 (14) [back to overview]Percent Change in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6
NCT00276458 (14) [back to overview]Percent Change in C-Reactive Protein (CRP) at Week 6
NCT00276458 (14) [back to overview]Percent Change in Apolipoprotein A-I at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Triglycerides (TG) at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Apolipoprotein B: Apolipoprotein A-I Ratio at Week 6
NCT00276458 (14) [back to overview]Percent Change in High Density Lipoprotein -Cholesterol (HDL-C)at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in C-Reactive Protein (CRP) at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00276458 (14) [back to overview]Percent Change From Baseline in Low Density Lipoprotein-Cholesterol (LDL-C) at Week 6
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Low-Density Lipoprotein-Cholesterol:High-Density Lipoprotein-Cholesterol (LDL-C:HDL-C) Ratio
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Low-Density Lipoprotein (LDL)-C
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in High-Density Lipoprotein Cholesterol (HDL-C)
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in C Reactive Protein (CRP)
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Apolipoprotein B (Apo B)
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Apolipoprotein A-I (Apo A-I)
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Apolipoprotein B:Apolipoprotein A-I (Apo B:Apo A-I) Ratio
NCT00276484 (13) [back to overview]Number of Patients Who Attained Target Low-Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 6
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Triglycerides (TG)
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Total-Cholesterol (TC):High-Density Lipoprotein Cholesterol (HDL-C) Ratio
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Total-Cholesterol
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Non-High-Density Lipoprotein-Cholesterol:High-Density Lipoprotein-Cholesterol (Non-HDL-C:HDL-C) Ratio
NCT00276484 (13) [back to overview]Percent Change From Baseline to Week 6 in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C)
NCT00279708 (1) [back to overview]The Steroid Sparing Period
NCT00289900 (25) [back to overview]Percentage Change From Baseline in TC/HDL-C Ratio
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Apolipoprotein (Apo) B
NCT00289900 (25) [back to overview]Percentage Change From Baseline in C-reactive Protein (CRP)
NCT00289900 (25) [back to overview]Percentage Change From Baseline in HDL-C
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Apo A-I
NCT00289900 (25) [back to overview]Percentage of Participants Who Experience at Least 1 Hepatitis-related Clinical AE
NCT00289900 (25) [back to overview]Percentage Change From Baseline in LDL-C
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Lipoprotein (a) (Lp[a])
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Non-HDL-C
NCT00289900 (25) [back to overview]Percentage Change From Baseline in the LDL-C/HDL-C Ratio
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Total Cholesterol (TC)
NCT00289900 (25) [back to overview]Percentage Change From Baseline in Triglycerides (TG)
NCT00289900 (25) [back to overview]Percentage of Participants Who Experience at Least 1 Clinical Adverse Event (AE)
NCT00289900 (25) [back to overview]Percentage of Participants Who Experience at Least 1 Laboratory Adverse Event (AE)
NCT00289900 (25) [back to overview]Percentage of Participants With New Diagnosis of Impaired Fasting Blood Glucose
NCT00289900 (25) [back to overview]Percentage of Participants With New Diagnosis of Diabetes
NCT00289900 (25) [back to overview]Percentage of Participants With Elevations in ALT and/or AST of >=5 x ULN
NCT00289900 (25) [back to overview]Percentage of Participants With Elevations in ALT and/or AST of >=10 x ULN
NCT00289900 (25) [back to overview]Percentage of Participants With Creatine Kinase (CK) >=10 x ULN
NCT00289900 (25) [back to overview]Percentage of Participants With Consecutive Elevations in Alanine Aminotransferase (ALT) and/or Aspartate Aminotransferase (AST) of >=3 x Upper Limit of Normal (ULN)
NCT00289900 (25) [back to overview]Percentage of Participants With CK >=10 x ULN With Muscle Symptoms - Drug Related
NCT00289900 (25) [back to overview]Percentage of Participants With CK >=10 x ULN With Muscle Symptoms
NCT00289900 (25) [back to overview]Percentage of Participants With a Confirmed Adjudicated Cardiovascular Event
NCT00289900 (25) [back to overview]Percentage of Participants Who Were Discontinued From the Study Due to a Laboratory AE
NCT00289900 (25) [back to overview]Percentage of Participants Who Were Discontinued From the Study Due to a Clinical AE
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoA1
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoA1
NCT00296374 (72) [back to overview]Correlation Coefficient Urinary Protein/Creatinine Ratio and Total Cholesterol [TC] Indicating the Relationship Between Renal Effects and Lipid Changes
NCT00296374 (72) [back to overview]Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 26
NCT00296374 (72) [back to overview]Change From Baseline in eGFR at Week 52 [LOCF]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and High Density Lipoprotein Cholesterol [HDL-C]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Low Density Lipoprotein Cholesterol [LDL-C]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Non-high Density Lipoprotein Cholesterol [nonHDL-C]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TG
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Triglyceride [TG]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio TC
NCT00296374 (72) [back to overview]Urinary Albumin/Creatinine Ratio at Week 26
NCT00296374 (72) [back to overview]Urinary Albumin/Creatinine Ratio at Week 52 [LOCF]
NCT00296374 (72) [back to overview]Urinary Protein/Creatinine Ratio at Week 26.
NCT00296374 (72) [back to overview]Urinary Protein/Creatinine Ratio in Patients With Type 1 or 2 Diabetes.
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TG
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Apolipoprotein A-1 [ApoA-1]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Apolipoprotein B [ApoB]
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and HDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TC
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TC
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoA-1
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoA-1
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoA-1
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and HDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and HDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and HDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TG
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and HDL-C
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and TG
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TG
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C/HDL-C Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB/ApoA-1 Ratio
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB
NCT00296374 (72) [back to overview]Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in TC at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in LDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in LDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in HDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in HDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TG at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TG
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TC/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TC/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB at Week 26
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoA1 at Week 52
NCT00296400 (72) [back to overview]Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoA1 at Week 26
NCT00296400 (72) [back to overview]Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TG at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Total Cholesterol [TC] at Week 26.
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Total Cholesterol [TC] at Week 52.
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Triglyceride [TG] at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline inUrinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C
NCT00296400 (72) [back to overview]Urinary Albumin/Creatinine Ratio at Week 26
NCT00296400 (72) [back to overview]Urinary Albumin/Creatinine Ratio at Week 52 [LOCF]
NCT00296400 (72) [back to overview]Urinary Protein/Creatinine Ratio at Week 26.
NCT00296400 (72) [back to overview]Urinary Protein/Creatinine Ratio at Week 52 [LOCF]
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Change From Baseline in eGFR at Week 52 [LOCF]
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TG at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TG at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Apolipoprotein A-1 [ApoA-1] at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Apolipoprotein B [ApoB] at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in High Density Lipoprotein Cholesterol [HDL-C] at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Non-high Density Lipoprotein Cholesterol [nonHDL-C] at Week 26
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52
NCT00296400 (72) [back to overview]Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in TC at Week 52
NCT00300430 (9) [back to overview]Mean Percent Change in Total Cholesterol From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Mean Percent Change in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 52 in This Open-label Study
NCT00300430 (9) [back to overview]Mean Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Mean Percent Change in Direct Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Median Percent Change in High-sensitivity C-reactive Protein (hsCRP) From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Mean Percent Change in Very Low-density Lipoprotein Cholesterol (VLDL-C) From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Median Percent Change in Triglycerides From Baseline to Week 52 of the Open-label Study
NCT00300430 (9) [back to overview]Percentage of Subjects Reporting Adverse Events During Combination Therapy, Either in the Preceding Double-blind Studies or in This Open-label Study
NCT00300430 (9) [back to overview]Mean Percent Change in Apolipoprotein B (Apo B) From Baseline to Week 52 of the Open-label Study
NCT00300469 (8) [back to overview]Mean Percent Change in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in Triglycerides From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in Total Cholesterol From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in Lipoprotein Apo B (Apo B) From Baseline to Final Visit
NCT00300469 (8) [back to overview]Median Percent Change in High-sensitivity C-reactive Protein (hsCRP) From Baseline to Final Visit
NCT00300469 (8) [back to overview]Mean Percent Change in Very Low-density Lipoprotein Cholesterol (VLDL-C) From Baseline to Final Visit
NCT00309751 (2) [back to overview]Percent Change From Baseline Low Density Lipoprotein Cholesterol (LDL-C)
NCT00309751 (2) [back to overview]Number of Patients Attaining National Cholesterol Education Program (NCEP) LDL-C Target
NCT00319449 (3) [back to overview]Number of Participants Who Achieve the Target LDL-C Concentration of < 3.3 mmol/L (130 mg/dL)
NCT00319449 (3) [back to overview]Low Density Lipoprotein-cholesterol (LDL-C) at Baseline and After 6 Weeks of Treatment With Ezetimibe 10 mg Added to Atorvastatin 10 mg Versus Placebo Added to Atorvastatin 10 mg
NCT00319449 (3) [back to overview]High Density Lipoprotein-cholesterol (HDL-C), Total Cholesterol and Triglycerides at Baseline and After 6 Weeks of Treatment With Ezetimibe 10 mg Added to Atorvastatin 10 mg Versus Placebo Added to Atorvastatin 10 mg
NCT00335504 (4) [back to overview]Effects on Apoptosis (Caspase-3 Expression).
NCT00335504 (4) [back to overview]Effects on Proliferation (Ki67 Expression).
NCT00335504 (4) [back to overview]Percent Change in Number of Rectal Aberrant Cryptic Foci (ACF) as Measured by Magnification Chromoendoscopy
NCT00335504 (4) [back to overview]Adverse Events.
NCT00344370 (2) [back to overview]Percent Change From Baseline in LDL-C
NCT00344370 (2) [back to overview]NCEP LDL-C Target Attainment
NCT00359281 (11) [back to overview]AUC0-t Atorvastatin Acid (Lomitapide 60 mg)
NCT00359281 (11) [back to overview]Area Under Concentration-time Curve From 0 to Last Measureable Concentration (AUC0-t) Atorvastatin Acid (Lomitapide 10 mg)
NCT00359281 (11) [back to overview]AUC0-t Simvastatin
NCT00359281 (11) [back to overview]AUC0-t Simvastatin Acid
NCT00359281 (11) [back to overview]AUC0-t Total Ezetimibe
NCT00359281 (11) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C)
NCT00359281 (11) [back to overview]AUC0-t Nicotinuric Acid
NCT00359281 (11) [back to overview]AUC0-t Nicotinic Acid
NCT00359281 (11) [back to overview]AUC0-t Rosuvastatin (Lomitapide 60 mg)
NCT00359281 (11) [back to overview]AUC0-t Fenofibric Acid
NCT00359281 (11) [back to overview]AUC0-t Rosuvastatin (Lomitapide 10 mg)
NCT00361283 (1) [back to overview]Mean Change in Level: Week 16-baseline in Ena-78
NCT00367458 (5) [back to overview]Number of Participants With Serious and Non-Serious Adverse Events
NCT00367458 (5) [back to overview]Change in Percentage of Cluster of Differentiation 8 (CD8+) Human Leukocyte Antigen DR (HLA-DR+), CD8+(CD8+HLADR+CD38+) in Peripheral Blood
NCT00367458 (5) [back to overview]Change in Percentage of Cluster of Differentiation 8 (CD8+) Human Leukocyte Antigen DR (HLA-DR+) in Peripheral Blood
NCT00367458 (5) [back to overview]Change in Percentage of Cluster of Differentiation 4 (CD4+) Human Leukocyte Antigen DR (HLA-DR+) in Peripheral Blood
NCT00367458 (5) [back to overview]Change in Human Immunodeficiency Virus 1 (HIV-1) Ribonucleic Acid (RNA) Levels
NCT00375518 (1) [back to overview]Determine the Postoperative Complications Found in Each Group
NCT00395486 (12) [back to overview]Percentage Change of Total Cholesterol (TC)
NCT00395486 (12) [back to overview]Percentage Reduction of Low-Density Lipoprotein-C (LDL-C)
NCT00395486 (12) [back to overview]Percentage of Subjects Reaching Their Low-Density Lipoprotein-C (LDL-C) and Non High-Density Lipoprotein-C (HDL-C) Target Goal
NCT00395486 (12) [back to overview]Percentage of Subjects Reaching Their LDL-C Target Goal
NCT00395486 (12) [back to overview]Percentage Change of Triglycerides (TG)
NCT00395486 (12) [back to overview]Percentage Change of Insulin Resistance Using QUICKI
NCT00395486 (12) [back to overview]Percentage Change of Insulin Resistance Using HOMA-R
NCT00395486 (12) [back to overview]Percentage Change of High-Density Lipoprotein-C (HDL-C)
NCT00395486 (12) [back to overview]Percentage Change of Glucose Level
NCT00395486 (12) [back to overview]Percentage Change of Apolipoprotein A1 (ApoA1)
NCT00395486 (12) [back to overview]Percentage Change of Apolipoprotein B (ApoB)
NCT00395486 (12) [back to overview]Percentage Change From Baseline in Ratio of Apolipoprotein (ApoB/ApoA1) at Week 6
NCT00407537 (22) [back to overview]European Systematic COronary Risk Evaluation (SCORE) 10-year Risk of Fatal Cardiovascular Disease (CVD) at Month 12
NCT00407537 (22) [back to overview]Framingham 10-year Risk of Stroke at Month 12
NCT00407537 (22) [back to overview]Framingham 10-year Risk of Stroke at Month 4
NCT00407537 (22) [back to overview]Framingham 10-year Risk of Total CHD at Month 4
NCT00407537 (22) [back to overview]Framingham 10-year Risk of Total Coronary Heart Disease (CHD) at Month 12
NCT00407537 (22) [back to overview]Change From Baseline European SCORE 10-year Risk of Developing Fatal CVD
NCT00407537 (22) [back to overview]Change From Baseline in Framingham 10-year Risk of Developing Total CHD
NCT00407537 (22) [back to overview]Change From Baseline in Lipid Parameters at Month 12
NCT00407537 (22) [back to overview]Change From Baseline in Lipid Parameters at Month 4
NCT00407537 (22) [back to overview]Mean Lipid Parameters at Month 12
NCT00407537 (22) [back to overview]Mean Lipid Parameters at Month 4
NCT00407537 (22) [back to overview]Mean Systolic and Diastolic Blood Pressure at Month 12
NCT00407537 (22) [back to overview]Mean Systolic and Diastolic Blood Pressure at Month 4
NCT00407537 (22) [back to overview]Number of Participants With Increase of Treatment Dosages After 4 Months.
NCT00407537 (22) [back to overview]Number of Participants With Lipid and Antihypertensive Treatments Used at 4 and 12 Months
NCT00407537 (22) [back to overview]Percentage of Participants at Conventional Treatment Goals According to Global and Local Guidelines for Blood Pressure at 4 and 12 Months
NCT00407537 (22) [back to overview]Percentage of Participants at Conventional Treatment Goals According to Global and Local Guidelines for LDL at 4 and 12 Months
NCT00407537 (22) [back to overview]Change From Baseline in SBP at Month 12
NCT00407537 (22) [back to overview]Change From Baseline in DBP at Month 12
NCT00407537 (22) [back to overview]Change From Baseline in Diastolic Blood Pressure (DBP) at Month 4
NCT00407537 (22) [back to overview]Change From Baseline in Systolic Blood Pressure (SBP) at Month 4
NCT00407537 (22) [back to overview]European SCORE 10-year Risk of Fatal CVD at Month 4
NCT00409773 (15) [back to overview]Percent Change From Baseline in Non- High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol: High Density Lipoprotein Cholesterol (Non-HDL-C:HDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Apolipoprotein-B: Apolipoprotein-A1 (Apo-B:Apo-A1) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Apolipoprotein-A1 (Apo-A1) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Apolipoprotein- B (Apo-B) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in High-Sensitivity C-reactive (Hs-CRP) (mg/dL) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Total-Cholesterol: High Density Lipoprotein-Cholesterol (Total-C:HDL- C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Total Cholesterol(mg/dL) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Very Low Density Lipoprotein Cholesterol (VLDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Low Density Lipoprotein (LDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 6 in Patients With Atherosclerotic Vascular Disease (AVD)
NCT00409773 (15) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 6 in Patients Without Atherosclerotic Vascular Disease (AVD)
NCT00409773 (15) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol: High Density Lipoprotein Cholesterol (LDL-C: HDL-C) at Week 6
NCT00409773 (15) [back to overview]Percent Change From Baseline in Triglyceride (TG) (mg/dL) at Week 6
NCT00412113 (24) [back to overview]Subjects With LDL-C < 100 mg/dL at Week 6
NCT00412113 (24) [back to overview]Subjects With BP <140/90 mmHg and LDL-C <130 mg/dL at Week 4.
NCT00412113 (24) [back to overview]Change From Baseline in HDL at Week 6.
NCT00412113 (24) [back to overview]Change From Baseline in High Density Lipoprotein (HDL) at Week 4.
NCT00412113 (24) [back to overview]Change From Baseline in LDL at Week 4.
NCT00412113 (24) [back to overview]Change From Baseline in LDL at Week 6.
NCT00412113 (24) [back to overview]Change From Baseline in Total Cholesterol (TC) to Week 6.
NCT00412113 (24) [back to overview]Change From Baseline in Triglycerides (TG) at Week 6.
NCT00412113 (24) [back to overview]Change From Baseline in Triglycerides (TG) to Week 4.
NCT00412113 (24) [back to overview]Change From Baseline to Week 4 in Diastolic Blood Pressure (DBP)
NCT00412113 (24) [back to overview]Change From Baseline to Week 4 in Framingham Predicted Absolute 10-year Risk.
NCT00412113 (24) [back to overview]Change From Baseline to Week 4 in Pulse Rate
NCT00412113 (24) [back to overview]Change From Baseline to Week 4 in Systolic Blood Pressure (SBP).
NCT00412113 (24) [back to overview]Change From Baseline to Week 6 in Diastolic Blood Pressue (DBP)
NCT00412113 (24) [back to overview]Change From Baseline to Week 6 in Framingham Predicted Absolute 10-year Risk
NCT00412113 (24) [back to overview]Change From Baseline to Week 6 in Pulse Rate
NCT00412113 (24) [back to overview]Change From Baseline to Week 6 in Systolic Blood Pressure (SBP)
NCT00412113 (24) [back to overview]Change in Total Cholesterol (TC) From Baseline to Week 4.
NCT00412113 (24) [back to overview]Subjects With Blood Pressure (BP) <140/90 Millimeters of Mercury (mmHg) and Low Density Lipoprotein Cholesterol (LDL-C) <100 Milligrams Per Deciliter(mg/dL) at Week 6
NCT00412113 (24) [back to overview]Subjects With Blood Pressure of <140/90 mmHg and LDL-C <100 mg/dL at Week 4
NCT00412113 (24) [back to overview]Subjects With BP < 140/90 mmHg at Week 4
NCT00412113 (24) [back to overview]Subjects With BP < 140/90 mmHg at Week 6
NCT00412113 (24) [back to overview]Subjects With BP <140/90 mmHg and LDL-C <130 mg/dL at Week 6.
NCT00412113 (24) [back to overview]Subjects With LDL-C < 100 mg/dL at Week 4
NCT00412841 (2) [back to overview]Number of Participants With AVN After 9 Months
NCT00412841 (2) [back to overview]Number of Participants With AVN After 4 Months
NCT00418834 (28) [back to overview]Number of Patients Who Achieved Low Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 6
NCT00418834 (28) [back to overview]Number of Patients Who Achieved Low Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 12
NCT00418834 (28) [back to overview]Number of Patients Who Achieved LDL-C<100 mg/dL for Patients Without AVD and LDL-C<70 mg/dL for Patients With AVD at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein B (Apo B) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Triglycerides (TG) at Week 6
NCT00418834 (28) [back to overview]Number of Patients Who Achieved LDL-C <100 mg/dL for Patients Without Atherosclerotic Vascular Disease (AVD) and LDL-C <70 mg/dL for Patients With Atherosclerotic Vascular Disease (AVD) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein B (Apo B) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein A-I (Apo A-I) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein A-I (Apo A-I) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Ratio of Highly Selective C-Reactive Protein (Hs-CRP) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Triglycerides (TG) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC): High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in LDL-C at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 12
NCT00418834 (28) [back to overview]Percent Change From Baseline in Ratio of Highly Selective C-Reactive Protein (Hs-CRP) at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein B (Apo B):Apo Lipoprotein A-I (Apo A-I) Ratio at Week 6
NCT00418834 (28) [back to overview]Percent Change From Baseline in Apo Lipoprotein B (Apo B):Apo Lipoprotein A-I (Apo A-I) Ratio at Week 12
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6) in Apolipoprotein-B (ApoB)
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6) in TC/HDL-C Ratio
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6)in LDL-C/HDL-C Ratio
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6)in Non-HDL-C
NCT00427960 (15) [back to overview]The Percentage Change From Baseline(Week 6) in Non-HDL-C/HDL-C Ratio
NCT00427960 (15) [back to overview]The Percentage Change From Baseline(week6) in TC
NCT00427960 (15) [back to overview]The Percentage of Participants Reaching the European (EAS) Targets of LDL-C<2.5 or 3.00 mmol/L, Depending on Risk Category, and the Combined LDL-C and TC Target of LDL-C<2.5 or 3.0 mmol/L and TC<4.5 or 5.0 mmol/L, Both Depending on Risk Category.
NCT00427960 (15) [back to overview]The Percentage of Participants Reaching the European (EAS) Targets of LDL-C<2.5 or 3.00 mmol/L, Depending on Risk Category.
NCT00427960 (15) [back to overview]The Percentage of Participants Reaching the General Medical Services (GMS) Contract Target of Total Cholesterol (TC) <5 mmol/L
NCT00427960 (15) [back to overview]The Percentage of Participants Reaching the Joint British Societies' Guideline (JBS 2) Targets of TC <4 mmol/L and LDL-C <2 mmol/L
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6) in High-density Lipoprotein Cholesterol (HDL-C)
NCT00427960 (15) [back to overview]The Percentage of Participants Reaching the Joint British Societies Guideline (JBS 2) Target of TC <4 mmol/L
NCT00427960 (15) [back to overview]Percentage Change in Low Density Lipoprotein - Cholesterol (LDL-C)
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6) in ApoB/ApoA1 Ratio
NCT00427960 (15) [back to overview]The Percentage Change From Baseline (Week 6) in Apolipoprotein-A1 (ApoA1)
NCT00435045 (25) [back to overview]Percent Change in Low Density Lipoprotein Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Low Density Lipoprotein Particle Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Non-High Density Lipoprotein Cholesterol From Baseline to Week 12 During 20 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Intermediate Density Lipoprotein Particle Concentration From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in High Density Lipoprotein (HDL)Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in High Density Lipoprotein (HDL) Particle Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in High Density Lipoprotein (HDL) Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Docosahexaenoic Acid (DHA) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Apolipoprotein-B From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Apolipoprotein-A-1 From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Triglycerides From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Eicosapentaenoic Acid (EPA) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Apolipoprotein C-III From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Low Density Lipoprotein (LDL) Cholesterol (Beta-quantification) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Total Adiponectin From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Total Cholesterol (TC) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Remnant-like Particle Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Total Cholesterol/High Density Lipoprotein Cholesterol Ratio From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Triglycerides/High Density Lipoprotein Cholesterol Ratio From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Very Low Density Lipoproteins (VLDL) Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Lipoprotein-Phosphoslipase A2 From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Non-High Density Lipoprotein Cholesterol From Baseline to Week 16 During 40 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Very Low Density Lipoproteins and Chylomicron Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00435045 (25) [back to overview]Percent Change in Very Low Density Lipoproteins Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period
NCT00442897 (2) [back to overview]Number of Participants Reaching the LDL-C (Low Density Lipoprotein-Cholesterol) Goal (< 100 mg/dl) After 6 Weeks of Treatment
NCT00442897 (2) [back to overview]Number of Participants Reaching the LDL-C Goal (< 100 mg/dl) After 12 Weeks of Treatment
NCT00462748 (1) [back to overview]Percentage of Patients Achieving a Target of Fasting LDL-C of <2mmol/l at Study End
NCT00465088 (14) [back to overview]Percent Change in Triglycerides From Baseline to Week 12
NCT00465088 (14) [back to overview]Percent Change in Total Cholesterol:HDL-C Ratio
NCT00465088 (14) [back to overview]Percent Change in Total Cholesterol From Baseline to Week 12
NCT00465088 (14) [back to overview]Percent Change in Non-HDL-C From Baseline to Week 8
NCT00465088 (14) [back to overview]Percent Change in Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 12
NCT00465088 (14) [back to overview]Percent Change in Lipoprotein A From Baseline to Week 12
NCT00465088 (14) [back to overview]Percent Change in LDL-C:HDL-C Ratio
NCT00465088 (14) [back to overview]Percent Change in Non-HDL-C From Baseline to Week 12
NCT00465088 (14) [back to overview]Percent Change in HDL-C From Baseline to Week 8
NCT00465088 (14) [back to overview]Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 12
NCT00465088 (14) [back to overview]Percentage of Subjects With Triglycerides < 150 mg/dL at Week 12
NCT00465088 (14) [back to overview]Percentage of Subjects With HDL-C >/= 40 mg/dL, LDL-C Meeting NCEP ATP III Goal, and Triglycerides < 150 mg/dL at Week 12
NCT00465088 (14) [back to overview]Percentage of Subjects Meeting With HDL-C >/= 40 mg/dL at Week 12
NCT00465088 (14) [back to overview]Percentage of Subjects Meeting National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III Goal for LDL-C at Week 12
NCT00474240 (2) [back to overview]Percent Change From Baseline of Other Lipids
NCT00474240 (2) [back to overview]Percent Change From Baseline in LDL-C at 8 Weeks
NCT00479388 (3) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12
NCT00479388 (3) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12
NCT00479388 (3) [back to overview]Percent Change From Baseline in Triglycerides at Week 12
NCT00490698 (1) [back to overview]Median Time to First Skeletal-related Event
NCT00491530 (7) [back to overview]Mean Percent Change in Direct Low-Density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Mean Percent Change in Total Cholesterol (Total-C) From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Mean Percent Change in Very Low-Density Lipoprotein Cholesterol (VLDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Mean Percent Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Median Percent Change in Triglycerides From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Mean Percent Change in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study
NCT00491530 (7) [back to overview]Percentage of Subjects Reporting Adverse Events During Combination Therapy in the Preceding Double-Blind Studies or in the Preceding Open-Label Year 1 Study or in This Open-Label Year 2 Study
NCT00491751 (2) [back to overview]Percentage Change in FMD in All Participants With and Without a CVD Event (Not by Treatment Group)
NCT00491751 (2) [back to overview]Change in FMD
NCT00496730 (3) [back to overview]Mean Percent Change of Low Density Lipoprotein-Cholesterol (LDL-C) From Baseline After 8 Weeks.
NCT00496730 (3) [back to overview]Number of Patients Attaining LDL-C Goal After 8 Weeks Treatment.
NCT00496730 (3) [back to overview]Change in Lower Density Lipoprotein Cholesterol From Baseline After 8 Weeks.
NCT00504829 (2) [back to overview]Percent Changes From Baseline to End-of-treatment in Non-HDL, HDL and LDL Cholesterol by LCP-AtorFen Versus Fenofibrate Monotherapy
NCT00504829 (2) [back to overview]Percent Changes From Baseline to End-of-treatment in Non-HDL Cholesterol, HDL Cholesterol, and Triglycerides by LCP-AtorFen Versus Atorvastatin Monotherapy
NCT00529191 (8) [back to overview]Number of Episodes of Hypoglycemia Requiring Any Treatment
NCT00529191 (8) [back to overview]Blood Glucose Control (Number of Participants With Hypoglycemia)
NCT00529191 (8) [back to overview]HDL and LDL Cholesterol Levels in Participants Stratified by the Preservation of Islet Cell Function
NCT00529191 (8) [back to overview]Levels of HbA1c at Months 3, 6, 9, 12 and 18
NCT00529191 (8) [back to overview]% Subjects Without Change in 2-hour C-peptide AUC in Response to the MMTT at Baseline vs. 12 Months
NCT00529191 (8) [back to overview]Mean Daily Insulin Dose Per kg Body Weight for 7 Days
NCT00529191 (8) [back to overview]Efficacy of a Daily Dose of Atorvastatin to Maintain Islet Cell Function as Measured by a 4-hour C-peptide Area Under Curve (AUC) in Patients With Newly Diagnosed Type 1 Diabetes Mellitus
NCT00529191 (8) [back to overview]Study Drug Compliance Rate Overall
NCT00529542 (18) [back to overview]Body Mass Index
NCT00529542 (18) [back to overview]Brachial Artery Flow-mediated Dilation (FMD)
NCT00529542 (18) [back to overview]Triglycerides
NCT00529542 (18) [back to overview]LDL Cholesterol
NCT00529542 (18) [back to overview]Systolic Blood Pressure
NCT00529542 (18) [back to overview]HDL Cholesterol
NCT00529542 (18) [back to overview]Peak Brachial Artery Conductance (BAC)
NCT00529542 (18) [back to overview]High-sensitivity C-reactive Protein (hsCRP)
NCT00529542 (18) [back to overview]Total Cholesterol
NCT00529542 (18) [back to overview]Fasting Insulin
NCT00529542 (18) [back to overview]Area Under the Curve (AUC) for Glucose During OGTT
NCT00529542 (18) [back to overview]Fasting Glucose
NCT00529542 (18) [back to overview]Diastolic Blood Pressure
NCT00529542 (18) [back to overview]DHEAS
NCT00529542 (18) [back to overview]Androstenedione
NCT00529542 (18) [back to overview]Mean Ovarian Volume
NCT00529542 (18) [back to overview]Total Testosterone
NCT00529542 (18) [back to overview]AUC for Insulin
NCT00530946 (11) [back to overview]Percent Change in High Density Lipoprotein-Cholesterol From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Percent Change in Low Density Lipoprotein-Cholesterol From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Percent Change in Total Cholesterol From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Percent Change in Triglycerides From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Change in Low Density Lipoprotein-Cholesterol/ High Density Lipoprotein-Cholesterol Ratio (LDL-C/HDL-C) From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Change in Total Cholesterol/ High Density Lipoprotein-Cholesterol Ratio (TC/HDL-C) From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Change in Systolic Blood Pressure From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Change in Diastolic Blood Pressure From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Change in Apolipoprotein B From Baseline to Each Observation Point
NCT00530946 (11) [back to overview]Percent Change in Low Density Lipoprotein-Cholesterol
NCT00530946 (11) [back to overview]Change in Systolic Blood Pressure
NCT00535405 (6) [back to overview]Percentage of Patients With AVD Who Achieved LDL-C <70 mg/dL at Week 12
NCT00535405 (6) [back to overview]Percentage of Patients Who Achieved LDL-C <70 mg/dL at Week 12
NCT00535405 (6) [back to overview]Percentage of Patients Who Achieved LDL-C <100 mg/dL at Week 12
NCT00535405 (6) [back to overview]Percent Change From Baseline in Low Density Lipoprotein (LDL-C) at Week 12
NCT00535405 (6) [back to overview]Percentage of Patients Without Atherosclerosis Vascular Disease (AVD) Who Achieved LDL-C <100 mg/dL or Patients With AVD Who Achieved LDL-C <70 mg/dL at Week 12
NCT00535405 (6) [back to overview]Percentage of Patients With High Risk for CHD Who Achieved LDL-C <70 mg/dL at Week 12
NCT00540293 (10) [back to overview]Percent of Subjects in the Total Group and Each Cardiovascular Risk Group Achieving LDL-C Target After 4 Weeks of Treatment.
NCT00540293 (10) [back to overview]Changes From Baseline in Selected Inflammatory Markers After 8 Weeks of Treatment.
NCT00540293 (10) [back to overview]Percent of Subjects in the Total and Each Cardiovascular Risk Group Achieving Low Density Lipoprotein-cholesterol (LDL-C) Target After 8 Weeks of Treatment.
NCT00540293 (10) [back to overview]Subjects Who Achieved LDL-C Target With no Titration of Atorvastatin and After One Step Titration of Atorvastatin.
NCT00540293 (10) [back to overview]Percent of Subjects Who Achieved LDL-C Target With no Titration of Atorvastatin and After One Step Titration of Atorvastatin.
NCT00540293 (10) [back to overview]Percent Changes From Baseline in Selected Inflammatory Markers After 8 Weeks of Treatment.
NCT00540293 (10) [back to overview]Percent Changes From Baseline in Lipid Parameters in Subjects in the Total Group and Each Cardiovascular Risk Group After 4 and 8 Weeks of Treatment
NCT00540293 (10) [back to overview]Percent Change From Baseline in High Sensitive Circulating C-reactive Protein (Hs-CRP) After 4 and 8 Weeks of Treatment
NCT00540293 (10) [back to overview]Changes in Lipid Parameters in Subjects in the Total Group and Each Cardiovascular Risk Group After 4 and 8 Weeks of Treatment
NCT00540293 (10) [back to overview]Change From Baseline in High Sensitive Circulating C-reactive Protein (Hs-CRP) After 4 and 8 Weeks of Treatment
NCT00559962 (1) [back to overview]Absolute Change From Baseline in Percent Hepatic Fat
NCT00576576 (3) [back to overview]Change in Fibrous Plaque Volume
NCT00576576 (3) [back to overview]Change in Necrotic Core Volume
NCT00576576 (3) [back to overview]Change in Atheroma Volume
NCT00579098 (5) [back to overview]Change in Mean C-Reactive Protein Level
NCT00579098 (5) [back to overview]Change in Mean Quality of Life Score
NCT00579098 (5) [back to overview]Percentage of Subjects Without Atrial Arrhythmia at 3 Months
NCT00579098 (5) [back to overview]Percentage of Subjects Without Symptoms of Atrial Fibrillation at 3 Months
NCT00579098 (5) [back to overview]Change in Lipid Levels
NCT00616772 (5) [back to overview]Rate of Change in Mean of Maximal Posterior-wall Carotid Intima-media Thickness (cIMT)
NCT00616772 (5) [back to overview]Rate of Change in Composite of Mean of Maximal Posterior-wall Intima-media Thickness (IMT)
NCT00616772 (5) [back to overview]Rate of Change in Composite of Mean of the Mean Posterior-wall Intima-media Thickness (IMT)
NCT00616772 (5) [back to overview]Rate of Change in Composite of Mean of Maximal Posterior-wall and Anterior-wall Intima-media Thickness (IMT)
NCT00616772 (5) [back to overview]Rate of Change in Mean Posterior-wall Carotid Intima-media Thickness (cIMT)
NCT00620542 (16) [back to overview]Non-HDL-C Blood Level
NCT00620542 (16) [back to overview]VLDL-C During the 104 Week Treatment Period
NCT00620542 (16) [back to overview]Apolipoprotein A-1 Blood Level
NCT00620542 (16) [back to overview]Apolipoprotein B Blood Level
NCT00620542 (16) [back to overview]Apoliprotein B/Apolipoprotein A-1 Blood Level
NCT00620542 (16) [back to overview]Change From Baseline to End of Study (Week 104) in Total Atheroma Volume (TAV)
NCT00620542 (16) [back to overview]HDL-C Blood Level
NCT00620542 (16) [back to overview]LDL-C Blood Level
NCT00620542 (16) [back to overview]LDL-C/HDL-C Blood Level
NCT00620542 (16) [back to overview]Change From Baseline to End of Study (Week 104) in Percent Atheroma Volume (PAV)
NCT00620542 (16) [back to overview]Non-HDL-C/HDL-C Blood Level
NCT00620542 (16) [back to overview]Numbers of Patients Showing Regression in PAV
NCT00620542 (16) [back to overview]Numbers of Patients Showing Regression in TAV
NCT00620542 (16) [back to overview]Total Cholesterol Blood Level
NCT00620542 (16) [back to overview]Total Cholesterol/HDL-C Blood Level
NCT00620542 (16) [back to overview]Triglycerides Blood Level
NCT00631189 (9) [back to overview]Compare the Percentage of Variation From Baseline Apolipoprotein B/Apolipoprotein A1 Ratio and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]Compare the Numbers of Patients Achieving the LDL-C Goal According to the National Cholesterol Education Program Adult Treatment Panel III (NCEP) ATP III) Guidelines for the Management of Dyslipidaemic Patients
NCT00631189 (9) [back to overview]To Evaluate Clinical and Laboratory Safety
NCT00631189 (9) [back to overview]Compare the Percentage of HDL-C (High Density Lipoprotein Cholesterol) Variation From Baseline and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]Compare the Percentage of Total Cholesterol Variation From Baseline and After 8 Weeks of Treatment
NCT00631189 (9) [back to overview]Compare the Percentage of Variation of C-reactive Protein (CRP)
NCT00631189 (9) [back to overview]Compare the Percentage of Variation of Phospholipase A2 (PLA2)
NCT00631189 (9) [back to overview]Compare the Percentage of Variation From Baseline Triglycerides Values and After 8 Weeks
NCT00631189 (9) [back to overview]Change in Low Density Lipoprotein Cholesterol (LDL-C) Level After 8 Weeks
NCT00639158 (8) [back to overview]Mean Percent Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Mean Percent Change in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Mean Percent Change in Apolipoprotein AI (apoAI) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Mean Percent Change in Apolipoprotein B (apoB) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Median Percent Change in Triglycerides From Baseline to Final Visit
NCT00639158 (8) [back to overview]Mean Percent Change in Very Low-Density Lipoprotein Cholesterol (VLDL-C) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Median Percent Change in High-Sensitivity C-Reactive Protein (hsCRP) From Baseline to Final Visit
NCT00639158 (8) [back to overview]Mean Percent Change in Apolipoprotein CIII (apoCIII) From Baseline to Final Visit
NCT00652327 (1) [back to overview]Percentage Change in Low Density Lipoprotein-Cholesterol (LDL-C) From Baseline at Study Endpoint, After 8 Weeks of Treatment
NCT00654095 (1) [back to overview]Number of Participants With Adverse Events and Adverse Reactions
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Data Available)
NCT00663234 (19) [back to overview]Percentage of Participants Experiencing at Least One Adverse Event (AE)
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Per Protocol)
NCT00663234 (19) [back to overview]Percentage of Participants With Undetectable Plasma HIV-1 RNA
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria by NNRTI Treatment
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria by Age Group
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria and Did Not Experience a Primary Safety Endpoint Attributable to Study Drug
NCT00663234 (19) [back to overview]Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Intention to Treat)
NCT00663234 (19) [back to overview]Percentage of Participants Experiencing at Least One Treatment-related Adverse Event (AE) by Age Group
NCT00663234 (19) [back to overview]Percentage of Participants Experiencing at Least One Treatment-related Adverse Event (AE)
NCT00663234 (19) [back to overview]Percentage of Participants Experiencing at Least One Adverse Event (AE) by Age Group
NCT00663234 (19) [back to overview]Percent Change in Triglycerides (TG) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in LDL Cholesterol (LDL-C) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in Interleukin 6 (IL-6) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in High-sensitivity CRP (Hs-CRP) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in HDL-cholesterol (HDL-C) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in Fasting Total Cholesterol (TC) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in Apolipoprotein B (Apo B) From Study Entry
NCT00663234 (19) [back to overview]Percent Change in Apolipoprotein A1 (Apo A-1) From Study Entry
NCT00664859 (2) [back to overview]Change in Non-HDL Cholesterol, HDL Cholesterol, TG Levels From Baseline to End of Treatment
NCT00664859 (2) [back to overview]Change in LDL Cholesterol, VLDL, Total Cholesterol, Apo A-1, and Apo B From Baseline to End of Treatment
NCT00666029 (2) [back to overview]Insulin Sensitivity Index
NCT00666029 (2) [back to overview]Muscle Microvascular Function
NCT00683618 (15) [back to overview]Percentage of Patients Achieved National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III Guideline (2001) Low Density Lipoprotein-Cholesterol (LDL-C) Goal After Titration
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Apolipoprotein A-I (ApoA-I) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Non High Density Lipoprotein Cholesterol/High Density Lipoprotein Cholesterol (nonHDL-C/HDL-C) at Week 6
NCT00683618 (15) [back to overview]6 weeksPercentage of Patients Achieved ATP III Guideline (2001) Non High Density Lipoprotein-Cholesterol (nonHDL-C) Goal at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Apolipoprotein B (ApoB) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Apolipoprotein B/Apolipoprotein A I (ApoB/ApoA-I) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in High Density Lipoprotein-Cholesterol (HDL-C) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) Concentration After 6 Weeks of Treatment Comparing Rosuvastatin 10mg With Atorvastatin 10mg
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) Concentration After 6 Weeks of Treatment Comparing Rosuvastatin 5mg With Atorvastatin 10mg
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Low Density Lipoprotein Cholesterol/High Density Lipoprotein Cholesterol (LDL-C/HDL-C) at Week 6
NCT00683618 (15) [back to overview]Percentage of Patients Achieved ATP III Guideline (2001) Low Density Lipoprotein Cholesterol (LDL-C) Goal at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Non High Density Lipoprotein-Cholesterol (nonHDL-C) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Total Cholesterol (TC ) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Total Cholesterol/High Density Lipoprotein-Cholesterol (TC/HDL-C) at Week 6
NCT00683618 (15) [back to overview]Percentage Change From Baseline in Triglycerides (TG) at Week 6
NCT00687271 (8) [back to overview]Percentage of Participants Who Experience at Least 1 Adverse Event (AE)
NCT00687271 (8) [back to overview]Percentage of Participants That Had Study Drug Discontinued Due to an AE
NCT00687271 (8) [back to overview]Percentage Change From Baseline in Total Cholesterol (TC)
NCT00687271 (8) [back to overview]Percentage Change From Baseline in TG
NCT00687271 (8) [back to overview]Percentage Change From Baseline in Non-High-Density Lipoprotein-Cholesterol (Non-HDL-C)
NCT00687271 (8) [back to overview]Percentage Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C)
NCT00687271 (8) [back to overview]Percentage Change From Baseline in HDL-C
NCT00687271 (8) [back to overview]Percentage Change From Baseline in Apolipoprotein B (ApoB)
NCT00690443 (2) [back to overview]Percent Changes in LDL-C at Week 4 + Baseline Serum Lipoproteins (TC, Non-HDL, VLDL, TGs, HDL-C, Apolopoproteins A1 and B), High Sensitivity C-reactive Protein and Change in Body Weight.
NCT00690443 (2) [back to overview]Percent Change in LDL-C After 8 Weeks of Therapy
NCT00701220 (2) [back to overview]Percentage Aldofluor Positive Cells
NCT00701220 (2) [back to overview]Change in Endothelial Progenitor Cells
NCT00703261 (2) [back to overview]Percent Reduction From Baseline in TBRmeanmax of the Qualifying Segment in Statin-naive Participants
NCT00703261 (2) [back to overview]Percent Reduction From Baseline in TBRmeanmax of the Qualifying Segment
NCT00715273 (3) [back to overview]Composite of Cardiovascular Endpoints: Number of Participants With Cardiovascular Disease Death, Non-fatal Heart Attack, Stroke, and Worsening Ischemia Requiring Medical Interventions
NCT00715273 (3) [back to overview]Annualized LRNC and Wall Volume Changes in Carotid Plaque Composition, as Assessed by MRI
NCT00715273 (3) [back to overview]Annualized LRNC Volume Change in Carotid Plaque Composition, as Assessed by MRI
NCT00728910 (3) [back to overview]Apo-A1 Production Rate
NCT00728910 (3) [back to overview]Post-prandial Triglyceride Incremental Area Under the Curve (iAUC)
NCT00728910 (3) [back to overview]The Apolipoprotein A-I Fractional Catabolic Rate (FCR)
NCT00728988 (7) [back to overview]Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 30 Days Post-percutaneous Coronary Intervention (PCI)
NCT00728988 (7) [back to overview]Percentage of Participants With Elevated Troponin I
NCT00728988 (7) [back to overview]Percentage of Participants With Elevated Myoglobin
NCT00728988 (7) [back to overview]Percentage of Participants With Elevated Creatine Kinase-MB (CK-MB)
NCT00728988 (7) [back to overview]Percent Change From Baseline in C-Reactive Protein (CRP)
NCT00728988 (7) [back to overview]Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 24 Hours Post-PCI
NCT00728988 (7) [back to overview]Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 8 Hours Post-PCI
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Apolipoprotein B (Apo B)
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Flow-Mediated Dilatation at Week 8
NCT00739999 (18) [back to overview]Absolute Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C)
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Pharmacodynamic Responses of Low-density Lipoprotein Cholesterol (LDL-C)
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Total Cholesterol (TC)
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Triglycerides (TG)
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Very Low-density Lipoprotein-cholesterol (VLDL-C)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo B)
NCT00739999 (18) [back to overview]Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Pharmacodynamic Responses of Low-density Lipoprotein Cholesterol (LDL-C)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Total Cholesterol (TC)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Triglycerides (TG)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Very Low-density Lipoprotein-cholesterol (VLDL-C)
NCT00739999 (18) [back to overview]Parent-metabolite Population Pharmacokinetic (PK) Model for Atorvastatin and Its Metabolites: Atorvastatin Apparent Clearance (CL/F)
NCT00739999 (18) [back to overview]Parent-metabolite Population Pharmacokinetic (PK) Model for Atorvastatin and Its Metabolites: Apparent Volume of Distribution of the Central Compartment (Vc/F)
NCT00739999 (18) [back to overview]Percent Change From Baseline in Flow-Mediated Dilatation at Week 8
NCT00739999 (18) [back to overview]Absolute Change From Baseline in Apolipoprotein A-1 (Apo A-1)
NCT00756886 (1) [back to overview]Atrial Fibrillation
NCT00767572 (1) [back to overview]Pre-post Change in Brachial Artery Reactivity
NCT00770679 (1) [back to overview]Mean Change in Low Density Lipoprotein (LDL)
NCT00782184 (15) [back to overview]Percent Change From Baseline in Apolipoprotein B/A-1 Ratio
NCT00782184 (15) [back to overview]Percent Change From Baseline in Apolipoprotein B
NCT00782184 (15) [back to overview]Percent Change From Baseline in High-Density Lipoprotein (HDL) Cholesterol
NCT00782184 (15) [back to overview]Percent Change From Baseline in Triglycerides
NCT00782184 (15) [back to overview]Percent Change From Baseline in Total Cholesterol/HDL-Cholesterol Ratio
NCT00782184 (15) [back to overview]Percent Change From Baseline in Total Cholesterol
NCT00782184 (15) [back to overview]Percent Change From Baseline in Non-HDL Cholesterol/HDL-Cholesterol Ratio
NCT00782184 (15) [back to overview]Percent Change From Baseline in Non-HDL Cholesterol
NCT00782184 (15) [back to overview]Number of Participants Reaching LDL-C Target Goal <100 mg/dL
NCT00782184 (15) [back to overview]Number of Participants Reaching LDL-C Target Goal <77 mg/dL
NCT00782184 (15) [back to overview]Number of Participants Reaching LDL-C Target Goals of <70 mg/dL
NCT00782184 (15) [back to overview]Percent Change From Baseline in Apolipoprotein A-1
NCT00782184 (15) [back to overview]Percent Change From Baseline in Low Density Lipoprotein (LDL)-C
NCT00782184 (15) [back to overview]Percent Change From Baseline in LDL-Cholesterol/HDL-Cholesterol Ratio
NCT00782184 (15) [back to overview]Percent Change From Baseline in High-sensitivity C-Reactive Protein (Hs-CRP)
NCT00791648 (16) [back to overview]Plasma Markers of Oxidative Stress: f2-Isoprostanes
NCT00791648 (16) [back to overview]Plasma Markers of Inflammation: Measurements of Neuronal Injury (Ubiquitin C-terminal Hydrolase-1)
NCT00791648 (16) [back to overview]Plasma Markers of Inflammation: Blood Brain Barrier Disruption (S100 Calcium-binding Protein B)
NCT00791648 (16) [back to overview]Mitochondrial Function--PGC-1alpha RNA Expression
NCT00791648 (16) [back to overview]Mitochondrial Function--mtDNA Copy Number
NCT00791648 (16) [back to overview]Number of Participants With Stroke
NCT00791648 (16) [back to overview]Number of Participants With Delirium
NCT00791648 (16) [back to overview]Number of Participants With Acute Kidney Injury
NCT00791648 (16) [back to overview]Urine Markers of Oxidative Stress: f2-Isoprostanes
NCT00791648 (16) [back to overview]Urine Markers of Renal Injury
NCT00791648 (16) [back to overview]Liver Enzyme: Aspartate Aminotransferase Level
NCT00791648 (16) [back to overview]Plasma Markers of Oxidative Stress: Isofurans
NCT00791648 (16) [back to overview]Mitochondrial Function--lactate / Pyruvate Ratio
NCT00791648 (16) [back to overview]Number of Participants Requiring Dialysis
NCT00791648 (16) [back to overview]Number of Participants That Died
NCT00791648 (16) [back to overview]Urine Markers of Oxidative Stress: Isofurans
NCT00804843 (2) [back to overview]Composite Score of Plaque Inflammation/Stability Gene Expression as Assayed by Ribonucleic Acid (RNA) Taqman Analysis
NCT00804843 (2) [back to overview]Plaque Instability Protein Composite Score
NCT00814255 (2) [back to overview]Number of Participants With Adverse Events
NCT00814255 (2) [back to overview]Number of Participants With a Reduction in Proteinuria at 6 Months by > 50% of the Value at Screening AND Stable GFR Defined as Greater Than 75 ml/Min/1.73m2 in Those With an Initial Value Above 90 OR Within 25% of Baseline for Remaining Patients
NCT00827606 (35) [back to overview]Percent Change From Baseline in Apo B
NCT00827606 (35) [back to overview]Age (Years) During the Study: Females
NCT00827606 (35) [back to overview]Age (Years) During the Study: Males
NCT00827606 (35) [back to overview]Apoliprotein A-1 (Apo A-1; Grams Per Liter [g/L]) During the Study
NCT00827606 (35) [back to overview]Apoliprotein B (Apo B; g/L) During the Study
NCT00827606 (35) [back to overview]BMI (kg/m^2) During the Study: Females
NCT00827606 (35) [back to overview]Body Mass Index (BMI in kg Per Square Meter [kg/m^2]) During the Study: Males
NCT00827606 (35) [back to overview]Flow-Mediated Dilatation (FMD) During the Study
NCT00827606 (35) [back to overview]Height (Centimeters [cm]) During the Study: Males
NCT00827606 (35) [back to overview]Height (cm) During the Study: Females
NCT00827606 (35) [back to overview]High-Density Lipoprotein Cholesterol (HDL-C; mMol/L) During the Study
NCT00827606 (35) [back to overview]Number of Participants With Shift From Baseline in Tanner_Stage by Timepoint and Baseline Tanner_Stage
NCT00827606 (35) [back to overview]Percent Change From Baseline in Age: Females
NCT00827606 (35) [back to overview]Percent Change From Baseline in Age: Males
NCT00827606 (35) [back to overview]Percent Change From Baseline in Apo A-1
NCT00827606 (35) [back to overview]Percent Change From Baseline in BMI: Females
NCT00827606 (35) [back to overview]Percent Change From Baseline in BMI: Males
NCT00827606 (35) [back to overview]Percent Change From Baseline in FMD
NCT00827606 (35) [back to overview]Percent Change From Baseline in HDL-C
NCT00827606 (35) [back to overview]Percent Change From Baseline in Height: Females
NCT00827606 (35) [back to overview]Percent Change From Baseline in Height: Males
NCT00827606 (35) [back to overview]Percent Change From Baseline in LDL-C
NCT00827606 (35) [back to overview]Percent Change From Baseline in Total Cholesterol
NCT00827606 (35) [back to overview]Percent Change From Baseline in Trigylcerides
NCT00827606 (35) [back to overview]Percent Change From Baseline in VLDL
NCT00827606 (35) [back to overview]Percent Change From Baseline in Weight: Females
NCT00827606 (35) [back to overview]Percent Change From Baseline in Weight: Males
NCT00827606 (35) [back to overview]Percentage of Participants by Study Drug Compliance Category
NCT00827606 (35) [back to overview]Percentage of Participants With Overall Expected Maturation and Development Consistent With Expectations as Assessed by the Investigator
NCT00827606 (35) [back to overview]Total Cholesterol (mMol/L) During the Study
NCT00827606 (35) [back to overview]Trigylcerides (mMol/L) During the Study
NCT00827606 (35) [back to overview]Very Low-Density Lipoprotein (VLDL; mMol/L) During the Study
NCT00827606 (35) [back to overview]Weight (kg) During the Study: Females
NCT00827606 (35) [back to overview]Weight (Kilograms [kg]) During the Study: Males
NCT00827606 (35) [back to overview]Low Density Lipoprotein Cholesterol (LDL-C; Millimoles Per Liter [mMol/L]) During the Study
NCT00844376 (7) [back to overview]Area Under the Curve From Predose (Time Zero) to 48 Hours Post-dose (AUC48)
NCT00844376 (7) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax)
NCT00844376 (7) [back to overview]Area Under the Curve From Predose (Time Zero) to Last Quantifiable Concentration (AUClast)
NCT00844376 (7) [back to overview]Area Under the Curve From Predose (Time Zero) to Extrapolated Infinite Time (AUC Infinity)
NCT00844376 (7) [back to overview]Maximum Observed Plasma Concentration (Cmax)
NCT00844376 (7) [back to overview]Plasma Elimination Half-life (t1/2)
NCT00844376 (7) [back to overview]Terminal Phase Rate Constant (Kel)
NCT00850460 (2) [back to overview]Individualized Short Form-36 (SF-36) Mean Scores (Physical Component) From Week 0 to Week 8
NCT00850460 (2) [back to overview]Individualized Neuromuscular Quality of Life (INQoL) Mean Scores From Week 0 to Week 8
NCT00862251 (18) [back to overview]Percent Change From Baseline in Triglycerides
NCT00862251 (18) [back to overview]Percent Change From Baseline in Non-HDL-C/HDL-C Ratio
NCT00862251 (18) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Statin (Simvastatin or Atorvastatin).
NCT00862251 (18) [back to overview]Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C)
NCT00862251 (18) [back to overview]Percent Change From Baseline in TC/HDL-C Ratio
NCT00862251 (18) [back to overview]Percent Change From Baseline in Total Cholesterol (TC)
NCT00862251 (18) [back to overview]In Participants Treated With Atorvastatin at Baseline, Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Atorvastatin
NCT00862251 (18) [back to overview]In Participants Treated With Simvastatin at Baseline, Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)
NCT00862251 (18) [back to overview]In Participants Treated With Simvastatin at Baseline, Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Simvastatin
NCT00862251 (18) [back to overview]Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)
NCT00862251 (18) [back to overview]Percent Change From Baseline Apolipoprotein A-I (Apo A-I)
NCT00862251 (18) [back to overview]Percent Change From Baseline in Apo B/Apo A-I Ratio
NCT00862251 (18) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo B)
NCT00862251 (18) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C)
NCT00862251 (18) [back to overview]In Participants Treated With Atorvastatin at Baseline, Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)
NCT00862251 (18) [back to overview]Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP)
NCT00862251 (18) [back to overview]Percent Change From Baseline in LDL-C/HDL-C Ratio
NCT00862251 (18) [back to overview]Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Switching Treatment to Rosuvastatin
NCT00871351 (5) [back to overview]Percent Change in Total Lipids and Hs-CRP
NCT00871351 (5) [back to overview]Percent Change in Total Lipids and High Sensitivity C-reactive Protein (Hs-CRP)
NCT00871351 (5) [back to overview]Percent Change in Low-Density Lipoprotein - Cholesterol (LDL-C) Values
NCT00871351 (5) [back to overview]Percent Change in LDL-C
NCT00871351 (5) [back to overview]Number of Participants Whose LDL-C Levels Reached the Lipid Management Target Values
NCT00889226 (2) [back to overview]The Change of LDL-C
NCT00889226 (2) [back to overview]Proportion of Patients Achieving LDL- C<100mg/dL
NCT00917579 (5) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time (AUC Infinity)
NCT00917579 (5) [back to overview]Plasma Elimination Half-life (t1/2)
NCT00917579 (5) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax)
NCT00917579 (5) [back to overview]Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast)
NCT00917579 (5) [back to overview]Maximum Observed Plasma Concentration (Cmax)
NCT00917644 (5) [back to overview]Area Under the Curve From Time Zero to Extrapolated Infinite Time (AUC Infinity)
NCT00917644 (5) [back to overview]Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast)
NCT00917644 (5) [back to overview]Maximum Observed Plasma Concentration (Cmax)
NCT00917644 (5) [back to overview]Plasma Elimination Half-life (t1/2)
NCT00917644 (5) [back to overview]Time to Reach Maximum Plasma Concentration (Tmax)
NCT00960323 (3) [back to overview]Maximum Plasma Concentration (Cmax) of Colchicine
NCT00960323 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 Extrapolated to Infinity [AUC(0-∞)]
NCT00960323 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]
NCT00965185 (7) [back to overview]Coronary and Aortic Plaque Inflammation
NCT00965185 (7) [back to overview]Lipid Profile
NCT00965185 (7) [back to overview]Plaque Progression
NCT00965185 (7) [back to overview]Adipocytokines
NCT00965185 (7) [back to overview]C-reactive Protein (CRP)
NCT00965185 (7) [back to overview]Immune Function
NCT00965185 (7) [back to overview]Liver Function Tests (LFTs)
NCT00979940 (1) [back to overview]Periprocedural Myonecrosis
NCT00993915 (3) [back to overview]Percent Change From Baseline in Lipid Parameters
NCT00993915 (3) [back to overview]Change From Baseline in Lipid Parameters
NCT00993915 (3) [back to overview]Percentage of Participants Achieving LDL Level Less Than or Equal to (≤) 100 mg/dL at the 6 Month Visit
NCT01004406 (4) [back to overview]Major Adverse Cardiovascular Events
NCT01004406 (4) [back to overview]Change in % Necrotic Core (NC) Component of Atheroma From Baseline to 12 Weeks Post-PCI as Assessed Via IVUS-VH
NCT01004406 (4) [back to overview]Endothelial Progenitor Cell Colony Forming Units (EPC-CFU) Per Milliliter of Peripheral Blood Across Time
NCT01004406 (4) [back to overview]Change in the Total Atheroma Volume of the Target Coronary Artery From Baseline to 12 Weeks Post-PCI as Assessed Via Intravascular Ultrasound With Virtual Histology (IVUS-VH)
NCT01013870 (9) [back to overview]Symbol Digit Modalities Test - Written Score
NCT01013870 (9) [back to overview]Brief Visuospatial Memory Test - Revised
NCT01013870 (9) [back to overview]Rivermead Post-Concussion Symptoms Questionnaire, at 3 Months After Injury.
NCT01013870 (9) [back to overview]Post-traumatic Stress Checklist - Civilian Form
NCT01013870 (9) [back to overview]Medical Outcome Study Short Form 12 - Physical Score
NCT01013870 (9) [back to overview]Medical Outcome Study Short Form 12 - Mental Score
NCT01013870 (9) [back to overview]Connor Davidson Resilience Measure
NCT01013870 (9) [back to overview]Center for Epidemiological Study Depression Scale
NCT01013870 (9) [back to overview]Symbol Digit Modalities Test - Oral Score
NCT01059864 (19) [back to overview]C-Reactive Protein (CRP)
NCT01059864 (19) [back to overview]Swollen-Joint Count
NCT01059864 (19) [back to overview]Physician's Global Assessment (PhysGA) of Arthritis Pain
NCT01059864 (19) [back to overview]Percentage of Participants Achieving American College of Rheumatology 70% (ACR70) Response
NCT01059864 (19) [back to overview]Percentage of Participants Achieving American College of Rheumatology 50% (ACR50) Response
NCT01059864 (19) [back to overview]Percentage of Participants Achieving American College of Rheumatology 20% (ACR20) Response
NCT01059864 (19) [back to overview]Patient's Global Assessment (PtGA) of Arthritis Pain
NCT01059864 (19) [back to overview]Change From Baseline in Low Density Lipoprotein-Cholesterol (LDL-C) at Week 12
NCT01059864 (19) [back to overview]Patient Assessment of Arthritis Pain
NCT01059864 (19) [back to overview]Health Assessment Questionnaire Disability Index (HAQ-DI)
NCT01059864 (19) [back to overview]Percent Change From Baseline (Week 6) in Low Density Lipoprotein-Cholesterol (LDL-C) Level at Week 12
NCT01059864 (19) [back to overview]Tender-Joint Count
NCT01059864 (19) [back to overview]Erythrocyte Sedimentation Rate (ESR)
NCT01059864 (19) [back to overview]Disease Activity Score Using 28-Joint Count and Erythrocyte Sedimentation Rate (4 Variables) (DAS28-4 [ESR])
NCT01059864 (19) [back to overview]12-Hours Fasting Lipid Profile: Level of Lipoprotein Particles
NCT01059864 (19) [back to overview]12-Hours Fasting Lipid Profile: Level of High Density Lipoprotein Cholesterol (HDL-C) Particles
NCT01059864 (19) [back to overview]12-Hours Fasting Lipid Profile
NCT01059864 (19) [back to overview]Disease Activity Score Using 28-Joint Count and C-Reactive Protein (3 Variables) (DAS28-3 [CRP])
NCT01059864 (19) [back to overview]12-Hours Fasting Lipid Profile: Particle Size of Lipoproteins
NCT01096875 (4) [back to overview]High Sensitive C-reactive Protein (hsCRP mg/L)
NCT01096875 (4) [back to overview]Left Ventricular Ejection Fraction (LVEF %) Measured at 30 Days Postoperatively
NCT01096875 (4) [back to overview]Endothelial Progenitor Cells (EPCs) Count (Cells/µl)
NCT01096875 (4) [back to overview]High Sensitive C-reactive Protein (hsCRP mg/L)
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Simvastatin or Rosuvastatin and Simvastatin/Rosuvastatin Monotherapy
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in Plasma Cholesteryl Ester Transfer Protein (CETP) Activity
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in Plasma Cholesteryl Ester Transfer Protein (CETP) Mass
NCT01105975 (17) [back to overview]Pharmacokinetics - LY2484595 Area Under the Concentration-Time Curve (AUC) at Steady-State
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Blood Pressure (BP)
NCT01105975 (17) [back to overview]The Number of Episodes of Rashes at Any Time From Baseline Through Week 12
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Serum Sodium
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Serum Potassium
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Serum Bicarbonate
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Serum Aldosterone
NCT01105975 (17) [back to overview]Change From Baseline to 12 Weeks Endpoint in Plasma Renin Activity
NCT01105975 (17) [back to overview]Change From Baseline to 18 Weeks Endpoint in EuroQoL Questionnaire - 5 Dimensions (EQ-5D) Score
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 in Combination With Atorvastatin and Atorvastatin Monotherapy
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 and Placebo
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 and Placebo
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Atorvastatin and Atorvastatin Monotherapy
NCT01105975 (17) [back to overview]Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 in Combination With Simvastatin or Rosuvastatin and Simvastatin/Rosuvastatin Monotherapy
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Hepatic Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Renal Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Age.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Complications.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Concomitant Drugs.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Gender.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Hepatic Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Hypertension Severity.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypertension -Renal Dysfunction.
NCT01107743 (38) [back to overview]Number of Treatment Related Unlisted Adverse Events in Japanese Package Insert.
NCT01107743 (38) [back to overview]Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Angina Pectoris.
NCT01107743 (38) [back to overview]Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Hypercholesterolemia or Familial Hypercholesterolemia.
NCT01107743 (38) [back to overview]Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Hypertension.
NCT01107743 (38) [back to overview]Number of Treatment Related Adverse Events.
NCT01107743 (38) [back to overview]Risk Factor for the Proportion of Responders of Amlodipine/Atorvastatin Combination Tablets for Hypercholesterolemia or Familial Hypercholesterolemia - Hypercholesterolemia Expression Type.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Age.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Angina Pectoris.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Complications.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Concomitant Drugs.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Familial Hypercholesterolemia.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Gender.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Hepatic Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Hypercholesterolemia Expression Type.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Hypercholesterolemia.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Hypertension Severity.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Hypertension.
NCT01107743 (38) [back to overview]Risk Factors for Incidence Rate of Treatment Related Adverse Events(TRAEs) of Amlodipine/Atorvastatin Combination Tablets -Renal Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Age.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Angina Pectoris Severity.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Complications.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Concomitant Drugs.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Gender.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Hepatic Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Angina Pectoris -Renal Dysfunction.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Age.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Complications.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Concomitant Drugs.
NCT01107743 (38) [back to overview]Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Gender.
NCT01112670 (11) [back to overview]Sitagliptin + Atorvastatin: Sitagliptin Maximum Plasma Concentration (Cmax)
NCT01112670 (11) [back to overview]Sitagliptin + Atorvastatin: Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity
NCT01112670 (11) [back to overview]Relative Change in Sitagliptin Renal Clearance (CLr)
NCT01112670 (11) [back to overview]Sitagliptin Monotherapy: Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity
NCT01112670 (11) [back to overview]Relative Change in Sitagliptin Maximum Plasma Concentration (Cmax)
NCT01112670 (11) [back to overview]Relative Change in Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity
NCT01112670 (11) [back to overview]Atorvastatin Maximum Plasma Concentration (Cmax)
NCT01112670 (11) [back to overview]Atorvastatin Area Under the Plasma Concentration Time Curve (AUC) Over the Dosing Interval (0-24 Hours)
NCT01112670 (11) [back to overview]Sitagliptin Monotherapy: Sitagliptin Renal Clearance (CLr)
NCT01112670 (11) [back to overview]Sitagliptin Monotherapy: Sitagliptin Maximum Plasma Concentration (Cmax)
NCT01112670 (11) [back to overview]Sitagliptin + Atorvastatin: Sitagliptin Renal Clearance (CLr)
NCT01154036 (28) [back to overview]Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Non-HDL-C/HDL-C Ratio (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apo B/Apo A-I Ratio (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apo B/Apo A-I Ratio (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apo B (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apo A-I (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apolipoprotein A-I (Apo A-I) (Phase I)
NCT01154036 (28) [back to overview]Percentage of Participants That Reach Target LDL-C Level of < 70 mg/dL (Phase II)
NCT01154036 (28) [back to overview]Percentage of Participants That Reach Target LDL-C Level of < 70 mg/dL (Phase I)
NCT01154036 (28) [back to overview]Percentage of Participants That Reach Target LDL-C Level of < 100 mg/dL (Phase II)
NCT01154036 (28) [back to overview]Percentage of Participants That Reach Target LDL-C Level of < 100 mg/dL (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Triglycerides (TG) (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo B) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Triglycerides (TG) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in TC/HDL-C Ratio (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in TC/HDL-C Ratio (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Non-HDL-C/HDL-C Ratio (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Non-HDL-C (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Non-HDL-C (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein-Cholesterol (LDL-C) (Phase II).
NCT01154036 (28) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein-Cholesterol (LDL-C) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in LDL-C/HDL-C Ratio (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in LDL-C/HDL-C Ratio (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in Hs-CRP (Phase II)
NCT01154036 (28) [back to overview]Percent Change From Baseline in High-density Lipoprotein-Cholesterol (HDL-C) (Phase I)
NCT01154036 (28) [back to overview]Percent Change From Baseline in HDL-C (Phase II)
NCT01175148 (1) [back to overview]Cummalative Incidence of Grade 2 to 4 Acute Graft vs Host Diesease (GVHD) at Day 100 Post Transplant in HSCT Recipients
NCT01218204 (45) [back to overview]Time of Occurrence of Cmax (Tmax) and Terminal Phase Half-life (t1/2) GSK1292263- Part A
NCT01218204 (45) [back to overview]Tmax and t1/2 of GSK1292263- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Tmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A
NCT01218204 (45) [back to overview]AUC (0-24) of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A
NCT01218204 (45) [back to overview]Tmax of Atorvastatin- Part A
NCT01218204 (45) [back to overview]Tmax of Atorvastatin- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part A
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Run-in)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal- Clinically Significant Electrocardiogram (ECG) Findings- Part A
NCT01218204 (45) [back to overview]Percent Change From Baseline in Lipid Metabolism: Apolipoprotein E at Day 14 (24 Hours)
NCT01218204 (45) [back to overview]Percent Change From Baseline in Lipid Metabolism: LDL/HDL Ratio at Day 14 (24 Hours)
NCT01218204 (45) [back to overview]Tmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Tlag of GSK1292263- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Weighted Mean Area Under Concentration Curve From 0 to 24 Hours (AUC [0-24]) Change From Baseline for Triglycerides at Day 14
NCT01218204 (45) [back to overview]Area Under the Concentration-time Curve From Time Zero (Pre-dose) to 24 Hours [AUC(0-24)] of GSK1292263- Part A
NCT01218204 (45) [back to overview]AUC (0-24) of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]AUC (0-24) of Atorvastatin- Part A
NCT01218204 (45) [back to overview]AUC (0-24) of Atorvastatin- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]AUC(0-24) of GSK1292263- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Cmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A
NCT01218204 (45) [back to overview]Lag Time Before Observation of Drug Concentrations in Sampled Matrix (Tlag) of GSK1292263- Part A
NCT01218204 (45) [back to overview]Cmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Cmax of Atorvastatin- Part A
NCT01218204 (45) [back to overview]Cmax of Atorvastatin- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Cmax of GSK1292263- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Maximum Observed Concentration (Cmax) of GSK1292263- Part A
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (run-in)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (Washout)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Washout)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Hematology Value of PCI- Part A
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Hematology Value of PCI- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Hematology Value of PCI- Part B (Run-in)
NCT01218204 (45) [back to overview]Number of Participants With Any AEs and SAEs- Part B (Washout)
NCT01218204 (45) [back to overview]Number of Participants With Abnormal Hematology Value of PCI- Part B (Washout)
NCT01218204 (45) [back to overview]Number of Participants With Any Adverse Events (AEs) and Serious Adverse Events (SAEs)- Part A
NCT01218204 (45) [back to overview]Number of Participants With Any AEs and SAEs- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Any AEs and SAEs- Part B (Run-in)
NCT01218204 (45) [back to overview]Number of Participants With Vital Signs of PCI- Part B (Washout)
NCT01218204 (45) [back to overview]Number of Participants With Vital Signs of Potential Clinical Importance (PCI)- Part A
NCT01218204 (45) [back to overview]Number of Participants With Vital Signs of Potential Clinical Importance- Part B (Pooled Treatment Arm)
NCT01218204 (45) [back to overview]Number of Participants With Vital Signs of Potential Clinical Importance- Part B (Run-in)
NCT01218204 (45) [back to overview]Percent Change From Baseline for Lipid Metabolism: Apolipoprotein A1 and Apolipoprotein B100 at Day 14
NCT01218204 (45) [back to overview]Percent Change From Baseline in Lipid Metabolism: High Density Lipids Cholesterol (HDLc), Low Density Lipids Cholesterol (LDLc), Tryglycerides, Non-HDLc and Total Cholesterol at Day 14 (24 Hours)
NCT01220973 (1) [back to overview]PSA Response
NCT01236365 (5) [back to overview]Hs-CRP Levels Assessed at Randomization and 6 Months
NCT01236365 (5) [back to overview]LDL-C Levels Assessed at Randomization and 6 Months
NCT01236365 (5) [back to overview]MAGE
NCT01236365 (5) [back to overview]RAGE
NCT01236365 (5) [back to overview]Descending Aortic Strain
NCT01250834 (5) [back to overview]Pharmacokinetics of Atorvastatin: Maximum Plasma Concentration (Cmax)
NCT01250834 (5) [back to overview]Pharmacokinetics of Atorvastatin: Area Under the Curve (AUC)
NCT01250834 (5) [back to overview]Pharmacokinetics of Ortho-Hydroxyatorvastatin: Area Under the Curve (AUC)
NCT01250834 (5) [back to overview]Pharmacokinetics of Ortho-Hydroxyatorvastatin: Maximum Concentration (Cmax)
NCT01250834 (5) [back to overview]Pharmacokinetics of Para-Hydroxyatorvastatin: Maximum Concentration (Cmax)
NCT01263938 (4) [back to overview]Change in Monocyte Surface Markers Expression (Expressed as Percentage), Following Treatment of Chronic HIV+/ HAART+ Subjects With Atorvastatin (T=12wks Versus T=0wk).
NCT01263938 (4) [back to overview]Change From Baseline in Levels of Plasma Inflammatory Marker sCD14 of Chronic HIV+/ HAART+ Subjects.
NCT01263938 (4) [back to overview]Change From Baseline in Levels of Plasma Inflammatory Marker sCD163 of Chronic HIV+/ HAART+ Subjects.
NCT01263938 (4) [back to overview]Change From Baseline in Levels of Plasma Inflammatory Marker MCP-1 of Chronic HIV+/ HAART+ Subjects.
NCT01288443 (7) [back to overview]Percent Change From Baseline in Total Cholesterol, High-density Lipoprotein Cholesterol (HDL-C), Non-HDL-C and Apolipoprotein B (Apo-B) at Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Percent Change From Baseline in Fasting Triglycerides and Lipoprotein(a) at Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and <70 mg/dL (1.81 mmol/L) at Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Absolute Change in the Ratio Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) From Baseline to Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 12 - On-Treatment Analysis
NCT01288443 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 12 - On-Treatment Analysis
NCT01288469 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Absolute Change in the Ratio Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) From Baseline to Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and < 70 mg/dL (1.81 mmol/L) at Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 8 - On-treatment Analysis
NCT01288469 (7) [back to overview]Percent Change From Baseline in Total Cholesterol, Fasting Triglycerides, Non-high-Density Lipoprotein Cholesterol (Non-HDL-C), Apolipoprotein B (Apo-B) and Lipoprotein(a) at Week 8 - On-treatment Analysis
NCT01304641 (7) [back to overview]Number of Participants With Post-index Cardiovascular (CV) Events
NCT01304641 (7) [back to overview]Hazard Ratio for First Cardiovascular (CV) Event
NCT01304641 (7) [back to overview]Number of Participants Per Dose
NCT01304641 (7) [back to overview]Mean Dose
NCT01304641 (7) [back to overview]Percentage of Participants Who Adhered to Index Therapy
NCT01304641 (7) [back to overview]Low-density Lipoprotein Cholesterol (LDL-C)
NCT01304641 (7) [back to overview]Length of Post-index Period
NCT01341730 (1) [back to overview]Difference of Standardized Uptake Value (SUV) of Atherosclerotic Plaque in Carotid Artery by PET CT
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in CD4+ T-cell Activation Percent
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in CD40L (log10 Transformed)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in CD8+ T-cell Activation Percent
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in log10 D-dimer
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in log10 IL-6
NCT01351025 (12) [back to overview]Number of Participants With Safety Endpoints After Study Treatment Cross-over (Week 24 to Week 48)
NCT01351025 (12) [back to overview]Number of Participants With Safety Endpoints Before Study Treatment Cross-over (Baseline to Week 24)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in IP-10 (log10 Transformed)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in MCP-1 (log10 Transformed)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in P-selectin (log10 Transformed)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in sCD14 (log10 Transformed)
NCT01351025 (12) [back to overview]Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in sCD163 (log10 Transformed)
NCT01363999 (4) [back to overview]Plasma Concentration of Atorvastatin Metabolites
NCT01363999 (4) [back to overview]Plasma Concentration of Atorvastatin
NCT01363999 (4) [back to overview]Safety: Incidence of Serious Adverse Events
NCT01363999 (4) [back to overview]Plasma Concentration of Dalcetrapib Active Form
NCT01370590 (6) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After 6 Weeks of Treatment
NCT01370590 (6) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B After 6 Weeks of Treatment
NCT01370590 (6) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) After 6 Weeks of Treatment
NCT01370590 (6) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) After 6 Weeks of Treatment
NCT01370590 (6) [back to overview]Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) After 6 Weeks of Treatment
NCT01370590 (6) [back to overview]Percent Change From Baseline in Triglycerides (TG) After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in Total Cholesterol (TC) After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in Triglycerides (TG) After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B After 6 Weeks of Treatment
NCT01370603 (6) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) After 6 Weeks of Treatment
NCT01375075 (13) [back to overview]Change From Baseline in Plasma CETP Mass
NCT01375075 (13) [back to overview]Pharmacokinetics - Area Under the Curve (AUC) of LY2484595 and Atorvastatin
NCT01375075 (13) [back to overview]Change From Baseline to 12 Weeks in Serum Sodium
NCT01375075 (13) [back to overview]Change From Baseline to 12 Weeks in Serum Bicarbonate
NCT01375075 (13) [back to overview]Change From Baseline to 12 Weeks in Plasma Renin Activity
NCT01375075 (13) [back to overview]Change From Baseline to 12 Week Endpoint in Highly-Sensitive C-Reactive Protein (hsCRP)
NCT01375075 (13) [back to overview]The Number and Severity of Episodes of Rashes at Any Time From Baseline Through Week 12
NCT01375075 (13) [back to overview]Percent Change From Baseline to 12 Weeks in High Density Lipoprotein Cholesterol (HDL-C) and Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 and Placebo
NCT01375075 (13) [back to overview]Percent Change From Baseline in Plasma Cholesteryl Ester Transfer Protein (CETP) Activity
NCT01375075 (13) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) and Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Atorvastatin
NCT01375075 (13) [back to overview]Change From Baseline to 12 Weeks in Aldosterone
NCT01375075 (13) [back to overview]Number of Myopathy and Liver Injury Events
NCT01375075 (13) [back to overview]Change From Baseline to 12 Weeks in Blood Pressure
NCT01431105 (1) [back to overview]Number of Participants With SAE
NCT01477853 (11) [back to overview]Percent Change From Baseline in Triglycerides at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in Non-high Density Lipoprotein Cholesterol (Non-HDL-C) at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 16
NCT01477853 (11) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 16
NCT01477853 (11) [back to overview]Number of Participants Who Experienced at Least One Adverse Event
NCT01477853 (11) [back to overview]Number of Participants Who Discontinued Study Drug Due to an Adverse Event
NCT01477853 (11) [back to overview]Change From Baseline in Hemoglobin A1C (A1C) at Week 16
NCT01477853 (11) [back to overview]Change From Baseline in Fasting Plasma Glucose (FPG) at Week 16
NCT01491958 (5) [back to overview]Non Relapse Mortality (NRM) at One Year
NCT01491958 (5) [back to overview]Safety of Atorvastatin in Transplant Recipients in Terms of Adverse Events and Toxicities.
NCT01491958 (5) [back to overview]Percentage of Participants With Grades II to IV aGVHD at Day +100 of Atorvastatin Administration
NCT01491958 (5) [back to overview]Percentage of Patients With Chronic Graft Versus Host Disease (cGVHD)
NCT01491958 (5) [back to overview]Time to Neutrophil and Platelet Engraftment
NCT01516879 (15) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 12
NCT01516879 (15) [back to overview]Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in LDL-C at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in LDL-C at Week 12
NCT01516879 (15) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 52
NCT01516879 (15) [back to overview]Change From Baseline in LDL-C at Week 52
NCT01516879 (15) [back to overview]Percentage of Participants With an LDL-C Response at Week 52
NCT01516879 (15) [back to overview]Percent Change From Week 12 to Week 52 in LDL-C
NCT01516879 (15) [back to overview]Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Triglycerides at Week 52
NCT01516879 (15) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 52
NCT01525407 (10) [back to overview]Recurrent or Progressive Malignancy
NCT01525407 (10) [back to overview]Non-relapse Mortality
NCT01525407 (10) [back to overview]Non-relapse Mortality
NCT01525407 (10) [back to overview]Overall Survival
NCT01525407 (10) [back to overview]Proportion of Donors Who Have to Discontinue Atorvastatin Because of Toxicity
NCT01525407 (10) [back to overview]Chronic Extensive GVHD
NCT01525407 (10) [back to overview]Proportion of Patients Requiring Secondary Systemic Immunosuppressive Therapy
NCT01525407 (10) [back to overview]Disease-free Survival
NCT01525407 (10) [back to overview]Grade 3-4 Acute GVHD
NCT01525407 (10) [back to overview]Grades II-IV Acute GVHD
NCT01527045 (8) [back to overview]Number of Patients Requiring Secondary Systemic Immunosuppressive Therapy
NCT01527045 (8) [back to overview]Number of Patients Surviving Overall
NCT01527045 (8) [back to overview]Number of Patients With Chronic Extensive GVHD
NCT01527045 (8) [back to overview]Number of Patients With Grade III-IV Acute Graft-versus-host Disease (GVHD) Post-transplant
NCT01527045 (8) [back to overview]Number of Patients With Recurrent or Progressive Malignancy
NCT01527045 (8) [back to overview]Number of Patients With Grades II-IV Acute Graft-versus-host-disease (GVHD)
NCT01527045 (8) [back to overview]Number of Donors Discontinuing Atorvastatin Due to Toxicity
NCT01527045 (8) [back to overview]Number of Non-relapse Mortalities
NCT01528709 (2) [back to overview]Saphenous Vein Graft Occlusion (Percentage of Vein Grafts Occluded) Based on CT Coronary Angiography at 1 Year
NCT01528709 (2) [back to overview]Vein Graft Stenosis 1 Year After CABG Based on CT Coronary Angiography
NCT01544309 (16) [back to overview]Frequency of Serious Adverse Events (SAE)
NCT01544309 (16) [back to overview]Percent Change in 1,5-AG Level
NCT01544309 (16) [back to overview]Number of Participants Stratified by Time to the Occurrence of Deterioration of Diabetic Treatment Status
NCT01544309 (16) [back to overview]Percent Change in Blood Glucose Level (Fasting)
NCT01544309 (16) [back to overview]Occurrence of Deterioration of Diabetic Treatment Status
NCT01544309 (16) [back to overview]Percent Change in Non-high-density Lipoprotein Cholesterol (HDL-C) Level
NCT01544309 (16) [back to overview]Change From Baseline in Insulin Level
NCT01544309 (16) [back to overview]Change in Blood Glucose Level (Fasting)
NCT01544309 (16) [back to overview]Rate of Patients Who Have Reached the Target LDL-C Level Specified in Japan Atherosclerosis Society Guidelines (JASGL) 2007
NCT01544309 (16) [back to overview]Percent Changes in Lipids (LDL-C, HDL-C, TC, TG, Non-HDL-C/HDL-C Ratio, and FFA)
NCT01544309 (16) [back to overview]Percent Change in Non-HDL-C Level
NCT01544309 (16) [back to overview]Frequency of Cardiovascular Events (Coronary Artery Disease, Heart Failure, Cerebrovascular Disease, Peripheral Artery Disease and Aortic Disease)
NCT01544309 (16) [back to overview]Change in HbA1c Level
NCT01544309 (16) [back to overview]Percent Change in Insulin Level
NCT01544309 (16) [back to overview]Change From Baseline in 1,5-AG Level
NCT01544309 (16) [back to overview]Change in HbA1c Level
NCT01567826 (10) [back to overview]Intravascular Ultrasound (IVUS) Parameters
NCT01567826 (10) [back to overview]LCBI4mm Max
NCT01567826 (10) [back to overview]Lipiscan - Lipid Core Burden Index (LCBI)
NCT01567826 (10) [back to overview]Major Adverse Cardiac Events (MACE)
NCT01567826 (10) [back to overview]Change in LCBI4mm Max
NCT01567826 (10) [back to overview]Change in LCBI, Lesion
NCT01567826 (10) [back to overview]Post PCI Cardiac Enzymes
NCT01567826 (10) [back to overview]Blood Chemistry - HsCRP
NCT01567826 (10) [back to overview]Diameter Stenosis
NCT01567826 (10) [back to overview]Fractional Flow Reserve (FFR) Value
NCT01600170 (9) [back to overview]Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CCR2 at 12 Weeks, as a Result of Treatment.
NCT01600170 (9) [back to overview]Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CD16 at 12 Weeks, as a Result of Treatment.
NCT01600170 (9) [back to overview]Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CD163 at 12 Weeks, as a Result of Treatment.
NCT01600170 (9) [back to overview]Change From Week 0 in Plasma sCD163 Levels, at Week 12 Following Treatment.
NCT01600170 (9) [back to overview]Change From Week 0 to Week 12 in Percentage of Blood Monocytes Expressing Surface Marker Tissue Factor (TF), Following Treatment.
NCT01600170 (9) [back to overview]Change From 0 Week in Levels of Plasma Inflammatory Marker hsCRP in Chronic HIV+/ HAART+ Subjects Over 12 Weeks, Following Treatment.
NCT01600170 (9) [back to overview]Change From Week 0 to Week 12 in Percentage of Blood Monocytes Expressing Surface Marker CD38, Following Treatment.
NCT01600170 (9) [back to overview]Change From Baseline Within Each Period in Levels of Plasma Inflammatory Marker MCP-1 in Chronic HIV+/ HAART+ Subjects Over 12 Weeks.
NCT01600170 (9) [back to overview]Change From Baseline Within Each Period in Levels of Plasma Inflammatory Marker sCD14 in Chronic HIV+/ HAART+ Subjects Over 12 Weeks.
NCT01645176 (1) [back to overview]Change in Synovitis
NCT01660191 (6) [back to overview]Changes in Major Lipid Parameters - VLDL Size
NCT01660191 (6) [back to overview]Changes in Plasma CoQ10 Levels
NCT01660191 (6) [back to overview]Changes to Glucose Metabolism - Fructosamine
NCT01660191 (6) [back to overview]Changes in HDL and LDL Size
NCT01660191 (6) [back to overview]Changes to Glucose Metabolism - HbA1c and Insulin
NCT01660191 (6) [back to overview]Changes HDL Particle Number and LDL Particle Number
NCT01665677 (4) [back to overview]Matched Related Transplants Who Develop Grade II-IV Chronic GVHD.
NCT01665677 (4) [back to overview]Matched Unrelated Donors Transplants Who Develop Grade II-IV Acute GVHD.
NCT01665677 (4) [back to overview]Matched Unrelated Donors Transplants Who Develop Grade II-IV Chronic GVHD.
NCT01665677 (4) [back to overview]Matched Related Transplants Who Develop Grade II-IV Acute Graft Versus Host Disease (GVHD).
NCT01702987 (1) [back to overview]Phosphocreatine Recovery
NCT01709500 (25) [back to overview]Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Apo A-1 at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - On- Treatment Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent--to--Treat (ITT) Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - On-Treatment Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 52 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Apo B at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in HDL-C at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Lipoprotein (a) at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 24 - On-Treatment Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Non-High -Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Total-C at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percentage of Participants Reaching Calculated LDL--C <70 mg/dL (1.81 mmol/L) at Week 52 - On-Treatment Analysis
NCT01709500 (25) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL--C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL--C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Lipoprotein (a) at Week 12 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Apo B at Week 24 - On-Treatment Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 - ITT Analysis
NCT01709500 (25) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - ITT Analysis
NCT01709513 (26) [back to overview]Percentage of Participants Who Experienced Skeletal Muscle-related Adverse Event (AE)
NCT01709513 (26) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or Moderate or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis
NCT01709513 (26) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or Moderate or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - On-Treatment Analysis
NCT01709513 (26) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change in Fasting Triglycerides From Baseline to Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Total Cholesterol (Total--C) at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Non--High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Apo B at Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Total-C at Week 12 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change in HDL-C From Baseline to Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Apo A--1 at Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Apo B at Week 24 -- On--Treatment Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Non--HDL-C at Week 24 -- On--Treatment Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Calculated LDL--C at Week 12 -- ITT Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - On--Treatment Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent--To-Treat (ITT) Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - On--Treatment Analysis
NCT01709513 (26) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 Versus Atorvastatin - Raw Data Description - Intent-To-Treat (ITT) Analysis
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
NCT01730040 (24) [back to overview]Percent Change From Baseline in Apo B at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Apo A-1 at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis
NCT01730040 (24) [back to overview]Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - On-Treatment Analysis
NCT01730040 (24) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Total-C at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Non-High-density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 24 - On-Treatment Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in HDL-C at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - On-Treatment Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent-to-treat (ITT) Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 - ITT Analysis
NCT01730040 (24) [back to overview]Percent Change From Baseline in Apo B at Week 24 - On-Treatment Analysis
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Renal Function
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Tricuspid Regurgitant (TR) Jet.
NCT01732718 (9) [back to overview]Occurrence of Adverse Events.
NCT01732718 (9) [back to overview]Mean Change From Baseline to Week 6 in Absolute Cell Counts
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Plasma Markers of Endothelial Activation
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Plasma Levels of Vascular Endothelial Growth Factor (VEGF)
NCT01732718 (9) [back to overview]Abnormal Physical Findings.
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Plasma Levels of Soluble Fms-like Tyrosine Kinase-1 (sFLT-1)
NCT01732718 (9) [back to overview]Change From Baseline to Week 6 in Endothelial Function
NCT01733953 (6) [back to overview]Change From Baseline in Brachial Artery Flow-Mediated Dilation at 6-months
NCT01733953 (6) [back to overview]Change From Baseline in Carotid Artery Compliance at 6-Months
NCT01733953 (6) [back to overview]Change From Baseline in Carotid Artery Distensibility at 6-Months
NCT01733953 (6) [back to overview]Change From Baseline in Carotid Intima-Media Thickness at 6-Months
NCT01733953 (6) [back to overview]Change From Baseline in Pulse Wave Velocity at 6-Months
NCT01733953 (6) [back to overview]Change From Baseline in Augmentation Index at 6-Months
NCT01763866 (22) [back to overview]Percentage of Participants Who Achieved LDL-C < 70 mg/dL at Week 12
NCT01763866 (22) [back to overview]Percentage of Participants Who Achieved a Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL
NCT01763866 (22) [back to overview]Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in LDL-C at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in HDL-C at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 12
NCT01763866 (22) [back to overview]Change From Baseline in LDL-C at at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Change From Baseline in LDL-C at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Triglycerides at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Very Low-Density Cholesterol (VLDL-C) at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Very Low-Density Cholesterol (VLDL-C) at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at the Mean of Weeks 10 and 12
NCT01763866 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 12
NCT01766076 (1) [back to overview]Percentage Change in Immune Activation Levels After 12 Weeks of Atorvastatin 80mg Daily
NCT01785615 (33) [back to overview]Mean Low Density Lipoprotein Cholesterol in Blood
NCT01785615 (33) [back to overview]Mean Myeloperoxidase in Blood
NCT01785615 (33) [back to overview]Mean Myeloperoxidase in Blood
NCT01785615 (33) [back to overview]Mean Plasminogen Activator Inhibitor-1 in Blood
NCT01785615 (33) [back to overview]Mean Soluble Intercellular Adhesion Molecule in Blood
NCT01785615 (33) [back to overview]Mean Soluble Vascular Adhesion Molecule in Blood
NCT01785615 (33) [back to overview]Mean Systolic Blood Pressure
NCT01785615 (33) [back to overview]Mean Triglycerides in Blood
NCT01785615 (33) [back to overview]Mean Triglycerides in Blood
NCT01785615 (33) [back to overview]Mean Vascular Adhesion Molecule in Blood
NCT01785615 (33) [back to overview]Mean Waist Circumference
NCT01785615 (33) [back to overview]Mean Waist Circumference
NCT01785615 (33) [back to overview]Mean Systolic Blood Pressure
NCT01785615 (33) [back to overview]Mean Fasting Plasma Glucose in Blood
NCT01785615 (33) [back to overview]Mean Plasminogen Activator Inhibitor-1 in Blood
NCT01785615 (33) [back to overview]Mean Alanine Aminotransferase in Blood
NCT01785615 (33) [back to overview]Mean Apolipoprotein A-1 in Blood
NCT01785615 (33) [back to overview]Mean Apolipoprotein B in Blood
NCT01785615 (33) [back to overview]Mean Apolipoprotein B in Blood
NCT01785615 (33) [back to overview]Mean Apolipoprotein B/ Apolipoprotein A1 Ratio in Blood
NCT01785615 (33) [back to overview]Mean Apolipoprotein B/ Apolipoprotein A1 Ratio in Blood
NCT01785615 (33) [back to overview]Mean Aspartate Aminotransferase in Blood
NCT01785615 (33) [back to overview]Mean Diastolic Blood Pressure
NCT01785615 (33) [back to overview]Mean Diastolic Blood Pressure
NCT01785615 (33) [back to overview]Mean Fasting Blood Glucose in Blood
NCT01785615 (33) [back to overview]Mean High Density Lipoprotein Cholesterol in Blood
NCT01785615 (33) [back to overview]Mean High Density Lipoprotein Cholesterol in Blood
NCT01785615 (33) [back to overview]Mean High Sensitivity C-reactive Protein in Blood
NCT01785615 (33) [back to overview]Mean Hs-C Reactive Protein in Blood
NCT01785615 (33) [back to overview]Mean Intercellular Adhesion Molecule in Blood
NCT01785615 (33) [back to overview]Mean Leptin in Blood
NCT01785615 (33) [back to overview]Mean Leptin in Blood
NCT01785615 (33) [back to overview]Mean Low Density Lipoprotein Cholesterol in Blood
NCT01795937 (10) [back to overview]Cmax of Rosuvastatin
NCT01795937 (10) [back to overview]Cmax of Atorvastatin (Statins Part)
NCT01795937 (10) [back to overview]AUCτ,ss (Itraconazole Part)
NCT01795937 (10) [back to overview]AUC0-tz of Atorvastatin
NCT01795937 (10) [back to overview]AUC0-tz of Rosuvastatin
NCT01795937 (10) [back to overview]AUC0-∞ of Rosuvastatin (Statins Part)
NCT01795937 (10) [back to overview]Cmax,ss of Faldaprevir (Statins Part)
NCT01795937 (10) [back to overview]AUC0-∞ of Atorvastatin (Statins Part)
NCT01795937 (10) [back to overview]Cmax,ss (Itraconazole Part)
NCT01795937 (10) [back to overview]AUCτ,ss of Faldaprevir (Statins Part)
NCT01812707 (7) [back to overview]Percent Change From Baseline in Fasting Triglycerides and Lipoprotein (a) at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Percent Change From Baseline in Total Cholesterol, High-Density Lipoprotein Cholesterol (HDL-C), Non-HDL-C, and Apolipoprotein B (Apo-B) at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and < 70 mg/dL (1.81 mmol/L) at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 12 - On-Treatment Analysis
NCT01812707 (7) [back to overview]Absolute Change From Baseline in Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) Ratio at Week 12 - On-Treatment Analysis
NCT01837069 (2) [back to overview]Number of Partipants That Experienced Death, Myocardial Infarction, Stroke, Transient Ischemic Attack, Myocardial Necrosis, or Venous Thromboembolism
NCT01837069 (2) [back to overview]Length of Stay
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Apolipoprotein A1 (Apo A1), Apolipoprotein B (Apo B)
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 Total Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
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 Lipoprotein(a) [Lp(a)]
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]Number of Participants With an Injection Site Reaction
NCT01890967 (10) [back to overview]Number of Participants Who Develop Treatment Emergent Anti-LY3015014 Antibodies
NCT01890967 (10) [back to overview]Change From Baseline in High Sensitivity C-Reactive Protein (hsCRP)
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
NCT01929135 (5) [back to overview]Change in Bleeding on Probing Index (BOP)
NCT01929135 (5) [back to overview]Change in Periodontal Inflammation Surface Area (PISA)
NCT01929135 (5) [back to overview]Change in Mean Pocket Depth (PD)
NCT01929135 (5) [back to overview]Change in Gingival Index
NCT01929135 (5) [back to overview]Change in Clinical Attachment Level (CAL)
NCT01953328 (24) [back to overview]Percent Change From Baseline in the Apolipoprotein B/Apolipoprotein A-1 Ratio at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Non-HDL-C at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in HDL-C at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A-1 Ratio at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Change From Baseline in LDL-C at Week 12
NCT01953328 (24) [back to overview]Change From Baseline in LDL-C at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percentage of Participants Who Achieved LDL-C < 70 mg/dL at Week 12
NCT01953328 (24) [back to overview]Percentage of Participants Who Achieved a Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL
NCT01953328 (24) [back to overview]Percent Change From Baseline in VLDL-C at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in VLDL-C at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Triglycerides at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 10 and 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 12
NCT01953328 (24) [back to overview]Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12
NCT01964326 (4) [back to overview]Percentage of Participants Who Complied With the Direction to Check Their Low-density Lipoprotein Cholesterol (LDL-C) Level
NCT01964326 (4) [back to overview]"Percentage of Participants Taking an Ask a Doctor or Pharmacist Before Use Medication Who Followed the Labeling and Contacted a Doctor or Pharmacist Before Using Study Medication"
NCT01964326 (4) [back to overview]"Percentage of Participants Who Stopped Study Medication Use and Asked a Doctor if They Experienced Any of the Labeled Stop Use and Ask a Doctor Symptoms"
NCT01964326 (4) [back to overview]Percentage of Participants Who Took Appropriate Action Based on Their LDL-C Results
NCT01984424 (24) [back to overview]Change From Baseline in LDL-C at Week 24
NCT01984424 (24) [back to overview]Change From Baseline in LDL-C at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in VLDL-C at Week 24
NCT01984424 (24) [back to overview]Percentage of Participants Who Achieved a Mean LDL-C at Weeks 22 and 24 of Less Than 70 mg/dL
NCT01984424 (24) [back to overview]Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percentage of Participants Who Achieved LDL-C at Week 24 of Less Than 70 mg/dL
NCT01984424 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Triglycerides at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Triglycerides at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in HDL-C at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in LDL-C at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in LDL-C at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 22 and 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 24
NCT01984424 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at the Mean of Weeks 22 and 24
NCT01988571 (10) [back to overview]Patient-reported Outcomes Measurement (PROMIS) Questionnaire - Fatigue Short Form 41
NCT01988571 (10) [back to overview]Left Ventricular Ejection Fraction (LVEF)
NCT01988571 (10) [back to overview]Stroke Volume
NCT01988571 (10) [back to overview]Pulse Wave Velocity
NCT01988571 (10) [back to overview]Patient-reported Outcomes Measurement (PROMIS) Questionnaire - Applied Cognition - General Concerns - Short Form 4a
NCT01988571 (10) [back to overview]Left Ventricular (LV) Mass
NCT01988571 (10) [back to overview]Hopkins Verbal Learning Test (HVLT) Total Recall
NCT01988571 (10) [back to overview]End Systolic Volume
NCT01988571 (10) [back to overview]End Diastolic Volume
NCT01988571 (10) [back to overview]Controlled Oral Word Association (COWA)
NCT02056340 (2) [back to overview]Change in Inflammatory Markers From Time Zero to 72 Hours
NCT02056340 (2) [back to overview]Severity of Illness Score Baseline to 72 Hours
NCT02080455 (10) [back to overview]AUC0-t
NCT02080455 (10) [back to overview]AUC0-∞
NCT02080455 (10) [back to overview]AUC0-∞
NCT02080455 (10) [back to overview]AUC0-t
NCT02080455 (10) [back to overview]Cmax
NCT02080455 (10) [back to overview]Tmax
NCT02080455 (10) [back to overview]Cmax
NCT02080455 (10) [back to overview]t1/2
NCT02080455 (10) [back to overview]t1/2
NCT02080455 (10) [back to overview]Tmax
NCT02081638 (2) [back to overview]Changes in sCD14 After 9 Months of Treatment With Aspirin or Atorvastatin
NCT02081638 (2) [back to overview]Changes in sCD14 in EC and ART <50 Groups Treated With Aspirin or Atorvastatin.
NCT02084069 (1) [back to overview]Atrial Fibrillation Incidence After Open Cardiac Valve Repair
NCT02093390 (17) [back to overview]Terminal Disposition Half-life (t1/2) of TAK-385
NCT02093390 (17) [back to overview]Tmax: Time to Reach the Maximum Plasma Concentration of TAK-385
NCT02093390 (17) [back to overview]AUC(0-inf): Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity of TAK-385 on Day 1
NCT02093390 (17) [back to overview]AUC(0-tlast): Area Under the Plasma Concentration Curve From Time Zero to the Time of the Last Quantifiable Concentration of TAK-385 on Day 10
NCT02093390 (17) [back to overview]Cmax: Maximum Observed Plasma Concentration of TAK-385 on Day 1
NCT02093390 (17) [back to overview]Cmax: Maximum Observed Plasma Concentration of TAK-385 on Day 10
NCT02093390 (17) [back to overview]AUC(0-inf): Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity of TAK-385 on Day 10
NCT02093390 (17) [back to overview]Number of Participants With at Least 1 Treatment Emergent Adverse Event (AE)
NCT02093390 (17) [back to overview]Number of Participants With Clinical Significant Changes in Electrocardiogram (ECG) Findings
NCT02093390 (17) [back to overview]Number of Participants With Clinical Significant Changes in Laboratory Tests
NCT02093390 (17) [back to overview]Number of Participants With Clinical Significant Changes in Vital Signs
NCT02093390 (17) [back to overview]AUC(0-tlast): Area Under the Plasma Concentration Curve From Time Zero to the Time of the Last Quantifiable Concentration of TAK-385 on Day 1
NCT02093390 (17) [back to overview]Apparent Total Body Clearance (CL/F) of TAK-385
NCT02093390 (17) [back to overview]AUC (0-120): Area Under the Plasma Concentration-Time Curve From Time 0 to 120 Hours of TAK-385
NCT02093390 (17) [back to overview]Fraction Excreted Unchanged (Fe) of TAK-385
NCT02093390 (17) [back to overview]Plasma Trough Concentrations for Atorvastatin
NCT02093390 (17) [back to overview]Plasma Trough Concentrations for Fluconazole
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Lipoprotein (A) (Lp[A]) at Week 12
NCT02135029 (26) [back to overview]Anti-drug Antibody (ADA) and Neutralizing Anti-body (nAb) Titer Level in Participants Who Tested Positive for ADA and nAb Respectively
NCT02135029 (26) [back to overview]Number of Participants With Adverse Events Related to Type 1 and 3 Hypersensitivity Reactions, Injection Site Reactions, Myalgia, Myopathy, Creatinine Kinase (CK) and Liver Function Tests (LFT) Elevations
NCT02135029 (26) [back to overview]Number of Participants With Positive Anti-drug Antibodies (ADA) and Neutralizing Antibodies (nAb)
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Apolipoprotein A-I (ApoA-I) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Apolipoprotein A-II (ApoA-II) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Apolipoprotein B (ApoB) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting High Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Lipoprotein (a) (Lp[a]) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Non High Density Lipoprotein Cholesterol (Non HDL-C) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Total Cholesterol (TC) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Triglycerides (TG) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Very Low Density Lipoprotein Cholesterol (VLDL-C) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percentage of Participants Achieving Fasting Low Density Lipoprotein Cholesterol (LDL-C) Less Than or Equal to (<=) 100 Milligram Per Deciliter (mg/dL) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting Low Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting Non High Density Lipoprotein Cholesterol (Non HDL-C) at Week 12
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting Total Cholesterol (TC) at Week 12
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting Total Cholesterol (TC)/ High Density Lipoprotein Cholesterol (HDL-C) Ratio at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percentage of Participants Discontinued Due to Myalgia, Myopathy, Creatinine Kinase (CK) and Liver Function Tests (LFT) Elevations
NCT02135029 (26) [back to overview]Plasma PF-04950615 Concentrations at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percentage of Participants Achieving Fasting Low Density Lipoprotein Cholesterol (LDL-C) Less Than or Equal to (<=) 70 Milligram Per Deciliter (mg/dL) at Weeks 12 and 24
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Low Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT02135029 (26) [back to overview]Percent Change From Baseline in Fasting Low Density Lipoprotein Cholesterol (LDL-C) at Week 24
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Apolipoprotein B (ApoB) at Week 12
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting Apolipoprotein B (ApoB)/Apolipoprotein A-I (ApoA-I) Ratio at Weeks 12 And 24
NCT02135029 (26) [back to overview]Absolute Change From Baseline in Fasting High Density Lipoprotein Cholesterol (HDL-C) at Week 12
NCT02156492 (7) [back to overview]Effect of Evacetrapib Single and Multiple Doses on High Density Lipoprotein Cholesterol (HDL-C), Low Density Lipoprotein Cholesterol (LDL-C), and Triglycerides (TG)
NCT02156492 (7) [back to overview]Pharmacokinetics (PK): Area Under Curve (AUC 0-inf) of Evacetrapib
NCT02156492 (7) [back to overview]PK: AUC of Evacetrapib Alone and With Simvastatin or Atorvastatin
NCT02156492 (7) [back to overview]PK: Cmax of Evacetrapib Alone and With Simvastatin or Atorvastatin
NCT02156492 (7) [back to overview]PK: Maximum Concentration (Cmax) of Evacetrapib
NCT02156492 (7) [back to overview]PK: Time to Maximum Concentration (Tmax) of Evacetrapib
NCT02156492 (7) [back to overview]PK: Tmax of Evacetrapib Alone and With Simvastatin or Atorvastatin
NCT02189837 (5) [back to overview]Percent Change From Baseline in Low-density Lipoprotein (LDL) Apolipoprotein B-100 Fractional Catabolic Rate (FCR)
NCT02189837 (5) [back to overview]Percent Change From Baseline in LDL-C at Day 50
NCT02189837 (5) [back to overview]Percent Change From Baseline in LDL Apolipoprotein B-100 Production Rate (PR)
NCT02189837 (5) [back to overview]Percent Change From Baseline in Lipoprotein (a) Fractional Catabolic Rate (FCR)
NCT02189837 (5) [back to overview]Percent Change From Baseline in Lipoprotein(a) Production Rate (PR)
NCT02197065 (3) [back to overview]Peri-operative Rise in Interleukin-6 (IL-6) Levels
NCT02197065 (3) [back to overview]Peri-operative Rise in High Sensitivity C-reactive Protein (Hs-CRP)
NCT02197065 (3) [back to overview]Percentage of All Enrolled Patients With a Peri-operative Rise in High-sensitivity Cardiac Troponin I
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Non-HDL-C
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Apolipoprotein AI (apoAI)
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Apolipoprotein B (apoB)
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Cholesterol Efflux Capacity
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in High-Density Lipoprotein Cholesterol (HDL-C)
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Lipoprotein(a) (Lp[a])
NCT02227784 (7) [back to overview]Percent Change From Baseline to 3 Months in Low-Density Lipoprotein Cholesterol (LDL-C)
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in Apolipoprotein B
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in High-Density Lipoprotein Cholesterol (HDL-C)
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in LDL-C (Direct)
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in Lipoprotein-a
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in Low-Density Lipoprotein Cholesterol (LDL-C) Measured by Beta Quantification
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in Non HDL-C
NCT02260648 (7) [back to overview]Percent Change From Baseline to Week 12 in Apolipoprotein A-I
NCT02278471 (6) [back to overview]Medication Adherence-Percentage of Pills Taken
NCT02278471 (6) [back to overview]Systolic Blood Pressure
NCT02278471 (6) [back to overview]Systolic Blood Pressure
NCT02278471 (6) [back to overview]Medication Adherence
NCT02278471 (6) [back to overview]LDL Cholesterol
NCT02278471 (6) [back to overview]LDL Cholesterol
NCT02331095 (11) [back to overview]The Reduction of Peak Thrombin Concentration
NCT02331095 (11) [back to overview]The Rate of Major, Non-major, and All Hemorrhages Defined by the International Society on Thrombosis and Haemostasis (ISTH) Criteria
NCT02331095 (11) [back to overview]The Reduction of Endogenous Thrombin Potential
NCT02331095 (11) [back to overview]The Reduction of Clinical Post-thrombotic Syndrome (PTS), as Objectively Evaluated With Villalta Scoring System
NCT02331095 (11) [back to overview]The Rate of Arterial Thrombotic Events
NCT02331095 (11) [back to overview]The Composite Rate of Recurrent Venous Thromboembolism (VTE) and VTE Related Mortality
NCT02331095 (11) [back to overview]Change in Triglyceride Levels at 3 Months
NCT02331095 (11) [back to overview]Change in the Levels of D-Dimer at 3 Months
NCT02331095 (11) [back to overview]Change in the Levels of C-Reactive Protein at 3 Months
NCT02331095 (11) [back to overview]Change in Low-Density Lipoproteins (LDL) at 3 Months
NCT02331095 (11) [back to overview]The Rate of Residual (Chronic) Vein Obstruction by Doppler Ultrasound
NCT02342015 (2) [back to overview]Change in Circulating Levels of Osteoprogenitor Cells (CD34+/OCN+/BAP+ Cells)
NCT02342015 (2) [back to overview]Relative Change in OPG/RANK/RANKL mRNA Expression in Isolated T Cells and Monocytes
NCT02347098 (4) [back to overview]Endothelial Progenitor Cell Colony Forming Units/ml of Peripheral Blood Across Time
NCT02347098 (4) [back to overview]Change in % Necrotic Core Component of Atheroma
NCT02347098 (4) [back to overview]Major Adverse CV Events
NCT02347098 (4) [back to overview]Change in the Total Atheroma Volume From Baseline to 12 Weeks
NCT02370784 (4) [back to overview]% of Patients Who Improved Their Brachial Flow-mediation Dilation (%FMD) at 16 Weeks
NCT02370784 (4) [back to overview]Change in the Raynaud Condition Score (RCS) at 16 Weeks (End-of-study) From Baseline
NCT02370784 (4) [back to overview]Proportion of Patients Improving Their EndoPAT Reactive Hyperemia Index (RHI) at the End-of-study (16 Weeks)
NCT02370784 (4) [back to overview]The Median Change in the Raynaud Phenomenon Visual Analog Scale (RP-VAS) Score at 16 Weeks (End-of-study) Compared to Baseline in the Atorvastatin and Placebo Groups.
NCT02432040 (8) [back to overview]Mean Change in hsCRP Levels
NCT02432040 (8) [back to overview]Adverse Events
NCT02432040 (8) [back to overview]Percentage of Patients Achieving PASI-50 at the End of 3 Months
NCT02432040 (8) [back to overview]Mean Gross Change in Psoriasis Area and Severity Index (PASI) Scores From Baseline to the End of 6 Months
NCT02432040 (8) [back to overview]Mean Change in Lipid Profile Levels
NCT02432040 (8) [back to overview]Monthly Mean Changes in PASI Scores
NCT02432040 (8) [back to overview]Mean Change in Dermatology Life Quality Index (DLQI) Scores After 6 Months
NCT02432040 (8) [back to overview]Percentage of Patients Achieving PASI-50 in Each Arm at the End of 6 Months
NCT02437084 (6) [back to overview]OGTT Insulin AUC
NCT02437084 (6) [back to overview]Steady-state Plasma Glucose (SSPG)
NCT02437084 (6) [back to overview]Fasting Plasma Insulin
NCT02437084 (6) [back to overview]Fasting Plasma Glucose
NCT02437084 (6) [back to overview]Insulin Secretion Rate Area Under the Curve (ISR-AUC)
NCT02437084 (6) [back to overview]OGTT Glucose AUC
NCT02476006 (11) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12
NCT02476006 (11) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12
NCT02476006 (11) [back to overview]Percentage of Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 12
NCT02476006 (11) [back to overview]Percentage of Participants With Treatment Emergent Adverse Events (TEAEs)
NCT02476006 (11) [back to overview]Assessment of Participant's Acceptability of Self-Injection Using Self Injection Assessment Questionnaire (SIAQ): Self Image, Injection-Site Reactions, Ease of Use
NCT02476006 (11) [back to overview]Assessment of Participant's Acceptability of Self-Injection Using Self Injection Assessment Questionnaire (SIAQ): Feeling About Injections, Self Confidence, Satisfaction With Self-Injections
NCT02476006 (11) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) and/or >=50% Reduction From Baseline in LDL-C at Week 12
NCT02476006 (11) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Week 12
NCT02476006 (11) [back to overview]Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 12
NCT02476006 (11) [back to overview]Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT02476006 (11) [back to overview]Percent Change From Baseline in Triglycerides at Week 12
NCT02503865 (5) [back to overview]Immunoassay Cortisole in Blood
NCT02503865 (5) [back to overview]Systolic/ Diastolic Blood Pressures (mm Hg)
NCT02503865 (5) [back to overview]Lipid Profile
NCT02503865 (5) [back to overview]Blood Glucose Level
NCT02503865 (5) [back to overview]Immunoassay Hormones in Blood
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience 1 or More Gastrointestinal-related Adverse Events (AEs)
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience 1 or More Gallbladder-related AEs
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience 1 or More Allergic Reaction or Rash AEs
NCT02550288 (18) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) at Week 12
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in AST ≥10 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in Alanine Aminotransferase (ALT) ≥3 Times Upper Limit of Normal (ULN)
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in ALT and/or AST ≥3 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants With Potential Hy's Law Condition
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in Aspartate Aminotransferase (AST) ≥3 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in AST ≥5 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Have Consecutive Elevations in ALT and/or AST ≥10 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Have Consecutive Elevations in ALT and/or AST ≥5 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Have Elevations in CK ≥10xULN and Drug-Related Muscle Symptoms
NCT02550288 (18) [back to overview]Percentage of Participants Who Have Elevations in CK ≥10xULN With Muscle Symptoms
NCT02550288 (18) [back to overview]Percentage of Participants Who Have Elevations in Creatine Kinase (CK) ≥10xULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in ALT ≥5 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience Consecutive Elevations in ALT ≥10 Times ULN
NCT02550288 (18) [back to overview]Percentage of Participants Who Experience 1 or More Hepatitis-related AEs
NCT02577042 (2) [back to overview]Changes in the Inflammatory Marker IL-6
NCT02577042 (2) [back to overview]Changes in Plasma Soluble Markers (D-dimer)
NCT02584504 (16) [back to overview]Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo-B) at Week 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12- Intent to Treat (ITT) Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 12- On-Treatment Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Calculated LDL-C to Averaged Week 10 to 12- On-Treatment Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Calculated LDL-C to Averaged Week 10 to 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Fasting Triglycerides (TGs) at Week 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12: ITT Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Week 12- ITT Analysis
NCT02584504 (16) [back to overview]Percentage of Participants Reaching Calculated LDL-C Goal at Week 12- ITT Analysis
NCT02584504 (16) [back to overview]Percentage of Participants Reaching Calculated LDL-C Goal at Week 12- On-Treatment Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Calculated LDL-C at Week 20, 24, 36, 48 and 64 -OLTP Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Apo-B at Week 12- On-Treatment Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12- On-treatment Analysis
NCT02584504 (16) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 12- ITT Analysis
NCT02586155 (15) [back to overview]Change in Glucose From Baseline Over Time Between and Within Treatment Groups
NCT02586155 (15) [back to overview]Change in Estimated Glomerular Filtration Rate (eGFR) From Baseline Over Time Within and Between Treatment Groups for Subjects With Impaired Renal Function at Baseline (eGFR <60 mL/Min/1.7m2)
NCT02586155 (15) [back to overview]Incidence of All-cause Mortality
NCT02586155 (15) [back to overview]Change in Apolipoprotein A1 (ApoA-I) Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Incidence of First Occurrence of Adjudication-Confirmed Four-Point MACE
NCT02586155 (15) [back to overview]Incidence of Hospitalization for Congestive Heart Failure (CHF)
NCT02586155 (15) [back to overview]Change in C Reactive Protein (CRP) Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Incidence of First Occurrence of Adjudication-confirmed Narrowly Defined MACE
NCT02586155 (15) [back to overview]Incidence of First Occurrence of Adjudication-confirmed Broadly Defined MACE
NCT02586155 (15) [back to overview]Change in Alkaline Phosphatase (ALP) From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Change in Triglyceride (TG) Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Change in LDL-C Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Change in Hemoglobin (Hb) A1c From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Change in HDL-C Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02586155 (15) [back to overview]Change in Apolipoprotein B (apoB) Concentration From Baseline Over Time Within and Between Treatment Groups
NCT02633956 (3) [back to overview]The Effect of Obeticholic Acid on LDL Particle Concentration (Total) (Least Squares Mean Change From Baseline at Week 16)
NCT02633956 (3) [back to overview]The Effect of Obeticholic Acid on LDL Particle Size (Least Squares Mean Change From Baseline at Week 16)
NCT02633956 (3) [back to overview]The Effect of Obeticholic Acid on Low-density Lipoprotein (LDL) Concentration (Least Squares Mean Change From Baseline at Week 16)
NCT02662569 (23) [back to overview]Percent Change From Baseline in LDL-C at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percentage of Participants With LDL-C Less Than 70 mg/dL (1.8 mmol/L) at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in HDL-C at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Apolipoprotein B100 at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Apolipoprotein B100 at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in LDL-C at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Apolipoprotein B100/Apolipoprotein A1 Ratio at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Apolipoprotein B100/Apolipoprotein A1 Ratio at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Non-HDL-C at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Non-HDL-C at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Lipoprotein(a) at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percentage of Participants With Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL (1.8 mmol/L)
NCT02662569 (23) [back to overview]Change From Baseline in LDL-C at Week 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in VLDL-C at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Triglycerides at Week 12
NCT02662569 (23) [back to overview]Change From Baseline in LDL-C at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12
NCT02662569 (23) [back to overview]Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at Week 12
NCT02714569 (19) [back to overview]Pharmacokinetics (PK): Maximum Plasma Concentration (Cmax) of LY3202328 (LY) in Part A After a Single Dose
NCT02714569 (19) [back to overview]PD: Change From Baseline to Last Day of Dosing in Fasting Total Triglycerides in Part B
NCT02714569 (19) [back to overview]PD: Change From Baseline to Last Day of Dosing in Fasting Total Cholesterol in Part B
NCT02714569 (19) [back to overview]PD: Change From Baseline to Last Day of Dosing in Fasting LDL-c in Part B
NCT02714569 (19) [back to overview]PD: Change From Baseline to Last Day of Dosing in Fasting HDL-c in Part B
NCT02714569 (19) [back to overview]Number of Participants With One or More Serious Adverse Event(s) (SAEs) Considered by the Investigator to be Related to Study Drug Administration Part A and Part B
NCT02714569 (19) [back to overview]PD: Change From Baseline to in Fasting Total Cholesterol in Part A
NCT02714569 (19) [back to overview]PK: Steady State Tmax of LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PK: Steady State Maximum Plasma Concentration (Cmax) of LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PK: Cmax of Atorvastatin With/Without LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PK: AUC (0-t) of Atorvastatin With/Without LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PK: Area Under Concentration Curve From Zero to Time (AUC [0-t]) of Simvastatin With/Without LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]Pharmacodynamics (PD): Change From Baseline in Fasting High-Density Lipoprotein Cholesterol (HDL-c) in Part A
NCT02714569 (19) [back to overview]PK: Cmax of Simvastatin With/Without LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PD: Change From Baseline in Fasting Low-Density Lipoprotein Cholesterol (LDL-c) in Part A
NCT02714569 (19) [back to overview]PK: Time to Maximum Concentration (Tmax) of LY3202328 (LY) in Part A
NCT02714569 (19) [back to overview]PK: Steady State Area Under the Serum Concentration-Time Curve During the Dosing Interval (AUCτ) of LY3202328 (LY) in Part B
NCT02714569 (19) [back to overview]PK: Area Under the Serum Concentration Time Curve From Zero to Infinity (AUC[0-∞]) of LY3202328 (LY) in Part A After a Single Dose
NCT02714569 (19) [back to overview]PD: Change From Baseline in Fasting Total Triglycerides Part A
NCT02715726 (22) [back to overview]Percentage of Participants Reaching Calculated Low Density Lipoprotein Cholesterol <70 mg/dL (1.81 mmol/L) at Week 24: On-Treatment Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 24: On-Treatment Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 24: On-Treatment Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 12: On-Treatment Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 24: On-Treatment Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Apolipoprotein A-1 at Week 12 : ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 24: Intent-to-treat (ITT) Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Lipoprotein (a) (Lp[a]) at Week 24: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 12: ITT Analysis
NCT02715726 (22) [back to overview]Percentage of Participants Reaching Calculated Low Density Lipoprotein Cholesterol <70 mg/dL (1.81 mmol/L) at Week 24: ITT Analysis
NCT02943590 (2) [back to overview]The Percentage of Participants in Each Group With New Onset Heart Failure.
NCT02943590 (2) [back to overview]The Percentage of Individuals in Each Group With a Significant Decline in the LVEF.
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Lumen Volume at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Lipoprotein (a) (Lp[a]) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in High-density Lipoprotein Cholesterol at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Fasting Triglycerides (TGs) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in External Elastic Membrane (EEM) Volume at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Apolipoprotein B (Apo B) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Lumen Volume at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36
NCT02984982 (24) [back to overview]Number of Participants With Cardiovascular (CV) Adverse Events
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Total Cholesterol at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Normalized Total Atheroma Volume (TAV) at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Non-High-density Lipoprotein Cholesterol at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Lipoprotein (a) at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in High-density Lipoprotein Cholesterol at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Fasting Triglycerides at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in External Elastic Membrane Volume at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Apolipoprotein B at Week 36
NCT02984982 (24) [back to overview]Percent Change From Baseline in Apolipoprotein A-1 at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Total Cholesterol (TC) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Percent Atheroma Volume (PAV) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Non-High-density Lipoprotein Cholesterol (Non-HDL-C) at Week 36
NCT02984982 (24) [back to overview]Absolute Change From Baseline in Normalized Total Atheroma Volume at Week 36
NCT03051100 (5) [back to overview]Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP) at Week 6
NCT03051100 (5) [back to overview]Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) at Week 6
NCT03051100 (5) [back to overview]Percent Change From Baseline in Lipid Profile Parameters at Week 6
NCT03051100 (5) [back to overview]Number of Participants With LDL-C <70 mg/dL at Week 6
NCT03051100 (5) [back to overview]Number of Participants With LDL-C Reduction ≥50% From Baseline at Week 6
NCT03228017 (4) [back to overview]Fold Change in Composite Endothelial Inflammation
NCT03228017 (4) [back to overview]Mean Fold Change in Brachial Vein Endothelial Inflammatory Transcript
NCT03228017 (4) [back to overview]Fold Change Change in Composite Endothelial Inflammation
NCT03228017 (4) [back to overview]Change in Levels of Circulating Thromboxane B2
NCT03311841 (18) [back to overview]Effect of Rifampin on t1/2 Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on Tmax Post-dose Period 2
NCT03311841 (18) [back to overview]Apparent Volume of Distribution During the Terminal Phase (Vz/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]Area Under the Plasma Concentration-time Curve From Time 0 to Infinity (AUC0-inf) Post-dose Period 1
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]Effect of Rifampin on AUC0-24 Post-dose Period 2
NCT03311841 (18) [back to overview]Effect of Rifampin on Vz/F Post-dose Period 2
NCT03311841 (18) [back to overview]Maximum Plasma Concentration (Cmax) Post-dose Period 1
NCT03311841 (18) [back to overview]Time to Maximum Plasma Concentration (Tmax) Post-dose Period 1
NCT03311841 (18) [back to overview]Effect of Rifampin on AUC0-inf Post-dose Period 2
NCT03311841 (18) [back to overview]Plasma Concentration at 24 Hours (C24) Post-dose Period 1
NCT03311841 (18) [back to overview]Effect of Rifampin on AUC0-last Post-dose Period 2
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]Effect of Rifampin on C24 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 Cmax Post-dose Period 2
NCT03415178 (21) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 4: Parallel-Arm Period
NCT03415178 (21) [back to overview]Area Under the Curve-During the Dosing Interval Tau (AUC [0-tau]) : Parallel-Arm Period
NCT03415178 (21) [back to overview]Area Under the Curve-During the Dosing Interval Tau (AUC [0-tau]) : Single-Arm Period
NCT03415178 (21) [back to overview]Free Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Parallel-Arm Period
NCT03415178 (21) [back to overview]Free Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Single-Arm Period
NCT03415178 (21) [back to overview]Injection Experience Questionnaire at Initial Supervised Injection: Overall Ease of Use Scores: Parallel-Arm Period
NCT03415178 (21) [back to overview]Injection-Treatment Acceptance Questionnaire (I-TAQ©) After Last Injection (at Week 12) - Overall Acceptance Scores: Single-Arm Period
NCT03415178 (21) [back to overview]Maximum Serum Alirocumab Concentration Observed - Cmax : Parallel-Arm Period
NCT03415178 (21) [back to overview]Maximum Serum Alirocumab Concentration Observed - Cmax : Single-Arm Period
NCT03415178 (21) [back to overview]Number of Participants With Treatment-Emergent Anti-Alirocumab Antibodies (ADA) Positive Response: Parallel-Arm Period
NCT03415178 (21) [back to overview]Percentage of SYDNEY-Associated Product Technical Complaints (PTCs) (Overall) at the Unsupervised Injections: Single-Arm Period
NCT03415178 (21) [back to overview]Time to Reach Maximum Observed Plasma Concentration (Tmax) of Alirocumab : Parallel-Arm Period
NCT03415178 (21) [back to overview]Time to Reach Maximum Observed Plasma Concentration (Tmax) of Alirocumab: Single-Arm Period
NCT03415178 (21) [back to overview]Total Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Parallel-Arm Period
NCT03415178 (21) [back to overview]Total Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Single-Arm Period
NCT03415178 (21) [back to overview]Percentage of Participants With SYDNEY-Associated Product Technical Complaint (PTCs) (Overall and by Type) at the Unsupervised Injections : Single-Arm Period
NCT03415178 (21) [back to overview]Percentage of Participants With a SYDNEY or Current Auto-Injector (AI)-Associated Product Technical Complaint (PTCs) (Overall and by Type) at the Supervised Injections on Week 0 (Day 1): Parallel-Arm Period
NCT03415178 (21) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 8, 12, 16: Single-Arm Period
NCT03415178 (21) [back to overview]Patient Perspective Questionnaire After the Last Injection (at Week 12): Single-Arm Period
NCT03415178 (21) [back to overview]Percentage of SYDNEY-Associated Product Technical Complaints (PTCs) (by Type) at the Unsupervised Injections: Single-Arm Period
NCT03415178 (21) [back to overview]Number of Participants With Treatment-Emergent Anti-Alirocumab Antibodies (ADA) Positive Response According to ADA Status During Parallel-Arm Period: Single Arm Period
NCT03510715 (13) [back to overview]Number of Participants With Tanner Staging at Baseline, Weeks 12, 24 and 48
NCT03510715 (13) [back to overview]Percent Change From Baseline in Apolipoprotein (Apo) B at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Total Cholesterol (Total-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Weeks 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Week 12: On-treatment Analysis
NCT03510715 (13) [back to overview]Percentage of Participants Reporting >=15 Percent (%) Reduction in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Absolute Change From Baseline in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Fasting Triglycerides (TG) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Lipoprotein a (Lp) (a) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Weeks 12, 24 and 48 - ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12: Intent-to-Treat (ITT) Analysis
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 130 mg/dL (3.37 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]Number of Participants With Tanner Staging at Baseline and Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein A1 at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Lipoprotein (a) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 24: Intent-to-treat (ITT) Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Weeks 12, and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level <130 mg/dL (3.37 mmol/L) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level Lower Than (<) 130 mg/dL (3.37 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: On-treatment Estimand
NCT03510884 (44) [back to overview]Change From Baseline in Cogstate Battery Test - Overall Composite Score at Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein A1 at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Achieved at Least 30% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved at Least 30 Percent (%) Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 110 mg/dL (2.84 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: ITT Estimand
NCT03611010 (9) [back to overview]Efficacy, Number of Participants With Day 15 HDL-C More Than or Equal to 75% Baseline HDL-C
NCT03611010 (9) [back to overview]Change in Baseline LDL-C Concentration
NCT03611010 (9) [back to overview]AUC Inf
NCT03611010 (9) [back to overview]t 1/2
NCT03611010 (9) [back to overview]VDss
NCT03611010 (9) [back to overview]Efficacy, Number of Participants With Day 15 LDL-C Less Than or Equal to 125% of Baseline LDL-C
NCT03611010 (9) [back to overview]AUC 0-24
NCT03611010 (9) [back to overview]Cmax IV
NCT03611010 (9) [back to overview]Tmax IV
NCT03768427 (3) [back to overview]Number of Participants Who Discontinued From Study Treatment
NCT03768427 (3) [back to overview]Percent Change From Baseline in LDL-C at Week 12
NCT03768427 (3) [back to overview]Percentage of Participants With An Adverse Event (AE)
NCT03830164 (3) [back to overview]Change in International Index of Erectile Function (IIEF) Scores
NCT03830164 (3) [back to overview]Number of Participants With Incidence of Adverse Events (AEs)
NCT03830164 (3) [back to overview]Choosing Other Erectile Dysfunction (ED) Treatments After Pentoxifylline, Atorvastatin and Vitamin E (PAVE)
NCT04608344 (8) [back to overview]PK Parameter: AUCinf of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]PK Parameter: Cmax of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]PK Parameter: Cmax of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]Percentage of Participants Experiencing Treatment Emergent Adverse Events (TEAEs)
NCT04608344 (8) [back to overview]Percentage of Participants With Severity Grade 3 or Above Treatment-Emergent Laboratory Abnormalities
NCT04608344 (8) [back to overview]Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS
NCT04608344 (8) [back to overview]PK Parameter: AUCinf of ATV, PRA, and ROS

Change in Mean-Max Bifurcation CIMT

For each side and wall of the bifurcation arterial segment, the maximum CIMT over the 4 angles of interrogation was selected to produce 4 summary variables (right bifurcation near wall max, right bifurcation far wall max, left bifurcation near wall max and left bifurcation far wall max). These summary variables were then averaged to estimate a single mean-max bifurcation CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0033
2 Placebo0.0072

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Change in Triglycerides

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmg/dl (Mean)
1 Atorvastatin-11.04
2 Placebo-5.62

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Change in Total Cholesterol

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmg/dl (Mean)
1 Atorvastatin-30.30
2 Placebo-0.72

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Change in Natural Log of mg/L for hsCRP

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionnatural log of mg/L (Mean)
1 Atorvastatin-0.13
2 Placebo0.27

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Change in Mean-Mean Near Wall CIMT

For the near wall measurements for each side and segment, mean CIMT values were averaged over the 4 angles of interrogation to produce 6 summary variables (right common near wall mean, right bifurcation near wall mean, right internal near wall mean, left common near wall mean, left bifurcation wall mean and left internal far wall mean). These 6 summary variables were then averaged to estimate a single mean-mean far wall CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0022
2 Placebo0.0028

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Change in Mean-Mean Internal CIMT

For the internal carotid arterial segment, mean CIMT values were averaged across angles by side and wall to produce 4 summary variables (right internal near wall mean, right internal far wall mean, left internal near wall mean and left internal far wall mean). These summary variables were then averaged to estimate a single mean-mean internal CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0067
2 Placebo0.0082

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Change in Mean-Mean Far Wall CIMT

For the far wall measurements for each side and segment, mean CIMT values were averaged over the 4 angles of interrogation to produce 6 summary variables (right common far wall mean, right bifurcation far wall mean, right internal far wall mean, left common far wall mean, left bifurcation far wall mean and left internal far wall mean). These 6 summary variables were then averaged to estimate a single mean-mean far wall CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0042
2 Placebo0.0064

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Change in Mean-Max Common CIMT

For each side and wall of the common carotid arterial segment, the maximum CIMT over the 4 angles of interrogation was selected to produce 4 summary variables (right common near wall max, right common far wall max, left common near wall max and left common far wall max). These summary variables were then averaged to estimate a single mean-max common CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0006
2 Placebo0.0008

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Change in Mean-Max Far Wall CIMT

For the far wall measurements for each side and segment, the maximum CIMT over the 4 angles of interrogation was selected to produce 6 summary variables (right common far wall max, right bifurcation far wall max, right internal far wall max, left common far wall max, left bifurcation far wall max, and left internal far wall max). These 6 summary variables were then averaged to estimate a single mean-max far wall CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0045
2 Placebo0.0082

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Change in Mean-Max Internal CIMT

For each side and wall of the internal carotid arterial segment, the maximum CIMT over the 4 angles of interrogation was selected to produce 4 summary variables (right internal near wall max, right internal far wall max, left internal near wall max and left internal far wall max). These summary variables were then averaged to estimate a single mean-max internal CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0090
2 Placebo0.0144

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Change in Mean-Max Near Wall CIMT

For the near wall measurements for each side and segment, the maximum CIMT over the 4 angles of interrogation was selected to produce 6 summary variables (right common near wall max, right bifurcation near wall max, right internal near wall max, left common near wall max, left bifurcation near wall max, and left internal near wall max). These 6 summary variables were then averaged to estimate a single mean-max near wall CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0024
2 Placebo0.0038

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Change in Mean-Max CIMT

For each side, segment and wall, the maximum CIMT over the 4 angles of interrogation was selected to produce 12 summary variables (right common near wall max, right common far wall max, right bifurcation near wall max, right bifurcation far wall max, right internal near wall max, right internal far wall max, left common near wall max, left common far wall max, left bifurcation near wall max, left bifurcation far wall max, left internal near wall max and left internal far wall max). These 12 summary variables were then averaged to estimate a single mean-max CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0037
2 Placebo0.0064

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Change in Lipoprotein A

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmg/dl (Mean)
1 Atorvastatin2.00
2 Placebo6.34

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Change in LDL Cholesterol

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmg/dl (Mean)
1 Atorvastatin-27.63
2 Placebo-1.48

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Change in Homocysteine

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionμmoles/liter (Mean)
1 Atorvastatin1.84
2 Placebo1.76

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Change in HDL Cholesterol

(NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmg/dl (Mean)
1 Atorvastatin-0.43
2 Placebo0.89

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Change in Mean-Mean Common Carotid IMT (CIMT)

For the common carotid arterial segment, mean CIMT values were averaged across angles by side and wall to produce 4 summary variables (right common near wall mean, right common far wall mean, left common near wall mean and left common far wall mean). These summary variables were then averaged to estimate a single mean-mean common CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0010
2 Placebo0.0024

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Change in Mean-Mean Bifurcation CIMT

For the bifurcation arterial segment, mean CIMT values were averaged across angles by side and wall to produce 4 summary variables (right bifurcation near wall mean, right bifurcation far wall mean, left bifurcation near wall mean and left bifurcation far wall mean). These summary variables were then averaged to estimate a single mean-mean bifurcation CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0030
2 Placebo0.0055

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Change in Mean-Mean CIMT

For each side, segment and wall, mean CIMT values were averaged over the 4 angles of interrogation to produce 12 summary variables (right common near wall mean, right common far wall mean, right bifurcation near wall mean, right bifurcation far wall mean, right internal near wall mean, right internal far wall mean, left common near wall mean, left common far wall mean, left bifurcation near wall mean, left bifurcation far wall mean, left internal near wall mean and left internal far wall mean). These 12 summary variables were then averaged to estimate a single mean-mean CIMT for each participant visit. (NCT00065806)
Timeframe: Change from baseline to 36 months

Interventionmm (Mean)
1 Atorvastatin0.0033
2 Placebo0.0049

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The Occurrence of ≥ 3 New T2 Lesions With or Without Gd+ Enhancement or Clinical Exacerbation Through 12 Months.

"The occurrence of ≥ T2 lesions[1] with or without gadolinium lesion (Gd+) enhancement[2] or clinical exacerbation[3] through 12 months. A higher score indicates more severe disease~A new T2 lesion is an abnormal, hyperintense white-matter area visible on T2 weighted images that were not present on the baseline scan~A Gd+ enhancement is defined as a contrast enhancement visible on a new T2 lesion~A clinical exacerbation is a new neurological symptom that lasts more than 48 hours in a participant who has been neurologically stable for 30 days following start of study medication" (NCT00094172)
Timeframe: 12 months post-randomization

InterventionParticipants (Number)
Atorvastatin26
Placebo18

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Proportion of Participants Who Are Diagnosed With Multiple Sclerosis According to the McDonald Criteria

"Number of participants diagnosed with Multiple Sclerosis (MS) according to the McDonald criteria[1]~The McDonald criteria uses dissemination in time and space[2] established by Magnetic Resonance Image (MRI) findings to provide a clinical diagnosis for MS~Dissemination in time is established by a new T2 or gadolinium-enhancing (Gd+) lesion found on a repeat MRI. The presence of any 3 of the following establishes dissemination in space: 1 Gd+ lesion or 9 T2 bright lesions if there is no enhancement; ≥1 infratentorial lesion; ≥1 juxtacortical lesion; ≥3 periventricular lesions" (NCT00094172)
Timeframe: 12 months post-randomization

InterventionParticipants (Number)
Atorvastatin29
Placebo24

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Proportion of Participants Diagnosed With Multiple Sclerosis According to the McDonald Criteria

"Number of participants diagnosed with Multiple Sclerosis (MS) according to the McDonald criteria[1]~The McDonald criteria uses dissemination in time and space[2] established by Magnetic Resonance Image (MRI) findings to provide a clinical diagnosis for MS~Dissemination in time is established by a new T2 or gadolinium-enhancing (Gd+) lesion found on a repeat MRI. The presence of any 3 of the following establishes dissemination in space: 1 Gd+ lesion or 9 T2 bright lesions if there is no enhancement; ≥1 infratentorial lesion; ≥1 juxtacortical lesion; ≥3 periventricular lesions" (NCT00094172)
Timeframe: 18 months post-randomization

InterventionParticipants (Number)
Atorvastatin37
Placebo24

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

The primary endpoint is Changes in plaque architecture and composition directly measured by magnetic resonance imaging (MRI) in the aorta and carotid arteries. (NCT00127218)
Timeframe: 18 months

Interventionpercentage of internal carotid artery (Mean)
Niacin Plus Statin7
Placebo Plus Statin5

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

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

InterventionParticipants (Count of Participants)
Any Statin Plus Niacin6
Any Statin Plus Placebo2

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Lower Extremity Skeletal Muscle Glucose Uptake

Net calf skeletal muscle glucose uptake determined by Patlak modeling. (NCT00153166)
Timeframe: 60 minutes

Interventionumol/kg/min (Mean)
Healthy Controls62.9
Patients With PAD48.6
PAD (Excluding Diabetes)49.5

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'M' = Whole Body Insulin Sensitivity

"A hyperinsulinemic-euglycemic clamp was performed prior to and during FDG-PET imaging to measure insulin sensitivity and to standardize metabolic conditions. Subjects were required to fast for 8 hours prior to the study. Patients were given a primed insulin infusion of 2 mU/kg/min. Serum glucose measurements were made at five-minute intervals from an arterialized venous sample achieved by placing the hand in a warming box at 50°C. Blood glucose levels are checked every 5 minutes and 20% dextrose infusion is adjusted to maintain a serum glucose level of approximately 80 mg/dL. Subjects were considered to have achieved steady state when the dextrose infusion rate required to maintain a serum glucose level of 80 mg/dL varied by no greater than 5%. To compute the steady-state glucose disposal rate, we averaged the glucose infusion rates over the last 20 minutes of the clamp and applied a space correction to account for small changes in serum glucose levels over that time period." (NCT00153166)
Timeframe: every 5 minutes for 20 minutes

Interventionmg/kg/min (Median)
Healthy Controls5.0
Patients With PAD3.4
PAD (Excluding Diabetes)3.4

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Change in Plasma Thiobarbituric Acid Reactive Substance (TBARS) Levels

Oxidative stress was assessed with plasma thiobarbituric acid reactive substance (TBARS) levels (an index of lipid peroxidation).Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.We hypothesized that equipotent doses of these two statins will have divergent effects on markers of oxidative stress and endothelial function. (NCT00166036)
Timeframe: Baseline &12 Weeks

Interventionnmol/mL (Mean)
Atorvastatin 10 mg2.1
Pravastatin 80 mg2.5

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Change in Flow-mediated Dilatation (FMD)

Flow-mediated dilatation (FMD) of the brachial artery was used to asses Endothelial Function. The endothelium, by releasing nitric oxide (NO), promotes vasodilation and inhibits inflammation, thrombosis, and vascular smooth muscle cell proliferation.We hypothesized that equipotent doses of these two statins will have divergent effects on markers of oxidative stress and endothelial function. (NCT00166036)
Timeframe: Baseline & 12 Weeks

InterventionPercentage of brachial artery diameter (Mean)
Atorvastatin 10 mg5.9
Pravastatin 80 mg6.0

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LDL-C Lowering Efficacy

LDL-C = low density lipoprotein cholesterol, measured in mg/dl. (NCT00166504)
Timeframe: 6 weeks

InterventionPercent Change from Baseline (Least Squares Mean)
Vytorin-51
Atorvastatin-41

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Correlation of Tumor Apoptosis to Clinical Response

The validity of tumor apoptosis as a biologic endpoint was assessed by correlation to clinical response. A correlation substantially less than 1 is interpreted as a poor correlation, while a correlation near +1 or -1 is interpreted as a strong correlation. (NCT00185731)
Timeframe: 1 year

InterventionPearson Correlation Coefficient (Number)
80 mg-0.26

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Atorvastatin Toxicity

Assessed as the number of study participants with atorvastatin-related serious adverse events (SAEs). (NCT00185731)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
80 mg Atorvastatin4

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Tumor Apoptosis

Expressed as the number of participants whose tumor cells showed an increase in apoptosis during atorvastatin treatment (NCT00185731)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Atorvastatin7

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High-sensitivity C-reactive Protein (hsCRP) as a Cardiac Biomarker

(NCT00233480)
Timeframe: Baseline, Three months

,
Interventionmg/L (Mean)
BaselineThree months
Active Treatment1.61.9
Placebo1.93.4

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Cardiac Biomarker Level BNP

B-type natriuretic peptide, measured pg/mL at baseline and post-treatment (NCT00233480)
Timeframe: Baseline, 3 months

,
Interventionpg/mL (Mean)
BaselineThree Months
Active Treatment175107
Placebo6667

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Cardiac Troponin I (cTnI)

Participants with cTnI ≥0.04 ng/mL (NCT00233480)
Timeframe: Baseline, Three months

,
Interventionpercent of participants (Number)
BaselineThree Months
Active Treatment80
Placebo2115

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Left Ventricular End-diastolic Dimension (LVEDD)

The end-diastolic dimension of the left ventricle (in mm) was measured with 2D echocardiography performed by experienced technicians using Acuson Sequoia Echocardiography System (NCT00233480)
Timeframe: Baseline and three months

,
InterventionMillimeters (mm) (Mean)
Baseline LVEDDThree months LVEDD
Active Treatment6525
Placebo2824

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LVEF (Left Ventricular Ejection Fraction)

Left ventricular ejection fraction was assessed by transthoracic echocardiography according to Simpson's rule (biplane method of disks). (NCT00233480)
Timeframe: baseline and three months

,
Interventionpercent ejection fraction (Mean)
Baseline LVEF3 month LVEF
Active Treatment2425
Placebo2824

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Muscle Sympathetic Nerve Activity (by Sympathetic Microneurography)

(NCT00233480)
Timeframe: Baseline and three months

,
Interventionbursts per minute (Mean)
BaselineThree months
Active Treatment4336
Placebo3938

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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 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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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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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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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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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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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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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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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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Comparison of Derivatives of Reactive Oxygen Metabolites Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
InterventionCarr (Median)
Baseline1 month (30 day follow-up)
Atorvastatin382345
Placebo384400

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Comparison of Interleukin-1 Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
Interventionng/mL (Median)
Baseline1 month (30 day follow-up)
Atorvastatin0.300.28
Placebo0.290.25

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Comparison of High Sensitivity C-reactive Protein

(NCT00252967)
Timeframe: Baseline and 30 days

,
Interventionmg/L (Median)
Baseline1 month (30 day follow-up)
Atorvastatin6.32.3
Placebo9.612.3

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Comparison of Interleukin-6 Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
Interventionng/mL (Median)
Baseline1 month (30 day follow-up)
Atorvastatin4.02.2
Placebo5.35.6

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Comparison of Isoprostanes Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
Interventionpg/mL (Median)
Baseline1 month (30 day follow-up)
Atorvastatin10621240
Placebo12591146

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Comparison of Redox Potential for Cysteine Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
InterventionmV (Median)
Baseline1 month (30 day follow-up)
Atorvastatin-65.3-62.6
Placebo-61.2-64.5

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Comparison of Redox Potential for Glutathione Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
InterventionmV (Median)
Baseline1 month (30 day follow-up)
Atorvastatin-125.3-129.0
Placebo-116.7-124.3

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Comparison of Tumor Necrosis Factor Alpha Values

(NCT00252967)
Timeframe: Baseline and 30 days

,
Interventionng/mL (Median)
Baseline1 month (30 day follow-up)
Atorvastatin1.81.5
Placebo2.02.6

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Time of Atrial Fibrillation Recurrence

(NCT00252967)
Timeframe: Upon recurrence, up to 12 months

Interventiondays (Median)
Placebo22
Atorvastatin29

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Percent Change From Baseline in Total-Cholesterol:High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-20.6
Atorvastatin-7.5

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (HDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-27.2
Atorvastatin-9.9

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Percent Change From Baseline in Total-Cholesterol at Week 6

([6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

Interventionpercent (Least Squares Mean)
Atorvastatin + Ezetimibe-19.7
Atorvastatin-7.4

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Number of Participants Who Attained Target LDL-C <100 mg/dL at Week 6

(NCT00276458)
Timeframe: 6 weeks

,
InterventionParticipants (Number)
<100 mg/dL≥100 mg/dL
Atorvastatin4547
Atorvastatin + Ezetimibe7715

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Percent Change in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-26.7
Atorvastatin-10.2

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Percent Change in C-Reactive Protein (CRP) at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-19.2
Atorvastatin-9.1

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Percent Change in Apolipoprotein A-I at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-1.9
Atorvastatin-1.2

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Percent Change From Baseline in Triglycerides (TG) at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-17.8
Atorvastatin-5.5

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Percent Change From Baseline in Apolipoprotein B at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-21.4
Atorvastatin-7.7

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Percent Change From Baseline in Apolipoprotein B: Apolipoprotein A-I Ratio at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-19.0
Atorvastatin-5.8

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Percent Change in High Density Lipoprotein -Cholesterol (HDL-C)at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe3.2
Atorvastatin0.8

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Percent Change From Baseline in C-Reactive Protein (CRP) at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

Interventionpercent (Least Squares Mean)
Atorvastatin + Ezetimibe-6.7
Atorvastatin-9.2

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 Weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-31.9
Atorvastatin-11.0

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Percent Change From Baseline in Low Density Lipoprotein-Cholesterol (LDL-C) at Week 6

[(6 week value - baseline value)/baseline value]*100%. (NCT00276458)
Timeframe: 6 weeks

InterventionPercent (Least Squares Mean)
Atorvastatin + Ezetimibe-30.8
Atorvastatin-10.9

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Percent Change From Baseline to Week 6 in Low-Density Lipoprotein-Cholesterol:High-Density Lipoprotein-Cholesterol (LDL-C:HDL-C) Ratio

Percent Change in LDL-C:HDL-C Ratio = [(week 6 ratio - baseline ratio)/baseline ratio]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent change (Least Squares Mean)
Atorvastatin + Ezetemibe-26.4
Atorvastatin-9.9

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Percent Change From Baseline to Week 6 in Low-Density Lipoprotein (LDL)-C

Percent Change in LDL-C = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-27.4
Atorvastatin-11.0

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Percent Change From Baseline to Week 6 in High-Density Lipoprotein Cholesterol (HDL-C)

Percent Change in HDL-C = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-0.5
Atorvastatin-1.0

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Percent Change From Baseline to Week 6 in C Reactive Protein (CRP)

Percent Change in CRP = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-18.3
Atorvastatin-11.5

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Percent Change From Baseline to Week 6 in Apolipoprotein B (Apo B)

Percent Change in Apo B = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-17.8
Atorvastatin-7.7

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Percent Change From Baseline to Week 6 in Apolipoprotein A-I (Apo A-I)

Percent Change in Apo A-I = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-0.3
Atorvastatin-1.2

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Percent Change From Baseline to Week 6 in Apolipoprotein B:Apolipoprotein A-I (Apo B:Apo A-I) Ratio

Percent Change in Apo B:Apo A-I Ratio = [(week 6 ratio - baseline ratio)/baseline ratio]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-16.9
Atorvastatin-5.9

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Number of Patients Who Attained Target Low-Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 6

(NCT00276484)
Timeframe: 6 Weeks

,
InterventionParticipants (Number)
<70 mg/dL>=70 mg/dL
Atorvastatin88191
Atorvastatin + Ezetemibe20473

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Percent Change From Baseline to Week 6 in Triglycerides (TG)

Percent Change in TG = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-12.3
Atorvastatin-5.9

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Percent Change From Baseline to Week 6 in Total-Cholesterol (TC):High-Density Lipoprotein Cholesterol (HDL-C) Ratio

Percent Change in TC:HDL-C Ratio = [(week 6 ratio - baseline ratio)/baseline ratio]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-16.0
Atorvastatin-5.6

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Percent Change From Baseline to Week 6 in Total-Cholesterol

Percent Change in Total-C = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-16.9
Atorvastatin-6.9

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Percent Change From Baseline to Week 6 in Non-High-Density Lipoprotein-Cholesterol:High-Density Lipoprotein-Cholesterol (Non-HDL-C:HDL-C) Ratio

Percent Change in non-HDL-C:HDL-C Ratio = [(week 6 ratio - baseline ratio)/baseline ratio]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-22.2
Atorvastatin-7.6

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Percent Change From Baseline to Week 6 in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C)

Percent Change in Non-HDL-C = [(week 6 value - baseline value)/baseline value]*100% (NCT00276484)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorvastatin + Ezetemibe-23.3
Atorvastatin-9.0

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The Steroid Sparing Period

The duration of steroid sparing was defined as the date when the target dose of prednisone was reached until the date at which the dose was increased and/or met the relapse (flare) criteria; or until the 12 month study phase ended if no prednisone dose increase was required. The steroid sparing period was measured in units of days. The prednisone target dose was defined as a 90% reduction of the baseline dose or an absolute prednisone dose of 4 mg/day or less. (NCT00279708)
Timeframe: 1 year

Interventiondays (Mean)
Intervention Group (Atorvastatin)301
Control Group (Placebo)257

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Percentage Change From Baseline in TC/HDL-C Ratio

Blood samples taken at baseline and after 12 weeks of treatment to determine the TC and HDL-C levels. The TC/HDL-C ratio was then calculated for baseline and Week 12 and the change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg-41.0
MK-0524B 2g/40mg-42.3
Atorvastatin 10 mg-28.2
Atorvastatin 20 mg-31.5
Atorvastatin 40 mg-36.0
Atorvastatin 80 mg-36.7

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Percentage Change From Baseline in Apolipoprotein (Apo) B

Blood samples taken at baseline and after 12 weeks of treatment to determine the Apo B levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg-36.1
MK-0524B 2g/40mg-38.0
Atorvastatin 10 mg-26.9
Atorvastatin 20 mg-32.8
Atorvastatin 40 mg-37.2
Atorvastatin 80 mg-38.3

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Percentage Change From Baseline in C-reactive Protein (CRP)

Blood samples taken at baseline and after 12 weeks of treatment to determine the CRP levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Median)
MK-0524B 2g/20 mg-15.4
MK-0524B 2g/40mg-20.0
Atorvastatin 10 mg-19.5
Atorvastatin 20 mg-28.6
Atorvastatin 40 mg-33.3
Atorvastatin 80 mg-38.1

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Percentage Change From Baseline in HDL-C

Blood samples taken at baseline and after 12 weeks of treatment to determine the HDL-C levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg26.9
MK-0524B 2g/40mg26.6
Atorvastatin 10 mg7.0
Atorvastatin 20 mg5.3
Atorvastatin 40 mg4.5
Atorvastatin 80 mg3.6

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Percentage Change From Baseline in Apo A-I

Blood samples taken at baseline and after 12 weeks of treatment to determine the Apo A-I levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg10.7
MK-0524B 2g/40mg8.2
Atorvastatin 10 mg1.7
Atorvastatin 20 mg0.4
Atorvastatin 40 mg-0.8
Atorvastatin 80 mg-2.5

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Percentage Change From Baseline in LDL-C

Blood samples taken at baseline and after 12 weeks of treatment to determine the LDL-C levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg-40.4
MK-0524B 2g/40mg-42.8
Atorvastatin 10 mg-33.6
Atorvastatin 20 mg-39.8
Atorvastatin 40 mg-45.6
Atorvastatin 80 mg-47.5

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

Blood samples taken at baseline and after 12 weeks of treatment to determine the Lp(a) levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Median)
MK-0524B 2g/20 mg-15.2
MK-0524B 2g/40mg-14.6
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Atorvastatin 40 mg7.8
Atorvastatin 80 mg8.8

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Percentage Change From Baseline in Non-HDL-C

Blood samples taken at baseline and after 12 weeks of treatment to determine the non-HDL-C levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg-40.4
MK-0524B 2g/40mg-42.2
Atorvastatin 10 mg-31.3
Atorvastatin 20 mg-36.8
Atorvastatin 40 mg-42.6
Atorvastatin 80 mg-44.6

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Percentage Change From Baseline in the LDL-C/HDL-C Ratio

Blood samples taken at baseline and after 12 weeks of treatment to determine the LDL-C and HDL-C levels. The LDL-C/HDL-C ratio was then calculated for baseline and Week 12 and the change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage Change (Least Squares Mean)
MK-0524B 2g/20 mg-50.9
MK-0524B 2g/40mg-53.0
Atorvastatin 10 mg-37.6
Atorvastatin 20 mg-42.4
Atorvastatin 40 mg-47.9
Atorvastatin 80 mg-48.8

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Percentage Change From Baseline in Total Cholesterol (TC)

Blood samples taken at baseline and after 12 weeks of treatment to determine the TC levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Least Squares Mean)
MK-0524B 2g/20 mg-28.1
MK-0524B 2g/40mg-30.0
Atorvastatin 10 mg-24.6
Atorvastatin 20 mg-29.4
Atorvastatin 40 mg-34.2
Atorvastatin 80 mg-36.1

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Percentage Change From Baseline in Triglycerides (TG)

Blood samples taken at baseline and after 12 weeks of treatment to determine the TG levels. The change from baseline at Week 12 was recorded. (NCT00289900)
Timeframe: Baseline and Week 12

InterventionPercentage change (Median)
MK-0524B 2g/20 mg-40.3
MK-0524B 2g/40mg-42.0
Atorvastatin 10 mg-21.9
Atorvastatin 20 mg-23.8
Atorvastatin 40 mg-30.4
Atorvastatin 80 mg-33.8

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Percentage of Participants Who Experience at Least 1 Clinical Adverse Event (AE)

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the product, was also an AE. A clinical AE was an AE reported as a result of a clinical examination or reported by the participant. (NCT00289900)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)59.6
Atorvastatin 10, 20, 40, or 80 mg (Pooled)45.9

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Percentage of Participants Who Experience at Least 1 Laboratory Adverse Event (AE)

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the product, was also an AE. A laboratory AE was an AE reported as a result of a laboratory assessment or test. (NCT00289900)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)5.2
Atorvastatin 10, 20, 40, or 80 mg (Pooled)5.9

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Percentage of Participants With New Diagnosis of Impaired Fasting Blood Glucose

Participants had blood glucose levels assessed throughout the 12 week treatment period. Participants who had the new diagnosis of impaired fasting blood glucose were recorded. A pre-defined set of MedDRA terms was used to identify participants whose glycemic status became 'impaired' during the course of treatment (from clinical adverse experience reports). The MedDRA terms were as follows: blood glucose increased, blood glucose abnormal, glucose tolerance decreased, glucose tolerance test abnormal, carbohydrate tolerance decreased, glucose tolerance impaired, hyperglycaemia, impaired fasting glucose, impaired insulin secretion, metabolic syndrome, insulin resistance, insulin resistance syndrome. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.2
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.1

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Percentage of Participants With New Diagnosis of Diabetes

Participants had blood glucose levels assessed throughout the 12 week treatment period. Participants who with newly diagnosed of diabetes were recorded. A participant was classified as having new onset diabetes if they experienced an adverse Event (AE) related to a diagnosis of diabetes (based on a pre-defined set of Medical Dictionary for Regulatory Activities [MedDRA] terms), or if they started taking an anti-diabetic medication during the course of the study. The MedDRA terms were as follows: diabetes mellitus, diabetes mellitus insulin-dependent, diabetes mellitus non-insulin dependent, insulin-requiring type II diabetes mellitus, insulin resistant diabetes, diabetes with hyperosmolarity, latent autoimmune diabetes in adults. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.9
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.2

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Percentage of Participants With Elevations in ALT and/or AST of >=5 x ULN

Participants had AST and ALT levels assessed throughout the 12 week treatment period. Participants who had an assessment of either AST or ALT that was 5 x ULN or greater were recorded. The AST UNLs for males and females were 43 U/L and 36 U/L, respectively. The ALT UNLs for males and females were 40 U/L and 33 U/L, respectively. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg and MK-0524B 2g/40mg (Pooled)0.1
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.9

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Percentage of Participants With Elevations in ALT and/or AST of >=10 x ULN

Participants had AST and ALT levels assessed throughout the 12 week treatment period. Participants who had an assessment of either AST or ALT that was 10 x ULN or greater were recorded. The AST UNLs for males and females were 43 U/L and 36 U/L, respectively. The ALT UNLs for males and females were 40 U/L and 33 U/L, respectively. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.0
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.1

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Percentage of Participants With Creatine Kinase (CK) >=10 x ULN

Participants had CK assessed throughout the 12 week treatment period. Participants who had any CK level that was >=10 x ULN were recorded. The UNLs for males and females were 207 U/L and 169 U/L, respectively. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.1
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.1

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Percentage of Participants With Consecutive Elevations in Alanine Aminotransferase (ALT) and/or Aspartate Aminotransferase (AST) of >=3 x Upper Limit of Normal (ULN)

Participants had AST and ALT levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of either AST or ALT that were 3 x ULN or greater were recorded. The AST UNLs for males and females were 43 U/L and 36 U/L, respectively. The ALT UNLs for males and females were 40 U/L and 33 U/L, respectively. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg and MK-0524B 2g/40mg (Pooled)0.4
Atorvastatin 10, 20, 40, or 80 mg (Pooled)1.8

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Percentage of Participants With CK >=10 x ULN With Muscle Symptoms

Participants had CK assessed throughout the 24 week treatment period. Participants who had any CK level that was >=10 x ULN and had associated muscle symptoms present within +/- 7 days were recorded. The UNLs for males and females were 207 U/L and 169 U/L, respectively. (NCT00289900)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.1
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.0

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Percentage of Participants With a Confirmed Adjudicated Cardiovascular Event

Select serious adverse cardiovascular events and all-cause mortality that occurred during the treatment phase of the study were adjudicated by an expert committee external to the sponsor. Those events confirmed by the committee a cardiovascular events were recorded. (NCT00289900)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.1
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.2

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Percentage of Participants Who Were Discontinued From the Study Due to a Laboratory AE

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the product, was also an AE. A laboratory AE was an AE reported as a result of a laboratory assessment or test. Participants who were discontinued from the study due to a laboratory AE were recorded. (NCT00289900)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)0.7
Atorvastatin 10, 20, 40, or 80 mg (Pooled)0.7

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Percentage of Participants Who Were Discontinued From the Study Due to a Clinical AE

An AE was defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which was temporally associated with the use of the product, was also an AE. A clinical AE was an AE reported as a result of a clinical examination or reported by the participant. Participants who were discontinued from the study due to a clinical AE were recorded. (NCT00289900)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
MK-0524B 2g/20 mg or MK-0524B 2g/40mg (Pooled)16.5
Atorvastatin 10, 20, 40, or 80 mg (Pooled)4.9

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Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.01427
Atorvastatin0.08821
All Treatment0.00737

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Relationship Between Renal Effects and Lipid Changes: eGFR and ApoA1

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.17909
Atorvastatin0.08090
All Treatment0.12787

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Relationship Between Renal Effects and Lipid Changes: eGFR and ApoA1

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08146
Atorvastatin0.05333
All Treatment0.05845

[back to top]

Correlation Coefficient Urinary Protein/Creatinine Ratio and Total Cholesterol [TC] Indicating the Relationship Between Renal Effects and Lipid Changes

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (LOCF). (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.03507
Atorvastatin0.14258
All Treatment0.01600

[back to top]

Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 26

(NCT00296374)
Timeframe: Assessed at Baseline and Week 26

InterventionmL/min (Mean)
Rosuvastatin 10mg-2.73
Rosuvastatin 40mg-5.46
Atorvastatin 80mg-1.78

[back to top]

Change From Baseline in eGFR at Week 52 [LOCF]

(NCT00296374)
Timeframe: Assessed at Baseline and Week 52 [LOCF]

InterventionmL/min (Mean)
Rosuvastatin 10 mg-3.70
Rosuvastatin 40 mg-7.29
Atorvastatin 80 mg-1.61

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and High Density Lipoprotein Cholesterol [HDL-C]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.15614
Atorvastatin0.06987
All Treatment0.14226

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04510
Atorvastatin0.16280
All Treatment0.06739

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TC/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.05945
Atorvastatin0.12132
All Treatment-0.02666

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.13689
Atorvastatin0.12931
All Treatment-0.08108

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and LDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.02775
Atorvastatin0.06535
All Treatment-0.01569

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Low Density Lipoprotein Cholesterol [LDL-C]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.08588
Atorvastatin0.18570
All Treatment-0.02491

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Non-high Density Lipoprotein Cholesterol [nonHDL-C]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.12068
Atorvastatin0.15929
All Treatment-0.05186

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.02594
Atorvastatin0.24018
All Treatment0.07381

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.01040
Atorvastatin0.00241
All Treatment0.00189

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.06085
Atorvastatin0.12507
All Treatment-0.02841

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TG

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.05251
Atorvastatin0.11755
All Treatment0.01345

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Triglyceride [TG]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.14569
Atorvastatin0.04948
All Treatment-0.08471

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio TC

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: Assessed at 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.07019
Atorvastatin0.26855
All Treatment0.12013

[back to top]

Urinary Albumin/Creatinine Ratio at Week 26

Urinary albumin/creatinine ratio (mg/g) =urine albumin concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 26 urine albumin/creatinine ratio over baseline urine albumin/creatinine ratio. (NCT00296374)
Timeframe: Assessed at Week 26

Interventionmg/g (Geometric Mean)
Rosuvastatin 10mg0.927
Rosuvastatin 40mg0.913
Atorvastatin 80mg0.831

[back to top]

Urinary Albumin/Creatinine Ratio at Week 52 [LOCF]

Urinary albumin/creatinine ratio (mg/g) =urine albumin concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 52 [LOCF] urine albumin/creatinine ratio over baseline urine albumin/creatinine ratio. (NCT00296374)
Timeframe: Assessed at Week 52 LOCF

Interventionmg/g (Geometric Mean)
Rosuvastatin 10mg1.016
Rosuvastatin 40mg0.836
Atorvastatin 80mg0.823

[back to top]

Urinary Protein/Creatinine Ratio at Week 26.

Urinary protein/creatinine ratio (mg/g) =urine protein concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 26 urine protein/creatinine ratio over baseline urine protein/creatinine ratio. (NCT00296374)
Timeframe: Assessed at Week 26

Interventionmg/g (Geometric Mean)
Rosuvastatin 10mg1.007
Rosuvastatin 40mg0.994
Atorvastatin 80mg0.876

[back to top]

Urinary Protein/Creatinine Ratio in Patients With Type 1 or 2 Diabetes.

Urinary protein/creatinine ratio (mg/g) =urine protein concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 52 [LOCF] urine protein/creatinine ratio over baseline urine protein/creatinine ratio. (NCT00296374)
Timeframe: Assessed at Week 52, Last observation carried forward (LOCF)

Interventionmg/g (Geometric Mean)
Rosuvastatin 10mg1.016
Rosuvastatin 40mg0.955
Atorvastatin 80mg0.874

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TG

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.07271
Atorvastatin0.08654
All Treatment-0.02876

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.05397
Atorvastatin0.29486
All Treatment0.11079

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.16755
Atorvastatin0.08891
All Treatment-0.11221

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.07846
Atorvastatin0.13910
All Treatment-0.02825

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.00600
Atorvastatin0.22710
All Treatment0.03684

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Apolipoprotein A-1 [ApoA-1]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.15859
Atorvastatin0.13133
All Treatment0.15516

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and Apolipoprotein B [ApoB]

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.02276
Atorvastatin0.21405
All Treatment0.04578

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and HDL-C

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16111
Atorvastatin0.26194
All Treatment0.18918

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.19850
Atorvastatin-0.06481
All Treatment-0.17579

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.11072
Atorvastatin-0.12835
All Treatment-0.11378

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.01709
Atorvastatin-0.05610
All Treatment-0.02569

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.17729
Atorvastatin-0.19501
All Treatment-0.17911

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and TC/HDL-C Ratio

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.13572
Atorvastatin0.07339
All Treatment-0.08855

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.06356
Atorvastatin-0.04402
All Treatment-0.05499

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.26802
Atorvastatin-0.11804
All Treatment-0.24204

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TC

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.01586
Atorvastatin-0.03124
All Treatment0.00101

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TC

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.13489
Atorvastatin-0.18105
All Treatment-0.14690

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoA-1

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14207
Atorvastatin0.11171
All Treatment0.13429

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoA-1

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16085
Atorvastatin0.15933
All Treatment0.17306

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.00569
Atorvastatin0.20008
All Treatment0.04833

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.10997
Atorvastatin0.30537
All Treatment0.15652

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.05906
Atorvastatin0.13706
All Treatment-0.01775

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04760
Atorvastatin0.25636
All Treatment0.07766

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and LDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.03010
Atorvastatin-0.00944
All Treatment0.02609

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TC/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.05426
Atorvastatin-0.01643
All Treatment-0.04256

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Protein/Creatinine Ratio and ApoA-1

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16587
Atorvastatin0.18469
All Treatment0.18832

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and HDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.11373
Atorvastatin0.01123
All Treatment0.07576

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.26146
Atorvastatin0.05248
All Treatment-0.22109

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and HDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08593
Atorvastatin0.00032
All Treatment0.06930

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and HDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14758
Atorvastatin0.26805
All Treatment0.17550

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.05514
Atorvastatin0.19842
All Treatment0.00038

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.10037
Atorvastatin0.21205
All Treatment0.12270

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.08211
Atorvastatin0.16654
All Treatment-0.03001

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TG

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.24494
Atorvastatin-0.07059
All Treatment-0.15586

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and LDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.03476
Atorvastatin0.10902
All Treatment0.04508

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.06694
Atorvastatin0.17296
All Treatment-0.01144

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and HDL-C

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14457
Atorvastatin-0.15546
All Treatment0.08841

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TC/HDL-C Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.26268
Atorvastatin-0.08593
All Treatment-0.23226

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and TG

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.10533
Atorvastatin-0.00604
All Treatment-0.09437

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TG

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.02947
Atorvastatin0.27198
All Treatment0.08787

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.01798
Atorvastatin0.20127
All Treatment0.05369

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.04785
Atorvastatin0.11256
All Treatment-0.01362

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.13220
Atorvastatin0.35715
All Treatment0.18971

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and TC

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.00642
Atorvastatin0.14331
All Treatment0.04311

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.01528
Atorvastatin0.21198
All Treatment0.05251

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C/HDL-C Ratio

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.08468
Atorvastatin0.12805
All Treatment-0.04102

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB/ApoA-1 Ratio

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (NCT00296374)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.04088
Atorvastatin0.06598
All Treatment-0.01652

[back to top]

Relationship Between Renal Effects and Lipid Changes: eGFR and ApoB

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.15146
Atorvastatin0.04886
All Treatment-0.12168

[back to top]

Relationship Between Renal Effects and Lipid Changes: Urinary Albumin/Creatinine Ratio and nonHDL-C

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52 (NCT00296374)
Timeframe: 52 Weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.09189
Atorvastatin0.33769
All Treatment0.14988

[back to top]

Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in TC at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.06641
Atorvastatin-0.07964
All Treatments0.02900

[back to top]

Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in LDL-C at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.15731
Atorvastatin0.15368
All Treatments-0.06310

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Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in LDL-C at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.02679
Atorvastatin-0.07603
All Treatments-0.00171

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Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in HDL-C at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14080
Atorvastatin0.02750
All Treatments0.09472

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Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in HDL-C at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.01684
Atorvastatin0.01755
All Treatments0.01758

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TG at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04160
Atorvastatin0.00531
All Treatments0.03430

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TG

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.12643
Atorvastatin0.00486
All Treatments-0.08301

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TC/HDL-C Ratio at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.23597
Atorvastatin0.19933
All Treatments-0.10205

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in TC/HDL-C Ratio at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08194
Atorvastatin-0.06576
All Treatments0.04477

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.23887
Atorvastatin0.17170
All Treatments-0.10817

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08263
Atorvastatin-0.06860
All Treatments0.04337

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.19532
Atorvastatin0.14967
All Treatments-0.09001

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in nonHDL-C at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.06029
Atorvastatin-0.08151
All Treatments0.02283

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.20805
Atorvastatin0.18299
All Treatments-0.07681

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04858
Atorvastatin-0.05535
All Treatments0.02023

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.15415
Atorvastatin0.10486
All Treatments-0.06121

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.02907
Atorvastatin-0.09476
All Treatments-0.00160

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.11217
Atorvastatin0.11006
All Treatments-0.03932

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoB at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.06098
Atorvastatin-0.03181
All Treatments0.03861

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoA1 at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.11047
Atorvastatin0.07751
All Treatments0.08580

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Correlation of Change From Baseline in eGFR With Percent Change From Baseline in ApoA1 at Week 26

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.13029
Atorvastatin0.17554
All Treatments0.14191

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Change From Baseline in Estimated Glomerular Filtration Rate (eGFR) at Week 26

The change from baseline in eGFR at Week 26 is the Week 26 value minus baseline value. (NCT00296400)
Timeframe: Assessed at baseline and Week 26

InterventionmL/min (Mean)
Rosuvastatin 10 mg1.39
Rosuvastatin 40 mg-3.41
Atorvastatin 80 mg-1.61

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04652
Atorvastatin0.06344
All Treatments0.04149

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.03957
Atorvastatin-0.17644
All Treatments-0.01549

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in TG at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20659
Atorvastatin0.23989
All Treatments0.21728

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Total Cholesterol [TC] at Week 26.

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.17601
Atorvastatin0.21701
All Treatments0.19643

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Total Cholesterol [TC] at Week 52.

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20462
Atorvastatin0.03480
All Treatments0.16077

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Triglyceride [TG] at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.15348
Atorvastatin-0.06049
All Treatments0.10089

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Correlation of Changes From Baseline inUrinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16868
Atorvastatin-0.09428
All Treatments0.10679

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Urinary Albumin/Creatinine Ratio at Week 26

Urinary albumin/creatinine ratio (mg/g) =urine albumin concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 26 urine albumin/creatinine ratio over baseline urine albumin/creatinine ratio. (NCT00296400)
Timeframe: Assessed at baseline and Week 26

Interventionratio (Geometric Mean)
Rosuvastatin 10 mg0.850
Rosuvastatin 40 mg0.946
Atorvastatin 80 mg0.731

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Urinary Albumin/Creatinine Ratio at Week 52 [LOCF]

Urinary albumin/creatinine ratio (mg/g) =urine albumin concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 52 [LOCF] urine albumin/creatinine ratio over baseline urine albumin/creatinine ratio. (NCT00296400)
Timeframe: Assessed at baseline and Week 52 [LOCF]

Interventionratio (Geometric Mean)
Rosuvastatin 10 mg0.879
Rosuvastatin 40 mg0.967
Atorvastatin 80 mg0.719

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Urinary Protein/Creatinine Ratio at Week 26.

Urinary protein/creatinine ratio (mg/g) =urine protein concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 26 urine protein/creatinine ratio over baseline urine protein/creatinine ratio. (NCT00296400)
Timeframe: Assessed at baseline and Week 26

Interventionratio (Geometric Mean)
Rosuvastatin 10 mg0.932
Rosuvastatin 40 mg1.057
Atorvastatin 80 mg0.762

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Urinary Protein/Creatinine Ratio at Week 52 [LOCF]

Urinary protein/creatinine ratio (mg/g) =urine protein concentration (mg/dL)/ urine creatinine concentration (g/dL). Outcome measure is the ratio of Week 52 [LOCF] urine protein/creatinine ratio over baseline urine protein/creatinine ratio. (NCT00296400)
Timeframe: Assessed at baseline and Week 52 (LOCF)

Interventionratio (Geometric Mean)
Rosuvastatin 10 mg0.938
Rosuvastatin 40 mg1.082
Atorvastatin 80 mg0.759

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16499
Atorvastatin0.02609
All Treatments0.15049

[back to top]

Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.06794
Atorvastatin0.05410
All Treatments0.05465

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20021
Atorvastatin0.12953
All Treatments0.18870

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.18720
Atorvastatin0.16167
All Treatments0.18717

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.21082
Atorvastatin-0.04379
All Treatments0.14085

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.10258
Atorvastatin0.13505
All Treatments0.11103

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08108
Atorvastatin-0.16753
All Treatments0.00479

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.23547
Atorvastatin0.25043
All Treatments0.25208

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.17479
Atorvastatin0.18677
All Treatments0.18203

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14783
Atorvastatin0.21561
All Treatments0.16899

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20285
Atorvastatin-0.13565
All Treatments0.12568

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.05037
Atorvastatin0.09779
All Treatments0.05936

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.10365
Atorvastatin-0.24717
All Treatments0.01386

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16080
Atorvastatin0.17150
All Treatments0.16578

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.24107
Atorvastatin-0.08640
All Treatments0.16525

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.04955
Atorvastatin0.02740
All Treatments0.03798

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.11997
Atorvastatin-0.21073
All Treatments0.03955

[back to top]

Change From Baseline in eGFR at Week 52 [LOCF]

The change from baseline in eGFR at Week 52 [LOCF] is the Week 52 value or last observation carried forward minus baseline value. (NCT00296400)
Timeframe: Assessed at baseline and Week 52 [LOCF]

InterventionmL/min (Mean)
Rosuvastatin 10 mg-2.71
Rosuvastatin 40 mg-3.30
Atorvastatin 80 mg-1.74

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.18188
Atorvastatin0.17503
All Treatments0.18566

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.23734
Atorvastatin0.01311
All Treatments0.17958

[back to top]

Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.02506
Atorvastatin0.02201
All Treatments0.01860

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TC/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.08954
Atorvastatin-0.20870
All Treatments0.01926

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TG at Week 26

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.11526
Atorvastatin-0.06890
All Treatments0.07248

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Correlation of Changes From Baseline in Urinary Albumin/Creatinine Ratio With Percent Change From Baseline in TG at Week 52

Correlation of changes from baseline in urinary albumin/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.21730
Atorvastatin0.21151
All Treatments0.21477

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoA-1 at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.19626
Atorvastatin0.09835
All Treatments0.18349

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.18473
Atorvastatin-0.02690
All Treatments0.12496

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.10698
Atorvastatin0.13814
All Treatments0.11414

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in ApoB/ApoA-1 Ratio at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.05859
Atorvastatin-0.12938
All Treatments-0.00540

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Apolipoprotein A-1 [ApoA-1] at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.12595
Atorvastatin0.05628
All Treatments0.13754

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Apolipoprotein B [ApoB] at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.18504
Atorvastatin0.17259
All Treatments0.19146

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in HDL-C at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20346
Atorvastatin0.18041
All Treatments0.20818

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in High Density Lipoprotein Cholesterol [HDL-C] at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.18055
Atorvastatin0.24987
All Treatments0.22094

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.06383
Atorvastatin0.12687
All Treatments0.07462

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in LDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.05881
Atorvastatin-0.20262
All Treatments-0.01340

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 26

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.14302
Atorvastatin0.24393
All Treatments0.17632

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in Non-high Density Lipoprotein Cholesterol [nonHDL-C] at Week 26

"Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 26. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.~)" (NCT00296400)
Timeframe: Baseline and 26 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.16206
Atorvastatin0.20032
All Treatments0.17628

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.20386
Atorvastatin-0.04698
All Treatments0.14495

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Correlation of Changes From Baseline in Urinary Protein/Creatinine Ratio With Percent Change From Baseline in nonHDL-C/HDL-C Ratio at Week 52

Correlation of changes from baseline in urinary protein/creatinine ratio with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin0.07188
Atorvastatin-0.16669
All Treatments0.00955

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Correlation of Changes From Baseline in eGFR With Percent Change From Baseline in TC at Week 52

Correlation of changes from baseline in eGFR with percent change from baseline in lipids and lipoprotein concentrations at Week 52. (Correlation values range from -1 to +1. -1 indicates a perfect negative linear relationship while a +1 indicates a perfect linear positive relationship. A value of zero indicates no relationship.) (NCT00296400)
Timeframe: Baseline and 52 weeks

InterventionCorrelation coefficient (Number)
Rosuvastatin-0.15721
Atorvastatin0.16110
All Treatments-0.05794

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Mean Percent Change in Total Cholesterol From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-37.9
ABT-335 + 40 mg Simvastatin-27.5
ABT-335 + 40 mg Atorvastatin-35.0

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Mean Percent Change in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 52 in This Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 in this open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-48.8
ABT-335 + 40 mg Simvastatin-36.6
ABT-335 + 40 mg Atorvastatin-44.3

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Mean Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin25.2
ABT-335 + 40 mg Simvastatin25.1
ABT-335 + 40 mg Atorvastatin19.4

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Mean Percent Change in Direct Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-41.6
ABT-335 + 40 mg Simvastatin-30.2
ABT-335 + 40 mg Atorvastatin-38.1

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Median Percent Change in High-sensitivity C-reactive Protein (hsCRP) From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Median)
ABT-335 + 20 mg Rosuvastatin-38.87
ABT-335 + 40 mg Simvastatin-27.72
ABT-335 + 40 mg Atorvastatin-39.13

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Mean Percent Change in Very Low-density Lipoprotein Cholesterol (VLDL-C) From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-56.9
ABT-335 + 40 mg Simvastatin-37.7
ABT-335 + 40 mg Atorvastatin-52.2

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Median Percent Change in Triglycerides From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Median)
ABT-335 + 20 mg Rosuvastatin-53.0
ABT-335 + 40 mg Simvastatin-47.7
ABT-335 + 40 mg Atorvastatin-56.2

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Percentage of Subjects Reporting Adverse Events During Combination Therapy, Either in the Preceding Double-blind Studies or in This Open-label Study

(NCT00300430)
Timeframe: Anytime after initiation of combination therapy (either in the double-blind or open-label study) to within 30 days after the last dose of combination therapy

Interventionpercentage of participants (Number)
ABT-335 + 20 mg Rosuvastatin83
ABT-335 + 40 mg Simvastatin86
ABT-335 + 40 mg Atorvastatin85

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Mean Percent Change in Apolipoprotein B (Apo B) From Baseline to Week 52 of the Open-label Study

(NCT00300430)
Timeframe: Baseline to Week 52 of the open-label study

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-44.8
ABT-335 + 40 mg Simvastatin-35.5
ABT-335 + 40 mg Atorvastatin-42.9

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Mean Percent Change in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Final Visit

[(Week 12 non-HDL-C minus baseline non-HDL-C)/baseline non-HDL-C] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-40.8
ABT-335 + 40 mg Atorvastatin-42.5
ABT-335-14.8
20 mg Atorvastatin-35.7
40 mg Atorvastatin-41.7
80 mg Atorvastatin-45.2

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Mean Percent Change in Low-density Lipoprotein Cholesterol (LDL-C) From Baseline to Final Visit

[(Week 12 LDL-C minus baseline LDL-C)/baseline LDL-C] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-33.7
ABT-335 + 40 mg Atorvastatin-35.4
ABT-335-3.4
20 mg Atorvastatin-37.1
40 mg Atorvastatin-39.7
80 mg Atorvastatin-46.0

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Mean Percent Change in Triglycerides From Baseline to Final Visit

[(Week 12 triglycerides minus baseline triglycerides)/baseline triglycerides] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-45.6
ABT-335 + 40 mg Atorvastatin-42.1
ABT-335-29.6
20 mg Atorvastatin-16.5
40 mg Atorvastatin-23.2
80 mg Atorvastatin-30.4

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Mean Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Final Visit

[(Week 12 HDL-C minus baseline HDL-C)/baseline HDL-C] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin14.0
ABT-335 + 40 mg Atorvastatin12.6
ABT-33519.9
20 mg Atorvastatin6.3
40 mg Atorvastatin5.3
80 mg Atorvastatin6.2

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Mean Percent Change in Total Cholesterol From Baseline to Final Visit

[(Week 12 total cholesterol minus baseline total cholesterol)/baseline total cholesterol] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-32.8
ABT-335 + 40 mg Atorvastatin-34.6
ABT-335-10.1
20 mg Atorvastatin-29.6
40 mg Atorvastatin-33.8
80 mg Atorvastatin-38.2

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Mean Percent Change in Lipoprotein Apo B (Apo B) From Baseline to Final Visit

[(Week 12 Apo B minus baseline Apo B)/baseline Apo B] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-37.0
ABT-335 + 40 mg Atorvastatin-37.1
ABT-335-12.4
20 mg Atorvastatin-32.9
40 mg Atorvastatin-35.3
80 mg Atorvastatin-40.3

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Median Percent Change in High-sensitivity C-reactive Protein (hsCRP) From Baseline to Final Visit

[(Week 12 hsCRP minus baseline hsCRP)/baseline hsCRP] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Median)
ABT-335 + 20 mg Atorvastatin-26.2
ABT-335 + 40 mg Atorvastatin-42.9
ABT-335-12.4
20 mg Atorvastatin-29.6
40 mg Atorvastatin-30.3
80 mg Atorvastatin-31.9

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Mean Percent Change in Very Low-density Lipoprotein Cholesterol (VLDL-C) From Baseline to Final Visit

[(Week 12 VLDL-C minus baseline VLDL-C)/baseline VLDL-C] x 100 (NCT00300469)
Timeframe: Baseline to 12 Weeks (Final Visit)

Interventionpercent change (Mean)
ABT-335 + 20 mg Atorvastatin-48.3
ABT-335 + 40 mg Atorvastatin-53.5
ABT-335-36.5
20 mg Atorvastatin-26.2
40 mg Atorvastatin-35.6
80 mg Atorvastatin-38.9

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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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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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Number of Participants Who Achieve the Target LDL-C Concentration of < 3.3 mmol/L (130 mg/dL)

12-hour fasting blood samples were collected in participants to measure high density lipoprotein-cholesterol (HDL-C), triglycerides and total cholesterol. LDL-C was measured using Friedewald calculation (LDL-C = Total C - [HDL-C + TG/5] after treatment for 6 weeks. (NCT00319449)
Timeframe: 6 weeks post treatment

InterventionParticipants (Number)
Ezetimibe 10 mg7
Placebo 10 mg8

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Low Density Lipoprotein-cholesterol (LDL-C) at Baseline and After 6 Weeks of Treatment With Ezetimibe 10 mg Added to Atorvastatin 10 mg Versus Placebo Added to Atorvastatin 10 mg

12-hour fasting blood samples were collected in participants to measure high density lipoprotein-cholesterol (HDL-C), triglycerides and total cholesterol. LDL-C was measured using Friedewald calculation (LDL-C = Total C - [HDL-C + TG/5]) before and after treatment. (NCT00319449)
Timeframe: Baseline and 6 weeks

,
Interventionmg/dL (Mean)
Baseline6 weeks post treatment
Ezetimibe 10 mg148.125106.000
Placebo 10 mg151.083108.273

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High Density Lipoprotein-cholesterol (HDL-C), Total Cholesterol and Triglycerides at Baseline and After 6 Weeks of Treatment With Ezetimibe 10 mg Added to Atorvastatin 10 mg Versus Placebo Added to Atorvastatin 10 mg

12-hour fasting blood samples were collected in participants and the high density lipoprotein-cholesterol (HDL-C), triglycerides and total cholesterol was measured with the basic lipid panel test. (NCT00319449)
Timeframe: 6 weeks post treatment

,
Interventionmg/dL (Mean)
HDL-C at baselineHDL-C at 6 weeksTotal Cholesterol at baselineTotal Cholesterol at 6 weeksTriglycerides at baselineTriglycerides at 6 weeks
Ezetimibe 10 mg53.25052.625219.125156.375139.500115.250
Placebo 10 mg57.66753.500226.000185.667131.667120.250

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Effects on Apoptosis (Caspase-3 Expression).

Tissue is examined by immunohistochemistry for cleaved caspase-3. Measured by biopsy samples obtained from normal-appearing rectal mucosa at baseline and after completion of study treatment. Wilcoxon will be used to assess significant differences between the intervention arms. (NCT00335504)
Timeframe: Up to 6 months

InterventionPercent change of caspase-3 (Mean)
Arm I (Atorvastatin Calcium)106.0
Arm II (Sulindac)131.9
Arm III (Oligofructose-enriched Inulin)120.5
Arm IV (Placebo)130.6

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Effects on Proliferation (Ki67 Expression).

Tissue is examined by immunohistochemistry for Ki67. Measured by biopsy samples obtained from normal-appearing rectal mucosa at baseline and after completion of study treatment. Wilcoxon will be used to assess significant differences between the intervention arms. (NCT00335504)
Timeframe: Up to 6 months

InterventionPercent change (Mean)
Arm I (Atorvastatin Calcium)6.5
Arm II (Sulindac)12.2
Arm III (Oligofructose-enriched Inulin)34.7
Arm IV (Placebo)13.6

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Percent Change in Number of Rectal Aberrant Cryptic Foci (ACF) as Measured by Magnification Chromoendoscopy

At the Pre-Intervention Evaluation, rectal ACF will be classified with respect to ACF number, crypt number, crypt size, tissue plane, staining intensity, and (optional) lumen shape for each subject. At the Post- Intervention Evaluation, these same parameters will be recorded and incident vs prevalent rectal ACF status will also be recorded. Compare each non-placebo arms versus the placebo arm to screen the three active study agents for possible phase III testing. (NCT00335504)
Timeframe: 6 months

Interventionpercent change in number of ACF (Mean)
Arm I (Atorvastatin Calcium)8.4
Arm II (Sulindac)-13.3
Arm III (Oligofructose-enriched Inulin)-8.8
Arm IV (Placebo)-8.6

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Adverse Events.

Defined as any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with participation in a study, whether or not related to that participation. Graded using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events version 3.0. Number of adverse events per grade level. (NCT00335504)
Timeframe: Up to 30 days after completion of study treatment

,,,
Interventionadverse events (Number)
Grade 1Grade 2Grade 3
Arm I (Atorvastatin Calcium)1152
Arm II (Sulindac)1242
Arm III (Oligofructose-enriched Inulin)1040
Arm IV (Placebo)15131

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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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AUC0-t Atorvastatin Acid (Lomitapide 60 mg)

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for atorvastatin acid (Lomitapide 60 mg) (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Atorvastatin 20 mg + Lomitapide 60 mg152.32

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Area Under Concentration-time Curve From 0 to Last Measureable Concentration (AUC0-t) Atorvastatin Acid (Lomitapide 10 mg)

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for atorvastatin acid (Lomitapide 10 mg) (NCT00359281)
Timeframe: 0 to 24 hour

InterventionRatio (Geometric Mean)
Atorvastatin 20 mg + Lomitapide 10 mg110.97

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AUC0-t Simvastatin

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for simvastatin (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Simvastatin 20 mg + Lomitapide 10 mg162.25

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AUC0-t Simvastatin Acid

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for simvastatin acid (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Simvastatin 20 mg + Lomitapide 10 mg138.76

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AUC0-t Total Ezetimibe

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for total ezetimibe (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Ezetimibe 10 mg + Lomitapide 10 mg105.71

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

Percent change from Baseline in LDL-C (NCT00359281)
Timeframe: Baseline to Day 8

InterventionPercent Change (Mean)
Atorvastatin 20 mg + Lomitapide 10 mg-30.99
Simvastatin 20 mg + Lomitapide 10 mg-26.43
Ezetimibe 10 mg + Lomitapide 10 mg-28.36
Rosuvastatin 20 mg + Lomitapide 10 mg-41.74
Fenofibrate 145 mg + Lomitapide 10 mg-20.12
Atorvastatin 20 mg + Lomitapide 60 mg-66.02
Rosuvastatin 20 mg + Lomitapide 60 mg-63.20
Dextrometh-rophan 30 mg + Lomitapide 60 mg-46.07
ER Niacin 1000 mg + Lomitapide 10 mg-20.89

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AUC0-t Nicotinuric Acid

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for nicotinuric acid (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
ER Niacin 1000 mg + Lomitapide 10 mg79.15

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AUC0-t Nicotinic Acid

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for nicotinic acid (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
ER Niacin 1000 mg + Lomitapide 10 mg110.22

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AUC0-t Rosuvastatin (Lomitapide 60 mg)

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for rosuvastatin (Lomitapide 60 mg) (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Rosuvastatin 20 mg + Lomitapide 60 mg132.21

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AUC0-t Fenofibric Acid

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for fenofibric acid (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Fenofibrate 145 mg + Lomitapide 10 mg89.62

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AUC0-t Rosuvastatin (Lomitapide 10 mg)

Geometric Mean Ratio ln(AUC0-t) Day 8/Day 1 for rosuvastatin (Lomitapide 10 mg) (NCT00359281)
Timeframe: 0 to 24 hours

InterventionRatio (Geometric Mean)
Rosuvastatin 20 mg + Lomitapide 10 mg102.05

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Mean Change in Level: Week 16-baseline in Ena-78

We take difference week 16 minus week 0 for ENA-78 and use a one sample t comparison. (NCT00361283)
Timeframe: 16 weeks after baseline

Interventionpg/ml (Mean)
Atorvastatin 80 MG/Day-111.2

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Number of Participants With Serious and Non-Serious Adverse Events

Here is the count of participants with serious and non-serious adverse events. A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT00367458)
Timeframe: Date treatment consent signed to date off study, approximately 26 weeks.

InterventionParticipants (Count of Participants)
Atorvastatin12
Placebo12

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Change in Percentage of Cluster of Differentiation 8 (CD8+) Human Leukocyte Antigen DR (HLA-DR+), CD8+(CD8+HLADR+CD38+) in Peripheral Blood

CD8+HLADR+CD38+ are cellular markers of immune activation that is present in HIV infected individuals. This marker was measured before and after the statin/placebo intervention by standard lymphocyte phenotyping. (NCT00367458)
Timeframe: Baseline and 8 weeks

,
Interventionpercent T cell subset (Mean)
Baseline CD8+HLADR+CD38+CD8+HLADR+CD38+ at 8 Weeks
Atorvastatin0-3.75
Placebo0-3.3

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Change in Percentage of Cluster of Differentiation 8 (CD8+) Human Leukocyte Antigen DR (HLA-DR+) in Peripheral Blood

CD8+HLA-DR+ are cellular markers of immune activation that is present in HIV infected individuals. This marker was measured before and after the statin/placebo intervention by standard lymphocyte phenotyping. (NCT00367458)
Timeframe: Baseline and 8 weeks

,
Interventionpercent T cell subset (Mean)
Baseline CD8+HLA-DR+CD8+HLA-DR+ at 8 Weeks
Atorvastatin0-3.8
Placebo0-3.5

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Change in Percentage of Cluster of Differentiation 4 (CD4+) Human Leukocyte Antigen DR (HLA-DR+) in Peripheral Blood

CD4+HLA-DR+ are cellular markers of immune activation that is present in HIV infected individuals. This marker was measured before and after the statin/placebo intervention by standard lymphocyte phenotyping. (NCT00367458)
Timeframe: Baseline and 8 weeks

,
Interventionpercent T cell subset (Mean)
Baseline CD4+HLA-DR+CD4+HLA-DR+ at 8 Weeks
Atorvastatin0-2
Placebo0-1.8

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Change in Human Immunodeficiency Virus 1 (HIV-1) Ribonucleic Acid (RNA) Levels

The change in HIV viral RNA level in plasma in response to lipid lowering agents was measured as log10 plasma RNA copy number, and the change in the log10 viral RNA level is included in table. (NCT00367458)
Timeframe: Baseline and 8 weeks

,
InterventionLog10 copies/ml plasma (Median)
Baseline8 Weeks
Atorvastatin0-0.03
Placebo0-0.08

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Determine the Postoperative Complications Found in Each Group

To determine whether one week of preventive therapy with atorvastatin prior to surgery and one week after surgery reduced the composite rate of cardiovascular morbidity when compared to placebo. (NCT00375518)
Timeframe: one week (minimum of 5 days) before surgery and continued for one week (minimum of 5 days) after surgery

,
Interventionparticipants (Number)
With Post Operative ComplicationsWithout Post Operative Complications
Atorvastatin1656
Placebo857

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Percentage Change of Total Cholesterol (TC)

Calculate the percentage change of total cholesterol level (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin-34.10
Atorvastatin-28.80

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Percentage Reduction of Low-Density Lipoprotein-C (LDL-C)

Calculate the percentage reduction of LDL-C (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage reduction (Mean)
Rosuvastatin-45.50
Atorvastatin-37.90

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Percentage of Subjects Reaching Their Low-Density Lipoprotein-C (LDL-C) and Non High-Density Lipoprotein-C (HDL-C) Target Goal

Based on NCEP ATP III guideline, calculate the percentage of subjects reaching their LDL-C & non HDL-C target goal. (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage of participants (Number)
Rosuvastatin78.80
Atorvastatin66.70

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Percentage of Subjects Reaching Their LDL-C Target Goal

Based on NCEP ATP III guideline, calculate the percentage of subjects reaching their LDL-C target goal. LDL-C target goals are <70mg/dl, <100mg/dl and <130mg/dl according to their baseline conditions (presence of Coronary heart disease and risk factors and grade of Framingham 10-Year risk). (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage of participants (Number)
Rosuvastatin88.20
Atorvastatin75.40

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Percentage Change of Triglycerides (TG)

Calculate the percentage change of Triglycerides. (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin-17.20
Atorvastatin-15.10

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Percentage Change of Insulin Resistance Using QUICKI

QUICKI was calculated using insulin and glucose levels derived by laboratory test. The formula is as following: QUICKI = 1/[log(insulin) + log(glucose)]. (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin-1.27
Atorvastatin-1.03

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Percentage Change of Insulin Resistance Using HOMA-R

HOMA-R was calculated using insulin and glucose levels derived by laboratory test. The formula is as following: HOMA-R = insulin* glucose/22.5 (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin28.00
Atorvastatin50.30

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Percentage Change of High-Density Lipoprotein-C (HDL-C)

Calculate the percentage change of HDL-C level (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin9.90
Atorvastatin8.20

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Percentage Change of Glucose Level

Using laboratory test, mean change of glucose level was investigated. (NCT00395486)
Timeframe: Baseline and 6 weeks

InterventionPercentage change (Mean)
Rosuvastatin-0.60
Atorvastatin2.78

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Percentage Change of Apolipoprotein A1 (ApoA1)

Calculate the percentage change of Apolipoprotein A1 (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin8.50
Atorvastatin4.20

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Percentage Change of Apolipoprotein B (ApoB)

Calculate the percentage change of apolipoprotein B (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercentage change (Mean)
Rosuvastatin-40.50
Atorvastatin-34.60

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Percentage Change From Baseline in Ratio of Apolipoprotein (ApoB/ApoA1) at Week 6

Samples for evaluation from all investigational sites will be delivered by courier to the central laboratory within 24 hours of blood being drawn. This outcome will be calculated by using the result of ApoB and ApoA1. (NCT00395486)
Timeframe: Baseline and 6 weeks

Interventionpercent change (Mean)
Rosuvastatin-44.40
Atorvastatin-36.50

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European Systematic COronary Risk Evaluation (SCORE) 10-year Risk of Fatal Cardiovascular Disease (CVD) at Month 12

European SCORE: designed to measure cardiovascular disease mortality; computed using age, gender, whether a person lives in a low risk or high risk region, measured total cholesterol, measured HDL cholesterol, systolic blood pressure, and current smoking status. The coefficients were used to derive the score calculated after 12 months of study treatment (Month 12). (NCT00407537)
Timeframe: Baseline, Month 12

Interventionpercent risk (Mean)
Caduet3.0
Usual Care3.7

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Framingham 10-year Risk of Stroke at Month 12

"Stroke risk calculated from the Framingham risk for CVD (CHD, stroke, intermittent claudication, congestive heart failure) multiplied by a gender-specific calibration factor for the stroke component risk. Coefficients were used to derive the score calculated at the end of study treatment (Month 12)." (NCT00407537)
Timeframe: Baseline, Month 12

Interventionpercent risk (Mean)
Caduet3.7
Usual Care4.9

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Framingham 10-year Risk of Stroke at Month 4

"Stroke risk calculated from the Framingham risk for CVD (CHD, stroke, intermittent claudication, congestive heart failure) multiplied by a gender-specific calibration factor for the stroke component risk. Coefficients were used to derive the score calculated at the end of study treatment (Month 12)." (NCT00407537)
Timeframe: Baseline, Month 4

Interventionpercent risk (Mean)
Caduet3.7
Usual Care4.9

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Framingham 10-year Risk of Total CHD at Month 4

Framingham prediction of 10-year risk of CHD: Gender-specific prediction equations formulated to predict CHD risk according to age, diabetes, smoking, blood pressure categories, and total cholesterol and low density lipoprotein (LDL) cholesterol categories. The coefficients were used to derive the score calculated after 4 months of treatment (Month 4). (NCT00407537)
Timeframe: Baseline, Month 4

Interventionpercent risk (Mean)
Caduet12.5
Usual Care16.3

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Framingham 10-year Risk of Total Coronary Heart Disease (CHD) at Month 12

Framingham prediction of 10-year risk of CHD: Gender-specific prediction equations formulated to predict CHD risk according to age, diabetes, smoking, blood pressure categories, and total cholesterol and low density lipoprotein (LDL) cholesterol categories. The coefficients were used to derive the score calculated at the end of study treatment (Month 12). (NCT00407537)
Timeframe: Baseline, Month 12

Interventionpercent risk (Mean)
Caduet12.5
Usual Care16.3

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Change From Baseline European SCORE 10-year Risk of Developing Fatal CVD

European SCORE: designed to measure cardiovascular disease mortality; computed using age, gender, whether a person lives in a low risk or high risk region, measured total cholesterol, measured HDL cholesterol, systolic blood pressure, and current smoking status. Change from baseline calculated as mean at observation minus mean at Baseline. (NCT00407537)
Timeframe: Baseline, Month 4, Month 12

,
Interventionpercent risk (Least Squares Mean)
Month 4Month 12
Caduet-1.8438-1.9693
Usual Care-0.9678-0.9963

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Change From Baseline in Framingham 10-year Risk of Developing Total CHD

Framingham prediction of 10-year risk of CHD: Gender-specific prediction equations formulated to predict CHD risk according to age, diabetes, smoking, blood pressure categories, and total cholesterol and low density lipoprotein (LDL) cholesterol categories. Change from baseline calculated as mean at observation minus mean at Baseline. (NCT00407537)
Timeframe: Baseline, Month 4, Month 12

,
Interventionpercent risk (Least Squares Mean)
Month 4Month 12
Caduet-7.2705-7.2374
Usual Care-2.5155-2.5167

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Change From Baseline in Lipid Parameters at Month 12

Mean Total Cholesterol (TC), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), and Triglyceride blood concentrations. (NCT00407537)
Timeframe: Baseline, Month 12

,
Interventionmg/dL (Least Squares Mean)
TCLDLHDLTriglycerides
Caduet-37.1024-33.2420-0.4339-15.2270
Usual Care-4.0368-3.4168-1.01053.0398

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Change From Baseline in Lipid Parameters at Month 4

Mean Total Cholesterol (TC), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), and Triglyceride blood concentrations. Change from baseline measured as mean at Month 4 minus mean at Baseline. (NCT00407537)
Timeframe: Baseline, Month 4

,
Interventionmg/dL (Least Squares Mean)
TCLDLHDLTriglycerides
Caduet-42.7542-38.2765-0.2060-20.5645
Usual Care-3.8144-2.9628-1.19783.0828

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Mean Lipid Parameters at Month 12

Mean Total Cholesterol (TC), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), and Triglyceride blood concentrations. (NCT00407537)
Timeframe: Month 12

,
Interventionmg/dL (Mean)
TCLDLHDLTriglycerides
Caduet163.387.147.3151.5
Usual Care196.6117.347.1166.4

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Mean Lipid Parameters at Month 4

Mean Total Cholesterol (TC), Low Density Lipoprotein (LDL), High Density Lipoprotein (HDL), and Triglyceride blood concentrations. (NCT00407537)
Timeframe: Month 4

,
Interventionmg/dL (Mean)
TCLDLHDLTriglycerides
Caduet156.080.947.6143.5
Usual Care195.2116.446.8164.8

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Mean Systolic and Diastolic Blood Pressure at Month 12

(NCT00407537)
Timeframe: Month 12

,
InterventionmmHg (Mean)
SystolicDiastolic
Caduet130.679.2
Usual Care134.381.1

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Mean Systolic and Diastolic Blood Pressure at Month 4

(NCT00407537)
Timeframe: Month 4

,
InterventionmmHg (Mean)
SystolicDiastolic
Caduet133.580.7
Usual Care134.581.1

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Number of Participants With Increase of Treatment Dosages After 4 Months.

Treatments indicative of prescribed medications other than study provided Caduet. (NCT00407537)
Timeframe: Month 4

,
InterventionParticipants (Number)
Increased doseincreased dose of anti-hypertensive medicationsincreased dose of lipid lowering medicationsincrease in either medicationincrease in both medications
Caduet3030040
Usual Care90882450

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Number of Participants With Lipid and Antihypertensive Treatments Used at 4 and 12 Months

Treatments indicative of prescribed medications other than study provided Caduet. (NCT00407537)
Timeframe: Month 4, Month 12

,
Interventionparticipants (Number)
Month 4: anti-hypertensive and/or lipid loweringMonth 4: anti-hypertensiveMonth 4: lipid loweringMonth 4: anti-hypertensive and lipid loweringMonth 12: anti-hypertensive and/or lipid loweringMonth 12: anti-hypertensiveMonth 12: lipid loweringMonth 12: anti-hypertensive and lipid lowering
Caduet64864745446556544645
Usual Care642637202197642638208204

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Percentage of Participants at Conventional Treatment Goals According to Global and Local Guidelines for Blood Pressure at 4 and 12 Months

Goals set at <140/90 mmHg according to the seventh Joint National Committee (JNC) on prevention, detection, evaluation, and treatment of high blood pressure and <140/90 mm Hg or <130/80 mm Hg for diabetics ccording to the European Society of Cardiology (ESC) guidelines. (NCT00407537)
Timeframe: Month 4, Month 12

,
Interventionpercentage of participants (Number)
JNC Month 4JNC Month 12ESC Month 4ESC Month 12
Caduet65.276.148.658.2
Usual Care62.660.646.047.5

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Percentage of Participants at Conventional Treatment Goals According to Global and Local Guidelines for LDL at 4 and 12 Months

Goal set at <100 mg/dL according to the United States (US) National Cholesterol Education Program Adult Treatment Panel 3 and at <80 mg/dL according to the European (EU) Society of Cardiology guidelines. (NCT00407537)
Timeframe: Month 4, Month 12

,
InterventionPercentage of participants (Number)
US Month 4US Month 12EU Month 4EU Month 12
Caduet77.371.952.446.7
Usual Care28.228.813.311.5

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Change From Baseline in SBP at Month 12

(NCT00407537)
Timeframe: Baseline, Month 12

InterventionmmHg (Least Squares Mean)
Caduet-18.2409
Usual Care-12.4903

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Change From Baseline in DBP at Month 12

(NCT00407537)
Timeframe: Baseline, Month 12

InterventionmmHg (Least Squares Mean)
Caduet-10.0128
Usual Care-6.8429

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Change From Baseline in Diastolic Blood Pressure (DBP) at Month 4

(NCT00407537)
Timeframe: Baseline, Month 4

InterventionmmHG (Least Squares Mean)
Caduet-8.3024
Usual Care-6.6908

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Change From Baseline in Systolic Blood Pressure (SBP) at Month 4

(NCT00407537)
Timeframe: Baseline, Month 4

InterventionmmHG (Least Squares Mean)
Caduet-15.3088
Usual Care-12.1619

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European SCORE 10-year Risk of Fatal CVD at Month 4

European SCORE: designed to measure cardiovascular disease mortality; computed using age, gender, whether a person lives in a low risk or high risk region, measured total cholesterol, measured HDL cholesterol, systolic blood pressure, and current smoking status. The coefficients were used to derive the score calculated after 4 months of study treatment (Month 4). (NCT00407537)
Timeframe: Baseline, Month 4

Interventionpercent risk (Mean)
Caduet3.1
Usual Care3.7

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Percent Change From Baseline in Non- High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-33.5
EZ/Simva 10 mg/20 mg-43.8
Atorva 20mg-36.5
EZ/Simva 10 mg/40 mg-48.3
Atorva 40 mg-41.4

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol: High Density Lipoprotein Cholesterol (Non-HDL-C:HDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-34.7
EZ/Simva 10 mg/20 mg-46.2
Atorva 20mg-39.2
EZ/Simva 10 mg/40 mg-51.2
Atorva 40 mg-43.5

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Percent Change From Baseline in Apolipoprotein-B: Apolipoprotein-A1 (Apo-B:Apo-A1) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-27.4
EZ/Simva 10 mg/20 mg-38.4
Atorva 20mg-32.0
EZ/Simva 10 mg/40 mg-41.9
Atorva 40 mg-36.2

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Percent Change From Baseline in Apolipoprotein-A1 (Apo-A1) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg0.8
EZ/Simva 10 mg/20 mg3.2
Atorva 20mg1.0
EZ/Simva 10 mg/40 mg3.0
Atorva 40 mg1.4

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg3.4
EZ/Simva 10 mg/20 mg6.8
Atorva 20mg5.6
EZ/Simva 10 mg/40 mg8.8
Atorva 40 mg4.9

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Percent Change From Baseline in Apolipoprotein- B (Apo-B) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-27.9
EZ/Simva 10 mg/20 mg-37.2
Atorva 20mg-31.9
EZ/Simva 10 mg/40 mg-41.1
Atorva 40 mg-35.8

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Percent Change From Baseline in High-Sensitivity C-reactive (Hs-CRP) (mg/dL) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Median)
Atorva 10 mg-16.8
EZ/Simva 10 mg/20 mg-17.2
Atorva 20mg-22.4
EZ/Simva 10 mg/40 mg-27.6
Atorva 40 mg-30.0

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Percent Change From Baseline in Total-Cholesterol: High Density Lipoprotein-Cholesterol (Total-C:HDL- C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-28.1
EZ/Simva 10 mg/20 mg-36.9
Atorva 20mg-31.5
EZ/Simva 10 mg/40 mg-41.2
Atorva 40 mg-35.3

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Percent Change From Baseline in Total Cholesterol(mg/dL) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-26.5
EZ/Simva 10 mg/20 mg-33.7
Atorva 20mg-28.3
EZ/Simva 10 mg/40 mg-37.3
Atorva 40 mg-32.8

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Percent Change From Baseline in Very Low Density Lipoprotein Cholesterol (VLDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-17.7
EZ/Simva 10 mg/20 mg-18.3
Atorva 20mg-21.6
EZ/Simva 10 mg/40 mg-23.4
Atorva 40 mg-22.7

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Percent Change From Baseline in Low Density Lipoprotein (LDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-36.5
EZ/Simva 10 mg/20 mg-49.6
Atorva 20mg-39.4
EZ/Simva 10 mg/40 mg-53.9
Atorva 40 mg-46.0

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 6 in Patients With Atherosclerotic Vascular Disease (AVD)

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-37.1
EZ/Simva 10 mg/20 mg-48.7
Atorva 20mg-36.9
EZ/Simva 10 mg/40 mg-56.1
Atorva 40 mg-45.8

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 6 in Patients Without Atherosclerotic Vascular Disease (AVD)

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-36.3
EZ/Simva 10 mg/20 mg-50.1
Atorva 20mg-40.3
EZ/Simva 10 mg/40 mg-53.2
Atorva 40 mg-46.1

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol: High Density Lipoprotein Cholesterol (LDL-C: HDL-C) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg-37.8
EZ/Simva 10 mg/20 mg-51.8
Atorva 20mg-42.1
EZ/Simva 10 mg/40 mg-56.6
Atorva 40 mg-48.2

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Percent Change From Baseline in Triglyceride (TG) (mg/dL) at Week 6

(NCT00409773)
Timeframe: Baseline and 6 Weeks

InterventionPercent Change (Median)
Atorva 10 mg-21.7
EZ/Simva 10 mg/20 mg-23.3
Atorva 20mg-27.5
EZ/Simva 10 mg/40 mg-29.5
Atorva 40 mg-30.0

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Subjects With LDL-C < 100 mg/dL at Week 6

Subjects Who achieve a goal of LDL-C < 100 mg/dL at Week 6. (NCT00412113)
Timeframe: Week 6

Interventionparticipants (Number)
Norvasc + TLC13
Caduet + TLC99

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Subjects With BP <140/90 mmHg and LDL-C <130 mg/dL at Week 4.

Subjects achieving both JNC-7 blood pressure goal of <140/90 mmHg and NCEP/ATP III LDL-C goal <130 mg/dL at Week 4. (NCT00412113)
Timeframe: Week 4

Interventionparticipants (Number)
Norvasc + TLC41
Caduet + TLC85

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Change From Baseline in HDL at Week 6.

Mean change at observation minus baseline. (NCT00412113)
Timeframe: Week 6, baseline

Interventionmg/dL (Mean)
Norvasc + TLC1.2
Caduet + TLC0.4

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Change From Baseline in High Density Lipoprotein (HDL) at Week 4.

Mean change at observation minus baseline. (NCT00412113)
Timeframe: Week 4, baseline

Interventionmg/dL (Mean)
Norvasc + TLC0.6
Caduet + TLC0.6

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Change From Baseline in LDL at Week 4.

Change: mean of observation minus mean at baseline. (NCT00412113)
Timeframe: Week 4, baseline

Interventionmg/dL (Mean)
Norvasc + TLC-0.5
Caduet + TLC-47.8

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Change From Baseline in LDL at Week 6.

Mean change at observation minus baseline. (NCT00412113)
Timeframe: Week 6, baseline

Interventionmg/dL (Mean)
Norvasc + TLC0.3
Caduet + TLC-49.2

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Change From Baseline in Total Cholesterol (TC) to Week 6.

Mean change at observation minus baseline. (NCT00412113)
Timeframe: Week 6, baseline

Interventionmg/dL (Mean)
Norvasc + TLC3.7
Caduet + TLC-56.8

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Change From Baseline in Triglycerides (TG) at Week 6.

Mean change at observation minus mean baseline. (NCT00412113)
Timeframe: Week 6 , baseline

Interventionmg/dL (Mean)
Norvasc + TLC11.6
Caduet + TLC-42.6

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Change From Baseline in Triglycerides (TG) to Week 4.

Mean change at observation minus baseline (NCT00412113)
Timeframe: Week 4, baseline

Interventionmg/dL (Mean)
Norvasc + TLC2.4
Caduet + TLC-45.7

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Change From Baseline to Week 4 in Diastolic Blood Pressure (DBP)

Mean at observation minus mean at baseline (NCT00412113)
Timeframe: Week 4, baseline

InterventionmmHg (Mean)
Norvasc + TLC-1.5
Caduet + TLC-1.2

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Change From Baseline to Week 4 in Framingham Predicted Absolute 10-year Risk.

Framingham prediction of absolute 10-year risk of CHD outcomes (MI or CHD death) are calculations based on total point score (range less than negative 3 [best] to greater than or equal to 14 [worst] for men; less than or equal to negative 2 [best] and greater than or equal to 17 [worst] for women) of subject age, sex, current blood pressure treatment status, current smoking status, total cholesterol, high-density lipoprotein cholesterol and systolic blood pressure calculated at Week 4. Mean at observation minus mean at baseline. (NCT00412113)
Timeframe: Week 4, baseline

Interventionscore on scale (Least Squares Mean)
Norvasc + TLC-0.3
Caduet + TLC-2.8

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Change From Baseline to Week 4 in Pulse Rate

Mean at observation minus mean at baseline measured in beats per minute (bpm). (NCT00412113)
Timeframe: Week 4, baseline

Interventionbpm (Mean)
Norvasc + TLC-0.1
Caduet + TLC-0.9

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Change From Baseline to Week 4 in Systolic Blood Pressure (SBP).

Mean at observation minus mean at baseline (NCT00412113)
Timeframe: Week 4, baseline

InterventionmmHg (Mean)
Norvasc + TLC-2.6
Caduet + TLC-1.5

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Change From Baseline to Week 6 in Diastolic Blood Pressue (DBP)

Change from mean at observation minus mean at baseline (NCT00412113)
Timeframe: Week 6, baseline

InterventionmmHg (Median)
Norvasc + TLC-1.1
Caduet + TLC-1.7

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Change From Baseline to Week 6 in Framingham Predicted Absolute 10-year Risk

Framingham prediction of absolute 10-year risk of Coronary Heart Disease (CHD) outcomes (myocardial infarction [MI] or CHD death) are calculations based on total point score (range less than negative 3 [best] to greater than or equal to 14 [worst] for men; less than or equal to negative 2 [best] and greater than or equal to 17 [worst] for women) of subject age, sex, current blood pressure treatment status, current smoking status, total cholesterol, high-density lipoprotein cholesterol, and systolic blood pressure calculated at Week 6. Mean at observation minus mean at baseline. (NCT00412113)
Timeframe: Week 6, baseline

Interventionscore on scale (Least Squares Mean)
Norvasc + TLC-0.1
Caduet + TLC-2.9

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Change From Baseline to Week 6 in Pulse Rate

Mean at observation minus mean at baseline (NCT00412113)
Timeframe: Week 6, baseline

Interventionbpm (Mean)
Norvasc + TLC0.9
Caduet + TLC1.1

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Change From Baseline to Week 6 in Systolic Blood Pressure (SBP)

Mean change at observation minus mean baseline. (NCT00412113)
Timeframe: Week 6, baseline

InterventionmmHg (Mean)
Norvasc + TLC-1.0
Caduet + TLC-4.0

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Change in Total Cholesterol (TC) From Baseline to Week 4.

Mean change at observation minus baseline. (NCT00412113)
Timeframe: Week 4, baseline

Interventionmg/dL (Mean)
Norvasc + TLC0.5
Caduet + TLC-55.9

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Subjects With Blood Pressure (BP) <140/90 Millimeters of Mercury (mmHg) and Low Density Lipoprotein Cholesterol (LDL-C) <100 Milligrams Per Deciliter(mg/dL) at Week 6

Number of subjects reaching dual goal of systolic blood pressure <140 millimeters of mercury (mmHg) and diastolic blood pressue of <90 mmHg and low density lipoprotein-cholesterol(LDL-C) <100 milligrams per deciliter(mg/dL) (NCT00412113)
Timeframe: Week 6

Interventionparticipants (Number)
Norvasc + TLC11
Caduet + TLC80

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Subjects With Blood Pressure of <140/90 mmHg and LDL-C <100 mg/dL at Week 4

Subjects achieving both the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC)-7 blood pressure goal of <140/90 mmHg and the National Cholesterol Education Program Adult Treatment Panel (NCEP/ATP) III Update low density lipoprotein-cholesterol (LDL-C) goal <100 mg/dL at Week 4. (NCT00412113)
Timeframe: Week 4

Interventionparticipants (Number)
Norvasc + TLC6
Caduet + TLC73

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Subjects With BP < 140/90 mmHg at Week 4

Subjects achieving BP goal of <140/90 mmHg at week 4 (NCT00412113)
Timeframe: Week 4

Interventionparticipants (Number)
Norvasc + TLC84
Caduet + TLC87

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Subjects With BP < 140/90 mmHg at Week 6

Subjects achieving BP goal of <140/90 mmHg at week 6 (NCT00412113)
Timeframe: Week 6

Interventionparticipants (Number)
Norvasc + TLC83
Caduet + TLC94

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Subjects With BP <140/90 mmHg and LDL-C <130 mg/dL at Week 6.

Subjects achieving both JNC-7 blood pressure goal of <140/90 mmHg and NCEP/ATP III LDL-C goal <130 mg/dL at Week 6. (NCT00412113)
Timeframe: Week 6

Interventionparticipants (Number)
Norvasc + TLC45
Caduet + TLC90

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Subjects With LDL-C < 100 mg/dL at Week 4

Subjects Who achieve a goal of LDL-C < 100 mg/dL at Week 4. (NCT00412113)
Timeframe: Week 4

Interventionparticipants (Number)
Norvasc + TLC8
Caduet + TLC96

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Number of Participants With AVN After 9 Months

(NCT00412841)
Timeframe: 9 months

Interventionparticipants (Number)
Atorvastatin12
Placebo16

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Number of Participants With AVN After 4 Months

(NCT00412841)
Timeframe: 4 months

Interventionparticipants (Number)
Atorvastatin14
Placebo19

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Number of Patients Who Achieved Low Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 6

(NCT00418834)
Timeframe: Week 6

,
InterventionParticipants (Number)
<70 mg/dL≥70 mg/dL
Atorva 10 mg + EZ244271
Atorva 20 mg / Atorva 40 mg92423

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Number of Patients Who Achieved Low Density Lipoprotein Cholesterol (LDL-C) <70 mg/dL at Week 12

(NCT00418834)
Timeframe: Week 12

,
InterventionParticipants (Number)
<70 mg/dL≥70 mg/dL
Atorva 10 mg + EZ225291
Atorva 20 mg / Atorva 40 mg164345

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Number of Patients Who Achieved LDL-C<100 mg/dL for Patients Without AVD and LDL-C<70 mg/dL for Patients With AVD at Week 12

(NCT00418834)
Timeframe: Week 12

,
InterventionParticipants (Number)
<100 mg/dL (w/o AVD) and <70 mg/dL (w/ AVD)≥100 mg/dL (w/o AVD) and ≥70 mg/dL (w/ AVD)
Atorva 10 mg + EZ255261
Atorva 20 mg / Atorva 40 mg200309

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Percent Change From Baseline in Apo Lipoprotein B (Apo B) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-16.8
Atorva 20 mg / Atorva 40 mg-7.7

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Percent Change From Baseline in Triglycerides (TG) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-12.9
Atorva 20 mg / Atorva 40 mg-5.7

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Number of Patients Who Achieved LDL-C <100 mg/dL for Patients Without Atherosclerotic Vascular Disease (AVD) and LDL-C <70 mg/dL for Patients With Atherosclerotic Vascular Disease (AVD) at Week 6

(NCT00418834)
Timeframe: Week 6

,
InterventionParticipants (Number)
<100 mg/dL (w/o AVD) and <70 mg/dL (w/ AVD)>100 mg/dL (w/o AVD) and ≥70 mg/dL (w/AVD)
Atorva 10 mg + EZ274241
Atorva 20 mg / Atorva 40 mg127388

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Percent Change From Baseline in Apo Lipoprotein B (Apo B) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-14.0
Atorva 20 mg / Atorva 40 mg-10.8

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Percent Change From Baseline in Apo Lipoprotein A-I (Apo A-I) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-1.1
Atorva 20 mg / Atorva 40 mg-1.7

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Percent Change From Baseline in Apo Lipoprotein A-I (Apo A-I) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ0.7
Atorva 20 mg / Atorva 40 mg-2.0

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Percent Change From Baseline in Ratio of Highly Selective C-Reactive Protein (Hs-CRP) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-21.7
Atorva 20 mg / Atorva 40 mg-14.6

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Percent Change From Baseline in Total Cholesterol (TC) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-13.6
Atorva 20 mg / Atorva 40 mg-11.6

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Percent Change From Baseline in Triglycerides (TG) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-11.8
Atorva 20 mg / Atorva 40 mg-8.5

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Percent Change From Baseline in Total Cholesterol (TC):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-14.4
Atorva 20 mg / Atorva 40 mg-9.8

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Percent Change From Baseline in Total Cholesterol (TC): High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-16.9
Atorva 20 mg / Atorva 40 mg-7.9

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Percent Change From Baseline in Total Cholesterol (TC) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-15.9
Atorva 20 mg / Atorva 40 mg-8.0

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-27.2
Atorva 20 mg / Atorva 40 mg-12.6

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-22.9
Atorva 20 mg / Atorva 40 mg-16.0

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12

(NCT00418834)
Timeframe: Baseine and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-20.0
Atorva 20 mg / Atorva 40 mg-15.8

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-23.5
Atorva 20 mg / Atorva 40 mg-11.2

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-20.4
Atorva 20 mg / Atorva 40 mg-13.8

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL):High Density Lipoprotein Cholesterol (HDL-C) Ratio at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-24.0
Atorva 20 mg / Atorva 40 mg-11.1

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

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-22.5
Atorva 20 mg / Atorva 40 mg-17.9

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Percent Change From Baseline in LDL-C at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-26.7
Atorva 20 mg / Atorva 40 mg-12.8

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ2.5
Atorva 20 mg / Atorva 40 mg0.7

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ2.4
Atorva 20 mg / Atorva 40 mg-0.8

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Percent Change From Baseline in Ratio of Highly Selective C-Reactive Protein (Hs-CRP) at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-13.5
Atorva 20 mg / Atorva 40 mg-10.7

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Percent Change From Baseline in Apo Lipoprotein B (Apo B):Apo Lipoprotein A-I (Apo A-I) Ratio at Week 6

(NCT00418834)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-14.8
Atorva 20 mg / Atorva 40 mg-5.2

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Percent Change From Baseline in Apo Lipoprotein B (Apo B):Apo Lipoprotein A-I (Apo A-I) Ratio at Week 12

(NCT00418834)
Timeframe: Baseline and Week 12

InterventionPercent Change (Least Squares Mean)
Atorva 10 mg + EZ-13.5
Atorva 20 mg / Atorva 40 mg-8.2

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The Percentage Change From Baseline (Week 6) in Apolipoprotein-B (ApoB)

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in ApoB (Number)
Rosuvastatin-25.96
Atorvastatin-28.67

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The Percentage Change From Baseline (Week 6) in TC/HDL-C Ratio

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in TC/HDL-C Ratio (Number)
Rosuvastatin-24.99
Atorvastatin-28.42

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The Percentage Change From Baseline (Week 6)in LDL-C/HDL-C Ratio

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in LDL-C/HDL-C Ratio (Number)
Rosuvastatin-34.75
Atorvastatin-38.45

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The Percentage Change From Baseline (Week 6)in Non-HDL-C

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in Non-HDL-C (Number)
Rosuvastatin-29.72
Atorvastatin-34.09

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The Percentage Change From Baseline(Week 6) in Non-HDL-C/HDL-C Ratio

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in Non-HDL-C/HDL-C Ratio (Number)
Rosuvastatin-31.05
Atorvastatin-35.48

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The Percentage Change From Baseline(week6) in TC

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in TC (Number)
Rosuvastatin-23.03
Atorvastatin-26.88

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The Percentage of Participants Reaching the European (EAS) Targets of LDL-C<2.5 or 3.00 mmol/L, Depending on Risk Category, and the Combined LDL-C and TC Target of LDL-C<2.5 or 3.0 mmol/L and TC<4.5 or 5.0 mmol/L, Both Depending on Risk Category.

"Risk categories are:~Symptomatic Asymptomatic, total risk <5% Asymptomatic, total risk ≥5%, baseline LDL-C<3 mmol/L and baseline TC<5 mmol/L Asymptomatic, total risk ≥5%, baseline LDL-C ≥3 mmol/L or baseline TC ≥5 mmol/L~Patients are defined as symptomatic if they meet at least 1 of the following criteria:~History of cardiovascular disease Type II diabetes or diabetes of unknown type Baseline TC ≥8 mmol/l Baseline LDL-C ≥6 mmol/l Baseline systolic BP ≥180 mmHg Baseline diastolic BP ≥110 mmHg~Total risk is derived from age, sex, TC, systolic BP and smoking status." (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercentage of Participants (Number)
Rosuvastatin43
Atorvastatin48

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The Percentage of Participants Reaching the European (EAS) Targets of LDL-C<2.5 or 3.00 mmol/L, Depending on Risk Category.

"Risk categories are:~Symptomatic Asymptomatic, total risk <5% Asymptomatic, total risk ≥5%, baseline LDL-C<3 mmol/L and baseline TC<5 mmol/L Asymptomatic, total risk ≥5%, baseline LDL-C ≥3 mmol/L or baseline TC ≥5 mmol/L~Patients are defined as symptomatic if they meet at least 1 of the following criteria:~History of cardiovascular disease Type II diabetes or diabetes of unknown type Baseline TC ≥8 mmol/l Baseline LDL-C ≥6 mmol/l Baseline systolic BP ≥180 mmHg Baseline diastolic BP ≥110 mmHg~Total risk is derived from age, sex, TC, systolic BP and smoking status." (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercentage of Participants (Number)
Rosuvastatin56.7
Atorvastatin56.0

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The Percentage of Participants Reaching the General Medical Services (GMS) Contract Target of Total Cholesterol (TC) <5 mmol/L

(NCT00427960)
Timeframe: 6 weeks (Baseline) and 12 weeks

InterventionPercentage of Participants (Number)
Rosuvastatin50
Atorvastatin64

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The Percentage of Participants Reaching the Joint British Societies' Guideline (JBS 2) Targets of TC <4 mmol/L and LDL-C <2 mmol/L

(NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercentage of Participants (Number)
Rosuvastatin16
Atorvastatin28

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The Percentage Change From Baseline (Week 6) in High-density Lipoprotein Cholesterol (HDL-C)

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in HDL-C (Number)
Rosuvastatin4.46
Atorvastatin3.15

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The Percentage of Participants Reaching the Joint British Societies Guideline (JBS 2) Target of TC <4 mmol/L

(NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercentage of Participants (Number)
Rosuvastatin13
Atorvastatin12

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

Calculated as LDL-C at Week 6 - LDL-C at Week 12] * 100 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in LDL-C (Number)
Rosuvastatin33.28
Atorvastatin36.92

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The Percentage Change From Baseline (Week 6) in ApoB/ApoA1 Ratio

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in ApoB/ApoA1 Ratio (Number)
Rosuvastatin-22.89
Atorvastatin-28.75

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The Percentage Change From Baseline (Week 6) in Apolipoprotein-A1 (ApoA1)

Derived according to the following formula: 100*[Lipid at week 12 - Lipid at week 6]/Lipid at week 6 (NCT00427960)
Timeframe: 6 weeks (baseline) and 12 weeks

InterventionPercent Change in ApoA1 (Number)
Rosuvastatin-0.55
Atorvastatin1.89

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Percent Change in Low Density Lipoprotein Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Low-density lipoproteins - A complex of lipids and proteins, with greater amounts of lipid than protein, that transports cholesterol in the blood. High levels are associated with an increased risk of atherosclerosis and coronary heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-34.6
Placebo + Atorvastatin-32.2

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Percent Change in Low Density Lipoprotein Particle Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Low-density lipoproteins - A complex of lipids and proteins, with greater amounts of lipid than protein, that transports cholesterol in the blood. High levels are associated with an increased risk of atherosclerosis and coronary heart disease. Researchers have linked LDL particle size to the subsequent development of heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin1.5
Placebo + Atorvastatin0.5

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Percent Change in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Non-high density lipoprotein cholesterol is the Total Cholesterol minus the HDL(high density lipoproteins or the sum of the LDL, VLDL and IDL. That is, Low Density Lipoproteins, Very Low Density Lipoproteins and Intermediate Density Lipoproteins. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-40.2
Placebo + Atorvastatin-33.7

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Percent Change in Non-High Density Lipoprotein Cholesterol From Baseline to Week 12 During 20 mg Atorvastatin Treatment Period

Non-high density lipoprotein cholesterol is the Total Cholesterol minus the HDL(high density lipoproteins or the sum of the LDL, VLDL and IDL. That is, Low Density Lipoproteins, Very Low Density Lipoproteins and Intermediate Density Lipoproteins. (NCT00435045)
Timeframe: Baseline and Week 12

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-46.9
Placebo + Atorvastatin-39.0

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Percent Change in Intermediate Density Lipoprotein Particle Concentration From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Intermediate Density Lipoprotein, or IDLs, transport cholesterol and triglycerides through the body. IDLs are a type of cholesterol that are a product of VLDL degradation and result in LDL cholesterol when broken down. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-60.4
Placebo + Atorvastatin-50.3

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Percent Change in High Density Lipoprotein (HDL)Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

"HDL - A complex of lipids and proteins in approximately equal amounts that functions as a transporter of cholesterol in the blood. High levels are associated with a decreased risk of atherosclerosis and coronary heart disease.~High density lipoprotein cholesterol is the Total Cholesterol minus the sum of the LDL, VLDL and IDL." (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin12.4
Placebo + Atorvastatin10.0

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Percent Change in High Density Lipoprotein (HDL) Particle Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Partical size suggests the bigger the better. HDL is a complex of lipids and proteins in approximately equal amounts that functions as a transporter of cholesterol in the blood. High levels are associated with a decreased risk of atherosclerosis and coronary heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin0.0
Placebo + Atorvastatin1.2

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Percent Change in High Density Lipoprotein (HDL) Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

High Density Lipoprotein partical size suggests the bigger the better. HDL is a complex of lipids and proteins in approximately equal amounts that functions as a transporter of cholesterol in the blood. High levels are associated with a decreased risk of atherosclerosis and coronary heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin1.0
Placebo + Atorvastatin5.1

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Percent Change in Docosahexaenoic Acid (DHA) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Docosahexaenoic Acid is an omega-3 essential fatty acid. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin85.5
Placebo + Atorvastatin4.2

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Percent Change in Apolipoprotein-B From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

"Apolipoprotein B is the primary apolipoprotein of low density lipoproteins (LDL or bad cholesterol), which is responsible for carrying cholesterol to tissues." (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-32.1
Placebo + Atorvastatin-30.7

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Percent Change in Apolipoprotein-A-1 From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Apolipoprotein A1 - major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-0.3
Placebo + Atorvastatin1.5

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Percent Change in Triglycerides From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Triglycerides - A naturally occurring ester of three fatty acids and glycerol that is the chief constituent of fats and oils. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-45.4
Placebo + Atorvastatin-26.9

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Percent Change in Eicosapentaenoic Acid (EPA) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Eicosapentaenoic acid (EPA) is one of several omega-3 fatty acids used by the body. It is found in cold water fatty fish and in fish oil supplements, along with docosahexaenoic acid (DHA). Omega-3 fatty acids are part of a healthy diet that helps lower risk of heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin402.2
Placebo + Atorvastatin-5.6

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Percent Change in Apolipoprotein C-III From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Apolipoprotein C-III (APOC3) is a very low density lipoprotein (VLDL) protein. APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to delay catabolism of triglyceride-rich particles. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-29.4
Placebo + Atorvastatin-16.0

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Percent Change in Low Density Lipoprotein (LDL) Cholesterol (Beta-quantification) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

LDL - A complex of lipids and proteins, with greater amounts of lipid than protein, that transports cholesterol in the blood. High levels are associated with an increased risk of atherosclerosis and coronary heart disease. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-29.3
Placebo + Atorvastatin-31.5

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Percent Change in Total Adiponectin From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid catabolism. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-5.1
Placebo + Atorvastatin-1.6

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Percent Change in Total Cholesterol (TC) From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Total Cholesterol is the sum of the High Density Lipoproteins (HDL), Low Density Lipoproteins (LDL), Very Low Density Lipoproteins (VLDL), and Intermediate Density Lipoproteins (IDL). (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-31.5
Placebo + Atorvastatin-27.4

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Percent Change in Remnant-like Particle Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Remnant-like particle cholesterol within the plasma has been identified as a cardiovascular risk factor. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-50.0
Placebo + Atorvastatin-38.9

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Percent Change in Total Cholesterol/High Density Lipoprotein Cholesterol Ratio From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Total cholesterol/High density lipoprotein cholesterol (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-38.3
Placebo + Atorvastatin-34.5

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Percent Change in Triglycerides/High Density Lipoprotein Cholesterol Ratio From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

(NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-51.9
Placebo + Atorvastatin-34.0

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Percent Change in Very Low Density Lipoproteins (VLDL) Cholesterol From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

VLDL - very-low-density lipoprotein: a plasma lipoprotein with a high lipid content, associated with atherosclerosis. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-54.3
Placebo + Atorvastatin-37.0

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Percent Change in Lipoprotein-Phosphoslipase A2 From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Lipoprotein Phosphoslipase A2 - modified form of LDL. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-20.7
Placebo + Atorvastatin-9.7

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Percent Change in Non-High Density Lipoprotein Cholesterol From Baseline to Week 16 During 40 mg Atorvastatin Treatment Period

Non-high density lipoprotein cholesterol is the Total Cholesterol minus the HDL(high density lipoproteins or the sum of the LDL, VLDL and IDL. That is, Low Density Lipoproteins, Very Low Density Lipoproteins and Intermediate Density Lipoproteins. (NCT00435045)
Timeframe: Baseline and Week 16

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-50.4
Placebo + Atorvastatin-46.3

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Percent Change in Very Low Density Lipoproteins and Chylomicron Particle Concentration Total From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Very low density lipoproteins are plasma lipoproteins with a high lipid content, associated with atherosclerosis. Chylomicrons are One of the microscopic particles of emulsified fat found in the blood and lymph and formed during the digestion of fats. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-32.4
Placebo + Atorvastatin-25.9

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Percent Change in Very Low Density Lipoproteins Size From Baseline to Week 8 During 10 mg Atorvastatin Treatment Period

Very low density lipoproteins are plasma lipoproteins with a high lipid content, associated with atherosclerosis. (NCT00435045)
Timeframe: Baseline and Week 8

Interventionpercent change (Median)
Lovaza(Omacor) + Atorvastatin-17.5
Placebo + Atorvastatin-3.3

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Number of Participants Reaching the LDL-C (Low Density Lipoprotein-Cholesterol) Goal (< 100 mg/dl) After 6 Weeks of Treatment

Primary objective is to evaluate the proportion of patients achieving LDL-C target <100 mg/dl recommend in National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) after 6 weeks of treatment(vytorin 10/20 vs. atorvastatin 10 mg) (NCT00442897)
Timeframe: After 6 weeks of treatment

InterventionParticipants (Number)
Vytorin89
Atorvastatin63

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Number of Participants Reaching the LDL-C Goal (< 100 mg/dl) After 12 Weeks of Treatment

If patients didn't achieve LDL-C <100 mg/dl after 6 weeks of treatment, they received the double dosage of study drug for the next 6 weeks (vytorin 10/40 or atorvastatin 20 mg) and If achieved LDL-C < 100 mg/dl, they received the same dosage of study drug for the next 6 weeks. (NCT00442897)
Timeframe: After 12 weeks of the treatment

InterventionParticipants (Number)
Vytorin85
Atorvastatin63

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Percentage of Patients Achieving a Target of Fasting LDL-C of <2mmol/l at Study End

Fasting LDL-C was the primary efficacy variable. The primary efficacy analysis was based on the proportion of patients achieving a target of <2mmol/l in fasting LDL-C at study end. (NCT00462748)
Timeframe: 6 Weeks

InterventionPercent (Number)
Ezetimibe/Simvastatin67.4
Atorvostatin36.3
Rosuvastatin17.4

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Percent Change in Triglycerides From Baseline to Week 12

(Week 12 triglycerides minus baseline triglycerides) x 100/baseline triglycerides (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Median)
Niacin Extended-release Plus Simvastatin-44.0
Atorvastatin-37.0

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Percent Change in Total Cholesterol:HDL-C Ratio

(Week 12 total cholesterol:HDL-C ratio minus baseline total cholesterol:HDL-C ratio) x 100/baseline total cholesterol:HDL-C ratio (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-45.2
Atorvastatin-40.3

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Percent Change in Total Cholesterol From Baseline to Week 12

(Week 12 total cholesterol minus baseline total cholesterol) x 100/baseline total cholesterol (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-31.3
Atorvastatin-35.1

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Percent Change in Non-HDL-C From Baseline to Week 8

(Week 8 non-HDL-C minus baseline non-HDL-C) x 100/baseline non-HDL-C (NCT00465088)
Timeframe: From baseline to Week 8

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-45.0
Atorvastatin-44.3

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

(Week 12 LDL-C minus baseline LDL-C) x 100/baseline LDL-C (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-43.8
Atorvastatin-46.0

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Percent Change in Lipoprotein A From Baseline to Week 12

(Week 12 lipoprotein A minus baseline lipoprotein A) x 100/baseline lipoprotein A (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Median)
Niacin Extended-release Plus Simvastatin-15.8
Atorvastatin16.0

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Percent Change in LDL-C:HDL-C Ratio

(Week 12 LDL-C:HDL-C ratio minus baseline LDL-C:HDL-C ratio) x 100/baseline LDL-C:HDL-C ratio (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-54.5
Atorvastatin-50.5

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Percent Change in Non-HDL-C From Baseline to Week 12

(Week 12 non-HDL-C minus baseline non-HDL-C) x 100/baseline non-HDL-C (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin-43.4
Atorvastatin-43.3

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Percent Change in HDL-C From Baseline to Week 8

(Week 8 HDL-C minus baseline HDL-C) x 100/baseline HDL-C (NCT00465088)
Timeframe: From baseline to Week 8

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin26.7
Atorvastatin1.4

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Percent Change in High-density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 12

(Week 12 HDL-C minus baseline HDL-C) x 100/baseline HDL-C (NCT00465088)
Timeframe: From baseline to Week 12

Interventionpercent change (Least Squares Mean)
Niacin Extended-release Plus Simvastatin30.1
Atorvastatin9.4

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Percentage of Subjects With Triglycerides < 150 mg/dL at Week 12

(NCT00465088)
Timeframe: 12 weeks

InterventionPercentage of subjects (Number)
Niacin Extended-release Plus Simvastatin79
Atorvastatin70

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Percentage of Subjects With HDL-C >/= 40 mg/dL, LDL-C Meeting NCEP ATP III Goal, and Triglycerides < 150 mg/dL at Week 12

NCEP ATP III goals for LDL-C are as follows: For high-risk patients, LDL-C < 100 mg/dL; for moderate risk patients, LDL-C < 130 mg/dL; for low-risk patients: LDL-C < 160 mg/dL. High-risk means coronary heart disease or risk equivalents; moderate risk means having at least 2 risk factors; low-risk means having no or 1 risk factor. (NCT00465088)
Timeframe: 12 weeks

InterventionPercentage of subjects (Number)
Niacin Extended-release Plus Simvastatin65
Atorvastatin34

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Percentage of Subjects Meeting With HDL-C >/= 40 mg/dL at Week 12

(NCT00465088)
Timeframe: 12 weeks

InterventionPercentage of subjects (Number)
Niacin Extended-release Plus Simvastatin78
Atorvastatin28

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Percentage of Subjects Meeting National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III Goal for LDL-C at Week 12

For high-risk patients (coronary heart disease or equivalent), LDL-C < 100 mg/dL and non-HDL-C < 130 mg/dL; for moderate risk patients (having 2 risk factors), LDL-C < 130 mg/dL and non-HDL-C < 160 mg/dL; for low-risk patients (having 0 or 1 risk factor): LDL-C < 160 mg/dL and non-HDL-C < 190 mg/dL. (NCT00465088)
Timeframe: 12 weeks

InterventionPercentage of subjects (Number)
Niacin Extended-release Plus Simvastatin78
Atorvastatin84

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Percent Change From Baseline of Other Lipids

(NCT00474240)
Timeframe: After 8 weeks of study drug

,,,,,
InterventionPercent (Mean)
Percent change from baseline in total cholesterolPercent change from baseline in total Apo BPercent change from baseline in non-HDL-C
AEGR-733 10 mg-33-36-36
AEGR-733 10 mg + Atorvastatin 20 mg-40-46-48
AEGR-733 5 mg-18-17-19
AEGR-733 5 mg + Atorvastatin 20 mg-37-41-45
Atorvastatin 20 mg-30-34-38
Placebo202

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Percent Change From Baseline in LDL-C at 8 Weeks

(NCT00474240)
Timeframe: Atfer 8 weeks on study drug

InterventionPercent Change (Mean)
Placebo2
Atorvastatin 20 mg-42
AEGR-733 5 mg-16
AEGR-733 10 mg-37
AEGR-733 5 mg + Atorvastatin 20 mg-47
AEGR-733 10 mg + Atorvastatin 20 mg-50

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12

(NCT00479388)
Timeframe: Baseline and 12 Weeks

InterventionPercent (Least Squares Mean)
ER Niacin/Laropiprant + Run-in Statin-10.0
Run-in Statin Dose Doubled-5.5

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Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12

(NCT00479388)
Timeframe: Baseline and 12 Weeks

InterventionPercent (Least Squares Mean)
ER Niacin/Laropiprant + Run-in Statin15.8
Run-in Statin Dose Doubled0.2

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Percent Change From Baseline in Triglycerides at Week 12

(NCT00479388)
Timeframe: Baseline and 12 Weeks

InterventionPercent (Median)
ER Niacin/Laropiprant + Run-in Statin-17.6
Run-in Statin Dose Doubled-4.0

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Mean Percent Change in Direct Low-Density Lipoprotein Cholesterol (LDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 LDL-C minus baseline LDL-C)/baseline LDL-C] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-19.2
ABT-335 + 40 mg Simvastatin-20.2
ABT-335 + 40 mg Atorvastatin-20.5

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Mean Percent Change in Total Cholesterol (Total-C) From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 Total-C minus baseline Total-C)/baseline Total-C] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-20.1
ABT-335 + 40 mg Simvastatin-17.9
ABT-335 + 40 mg Atorvastatin-20.4

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Mean Percent Change in Very Low-Density Lipoprotein Cholesterol (VLDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 VLDL-C minus baseline VLDL-C)/baseline VLDL-C] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-33.7
ABT-335 + 40 mg Simvastatin-18.7
ABT-335 + 40 mg Atorvastatin-26.6

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Mean Percent Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 HDL-C minus baseline HDL-C)/baseline HDL-C] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin13.7
ABT-335 + 40 mg Simvastatin11.2
ABT-335 + 40 mg Atorvastatin5.2

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Median Percent Change in Triglycerides From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 triglycerides minus baseline triglycerides)/baseline triglycerides] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Median)
ABT-335 + 20 mg Rosuvastatin-36.9
ABT-335 + 40 mg Simvastatin-29.6
ABT-335 + 40 mg Atorvastatin-38.7

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Mean Percent Change in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Week 104 of This Open-Label Year 2 Study

[(Week 104 Non-HDL-C minus baseline Non-HDL-C)/baseline Non-HDL-C] X 100. Baseline is the last value prior to the first dose of combination therapy. (NCT00491530)
Timeframe: Baseline to Week 104 (may include weeks in preceding double-blind studies [combination treatment arms], plus 52 weeks in preceding open-label year 1 study, and open-label year 2 study, up to 104 weeks)

Interventionpercent change (Mean)
ABT-335 + 20 mg Rosuvastatin-26.9
ABT-335 + 40 mg Simvastatin-23.8
ABT-335 + 40 mg Atorvastatin-25.1

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Percentage of Subjects Reporting Adverse Events During Combination Therapy in the Preceding Double-Blind Studies or in the Preceding Open-Label Year 1 Study or in This Open-Label Year 2 Study

All serious and non-serious adverse events are reported from the time of combination study drug initiation until 30 days after discontinuation of study drug. Adverse events are unfavorable changes in health that occur in subjects during a clinical trial or within a specified period following a trial. Serious adverse events are those that result in death, require inpatient hospitalization or the prolongation of hospitalization, result in congenital anomaly/birth defect, or significant disability/incapacity or are life-threatening. (NCT00491530)
Timeframe: Anytime after initiation of combination therapy (in the preceding 12-week double-blind studies or in the preceding open-label year 1 study) up to 116 weeks, to within 30 days after the last dose of combination therapy.

Interventionpercentage of participants (Number)
ABT-335 + 20 mg Rosuvastatin94.8
ABT-335 + 40 mg Simvastatin90.0
ABT-335 + 40 mg Atorvastatin97.7

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Percentage Change in FMD in All Participants With and Without a CVD Event (Not by Treatment Group)

This outcome is independent of the treatment group so the groups are 'CVD event' and ' No CVD Event'. Cardiovascular events (CVD) included cardiovascular disease, myocardial infarction, congestive heart failure, stroke, and unstable angina. (NCT00491751)
Timeframe: 2 months

Interventionpercent change of flow-mediated dilation (Mean)
CVD Event0.5
No CVD Event0.7

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Change in FMD

Change in flow mediated dilation with treatment: FMD visit 2 - FMD visit 1 FMD is measured by using vascular ultrasound to determine the baseline diameter of the brachial artery. Endothelium-dependent vasodilation is induced by 5-minute arterial occlusion with a blood pressure cuff. When the cuff is released, the resultant increase in blood flow (reactive hyperemia) stimulates vasodilation of the brachial artery. This flow-mediated dilation (FMD) is expressed as the percent change from baseline. Healthy individuals typical dysplay a 10 to 12% dilation. Individuals with PAD had markedly impaired dilation of 6-7. The currernt study sought to determine whether a change in FMD would occur following intervention. (NCT00491751)
Timeframe: 1-4 weeks

Interventionpercent change of FMD (Mean)
Atorvastatin0.88
Ascorbic Acid0.41
Placebo0.88

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Mean Percent Change of Low Density Lipoprotein-Cholesterol (LDL-C) From Baseline After 8 Weeks.

(NCT00496730)
Timeframe: Baseline and 8 Weeks

InterventionPercent of Baseline Value (Mean)
Vytorin-49.29
Atorvastatin-38.05

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Number of Patients Attaining LDL-C Goal After 8 Weeks Treatment.

"Number of Patients Attaining LDL-C Goal After 8 Weeks Treatment.~LDL-C goal is based on National Cholesterol Education Program (NCEP) III guideline (LDL-C goals and cutpoints for therapeutic life changes and drug Therapy in different risk)." (NCT00496730)
Timeframe: Baseline and 8 weeks

InterventionParticipants attaining LDL-C goal (Number)
Vytorin105
Atorvastatin93

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Change in Lower Density Lipoprotein Cholesterol From Baseline After 8 Weeks.

(NCT00496730)
Timeframe: Baseline and Week 8

Interventionmg/dL (Mean)
Vytorin83.52
Atorvastatin98.27

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Percent Changes From Baseline to End-of-treatment in Non-HDL, HDL and LDL Cholesterol by LCP-AtorFen Versus Fenofibrate Monotherapy

Mean percent changes from baseline (Visit 3, Week 0) to end-of-treatment (Visit 6; Week 12) in non-HDL, HDL and LDL cholesterol by LCP-AtorFen versus fenofibrate monotherapy (NCT00504829)
Timeframe: baseline (week 0) to 12 weeks

,
Interventionpercent change from baseline (Mean)
non-HDLLDLHDL
Fenofibrate 145mg-16.1-13.918.2
LCP-AtorFen 40/100mg-44.8-42.319.7

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Percent Changes From Baseline to End-of-treatment in Non-HDL Cholesterol, HDL Cholesterol, and Triglycerides by LCP-AtorFen Versus Atorvastatin Monotherapy

Mean percent change from baseline to end-of-treatment (12 weeks) for non-HDL cholesterol and triglycerides and the mean percent change from baseline to end-of-treatment for HDL cholesterol for AtorFen 40/100mg fixed-dose combination tablet versus atorvastatin 40mg tablet. (NCT00504829)
Timeframe: baseline(randomization) to 12 weeks

,
Interventionpercent change from baseline (Mean)
non-HDLtriglyceridesHDL
Atorvastatin 40mg-40.2-28.96.5
LCP-AtorFen 40/100mg-44.8-49.119.7

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Number of Episodes of Hypoglycemia Requiring Any Treatment

number of episodes of hypoglycemia requiring any treatment, defined by the need for treatment with glucagon or third party intervention. (NCT00529191)
Timeframe: Baseline, Month 12, Month 18

,
Interventionepisodes (Mean)
BaselineMonth 12Month 18
Atorvastatin4.133.442.75
Placebo2.862.442.5

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Blood Glucose Control (Number of Participants With Hypoglycemia)

Blood glucose control as determined from home glucose meter downloads for the 1 week preceding the visit. The number of subjects with hypoglycemic episodes requiring treatment (BG < 70 mg/dl) (NCT00529191)
Timeframe: Baseline, Month 12, Month 18

,
InterventionParticipants (Count of Participants)
Baseline12 Month18 Month
Atorvastatin16168
Placebo798

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HDL and LDL Cholesterol Levels in Participants Stratified by the Preservation of Islet Cell Function

"Relationship between atorvastatin's effect on HDL and LDL cholesterol and the preservation of islet cell function.~Islet cell preservation defined as: <7.5% Reduction in C-Pep" (NCT00529191)
Timeframe: Baseline, Week 1, Month 3, Month 6, Month 9, Month 12,

,,,
Interventionmg/dl (Mean)
Baseline- HDL Cholesterol (mg/dL)Baseline - LDL Cholesterol (mg/dL)Week 1- HDL Cholesterol (mg/dL)Week 1 - LDL Cholesterol (mg/dL)Month 3- HDL Cholesterol (mg/dL)Month 3 - LDL Cholesterol (mg/dL)Month 6- HDL Cholesterol (mg/dL)Month 6 - LDL Cholesterol (mg/dL)Month 9- HDL Cholesterol (mg/dL)Month 9 - LDL Cholesterol (mg/dL)Month 12 - HDL Cholesterol (mg/dL)Month 12 - LDL Cholesterol (mg/dL)
Atorvastatin NO Islet Cell Preservation47.5899.0445.4368.9145.05614863.149.167.2447.9561.52
Atorvastatin YES Islet Cell Preservation47.3383.6752.3357.6743.334851.675455.3365.3357.3366
Placebo NO Islet Cell Preservation44.7596.1348.2597.6348.25106.2550.5102.545.889745.75102.75
Placebo YES Islet Cell Preservation53.29947.286.449.2591.554.7596.755090.754796.4

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Levels of HbA1c at Months 3, 6, 9, 12 and 18

(NCT00529191)
Timeframe: 3, 6, 9, 12, and 18 months

,
Interventionpercentage of glycated hemoglobin (Mean)
3 months6 months9 months12 months18 months
Atorvastatin6.687.137.477.388.04
Placebo6.396.626.867.267.94

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% Subjects Without Change in 2-hour C-peptide AUC in Response to the MMTT at Baseline vs. 12 Months

The C-peptide AUC measurements are collected over a 2 hour period (with 30 minute intervals) after a Mixed Meal Tolerance Test. The area under the curve from these combined measurements (from 0 to 120 or 0 to 240 minutes) is calculated and the unit of measure is nanogram*minutes/ml. The change in C-peptide AUC in response to a 2 hour MMTT at baseline vs 12 months were calculated, and efficacy (success) is defined as < 7.5% reduction. (NCT00529191)
Timeframe: Baseline vs 12 months

Intervention% of participants with efficacy (Number)
Atorvastatin14.8
Placebo38.4

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Mean Daily Insulin Dose Per kg Body Weight for 7 Days

Mean daily insulin dose per kg body weight for the 1 week preceding each scheduled study visit. (NCT00529191)
Timeframe: Visit 1, 2, 3, 4, 5, 6, 7

,
Interventionunits/kg (Mean)
Visit 1Visit 2Visit 3Visit 4Visit 5Visit 6Visit 7
Atorvastatin0.530.500.480.590.640.650.70
Placebo0.620.520.500.470.590.640.71

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Efficacy of a Daily Dose of Atorvastatin to Maintain Islet Cell Function as Measured by a 4-hour C-peptide Area Under Curve (AUC) in Patients With Newly Diagnosed Type 1 Diabetes Mellitus

The change in C-peptide measurements collected over a 4 hour period (0, 30, 60, 90, 120, 150, 180, 210 and 240 minutes) after a Mixed Meal Tolerance Test at baseline vs 12 months post-treatment were calculated. The area under the curve for these combined measurements is calculated and the unit of measure is nanogram x minutes / mL. Efficacy (success) is defined by < 7.5% reduction in AUC for 4-hr MMTT. (NCT00529191)
Timeframe: Baseline vs 12-month

Interventionnanogram*minutes/ml (Mean)
Atorvastatin345
Placebo178

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Study Drug Compliance Rate Overall

Compliance is defined as >=80% expected dosage consumed during the visit period. (NCT00529191)
Timeframe: 12 months treatment

Intervention% of compliant participants (Number)
Atorvastatin85.1
Placebo76.9

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Body Mass Index

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionkg/m2 (Mean)
Before treatmentAfter treatment
Atorvastatin40.138.2
Placebo36.035.8

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Brachial Artery Flow-mediated Dilation (FMD)

Brachial artery FMD, the percent change in brachial artery diameter following release of transient occlusion, was selected as the primary outcome because it is the most widely used research tool for evaluating the effects of interventions on endothelial function. FMD has been shown to predict longterm cardiovascular events, even in patients with no apparent heart disease. (NCT00529542)
Timeframe: baseline and 6 weeks

,
Intervention% change in brachial artery diameter (Mean)
Before treatmentAfter treatment
Atorvastatin12.010.4
Placebo9.810.2

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Triglycerides

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/dl (Mean)
Before treatmentAfter treatment
Atorvastatin153.378.5
Placebo125.5132.5

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LDL Cholesterol

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/dl (Mean)
Before treatmentAfter treatment
Atorvastatin140.768.5
Placebo131.3118.8

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Systolic Blood Pressure

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmm Hg (Mean)
Before treatmentAfter treatment
Atorvastatin119.8112.0
Placebo114.5111.4

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HDL Cholesterol

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/dl (Mean)
Before treatmentAfter treatment
Atorvastatin44.447.8
Placebo46.546.8

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Peak Brachial Artery Conductance (BAC)

Pneumatic cuffs were positioned on the upper arm and wrist of the experimental arm. The brachial artery was imaged using an ATL Doppler ultrasound probe (5-12MHz linear array scanhead, HDI 5000, Advanced Technology Laboratories, Bothell, WA). Mean blood flow velocity (MBV) and brachial artery diameter (BAD) were recorded at baseline. Then the wrist cuff was inflated to 200-250 mmHg. After a minute, with the wrist cuff still inflated, the arm cuff was inflated to 200-250 mmHg. After 10 minutes the arm cuff was released to induce reactive hyperemia in the brachial artery. Upon release of the arm cuff, we continuously measured blood pressure (BP), heart rate (HR), and MBV, and intermittently measured BAD in the experimental arm. Brachial artery conductance (BAC)was calculated as MBV/MAP and FMD was calculated as percent change in BAD from baseline. (NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionml/sec/mm Hg (Mean)
Before treatmentAfter treatment
Atorvastatin5.46.9
Placebo3.64.3

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High-sensitivity C-reactive Protein (hsCRP)

high sensitive C-reactive protein as a measure of inflammation (NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/L (Mean)
Before treatmentAfter treatment
Atorvastatin8.04.3
Placebo7.26.0

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Total Cholesterol

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/dl (Mean)
Before treatmentAfter treatment
Atorvastatin215.8132.0
Placebo202.8192.1

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Fasting Insulin

(NCT00529542)
Timeframe: baseline and 6 weeks

,
InterventionuU/ml (Mean)
Before treatmentAfter treatment
Atorvastatin18.621.0
Placebo16.815.9

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Area Under the Curve (AUC) for Glucose During OGTT

A 75 gram oral glucose tolerance test (OGTT) was performed with blood draws at 0, 30, 60, 90 and 120 minutes. (NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg*minute/dL (Mean)
Before treatmentAfter treatment
Atorvastatin1569316136
Placebo1530915448

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Fasting Glucose

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmg/dl (Mean)
Before treatmentAfter treatment
Atorvastatin87.787.8
Placebo85.388.9

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Diastolic Blood Pressure

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmm Hg (Mean)
Before treatmentAfter treatment
Atorvastatin70.864.3
Placebo64.665.4

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DHEAS

Dehydroepiandrosterone sulfate (NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionng/ml (Mean)
Before treatmentAfter treatment
Atorvastatin1630.01326.4
Placebo1701.51739.5

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Androstenedione

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionng/ml (Mean)
Before treatmentAfter treatment
Atorvastatin3.42.5
Placebo3.84.1

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Mean Ovarian Volume

Pelvic ultrasound was performed using the 6.5 megahertz (MHz) probe of an ATL 400 machine to characterize ovarian size and morphology. Since in vitro studies demonstrate that statins inhibit ovarian theca-interstitial cell proliferation, we hypothesized that statins might reduce ovarian volume in PCOS. (NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionmm3 (Mean)
Before treatmentAfter treatment
Atorvastatin15.119.2
Placebo25.425.2

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Total Testosterone

(NCT00529542)
Timeframe: baseline and 6 weeks

,
Interventionng/dl (Mean)
Before treatmentAfter treatment
Atorvastatin61.347.1
Placebo92.375.7

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AUC for Insulin

Area under the curve for insulin during OGTT: A 75 gram oral glucose tolerance test was performed with blood draws at 0, 30, 60, 90 and 120 minutes. (NCT00529542)
Timeframe: baseline and 6 weeks

,
InterventionuU*minute/mL (Mean)
Before treatmentAfter treatment
Atorvastatin1273817479
Placebo93389132

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Percent Change in High Density Lipoprotein-Cholesterol From Baseline to Each Observation Point

"Percent of value at Week 2, Week 4, or Week 8 minus value at baseline over value at baseline" (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
InterventionPercent Change (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg8.37.97.5
CI-1038 2.5 mg/5 mg7.77.27.2
CI-1038 5 mg/10 mg9.911.910.8
CI-1038 5 mg/5 mg6.69.39.7

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Percent Change in Low Density Lipoprotein-Cholesterol From Baseline to Each Observation Point

"Percent of value at Week 2, Week 4, or Week 8 minus value at baseline over value at baseline" (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
InterventionPercent Change (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-42.5-43.8-42.9
CI-1038 2.5 mg/5 mg-34.8-37.4-37.6
CI-1038 5 mg/10 mg-40.2-41.8-40.8
CI-1038 5 mg/5 mg-32.8-35.0-34.2

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Percent Change in Total Cholesterol From Baseline to Each Observation Point

"Percent of value at Week 2, Week 4, or Week 8 minus value at baseline over value at baseline" (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
InterventionPercent Change (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-30.5-31.5-30.0
CI-1038 2.5 mg/5 mg-24.2-26.6-26.1
CI-1038 5 mg/10 mg-28.3-28.6-28.2
CI-1038 5 mg/5 mg-23.0-24.7-23.4

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Percent Change in Triglycerides From Baseline to Each Observation Point

"Percent of value at Week 2, Week 4, or Week 8 minus value at baseline over value at baseline" (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
InterventionPercent Change (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-27.4-25.7-21.1
CI-1038 2.5 mg/5 mg-15.1-14.2-14.1
CI-1038 5 mg/10 mg-23.9-23.2-24.0
CI-1038 5 mg/5 mg-16.2-15.1-10.8

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Change in Low Density Lipoprotein-Cholesterol/ High Density Lipoprotein-Cholesterol Ratio (LDL-C/HDL-C) From Baseline to Each Observation Point

Value at Week 2, Week 4, or Week 8 minus value at baseline (NCT00530946)
Timeframe: 2 weeks, 4 weeks, and 8 weeks

,,,
InterventionRatio (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-1.4-1.4-1.4
CI-1038 2.5 mg/5 mg-1.2-1.3-1.2
CI-1038 5 mg/10 mg-1.3-1.4-1.4
CI-1038 5 mg/5 mg-1.1-1.2-1.2

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Change in Total Cholesterol/ High Density Lipoprotein-Cholesterol Ratio (TC/HDL-C) From Baseline to Each Observation Point

Value at Week 2, Week 4, or Week 8 minus value at baseline (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
InterventionRatio (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-1.6-1.6-1.5
CI-1038 2.5 mg/5 mg-1.3-1.4-1.3
CI-1038 5 mg/10 mg-1.5-1.6-1.5
CI-1038 5 mg/5 mg-1.2-1.4-1.4

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Change in Systolic Blood Pressure From Baseline to Each Observation Point

Value at Week 2, Week 4, or Week 8 minus value at baseline (NCT00530946)
Timeframe: 2 weeks, 4 weeks, and 8 weeks

,,,
Interventionmm Hg (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-13.5-14.6-15.3
CI-1038 2.5 mg/5 mg-12.8-14.2-16.8
CI-1038 5 mg/10 mg-16.0-19.6-18.7
CI-1038 5 mg/5 mg-19.2-20.2-21.3

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Change in Diastolic Blood Pressure From Baseline to Each Observation Point

Value at Week 2, Week 4, or Week 8 minus value at baseline (NCT00530946)
Timeframe: 2 weeks, 4 weeks , and 8 weeks

,,,
Interventionmm Hg (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-6.0-8.2-8.7
CI-1038 2.5 mg/5 mg-4.9-5.3-7.7
CI-1038 5 mg/10 mg-8.2-9.2-9.9
CI-1038 5 mg/5 mg-8.1-9.4-12.0

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Change in Apolipoprotein B From Baseline to Each Observation Point

Value at Week 2, Week 4, or Week 8 minus value at baseline (NCT00530946)
Timeframe: 2 weeks, 4 weeks, and 8 weeks

,,,
Interventionmg/dL (Mean)
Week 2Week 4Week 8
CI-1038 2.5 mg/10 mg-45.8-47.2-46.4
CI-1038 2.5 mg/5 mg-36.6-40.1-40.2
CI-1038 5 mg/10 mg-44.4-45.8-45.1
CI-1038 5 mg/5 mg-33.5-36.6-36.6

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Percent Change in Low Density Lipoprotein-Cholesterol

"Percent of value at Week 8 minus value at baseline over value at baseline" (NCT00530946)
Timeframe: 8 weeks

InterventionPercent Change (Least Squares Mean)
CI-1038 2.5 mg/5 mg-37.2
CI-1038 2.5 mg/10 mg-42.5
CI-1038 5 mg/5 mg-34.3
CI-1038 5 mg/10 mg-40.6

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Change in Systolic Blood Pressure

Value at Week 8 minus value at baseline (NCT00530946)
Timeframe: 8 weeks

Interventionmm Hg (Least Squares Mean)
CI-1038 2.5 mg/5 mg-16.6
CI-1038 2.5 mg/10 mg-15.9
CI-1038 5 mg/5 mg-21.8
CI-1038 5 mg/10 mg-18.9

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Percentage of Patients With AVD Who Achieved LDL-C <70 mg/dL at Week 12

Patients with AVD Who Achieved LDL-C <70 mg/dL. AVD was defined as a history of myocardial infarction, stable angina, coronary artery procedures or evidence of clinically significant myocardial ischemia. (NCT00535405)
Timeframe: 12 Weeks

InterventionPercent of Patients (Mean)
Atorvastatin 10 mg10.0
Ezetimibe 10 mg/Simvastatin 20 mg44.4
Atorvastatin 20 mg31.6
Ezetimibe 10 mg/Simvastatin 40 mg65.8
Atorva 40 mg44.4

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Percentage of Patients Who Achieved LDL-C <70 mg/dL at Week 12

(NCT00535405)
Timeframe: 12 weeks

InterventionPercent of Patients (Mean)
Atorvastatin 10 mg9.9
Ezetimibe 10 mg/Simvastatin 20 mg51.3
Atorvastatin 20 mg26.1
Ezetimibe 10 mg/Simvastatin 40 mg68.2
Atorva 40 mg38.1

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Percentage of Patients Who Achieved LDL-C <100 mg/dL at Week 12

(NCT00535405)
Timeframe: 12 Weeks

InterventionPercent of Patients (Mean)
Atorvastatin 10 mg58.7
Ezetimibe 10 mg/Simvastatin 20 mg83.6
Atorvastatin 20 mg76.9
Ezetimibe 10 mg/Simvastatin 40 mg90.3
Atorva 40 mg79.5

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

(NCT00535405)
Timeframe: Baseline and 12 weeks

InterventionPercent change in LDL-C (Least Squares Mean)
Atorvastatin 10 mg-39.5
Ezetimibe 10 mg/Simvastatin 20 mg-54.2
Atorvastatin 20 mg-46.6
Ezetimibe 10 mg/Simvastatin 40 mg-59.1
Atorva 40 mg-50.8

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Percentage of Patients Without Atherosclerosis Vascular Disease (AVD) Who Achieved LDL-C <100 mg/dL or Patients With AVD Who Achieved LDL-C <70 mg/dL at Week 12

Patients with AVD Who Achieved LDL-C <70 mg/dL. AVD was defined as a history of myocardial infarction, stable angina, coronary artery procedures or evidence of clinically significant myocardial ischemia. (NCT00535405)
Timeframe: 12 Weeks

InterventionPercent of Patients (Mean)
Atorvastatin 10 mg45.0
Ezetimibe 10 mg/Simvastatin 20 mg69.0
Atorvastatin 20 mg61.3
Ezetimibe 10 mg/Simvastatin 40 mg82.1
Atorva 40 mg69.9

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Percentage of Patients With High Risk for CHD Who Achieved LDL-C <70 mg/dL at Week 12

Risk was assessed utilizing a history of established CHD or CHD risk equivalent and Framingham Risk scoring. (NCT00535405)
Timeframe: 12 Weeks

InterventionPercent of Patients (Mean)
Atorvastatin 10 mg10.9
Ezetimibe 10 mg/Simvastatin 20 mg54.3
Atorvastatin 20 mg28.9
Ezetimibe 10 mg/Simvastatin 40 mg69.2
Atorva 40 mg38.2

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Percent of Subjects in the Total Group and Each Cardiovascular Risk Group Achieving LDL-C Target After 4 Weeks of Treatment.

LDL-C Responders by visit and by risk group - FAS (NCT00540293)
Timeframe: Week 4

InterventionPercent subjects achieved LDL-C target (Mean)
Total81.9
Low Risk85.7
Medium Risk95.5
High Risk79.9

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Changes From Baseline in Selected Inflammatory Markers After 8 Weeks of Treatment.

Median baseline, and change from baseline in monocyte chemoattractant protein (MCP-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by risk group - FAS (NCT00540293)
Timeframe: Baseline, and 8 weeks

,,,
Interventionpg/dL (Median)
MCP-1 baselineMCP-1 change from baseline (week 8)IL-6 baselineIL-6 change from baseline (week 8)TNF-alpha baselineTNF-alpha change from baseline (week 8)
High Risk301.659.40.500.000.100.00
Low Risk305.2-15.00.300.000.100.00
Medium Risk317.7-22.40.40-0.100.200.00
Total302.739.80.400.000.100.00

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Percent of Subjects in the Total and Each Cardiovascular Risk Group Achieving Low Density Lipoprotein-cholesterol (LDL-C) Target After 8 Weeks of Treatment.

LDL-C Responders by visit and by risk group - full analysis set (FAS) (NCT00540293)
Timeframe: Week 8

InterventionPercentage of participants (Mean)
Total86.0
Low Risk92.9
Medium Risk95.5
High Risk84.3

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Subjects Who Achieved LDL-C Target With no Titration of Atorvastatin and After One Step Titration of Atorvastatin.

LDL-C responders at week 8 by titration status and risk groups - FAS, efficacy evaluation (EVAL), and FAS (no last observation carried forward, LOCF) (NCT00540293)
Timeframe: 8 weeks

,,,
InterventionParticipants (Number)
FAS population responders no titrationFAS population responders 1-step titrationEVAL population responders no titrationEVAL population responders 1-step titrationFAS population (no LOCF) no titrationFAS population (no LOCF) 1-step titration
High Risk274522444927152
Low Risk243223243
Medium Risk411391411
Total339563055333656

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Percent of Subjects Who Achieved LDL-C Target With no Titration of Atorvastatin and After One Step Titration of Atorvastatin.

LDL-C responders at week 8 by titration status and risk groups - FAS, efficay evaluation (EVAL), and FAS (no last observation carried forward, LOCF) (NCT00540293)
Timeframe: 8 weeks

,,,
Interventionpercentage of participants (Mean)
FAS population, no titrationFAS population, 1-step titrationEVAL population, no titrationEVAL population, 1-step titrationFAS population (no LOCF), no titrationFAS population (no LOCF), 1-step titration
High Risk87.280.889.881.687.180.8
Low Risk95.8100.095.5100.095.8100.0
Medium Risk97.6100.097.4100.097.6100.0
Total89.182.191.183.089.082.1

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Percent Changes From Baseline in Selected Inflammatory Markers After 8 Weeks of Treatment.

Percent changes from baseline in monocyte chemoattractant protein (MCP-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by risk group - FAS (NCT00540293)
Timeframe: 8 weeks

,,,
Interventionpercent (Median)
MCP-1 % change (week 8)IL-6 % change (week 8)TNF-alpha % change (week 8)
High Risk18.20.000.00
Low Risk-5.60.000.00
Medium Risk-8.0-12.500.00
Total14.00.000.00

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Percent Changes From Baseline in Lipid Parameters in Subjects in the Total Group and Each Cardiovascular Risk Group After 4 and 8 Weeks of Treatment

Mean percent changes from baseline in lipid parameters by risk group - FAS. HDL-C: high density lipoprotein-cholesterol; TC: total cholesterol; TG: triglyceride (NCT00540293)
Timeframe: weeks 4 and 8

,,,
InterventionPercent (Mean)
LDL-C % change from baseline (week 4)LDL-C % change from baseline (week 8)HDL-C % change from baseline (week 4)HDL-C % change from baseline (week 8)Non-HDL-C % change from baseline (week 4)Non-HDL-C % change from baseline (week 8)LDL-C/HDL-C ratio % change from baseline (week 4)LDL-C/HDL-C ratio % change from baseline (week 8)TC % change from baseline (week 4)TC % change from baseline (week 8)TG % change from baseline (week 4)TG % change from baseline (week 8)
High Risk-41.2-42.51.11.8-39.1-39.7-41.4-42.6-30.6-31.0-9.3-10.5
Low Risk-39.5-41.2-0.25.6-35.5-38.2-36.7-41.6-29.7-30.44.4-6.3
Medium Risk-39.6-39.37.76.7-37.7-38.3-44.1-42.9-28.5-29.2-8.3-7.0
Total-40.9-42.01.72.6-38.7-39.4-41.3-42.6-30.3-30.7-8.2-9.8

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Percent Change From Baseline in High Sensitive Circulating C-reactive Protein (Hs-CRP) After 4 and 8 Weeks of Treatment

Percent change from baseline in hs-CRP by risk group - FAS (NCT00540293)
Timeframe: 4 and 8 weeks

,,,
Interventionpercentage (Median)
Median % change from baseline (week 4)Median % change from baseline (week 8)
High Risk-16.197-20.561
Low Risk-13.941-18.621
Medium Risk-2.553-1.472
Total-12.346-18.605

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Changes in Lipid Parameters in Subjects in the Total Group and Each Cardiovascular Risk Group After 4 and 8 Weeks of Treatment

Mean baseline, change and percent change from baseline in lipid parameters by risk group - FAS. HDL-C: high density lipoprotein-cholesterol; TC: total cholesterol; TG: triglyceride (NCT00540293)
Timeframe: Weeks 4 and 8

,,,
Interventionmg/dL (ratio for Scalar) (Mean)
LDL-C baselineLDL-C (week 4)LDL-C (week 8)HDL-C baselineHDL-C (week 4)HDL-C (week 8)Non-HDL-C baselineNon-HDL-C (week 4)Non-HDL-C (week 8)LDL-C/HDL-C ratio baselineLDL-C/HDL-C Ratio (Scalar) week 4LDL-C/HDL-C Ratio (Scalar) week 8TC baselineTC (week 4)TC (week 8)TG baselineTG (week 4)TG (week 8)
High Risk147.7-62.4-64.448.2-0.20.0171.1-68.6-69.73.2-1.3-1.4219.3-68.8-69.7154.7-32.1-31.4
Low Risk187.0-73.8-77.650.5-0.82.1209.9-75.4-80.93.7-1.4-1.6262.3-78.2-80.7150.7-11.5-20.9
Medium Risk160.6-65.1-64.248.03.33.0187.1-71.3-72.13.4-1.5-1.5235.1-68.0-69.1152.3-16.6-18.5
Total151.7-63.5-65.348.30.10.5175.5-69.4-70.73.2-1.4-1.4223.9-69.4-70.4154.1-29.1-29.3

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Change From Baseline in High Sensitive Circulating C-reactive Protein (Hs-CRP) After 4 and 8 Weeks of Treatment

Median baseline, and change from baseline in hs-CRP by risk group - FAS (NCT00540293)
Timeframe: 4 and 8 weeks

,,,
Interventionmg/dL (Median)
BaselineMedian change from baseline (week 4)Median change from baseline (week 8)
High Risk0.122-0.010-0.018
Low Risk0.082-0.008-0.011
Medium Risk0.075-0.002-0.001
Total0.108-0.008-0.015

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Absolute Change From Baseline in Percent Hepatic Fat

Absolute change from Baseline in percent hepatic fat (NCT00559962)
Timeframe: Baseline and 12 weeks on study drug

,
InterventionPercent of Hepatic Fat (Mean)
Placebo0.03
AEGR-733 5 mg4.72
Placebo0.03
AEGR-733 2.5 mg4.95
AEGR-733 5 mg4.72
AEGR-733 7.5 mg3.94
AEGR-733 10 mg7.86
AEGR-733 5 mg + Atorvastatin 20 mg3.68
AEGR-733 5 mg + Fenofibrate 145 mg7.70
AEGR-733 5 mg + Ezetimibe 10 mg7.55

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Change in Fibrous Plaque Volume

Change in fibrous plaque volume between baseline and follow-up. This was derived by subtracting the baseline value from the 6-month value. (NCT00576576)
Timeframe: 6 months

Interventionmm^3 (Median)
Atorvastatin-3.3

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Change in Necrotic Core Volume

Virtual Histology-Intravascular Ultrasound (VH-IVUS) defined necrotic core cross sectional area (CSA) measured in each VH-IVUS frame and averaged over length of studied vessel at baseline and follow -up. Change in necrotic core CSA between baseline and follow-up was calculated (subtracting the baseline value from the follow-up value). (NCT00576576)
Timeframe: 6 months

Interventionmm^2 (Mean)
Atorvastatin0.07

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Change in Atheroma Volume

Change in atheroma volume between baseline and follow-up is reported. This was derived by subtracting the baseline value from the 6-month value. (NCT00576576)
Timeframe: 6 months

Interventionmm^3 (Median)
Atorvastatin-4.0

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Change in Mean C-Reactive Protein Level

(NCT00579098)
Timeframe: Baseline and 3 months

Interventionmg/dL (Mean)
Atorvastatin-0.75
Placebo2.1

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Change in Mean Quality of Life Score

A visual analogue scale (VAS) was used to collect the subject's perception of their current state of health/quality of life. The VAS consists of a vertical 20 centimeter scored line (like a thermometer) with the ends labelled best imaginable health state at the top (100) and worst imaginable health state at the bottom (0). The subject marked a single line to grade his/her own current level of function at the baseline visit and again at the 3 month visit. The average change in VAS score from baseline to 3 months later is reported for each treatment group. (NCT00579098)
Timeframe: Baseline and 3 months

Interventionunits on a scale (Mean)
Atorvastatin13
Placebo11

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Percentage of Subjects Without Atrial Arrhythmia at 3 Months

Percentage of subjects without atrial arrhythmia (as opposed to atrial fibrillation) recurrence, irrespective of symptoms. Atrial arrhythmias included AF, atrial tachycardia and atrial flutter. (NCT00579098)
Timeframe: Baseline through 3 months

InterventionPercentage of subjects (Number)
Atorvastatin85
Placebo88

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Percentage of Subjects Without Symptoms of Atrial Fibrillation at 3 Months

Asymptomatic recurrence was defined as any atrial arrhythmia lasting more than 30 seconds. This was assessed by an electrocardiogram (ECG) and 72-hour Holter monitor recordings. At the end of the study, 336 ECG and Holter recordings were available for analysis (172 in the atorvastatin group and 164 in the placebo group). (NCT00579098)
Timeframe: Baseline through 3 months

InterventionPercentage of subjects (Number)
Atorvastatin95
Placebo93.5

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Change in Lipid Levels

The change from baseline to 3 months in blood cholesterol levels (total cholesterol, LDL or low-density lipoprotein and HDL or high-density lipoprotein) was calculated. (NCT00579098)
Timeframe: Baseline and 3 months

,
Interventionmg/dL (Mean)
Change in total cholesterolChange in LDL (low-density lipoprotein) cholesteroChange in HDL (high-density lipoprotein) cholest.
Atorvastatin-50-473
Placebo1593

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Rate of Change in Mean of Maximal Posterior-wall Carotid Intima-media Thickness (cIMT)

Rate of change (mm/year) from baseline in mean of maximal posterior-wall carotid intima-media thickness (cIMT) of the left and right common carotid artery. The statistical model used change from baseline as the dependent variable, with time of cIMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. cIMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.005
Placebo + Atorvastatin-0.003

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Rate of Change in Composite of Mean of Maximal Posterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of maximal posterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.014
Placebo + Atorvastatin-0.008

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Rate of Change in Composite of Mean of the Mean Posterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of the mean posterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.010
Placebo + Atorvastatin-0.004

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Rate of Change in Composite of Mean of Maximal Posterior-wall and Anterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of maximal posterior-wall and anterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.003
Placebo + Atorvastatin-0.019

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Rate of Change in Mean Posterior-wall Carotid Intima-media Thickness (cIMT)

Rate of change (mm/year) from baseline in mean of posterior-wall carotid intima-media thickness (cIMT) of the left and right common carotid artery. The statistical model used change from baseline as the dependent variable, with time of cIMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. cIMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.006
Placebo + Atorvastatin0.000

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Non-HDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg88.95
Atorvastatin 80 mg95.41

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VLDL-C During the 104 Week Treatment Period

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg26.05
Atorvastatin 80 mg25.03

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Apolipoprotein A-1 Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg146.81
Atorvastatin 80 mg137.68

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Apolipoprotein B Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg72.55
Atorvastatin 80 mg75.12

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Apoliprotein B/Apolipoprotein A-1 Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

InterventionRatio (Least Squares Mean)
Rosuvastatin 40 mg0.51
Atorvastatin 80 mg0.56

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Change From Baseline to End of Study (Week 104) in Total Atheroma Volume (TAV)

Change in TAV, as measured by IVUS, computed as TAV(Week 104)-TAV(baseline) where TAV is the sum(EEMcsa-LUMENcsa)/n. n is the number of cross-sections measured. TAV for each patient is calculated as the average area of atheroma per cross-section multiplied by the median number of cross-sections measured for all patients in the analysis population. (NCT00620542)
Timeframe: End of study (Week 104)

Interventionmm^3 (Median)
Rosuvastatin 40 mg-6.39
Atorvastatin 80 mg-4.42

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HDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg50.43
Atorvastatin 80 mg48.64

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LDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg62.64
Atorvastatin 80 mg70.18

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LDL-C/HDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

InterventionRatio (Least Squares Mean)
Rosuvastatin 40 mg1.30
Atorvastatin 80 mg1.50

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Change From Baseline to End of Study (Week 104) in Percent Atheroma Volume (PAV)

"Change in PAV computed as PAV(Week 104)-PAV(baseline) where PAV is calculated as:~[sum(EEMcsa-LUMENcsa)/sum EEMcsa]*100 where EEMcsa is the cross-sectional area of the external elastic membrane and LUMENcsa is the cross-sectional area of the lumen, as measured by intravascular ultrasound IVUS of a coronary artery in patients with CAD." (NCT00620542)
Timeframe: End of study (Week 104)

InterventionPercent change (Median)
Rosuvastatin 40 mg-1.22
Atorvastatin 80 mg-0.99

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Non-HDL-C/HDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

InterventionRatio (Least Squares Mean)
Rosuvastatin 40 mg1.88
Atorvastatin 80 mg2.08

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Numbers of Patients Showing Regression in PAV

Regression defined as a change from baseline in PAV < 0 (NCT00620542)
Timeframe: End of study (Week 104)

InterventionParticipants (Number)
Rosuvastatin 40 mg356
Atorvastatin 80 mg328

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Numbers of Patients Showing Regression in TAV

Regression defined as a change from baseline in TAV < 0 (NCT00620542)
Timeframe: End of study (Week 104)

InterventionParticipants (Number)
Rosuvastatin 40 mg371
Atorvastatin 80 mg336

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Total Cholesterol Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg139.38
Atorvastatin 80 mg144.05

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Total Cholesterol/HDL-C Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

InterventionRatio (Least Squares Mean)
Rosuvastatin 40 mg2.88
Atorvastatin 80 mg3.08

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Triglycerides Blood Level

Time-weighted average is calculated as the lipid value times the number of days since last lipid assessment, summed for all and divided by the number of days from Part B randomization to date of the last lipid evaluation. (NCT00620542)
Timeframe: 104 weeks

Interventionmg/dL (Least Squares Mean)
Rosuvastatin 40 mg132.50
Atorvastatin 80 mg126.58

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

To Compare the percentage of variation from baseline Apolipoprotein B/Apolipoprotein A1 ratio and after 8 weeks of treatment. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: baseline and after 8 weeks of treatment

Interventionpercent. Apolipoprotein B/A1 decrease (Mean)
Atorvastatin-30.9
Pravastatin-26
Rosuvastatin-31.9

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

To Compare numbers of patients achieving the LDL-C goal according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP). As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data. The percentage of patients achieving the NCEP-ATP III LDL-C goal. ATP III is categorized into 3 risk categories:(1) established CHD and CHD risk equivalents(2) multiple risk factors(3) zero to one (0-1) risk factor (NCT00631189)
Timeframe: from baseline and after 8 weeks of treatment

InterventionParticipants (Number)
Atorvastatin42
Pravastatin22
Rosuvastatin38

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To Evaluate Clinical and Laboratory Safety

Serious Adverse Event and Adverse Event reported throughout the study (NCT00631189)
Timeframe: duration of study

InterventionAdverse Events (Number)
Initial Phase8
Atorvastatin9
Pravastatin8
Rosuvastatin5

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

Compare the percentage of HDL-C (High Density Lipoprotein Cholesterol) variation taking baseline value as a reference and after 8 weeks of treatment. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: After 8 weeks of treatment

Interventionpercentage of HDL-C increase (Mean)
Atorvastatin4.4
Pravastatin7.9
Rosuvastatin11.3

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

To compare the percentage of total cholesterol variation taking baseline value as a reference. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: from baseline and after 8 weeks of treatment

Interventionpercentage of total cholesterol decrease (Mean)
Atorvastatin-28.6
Pravastatin-20.4
Rosuvastatin-25.2

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

To compare the percentage of variation of C-reactive protein (CRP) taking baseline values as reference. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: baseline and after 8 weeks of treatment

Interventionpercent of variation of C-reactive prot. (Mean)
Atorvastatin37.3
Pravastatin33.1
Rosuvastatin15.2

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Compare the Percentage of Variation of Phospholipase A2 (PLA2)

To Compare the percentage of variation of phospholipase A2 (PLA2) taking baseline value as a reference. As the recruitment target was not reached at the date initially planned, and view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: from baseline and after 8 weeks of treatment

Interventionpercent of variation of phospholipase A2 (Mean)
Atorvastatin5.6
Pravastatin13
Rosuvastatin2.9

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

To compare the percentage of variation from baseline triglycerides values and after 8 weeks. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: Baseline and after 8 weeks of treatment

Interventionpercentage of triglycerides decrease (Mean)
Atorvastatin-19.2
Pravastatin-6.1
Rosuvastatin-8.7

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

To compare the percentages of LDL-C level variation. As the recruitment target was not reached at the date initially planned, and in view of the recruitment difficulties, AstraZeneca decided not to extend the patient recruitment period and to perform only a descriptive analysis of the data (NCT00631189)
Timeframe: Change from baseline and after 8 weeks of treatment

Interventionpercentage of LDL-C decrease (Mean)
Atorvastatin-39.4
Pravastatin-30.3
Rosuvastatin-37.6

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Mean Percent Change in High-Density Lipoprotein Cholesterol (HDL-C) From Baseline to Final Visit

[(Week 12 HDL-C minus baseline HDL-C)/baseline HDL-C] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe13.0
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe4.2

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Mean Percent Change in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) From Baseline to Final Visit

[(Week 12 non-HDL-C minus baseline non-HDL-C)/baseline non-HDL-C] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-55.6
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-51.0

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Mean Percent Change in Apolipoprotein AI (apoAI) From Baseline to Final Visit

[(Week 12 apoAI minus baseline apoAI)/baseline apoAI] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe1.8
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-1.3

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Mean Percent Change in Apolipoprotein B (apoB) From Baseline to Final Visit

[(Week 12 apoB minus baseline apoB)/baseline apoB] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-49.1
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-44.7

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Median Percent Change in Triglycerides From Baseline to Final Visit

[(Week 12 triglycerides minus baseline triglycerides)/baseline triglycerides] x 100 (NCT00639158)
Timeframe: Baseline to 12 Weeks (Final Visit)

InterventionPercent change (Median)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-57.3
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-39.7

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Mean Percent Change in Very Low-Density Lipoprotein Cholesterol (VLDL-C) From Baseline to Final Visit

[(Week 12 VLDL-C minus baseline VLDL-C)/baseline VLDL-C] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (final visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-57.8
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-41.1

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Median Percent Change in High-Sensitivity C-Reactive Protein (hsCRP) From Baseline to Final Visit

[(Week 12 hsCRP minus baseline hsCRP)/baseline hSCRP] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Median)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-52.1
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-40.3

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Mean Percent Change in Apolipoprotein CIII (apoCIII) From Baseline to Final Visit

[(Week 12 apoCIII minus baseline apoCIII)/baseline apoCIII] x 100 (NCT00639158)
Timeframe: Baseline to 12 weeks (Final Visit)

InterventionPercent change (Mean)
ABT-335 + 40 mg Atorvastatin + 10 mg Ezetimibe-42.5
Placebo + 40 mg Atorvastatin + 10 mg Ezetimibe-25.3

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

(NCT00652327)
Timeframe: Assessed at the end of 8 weeks of treatment (from baseline to endpoint)

InterventionPercentage change (Mean)
Ezetimibe + Statin-26.56
Double Statin-9.7

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Number of Participants With Adverse Events and Adverse Reactions

"An adverse event is any unfavorable medical event occurring in a subject to whom an investigational product is administered, and a causal relationship between the administered investigational product and an adverse event is not always clarified.~That is, an adverse event is any unfavorable or unintended sign (including an abnormal change in laboratory test values), symptom, or disease, and a causal relationship to the relevant investigational product is not considered.~Any adverse event that was considered treatment-related was considered an adverse reaction." (NCT00654095)
Timeframe: Throughout 1 year of study

InterventionParticipants (Number)
Adverse EventsAdverse Reactions
Ezetimibe + Atorvastatin14161

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Data Available)

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of participants (Number)
Week 4 (N=27)Week 12 (N=27)Week 24 (N=26)Week 48 (N=26)
Atorvastatin63.048.261.557.7

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Percentage of Participants Experiencing at Least One Adverse Event (AE)

AEs were graded by the clinicians according to the Division of AIDS (DAIDS) AE Grading Table (see references in the Protocol Section) as follows: Grade 1=Mild, Grade 2=Moderate, Grade 3=Severe, Grade 4=Potentially Life-Threatening, Grade 5=Death. The primary outcome measure includes any AE of grade 3 or higher and liver function tests (LFTs) of grade 2 or higher. (NCT00663234)
Timeframe: Study entry to weeks 12, 24, and 48

Interventionpercentage of participants (Number)
Week 12Week 24Week 48
Atorvastatin21.421.428.6

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Per Protocol)

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of participants (Number)
Week 4Week 12Week 24Week 48
Atorvastatin69.269.284.653.9

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Percentage of Participants With Undetectable Plasma HIV-1 RNA

Undetectable is defined as plasma HIV-1 RNA below the lower limit of quantification of the assay used. (NCT00663234)
Timeframe: Study entry and weeks 12, 24, and 48

Interventionpercentage of participants (Number)
Week 0 (N=28)Week 12 (N=26)Week 24 (N=26)Week 48 (N=26)
Atorvastatin71.069.062.069.0

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria by NNRTI Treatment

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

,
Interventionpercentage of participants (Number)
Week 4Week 12Week 24Week 48
NNRTI-exposed66.755.644.455.6
NNRTI-unexposed57.942.163.252.6

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria by Age Group

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

,
Interventionpercentage of participants (Number)
Week 4Week 12Week 24Week 48
10 to 14 Years Old71.428.671.471.4
15 to 23 Years Old57.152.452.447.6

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria and Did Not Experience a Primary Safety Endpoint Attributable to Study Drug

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of participants (Number)
Week 4Week 12Week 24Week 48
Atorvastatin57.750.057.753.9

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Percentage of Participants Who Met the LDL Cholesterol (LDL-C) Efficacy Criteria (Intention to Treat)

Efficacy was defined as having LDL-C of 110 mg/dL or less or at least 30% decline in LDL-C from baseline to the specified week. (NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of participants (Number)
Week 4Week 12Week 24Week 48
Atorvastatin60.746.457.153.6

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Percentage of Participants Experiencing at Least One Adverse Event (AE) by Age Group

AEs were graded by the clinicians according to the Division of AIDS (DAIDS) AE Grading Table (see references in the Protocol Section) as follows: Grade 1=Mild, Grade 2=Moderate, Grade 3=Severe, Grade 4=Potentially Life-Threatening, Grade 5=Death. The primary outcome measure includes any AE of grade 3 or higher and liver function tests (LFTs) of grade 2 or higher. (NCT00663234)
Timeframe: Study entry to weeks 12, 24, and 48

,
Interventionpercentage of participants (Number)
Week 12Week 24Week 48
10 to 14 Years Old14.314.328.6
15 to 23 Years Old23.823.828.6

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Percent Change in Triglycerides (TG) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of TG at study entry (Mean)
Percent change in TG at Week 4 (N=27)Percent change in TG at Week 12 (N=27)Percent change in TG at Week 24 (N=26)Percent change in TG at Week 48 (N=26)
Atorvastatin-9.5-12.6-11.3-12.6

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Percent Change in LDL Cholesterol (LDL-C) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of LDL-C at study entry (Mean)
Percent change in LDL-C at Week 4 (N=27)Percent change in LDL-C at Week 12 (N=27)Percent change in LDL-C at Week 24 (N=26)Percent change in LDL-C at Week 48 (N=26)
Atorvastatin-30.3-26.5-28.0-26.4

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Percent Change in Interleukin 6 (IL-6) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 12, 24, and 48

Interventionpercentage of IL-6 at study entry (Median)
Percent change in IL-6 at Week 12 (N=24)Percent change in IL-6 at Week 24 (N=23)Percent change in IL-6 at Week 48 (N=24)
Atorvastatin-1-19-11.5

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Percent Change in High-sensitivity CRP (Hs-CRP) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 12, 24, and 48

Interventionpercentage of hs-CRP at study entry (Median)
Percent change in hs-CRP at Week 12 (N=25)Percent change in hs-CRP at Week 24 (N=23)Percent change in hs-CRP at Week 48 (N=24)
Atorvastatin0-200

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Percent Change in HDL-cholesterol (HDL-C) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of HDL-C at study entry (Mean)
Percent change in HDL-C at Week 4 (N=27)Percent change in HDL-C at Week 12 (N=27)Percent change in HDL-C at Week 24 (N=26)Percent change in HDL-C at Week 48 (N=26)
Atorvastatin1.82.33.04.2

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Percent Change in Fasting Total Cholesterol (TC) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 4, 12, 24, and 48

Interventionpercentage of TC at study entry (Mean)
Percent change in TC at Week 4 (N=27)Percent change in TC at Week 12 (N=27)Percent change in TC at Week 24 (N=26)Percent change in TC at Week 48 (N=26)
Atorvastatin-23.8-21.1-22.5-21.5

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Percent Change in Apolipoprotein B (Apo B) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 12, 24, and 48

Interventionpercentage of Apo B at study entry (Mean)
Percent change in Apo B at Week 12 (N=24)Percent change in Apo B at Week 24 (N=23)Percent change in Apo B at Week 48 (N=24)
Atorvastatin-27.2-25.1-23.8

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Percent Change in Apolipoprotein A1 (Apo A-1) From Study Entry

(NCT00663234)
Timeframe: Study entry and weeks 12, 24, and 48

Interventionpercentage of Apo A-1 at study entry (Mean)
Percent change in Apo A-1 at Week 12 (N=24)Percent change in Apo A-1 at Week 24 (N=23)Percent change in Apo A-1 at Week 48 (N=24)
Atorvastatin0.82.40.3

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Change in Non-HDL Cholesterol, HDL Cholesterol, TG Levels From Baseline to End of Treatment

Mean percent changes in non-HDL cholesterol, HDL cholesterol, TG levels from the double-blind (DB) baseline (Week 0) to end-of-treatment (Week 52), and from the open-label (OL) baseline (week 12 of DB study) to end of treatment (Week 52) (NCT00664859)
Timeframe: 52 weeks from DB baseline and 40 weeks from OL baseline

,,
Interventionpercent change (Mean)
Non-HDL cholesterol, change from DB baselineNon-HDL cholesterol change from OL baselineTriglycerides change from DB baselineTriglycerides change from OL baselineHDL cholesterol change from DB baselineHDL cholesterol change from OL baseline
Atorvastatin 40 mg-43.62.8-51.2-19.116.310.1
Fenofibrate 145 mg-42.0-29.6-42.1-5.217.5-2.4
LCP-AtorFen 40/100mg-48.22.6-53.111.422.12.1

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Change in LDL Cholesterol, VLDL, Total Cholesterol, Apo A-1, and Apo B From Baseline to End of Treatment

Mean percent changes in LDL cholesterol, VLDL, total cholesterol, Apo A-1, and Apo B from the double-blind (DB) baseline (Week 0) to end-of-treatment (Week 52), and from the open-label (OL) baseline (week 12) to end-of-treatment (Week 52) (NCT00664859)
Timeframe: 52 weeks from DB baseline and 40 weeks from OL baseline

,,
InterventionPercent change (Mean)
LDL-C change from DB baselineLDL-C change from OL baselineVLDL-C change from DB baselineVLDL-C change from OL baselineTotal-C change from DB baselineTotal-C change from OL baselineApo A-1 change from DB baselineApo-A-1 change from OL baselineApo B change from DB baselineApo B change from OL baseline
Atorvastatin 40 mg-39.314-51.1-18.7-33.84.61.01.9-38.9-1.5
Fenofibrate 145 mg-40.9-33.6-42.0-5.5-32.8-24.40.4-5.1-36.8-25.5
LCP-AtorFen 40/100mg-44.82.1-53.612.7-36.51.53.2-1.4-42.43.1

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Insulin Sensitivity Index

Insulin sensitivity index was assessed during the final steady state 30 minutes of a high dose hyperinsulinaemic euglycaemic clamp (insulin infusion rate 1.5 mIU/kg/min). During this part of the clamp, insulin was infused at 1.5mIU/kg/min and the glucose concentration was maintained at 5 mmol/L using a dextrose infusion. The whole body insulin mediated glucose disposal rate (M value - mg/kg/min) was estimated from the total amount of glucose infused during the last 30 minutes of the clamp. The mean of four serum insulin concentrations was taken during this 30 minutes to determine the steady state insulin concentration (I value - milliunits/litre). M value/I value defined the insulin sensitivity index. (NCT00666029)
Timeframe: 6 months

Interventionmg*kg^-1*min^-1*mIU^-1*L^-1 (Mean)
Atorvastatin0.56
Placebo0.41

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Muscle Microvascular Function

Skeletal muscle microvascular function assessed (Filtrass plethysmographic system) using a passive inductive transducer (Compumedics.dwl, Singen, Germany) and a small pressure step venous congestion protocol. Fluid filtration rate (Jv mL min-1 100 mL-1), measured from the slope of limb volume change in response to each pressure step (10 mmHg steps to 60 mmHg around the thigh) over the last 2 minutes of its application, to allow for completion of vascular filling, and plotted against cuff pressure (Pcuff). The slope of this relationship, at pressures above those giving rise to net filtration, is a measure of Kf, microvascular filtration capacity, a function of exchange surface area and permeability. The CV for Kf measurement was 14.5%. (NCT00666029)
Timeframe: 6 months

Intervention10^3 mL*min^-1*100ml^-1*mmHg^-1 (Mean)
Atorvastatin3.7
Placebo4.0

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Percentage of Patients Achieved National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III Guideline (2001) Low Density Lipoprotein-Cholesterol (LDL-C) Goal After Titration

"The percentage of patients achieved LDL-C goal is done in ITT population.~National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guideline (2001) LDL-C goal:~Moderately high risk: 2+ risk factors (10-year risk 10%-20%): LDL-C goal < 3.36mmol/L(130mg/dL), non-HDL-C goal < 4.14mmol/L (160mg/dL) ; High risk: Coronary Heart Disease (CHD) or CHD risk equivalents (10-year risk >20%): LDL-C goal< 2.60mmol/L (100mg/dL), non-HDL-C goal < 3.36mmol/L (130mg/dL)" (NCT00683618)
Timeframe: from week 6 to week 12

Interventionpercentage of patients (Number)
Rosuvastatin 5mg41.2
Rosuvastatin 10mg47.6

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Percentage Change From Baseline in Apolipoprotein A-I (ApoA-I) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg3.67
Rosuvastatin 10mg4.25
Atorvastatin 10mg1.79

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Percentage Change From Baseline in Non High Density Lipoprotein Cholesterol/High Density Lipoprotein Cholesterol (nonHDL-C/HDL-C) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-41.79
Rosuvastatin 10mg-56.63
Atorvastatin 10mg-48.33

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6 weeksPercentage of Patients Achieved ATP III Guideline (2001) Non High Density Lipoprotein-Cholesterol (nonHDL-C) Goal at Week 6

"The percentage of patients achieved LDL-C goal is done in ITT population.~National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guideline (2001) LDL-C goal:~Moderately high risk: 2+ risk factors (10-year risk 10%-20%): LDL-C goal < 3.36mmol/L(130mg/dL); non-HDL-C goal < 4.14mmol/L (160mg/dL) ; High risk: Coronary Heart Disease (CHD) or CHD risk equivalents (10-year risk >20%): LDL-C goal< 2.60mmol/L (100mg/dL),non-HDL-C goal < 3.36mmol/L (130mg/dL)" (NCT00683618)
Timeframe: week 6

Interventionpercentage of patients (Number)
Rosuvastatin 5mg66.9
Rosuvastatin 10mg78.4
Atorvastatin 10mg60.4

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Percentage Change From Baseline in Apolipoprotein B (ApoB) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-36.55
Rosuvastatin 10mg-41.21
Atorvastatin 10mg-34.67

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Percentage Change From Baseline in Apolipoprotein B/Apolipoprotein A I (ApoB/ApoA-I) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-37.62
Rosuvastatin 10mg-41.87
Atorvastatin 10mg-35.15

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Percentage Change From Baseline in High Density Lipoprotein-Cholesterol (HDL-C) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg5.63
Rosuvastatin 10mg6.82
Atorvastatin 10mg3.64

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Percentage Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) Concentration After 6 Weeks of Treatment Comparing Rosuvastatin 10mg With Atorvastatin 10mg

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.025 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

InterventionPercent change (Least Squares Mean)
Rosuvastatin 10mg-46.28
Atorvastatin 10mg-38.67

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Percentage Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) Concentration After 6 Weeks of Treatment Comparing Rosuvastatin 5mg With Atorvastatin 10mg

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a two-sided significance level of 0.025 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-41.70
Atorvastatin 10mg-38.67

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Percentage Change From Baseline in Low Density Lipoprotein Cholesterol/High Density Lipoprotein Cholesterol (LDL-C/HDL-C) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-44.07
Rosuvastatin 10mg-50.27
Atorvastatin 10mg-41.04

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Percentage of Patients Achieved ATP III Guideline (2001) Low Density Lipoprotein Cholesterol (LDL-C) Goal at Week 6

"The percentage of patients achieved LDL-C goal is done in ITT population.~National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guideline (2001) LDL-C goal:~Moderately high risk: 2+ risk factors (10-year risk 10%-20%): LDL-C goal < 3.36mmol/L(130mg/dL), non-HDL-C goal < 4.14mmol/L (160mg/dL) ; High risk: Coronary Heart Disease (CHD) or CHD risk equivalents (10-year risk >20%): LDL-C goal< 2.60mmol/L (100mg/dL), non-HDL-C goal < 3.36mmol/L (130mg/dL)" (NCT00683618)
Timeframe: week 6

Interventionpercentage of patients (Number)
Rosuvastatin 5mg61.0
Rosuvastatin 10mg79.1
Atorvastatin 10mg58.3

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Percentage Change From Baseline in Non High Density Lipoprotein-Cholesterol (nonHDL-C) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-38.60
Rosuvastatin 10mg-46.08
Atorvastatin 10mg-38.50

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Percentage Change From Baseline in Total Cholesterol (TC ) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-29.62
Rosuvastatin 10mg-33.14
Atorvastatin 10mg-28.06

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Percentage Change From Baseline in Total Cholesterol/High Density Lipoprotein-Cholesterol (TC/HDL-C) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

Interventionpercent change (Least Squares Mean)
Rosuvastatin 5mg-32.95
Rosuvastatin 10mg-38.04
Atorvastatin 10mg-31.92

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Percentage Change From Baseline in Triglycerides (TG) at Week 6

Analyzed with analysis of covariance (ANCOVA) model with factors fitted for treatment, centre, risk factor, lipid concentration at baseline, treatment by centre and treatment by risk factor with a significance level of 0.05 on ITT population. (NCT00683618)
Timeframe: baseline, 6 weeks

InterventionPercent change (Least Squares Mean)
Rosuvastatin 5mg-20.09
Rosuvastatin 10mg-22.05
Atorvastatin 10mg-20.67

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Percentage of Participants Who Experience at Least 1 Adverse Event (AE)

An AE was any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with use of a medicinal product, regardless of whether or not it was considered related to the medicinal product. The percentage of participants that reported at least 1 AE was summarized (NCT00687271)
Timeframe: Up to 14 days post last dose of study drug (up to 6 weeks)

InterventionPercentage of Participants (Number)
MK-6213 160 mg + Atorvastatin 20 mg33.0
Atorvastatin 20 mg37.9
MK-6213 160 mg29.2
Placebo41.7

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Percentage of Participants That Had Study Drug Discontinued Due to an AE

An AE was defined as any untoward medical occurrence in a participant which does not necessarily have a causal relationship with the treatment. An AE was any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease temporally associated with use of a medicinal product, regardless of whether or not it was considered related to the medicinal product. The percentage of participants who had study drug discontinued due to an AE was summarized. (NCT00687271)
Timeframe: up to 4 weeks

InterventionPercentage of Participants (Number)
MK-6213 160 mg + Atorvastatin 20 mg1.1
Atorvastatin 20 mg3.1
MK-6213 160 mg1.0
Placebo0.0

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Percentage Change From Baseline in Total Cholesterol (TC)

Blood collected at baseline (predose) and after 4 weeks of treatment to determine TC levels. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage Change (Least Squares Mean)
MK-6213 160 mg + Atorvastatin 20 mg-35.1
Atorvastatin 20 mg-27.6
MK-6213 160 mg-8.5
Placebo2.5

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Percentage Change From Baseline in TG

Blood collected at baseline (predose) and after 4 weeks of treatment to determine TG levels. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage of Participants (Median)
MK-6213 160 mg + Atorvastatin 20 mg-24.2
Atorvastatin 20 mg-25.9
MK-6213 160 mg1.6
Placebo-7.1

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

Blood collected at baseline (predose) and after 4 weeks of treatment to determine non-HDL-C levels. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage Change (Least Squares Mean)
MK-6213 160 mg + Atorvastatin 20 mg-46.6
Atorvastatin 20 mg-38.0
MK-6213 160 mg-11.4
Placebo2.5

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

Blood collected at baseline (predose) and after 4 weeks of treatment to determine LDL-C levels. LDL-C was calculated using the Friedewald equation. If triglycerides (TG) exceeded 400 mg/dL (4.6 mmol/L), LDL-C was determined by reflex beta-quantitation method. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage Change (Least Squares Mean)
MK-6213 160 mg + Atorvastatin 20 mg-50.7
Atorvastatin 20 mg-40.6
MK-6213 160 mg-13.3
Placebo4.6

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Percentage Change From Baseline in HDL-C

Blood collected at baseline (predose) and after 4 weeks of treatment to determine HDL-C levels. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage Change (Least Squares Mean)
MK-6213 160 mg + Atorvastatin 20 mg3.8
Atorvastatin 20 mg6.2
MK-6213 160 mg1.4
Placebo2.1

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Percentage Change From Baseline in Apolipoprotein B (ApoB)

Blood collected at baseline (predose) and after 4 weeks of treatment to determine ApoB levels. The percentage change from baseline at Week 4 was summarized. (NCT00687271)
Timeframe: Baseline (predose) and Week 4

InterventionPercentage Change (Least Squares Mean)
MK-6213 160 mg + Atorvastatin 20 mg-40.4
Atorvastatin 20 mg-32.7
MK-6213 160 mg-8.8
Placebo3.5

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Percent Changes in LDL-C at Week 4 + Baseline Serum Lipoproteins (TC, Non-HDL, VLDL, TGs, HDL-C, Apolopoproteins A1 and B), High Sensitivity C-reactive Protein and Change in Body Weight.

(NCT00690443)
Timeframe: Baseline and 4 weeks

,
InterventionPercent (Mean)
Change in LDL-CChange in TCChange in TGsChange in HDL-CChange in non-HDL-CChange in Apo BChange in Apo A-1Change in hs-CRPChange in body weight
Atorvastatin 20 mg-42.5-31.3-21.56.7-39.6-33.64.8-12.00.0
Atorvastatin 20 mg + Lomitapide-51.0-38.1-17.8-1.9-45.8-37.7-7.860.5-0.7

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Percent Change in LDL-C After 8 Weeks of Therapy

(NCT00690443)
Timeframe: Baseline and 8 weeks of treatment

InterventionPercent Change (Mean)
Atorvastatin 20 mg-39.6
Atorvastatin 20 mg + Lomitapide-49.9

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Percentage Aldofluor Positive Cells

The primary outcome measure is the percentage of cells of total analyzed that are positive for the Aldofluor assay. This commercially available assay tests cells for the enzyme aldehyde dehydrogenase that is expressed in stem cells and other early life cycle undifferentiated cells. It thus provides a measure of circulating primordial cells or cells that may serve as progenitors of destination mature cells. The percentages are designed from Facscan analysis of prepared blood cells and are quantified by quadrants defined by specific fluorescent bands and cell size distribution. The quantification of cells thus defined in the four quadrants is automatically determined by software resident in the facscan analysis system. (NCT00701220)
Timeframe: Baseline - 6 months

InterventionPercentage Aldefluor positive cells (Mean)
Ischemic Cardiomyopathy6.37
NonIschemic Cardiomyopathy5.7

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Change in Endothelial Progenitor Cells

Change in Endothelial Progenitor Cells (EPC) was assessed by extracting white blood cells from blood samples and labeling the white blood cells using the ALDEFLOUR system. Facscan analysis was then performed first isolating lymphocytic and monocytic cell lines, which contain the EPC populations, using forward versus side scatter plots. These cells were then scanned for fluorescence in the ALDEFLUOR frequency range allowing enumeration of progenitor cell lines. The measures of fluorescent cells was compared to numbers of unstained cells having the same back scatter range to correct for any background fluorescence. (NCT00701220)
Timeframe: Baseline - 6 months

InterventionPercentage of EPCs (Mean)
Ischemic Cardiomyopathy-10.01
NonIschemic Cardiomyopathy5.19

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Percent Reduction From Baseline in TBRmeanmax of the Qualifying Segment in Statin-naive Participants

Vascular plaque inflammation was measured by 18FDG-PET imaging. Uptake of FDG by the carotid and thoracic aorta is expressed as the target, vessel wall to background, lumen ratio (TBR). TBRmax of an axial cross section of a vessel (a slice) is defined as the maximum TBR within a slice and TBRmeanmax is the mean of TBRmax for all slices in the qualifying segment. The qualifying segment is the left or right carotid or thoracic aorta with the greatest FDG uptake value at Baseline. (NCT00703261)
Timeframe: Baseline and Week 12

InterventionPercent reduction (Geometric Mean)
Statin-Naive Participants2.3

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Percent Reduction From Baseline in TBRmeanmax of the Qualifying Segment

Vascular plaque inflammation was measured by 18FDG-PET imaging. Uptake of FDG by the carotid and thoracic aorta is expressed as the target, vessel wall to background, lumen ratio (TBR). TBRmax of an axial cross section of a vessel (a slice) is defined as the maximum TBR within a slice and TBRmeanmax is the mean of TBRmax for all slices in the qualifying segment. The qualifying segment is the left or right carotid or thoracic aorta with the greatest FDG uptake value at Baseline. (NCT00703261)
Timeframe: Baseline and Week 12

InterventionPercent reduction (Geometric Mean)
10 mg Atorvastatin1.4
80 mg Atorvastatin5.8

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Composite of Cardiovascular Endpoints: Number of Participants With Cardiovascular Disease Death, Non-fatal Heart Attack, Stroke, and Worsening Ischemia Requiring Medical Interventions

Any cardiovascular events such as death from any cause, nonfatal myocardial infarction, stroke, and revascularization procedures (PCI or CABG) due to unstable ischemia will be recorded and verified. (NCT00715273)
Timeframe: Measured at Years 3, 4, and 5

,,
InterventionParticipants (Count of Participants)
Composite Measured at Year 3Composite Measured at Year 4 (cumulative)Composite Measured at Year 5 (cumulative)
1 - Single Therapy Group679
2 - Double Therapy Group61111
3 - Triple Therapy Group799

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Annualized LRNC and Wall Volume Changes in Carotid Plaque Composition, as Assessed by MRI

"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3

,,
Interventionpercentage change/year (Mean)
LRNC changeWall Volume change
1 - Single Therapy Group-1.6-0.6
2 - Double Therapy Group-3.6-1.4
3 - Triple Therapy Group-2.8-1.2

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Annualized LRNC Volume Change in Carotid Plaque Composition, as Assessed by MRI

"The primary endpoint of this study is carotid plaque lipid composition identified by MRI. The determination of plaque lipid content for each carotid artery will be performed using the automated interactive system. These measurements will be performed from the MRI scans at four time points blinded to time sequence of MRI examinations, patient treatment, lipid levels and clinical course.~Volume Measurements: Contours were placed around the lumen, outer-wall boundaries, and plaque features of carotid artery. (Arterial wall area) = (outer-wall area) - (lumen area). Volume calculated as: area x 2 mm (slice thickness). Tissue volume/wall volume x (100%) is presented as percentage. Annualized change presented mm^3/year (for volume) and as percentage change/year." (NCT00715273)
Timeframe: Measured at Years 1, 2, and 3

Interventionmm^3/year (Mean)
1 - Single Therapy Group-4.6
2 - Double Therapy Group-15.1
3 - Triple Therapy Group-9.4

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Apo-A1 Production Rate

The apolipoprotein A-I production rate using (5,5,5-2H3-L-leucine) was measured following each of the three study periods i.e following 4 weeks of atorvastatin 10 mg/day, following 8 further weeks of ABT335 135 mg/day added to atorvastatin and following 10 further weeks of ER niacin 2000 mg/day and aspirin 325 mg/day added to atorvastatin+ABT335. (NCT00728910)
Timeframe: 4 weeks, 12 weeks and 22 weeks

Interventionmg/kg/day (Mean)
Atorvastatin14.2
Atorvastatin+ABT33514.2
Atorvastatin+ABT335+Niaspan13.8

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Post-prandial Triglyceride Incremental Area Under the Curve (iAUC)

Triglyceride iAUC was measured during an oral fat tolerance test administered after 4 weeks of atorvastatin 10 mg/day , a further 8 weeks of atorvastatin 10mg /day+ABT335 135mg/day and then after a further 10 weeks of atorvastatin 10 mg/day+ABT335 135 mg/day+Niaspan 2000 mg/day. The standardized oral fat load was administered one hour post medication dosing and blood was collected prior to drug dosing, prior to the oral fat load and hourly thereafter for 10 hours (0,1,2,3,4,5,6,7,8,9,10,12 hrs post drug dosing) (NCT00728910)
Timeframe: 4 weeks, 12 weeks, 22 weeks

Interventionmg/dl*h (Mean)
Atorvastatin770
Atorvastatin+ABT335515
Atorvastatin+ABT335+Niaspan381

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The Apolipoprotein A-I Fractional Catabolic Rate (FCR)

After receiving total daily caloric intake over 20 hrs as 20 identical small meals, starting at 0600 hrs, subjects took study medications at 0800 hrs. Five hours after the first meal, i.v. 5,5,5-2H3-L-leucine was administered, followed by a primed-constant infusion at 10 mol/kg body weight per hr for 15 hrs during which 14 blood samples were collected. Isotopic enrichment of leucine in apoA1 band excised from polyacrylamide gel was calculated. Assuming steady state apo A-I metabolism, we used a compartment model to fit data, consisting a precursor compartment (Compartment 1), the plasma leucine pool, an intracellular compartment accounting for apoA1 synthesis and lipoprotein assembly (Compartment 2), and compartments to account for dispositional kinetics of the subfractions including a plasma pool compartment (Compartment 3). The apoA1 FCR corresponds to the rate of irreversible loss of leucine pools from Compartment 3. (NCT00728910)
Timeframe: 4 weeks, 12 weeks and 22 weeks

Interventionpools/day (Mean)
Atorvastatin0.294
Atorvastatin+ABT3350.294
Atorvastatin+ABT335+Niaspan0.295

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Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 30 Days Post-percutaneous Coronary Intervention (PCI)

Percentage calculated as: (number of participants who experienced MACE [death, myocardial infarction, target vessel revascularization] within 30 days post-PCI) divided by (number of participants who experienced PCI) * 100. Major Adverse Cardiac Events (MACE) that occurred after 33 days post PCI were excluded. (NCT00728988)
Timeframe: 30 days post PCI

,
Interventionpercentage of participants (Number)
Total MACEDeathMyocardial InfarctionTarget Vessel Revascularization
Atorvastatin14.70.614.10.0
Usual Care15.70.615.10.0

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Percentage of Participants With Elevated Troponin I

Troponin I above the upper limit of normal range from baseline (biomarker of myocardial injury): normal range: 0-0.5 nanograms per milliliter (ng/mL). (NCT00728988)
Timeframe: 8 hours, 24 hours and 30 days post PCI

,
Interventionpercentage of participants (Number)
8 hours post-PCI24 hours post-PCI30 days post-PCI
Atorvastatin40.449.71.9
Usual Care35.544.41.8

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Percentage of Participants With Elevated Myoglobin

Myoglobin above the upper limit of normal from baseline (biomarker of myocardial injury): normal range: 0-109 nanograms per milliliter (ng/mL). (NCT00728988)
Timeframe: 8 hours, 24 hours and 30 days post PCI

,
Interventionpercentage of participants (Number)
8 hours post-PCI24 hours post-PCI30 days post-PCI
Atorvastatin8.23.11.3
Usual Care10.84.20.6

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Percentage of Participants With Elevated Creatine Kinase-MB (CK-MB)

CK-MB above the upper limit of normal range from baseline (biomarker of myocardial injury); normal range: 0-5.0 nanograms per milliliter (ng/mL). (NCT00728988)
Timeframe: 8 hours, 24 hours and 30 days post PCI

,
Interventionpercentage of participants (Number)
8 Hours Post-PCI24 Hours Post-PCI30 Days Post-PCI
Atorvastatin11.315.61.3
Usual Care13.618.90.0

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Percent Change From Baseline in C-Reactive Protein (CRP)

C-reactive protein percent change from baseline = (post baseline value minus baseline value) divided by baseline value*100. Includes all CRP samples tested for the study, including samples unaffected and those samples affected by defective high-sensitivity (hs) CRP reagents. (NCT00728988)
Timeframe: Baseline, 8 hours, 24 hours and 30 days

,
Interventionpercent change in CRP (Least Squares Mean)
8 hours post-PCI24 hours post-PCI30 days post-PCI
Atorvastatin205.25594.079.01
Usual Care234.77543.5067.23

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Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 24 Hours Post-PCI

Percentage calculated as: (number of participants who experienced MACE within 24 hours post PCI) divided by (number of participants who experienced PCI) * 100. (NCT00728988)
Timeframe: 24 hours post PCI

Interventionpercentage of participants (Number)
Atorvastatin13.5
Usual Care15.1

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Percentage of Participants With Major Adverse Cardiac Events (MACE) (Incidence of MACE) at 8 Hours Post-PCI

Percentage calculated as: (number of participants who experienced MACE within 8 hours post-PCI) divided by (number of participants who experienced PCI) * 100. (NCT00728988)
Timeframe: 8 hours post PCI

Interventionpercentage of participants (Number)
Atorvastatin6.7
Usual Care6.4

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Absolute Change From Baseline in Apolipoprotein B (Apo B)

Change from baseline in Apolipoprotein B measured in grams per liter (g/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventiong/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+1.26-0.39-0.44-0.42-0.41
Stayed at 5 mg: Tanner Stage 11.09-0.23-0.33-0.27-0.30
Titrated to 10 mg: Tanner Stage 11.49-0.31-0.40-0.53-0.59
Titrated to 20 mg: Tanner Stage 2+1.52-0.42-0.47-0.52-0.49

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Absolute Change From Baseline in Flow-Mediated Dilatation at Week 8

Brachial artery flow-mediated dilatation (FMD) = (max minus baseline diameter divided by baseline diameter) x 100%. Standardized image acquisition: brachial artery images recorded for one minute at rest, blood pressure cuff inflated to 250 mm Hg for 5 minutes with brachial artery imaged continuously throughout cuff inflation, cuff released to produce reactive hyperaemia and the brachial artery imaged continuously for 3 minutes after release. Total duration of measurement approximately 25 minutes. Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 8

,,,
InterventionFMD (Mean)
BaselineWeek 8
Stayed at 10 mg: Tanner Stage 2+5.05-0.32
Stayed at 5 mg: Tanner Stage 14.34-0.16
Titrated to 10 mg: Tanner Stage 17.41-1.14
Titrated to 20 mg: Tanner Stage 2+3.671.35

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

Change from baseline in high-density lipoprotein cholesterol measured in millimoles per liter (mmol/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionmmol/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+1.17-0.050.020.040.08
Stayed at 5 mg: Tanner Stage 11.350.08-0.02-0.120.04
Titrated to 10 mg: Tanner Stage 11.45-0.100.00-0.01-0.07
Titrated to 20 mg: Tanner Stage 2+1.18-0.01-0.01-0.03-0.08

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Absolute Change From Baseline in Pharmacodynamic Responses of Low-density Lipoprotein Cholesterol (LDL-C)

Low-density lipoprotein cholesterol (LDL-C) measured in millimoles per liter (mmol/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionmmol/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+5.11-1.95-2.24-2.12-1.99
Stayed at 5 mg: Tanner Stage 14.87-1.75-2.07-1.89-1.80
Titrated to 10 mg: Tanner Stage 16.37-1.62-1.94-2.57-2.71
Titrated to 20 mg: Tanner Stage 2+6.23-1.90-2.27-2.55-2.60

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Absolute Change From Baseline in Total Cholesterol (TC)

Total Cholesterol measured in millimoles per liter (mmol/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionmmol/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+6.92-2.11-2.37-2.28-2.26
Stayed at 5 mg: Tanner Stage 16.76-1.89-2.27-2.03-1.89
Titrated to 10 mg: Tanner Stage 18.58-2.04-2.24-2.86-3.20
Titrated to 20 mg: Tanner Stage 2+8.40-2.28-2.66-2.95-3.22

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Absolute Change From Baseline in Triglycerides (TG)

Change from baseline in triglycerides measured in millimoles per liter (mmol/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionmmol/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+1.030.05-0.10-0.12-0.31
Stayed at 5 mg: Tanner Stage 10.760.05-0.050.400.02
Titrated to 10 mg: Tanner Stage 10.95-0.08-0.26-0.04-0.16
Titrated to 20 mg: Tanner Stage 2+1.200.00-0.10-0.04-0.28

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Absolute Change From Baseline in Very Low-density Lipoprotein-cholesterol (VLDL-C)

Change from baseline in very low-density lipoprotein-cholesterol (VLDL-C) measured in millimoles per liter (mmol/L). Change from baseline = value at observation minus baseline value. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionmmol/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+0.65-0.12-0.14-0.20-0.35
Stayed at 5 mg: Tanner Stage 10.54-0.22-0.18-0.01-0.13
Titrated to 10 mg: Tanner Stage 10.76-0.31-0.30-0.28-0.42
Titrated to 20 mg: Tanner Stage 2+0.99-0.38-0.39-0.36-0.55

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Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1)

Apolipoprotein A-1 (Apo A-1): percent (%) change from baseline by treatment over time = [Apo A-1 at observation minus Apo A-1 at Week 0] divided by Apo A-1 at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in Apo A-1 (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-5.96-3.73-4.21-2.60
Stayed at 5 mg: Tanner Stage 11.69-5.15-9.90-1.24
Titrated to 10 mg: Tanner Stage 1-5.24-3.30-0.97-3.37
Titrated to 20 mg: Tanner Stage 2+-0.537.54-2.82-4.82

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Percent Change From Baseline in Apolipoprotein B (Apo B)

Apolipoprotein B (Apo B): percent (%) change from baseline by treatment over time = [Apo B at observation minus Apo B at Week 0] divided by Apo B at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in Apo B (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-30.81-34.69-33.26-31.94
Stayed at 5 mg: Tanner Stage 1-21.92-29.89-24.58-27.39
Titrated to 10 mg: Tanner Stage 1-19.88-26.56-35.26-39.59
Titrated to 20 mg: Tanner Stage 2+-27.46-30.42-33.61-31.26

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

High-density lipoprotein cholesterol (HDL-C): percent (%) change by treatment over time = [HDL-C at observation minus HDL-C at Week 0] divided by HDL-C at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in HDL-C (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-4.111.043.285.99
Stayed at 5 mg: Tanner Stage 15.38-1.99-10.182.50
Titrated to 10 mg: Tanner Stage 1-6.451.59-0.64-2.84
Titrated to 20 mg: Tanner Stage 2+-0.771.77-2.78-5.19

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

Low-density Lipoprotein Cholesterol (LDL-C): percent (%) change from baseline by treatment over time = [LDL-C at observation minus LDL-C at Week 0] divided by LDL-C at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in LDL-C (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-38.14-43.66-41.22-38.45
Stayed at 5 mg: Tanner Stage 1-36.27-42.33-38.87-36.78
Titrated to 10 mg: Tanner Stage 1-25.70-30.27-40.01-42.70
Titrated to 20 mg: Tanner Stage 2+-30.27-35.13-39.73-40.39

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Percent Change From Baseline in Total Cholesterol (TC)

Total cholesterol (TC): percent (%) change from baseline by treatment over time = [TC at observation minus TC at Week 0] divided by TC at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in TC (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-30.60-33.98-32.80-32.43
Stayed at 5 mg: Tanner Stage 1-28.06-33.37-29.99-27.80
Titrated to 10 mg: Tanner Stage 1-24.11-26.12-33.12-37.17
Titrated to 20 mg: Tanner Stage 2+-26.78-30.54-34.06-37.45

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Percent Change From Baseline in Triglycerides (TG)

Triglycerides (TG): percent (%) change from baseline by treatment over time = [TG at observation minus TG at Week 0] divided by TG at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in TG (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+28.371.27-4.43-20.94
Stayed at 5 mg: Tanner Stage 15.66-6.2057.061.69
Titrated to 10 mg: Tanner Stage 1-6.87-21.43-1.27-9.88
Titrated to 20 mg: Tanner Stage 2+-0.56-7.60-2.72-21.11

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Percent Change From Baseline in Very Low-density Lipoprotein-cholesterol (VLDL-C)

Very low-density lipoprotein-cholesterol (VLDL-C): percent (%) change from baseline by treatment over time = [VLDL-C at observation minus VLDL-C at Week 0] divided by VLDL-C at Week 0 * 100. Assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventionpercent change in VLDL-C (Mean)
Week 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+-14.50-21.10-29.20-53.61
Stayed at 5 mg: Tanner Stage 1-42.20-30.664.10-12.31
Titrated to 10 mg: Tanner Stage 1-28.49-31.86-25.59-50.29
Titrated to 20 mg: Tanner Stage 2+-39.95-36.35-35.08-52.38

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Parent-metabolite Population Pharmacokinetic (PK) Model for Atorvastatin and Its Metabolites: Atorvastatin Apparent Clearance (CL/F)

Parent-metabolite population PK model built using sparse blood samples from both Tanner Stage 1 and Tanner Stage 2+. Blood sampling times: Weeks 2 and 6: single sample between 4 and 12 hours postdose; Weeks 4 and 8: predose, 1 hour, and 2 hours postdose. Plasma samples were analyzed for atorvastatin and active hydroxyacid metabolite (o-hydroxyatorvastatin) concentrations using a validated, sensitive, and specific high-performance liquid chromatography tandem mass spectrometric method. Data presented are the result of the model used. (NCT00739999)
Timeframe: Week 2, Week 4, Week 6, Week 8

InterventionL/hr (Number)
Atorvastatin (5 mg, 10 mg): Tanner Stage 1553
Atorvastatin (10 mg, 20 mg): Tanner Stage 2+543

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Parent-metabolite Population Pharmacokinetic (PK) Model for Atorvastatin and Its Metabolites: Apparent Volume of Distribution of the Central Compartment (Vc/F)

Parent-metabolite population PK model built using sparse blood samples from Tanner Stages 1 and 2+. Sampling times: Weeks 2 + 6: single sample between 4 -12 hours postdose; Weeks 4 + 8: predose, 1 + 2 hours postdose. Plasma samples analyzed for atorvastatin and active hydroxyacid metabolite (o-hydroxyatorvastatin) concentrations using validated, sensitive, specific high-performance liquid chromatography tandem mass spectrometric method. Vc/F value based on 70 kg body weight. Parameter estimation uncertainty (95% CI) by non-parametric bootstrap analysis. Data presented are result of model used. (NCT00739999)
Timeframe: Week 2, Week 4, Week 6, Week 8

Interventionliters (Number)
Atorvastatin (5 mg, 10 mg, 20 mg): Tanner Stages 1 and 2+1020

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Percent Change From Baseline in Flow-Mediated Dilatation at Week 8

"Brachial Flow-Mediated Dilatation (FMD) = (max minus baseline diameter divided by baseline diameter) x 100%.~." (NCT00739999)
Timeframe: Baseline, Week 8

Interventionpercent change in FMD (Mean)
Stayed at 5 mg: Tanner Stage 1-17.19
Titrated to 10 mg: Tanner Stage 1-20.77
Stayed at 10 mg: Tanner Stage 2+-9.77
Titrated to 20 mg: Tanner Stage 2+1.49

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Absolute Change From Baseline in Apolipoprotein A-1 (Apo A-1)

Change from baseline in Apolipoprotein A-1 measured in grams per liter (g/L); assessments were performed in the fasting state (minimum 10-hour fast [optional at Weeks 2 and 6]). Change from baseline = value at observation minus baseline value. (NCT00739999)
Timeframe: Baseline, Week 2, Week 4, Week 6, Week 8

,,,
Interventiong/L (Mean)
BaselineWeek 2Week 4Week 6Week 8
Stayed at 10 mg: Tanner Stage 2+1.29-0.09-0.06-0.07-0.04
Stayed at 5 mg: Tanner Stage 11.420.01-0.09-0.14-0.03
Titrated to 10 mg: Tanner Stage 11.45-0.08-0.06-0.02-0.05
Titrated to 20 mg: Tanner Stage 2+1.24-0.010.07-0.04-0.07

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Atrial Fibrillation

(NCT00756886)
Timeframe: 0-21 days post-operative

Interventionparticipants (Number)
Atorvastatin6
Placebo1

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Pre-post Change in Brachial Artery Reactivity

Brachial artery reactivity was assessed by Flow-mediated dilatation (FMD), performed before and after the 12 week period on therapy. FMD uses high-frequency ultrasound measurement of changes in brachial artery diameter after a 5-minute blood pressure cuff arterial occlusion. Brachial artery reactivity has been shown to predict long-term cardiovascular events. (NCT00767572)
Timeframe: Baseline, 12 weeks

Interventionmm (Mean)
Atorvastatin3
Sugar Pill3

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Mean Change in Low Density Lipoprotein (LDL)

Serum LDL, mg/dL (baseline LDL-follow-up LDL) (NCT00770679)
Timeframe: Change from baseline to follow-up, up to 5 weeks

Interventionmg/dL (Mean)
High-Dose Statin75.54

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Percent Change From Baseline in Apolipoprotein B/A-1 Ratio

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-18.59
Atorvastatin 40 mg-5.67

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Percent Change From Baseline in Apolipoprotein B

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-17.23
Atorvastatin 40 mg-9.53

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

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/405.37
Atorvastatin 40 mg2.89

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Percent Change From Baseline in Triglycerides

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-5.41
Atorvastatin 40 mg-7.54

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Percent Change From Baseline in Total Cholesterol/HDL-Cholesterol Ratio

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-18.63
Atorvastatin 40 mg-8.60

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Percent Change From Baseline in Total Cholesterol

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-15.97
Atorvastatin 40 mg-7.73

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Percent Change From Baseline in Non-HDL Cholesterol/HDL-Cholesterol Ratio

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-24.41
Atorvastatin 40 mg-11.20

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Percent Change From Baseline in Non-HDL Cholesterol

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-22.50
Atorvastatin 40 mg-10.88

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Number of Participants Reaching LDL-C Target Goal <100 mg/dL

Target LDL-C level of < 100 mg/dL (2.59 mmol/L) at study endpoint after 6 weeks of treatment for the Full Analysis Set (FAS) population. (NCT00782184)
Timeframe: Treatment Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin 10/4081
Atorvastatin 40 mg52

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Number of Participants Reaching LDL-C Target Goal <77 mg/dL

Target LDL-C level of < 77 mg/dL (2.00 mmol/L) at study endpoint after 6 weeks of treatment for the Full Analysis Set (FAS) population. (NCT00782184)
Timeframe: Treatment Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin 10/4045
Atorvastatin 40 mg11

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Number of Participants Reaching LDL-C Target Goals of <70 mg/dL

Target LDL-C level of < 70 mg/dL (1.81 mmol/L) at study endpoint after 6 weeks of treatment for the Full Analysis Set (FAS) population. (NCT00782184)
Timeframe: Treatment Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin 10/4034
Atorvastatin 40 mg6

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Percent Change From Baseline in Apolipoprotein A-1

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/402.56
Atorvastatin 40 mg-2.69

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

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-26.81
Atorvastatin 40 mg-11.81

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Percent Change From Baseline in LDL-Cholesterol/HDL-Cholesterol Ratio

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-28.77
Atorvastatin 40 mg-12.66

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Percent Change From Baseline in High-sensitivity C-Reactive Protein (Hs-CRP)

(NCT00782184)
Timeframe: Baseline (Treatment Day 1), Treatment Week 6

Interventionpercent change from baseline (Least Squares Mean)
Ezetimibe/Simvastatin 10/40-6.18
Atorvastatin 40 mg-8.86

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Plasma Markers of Oxidative Stress: f2-Isoprostanes

(NCT00791648)
Timeframe: anesthesia induction, 30 minutes into cardiopulmonary bypass (CPB), after CPB, ICU admission, 6 hours postop, and POD 1, 2, 3.

,
Interventionpg/ml (Median)
at anesthesia induction30 minutes into cardiopulmonary bypass (CPB)after CPBICU admission6 hours post-opPOD 1POD 2POD 3
Placebo28.83931.531.64130.23726.5
Statin29.441.632.332.132.128.128.532.7

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Plasma Markers of Inflammation: Measurements of Neuronal Injury (Ubiquitin C-terminal Hydrolase-1)

measurements of neuronal injury (ubiquitin C-terminal hydrolase-1) (NCT00791648)
Timeframe: anesthesia induction, ICU admission, and POD 1

,
Interventionng/ml (Median)
at anesthesia inductionICU admissionPOD 1
Placebo6.711.612.2
Statin6.212.312.8

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Plasma Markers of Inflammation: Blood Brain Barrier Disruption (S100 Calcium-binding Protein B)

measurements of blood brain barrier disruption (S100 calcium-binding protein B) (NCT00791648)
Timeframe: anesthesia induction, ICU admission, and POD 1

,
Interventionpg/ml (Median)
at anesthesia inductionICU admissionPOD 1
Placebo17163.145
Statin17.5163.946.1

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Mitochondrial Function--PGC-1alpha RNA Expression

PGC-1alpha RNA expression (NCT00791648)
Timeframe: anesthesia induction and POD 1

,
Interventionau (Median)
at anesthesia inductionPOD 1
Placebo0.841.37
Statin0.541.02

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Mitochondrial Function--mtDNA Copy Number

mtDNA copy number (NCT00791648)
Timeframe: anesthesia induction and POD 1

,
Interventionau (Median)
at anesthesia inductionPOD 1
Placebo.480.43
Statin0.400.3

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Number of Participants With Stroke

(NCT00791648)
Timeframe: while in ICU (about 2 days)

InterventionParticipants (Count of Participants)
Statin10
Placebo7

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Number of Participants With Delirium

(NCT00791648)
Timeframe: while in ICU (about 2 days)

InterventionParticipants (Count of Participants)
Statin69
Placebo75

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Number of Participants With Acute Kidney Injury

(NCT00791648)
Timeframe: postoperative day 2

InterventionParticipants (Count of Participants)
Statin64
Placebo60

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Urine Markers of Oxidative Stress: f2-Isoprostanes

(NCT00791648)
Timeframe: anesthesia induction, 30 minutes into cardiopulmonary bypass (CPB), after CPB, ICU admission, 6 hours postop, and POD 1, 2, 3.

,
Interventionng/mg creatinine (Median)
at anesthesia induction30 minutes into cardiopulmonary bypass (CPB)after CPBICU admission6 hours post-opPOD 1POD 2POD 3
Placebo1.4782.292.7292.91.771.1430.880.875
Statin1.3691.7502.711.8161.4641.0560.7920.870

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Urine Markers of Renal Injury

tissue inhibitor metaloproteinase-2 x insulin-like growth factor binding protein-7 (NCT00791648)
Timeframe: anesthesia induction, 30 minutes into cardiopulm bypass (CPB), after CPB, ICU admission, 6 hours postop, and Post op Day (POD) 1, 2, 3

,
Intervention(ng/ml)^2/1000 (Median)
at anesthesia induction30 minutes into cardiopulmonary bypass (CPB)after CPBICU admission6 hours post-opPOD 1POD 2POD 3
Placebo0.0980.1690.2190.1120.2070.1860.1150.102
Statin0.1190.1710.2180.0960.2100.1890.1700.134

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Liver Enzyme: Aspartate Aminotransferase Level

(NCT00791648)
Timeframe: postoperative day 1

Interventionunits/liter (Median)
Statin49
Placebo52

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Plasma Markers of Oxidative Stress: Isofurans

(NCT00791648)
Timeframe: anesthesia induction, 30 minutes into cardiopulmonary bypass (CPB), after CPB, ICU admission, 6 hours postop, and POD 1, 2, 3.

,
Interventionpg/ml (Median)
at anesthesia induction30 minutes into cardiopulmonary bypass (CPB)after CPBICU admission6 hours post-opPOD 1POD 2POD 3
Placebo48.456.260.66440.450.93638
Statin4559.957.663.742.5484033.5

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Mitochondrial Function--lactate / Pyruvate Ratio

lactate / pyruvate ratio (NCT00791648)
Timeframe: anesthesia induction, after CPB, and POD 1

,
Interventionratio (Median)
at anesthesia inductionafter CPBPOD 1
Placebo0.040.060.04
Statin0.040.060.04

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Number of Participants Requiring Dialysis

(NCT00791648)
Timeframe: while in ICU (about 2 days)

InterventionParticipants (Count of Participants)
Statin5
Placebo3

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Number of Participants That Died

(NCT00791648)
Timeframe: until postoperative hospital discharge (about 7 days)

InterventionParticipants (Count of Participants)
Statin4
Placebo1

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Urine Markers of Oxidative Stress: Isofurans

(NCT00791648)
Timeframe: anesthesia induction, 30 minutes into cardiopulmonary bypass (CPB), after CPB, ICU admission, 6 hours postop, and POD 1, 2, 3.

,
Intervention(ng/ml)^2/1000 (Median)
at anesthesia induction30 minutes into cardiopulmonary bypass (CPB)after CPBICU admission6 hours post-opPOD 1POD 2POD 3
Placebo2.1462.483.7093.7343.0702.3442.22.16
Statin2.1462.483.7093.7343.3102.3442.22.16

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Composite Score of Plaque Inflammation/Stability Gene Expression as Assayed by Ribonucleic Acid (RNA) Taqman Analysis

"Excised carotid plaques were evaluated for the gene expression of 60 biomarkers associated with inflammation (Hot biomarkers) & 25 biomarkers associated with stability (Cold biomarkers). Each biomarker was assayed using a quantitative polymerase chain reaction method and results were reported as a Cycle Threshold, (Ct). A Composite Score was calculated by averaging the Ct for each of the 25 cold genes, and subtracting the average Ct for the 60 hot genes. A higher composite score was associated with greater inflammation and a lower score was associated with stability (non-inflamed)." (NCT00804843)
Timeframe: At time of carotid endarterectomy (after 4 to 12 weeks of dosing)

InterventionCycle threshold (Ct) (Mean)
Statin 80 mg + Niacin Extended-release (ER)1.36
Statin 10 mg0.82

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Plaque Instability Protein Composite Score

Each excised plaque was analyzed using an assay of 20 proteins that reflect plaque composition and inflammation. Each protein was assigned scaled signs, with a lower (negative) sign associated with plaque stability and a higher (positive) sign associated with plaque inflammation/instability. The Composite Score was the average amounts of all the 20 proteins with their associated signs. A higher Composite Score is associated with more plaque instability. (NCT00804843)
Timeframe: At time of carotid endarterectomy (after 4 to 12 weeks of dosing)

InterventionScore (Mean)
Statin 80 mg + Niacin Extended-release (ER)-7.19
Statin 10 mg-10.48

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Number of Participants With Adverse Events

(NCT00814255)
Timeframe: Up to 7 months

Interventionparticipants (Number)
Conservative Medical Therapy Plus Adalimumab7
Conservative Medical Therapy (Lisinopril, Losartan, Atorvastat7
Conservative Medical Therapy Plus Galactose7

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Number of Participants With a Reduction in Proteinuria at 6 Months by > 50% of the Value at Screening AND Stable GFR Defined as Greater Than 75 ml/Min/1.73m2 in Those With an Initial Value Above 90 OR Within 25% of Baseline for Remaining Patients

Number of participants with a reduction in proteinuria at 6 months by > 50% of the value at screening AND stable GFR defined as greater than 75 ml/min/1.73m2 in those with an initial value above 90 OR within 25% of baseline for remaining patients. (NCT00814255)
Timeframe: baseline and 6 months

Interventionparticipants (Number)
Conservative Medical Therapy Plus Adalimumab0
Conservative Medical Therapy (Lisinopril, Losartan, Atorvastat2
Conservative Medical Therapy Plus Galactose2

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Percent Change From Baseline in Apo B

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=132,130)Month 2 (n=131,123)Month 3 (n=126,117)Month 6 (n=123,110)Month 12 (n=120,108)Month 18 (n=114,100)Month 24 (n=113,95)Month 30 (n=112,95)Month 36/ET (n=125,118)
Atorvastatin (10-80 mg): Tanner_Stage 2+-29.851-33.959-35.849-34.740-36.842-36.211-36.677-36.453-31.362
Atorvastatin (5-80 mg): Tanner_Stage 1-26.933-31.867-35.163-35.900-36.624-38.158-36.426-36.668-34.507

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Age (Years) During the Study: Females

Investigator assessment of age during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionyears (Mean)
Baseline (n=125)Month 1 (n=125)Change at Month 1 (n=125)Month 2 (n=120)Change at Month 2 (n=120)Month 3 (n=115)Change at Month 3 (n=115)Month 6 (n=113)Change at Month 6 (n=113)Month 12 (n=107)Change at Month 12 (n=107)Month 18 (n=99)Change at Month 18 (n=99)Month 24 (n=95)Change at Month 24 (n=95)Month 30 (n=93)Change at Month 30 (n=93)Month 36/ET (n=121)Change at Month 36/ET (n=121)
Atorvastatin (5-80 mg)10.5510.660.1110.780.2010.750.2810.990.5211.500.9912.021.5212.421.9812.992.5213.072.54

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Age (Years) During the Study: Males

Investigator assessment of age during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionyears (Mean)
Baseline (n=146)Month 1 (n=141)Change at Month 1 (n=141)Month 2 (n=138)Change at Month 2 (n=138)Month 3 (n=133)Change at Month 3 (n=133)Month 6 (n=129)Change at Month 6 (n=129)Month 12 (n=123)Change at Month 12 (n=123)Month 18 (n=119)Change at Month 18 (n=119)Month 24 (n=114)Change at Month 24 (n=114)Month 30 (n=114)Change at Month 30 (n=114)Month 36/ET (n=134)Change at Month 36/ET (n=134)
Atorvastatin (5-80 mg)9.9410.050.1110.140.1810.210.2910.430.5510.961.0211.471.5411.932.0212.462.5412.692.67

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Apoliprotein A-1 (Apo A-1; Grams Per Liter [g/L]) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventiong/L (Mean)
Baseline (n=138,132)Month 1 (n=132,130)Change at Month 1 (n=132,130)Month 2 (n=131,123)Change at Month 2 (n=131,123)Month 3 (n=126,117)Change at Month 3 (n=126,117)Month 6 (n=123,110)Change at Month 6 (n=123,110)Month 12 (n=120,108)Change at Month 12 (n=120,108)Month 18 (n=114,100)Change at Month 18 (n=114,100)Month 24 (n=113,95)Change at Month 24 (n=113,95)Month 30 (n=112,95)Change at Month 30 (n=112,95)Month 36/ET (n=125,118)Change at Month 36/ET (n=125,118)
Atorvastatin (10-80 mg): Tanner_Stage 2+1.3081.3370.0321.3340.0251.3060.0061.3290.0261.271-0.0281.266-0.0381.275-0.0271.268-0.0361.272-0.040
Atorvastatin (5-80 mg): Tanner_Stage 11.3961.4190.0251.4110.0161.4050.0051.386-0.0071.347-0.0411.339-0.0491.364-0.0321.357-0.0401.327-0.073

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Apoliprotein B (Apo B; g/L) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventiong/L (Mean)
Baseline (n=138,132)Month 1 (n=132,130)Change at Month 1 (n=132,130)Month 2 (n=131,123)Change at Month 2 (n=131,123)Month 3 (n=126,117)Change at Month 3 (n=126,117)Month 6 (n=123,110)Change at Month 6 (n=123,110)Month 12 (n=120,108)Change at Month 12 (n=120,108)Month 18 (n=114,100)Change at Month 18 (n=114,100)Month 24 (n=113,95)Change at Month 24 (n=113,95)Month 30 (n=112,95)Change at Month 30 (n=112,95)Month 36/ET (n=125,118)Change at Month 36/ET (n=125,118)
Atorvastatin (10-80 mg): Tanner_Stage 2+1.3810.967-0.4150.916-0.4840.890-0.5180.910-0.5030.871-0.5300.882-0.5330.884-0.5350.885-0.5330.924-0.450
Atorvastatin (5-80 mg): Tanner_Stage 11.4541.062-0.3950.980-0.4710.930-0.5220.919-0.5350.918-0.5480.893-0.5780.918-0.5510.910-0.5600.926-0.520

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BMI (kg/m^2) During the Study: Females

Investigator assessment of BMI changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionkg/m^2 (Mean)
Baseline (n=125)Month 1 (n=124)Change at Month 1 (n=124)Month 2 (n=119)Change at Month 2 (n=119)Month 3 (n=115)Change at Month 3 (n=115)Month 6 (n=113)Change at Month 6 (n=113)Month 12 (n=107)Change at Month 12 (n=107)Month 18 (n=99)Change at Month 18 (n=99)Month 24 (n=95)Change at Month 24 (n=95)Month 30 (n=93)Change at Month 30 (n=93)Month 36/ET (n=121)Change at Month 36/ET (n=121)
Atorvastatin (5-80 mg)19.4419.45-0.0219.470.0019.540.1319.680.2419.980.6020.240.9220.501.3820.751.5920.711.46

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Body Mass Index (BMI in kg Per Square Meter [kg/m^2]) During the Study: Males

Investigator assessment of BMI changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionkg/m^2 (Mean)
Baseline (n=146)Month 1 (n=141)Change at Month 1 (n=141)Month 2 (n=138)Change at Month 2 (n=138)Month 3 (n=133)Change at Month 3 (n=133)Month 6 (n=129)Change at Month 6 (n=129)Month 12 (n=123)Change at Month 12 (n=123)Month 18 (n=119)Change at Month 18 (n=119)Month 24 (n=114)Change at Month 24 (n=114)Month 30 (n=114)Change at Month 30 (n=114)Month 36/ET (n=134)Change at Month 36/ET (n=134)
Atorvastatin (5-80 mg)18.9718.940.0119.060.0618.990.0719.040.1019.340.3719.650.7319.910.9920.181.2520.281.33

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Flow-Mediated Dilatation (FMD) During the Study

Percent (%) FMD was calculated as (hyperemic diameter minus resting diameter) divided by the resting diameter multiplied by 100. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 6, 12, 18, 24, 30 and 36/ET

,
Intervention% FMD (Mean)
Baseline (n=37,36)Month 6 (n=27,23)Change at Month 6 (n=27,23)Month 12 (n=32,29)Change at Month 12 (n=32,29)Month 18 (n=33,28)Change at Month 18 (n=33,28)Month 24 (n=33,28)Change at Month 24 (n=33,28)Month 30 (n=33,28)Change at Month 30 (n=33,28)Month 36/ET (n=34,33)Change at Month 36/ET (n=34,33)
Atorvastatin (10-80 mg): Tanner_Stage 2+6.6516.520-0.7596.363-0.7784.668-2.5565.679-1.5455.191-2.0335.360-1.563
Atorvastatin (5-80 mg): Tanner_Stage 15.5235.749-0.0634.732-0.9524.942-0.7624.538-1.1665.571-0.1344.987-0.550

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Height (Centimeters [cm]) During the Study: Males

Investigator assessment of height changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventioncm (Mean)
Baseline (n=146)Month 1 (n=141)Change at Month 1 (n=141)Month 2 (n=138)Change at Month 2 (n=138)Month 3 (n=133)Change at Month 3 (n=133)Month 6 (n=129)Change at Month 6 (n=129)Month 12 (n=123)Change at Month 12 (n=123)Month 18 (n=119)Change at Month 18 (n=119)Month 24 (n=114)Change at Month 24 (n=114)Month 30 (n=114)Change at Month 30 (n=114)Month 36/ET (n=134)Change at Month 36/ET (n=134)
Atorvastatin (5-80 mg)144.36145.210.68145.931.27146.001.72147.173.24150.756.67153.269.31156.0312.11158.7814.86160.5915.53

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Height (cm) During the Study: Females

Investigator assessment of height changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventioncm (Mean)
Baseline (n=125)Month 1 (n=124)Change at Month 1 (n=124)Month 2 (n=119)Change at Month 2 (n=119)Month 3 (n=115)Change at Month 3 (n=115)Month 6 (n=113)Change at Month 6 (n=113)Month 12 (n=107)Change at Month 12 (n=107)Month 18 (n=99)Change at Month 18 (n=99)Month 24 (n=95)Change at Month 24 (n=95)Month 30 (n=93)Change at Month 30 (n=93)Month 36/ET (n=121)Change at Month 36/ET (n=121)
Atorvastatin (5-80 mg)145.28146.060.71146.571.19146.811.68147.872.77150.845.50152.777.41154.799.61156.4311.23156.5211.23

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High-Density Lipoprotein Cholesterol (HDL-C; mMol/L) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
InterventionmMol/L (Mean)
Baseline (n=139,132)Month 1 (n=131,130)Change at Month 1 (n=131,130)Month 2 (n=132,122)Change at Month 2 (n=132,122)Month 3 (n=126,117)Change at Month 3 (n=126,117)Month 6 (n=127,115)Change at Month 6 (n=127,115)Month 12 (n=121,109)Change at Month 12 (n=121,109)Month 18 (n=116,102)Change at Month 18 (n=116,102)Month 24 (n=111,96)Change at Month 24 (n=111,96)Month 30 (n=112,94)Change at Month 30 (n=112,94)Month 36/ET (n=123,117)Change at Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+1.2771.2920.0161.2970.0251.2740.0111.2680.0101.241-0.0231.234-0.0271.2660.0071.2650.0061.2780.005
Atorvastatin (5-80 mg): Tanner_Stage 11.3491.3600.0101.3640.0141.3710.0151.337-0.0111.328-0.0121.3670.0241.3850.0271.3800.0321.335-0.024

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Number of Participants With Shift From Baseline in Tanner_Stage by Timepoint and Baseline Tanner_Stage

Tanner_Stage was assessed based on 2 components by gender, pubic hair and breasts for females and pubic hair and genitalia for males. If these values of components were not same, then the Tanner_Stage had the higher value of 2 components for each gender by visit. (NCT00827606)
Timeframe: Baseline, Months 6, 12, 18, 24, 30, and 36/ET

,,,,
Interventionparticipants (Number)
Tanner_Stage 1, Month 6 (n=126,48,25,27,15)Tanner_Stage 2 , Month 6 (n=126,48,25,27,15)Tanner_Stage 3, Month 6 (n=126,48,25,27,15)Tanner_Stage 4, Month 6 (n=126,48,25,27,15)Tanner_Stage 5, Month 6 (n=126,48,25,27,15)Tanner_Stage 1, Month 12 (n=121,43,23,26,15)Tanner_Stage 2, Month 12 (n=121,43,23,26,15)Tanner_Stage 3, Month 12 (n=121,43,23,26,15)Tanner_Stage 4, Month 12 (n=121,43,23,26,15)Tanner_Stage 5, Month 12 (n=121,43,23,26,15)Tanner_Stage 1, Month 18 (n=115,41, 21,25,14)Tanner_Stage 2, Month 18 (n=115,41, 21,25,14)Tanner_Stage 3, Month 18 (n=115,41, 21,25,14)Tanner_Stage 4, Month 18 (n=115,41, 21,25,14)Tanner_Stage 5, Month 18 (n=115,41, 21,25,14)Tanner_Stage 1, Month 24 (n=113,38,19,22,14)Tanner_Stage 2, Month 24 (n=113,38,19,22,14)Tanner_Stage 3, Month 24 (n=113,38,19,22,14)Tanner_Stage 4, Month 24 (n=113,38,19,22,14)Tanner_Stage 5, Month 24 (n=113,38,19,22,14)Tanner_Stage 1, Month 30 (n=111,38,19,23,14)Tanner_Stage 2, Month 30 (n=111,38,19,23,14)Tanner_Stage 3, Month 30 (n=111,38,19,23,14)Tanner_Stage 4, Month 30 (n=111,38,19,23,14)Tanner_Stage 5, Month 30 (n=111,38,19,23,14)Tanner_Stage 1, Month 36/ET (n=127,52,25,31,18)Tanner_Stage 2, Month 36/ET (n=127,52,25,31,18)Tanner_Stage 3, Month 36/ET (n=127,52,25,31,18)Tanner_Stage 4, Month 36/ET (n=127,52,25,31,18)Tanner_Stage 5, Month 36/ET (n=127,52,25,31,18)
Atorvastatin (10-80 mg): Baseline Tanner_Stage 20341040017215001516910914123031118606102412
Atorvastatin (10-80 mg): Baseline Tanner_Stage 300141100011102006114002134001990021310
Atorvastatin (10-80 mg): Baseline Tanner_Stage 400025200022400018700013900011120001219
Atorvastatin (10-80 mg): Baseline Tanner_Stage 5000114000114000113000113000113000018
Atorvastatin (5-80 mg): Baseline Tanner_Stage 110714500852510106331183051332090393226140413125255

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Percent Change From Baseline in Age: Females

Investigator assessment of age during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=125)Month 2 (n=120)Month 3 (n=115)Month 6 (n=113)Month 12 (n=107)Month 18 (n=99)Month 24 (n=95)Month 30 (n=93)Month 36/ET (n=121)
Atorvastatin (5-80 mg)1.102.002.745.1810.0015.2020.0825.3525.73

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Percent Change From Baseline in Age: Males

Investigator assessment of age during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=141)Month 2 (n=138)Month 3 (n=133)Month 6 (n=129)Month 12 (n=123)Month 18 (n=119)Month 24 (n=114)Month 30 (n=114)Month 36/ET (n=134)
Atorvastatin (5-80 mg)1.091.863.166.0611.1316.8221.9227.6728.90

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Percent Change From Baseline in Apo A-1

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=132,130)Month 2 (n=131,123)Month 3 (n=126,117)Month 6 (n=123,110)Month 12 (n=120,108)Month 18 (n=114,100)Month 24 (n=113,95)Month 30 (n=112,95)Month 36/ET (n=125,118)
Atorvastatin (10-80 mg): Tanner_Stage 2+3.3012.4991.1923.011-1.370-1.980-0.961-1.695-1.954
Atorvastatin (5-80 mg): Tanner_Stage 12.2291.7011.041-0.069-2.365-3.042-1.611-2.342-4.804

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Percent Change From Baseline in BMI: Females

Investigator assessment of BMI changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=124)Month 2 (n=119)Month 3 (n=115)Month 6 (n=113)Month 12 (n=107)Month 18 (n=99)Month 24 (n=95)Month 30 (n=93)Month 36/ET (n=121)
Atorvastatin (5-80 mg)-0.060.160.731.263.335.147.688.898.06

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Percent Change From Baseline in BMI: Males

Investigator assessment of BMI changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=141)Month 2 (n=138)Month 3 (n=133)Month 6 (n=129)Month 12 (n=123)Month 18 (n=119)Month 24 (n=114)Month 30 (n=114)Month 36/ET (n=134)
Atorvastatin (5-80 mg)0.030.310.390.552.103.985.456.807.31

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Percent Change From Baseline in FMD

Percent (%) FMD was calculated as (hyperemic diameter minus resting diameter) divided by the resting diameter multiplied by 100. (NCT00827606)
Timeframe: Months 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 6 (n=27,23)Month 12 (n=32,29)Month 18 (n=33,28)Month 24 (n=33,28)Month 30 (n=33,28)Month 36/ET (n=34,33)
Atorvastatin (10-80 mg): Tanner_Stage 2+-0.20515.444-24.3873.850-18.804-7.506
Atorvastatin (5-80 mg): Tanner_Stage 114.867-3.880-4.598-9.9927.0000.648

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Percent Change From Baseline in HDL-C

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=131,130)Month 2 (n=132,122)Month 3 (n=126,117)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=116,102)Month 24 (n=111,96)Month 30 (n=112,94)Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+2.1922.5441.6741.877-1.023-1.1651.7371.8681.602
Atorvastatin (5-80 mg): Tanner_Stage 11.5262.1951.929-0.016-0.0692.4723.0143.345-1.125

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Percent Change From Baseline in Height: Females

Investigator assessment of height changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=124)Month 2 (n=119)Month 3 (n=115)Month 6 (n=113)Month 12 (n=107)Month 18 (n=99)Month 24 (n=95)Month 30 (n=93)Month 36/ET (n=121)
Atorvastatin (5-80 mg)0.510.841.201.983.935.306.938.138.14

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Percent Change From Baseline in Height: Males

Investigator assessment of height changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=141)Month 2 (n=138)Month 3 (n=133)Month 6 (n=129)Month 12 (n=123)Month 18 (n=119)Month 24 (n=114)Month 30 (n=114)Month 36/ET (n=134)
Atorvastatin (5-80 mg)0.470.881.192.254.666.538.5310.4910.97

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Percent Change From Baseline in LDL-C

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36 (or ET)

,
Interventionpercent change (Mean)
Month 1 (n=131,130)Month 2 (n=132,122)Month 3 (n=126,117)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=116,101)Month 24 (n=111,96)Month 30 (n=112,94)Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+-37.516-41.939-44.887-43.697-45.727-44.818-46.417-47.734-39.863
Atorvastatin (5-80 mg): Tanner_Stage 1-34.995-40.371-43.568-45.647-45.530-47.101-46.944-46.631-43.785

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Percent Change From Baseline in Total Cholesterol

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=134,131)Month 2 (n=132,124)Month 3 (n=127,118)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=116,101)Month 24 (n=111,96)Month 30 (n=112,95)Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+-29.653-33.726-36.126-35.055-36.943-36.634-37.317-37.856-32.013
Atorvastatin (5-80 mg): Tanner_Stage 1-27.879-31.900-34.784-36.889-36.541-37.772-37.287-36.662-35.063

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Percent Change From Baseline in Trigylcerides

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=134,131)Month 2 (n=132,124)Month 3 (n=127,118)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=116,102)Month 24 (n=111,96)Month 30 (n=112,95)Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+-5.927-14.832-14.415-9.097-7.950-12.443-7.328-4.935-7.759
Atorvastatin (5-80 mg): Tanner_Stage 1-5.950-3.260-8.760-11.817-7.981-13.113-6.6970.657-0.703

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Percent Change From Baseline in VLDL

Assessments were performed in the fasting state (minimum 10-hour fast). (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
Interventionpercent change (Mean)
Month 1 (n=134,131)Month 2 (n=132,124)Month 3 (n=127,118)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=116,101)Month 24 (n=111,96)Month 30 (n=112,95)Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+-5.805-14.694-14.263-9.158-7.827-12.768-6.920-4.751-7.842
Atorvastatin (5-80 mg): Tanner_Stage 1-6.060-3.097-8.711-11.591-7.739-12.911-6.6540.627-0.520

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Percent Change From Baseline in Weight: Females

Investigator assessment of weight changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=125)Month 2 (n=120)Month 3 (n=115)Month 6 (n=113)Month 12 (n=107)Month 18 (n=99)Month 24 (n=95)Month 30 (n=93)Month 36/ET (n=121)
Atorvastatin (5-80 mg)0.971.853.165.3711.6516.7923.4327.8327.26

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Percent Change From Baseline in Weight: Males

Investigator assessment of weight changes during the study. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionpercent change (Mean)
Month 1 (n=141)Month 2 (n=138)Month 3 (n=133)Month 6 (n=129)Month 12 (n=123)Month 18 (n=119)Month 24 (n=114)Month 30 (n=114)Month 36/ET (n=134)
Atorvastatin (5-80 mg)0.942.042.735.0911.8518.0324.2830.4632.54

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Percentage of Participants by Study Drug Compliance Category

Compliance to study drug was categorized as <80%, 80% - 120%, and greater than (>) 120%. (NCT00827606)
Timeframe: Months 1, 2, 3, 6, 12, 18, 24, 30, and 36 (or early termination)

,
Interventionpercentage of participants (Number)
Month 1, <80% (n=135,132)Month 1, 80%-120% (n=135,132)Month 1, >120% (n=135,132)Month 2, <80% (n=132,126)Month 2, 80%-120% (n=132,126)Month 2, >120% (n=132,126)Month 3, <80% (n=130,118)Month 3, 80%-120% (n=130,118)Month 3, >120% (n=130,118)Month 6, <80% (n=127,115)Month 6, 80%-120% (n=127,115)Month 6, >120% (n=127,115)Month 12, <80% (n=121,109)Month 12, 80%-120% (n=121,109)Month 12, >120% (n=121,109)Month 18, <80% (n=116,102)Month 18, 80%-120% (n=116,102)Month 18, >120% (n=116,102)Month 24, <80% (n=113,95)Month 24, 80%-120% (n=113,95)Month 24, >120% (n=113,95)Month 30, <80% (n=112,94)Month 30, 80%-120% (n=112,94)Month 30, >120% (n=112,94)Month 36/ET, <80% (n=129,129)Month 36/ET, 80%-120% (n=129,129)Month 36/ET, >120% (n=129,129)
Atorvastatin (10-80 mg): Tanner_Stage 2+6.893.207.992.107.692.409.690.407.392.705.994.109.589.51.16.492.61.116.383.70
Atorvastatin (5-80 mg): Tanner_Stage 13.097.006.892.40.83.895.40.87.992.107.492.604.394.01.78.891.208.092.0011.686.81.6

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Percentage of Participants With Overall Expected Maturation and Development Consistent With Expectations as Assessed by the Investigator

(NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36 (or early termination)

,
Interventionpercentage of participants (Number)
Baseline (n=139,132)Month 1 (n=118,113)Month 2 (n=116,109)Month 3 (n=130,118)Month 6 (n=127,115)Month 12 (n=121,109)Month 18 (n=115,102)Month 24 (n=113,95)Month 30 (n=111,94)Month 36/Early Termination (n=128,127)
Atorvastatin (10-80 mg): Tanner_Stage 2+100.0100.0100.0100.099.199.1100.0100.098.999.2
Atorvastatin (5-80 mg): Tanner_Stage 199.3100.0100.0100.0100.0100.0100.0100.0100.099.2

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Total Cholesterol (mMol/L) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
InterventionmMol/L (Mean)
Baseline (n=139,132)Month 1 (n=134,131)Change at Month 1 (n=134,131)Month 2 (n=132,124)Change at Month 2 (n=132,124)Month 3 (n=127,118)Change at Month 3 (n=127,118)Month 6 (n=127,115)Change at Month 6 (n=127,115)Month 12 (n=121,109)Change at Month 12 (n=121,109)Month 18 (n=116,101)Change at Month 18 (n=116,101)Month 24 (n=111,96)Change at Month 24 (n=111,96)Month 30 (n=112,95)Change at Month 30 (n=112,95)Month 36/ET (n=123,117)Change at Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+7.6475.352-2.2975.061-2.6544.883-2.8834.982-2.8094.799-2.9454.845-2.9654.817-3.0094.795-3.0485.099-2.543
Atorvastatin (5-80 mg): Tanner_Stage 18.0565.785-2.2665.435-2.6205.195-2.8695.019-3.0635.081-3.0404.989-3.1685.032-3.1235.075-3.0965.134-2.923

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Trigylcerides (mMol/L) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
InterventionmMol/L (Mean)
Baseline (n=139,132)Month 1 (n=134,131)Change at Month 1 (n=134,131)Month 2 (n=132,124)Change at Month 2 (n=132,124)Month 3 (n=127,118)Change at Month 3 (n=127,118)Month 6 (n=127,115)Change at Month 6 (n=127,115)Month 12 (n=121,109)Change at Month 12 (n=121,109)Month 18 (n=116,102)Change at Month 18 (n=116,102)Month 24 (n=111,96)Change at Month 24 (n=111,96)Month 30 (n=112,95)Change at Month 30 (n=112,95)Month 36/ET (n=123,117)Change at Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+0.9800.815-0.1660.741-0.2460.748-0.2370.801-0.1880.789-0.1810.765-0.2190.790-0.1790.781-0.1870.794-0.171
Atorvastatin (5-80 mg): Tanner_Stage 10.8800.759-0.1210.772-0.1030.699-0.1660.691-0.183-0.747-0.1360.687-0.1900.725-0.1330.788-0.0820.764-0.092

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Very Low-Density Lipoprotein (VLDL; mMol/L) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

,
InterventionmMol/L (Mean)
Baseline (n=139,132)Month 1 (n=134,131)Change at Month 1 (n=134,131)Month 2 (n=132,124)Change at Month 2 (n=132,124)Month 3 (n=127,118)Change at Month 3 (n=127,118)Month 6 (n=127,115)Change at Month 6 (n=127,115)Month 12 (n=121,109)Change at Month 12 (n=121,109)Month 18 (n=116,101)Change at Month 18 (n=116,101)Month 24 (n=111,96)Change at Month 24 (n=111,96)Month 30 (n=112,95)Change at Month 30 (n=112,95)Month 36/ET (n=123,117)Change at Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+0.4490.374-0.0760.340-0.1130.344-0.1080.367-0.0860.362-0.0820.349-0.1020.363-0.0810.358-0.0860.364-0.079
Atorvastatin (5-80 mg): Tanner_Stage 10.4030.348-0.0560.354-0.0470.320-0.0760.317-0.0840.343-0.0620.315-0.0870.332-0.0610.361-0.0380.350-0.042

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Weight (kg) During the Study: Females

Investigator assessment of weight changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionkg (Mean)
Baseline (n=125)Month 1 (n=125)Change at Month 1 (n=125)Month 2 (n=120)Change at Month 2 (n=120)Month 3 (n=115)Change at Month 3 (n=115)Month 6 (n=113)Change at Month 6 (n=113)Month 12 (n=107)Change at Month 12 (n=107)Month 18 (n=99)Change at Month 18 (n=99)Month 24 (n=95)Change at Month 24 (n=95)Month 30 (n=93)Change at Month 30 (n=93)Month 36/ET (n=121)Change at Month 36/ET (n=121)
Atorvastatin (5-80 mg)42.1442.500.3642.860.6743.341.2444.262.1046.614.4148.326.2450.138.5551.7310.0251.559.77

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Weight (Kilograms [kg]) During the Study: Males

Investigator assessment of weight changes during the study. Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36/ET

Interventionkg (Mean)
Baseline (n=146)Month 1 (n=141)Change at Month 1 (n=141)Month 2 (n=138)Change at Month 2 (n=138)Month 3 (n=133)Change at Month 3 (n=133)Month 6 (n=129)Change at Month 6 (n=129)Month 12 (n=123)Change at Month 12 (n=123)Month 18 (n=119)Change at Month 18 (n=119)Month 24 (n=114)Change at Month 24 (n=114)Month 30 (n=114)Change at Month 30 (n=114)Month 36/ET (n=134)Change at Month 36/ET (n=134)
Atorvastatin (5-80 mg)40.7941.180.3641.830.8041.681.0842.472.0045.294.6547.537.0249.779.2752.1211.6153.5012.35

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Low Density Lipoprotein Cholesterol (LDL-C; Millimoles Per Liter [mMol/L]) During the Study

Assessments were performed in the fasting state (minimum 10-hour fast). Change from baseline was also determined. (NCT00827606)
Timeframe: Baseline, Months 1, 2, 3, 6, 12, 18, 24, 30 and 36 (or early termination [ET])

,
InterventionmMol/L (Mean)
Baseline (n=139,132)Month 1 (n=131,130)Change at Month 1 (n=131,130)Month 2 (n=132,122)Change at Month 2 (n=132,122)Month 3 (n=126,117)Change at Month 3 (n=126,117)Month 6 (n=127,115)Change at Month 6 (n=127,115)Month 12 (n=121,109)Change at Month 12 (n=121,109)Month 18 (n=116,101)Change at Month 18 (n=116,101)Month 24 (n=111,96)Change at Month 24 (n=111,96)Month 30 (n=112,94)Change at Month 30 (n=112,94)Month 36/ET (n=123,117)Change at Month 36/ET (n=123,117)
Atorvastatin (10-80 mg): Tanner_Stage 2+5.9213.675-2.2333.437-2.5543.270-2.7953.347-2.7323.196-2.8383.261-2.8353.189-2.9333.142-3.0083.457-2.468
Atorvastatin (5-80 mg): Tanner_Stage 16.3044.087-2.2143.719-2.5863.503-2.7983.366-2.9683.409-2.9663.309-3.1053.316-3.0883.335-3.0903.450-2.855

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Area Under the Curve From Predose (Time Zero) to 48 Hours Post-dose (AUC48)

Geometric means of AUC48 = area under the plasma concentration-time profile from time zero (0) to 48 hours postdose of atorvastatin (test versus [vs] reference); measured in nanograms times hour per milliliter (ng.hr/mL). (NCT00844376)
Timeframe: 5 days

Interventionng.h/mL (Geometric Mean)
Test135.05
Reference140.79

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Time to Reach Maximum Plasma Concentration (Tmax)

Median of Tmax = time to maximum plasma concentration (Cmax) (test vs reference); measured in hours (hr). (NCT00844376)
Timeframe: 5 days

Interventionhr (Median)
Test0.52
Reference0.50

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Area Under the Curve From Predose (Time Zero) to Last Quantifiable Concentration (AUClast)

Geometric mean of AUClast = area under the plasma concentration-time curve from time zero (0) to the last measurable concentration of atorvastatin (test vs reference); measured as ng.hr/mL (NCT00844376)
Timeframe: 5 days

Interventionng.hr/mL (Geometric Mean)
Test130.21
Reference137.49

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Area Under the Curve From Predose (Time Zero) to Extrapolated Infinite Time (AUC Infinity)

Geometric means of AUC infinity (AUCinf) = area under the plasma concentration-time curve from time zero (0) extrapolated to infinite time; measured in ng.hr/mL of atorvastatin (test vs reference). (NCT00844376)
Timeframe: 5 days

Interventionng.hr/mL (Geometric Mean)
Test135.88
Reference142.86

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Maximum Observed Plasma Concentration (Cmax)

Geometric mean of Cmax = maximum observed plasma concentration of atorvastatin (test vs reference); measured in nanograms per milliliter (ng/mL). (NCT00844376)
Timeframe: 5 days

Interventionng/mL (Geometric Mean)
Test38.74
Reference33.24

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Plasma Elimination Half-life (t1/2)

Mean of t1/2 = terminal elimination half-life of atorvastatin (test vs reference); measured in hours. (NCT00844376)
Timeframe: 5 days

Interventionhr (Mean)
Test5.95
Reference7.21

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Terminal Phase Rate Constant (Kel)

Geometric mean of Kel= termination phase rate constant for atorvastatin (test vs reference); measured as 1 per hour (1/hr). (NCT00844376)
Timeframe: 5 days

Intervention1/hr (Geometric Mean)
Test0.12
Reference0.10

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Individualized Short Form-36 (SF-36) Mean Scores (Physical Component) From Week 0 to Week 8

Scores from the self-administered SF-36 (Physical component) questionnaire were measured at the start (Week 0) of the study and at the end (Week 8) among patients in the placebo- and statin-treated group. Mean scores range from 0 (minimum) - 100 (maximum) with higher mean scores reflecting better outcomes. Measures reported are the means of Week 0 and week 8, measures of dispersion is the range of scores. (NCT00850460)
Timeframe: Week 0 to Week 8

,
Interventionunits on a scale (Mean)
Week 0 Mean ScoreWeek 8 Mean Score
Placebo5056
Statins5348

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Individualized Neuromuscular Quality of Life (INQoL) Mean Scores From Week 0 to Week 8

Scores from the self-administered INQoL questionnaire will be compared at the start of the study (Week 0) and at the end (Week 8) between the statin-treated group and the placebo group. Scores range from 0-100, with 100 being a better outcome. Measures reported are the means of Week 0 and week 8, measures of dispersion is the range of the results (3 per group). (NCT00850460)
Timeframe: Week 0 to Week 8

,
Interventionunits on a scale (Mean)
Week 0 Mean ScoreWeek 8 Mean Score
Placebo6567
Statins7650

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Percent Change From Baseline in Triglycerides

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-5.51
Doubling Statin Dose-2.63
Rosuvastatin-3.35

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Percent Change From Baseline in Non-HDL-C/HDL-C Ratio

(NCT00862251)
Timeframe: Baseline and Week 6

Interventionpercent change (Least Squares Mean)
Ezetimibe/Simvastatin-16.77
Doubling Statin Dose-5.32
Rosuvastatin-14.64

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Statin (Simvastatin or Atorvastatin).

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-23.13
Doubling Statin Dose-8.37

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Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C)

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-18.39
Doubling Statin Dose-6.77
Rosuvastatin-15.14

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Percent Change From Baseline in TC/HDL-C Ratio

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-12.52
Doubling Statin Dose-4.36
Rosuvastatin-10.70

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Percent Change From Baseline in Total Cholesterol (TC)

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent Change (Least Squares Mean)
Ezetimibe/Simvastatin-13.21
Doubling Statin Dose-4.88
Rosuvastatin-10.58

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In Participants Treated With Atorvastatin at Baseline, Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Atorvastatin

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-24.58
Doubling Atorvastatin Dose-8.85

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In Participants Treated With Simvastatin at Baseline, Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)

(NCT00862251)
Timeframe: Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin84
Doubling Simvastatin Dose19

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In Participants Treated With Simvastatin at Baseline, Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Doubling the Dose of Simvastatin

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-21.59
Doubling Simvastatin Dose-7.98

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Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)

(NCT00862251)
Timeframe: Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin171
Doubling Statin Dose43
Rosuvastatin134

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Percent Change From Baseline Apolipoprotein A-I (Apo A-I)

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin0.64
Doubling Statin Dose-0.93
Rosuvastatin0.86

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Percent Change From Baseline in Apo B/Apo A-I Ratio

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-13.67
Doubling Statin Dose-4.75
Rosuvastatin-11.14

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Percent Change From Baseline in Apolipoprotein B (Apo B)

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-14.98
Doubling Statin Dose-6.97
Rosuvastatin-12.03

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

(NCT00862251)
Timeframe: Baseline and Week 6

Interventionpercent change (Least Squares Mean)
Ezetimibe/Simvastatin1.47
Doubling Statin Dose1.00
Rosuvastatin1.99

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In Participants Treated With Atorvastatin at Baseline, Number of Participants Who Reached the Target LDL-Cholesterol Level of < 70 mg/dL (1.81 mmol/L)

(NCT00862251)
Timeframe: Week 6

Interventionparticipants (Number)
Ezetimibe/Simvastatin87
Doubling Atorvastatin Dose24

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Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP)

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-4.42
Doubling Statin Dose-1.64
Rosuvastatin-9.11

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Percent Change From Baseline in LDL-C/HDL-C Ratio

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-21.55
Doubling Statin Dose-7.39
Rosuvastatin-18.99

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Percent Change From Baseline in LDL-C After Switching to Treatment With Ezetimibe/Simvastatin vs Switching Treatment to Rosuvastatin

(NCT00862251)
Timeframe: Baseline and Week 6

InterventionPercent change (Least Squares Mean)
Ezetimibe/Simvastatin-23.13
Rosuvastatin-19.32

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Percent Change in Total Lipids and Hs-CRP

Total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, and hs-CRP were measured at the start of the treatment period (at start of administration of atorvastatin 10 mg alone) and at the end of study drug (Week 16 or discontinuation). (NCT00871351)
Timeframe: End of washout to Week 16 or discontinuation

,,
InterventionPercent change (Mean)
Total CholesterolTriglyceridesHigh-Density Lipoprotein Cholesterol (HDL-C)Non-HDL-CHigh Sensitivity C-reactive Protein (Hs-CRP)
Atorvastatin-32.8-18.87.4-41.4-2.9
Ezetimibe + Atorvastatin-39.9-25.310.3-50.173.0
Rosuvastatin-24.4-12.09.9-31.3-13.6

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Percent Change in Total Lipids and High Sensitivity C-reactive Protein (Hs-CRP)

Total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, and hs-CRP were measured at 4 weeks after the start of the treatment period (after completion of administration of atorvastatin 10 mg alone) and at Week 16 or at discontinuation. (NCT00871351)
Timeframe: End of Week 4 to Week 16 or discontinuation

,,
InterventionPercent change (Mean)
Total CholesterolTriglyceridesHigh-Density Lipoprotein Cholesterol (HDL-C)Non-HDL-CHigh Sensitivity C-Reactive Protein (Hs-CRP)
Atorvastatin-10.30.20.5-13.79.9
Ezetimibe + Atorvastatin-18.0-0.84.5-25.049.0
Rosuvastatin1.914.72.52.025.7

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Percent Change in Low-Density Lipoprotein - Cholesterol (LDL-C) Values

LDL-C was measured before group study drug administration (Week 4, end of atorvastatin single therapy) and at the end of study drug administration (after 12 weeks of study drug treatment, or at discontinuation). (NCT00871351)
Timeframe: End of Week 4 to Week 16 or discontinuation

InterventionPercent change (Mean)
Ezetimibe + Atorvastatin-25.8
Atorvastatin-15.1
Rosuvastatin0.8

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Percent Change in LDL-C

LDL-C was measured at the start of the atorvastatin 10 mg treatment period (end of the washout period) and at the end of administration of the study drug (Week 16 or discontinuation). (NCT00871351)
Timeframe: End of washout period to Week 16 or discontinuation

InterventionPercent change (Mean)
Ezetimibe + Atorvastatin-49.6
Atorvastatin-41.1
Rosuvastatin-30.5

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Number of Participants Whose LDL-C Levels Reached the Lipid Management Target Values

"LDL-C was measured at the end of administration of the study drug (Week 16 or discontinuation).~Target values:~For participants with history of coronary artery disease: <100 mg/dL;~for participants with at least 3 cardiovascular (CV) risk factors: <120 mg/dL;~for participants with 1-2 CV risk factors: <140 mg/dL;~for participants with no CV risk factors: <160 mg/dL." (NCT00871351)
Timeframe: Week 16 or discontinuation

InterventionParticipants (Number)
Ezetimibe + Atorvastatin37
Atorvastatin19
Rosuvastatin1

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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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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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Area Under the Curve From Time Zero to Extrapolated Infinite Time (AUC Infinity)

AUCinf = Area under the plasma concentration-time curve from time 0 (predose) extrapolated to infinite time; measured in nanograms times hour per milliliter (ng•hr/mL). (NCT00917579)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng•hr/mL (Mean)
Test Drug18.3206
Reference Drug19.2583

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Plasma Elimination Half-life (t1/2)

t1/2 = terminal elimination half-life in hours. (NCT00917579)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionhours (Mean)
Test Drug10.39
Reference Drug10.78

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Time to Reach Maximum Plasma Concentration (Tmax)

Tmax = time (hours) to maximum plasma concentration (Cmax). (NCT00917579)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionhours (Median)
Test Drug1.000
Reference Drug0.5000

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Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast)

AUClast = area under the plasma concentration-time curve from 0 (predose) to the time of the last measureable concentration (Clast); measured in nanograms times hour per milliliter (ng•hr/mL). (NCT00917579)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng•hr/mL (Mean)
Test Drug15.7382
Reference Drug16.5452

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Maximum Observed Plasma Concentration (Cmax)

Cmax = maximum observed plasma concentration. Measured in nanograms per milliter (ng/mL). (NCT00917579)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng/mL (Mean)
Test Drug2.6594
Reference Drug2.8086

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Area Under the Curve From Time Zero to Extrapolated Infinite Time (AUC Infinity)

AUCinf = Area under the plasma concentration-time curve from time 0 (predose) extrapolated to infinite time; measured in nanograms times hour per milliliter (ng*hr/mL). Pharmacokinetic (PK) parameters derived from subject's concentration data; collected Period 1, Day 1 to Day 4; Period 2, Day 1 to Day 4. (NCT00917644)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng*hr/mL (Mean)
Test Drug168.1355
Reference Drug176.1731

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Area Under the Curve From Time Zero to Last Quantifiable Concentration (AUClast)

AUClast = area under the plasma concentration-time curve from 0 (predose) to the time of the last measureable concentration (Clast). PK parameters derived from subject's concentration data; collected Period 1, Day 1 to Day 4; Period 2, Day 1 to Day 4. (NCT00917644)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng*hr/mL (Mean)
Test Drug162.5073
Reference Drug170.4735

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Maximum Observed Plasma Concentration (Cmax)

Cmax = maximum observed plasma concentration. Measured in nanograms per milliter (ng/mL); collected Period 1, Day 1 to Day 4; Period 2, Day 1 to Day 4. (NCT00917644)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionng/mL (Mean)
Test Drug43.1782
Reference Drug43.0534

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Plasma Elimination Half-life (t1/2)

t1/2 = terminal elimination half-life in hours; ln 2/kel, where kel is the termination phase rate constant calculated by a linear regression of the log-linear concentration-time curve. Only those data points judged to describe the terminal log-linear decline were used in the regression. PK parameters derived from subject's concentration data; collected Period 1, Day 1 to Day 4; Period 2, Day 1 to Day 4. (NCT00917644)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionhours (Mean)
Test Drug9.330
Reference Drug9.444

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Time to Reach Maximum Plasma Concentration (Tmax)

Tmax = time (hours) to maximum plasma concentration (Cmax). Observed directly from data as time of first occurrence; PK parameters derived from subject's concentration data; collected Period 1, Day 1 to Day 4; Period 2, Day 1 to Day 4. (NCT00917644)
Timeframe: 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 9, 10, 12, 24, 36, 48, 72 hours post dose

Interventionhours (Median)
Test Drug1.0
Reference Drug1.0

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Maximum Plasma Concentration (Cmax) of Colchicine

The maximum or peak concentration that colchicine reaches in the plasma. (NCT00960323)
Timeframe: serial pharmacokinetic blood samples drawn prior to dosing on Days 1 and 28 and then 0.5, 1, 1.5, 2, 3, 4, 5, 6, 8, 12 and 24 hours after dose administration.

Interventionpg/mL (Mean)
Colchicine Alone2,023.29
Colchicine With Atorvastatin2,487.96

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Area Under the Concentration Versus Time Curve From Time 0 Extrapolated to Infinity [AUC(0-∞)]

The area under the plasma concentration versus time curve from time 0 to infinity. [AUC(0-∞)] was calculated as the sum of AUC(0-t) plus the ratio of the last measurable plasma concentration to the elimination rate constant for colchicine. (NCT00960323)
Timeframe: Serial pharmacokinetic blood samples drawn prior to dosing on Days 1 and 28 and then 0.5, 1, 1.5, 2, 3, 4, 5, 6, 8, 12 and 24 hours after dose administration.

Interventionpg*hr/mL (Mean)
Colchicine Alone9,592.53
Colchicine With Atorvastatin11,043.58

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Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]

The area under the plasma concentration versus time curve from time 0 to the time of the last measurable concentration (t), as calculated by the linear trapezoidal rule for colchicine. (NCT00960323)
Timeframe: Serial pharmacokinetic blood samples drawn prior to dosing on Days 1 and 28 and then 0.5, 1, 1.5, 2, 3, 4, 5, 6, 8, 12 and 24 hours after dose administration.

Interventionpg*hr/mL (Mean)
Colchicine Alone8,717.33
Colchicine With Atorvastatin10,714.92

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Coronary and Aortic Plaque Inflammation

12 month change in mean FDG-PET TBR (18-fluorodeoxyglucose positron emission tomography target-to-background ratio) (NCT00965185)
Timeframe: Measured at baseline and 1 year

,
Interventionratio (Mean)
Mean FDG-PET TBR of aortaMean FDG-PET TBR of most diseased segment of aorta
Atorvastatin0.04-0.03
Placebo-0.05-0.06

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Lipid Profile

12 month change in lipid profile (NCT00965185)
Timeframe: Measured at baseline and 1 year

,
Interventionmmol/L (Mean)
12 month change in total cholesterol12 month change in HDL cholesterol12 month change in direct LDL12 month change in triglycerides
Atorvastatin-1.230.02-1.00-0.10
Placebo0.12-0.040.300.08

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Plaque Progression

12 month percent change in plaque volume (NCT00965185)
Timeframe: Measured at baseline and 1 year

,
InterventionPercent change (Mean)
12 month change in total plaque volume12 month change in non-calcified plaque volume
Atorvastatin-4.7-19.4
Placebo18.220.4

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Adipocytokines

12 month change in IL-6 (NCT00965185)
Timeframe: Measured at baseline and 1 year

Interventionpg/ml (Mean)
Atorvastatin-1.25
Placebo0.41

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C-reactive Protein (CRP)

12 month change in Log CRP concentration (NCT00965185)
Timeframe: Measured at baseline and 1 year

Interventionlog(mg/L) (Mean)
Atorvastatin-0.3
Placebo0.1

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Immune Function

12 month change in CD4 T-lymphocytes (NCT00965185)
Timeframe: Measured at baseline and 1 year

Interventioncells per microliter (Mean)
Atorvastatin17
Placebo4

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Liver Function Tests (LFTs)

"Number of participants with LFT abnormalities (greater than or equal to 3 times the upper limit of normal).~For reference, the normal ranges for AST and ALT are shown below. Please note that the normal range for ALT at Labcorp changed over the course of the study. AST and ALT elevations were determined based on the normal range at the time the lab test was performed.~ALT: 0-40 IU/L, 0-44 IU/L, or 0-55 IU/L AST: 0-40 IU/L" (NCT00965185)
Timeframe: Measured at baseline, 1, 3, 6, 9, and 12 months

Interventionparticipants (Number)
Atorvastatin3
Placebo2

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Periprocedural Myonecrosis

(NCT00979940)
Timeframe: 16-24 hours post PCI

Interventionparticipants (Number)
No Atorvastatin17
Atorvastatin15

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Percent Change From Baseline in Lipid Parameters

Percent change from baseline calculated as: 100*(change at Month X)/(baseline value). (NCT00993915)
Timeframe: Month 6

Interventionpercent change (Mean)
Change at Month 6 in Total cholesterol, n=593Change at Month 6 in LDL, n=583Change at Month 6 in HDL, n=562Change at Month 6 in Triglyceride, n=585
Atorvastatin-33.57-40.6614.49-23.05

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Change From Baseline in Lipid Parameters

Lipid parameters include HDL cholesterol, LDL cholesterol, total cholesterol, and total triglycerides. Change = Month 6 value minus baseline (NCT00993915)
Timeframe: Month 6

Interventionmg/dL (Mean)
Change at Month 6 in Total cholesterol, n=593Change at Month 6 in LDL, n=583Change at Month 6 in HDL, n=562Change at Month 6 in Triglycerides, n=585
Atorvastatin-98.06-76.843.15-70.57

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Percentage of Participants Achieving LDL Level Less Than or Equal to (≤) 100 mg/dL at the 6 Month Visit

(NCT00993915)
Timeframe: Month 6

Interventionpercentage of participants (Number)
Atorvastatin51.52

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Major Adverse Cardiovascular Events

The number of patients who experienced major adverse cardiovascular endpoints (MACE) including death, myocardial infarction, coronary revascularization, and stroke during the follow-up periods. (NCT01004406)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Intensive LDL-lowering Therapy (ILLT)1
Standard Statin Monotherapy (SMT)0

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Change in % Necrotic Core (NC) Component of Atheroma From Baseline to 12 Weeks Post-PCI as Assessed Via IVUS-VH

The %NC component of atheroma were obtained via IVUS-VH at 2 time points (baseline during index PCI and 12-week follow-up). (NCT01004406)
Timeframe: baseline and 12-week follow-up

Interventionpercentage of atheroma component (Mean)
Intensive LDL-lowering Therapy (ILLT)0.007
Standard Statin Monotherapy (SMT)-0.006

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Endothelial Progenitor Cell Colony Forming Units (EPC-CFU) Per Milliliter of Peripheral Blood Across Time

The cell culture assay and quantification of circulating EPC-CFU were performed for patients recruited at the Dallas VA center only. The assay were done at 4 time points (pre-PCI, post-PCI, 4-week follow-up, and 12-week follow-up). (NCT01004406)
Timeframe: pre-PCI, post-PCI, 4-week follow-up, and 12-week follow-up

,
Interventioncolonies/ml (Mean)
baseline pre-PCIbaseline post-PCI4-week follow-up12-week follow-up
Intensive LDL-lowering Therapy (ILLT)13.7115.8525.3927.62
Standard Statin Monotherapy (SMT)13.8913.3317.8621.50

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Change in the Total Atheroma Volume of the Target Coronary Artery From Baseline to 12 Weeks Post-PCI as Assessed Via Intravascular Ultrasound With Virtual Histology (IVUS-VH)

The primary effectiveness outcome measure was the change in the total atheroma volume within a ≥ 20 mm long segment of the target coronary artery from baseline to 12 weeks post-PCI. The measurement was done via IVUS-VH at 2 time points (baseline during index PCI and 12-week follow-up). (NCT01004406)
Timeframe: baseline and 12-week follow-up

Interventionmm^3 (Mean)
Intensive LDL-lowering Therapy (ILLT)-3.70
Standard Statin Monotherapy (SMT)10.79

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Symbol Digit Modalities Test - Written Score

The SDMT is a measure of divided attention, visual scanning and motor speed. This measure involves a coding key consisting of 9 abstract symbols, each paired with a number ranging from 1 to 9. The subject is required to scan the key and write down the number corresponding to each symbol as fast as possible. The number of correct substitution within 90 seconds is recorded. In the written version of the test the subject fills in the numbers that correspond to the symbols. In the oral version the examiner records the numbers spoken by the subject. The score is the number of correctly coded items from 0-110 in 90 seconds. A higher score indicates better performance. (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group55
mTBI-placebo Group55

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Brief Visuospatial Memory Test - Revised

The BVMT-R is a measure of visuospatial memory. Six equivalent, alternate stimulus forms consist of six geometric figures printed in a 2 x 3 array on separate pages. In three Learning Trials, the subject views the stimulus page for 10 seconds and is asked to draw as many of the figures as possible in their correct location. A Delayed Recall Trial is administered after a 25-minute delay. Last, a Recognition Trial, in which the respondent is asked to identify which of 12 figures were included among the original geometric figures, is administered. Scoring of the immediate and delayed recall are based on the accuracy of the drawings and the location of the figures. For each figure, one point is awarded to each satisfactory domain resulting in a maximum of 12-points per trial. (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group33
mTBI-placebo Group31

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Rivermead Post-Concussion Symptoms Questionnaire, at 3 Months After Injury.

The Rivermead Post-Concussive Symptoms Questionnaire (RPQ) is a 16-item self-report measure of the presence and severity of the 16 most commonly reported post-concussive symptoms found in the literature. The scale compares any current symptoms to pre-injury symptom levels to account for potential symptom exacerbation due to TBI. The range of scores is 0-64. Values for each of the 16 items include 0 (not experienced at all), 1 (no more of a problem than before the injury), 2 (mild problem), 3 (moderate problem), 4 (severe problem). The total score was a summation of symptoms that represented new symptom onset or an exacerbation of a symptom present pre-injury. (King, N.S., Crawford, S., Wenden, F.J., Moss, N.E., & Wade, D.T. [1995]. The Rivermead Post Concussion Symptoms Questionnaire: A Measure of Symptoms Commonly Experiences after Head Injury and its Reliability. Journal of Neurology 242: 587-92.) (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group2
mTBI-placebo Group3.5

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Post-traumatic Stress Checklist - Civilian Form

"The Post Traumatic Stress Disorder Checklist (PCL) is a 17-item self report measure of the DSM-IV symptoms of PTSD. Respondents rate how much they were bothered by a symptom on a 5-point scale ranging from 1 (not at all) to 5 (extremely). The PCL was scored as a total score (range 17-85), with higher total scores indicating more symptoms. (Weathers, F., Litz, B., Herman, D., Huska, J., & Keane, T. [October 1993]. The PTSD Checklist [PCL]: Reliability, Validity, and Diagnostic Utility. Paper presented at the Annual Convention of the International Society for Traumatic Stress Studies, San Antonio, TX.)" (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group24
mTBI-placebo Group21

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Medical Outcome Study Short Form 12 - Physical Score

SF-12 is a self-report questionnaire that assesses functional health and well-being. There are 12 items in 8 subscales, including physical, bodily pain, general health, vitality, social functioning, role-emotional, and mental health. Physical and Mental Health Composite Scores are computed using the scores of the 12 questions and range from 0 to 100, where a zero score indicates the lowest level of health measured by the scales and 100 indicates the highest level of health. Both Physical and Mental Health Composite Scales combine the 12 items in such a way that they compare to a national norm with a mean score of 50.0 and a standard deviation of 10.0. (Ware, J.E., Jr., Kosinski, M., Turner-Bowker, D.M., Gandek, B. How to Score Version 2 of the SF-12v2® Health Survey [With a Supplement Documenting SF-12® Health Survey] Lincoln, RI: QualityMetric Incorporated, 2002.) (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group55
mTBI-placebo Group56.5

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Medical Outcome Study Short Form 12 - Mental Score

SF-12 is a self-report questionnaire that assesses functional health and well-being. There are 12 items in 8 subscales, including physical, bodily pain, general health, vitality, social functioning, role-emotional, and mental health. Physical and Mental Health Composite Scores are computed using the scores of the 12 questions and range from 0 to 100, where a zero score indicates the lowest level of health measured by the scales and 100 indicates the highest level of health. Both Physical and Mental Health Composite Scales combine the 12 items in such a way that they compare to a national norm with a mean score of 50.0 and a standard deviation of 10.0. (Ware, J.E., Jr., Kosinski, M., Turner-Bowker, D.M., Gandek, B. How to Score Version 2 of the SF-12v2® Health Survey [With a Supplement Documenting SF-12® Health Survey] Lincoln, RI: QualityMetric Incorporated, 2002.) (NCT01013870)
Timeframe: 3 months

Interventionunits on a scale (Median)
mTBI-atorvastatin Group52
mTBI-placebo Group52

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Connor Davidson Resilience Measure

The Connor-Davidson Resilience scale (CD-RISC) has 25 items, each rated on a 5-point scale (0-4), with higher scores reflecting greater resilience. The sum score has a range from 0 to 100. (Conner KM, Davidson JR. Development of a new resilience scale: the Connor-Davidson Resilience Scale [CD-RISC]. Depress Anxiety 18[2]:76-82,2003]. (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group84
mTBI-placebo Group84

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Center for Epidemiological Study Depression Scale

The CES-D is a widely used screening scale for depression, assessing depressive feelings and behaviors occurring in the past week of a patient's life. The CES-D consists of 20 items, which make up six scales reflecting depressive symptomatology: depressed mood, feelings of guilt and worthlessness, feelings of helplessness and hopelessness, psychomotor retardation, loss of appetite, and sleep disturbance. Each item is scored on a 4-point scale ranging from 0 (rarely/none of the time) to 3 (most/all of the time). Scores for items 4, 8, 12, and 16 are reversed before summing all items to yield a total score, which can range from 0-60. Higher scores indicate more depressive symptoms. (Radloff, LS [1977]. The CES-D Scale: A self-report depression scale for research in the general population. App Psychol Meas, 1, 385-401.) (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group6
mTBI-placebo Group5.5

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Symbol Digit Modalities Test - Oral Score

The SDMT is a measure of divided attention, visual scanning and motor speed. This measure involves a coding key consisting of 9 abstract symbols, each paired with a number ranging from 1 to 9. The subject is required to scan the key and write down the number corresponding to each symbol as fast as possible. The number of correct substitution within 90 seconds is recorded. In the written version of the test the subject fills in the numbers that correspond to the symbols. In the oral version the examiner records the numbers spoken by the subject. The score is the number of correctly coded items from 0-110 in 90 seconds. A higher score indicates better performance. (NCT01013870)
Timeframe: 3 months after injury

Interventionunits on a scale (Median)
mTBI-atorvastatin Group60
mTBI-placebo Group68

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C-Reactive Protein (CRP)

The test for CRP is a laboratory measurement for evaluation of an acute phase reactant of inflammation. Normal range is 1-3 milligram per liter (mg/L). (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionmg/L (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin33.176.316.04
CP-690,550 + Placebo22.253.343.32

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Swollen-Joint Count

Swollen joint count (SJC): an assessment of 66 joints (upper body, upper extremity, and lower extremity). Each joint was assessed for swelling using the following scale: Present/Absent/Not Done/Not Applicable (for artificial joints). (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), Week 12

,
Interventionswollen joints (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin16.906.364.85
CP-690,550 + Placebo15.345.685.15

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Physician's Global Assessment (PhysGA) of Arthritis Pain

The physician evaluated participants disease signs, functional capacity and physical examination independent of the patient's global assessment of arthritis. Physician's response was recorded using 0-100 mm visual analog scale (VAS), where 0=no pain and 100=most severe pain. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), Week 12

,
Interventionmm (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin63.2830.8024.30
CP-690,550 + Placebo65.3831.8529.70

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Percentage of Participants Achieving American College of Rheumatology 70% (ACR70) Response

ACR70 responses were defined as greater than or equal to 70% improvement in tender or swollen joint counts and 70% improvement in 3 of the 5 remaining ACR-core set measures: 1) physician's global assessment of disease activity, 2) participants assessment of disease activity, 3) participants assessment of pain, 4) participants assessment of functional disability via a health assessment questionnaire, and 5) C-reactive protein at each visit. (NCT01059864)
Timeframe: Week 6 (Baseline), 12

,
Interventionpercentage of participants (Number)
Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin20.034.8
CP-690,550 + Placebo19.130.4

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Percentage of Participants Achieving American College of Rheumatology 50% (ACR50) Response

ACR50 responses were defined as greater than or equal to 50% improvement in tender or swollen joint counts and 50% improvement in 3 of the 5 remaining ACR-core set measures: 1) physician's global assessment of disease activity, 2) participants assessment of disease activity, 3) participants assessment of pain, 4) participants assessment of functional disability via a health assessment questionnaire, and 5) C-reactive protein at each visit. (NCT01059864)
Timeframe: Week 6 (Baseline), 12

,
Interventionpercentage of participants (Number)
Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin48.067.4
CP-690,550 + Placebo42.645.7

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Percentage of Participants Achieving American College of Rheumatology 20% (ACR20) Response

ACR20 responses were defined as greater than or equal to 20% improvement in tender or swollen joint counts and 20% improvement in 3 of the 5 remaining ACR-core set measures: 1) physician's global assessment of disease activity, 2) participants assessment of disease activity, 3) participants assessment of pain, 4) participants assessment of functional disability via a health assessment questionnaire, and 5) C-reactive protein at each visit. (NCT01059864)
Timeframe: Week 6 (Baseline), 12

,
Interventionpercentage of participants (Number)
Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin76.082.6
CP-690,550 + Placebo76.665.2

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Patient's Global Assessment (PtGA) of Arthritis Pain

"Participants answered: Considering all the ways your arthritis affects you, how are you feeling today? Participants responded by using a 0-100 mm visual analog scale where 0=no pain and 100=most severe pain." (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), Week 12

,
Interventionmm (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin68.1027.6623.33
CP-690,550 + Placebo61.6728.0824.15

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Change From Baseline in Low Density Lipoprotein-Cholesterol (LDL-C) at Week 12

(NCT01059864)
Timeframe: Baseline (Week 6), Week 12

Interventionmilligram per deciliter (mg/dL) (Least Squares Mean)
CP-690,550 + Atorvastatin-51.49
CP-690,550 + Placebo5.30

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Patient Assessment of Arthritis Pain

Participants assessed the severity of their arthritis pain using a 100 millimeter (mm) visual analog scale (VAS). The scale ranged from 0 (no pain) to 100 (most severe pain), measurement on a scale corresponds to the magnitude of their pain. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionmm (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin65.6630.1825.72
CP-690,550 + Placebo64.4131.2629.09

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Health Assessment Questionnaire Disability Index (HAQ-DI)

HAQ-DI: participant-reported assessment of ability to perform tasks in 8 functional categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week. Each item scored on 4-point scale from 0 to 3: 0=no difficulty; 1=some difficulty; 2=much difficulty; 3=unable to do. Overall score was computed as the sum of domain scores and divided by the number of domains answered. Total possible score range 0-3, 0=least functional difficulty and 3=extreme functional difficulty. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionunits on a scale (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin1.540.880.74
CP-690,550 + Placebo1.460.880.92

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Percent Change From Baseline (Week 6) in Low Density Lipoprotein-Cholesterol (LDL-C) Level at Week 12

(NCT01059864)
Timeframe: Baseline (Week 6), Week 12

Interventionpercent change (Least Squares Mean)
CP-690,550 + Atorvastatin-35.34
CP-690,550 + Placebo5.80

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Tender-Joint Count

Tender joint count (TJC) is an assessment of 68 joints (upper body, upper extremity, and lower extremity). Each joint's response to pressure/motion was assessed using the following scale: Present/Absent/Not Done/Not Applicable (for artificial joints). (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventiontender joints (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin23.2010.488.57
CP-690,550 + Placebo21.3810.997.83

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Erythrocyte Sedimentation Rate (ESR)

ESR is a laboratory test that provides a non-specific measure of inflammation. The test assesses the rate at which red blood cells fall in a test tube. Normal range is 0-30 mm/hr. A higher rate is consistent with inflammation. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionmm/hr (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin69.7637.4234.43
CP-690,550 + Placebo60.3229.9830.31

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Disease Activity Score Using 28-Joint Count and Erythrocyte Sedimentation Rate (4 Variables) (DAS28-4 [ESR])

DAS28-4 (ESR) was calculated from the number of swollen joints (SJC) and painful joints (PJC) using the 28 joints count, the erythrocyte sedimentation rate (ESR) [mm/hr] and patient's global assessment (PtGA) of disease activity (participant rated arthritis activity assessment with transformed scores ranging from 0 to 10; higher scores indicated greater affectation due to disease activity). DAS28-4 (ESR) <=3.2 indicated low disease activity, DAS28-4 (ESR) >3.2 to 5.1 indicated moderate to high disease activity. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionunits on a scale (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin6.604.333.84
CP-690,550 + Placebo6.444.263.81

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12-Hours Fasting Lipid Profile: Level of Lipoprotein Particles

Participants were required to fast for 12 hours prior to sampling for lipid profile which included following parameters: total and large VLDL-C and chylomicron particles (VLDLCP), medium and small VLDL-C particles; total, large, medium and small LDL-C particles; and intermediate density lipoprotein (IDL). (NCT01059864)
Timeframe: Day 0, Week 2, 6 (Baseline), 10, 12

,
Interventionnanomoles per liter (nmol/L) (Mean)
Day 0: Total VLDLCPWeek 2: Total VLDLCPWeek 6(Baseline): Total VLDLCPWeek 10: Total VLDLCPWeek 12: Total VLDLCPDay 0: Large VLDLCPWeek 2: Large VLDLCPWeek 6(Baseline): Large VLDLCPWeek 10: Large VLDLCPWeek 12: Large VLDLCPDay 0: Medium VLDL-C ParticlesWeek 2: Medium VLDL-C ParticlesWeek 6 (Baseline): Medium VLDL-C ParticlesWeek 10: Medium VLDL-C ParticlesWeek 12: Medium VLDL-C ParticlesDay 0: Small VLDL-C ParticlesWeek 2: Small VLDL-C ParticlesWeek 6 (Baseline): Small VLDL-C ParticlesWeek 10: Small VLDL-C ParticlesWeek 12: Small VLDL-C ParticlesDay 0: Total LDL-C ParticlesWeek 2: Total LDL-C ParticlesWeek 6 (Baseline): Total LDL-C ParticlesWeek 10: Total LDL-C ParticlesWeek 12: Total LDL-C ParticlesDay 0: IDL ParticlesWeek 2: IDL ParticlesWeek 6 (Baseline): IDL ParticlesWeek 10: IDL ParticlesWeek 12: IDL ParticlesDay 0: Large LDL-C ParticlesWeek 2: Large LDL-C ParticlesWeek 6 (Baseline): Large LDL-C ParticlesWeek 10: Large LDL-C ParticlesWeek 12: Large LDL-C ParticlesDay 0: Total Small LDL-C ParticlesWeek 2: Total Small LDL-C ParticlesWeek 6 (Baseline): Total Small LDL-C ParticlesWeek 10: Total Small LDL-C ParticlesWeek 12: Total Small LDL-C ParticlesDay 0: Medium Small LDL-C ParticlesWeek 2: Medium Small LDL-C ParticlesWeek 6 (Baseline): Medium Small LDL-C ParticlesWeek 10: Medium Small LDL-C ParticlesWeek 12: Medium Small LDL-C ParticlesDay 0: Very Small LDL-C ParticlesWeek 2: Very Small LDL-C ParticlesWeek 6 (Baseline): Very Small LDL-C ParticlesWeek 10: Very Small LDL-C ParticlesWeek 12: Very Small LDL-C Particles
CP-690,550 + Atorvastatin61.0068.8973.2353.2245.071.253.092.432.471.4522.1127.2026.5425.3620.6737.6438.6144.2625.3822.941111.81175.91154.3787.24801.3927.1236.5843.3724.4622.22451.88543.28581.73400.11424.26632.73596.12528.94362.72354.96127.08117.42104.9478.7877.96505.59478.62424.02283.76276.93
CP-690,550 + Placebo56.2065.2465.5170.0772.112.792.502.532.852.6323.2625.7524.5925.2725.4630.1536.9838.3941.9444.011222.21201.71195.01271.21264.930.9855.7453.9469.7866.91468.67589.28631.55582.04598.34722.46556.67509.45619.43599.77149.43114.74108.19130.57124.20572.98441.93401.21489.00475.55

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12-Hours Fasting Lipid Profile: Level of High Density Lipoprotein Cholesterol (HDL-C) Particles

Participants were required to fast for 12 hours prior to sampling for lipid profile which included following parameters: total, large, medium and small HDL-C particles. (NCT01059864)
Timeframe: Day 0, Week 2, 6 (Baseline), 10, 12

,
Interventionmicromole per liter (mcmol/L) (Mean)
Day 0: Total HDL-C ParticlesWeek 2: Total HDL-C ParticlesWeek 6 (Baseline): Total HDL-C ParticlesWeek 10: Total HDL-C ParticlesWeek 12: Total HDL-C ParticlesDay 0: Large HDL-C ParticlesWeek 2: Large HDL-C ParticlesWeek 6 (Baseline): Large HDL-C ParticlesWeek 10: Large HDL-C ParticlesWeek 12: Large HDL-C ParticlesDay 0: Medium HDL-C ParticlesWeek 2: Medium HDL-C ParticlesWeek 6 (Baseline): Medium HDL-C ParticlesWeek 10: Medium HDL-C ParticlesWeek 12: Medium HDL-C ParticlesDay 0: Small HDL-C ParticlesWeek 2: Small HDL-C ParticlesWeek 6 (Baseline): Small HDL-C ParticlesWeek 10: Small HDL-C ParticlesWeek 12: Small HDL-C Particles
CP-690,550 + Atorvastatin27.0830.8932.9034.5734.208.889.0810.0410.9811.233.743.873.894.573.8514.4417.9418.9719.0419.15
CP-690,550 + Placebo29.5833.6835.4436.0735.778.759.5610.639.9310.234.014.433.984.524.7416.8019.7020.8321.6320.79

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12-Hours Fasting Lipid Profile

Participants were required to fast for 12 hours prior to sampling for lipid profile which included following parameters: LDL-C, high-density lipoprotein-cholesterol (HDL-C), very low density lipoprotein-cholesterol (VLDL-C), total cholesterol, apolipoprotein A-1, apolipoprotein B, triglycerides (TGs) and Non-HDL-C. (NCT01059864)
Timeframe: Day 0, Week 2, 6 (Baseline), 10, 12

,
Interventionmg/dL (Mean)
Day 0: LDL-CWeek 2: LDL-CWeek 6 (Baseline): LDL-CWeek 10: LDL-CWeek 12: LDL-CDay 0: HDL-CWeek 2: HDL-CWeek 6 (Baseline): HDL-CWeek 10: HDL-CWeek 12: HDL-CDay 0: Total CholesterolWeek 2: Total CholesterolWeek 6 (Baseline): Total CholesterolWeek 10: Total CholesterolWeek 12: Total CholesterolDay 0: Apolipoprotein A-1Week 2: Apolipoprotein A-1Week 6 (Baseline): Apolipoprotein A-1Week 10: Apolipoprotein A-1Week 12: Apolipoprotein A-1Day 0: Apolipoprotein BWeek 2: Apolipoprotein BWeek 6 (Baseline): Apolipoprotein BWeek 10: Apolipoprotein BWeek 12: Apolipoprotein BDay 0: TGsWeek 2: TGsWeek 6 (Baseline): TGsWeek 10: TGsWeek 12: TGsDay 0: VLDL-CWeek 2: VLDL-CWeek 6 (Baseline): VLDL-CWeek 10: VLDL-CWeek 12: VLDL-CDay 0: Non-HDL-CWeek 2: Non-HDL-CWeek 6 (Baseline): Non-HDL-CWeek 10: Non-HDL-CWeek 12: Non-HDL-C
CP-690,550 + Atorvastatin111.99124.87135.8380.5884.0354.9661.1167.3970.1271.09189.62213.11228.22174.42175.18139.48153.80164.18171.87171.0290.3096.18100.2869.3270.35113.54135.69127.16117.90100.7857.7381.4876.1069.0051.59134.66152.00160.83104.30104.09
CP-690,550 + Placebo114.68132.94138.26141.52142.6156.2065.3570.5870.3171.73196.58222.85234.27238.16240.49148.36168.13171.81172.30178.3694.09101.74100.38103.96105.84128.76123.18127.63133.63131.4870.4174.8975.3079.4378.64140.39157.50163.69167.85168.76

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Disease Activity Score Using 28-Joint Count and C-Reactive Protein (3 Variables) (DAS28-3 [CRP])

DAS28-3 (CRP) was calculated from the number of swollen joints (SJC) and painful joints (PJC) using the 28 joints count and the CRP (milligram per liter [mg/L]). DAS28-3 (CRP) less than or equal to (<=)3.2 indicated low disease activity, DAS28-3 (CRP) more than (>) 3.2 to 5.1 indicated moderate to high disease activity. (NCT01059864)
Timeframe: Day 0, Week 6 (Baseline), 12

,
Interventionunits on a scale (Mean)
Day 0Week 6 (Baseline)Week 12
CP-690,550 + Atorvastatin5.383.443.06
CP-690,550 + Placebo5.233.332.99

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12-Hours Fasting Lipid Profile: Particle Size of Lipoproteins

Participants were required to fast for 12 hours prior to sampling for lipid profile which included following parameters: plasma lipoprotein VLDL-C, LDL-C and HDL-C particles size. (NCT01059864)
Timeframe: Day 0, Week 2, 6 (Baseline), 10, 12

,
Interventionnanometer (nm) (Mean)
Day 0: VLDL-C ParticlesWeek 2: VLDL-C ParticlesWeek 6 (Baseline): VLDL-C ParticlesWeek 10: VLDL-C ParticlesWeek 12: VLDL-C ParticlesDay 0: LDL-C ParticlesWeek 2: LDL-C ParticlesWeek 6 (Baseline): LDL-C ParticlesWeek 10: LDL-C ParticlesWeek 12: LDL-C ParticlesDay 0: HDL-C ParticlesWeek 2: HDL-C ParticlesWeek 6 (Baseline): HDL-C ParticlesWeek 10: HDL-C ParticlesWeek 12: HDL-C Particles
CP-690,550 + Atorvastatin42.0847.4144.7548.2947.3521.1921.4421.6521.6721.749.299.259.319.339.36
CP-690,550 + Placebo46.1547.3148.6747.4847.5821.1421.5521.6621.4521.519.219.269.309.229.25

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High Sensitive C-reactive Protein (hsCRP mg/L)

(NCT01096875)
Timeframe: 5 days postoperatively

Interventionmg/L (Mean)
Atorvastatin4.3
Placebo11.4

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Left Ventricular Ejection Fraction (LVEF %) Measured at 30 Days Postoperatively

(NCT01096875)
Timeframe: Change between statin and placebo groups at 30 days postoperatively

Interventionpercentage of LVEF (Mean)
Atorvastatin54.3
Placebo53.2

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Endothelial Progenitor Cells (EPCs) Count (Cells/µl)

(NCT01096875)
Timeframe: Postoperative 6th hours

Interventioncells/µl (Mean)
Atorvastatin5.00
Placebo2.19

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High Sensitive C-reactive Protein (hsCRP mg/L)

(NCT01096875)
Timeframe: Postoperative 6th hours

Interventionmg/L (Mean)
Atorvastatin72.9
Placebo96.0

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Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Simvastatin or Rosuvastatin and Simvastatin/Rosuvastatin Monotherapy

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
40 mg Simvastatin Monotherapy-34.9
100 mg LY2484595 + 40 mg Simvastatin-46.1
10 mg Rosuvastatin Monotherapy-38.8
100 mg LY2484595 + 10 mg Rosuvastatin-52.3

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Percent Change From Baseline to 12 Weeks Endpoint in Plasma Cholesteryl Ester Transfer Protein (CETP) Activity

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of picomoles/mL/minute (Least Squares Mean)
30 mg LY2484595 Monotherapy-49.48
100 mg LY2484595 Monotherapy-70.80
500 mg LY2484595 Monotherapy-89.10
Placebo12.12
20 mg Atorvastatin Monotherapy-0.01
100 mg LY2484595 + 20 mg Atorvastatin-72.00
40 mg Simvastatin Monotherapy-2.23
100 mg LY2484595 + 40 mg Simvastatin-64.64
10 mg Rosuvastatin Monotherapy-7.19
100 mg LY2484595 + 10 mg Rosuvastatin-73.24

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Percent Change From Baseline to 12 Weeks Endpoint in Plasma Cholesteryl Ester Transfer Protein (CETP) Mass

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of micrograms/mL (mcg/mL) (Least Squares Mean)
30 mg LY2484595 Monotherapy63.94
100 mg LY2484595 Monotherapy92.27
500 mg LY2484595 Monotherapy136.66
Placebo0.58
20 mg Atorvastatin Monotherapy-11.8
100 mg LY2484595 + 20 mg Atorvastatin62.98
40 mg Simvastatin Monotherapy-11.14
100 mg LY2484595 + 40 mg Simvastatin65.92
10 mg Rosuvastatin Monotherapy-16.58
100 mg LY2484595 + 10 mg Rosuvastatin64.08

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Pharmacokinetics - LY2484595 Area Under the Concentration-Time Curve (AUC) at Steady-State

(NCT01105975)
Timeframe: Baseline up to 12 weeks

Interventionnanograms*hour/milliliter (ng*h/mL) (Geometric Mean)
30 mg LY2484595 Monotherapy2300
100 mg LY2484595 Monotherapy5900
500 mg LY2484595 Monotherapy19700
100 mg LY2484595 + 20 mg Atorvastatin5500
100 mg LY2484595 + 40 mg Simvastatin5620
100 mg LY2484595 + 10 mg Rosuvastatin5960

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Change From Baseline to 12 Weeks Endpoint in Blood Pressure (BP)

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

,,,,,,,,,
Interventionmillimeters of mercury (mmHg) (Least Squares Mean)
Diastolic BPSystolic BP
10 mg Rosuvastatin Monotherapy2.20.0
100 mg LY2484595 + 10 mg Rosuvastatin-0.13.8
100 mg LY2484595 + 20 mg Atorvastatin1.22.1
100 mg LY2484595 + 40 mg Simvastatin2.32.3
100 mg LY2484595 Monotherapy0.84.3
20 mg Atorvastatin Monotherapy0.20.2
30 mg LY2484595 Monotherapy1.14.4
40 mg Simvastatin Monotherapy-1.50.0
500 mg LY2484595 Monotherapy1.21.4
Placebo1.62.8

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The Number of Episodes of Rashes at Any Time From Baseline Through Week 12

All rash cases were adjudicated by a central dermatologist blinded to treatment assignment according to a study-specific Clinical Events Committee (CEC) charter. Rash events were assessed according to clinical relevance (high risk, low risk, not a relevant dermatosis, or insufficient documentation for determination). A participant could be reported in multiple categories. (NCT01105975)
Timeframe: Baseline through Week 12

,,,,,,,,,
Interventionevents (Number)
High Risk (HR)- AngioedemaHR - Insufficient Documentation for DeterminationLow RiskNot a Relevant DermatosesInsufficient Documentation for Determination
10 mg Rosuvastatin Monotherapy00000
100 mg LY2484595 + 10 mg Rosuvastatin01210
100 mg LY2484595 + 20 mg Atorvastatin00020
100 mg LY2484595 + 40 mg Simvastatin00140
100 mg LY2484595 Monotherapy00050
20 mg Atorvastatin Monotherapy00010
30 mg LY2484595 Monotherapy00040
40 mg Simvastatin Monotherapy10060
500 mg LY2484595 Monotherapy00030
Placebo00000

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Change From Baseline to 12 Weeks Endpoint in Serum Sodium

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionmilliequivalents/Liter (Least Squares Mean)
30 mg LY2484595 Monotherapy0.3
100 mg LY2484595 Monotherapy0.3
500 mg LY2484595 Monotherapy0.5
Placebo0.1
20 mg Atorvastatin Monotherapy1.3
100 mg LY2484595 + 20 mg Atorvastatin0.6
40 mg Simvastatin Monotherapy0.8
100 mg LY2484595 + 40 mg Simvastatin0.9
10 mg Rosuvastatin Monotherapy0.5
100 mg LY2484595 + 10 mg Rosuvastatin0.3

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Change From Baseline to 12 Weeks Endpoint in Serum Potassium

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionmilliequivalents/Liter (Least Squares Mean)
30 mg LY2484595 Monotherapy-0.04
100 mg LY2484595 Monotherapy0.01
500 mg LY2484595 Monotherapy-0.02
Placebo-0.08
20 mg Atorvastatin Monotherapy0.09
100 mg LY2484595 + 20 mg Atorvastatin0.08
40 mg Simvastatin Monotherapy0.03
100 mg LY2484595 + 40 mg Simvastatin0.02
10 mg Rosuvastatin Monotherapy-0.07
100 mg LY2484595 + 10 mg Rosuvastatin-0.05

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Change From Baseline to 12 Weeks Endpoint in Serum Bicarbonate

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionmilliequivalents/Liter (Least Squares Mean)
30 mg LY2484595 Monotherapy0.40
100 mg LY2484595 Monotherapy0.60
500 mg LY2484595 Monotherapy0.51
Placebo0.27
20 mg Atorvastatin Monotherapy0.10
100 mg LY2484595 + 20 mg Atorvastatin0.58
40 mg Simvastatin Monotherapy1.04
100 mg LY2484595 + 40 mg Simvastatin0.58
10 mg Rosuvastatin Monotherapy0.78
100 mg LY2484595 + 10 mg Rosuvastatin1.25

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Change From Baseline to 12 Weeks Endpoint in Serum Aldosterone

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionnanogram/deciliter (ng/dL) (Least Squares Mean)
30 mg LY2484595 Monotherapy-0.5
100 mg LY2484595 Monotherapy1.0
500 mg LY2484595 Monotherapy-0.3
Placebo-1.0
20 mg Atorvastatin Monotherapy-1.0
100 mg LY2484595 + 20 mg Atorvastatin0.4
40 mg Simvastatin Monotherapy0.0
100 mg LY2484595 + 40 mg Simvastatin-1.7
10 mg Rosuvastatin Monotherapy-2.5
100 mg LY2484595 + 10 mg Rosuvastatin0.0

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Change From Baseline to 12 Weeks Endpoint in Plasma Renin Activity

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionnanograms/milliliter/hour (ng/mL/h) (Least Squares Mean)
30 mg LY2484595 Monotherapy-0.06
100 mg LY2484595 Monotherapy-0.11
500 mg LY2484595 Monotherapy-0.58
Placebo-0.30
20 mg Atorvastatin Monotherapy-0.58
100 mg LY2484595 + 20 mg Atorvastatin-0.26
40 mg Simvastatin Monotherapy-0.16
100 mg LY2484595 + 40 mg Simvastatin0.00
10 mg Rosuvastatin Monotherapy-0.86
100 mg LY2484595 + 10 mg Rosuvastatin-0.29

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Change From Baseline to 18 Weeks Endpoint in EuroQoL Questionnaire - 5 Dimensions (EQ-5D) Score

EQ-5D is a health-related, quality-of-life instrument. It allows participants to rate their health state in 5 domains: mobility, self-care, usual activities, pain/discomfort, and mood. A single score 1 -3 is generated for each domain, with 1=no problem and 3= extreme problems. The outcome ratings on the 5 domains are mapped to a single index through an algorithm. The index ranges 0-1, with the higher score indicating a better health state perceived by the participants. LS Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline up to Week 18

Interventionunits on a scale (Least Squares Mean)
30 mg LY2484595 Monotherapy0.008
100 mg LY2484595 Monotherapy0.002
500 mg LY2484595 Monotherapy0.012
Placebo-0.001
20 mg Atorvastatin Monotherapy-0.002
100 mg LY2484595 + 20 mg Atorvastatin-0.006
40 mg Simvastatin Monotherapy-0.001
100 mg LY2484595 + 40 mg Simvastatin-0.001
10 mg Rosuvastatin Monotherapy0.014
100 mg LY2484595 + 10 mg Rosuvastatin-0.047

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Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 in Combination With Atorvastatin and Atorvastatin Monotherapy

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
20 mg Atorvastatin Monotherapy1.4
100 mg LY2484595 + 20 mg Atorvastatin79.9

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Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 and Placebo

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
30 mg LY2484595 Monotherapy53.6
100 mg LY2484595 Monotherapy94.6
500 mg LY2484595 Monotherapy128.8
Placebo-3.0

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Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 and Placebo

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
30 mg LY2484595 Monotherapy-13.6
100 mg LY2484595 Monotherapy-22.3
500 mg LY2484595 Monotherapy-35.9
Placebo3.9

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Percent Change From Baseline to 12 Weeks Endpoint in Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Atorvastatin and Atorvastatin Monotherapy

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
20 mg Atorvastatin Monotherapy-33.6
100 mg LY2484595 + 20 mg Atorvastatin-47.6

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Percent Change From Baseline to 12 Weeks Endpoint in High Density Lipoprotein Cholesterol (HDL-C) With LY2484595 in Combination With Simvastatin or Rosuvastatin and Simvastatin/Rosuvastatin Monotherapy

Least Squares (LS) Mean values were controlled for region, baseline measurement, treatment, visit, and treatment by visit interaction. (NCT01105975)
Timeframe: Baseline, Week 12

Interventionpercent change of mg/dL (Least Squares Mean)
40 mg Simvastatin Monotherapy7.3
100 mg LY2484595 + 40 mg Simvastatin86.6
10 mg Rosuvastatin Monotherapy5.5
100 mg LY2484595 + 10 mg Rosuvastatin94.0

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Hepatic Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Hepatic Dysfunction is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Hepatic Dysfunction904
With Hepatic Dysfunction122

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Renal Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Renal Dysfunction is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Renal Dysfunction937
With Renal Dysfunction88

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Risk Factors for the Proportion of Responders for Hypertension -Age.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether <65 years or >=65 is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
<65 Years347
>=65 Years804

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Risk Factors for the Proportion of Responders for Hypertension -Complications.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Complications is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Complications527
With Complications624

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Risk Factors for the Proportion of Responders for Hypertension -Concomitant Drugs.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Concomitant Drugs is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Concomitant Drugs339
With Concomitant Drugs812

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Risk Factors for the Proportion of Responders for Hypertension -Gender.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether male or female is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Male415
Female736

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Risk Factors for the Proportion of Responders for Hypertension -Hepatic Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Hepatic Dysfunction is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Hepatic Dysfunction1008
With Hepatic Dysfunction131

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Risk Factors for the Proportion of Responders for Hypertension -Hypertension Severity.

"Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether Hypertension severity, ClassⅠ, ClassⅡ, or ClassⅢ is significant risk factor for Hypertension. Hypertension severity is defined by Guideline for the Management of hypertension (The Japan Society of Hypertension)." (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
ClassⅠ615
ClassⅡ325
ClassⅢ85

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Risk Factors for the Proportion of Responders for Hypertension -Renal Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Renal Dysfunction is significant risk factor for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Renal Dysfunction1036
With Renal Dysfunction102

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Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Angina Pectoris.

The physician performed efficacy evaluations at the end of the observation period (or the time of discontinuing administration), compared with the data before the start of administration of this drug, and enteterd the results for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Amlodipine and Atorvastatin Combination Tablet163

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Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Hypercholesterolemia or Familial Hypercholesterolemia.

The physician performed efficacy evaluations at the end of the observation period (or the time of discontinuing administration), compared with the data before the start of administration of this drug, and entered the results for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Amlodipine and Atorvastatin Combination Tablet1034

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Number of Participants That Responded to Amlodipine/Atorvastatin Treatment With Hypertension.

The physician performed efficacy evaluations at the end of the observation period (or the time of discontinuing administration), compared with the data before the start of administration of this drug, and entered the results for Hypertension. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Amlodipine and Atorvastatin Combination Tablet1151

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Risk Factor for the Proportion of Responders of Amlodipine/Atorvastatin Combination Tablets for Hypercholesterolemia or Familial Hypercholesterolemia - Hypercholesterolemia Expression Type.

"Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether Hypercholesterolemia expression type, Ⅰ, Ⅱa, Ⅱb, Ⅲ, Ⅳ, or Ⅴ is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. Hypercholesterolemia expression types are defined by Japan Atherosclerosis Society Guideline for Prevention of Atherosclerosis Cardiovascular Diseases." (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Type Ⅰ13
Type Ⅱa533
Type Ⅱb180
Type Ⅲ10
Type Ⅳ5

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Risk Factors for the Proportion of Responders for Angina Pectoris -Age.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether <65 years or >=65 is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
<65 Years45
>=65 Years118

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Risk Factors for the Proportion of Responders for Angina Pectoris -Angina Pectoris Severity.

"Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether Angina Pectoris functional classification Severity, Class1, Class2, Class3, or Class4 is significant risk factor for Angina Pectoris. Angina Pectoris functional classification Severity is defined by Canadian Cardiovascular Society functional Classification of Angina." (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Class1122
Class211
Class32
Class41

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Risk Factors for the Proportion of Responders for Angina Pectoris -Complications.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Angina Pectoris is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Complications57
With Complications106

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Risk Factors for the Proportion of Responders for Angina Pectoris -Concomitant Drugs.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Concomitant Drugs is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Concomitant Drugs22
With Concomitant Drugs141

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Risk Factors for the Proportion of Responders for Angina Pectoris -Gender.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether male or female is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Male75
Female88

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Risk Factors for the Proportion of Responders for Angina Pectoris -Hepatic Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Hepatic Dysfunction is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Hepatic Dysfunction145
With Hepatic Dysfunction18

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Risk Factors for the Proportion of Responders for Angina Pectoris -Renal Dysfunction.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Renal Dysfunction is significant risk factor for Angina Pectoris. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Renal Dysfunction137
With Renal Dysfunction25

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Age.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether <65 years or >=65 is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
<65 Years305
>=65 Years729

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Complications.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Complications is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Complications482
With Complications552

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Concomitant Drugs.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether with or without Concomitant Drugs is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Without Concomitant Drugs306
With Concomitant Drugs728

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Risk Factors for the Proportion of Responders for Hypercholesterolemia or Familial Hypercholesterolemia -Gender.

Number of Participants with responders of Amlodipine/Atorvastatin Combination Tablets to determine whether male or female is significant risk factor for Hypercholesterolemia or Familial Hypercholesterolemia. (NCT01107743)
Timeframe: 8 weeks

Interventionparticipants (Number)
Male380
Female654

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Sitagliptin + Atorvastatin: Sitagliptin Maximum Plasma Concentration (Cmax)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng/ml (Mean)
ABCB1 Group 1428
ABCB1 Group 2420
ABCB1 Group 3370

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Sitagliptin + Atorvastatin: Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng*h/ml (Mean)
ABCB1 Group 13501
ABCB1 Group 23430
ABCB1 Group 33117

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Relative Change in Sitagliptin Renal Clearance (CLr)

CLr of sitagliptin when administered with atorvastatin divided by CLr of sitagliptin when administered alone (NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours

Interventionratio (Mean)
ABCB1 Group 11.22
ABCB1 Group 20.99
ABCB1 Group 31.0

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Sitagliptin Monotherapy: Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng*hr/ml (Mean)
ABCB1 Group 13638
ABCB1 Group 23502
ABCB1 Group 33129

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Relative Change in Sitagliptin Maximum Plasma Concentration (Cmax)

Cmax of sitagliptin when administered with atorvastatin divided by Cmax of sitagliptin when administered alone (NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionratio (Mean)
ABCB1 Group 10.96
ABCB1 Group 21.0
ABCB1 Group 30.93

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Relative Change in Sitagliptin Area Under the Plasma Concentration-time Curve (AUC) From 0 to Infinity

AUC of sitagliptin when administered with atorvastatin divided by AUC of sitagliptin when administered alone (NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionratio (Mean)
ABCB1 Group 10.96
ABCB1 Group 20.98
ABCB1 Group 30.97

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Atorvastatin Maximum Plasma Concentration (Cmax)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng/ml (Mean)
ABCB1 Group 18.6
ABCB1 Group 27.5
ABCB1 Group 310.6

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Atorvastatin Area Under the Plasma Concentration Time Curve (AUC) Over the Dosing Interval (0-24 Hours)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng*h/ml (Mean)
ABCB1 Group 144.4
ABCB1 Group 235.4
ABCB1 Group 349.0

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Sitagliptin Monotherapy: Sitagliptin Renal Clearance (CLr)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionml/min (Mean)
ABCB1 Group 1254
ABCB1 Group 2232
ABCB1 Group 3359

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Sitagliptin Monotherapy: Sitagliptin Maximum Plasma Concentration (Cmax)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionng/ml (Mean)
ABCB1 Group 1454
ABCB1 Group 2438
ABCB1 Group 3394

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Sitagliptin + Atorvastatin: Sitagliptin Renal Clearance (CLr)

(NCT01112670)
Timeframe: 0, 0.5, 1, 2, 3, 4, 5, 6, 8, 10, 12, 16, 20, 24 hours post-dose

Interventionml/min (Mean)
ABCB1 Group 1280
ABCB1 Group 2226
ABCB1 Group 3339

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Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP) (Phase I)

hs-CRP measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4. Baseline and post-baseline measurements were log-transformed in the response vector, with fixed effects for treatment, time and the interaction of time by treatment. (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Least Squares Mean)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-10.5
Phase I: Atorvastatin 20 mg-6.6
Phase I: Rosuvastatin 10 mg-9.0

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Percent Change From Baseline in Non-HDL-C/HDL-C Ratio (Phase I)

Non HDL-C/HDL-C ratio calculated at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-18.9
Phase I: Atorvastatin 20 mg-6.3
Phase 1: Rosuvastatin 10 mg-12.2

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Percent Change From Baseline in Apo B/Apo A-I Ratio (Phase II)

Apo B/Apo A-I Ratio calculated at Baseline (Week 6; end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-11.2
Phase II: Atorva 40mg-6.4
Phase II: EZ 10mg + Atorva 20mg [R]-11.2
Phase II: Rosuvastatin 20mg-5.4
Phase II: EZ 10mg+Atorva 10mg-6.7

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Percent Change From Baseline in Apo B/Apo A-I Ratio (Phase I)

Apo B/Apo A-I ratio calculated at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-13.0
Phase I: Atorvastatin 20 mg-4.8
Phase 1: Rosuvastatin 10 mg-8.8

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Percent Change From Baseline in Apo B (Phase II)

Apo-B levels measured at Baseline (Week 6; end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-12.0
Phase II: Atorva 40mg-6.3
Phase II: EZ 10mg + Atorva 20mg [R]-14.0
Phase II: Rosuvastatin 20mg-4.9
Phase II: EZ 10mg+Atorva 10mg-4.0

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Percent Change From Baseline in Apo A-I (Phase II)

Apo-A-I levels measured at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase I) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]1.6
Phase II: Atorva 40mg1.4
Phase II: EZ 10mg + Atorva 20mg [R]-0.6
Phase II: Rosuvastatin 20mg0.0
Phase II: EZ 10mg+Atorva 10mg-0.7

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Percent Change From Baseline in Apolipoprotein A-I (Apo A-I) (Phase I)

Apo-A-I measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-0.6
Phase I: Atorvastatin 20 mg-1.9
Rosuvastatin 10 mg1.4

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Percentage of Participants That Reach Target LDL-C Level of < 70 mg/dL (Phase II)

(NCT01154036)
Timeframe: Week 12 (end of Phase II)

InterventionPercentage of Participants (Number)
Phase II: EZ 10mg + Atorva 20mg [A]18.3
Phase II: Atorva 40mg0.8
Phase II: EZ 10mg + Atorva 20mg [R]15.4
Phase II: Rosuvastatin 20mg3.0
Phase II: EZ 10mg+Atorva 10mgNA

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Percentage of Participants That Reach Target LDL-C Level of < 70 mg/dL (Phase I)

(NCT01154036)
Timeframe: Week 6 (End of Phase I)

InterventionPercentage of Participants (Number)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg19.3
Phase I: Atorvastatin 20 mg3.0
Rosuvastatin 10 mg6.6

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Percentage of Participants That Reach Target LDL-C Level of < 100 mg/dL (Phase II)

(NCT01154036)
Timeframe: Week 12 (End of Phase II)

InterventionPercentage of Participants (Number)
Phase II: EZ 10mg + Atorva 20mg [A]55.8
Phase II: Atorva 40mg34.1
Phase II: EZ 10mg + Atorva 20mg [R]53.5
Phase II: Rosuvastatin 20mg35.8
Phase II: EZ 10mg+Atorva 10mgNA

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Percentage of Participants That Reach Target LDL-C Level of < 100 mg/dL (Phase I)

(NCT01154036)
Timeframe: Week 6 (End of Phase I)

InterventionPercentage of Participants (Number)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg56.3
Phase I: Atorvastatin 20 mg37.4
Rosuvastatin 10 mg43.6

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Percent Change From Baseline in Triglycerides (TG) (Phase II)

TG levels measured at Baseline (Week 6: end of Phase I) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. Baseline and post-baseline measurements were log-transformed in the response vector, with fixed effects for treatment, time and the interaction of time by treatment. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase I) and Week 12 (end of Phase II)

InterventionPercentage Change (Least Squares Mean)
Phase II: EZ 10mg + Atorva 20mg [A]-5.9
Phase II: Atorva 40mg-3.1
Phase II: EZ 10mg + Atorva 20mg [R]-10.2
Phase II: Rosuvastatin 20mg-3.2
Phase II: EZ 10mg+Atorva 10mgNA

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Percent Change From Baseline in Apolipoprotein B (Apo B) (Phase I)

Apo-B measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-12.1
Phase I: Atorvastatin 20 mg-6.1
Rosuvastatin 10 mg-7.6

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Percent Change From Baseline in Triglycerides (TG) (Phase I)

TG measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4. Baseline and post-baseline measurements were log-transformed in the response vector, with fixed effects for treatment, time and the interaction of time by treatment. (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Least Squares Mean)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-6.0
Phase I: Atorvastatin 20 mg-3.9
Rosuvastatin 10 mg-1.1

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Percent Change From Baseline in Total Cholesterol (TC) (Phase II)

TC levels measured at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase I) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-10.2
Phase II: Atorva 40mg-2.9
Phase II: EZ 10mg + Atorva 20mg [R]-13.1
Phase II: Rosuvastatin 20mg-5.0
Phase II: EZ 10mg+Atorva 10mg2.2

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Percent Change From Baseline in Total Cholesterol (TC) (Phase I)

TC measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-13.6
Phase I: Atorvastatin 20 mg-6.3
Rosuvastatin 10 mg-8.2

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Percent Change From Baseline in TC/HDL-C Ratio (Phase II)

TC/HDL-C Ratio calculated at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-13.5
Phase II: Atorva 40mg-6.5
Phase II: EZ 10mg + Atorva 20mg [R]-11.7
Phase II: Rosuvastatin 20mg-4.0
Phase II: EZ 10mg+Atorva 10mg-1.0

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Percent Change From Baseline in TC/HDL-C Ratio (Phase I)

TC/HDL-C ratio calculated at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-14.3
Phase I: Atorvastatin 20 mg-4.5
Rosuvastatin 10 mg-9.0

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Percent Change From Baseline in Non-HDL-C/HDL-C Ratio (Phase II)

Non HDL-C/HDL-C Ratio calculated at baseline (Week 6; end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-18.2
Phase II: Atorva 40mg-8.8
Phase II: EZ 10mg + Atorva 20mg [R]-16.3
Phase II: Rosuvastatin 20mg-5.9
Phase II: EZ 10mg+Atorva 10mg-1.9

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Percent Change From Baseline in Non-HDL-C (Phase II)

Non-HDL-C levels calculated at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase I) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-17.5
Phase II: Atorva 40mg-5.5
Phase II: EZ 10mg + Atorva 20mg [R]-18.1
Phase II: Rosuvastatin 20mg-6.3
Phase II: EZ 10mg+Atorva 10mg-0.5

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Percent Change From Baseline in Non-HDL-C (Phase I)

Non-HDL-C measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-18.0
Phase I: Atorvastatin 20 mg-7.9
Rosuvastatin 10 mg-11.1

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Percent Change From Baseline in Low-Density Lipoprotein-Cholesterol (LDL-C) (Phase II).

LDL-C levels measured at Baseline (Week 6; end of Phase 1) and after 6 weeks of study drug administration (Week 12). Baseline was defined as the average of the values at Visits 5 and 6. LDL-C was calculated using the Friedewald method when triglyceride (TG)<350 mg/dL (3.95 mmol/L) and beta quantification ultracentrifugation when TG ≥350 mg/dL (3.95 mmol/L). (NCT01154036)
Timeframe: Baseline (Week 6) and Week 12

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-16.4
Phase II: Atorva 40mg-8.1
Phase II: EZ 10mg + Atorva 20mg [R]-19.3
Phase II: Rosuvastatin 20mg-8.4
Phase II: EZ 10mg+Atorva 10mg2.4

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

LDL-C levels measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4. LDL-C was calculated using the Friedewald method when triglyceride (TG)<350 mg/dL (3.95 mmol/L) and beta quantification ultracentrifugation when TG≥350 mg/dL (3.95 mmol/L). (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I )

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-24.8
Phase I: Atorvastatin 20 mg-10.1
Phase I: Rosuvastatin 10 mg-13.8

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Percent Change From Baseline in LDL-C/HDL-C Ratio (Phase II)

LDL-C/HDL-C Ratio calculated at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]-20.6
Phase II: Atorva 40mg-8.2
Phase II: EZ 10mg + Atorva 20mg [R]-18.2
Phase II: Rosuvastatin 20mg-7.5
Phase II: EZ 10mg+Atorva 10mg-4.5

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Percent Change From Baseline in LDL-C/HDL-C Ratio (Phase I)

LDL-C/HDL-C ratio calculated at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg-23.9
Phase I: Atorvastatin 20 mg-7.1
Phase 1: Rosuvastatin 10 mg-14.7

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Percent Change From Baseline in Hs-CRP (Phase II)

hs-CRP measured at Baseline (Week 6; end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. Baseline and post-baseline measurements were log-transformed in the response vector, with fixed effects for treatment, time and the interaction of time by treatment. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase 1) and Week 12 (end of Phase II)

InterventionPercentage Change (Least Squares Mean)
Phase II: EZ 10mg + Atorva 20mg [A]-19.5
Phase II: Atorva 40mg-6.4
Phase II: EZ 10mg + Atorva 20mg [R]-10.9
Phase II: Rosuvastatin 20mg0.7
Phase II: EZ 10mg+Atorva 10mgNA

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Percent Change From Baseline in High-density Lipoprotein-Cholesterol (HDL-C) (Phase I)

HDL-C measured at Baseline and after 6 weeks of treatment (Week 6; end of Phase I). Baseline was defined as the average value of the measurements taken at Visits 3 and 4 (NCT01154036)
Timeframe: Baseline and Week 6 (end of Phase I)

InterventionPercentage Change (Median)
Phase I: Ezetimibe (EZ) 10 mg + Atorvastatin (Atorva) 10 mg0.9
Phase I: Atorvastatin 20 mg-1.3
Rosuvastatin 10 mg1.0

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Percent Change From Baseline in HDL-C (Phase II)

HDL-C levels measured at Baseline (end of Phase 1) and after 6 weeks of study drug administration (Week 12; end of Phase II). Baseline was defined as the average of the values at Visits 5 and 6. (NCT01154036)
Timeframe: Baseline (Week 6; end of Phase I) and Week 12 (end of Phase II)

InterventionPercentage Change (Median)
Phase II: EZ 10mg + Atorva 20mg [A]0.9
Phase II: Atorva 40mg1.0
Phase II: EZ 10mg + Atorva 20mg [R]-0.8
Phase II: Rosuvastatin 20mg0.0
Phase II: EZ 10mg+Atorva 10mg0.0

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Cummalative Incidence of Grade 2 to 4 Acute Graft vs Host Diesease (GVHD) at Day 100 Post Transplant in HSCT Recipients

Cummalative incidence of grade 2 to 4 acute Graft vs Host Diesease (GVHD) at day 100 post transplant will be will be histologically confirmed and graded in Hematopoietic Stem Cell Transplantation Recipients (NCT01175148)
Timeframe: 100 days post transplant

Interventionpercentage of participants (Number)
Recipient Arm - Experimental3.3

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Time of Occurrence of Cmax (Tmax) and Terminal Phase Half-life (t1/2) GSK1292263- Part A

Serial blood samples for the determination of the PK for GSK1292263, on Days 1 and 14 were collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (no 48 hour sample on Day 1). (NCT01218204)
Timeframe: On Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,
Interventionhours (Median)
tmax, Day 1tmax, Day 14t1/2, Day 1t1/2, Day 14
Atorvastatin 80 mg + GSK1292263 800 mg6.0003.00011.18520.629
GSK1292263 800 mg5.0005.06716.16419.395

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Tmax and t1/2 of GSK1292263- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of GSK1292263 were taken on Days 1 and 14. For monotherapy arms, serial blood samples for the determination of the PK of GSK1292263 were collected on Days 1 and 14. Blood samples for PK were collected on Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hours PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. On Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionhours (Median)
tmax, Day 1tmax, Day 14t1/2, Day 1t1/2, Day 14
Atorvastatin 10 mg + GSK1292263 100 mg3.9835.00012.63026.453
Atorvastatin 10 mg + GSK1292263 300 mg5.0084.00010.27021.569
Atorvastatin 10 mg + GSK1292263 800 mg4.0004.00010.41621.846
Atorvastatin 80 mg + GSK1292263 800 mg4.0004.00012.37224.225
GSK1292263 100 mg4.0004.00015.30523.893
GSK1292263 300 mg4.0003.98314.34225.203
GSK1292263 800 mg3.4754.00014.46419.478

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Tmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A

Serial blood samples for the determination of the PK for atorvastatin metabolites on Day -1 was collected at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose (24 hour sample Day -1 = 0 hour sample Day 1). Serial blood samples for the determination of the PK for atorvastatin metabolites on Days 1 and 14 will be collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day -1 at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose. on Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose.

Interventionhours (Median)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg3.0004.0002.500

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AUC (0-24) of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A

Serial blood samples for the determination of the PK for atorvastatin metabolites on Day -1 was collected at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose (24 hour sample Day -1 = 0 hour sample Day 1). Serial blood samples for the determination of the PK for atorvastatin metabolites on Days 1 and 14 will be collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day -1 at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose. on Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose.

Interventionnanograms hour per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg119.66127.70139.78

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Tmax of Atorvastatin- Part A

Serial blood samples for the determination of the PK for atorvastatin on Day -1 was collected at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose (24 hour sample Day -1 = 0 hour sample Day 1). Serial blood samples for the determination of the PK for atorvastatin on Days 1 and 14 will be collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day -1 at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose. on Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose.

Interventionhours (Median)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg3.0004.0002.250

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Tmax of Atorvastatin- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin were collected on Day -1 and for atorvastatin on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionhours (Median)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg4.0004.0002.000
Atorvastatin 10 mg + GSK1292263 100 mg2.5004.9924.000
Atorvastatin 10 mg + GSK1292263 300 mg3.0006.0004.000
Atorvastatin 10 mg + GSK1292263 800 mg3.9833.0003.500
Atorvastatin 10 mg + Placebo3.0173.9923.525
Atorvastatin 80 mg + GSK1292263 800 mg2.5083.4922.067
Atorvastatin 80 mg + Placebo1.5172.0003.000

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Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part A

Samples were collected fasting on Day -1, and prior to breakfast (early in the morning, fasting) on Days 2, 4, 7, 11 and on Day 15 prior to checkout (24 hours post last-dose), and at Follow-up. When this resulted in multiple samples at the same time point, only one sample was collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). No parameter was found to have any value of PCI. (NCT01218204)
Timeframe: Up to Day 26

InterventionParticipants (Count of Participants)
Atorvastatin 80 mg + GSK1292263 800 mg0
GSK1292263 800 mg0

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Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Pooled Treatment Arm)

Single ECGs were taken after admission on Day -2, and pre-breakfast on Days -1, 4, 10, and at Follow-up. On Days 1, 7, and 14 single ECGS were taken pre-breakfast (fasting) and at 1, 3, 6, 8, 14 and 24 hours post-dose. ECGs were taken in supine position. Additional ECGs were taken at the discretion of the investigator as needed based on symptoms or ECG findings. The data was found to be abnormal clinically significant in treatment phase. (NCT01218204)
Timeframe: Up to Day 26

InterventionParticipants (Count of Participants)
Atorvastatin 10 mg + GSK1292263 100 mg0
Atorvastatin 10 mg + GSK1292263 300 mg0
Atorvastatin 10 mg + GSK1292263 800 mg0
Atorvastatin 10 mg + Placebo0
Atorvastatin 10 mg + Ezetimibe 10 mg0
Atorvastatin 80 mg + GSK1292263 800 mg0
Atorvastatin 80 mg + Placebo0
GSK1292263 100 mg0
GSK1292263 300 mg0
GSK1292263 800 mg0
Placebo0

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Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Run-in)

ECGs were taken on Day 28. Single assessments were made. ECGs were taken in supine position. Additional ECGs were taken at the discretion of the investigator as needed based on symptoms or ECG findings. No data found to be abnormal clinically significant in run-in phase. (NCT01218204)
Timeframe: Day 28

InterventionParticipants (Count of Participants)
Atorvastatin 10 mg0
Atorvastatin 80 mg0

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Number of Participants With Abnormal- Clinically Significant Electrocardiogram (ECG) Findings- Part A

Single ECGs were taken after admission on Day -1 and at Follow-up (up to Day 26). On Days 1, 7, and 14 single ECGS were taken pre-breakfast (fasting) and at 1, 3, 6, 8, 14 and 24 hours post-dose. ECGs were taken in supine position. Additional ECGs were taken at the discretion of the investigator as needed based on symptoms or ECG findings. No value found to be abnormal clinically significant in Part A of the study. (NCT01218204)
Timeframe: Up to Day 26

InterventionParticipants (Count of Participants)
Atorvastatin 80 mg + GSK1292263 800 mg0
GSK1292263 800 mg0

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Percent Change From Baseline in Lipid Metabolism: Apolipoprotein E at Day 14 (24 Hours)

Blood samples were collected fasting on Days 1 (pre-dose), 7 and 15 prior to checkout (24 hours post-dose), and at Follow-up. When this results in multiple samples at the same time point, only one sample will be collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Baseline was the closest scheduled value prior to dosing. The change from Baseline was calculated by subtracting the Baseline values from the individual post-randomization values. If either the Baseline or post-randomization value is missing, the change from Baseline was set to missing as well. Percent change from Baseline was calculated as the change from Baseline divided by the Baseline value then multiplied by 100. (NCT01218204)
Timeframe: Baseline and Day 14

InterventionPerecent change (Mean)
Atorvastatin 10 mg + GSK1292263 100 mg-21.97
Atorvastatin 10 mg + GSK1292263 300 mg-3.92
Atorvastatin 10 mg + GSK1292263 800 mg-31.41
Atorvastatin 10 mg + Placebo34.28
Atorvastatin 10 mg + Ezetimibe 10 mg-12.27
Atorvastatin 80 mg + GSK1292263 800 mg-13.19
Atorvastatin 80 mg + Placebo-13.41
GSK1292263 100 mg1.35
GSK1292263 300 mg-21.98
GSK1292263 800 mg-33.75
Placebo-1.58

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Percent Change From Baseline in Lipid Metabolism: LDL/HDL Ratio at Day 14 (24 Hours)

Blood samples were collected fasting on Days 1 (pre-dose), 7 and 15 prior to checkout (24 hours post-dose), and at Follow-up. When this results in multiple samples at the same time point, only one sample will be collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Baseline was the closest scheduled value prior to dosing. The change from Baseline was calculated by subtracting the Baseline values from the individual post-randomization values. If either the Baseline or post-randomization value is missing, the change from Baseline was set to missing as well. Percent change from Baseline was calculated as the change from Baseline divided by the Baseline value then multiplied by 100. (NCT01218204)
Timeframe: Baseline and Day 14

InterventionPercent change (Mean)
Atorvastatin 10 mg + GSK1292263 100 mg-12.25
Atorvastatin 10 mg + GSK1292263 300 mg-21.12
Atorvastatin 10 mg + GSK1292263 800 mg-41.61
Atorvastatin 10 mg + Placebo0.94
Atorvastatin 10 mg + Ezetimibe 10 mg-28.69
Atorvastatin 80 mg + GSK1292263 800 mg-34.35
Atorvastatin 80 mg + Placebo10.84
GSK1292263 100 mg-16.78
GSK1292263 300 mg-17.63
GSK1292263 800 mg-32.01
Placebo2.55

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Tmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin metabolites were collected on Day -1 and for atorvastatin metabolites on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose and on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionhours (Median)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg4.0004.0006.000
Atorvastatin 10 mg + GSK1292263 100 mg4.5006.0006.000
Atorvastatin 10 mg + GSK1292263 300 mg4.0006.0004.000
Atorvastatin 10 mg + GSK1292263 800 mg5.0004.0004.025
Atorvastatin 10 mg + Placebo4.0004.0005.000
Atorvastatin 80 mg + GSK1292263 800 mg3.9924.0004.000
Atorvastatin 80 mg + Placebo3.0003.0003.983

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Tlag of GSK1292263- Part B (Pooled Treatment Arm)

Blood samples for PK were collected on Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. (NCT01218204)
Timeframe: On Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose.

Interventionhours (Median)
Atorvastatin 10 mg + GSK1292263 100 mg0.000
Atorvastatin 10 mg + GSK1292263 300 mg0.000
Atorvastatin 10 mg + GSK1292263 800 mg0.000
Atorvastatin 80 mg + GSK1292263 800 mg0.000
GSK1292263 100 mg0.000
GSK1292263 300 mg0.000
GSK1292263 800 mg0.000

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Weighted Mean Area Under Concentration Curve From 0 to 24 Hours (AUC [0-24]) Change From Baseline for Triglycerides at Day 14

Blood samples were collected fasting on Days 1 (pre-dose), 7 and 15 prior to checkout (24 hours post-dose), and at Follow-up. When this results in multiple samples at the same time point, only one sample will be collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Baseline was Day -1 value. The change from Baseline was calculated by subtracting the Baseline values from the individual post-randomization values. If either the Baseline or post-randomization value is missing, the change from Baseline was set to missing as well. Percent change from Baseline was calculated as the change from Baseline divided by the Baseline value then multiplied by 100. (NCT01218204)
Timeframe: Baseline and Day 14

Interventionmillimoles per liter (Geometric Mean)
Atorvastatin 10 mg + GSK1292263 100 mg0.13341
Atorvastatin 10 mg + GSK1292263 300 mg0.30812
Atorvastatin 10 mg + GSK1292263 800 mg0.12845
Atorvastatin 10 mg + Placebo0.25228
Atorvastatin 10 mg + Ezetimibe 10 mg0.09060
Atorvastatin 80 mg + GSK1292263 800 mg0.04974
Atorvastatin 80 mg + Placebo0.20164
GSK1292263 100 mg0.30543
GSK1292263 300 mg0.37442
GSK1292263 800 mg0.13079
Placebo0.28863

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Area Under the Concentration-time Curve From Time Zero (Pre-dose) to 24 Hours [AUC(0-24)] of GSK1292263- Part A

Serial blood samples for the determination of the PK for GSK1292263, on Days 1 and 14 were collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (no 48 hour sample on Day 1). (NCT01218204)
Timeframe: On Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,
Interventionnanograms hour per milliliter (Geometric Mean)
Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg12953.8913206.52
GSK1292263 800 mg12032.2111890.40

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AUC (0-24) of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin metabolites were collected on Day -1 and for atorvastatin metabolites on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms hour per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg12.4115.1018.18
Atorvastatin 10 mg + GSK1292263 100 mg16.7216.0210.07
Atorvastatin 10 mg + GSK1292263 300 mg20.2518.2816.54
Atorvastatin 10 mg + GSK1292263 800 mg14.3714.8913.82
Atorvastatin 10 mg + Placebo12.3813.6012.03
Atorvastatin 80 mg + GSK1292263 800 mg163.16146.23144.23
Atorvastatin 80 mg + Placebo133.96150.41156.41

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AUC (0-24) of Atorvastatin- Part A

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin were collected on Day -1 and for atorvastatin on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

Interventionnanograms hour per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg219.27199.15187.25

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AUC (0-24) of Atorvastatin- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin were collected on Day -1 and for atorvastatin on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms hour per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg19.5919.0520.24
Atorvastatin 10 mg + GSK1292263 100 mg23.1617.8415.58
Atorvastatin 10 mg + GSK1292263 300 mg28.7826.1923.77
Atorvastatin 10 mg + GSK1292263 800 mg19.2620.8320.41
Atorvastatin 10 mg + Placebo18.7719.3318.60
Atorvastatin 80 mg + GSK1292263 800 mg188.88174.13174.93
Atorvastatin 80 mg + Placebo173.62186.73188.31

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AUC(0-24) of GSK1292263- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of GSK1292263 were taken on Days 1 and 14. For monotherapy arms, serial blood samples for the determination of the PK of GSK1292263 were collected on Days 1 and 14. Blood samples for PK were collected on Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hours PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. On Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms hour per milliliter (Geometric Mean)
Day 1Day 14
Atorvastatin 10 mg + GSK1292263 100 mg4218.024968.29
Atorvastatin 10 mg + GSK1292263 300 mg5373.787484.67
Atorvastatin 10 mg + GSK1292263 800 mg10384.2411224.58
Atorvastatin 80 mg + GSK1292263 800 mg9812.2110760.74
GSK1292263 100 mg2753.614061.78
GSK1292263 300 mg5342.776737.82
GSK1292263 800 mg8937.998837.31

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Cmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part A

Serial blood samples for the determination of the PK for atorvastatin metabolites on Day -1 was collected at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose (24 hour sample Day -1 = 0 hour sample Day 1). Serial blood samples for the determination of the PK for atorvastatin metabolites on Days 1 and 14 will be collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day -1 at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose. on Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose.

Interventionnanograms per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg17.52115.53521.271

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Lag Time Before Observation of Drug Concentrations in Sampled Matrix (Tlag) of GSK1292263- Part A

Serial blood samples for the determination of the PK for GSK1292263 on Days 1 were collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

Interventionhours (Median)
Atorvastatin 80 mg + GSK1292263 800 mg0.250
GSK1292263 800 mg0.000

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Cmax of Atorvastatin Metabolite (2-Hydroxyatorvastatin)- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin metabolites were collected on Day -1 and for atorvastatin metabolites on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg1.1851.2341.349
Atorvastatin 10 mg + GSK1292263 100 mg1.2981.0730.634
Atorvastatin 10 mg + GSK1292263 300 mg1.3881.2171.152
Atorvastatin 10 mg + GSK1292263 800 mg0.9471.0481.084
Atorvastatin 10 mg + Placebo0.9521.0280.869
Atorvastatin 80 mg + GSK1292263 800 mg26.10619.99122.645
Atorvastatin 80 mg + Placebo21.14926.40027.236

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Cmax of Atorvastatin- Part A

Serial blood samples for the determination of the PK for atorvastatin on Day -1 was collected at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose (24 hour sample Day -1 = 0 hour sample Day 1). Serial blood samples for the determination of the PK for atorvastatin on Days 1 and 14 will be collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose (no 48h sample on Day 1). (NCT01218204)
Timeframe: On Day -1 at immediately pre-morning dose=pre-breakfast (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14 and 24 hours post-morning dose. on Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hour post-morning dose.

Interventionnanograms per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg45.58725.86738.443

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Cmax of Atorvastatin- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of atorvastatin were collected on Day -1 and for atorvastatin on Days 1 and 14. Blood samples for PK were collected on Days -1 (co-dosing arms only) and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hour PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Days -1 and 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms per milliliter (Geometric Mean)
Day -1Day 1Day 14
Atorvastatin 10 mg + Ezetimibe 10 mg2.0031.8721.949
Atorvastatin 10 mg + GSK1292263 100 mg2.0451.2921.453
Atorvastatin 10 mg + GSK1292263 300 mg2.4542.1952.154
Atorvastatin 10 mg + GSK1292263 800 mg1.6831.9262.139
Atorvastatin 10 mg + Placebo1.8161.8521.640
Atorvastatin 80 mg + GSK1292263 800 mg42.37631.01838.419
Atorvastatin 80 mg + Placebo37.05845.78141.092

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Cmax of GSK1292263- Part B (Pooled Treatment Arm)

For co-dosing arms, serial blood samples for the determination of the PK of GSK1292263 were taken on Days 1 and 14. For monotherapy arms, serial blood samples for the determination of the PK of GSK1292263 were collected on Days 1 and 14. Blood samples for PK were collected on Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. Blood samples for PK were collected on Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (48 hours PK sample was collected on Day 16). (NCT01218204)
Timeframe: On Day 1 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, and 24 hours post-morning dose. On Day 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,,,,,,
Interventionnanograms per milliliter (Geometric Mean)
Day 1Day 14
Atorvastatin 10 mg + GSK1292263 100 mg281.321361.595
Atorvastatin 10 mg + GSK1292263 300 mg475.297639.687
Atorvastatin 10 mg + GSK1292263 800 mg808.278886.418
Atorvastatin 80 mg + GSK1292263 800 mg790.315848.082
GSK1292263 100 mg263.279364.936
GSK1292263 300 mg478.676590.949
GSK1292263 800 mg787.922782.914

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Maximum Observed Concentration (Cmax) of GSK1292263- Part A

Serial blood samples for the determination of the PK for GSK1292263 on Days 1 and 14 were collected at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose (no 48 hour sample on Day 1). (NCT01218204)
Timeframe: On Days 1 and 14 at immediately pre-morning dose (time 0), 0.5, 1, 1.5, 2, 3, 4, 6, 8, 14, 24 and 48 hours post-morning dose

,
Interventionnanograms per milliliter (Geometric Mean)
Day 1Day 14
Atorvastatin 80 mg + GSK1292263 800 mg976.3351118.344
GSK1292263 800 mg986.811948.764

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Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (Pooled Treatment Arm)

Samples were collected fasting on Day -2, and prior to breakfast (early in the morning, fasting) on Days 2 (pre-dose), 4, 7, 10, 13 and on Day 15 prior to checkout (24 hours post-dose), and at Follow-up. When this resulted in multiple samples at the same time point, only one sample was collected (example, when 24 hours post dose = pre-dose (time 0) for the next dose). Data for only those parameters (Glucose, Total bilirubin, Albumin, Magnesium, CO2/HCO3, Calcium, ALT, AST, Inorganic phosphorus, Potassium and Sodium) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 26

,,,,,,,,,,
InterventionParticipants (Count of Participants)
Glucose, highGlucose, lowTotal bilirubin, highAlbumin, lowMagnesium, highCO2/HCO3, highCO2/HCO3, lowCalcium, highCalcium, lowALT, highAST, highInorganic phosphorus, highPotassium, lowSodium, high
Atorvastatin 10 mg + Ezetimibe 10 mg10101000100200
Atorvastatin 10 mg + GSK1292263 100 mg20200000000000
Atorvastatin 10 mg + GSK1292263 300 mg00011010100000
Atorvastatin 10 mg + GSK1292263 800 mg00002000011000
Atorvastatin 10 mg + Placebo00111000000000
Atorvastatin 80 mg + GSK1292263 800 mg00102000000000
Atorvastatin 80 mg + Placebo00003001000000
GSK1292263 100 mg10002000000000
GSK1292263 300 mg01003000000010
GSK1292263 800 mg00012000100001
Placebo00102100000000

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Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (run-in)

Samples were collected on Day 14 and 28 prior to breakfast (early in the morning, fasting). Data for only those parameters (Glucose, Magnesium, ALT, AST, Calcium, Inorganic phosphorus and Total bilirubin) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Days 14 and 28

,
InterventionParticipants (Count of Participants)
Glucose, highMagnesium, highALT, highAST, highCalcium, highInorganic phosphorus, lowTotal bilirubin, high
Atorvastatin 10 mg1511000
Atorvastatin 80 mg0500111

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Number of Participants With Abnormal Clinical Chemistry Value of PCI- Part B (Washout)

Samples were collected at screening, and on Days1 (first day of washout), 14 and 28 prior to breakfast (early in the morning, fasting). Data for only those parameters (Inorganic phosphorus, Sodium, Alanine aminotransferase [ALT], Potassium, Creatinine, Calcium, magnesium, Glucose, Total Bilirubin, Carbon dioxide/bicarbonate [CO2/HCO3] and Aspartate aminotransferase [AST]) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 28

InterventionParticipants (Count of Participants)
Inorganic phosphorus, highInorganic phosphorus, lowSodium, highSodium, lowALT, highPotassium, highPotassium, lowCreatinine, highCalcium, highMagnesium, highGlucose, highGlucose, lowTotal bilirubin, highCO2/bicarbonate, lowAST, high
Washout3211331123241611

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Number of Participants With Abnormal Clinically Significant ECG Findings- Part B (Washout)

ECGs were taken at Screening, and on Day1 and Day 28. Single assessments were made. ECGs were taken in supine position. Additional ECGs were taken at the discretion of the investigator as needed based on symptoms or ECG findings. (NCT01218204)
Timeframe: Up to Day 28

InterventionParticipants (Count of Participants)
Day 1Day 28
Washout11

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Number of Participants With Abnormal Hematology Value of PCI- Part A

Blood samples were collected fasting on Day -1, and prior to breakfast (early in the morning, fasting) on Days 2, 4, 7, 11 and on Day 15 prior to checkout (24 hours post last-dose), and at Follow-up. When this resulted in multiple samples at the same time point, only one sample was collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Data for only those parameters (Hematocrit, Hemoglobin and Total neutrophils) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 26

,
InterventionParticipants (Count of Participants)
Hematocrit, highHemoglobin, highTotal neutrophil, low
Atorvastatin 80 mg + GSK1292263 800 mg221
GSK1292263 800 mg100

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Number of Participants With Abnormal Hematology Value of PCI- Part B (Pooled Treatment Arm)

Blood samples were collected fasting on Day -2, and prior to breakfast (early in the morning, fasting) on Days 2 (pre-dose), 4, 7, 10, 13 and on Day 15 prior to checkout (24hrs post-dose), and at Follow-up. When this resulted in multiple samples at the same time point, only one sample was collected (example, when 24hrs post dose = pre-dose (time 0) for the next dose). Data for only those parameters (Platelet count, Total neutrophils and Lymphocytes) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 26

,,,,,,,,,,
InterventionParticipants (Count of Participants)
Platelet count, lowTotal neutrophils, lowLymphocytes, low
Atorvastatin 10 mg + Ezetimibe 10 mg000
Atorvastatin 10 mg + GSK1292263 100 mg000
Atorvastatin 10 mg + GSK1292263 300 mg110
Atorvastatin 10 mg + GSK1292263 800 mg010
Atorvastatin 10 mg + Placebo000
Atorvastatin 80 mg + GSK1292263 800 mg000
Atorvastatin 80 mg + Placebo001
GSK1292263 100 mg001
GSK1292263 300 mg000
GSK1292263 800 mg000
Placebo010

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Number of Participants With Abnormal Hematology Value of PCI- Part B (Run-in)

Blood samples were collected on Day 14 and 28 prior to breakfast (early in the morning, fasting). Data for only those parameters (Lymphocytes) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Days 14 and 28

,
InterventionParticipants (Count of Participants)
Lymphocytes, lowLymphocytes, high
Atorvastatin 10 mg00
Atorvastatin 80 mg10

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Number of Participants With Any AEs and SAEs- Part B (Washout)

An AE is defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect, or is an important medical events that jeopardize the participants or may require medical or surgical intervention to prevent one of the other outcomes listed in the above definition, or a drug-induced liver injury. (NCT01218204)
Timeframe: Up to Day 28

,
InterventionParticipants (Count of Participants)
Any AEAny SAE
Pre-treatment140
Washout370

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Number of Participants With Abnormal Hematology Value of PCI- Part B (Washout)

Blood samples were collected at screening, and on Days 1 (first day of washout), 14 and 28 prior to breakfast (early in the morning, fasting). Data for only those parameters (White blood cells [WBC], Total neutrophils, Hematocrit and Lymphocytes) are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 28

InterventionParticipants (Count of Participants)
WBC, highWBC, lowTotal neutrophil, lowHematocrit, highLymphocytes, low
Washout11122

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Number of Participants With Any Adverse Events (AEs) and Serious Adverse Events (SAEs)- Part A

An AE is defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect, or is an important medical events that jeopardize the participants or may require medical or surgical intervention to prevent one of the other outcomes listed in the above definition, or a drug-induced liver injury. (NCT01218204)
Timeframe: Up to Day 26

,
InterventionParticipants (Count of Participants)
Any AEAny SAE
80 mg Atorvastatin + 800 mg GSK129226300
800 mg GSK129226320

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Number of Participants With Any AEs and SAEs- Part B (Pooled Treatment Arm)

An AE is defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect, or is an important medical events that jeopardize the participants or may require medical or surgical intervention to prevent one of the other outcomes listed in the above definition, or a drug-induced liver injury. (NCT01218204)
Timeframe: Up to Day 26

,,,,,,,,,,
InterventionParticipants (Count of Participants)
Any AEAny SAE
Atorvastatin 10 mg + Ezetimibe 10 mg40
Atorvastatin 10 mg + GSK1292263 100 mg60
Atorvastatin 10 mg + GSK1292263 300 mg20
Atorvastatin 10 mg + GSK1292263 800 mg30
Atorvastatin 10 mg + Placebo30
Atorvastatin 80 mg + GSK1292263 800 mg60
Atorvastatin 80 mg + Placebo40
GSK1292263 100 mg50
GSK1292263 300 mg70
GSK1292263 800 mg80
Placebo40

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Number of Participants With Any AEs and SAEs- Part B (Run-in)

An AE is defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. An SAE is defined as any untoward medical occurrence that, at any dose, results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect, or is an important medical events that jeopardize the participants or may require medical or surgical intervention to prevent one of the other outcomes listed in the above definition, or a drug-induced liver injury. (NCT01218204)
Timeframe: Up to Day 28

,
InterventionParticipants (Count of Participants)
Any AEAny SAE
Atorvastatin 10 mg190
Atorvastatin 80 mg80

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Number of Participants With Vital Signs of PCI- Part B (Washout)

Assessment of vital signs including SBP, DBP heart rate was performed at Screening, on Days 1, 14 and 28 in the morning. At each time point, assessment was performed after resting in a supine or semi-supine position for at least 10 minutes. Data for only those parameters are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to day 28

InterventionParticipants (Count of Participants)
SBP, highHeart rate, high
Washout41

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Number of Participants With Vital Signs of Potential Clinical Importance (PCI)- Part A

Assessment of vital signs including systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate was performed after admission on Day -1 and at Follow-up. On Days 1, 7 and 14, they were taken at pre-dose, 1, 3, 6, 8, 14 and 24 hours after the morning dose. At each time point, assessment was performed after resting in a supine or semi-supine position for at least 10 minutes. Data for only those parameters are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 26

,
InterventionParticipants (Count of Participants)
DBP, highDBP, low
Atorvastatin 80 mg + GSK1292263 800 mg00
GSK1292263 800 mg10

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Number of Participants With Vital Signs of Potential Clinical Importance- Part B (Pooled Treatment Arm)

Assessment of vital signs including SBP, DBP and heart rate was performed after admission on Day-2, and pre-breakfast on Days -1, 4, and 10 in a fasting state early in the morning (prior to dosing), and at Follow-up. On Days 1, 7 and 14, they were also be taken at 1, 3, 6, 9, 12 and 24 hours after the morning dose. At each time point, assessment was performed after resting in a supine or semi-supine position for at least 10 minutes. Data for only those parameters are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to Day 26

,,,,,,,,,,
InterventionParticipants (Count of Participants)
SBP, highDBP, highDBP, lowHeart rate, high
Atorvastatin 10 mg + Ezetimibe 10 mg2010
Atorvastatin 10 mg + GSK1292263 100 mg0000
Atorvastatin 10 mg + GSK1292263 300 mg0000
Atorvastatin 10 mg + GSK1292263 800 mg1000
Atorvastatin 10 mg + Placebo3101
Atorvastatin 80 mg + GSK1292263 800 mg1110
Atorvastatin 80 mg + Placebo2000
GSK1292263 100 mg1110
GSK1292263 300 mg2000
GSK1292263 800 mg0000
Placebo0000

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Number of Participants With Vital Signs of Potential Clinical Importance- Part B (Run-in)

Assessment of vital signs including SBP, DBP and heart rate was performed on Days 1, 14 and 28 in the morning. At each time point, assessment was performed after resting in a supine or semi-supine position for at least 10 minutes. Data for only those parameters are presented for which findings are of PCI either high or low. (NCT01218204)
Timeframe: Up to day 28

,
InterventionParticipants (Count of Participants)
SBP, highSBP, low
Atorvastatin 10 mg10
Atorvastatin 80 mg00

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Percent Change From Baseline for Lipid Metabolism: Apolipoprotein A1 and Apolipoprotein B100 at Day 14

Blood samples were collected fasting on Days 1 (pre-dose), 7 and 15 prior to checkout (24 hours post-dose), and at Follow-up. When this results in multiple samples at the same time point, only one sample will be collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Baseline was the closest scheduled value prior to dosing. The change from Baseline was calculated by subtracting the Baseline values from the individual post-randomization values. If either the Baseline or post-randomization value is missing, the change from Baseline was set to missing as well. Percent change from Baseline was calculated as the change from Baseline divided by the Baseline value then multiplied by 100. (NCT01218204)
Timeframe: Baseline and Day 14

,,,,,,,,,,
InterventionPercent change (Mean)
Apolipoprotein A1, 24 hoursApolipoprotein B100, 24 hours
Atorvastatin 10 mg + Ezetimibe 10 mg-3.88-15.49
Atorvastatin 10 mg + GSK1292263 100 mg-1.932.85
Atorvastatin 10 mg + GSK1292263 300 mg-8.72-17.93
Atorvastatin 10 mg + GSK1292263 800 mg4.17-22.22
Atorvastatin 10 mg + Placebo-7.19-5.03
Atorvastatin 80 mg + GSK1292263 800 mg-1.00-27.08
Atorvastatin 80 mg + Placebo-5.814.25
GSK1292263 100 mg3.76-10.21
GSK1292263 300 mg29.90-7.62
GSK1292263 800 mg-0.15-10.95
Placebo-0.18-2.39

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Percent Change From Baseline in Lipid Metabolism: High Density Lipids Cholesterol (HDLc), Low Density Lipids Cholesterol (LDLc), Tryglycerides, Non-HDLc and Total Cholesterol at Day 14 (24 Hours)

Blood samples were collected fasting on Days 1 (pre-dose), 7 and 15 prior to checkout (24 hours post-dose), and at Follow-up. When this results in multiple samples at the same time point, only one sample will be collected (example, when 24 hours post-dose = pre-dose (time 0) for the next dose). Baseline was the closest scheduled value prior to dosing. The change from Baseline was calculated by subtracting the Baseline values from the individual post-randomization values. If either the Baseline or post-randomization value is missing, the change from Baseline was set to missing as well. Percent change from Baseline was calculated as the change from Baseline divided by the Baseline value then multiplied by 100. (NCT01218204)
Timeframe: Baseline and Day 14

,,,,,,,,,,
InterventionPercent change (Mean)
HDLcLDLcTriglyceidesNon-HDLcTotal cholesterol
Atorvastatin 10 mg + Ezetimibe 10 mg6.03-24.81-10.44-21.19-14.23
Atorvastatin 10 mg + GSK1292263 100 mg7.50-6.80-18.67-9.53-5.17
Atorvastatin 10 mg + GSK1292263 300 mg14.97-10.01-15.98-11.67-3.61
Atorvastatin 10 mg + GSK1292263 800 mg31.09-24.09-32.81-26.59-10.31
Atorvastatin 10 mg + Placebo-0.03-0.3710.702.080.89
Atorvastatin 80 mg + GSK1292263 800 mg26.22-18.63-21.39-21.88-5.52
Atorvastatin 80 mg + Placebo4.5015.012.27-0.941.09
GSK1292263 100 mg9.17-10.24-3.95-9.32-5.81
GSK1292263 300 mg9.76-11.86-30.84-17.02-12.06
GSK1292263 800 mg18.95-19.94-34.66-22.62-14.05
Placebo-1.370.7718.903.172.18

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PSA Response

PSA response was defined as a decrease in slope of at least 25%, when log (PSA) is plotted vs. time. (NCT01220973)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Atorvastatin and Celecoxib14

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Hs-CRP Levels Assessed at Randomization and 6 Months

To assess if the use of statins in children with type 1 DM decreases the concentration of inflammatory markers. (NCT01236365)
Timeframe: Randomization and 6 months

Interventionmg/dL (Median)
Atorvastatin hsCRP at Randomization0.363
Atorvastatin hsCRP at 6 Months0.419
Placebo hsCRP at Randomization0.248
Placebo hsCRP at 6 Months0.446

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LDL-C Levels Assessed at Randomization and 6 Months

To assess if the use of statins in children with type 1 DM is safe, improves measures of LDL-C. Subjects will have a physical exam, laboratories, nutritional counseling and moderate aerobic exercise recommended. Diabetes management will be intensified. At 3 months fasting lipoprotein fractions (ion mobility)re-drawn and if LDL-C >100mg/dl patients will be randomized to treatment with statins or placebo for 6 months, randomization stratified by BP and microalbuminuria, duration of diabetes and HgA1C. At 1 month safety labs will be repeated and blood withdrawn again at 3 and 6 months from baseline. (NCT01236365)
Timeframe: Randomization and 6 months

Interventionmg/dL (Mean)
Atorvastatin LDL-C at Randomization128
Atorvastatin LDL-C at 6 Months87
Placebo LDL-C at Randomization126
Placebo LDL-C at 6 Months133

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MAGE

Mean amplitude of glycemic excursion (MAGE) with continuous glucose monitoring (CGM - IPro®, Medtronic Minimed) worn blindly for 6d to assess glucose variability (NCT01236365)
Timeframe: Randomization and 6 months

Interventionmg/dL (Mean)
Atorvastatin MAGE at Randomization150
Atorvastatin MAGE at 6 Months156
Placebo MAGE at Randomization156
Placebo MAGE at 6 Months152

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RAGE

Receptor for Advanced Glycation End Products (NCT01236365)
Timeframe: Randomization and 6 months

Interventionpg/mL (Mean)
Atorvastatin LDL-C at Randomization49
Atorvastatin LDL-C at 6 Months35
Placebo LDL-C at Randomization50
Placebo LDL-C at 6 Months58

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Descending Aortic Strain

Subclinical atherosclerosis and arterial stiffness of abdominal aortic MRI (NCT01236365)
Timeframe: Randomization

Interventionpercent area change (Mean)
Atorvastatin at Randomization27.2
Placebo at Randomization29

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Pharmacokinetics of Atorvastatin: Maximum Plasma Concentration (Cmax)

(NCT01250834)
Timeframe: Pre-dose to 56 hours post-dose

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
40 mg Atorvastatin Alone19.5
1.5 mg LY2189265 + 40 mg Atorvastatin5.78

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Pharmacokinetics of Atorvastatin: Area Under the Curve (AUC)

This measure is based on the pharmacokinetic area under the atorvastatin plasma concentration-time curve from time 0 to infinity. (NCT01250834)
Timeframe: Pre-dose to 56 hours post-dose

Interventionnanogram*hour per milliliter (ng*h/mL) (Geometric Mean)
40 mg Atorvastatin Alone82.8
1.5 mg LY2189265 + 40 mg Atorvastatin65.9

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Pharmacokinetics of Ortho-Hydroxyatorvastatin: Area Under the Curve (AUC)

This measure is based on the pharmacokinetic area under the ortho-hydroxyatorvastatin concentration-time curve from time 0 to infinity. (NCT01250834)
Timeframe: Pre-dose to 56 hours post-dose

Interventionnanogram*hour per milliliter (ng*h/mL) (Geometric Mean)
40 mg Atorvastatin Alone102
1.5 mg LY2189265 + 40 mg Atorvastatin95.9

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Pharmacokinetics of Ortho-Hydroxyatorvastatin: Maximum Concentration (Cmax)

(NCT01250834)
Timeframe: Pre-dose to 56 hours post-dose

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
40 mg Atorvastatin Alone14.4
1.5 mg LY2189265 + 40 mg Atorvastatin5.66

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Pharmacokinetics of Para-Hydroxyatorvastatin: Maximum Concentration (Cmax)

(NCT01250834)
Timeframe: Pre-dose to 56 hours post-dose

Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
40 mg Atorvastatin Alone0.473
1.5 mg LY2189265 + 40 mg Atorvastatin0.360

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Change in Monocyte Surface Markers Expression (Expressed as Percentage), Following Treatment of Chronic HIV+/ HAART+ Subjects With Atorvastatin (T=12wks Versus T=0wk).

Effects of Atorvastatin on immune activation associated surface markers (CD16, CD163 and CCR2) of monocytes were assessed in chronic HIV+/HAART+ subjects following 12 weeks of treatment. Whole blood drawn from these subjects were stained with fluorochrome tagged antibodies to the surface markers. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the percentage of cells (monocytes) expressing the specific marker. This was done before starting and after completing drug treatment to assess the effect of drug. (NCT01263938)
Timeframe: Subjects enrolled in the study following the screening visit were assessed for the primary outcome measures at T=0 (drug intervention begins); T=12wks (intervention ends)

InterventionChange T=0 to T=12 (percentage change) (Mean)
Total CD14+CD16+ monocytesCD14+CD163+ monocytesCD14+CCR2+ monocytes
Atorvastatin1.5-4.40.5

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Change From Baseline in Levels of Plasma Inflammatory Marker sCD14 of Chronic HIV+/ HAART+ Subjects.

Monocyte specific inflammatory soluble factor sCD14 was measured by ELISA in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following atorvastatin treatment. (NCT01263938)
Timeframe: Subjects enrolled in the study following the screening visit were assessed for the primary outcome measures at T=0 (drug intervention begins); T=12wks (intervention ends)

Interventionug/ml (Change fromT=0 to T=12wk) (Mean)
Atorvastatin-0.22

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Change From Baseline in Levels of Plasma Inflammatory Marker sCD163 of Chronic HIV+/ HAART+ Subjects.

Monocyte specific inflammatory soluble factor sCD163 was measured by ELISA in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following atorvastatin treatment. (NCT01263938)
Timeframe: Subjects enrolled in the study following the screening visit were assessed for the primary outcome measures at T=0 (drug intervention begins); T=12wks (intervention ends)

Interventionng/ml (Change fromT=0 to T=12wk) (Mean)
Atorvastatin-18

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Change From Baseline in Levels of Plasma Inflammatory Marker MCP-1 of Chronic HIV+/ HAART+ Subjects.

Monocyte specific inflammatory soluble factor MCP-1 was measured by ELISA in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following atorvastatin treatment. (NCT01263938)
Timeframe: Subjects enrolled in the study following the screening visit were assessed for the primary outcome measures at T=0 (drug intervention begins); T=12wks (intervention ends)

Interventionpg/ml (Change from T0 to T12) (Mean)
Atorvastatin10

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Percent Change From Baseline in Total Cholesterol, High-density Lipoprotein Cholesterol (HDL-C), Non-HDL-C and Apolipoprotein B (Apo-B) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

,,,,,
Interventionpercent change (Least Squares Mean)
Total Cholesterol (n= 31, 30, 31, 29, 28, 30)HDL-C (n= 31, 30, 31, 29, 28, 30)Non-HDL-C (n= 31, 30, 31, 29, 28, 30)Apo-B (n= 30, 30, 30, 29, 27, 30)
Alirocumab 100 mg Q2W-39.74.1-55.6-48.1
Alirocumab 150 mg Q2W-45.25.5-62.5-56.1
Alirocumab 200 mg Q4W-28.06.3-37.4-28.7
Alirocumab 300 mg Q4W-29.88.5-40.7-33.1
Alirocumab 50 mg Q2W-23.06.7-33.6-27.3
Placebo-1.6-1.0-2.22.2

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Percent Change From Baseline in Fasting Triglycerides and Lipoprotein(a) at Week 12 - On-Treatment Analysis

Since the assumptions of normal distribution and equality of variances were not verified for the lipid parameters, percent changes were expressed as median (inter-quartile range). (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

,,,,,
Interventionpercent change (Median)
Fasting Triglycerides (n= 31, 30, 31, 29, 28, 30)Lipoprotein(a) (n= 30, 30, 30, 29, 27, 30)
Alirocumab 100 mg Q2W-5.5-26.1
Alirocumab 150 mg Q2W-18.9-28.6
Alirocumab 200 mg Q4W-10.8-16.7
Alirocumab 300 mg Q4W-8.4-7.9
Alirocumab 50 mg Q2W-6.6-13.3
Placebo9.70.0

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Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and <70 mg/dL (1.81 mmol/L) at Week 12 - On-Treatment Analysis

(NCT01288443)
Timeframe: Week 12 (LOCF)

,,,,,
Interventionpercentage of participants (Number)
LDL-C <100 mg/dL (2.59 mmol/L)LDL-C <70 mg/dL (1.81 mmol/L)
Alirocumab 100 mg Q2W96.883.9
Alirocumab 150 mg Q2W100.0100.0
Alirocumab 200 mg Q4W89.346.4
Alirocumab 300 mg Q4W96.756.7
Alirocumab 50 mg Q2W93.346.7
Placebo16.13.2

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Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Baseline adjusted least squares (LS) means and standard errors were estimated using an analysis of covariance (ANCOVA) model including available post-baseline data on treatment from first study drug injection up to 21 days after last study drug injection (on-treatment analysis). Missing Week 12 data were imputed by last observation carried forward [LOCF] method. (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

Interventionpercent change (Least Squares Mean)
Placebo-5.1
Alirocumab 50 mg Q2W-39.6
Alirocumab 100 mg Q2W-64.2
Alirocumab 150 mg Q2W-72.4
Alirocumab 200 mg Q4W-43.2
Alirocumab 300 mg Q4W-47.7

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Absolute Change in the Ratio Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) From Baseline to Week 12 - On-Treatment Analysis

Adjusted LS mean and standard errors were estimated using the same ANCOVA as for primary endpoint. (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

Interventionratio (Least Squares Mean)
Placebo0.05
Alirocumab 50 mg Q2W-0.23
Alirocumab 100 mg Q2W-0.35
Alirocumab 150 mg Q2W-0.42
Alirocumab 200 mg Q4W-0.23
Alirocumab 300 mg Q4W-0.29

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Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

Interventionmmol/L (Least Squares Mean)
Placebo-0.20
Alirocumab 50 mg Q2W-1.37
Alirocumab 100 mg Q2W-2.10
Alirocumab 150 mg Q2W-2.38
Alirocumab 200 mg Q4W-1.46
Alirocumab 300 mg Q4W-1.62

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Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288443)
Timeframe: Baseline to Week 12 (LOCF)

Interventionmg/dL (Least Squares Mean)
Placebo-7.6
Alirocumab 50 mg Q2W-53.0
Alirocumab 100 mg Q2W-81.2
Alirocumab 150 mg Q2W-92.0
Alirocumab 200 mg Q4W-56.4
Alirocumab 300 mg Q4W-62.5

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Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 8 - On-treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288469)
Timeframe: From baseline to Week 8 (LOCF)

Interventionmmol/L (Least Squares Mean)
Placebo + Atorvastatin 80 mg-0.56
Alirocumab + Atorvastatin 10 mg-2.09
Alirocumab + Atorvastatin 80 mg-2.31

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Absolute Change in the Ratio Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) From Baseline to Week 8 - On-treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA as for primary endpoint. (NCT01288469)
Timeframe: From Baseline to Week 8 (LOCF)

Interventionratio (Median)
Placebo + Atorvastatin 80 mg-0.03
Alirocumab + Atorvastatin 10 mg-0.34
Alirocumab + Atorvastatin 80 mg-0.36

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Percent Change From Baseline in Calculated LDL-C at Week 8 - On-treatment Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Baseline adjusted least squares (LS) means and standard errors were estimated using an analysis of covariance (ANCOVA) model including available post-baseline data on treatment from first investigational product (IP) injection up to 21 days after last IP injection (on-treatment analysis). Missing Week 8 data were imputed by last observation carried forward [LOCF] method. (NCT01288469)
Timeframe: From Baseline to Week 8 (LOCF)

Interventionpercent change (Least Squares Mean)
Placebo + Atorvastatin 80 mg-17.3
Alirocumab + Atorvastatin 10 mg-66.2
Alirocumab + Atorvastatin 80 mg-73.2

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Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 8 - On-treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288469)
Timeframe: From Baseline to Week 8 (LOCF)

Interventionpercent change (Least Squares Mean)
Placebo + Atorvastatin 80 mg-3.6
Alirocumab + Atorvastatin 10 mg2.6
Alirocumab + Atorvastatin 80 mg5.8

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Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and < 70 mg/dL (1.81 mmol/L) at Week 8 - On-treatment Analysis

(NCT01288469)
Timeframe: Week 8 (LOCF)

,,
Interventionpercentage of participants (Number)
LDL-C < 100 mg/dL (2.59 mmol/L)LDL-C < 70 mg/dL (1.81 mmol/L)
Alirocumab + Atorvastatin 10 mg100.096.6
Alirocumab + Atorvastatin 80 mg100.090.0
Placebo + Atorvastatin 80 mg51.717.2

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Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 8 - On-treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01288469)
Timeframe: From baseline to Week 8 (LOCF)

Interventionmg/dL (Least Squares Mean)
Placebo + Atorvastatin 80 mg-21.5
Alirocumab + Atorvastatin 10 mg-80.7
Alirocumab + Atorvastatin 80 mg-89.3

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Percent Change From Baseline in Total Cholesterol, Fasting Triglycerides, Non-high-Density Lipoprotein Cholesterol (Non-HDL-C), Apolipoprotein B (Apo-B) and Lipoprotein(a) at Week 8 - On-treatment Analysis

Since the assumptions of normal distribution and equality of variances were not verified for the lipid parameters, percent changes were expressed as median (interquartile range). (NCT01288469)
Timeframe: From baseline to Week 8 (LOCF)

,,
Interventionpercent change (Median)
Total Cholesterol (n=29, 29, 30)Fasting Triglycerides (n=29, 29, 30)Non-HDL-C (n= 29, 29, 30)Apo-B (n = 29, 28, 29)Lipoprotein(a) (n= 29, 28, 29)
Alirocumab + Atorvastatin 10 mg-40.5-4.0-58.3-54.4-34.7
Alirocumab + Atorvastatin 80 mg-47.2-24.7-63.9-58.0-31.0
Placebo + Atorvastatin 80 mg-16.6-11.9-22.3-12.0-2.7

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Number of Participants With Post-index Cardiovascular (CV) Events

CV events were defined as an inpatient or emergency department admission for heart failure (HF), myocardial infarction (MI), ischemic heart disease (IHD), cerebrovascular disease, peripheral vascular disease (PVD), aortic aneurysm, and/or revascularization. CV events were identified using medical claims. (NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

InterventionParticipants (Number)
Atorvastatin700
Simvastatin1012

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Hazard Ratio for First Cardiovascular (CV) Event

Hazard ratio of atorvastatin versus simvastatin for first CV event. Hazard ratio of atorvastatin versus simvastatin was obtained from a Cox proportional hazards model. (NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

,
InterventionParticipants (Number)
Number of participants with eventNumber of participants without event
Atorvastatin70010770
Simvastatin101219120

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Number of Participants Per Dose

Index dose was categorized as low dose (atorvastatin 10 mg, simvastatin up to 20 mg), medium dose (atorvastatin 20 mg, simvastatin 40 mg), and high dose (atorvastatin 40 or 80 mg, simvastatin 80 mg). (NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

,
InterventionParticipants (Number)
Low doseMedium doseHigh dose
Atorvastatin563939401891
Simvastatin1234467681020

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Mean Dose

The first observed study medication fill during the participation identification period was defined as the index drug. The initial dose of the index drug was determined based on the pharmacy claims. (NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

Interventionmg (Mean)
Atorvastatin19.46
Simvastatin28.36

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Percentage of Participants Who Adhered to Index Therapy

Percentage of participants who adhered to index therapy was evaluated. Treatment adherence was defined as the number of days covered by index medication divided by the number of days in the post-index period, expressed as a percentage. (NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

,
InterventionPercentage of participants (Number)
Less than 80 percentGreater than or equal to 80 percent
Atorvastatin64.9235.08
Simvastatin57.3242.68

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Low-density Lipoprotein Cholesterol (LDL-C)

(NCT01304641)
Timeframe: At least 3 months from the post-index date (baseline) or end of study (28 February 2009)

Interventionmilligram/deciliter (mg/dL) (Mean)
Atorvastatin94.07
Simvastatin98.03

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Length of Post-index Period

Post-index period included time during which participants were observed for a minimum of 3 months following index date (fill date on which first observed atorvastatin or simvastatin was filled during the participant identification period) until disenrollment or end of study treatment (28 February 2009). (NCT01304641)
Timeframe: Index date (baseline) up to end of study (28 February 2009)

InterventionDays (Mean)
Atorvastatin519.10
Simvastatin448.41

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Difference of Standardized Uptake Value (SUV) of Atherosclerotic Plaque in Carotid Artery by PET CT

(NCT01341730)
Timeframe: 3 months

Interventionstandardized uptake value (SUV) (Mean)
Atorvastatin 20 mg-0.06
Atorvastatin 20 mg + Pioglitazone 30 mg-0.10

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Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in CD4+ T-cell Activation Percent

CD4+ T-cell activation percent (% CD38+/DR+ of CD4+): Difference between [change from week 24 to week 44] and [change from baseline to week 20] (i.e. [week 44 - week 24] - [week 20 - baseline]) (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionpercent (Median)
Arm A: Atorvastatin / Placebo-0.20
Arm B: Placebo / Atorvastatin0.60

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in CD40L (log10 Transformed)

"Cluster of differentiation 40 (CD40L) is a costimulatory protein found on antigen presenting cells and is required for their activation.~Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]." (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 pg/ml (Median)
Arm A: Atorvastatin / Placebo0.01
Arm B: Placebo / Atorvastatin-0.03

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Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in CD8+ T-cell Activation Percent

CD8+ T-cell activation percent (% CD38+/DR+ of CD8+): Difference between [change from week 24 to week 44] and [change from baseline to week 20] (i.e. [week 44 - week 24] - [week 20 - baseline]) (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionpercent (Median)
Arm A: Atorvastatin / Placebo1.10
Arm B: Placebo / Atorvastatin-1.15

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Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in log10 D-dimer

D-dimer in log10 ng/mL: Difference between [change from week 24 to week 44] and [change from baseline to week 20] (i.e. [week 44 - week 24] - [week 20 - baseline]) (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 ng/mL (Median)
Arm A: Atorvastatin / Placebo-0.02
Arm B: Placebo / Atorvastatin0.00

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Difference Between [Change From Week 24 to Week 44] and [Change From Baseline to Week 20] in log10 IL-6

IL-6 (Interleukin 6) in log10 pg/mL: Difference between [change from week 24 to week 44] and [change from baseline to week 20] (i.e. [week 44 - week 24] - [week 20 - baseline]) (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 pg/mL (Median)
Arm A: Atorvastatin / Placebo-0.08
Arm B: Placebo / Atorvastatin-0.08

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Number of Participants With Safety Endpoints After Study Treatment Cross-over (Week 24 to Week 48)

"Safety endpoints are defined as grade ≥ 2 signs and symptoms, laboratory abnormalities, AST/ALT > 3 X ULN, and adverse events after study treatment cross-over (week 24 to week 48).~The DAIDS Adverse Event (AE) Grading Table, Version 1.0, December 2004 (Clarification, August 2009) was used for grading of AEs." (NCT01351025)
Timeframe: week 24 to week 48

Interventionparticipants (Number)
Arm A: Atorvastatin / Placebo20
Arm B: Placebo / Atorvastatin14

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Number of Participants With Safety Endpoints Before Study Treatment Cross-over (Baseline to Week 24)

"Safety endpoints are defined as grade ≥ 2 signs and symptoms, laboratory abnormalities, AST/ALT > 3 X ULN, and adverse events prior to study treatment cross-over (baseline to week 24).~The DAIDS Adverse Event (AE) Grading Table, Version 1.0, December 2004 (Clarification, August 2009) was used for grading of AEs." (NCT01351025)
Timeframe: week 0 to week 24

Interventionparticipants (Number)
Arm A: Atorvastatin / Placebo20
Arm B: Placebo / Atorvastatin22

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in IP-10 (log10 Transformed)

"IFN-gamma-inducible protein 10 (IP-10 or CXCL10) is a chemokine secreted from cells stimulated with type I and II IFNs and LPS, is also a chemoattractant for activated T cells.~Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]." (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 pg/ml (Median)
Arm A: Atorvastatin / Placebo-0.03
Arm B: Placebo / Atorvastatin-0.04

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in MCP-1 (log10 Transformed)

"Monocyte chemoattractant protein-1 (MCP-1/CCL2) is one of the key chemokines that regulate migration and infiltration of monocytes/macrophages.~Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]." (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 pg/ml (Median)
Arm A: Atorvastatin / Placebo0.03
Arm B: Placebo / Atorvastatin-0.04

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in P-selectin (log10 Transformed)

"P-selectin is a protein that in humans encoded by the SELP gene. P-selectin functions as a cell adhesion molecule (CAM) on the surfaces of activated endothelial cells, which line the inner surface of blood vessels, and activated platelets.~Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]." (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 ng/ml (Median)
Arm A: Atorvastatin / Placebo0.01
Arm B: Placebo / Atorvastatin-0.06

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in sCD14 (log10 Transformed)

Soluble cluster of differentiation 14 (sCD14) is a human gene. Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]. (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 ng/ml (Median)
Arm A: Atorvastatin / Placebo0.00
Arm B: Placebo / Atorvastatin0.00

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Difference Between [Change From Week 24 to Week 44] and Change From [Baseline to Week 20] in sCD163 (log10 Transformed)

"CD163 (Cluster of Differentiation 163) is a protein that in humans encoded by the CD163 gene; and sCD163 is soluble CD163.~Difference between [change from week 24 to week 44] and change from [baseline to week 20] is defined as [week 44 - week 24] - [week 20 - baseline]." (NCT01351025)
Timeframe: baseline, week 20, week 24, and week 44

Interventionlog10 ng/ml (Median)
Arm A: Atorvastatin / Placebo-0.04
Arm B: Placebo / Atorvastatin0.03

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Plasma Concentration of Atorvastatin Metabolites

Measuring the amount of byproducts of the metabolization of Atorvastatin in the blood plasma. (NCT01363999)
Timeframe: 3 days

Interventionng/ml (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet2.50
B, RO5317116/F03 Bilayer Tablet2.51
C, RO5317116/F04 Active-coated Tablet2.95
D, RO4607381/F49 Tablet2.77

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Plasma Concentration of Atorvastatin

(NCT01363999)
Timeframe: 3 days

Interventionng/mL (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet3.56
B, RO5317116/F03 Bilayer Tablet3.55
C, RO5317116/F04 Active-coated Tablet4.26
D, RO4607381/F49 Tablet3.86

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Safety: Incidence of Serious Adverse Events

(NCT01363999)
Timeframe: 9 weeks

InterventionEvents (Number)
A, RO5317116/F01 Bilayer Tablet0
B, RO5317116/F03 Bilayer Tablet0
C, RO5317116/F04 Active-coated Tablet0
D, RO4607381/F49 Tablet0

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Plasma Concentration of Dalcetrapib Active Form

(NCT01363999)
Timeframe: 3 days

Interventionng/mL (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet285
B, RO5317116/F03 Bilayer Tablet272
C, RO5317116/F04 Active-coated Tablet294
D, RO4607381/F49 Tablet231

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After 6 Weeks of Treatment

Serum LDL-C calculated using Friedewald formula at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination-54.0
Co-Administration Ezetimibe and Atorvastin-53.8

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Percent Change From Baseline in Apolipoprotein (Apo) B After 6 Weeks of Treatment

Serum Apo B measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination-42.6
Co-Administration Ezetimibe and Atorvastin-43.3

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Percent Change From Baseline in Total Cholesterol (TC) After 6 Weeks of Treatment

Serum TC measured at baseline and after 6 week of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination-38.1
Co-Administration Ezetimibe and Atorvastin-38.5

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Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) After 6 Weeks of Treatment

Serum HDL-C calculated at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination5.4
Co-Administration Ezetimibe and Atorvastin4.6

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Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) After 6 Weeks of Treatment

Non-HDL-C measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination-50.1
Co-Administration Ezetimibe and Atorvastin-50.2

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Percent Change From Baseline in Triglycerides (TG) After 6 Weeks of Treatment

Serum TG measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370590)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorva Fixed Dose Combination-28.3
Co-Administration Ezetimibe and Atorvastin-29.9

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Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) After 6 Weeks of Treatment

Non-HDL-C calculated at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination-55.4
Co-Administration Ezetimibe and Atorvastatin-55.2

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Percent Change From Baseline in Total Cholesterol (TC) After 6 Weeks of Treatment

Serum TC measured at baseline and after 6 week of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination-43.0
Co-Administration Ezetimibe and Atorvastatin-42.9

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Percent Change From Baseline in Triglycerides (TG) After 6 Weeks of Treatment

Serum TG measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination-36.2
Co-Administration Ezetimibe and Atorvastatin-36.2

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) After 6 Weeks of Treatment

Serum LDL-C calculated using Friedewald formula at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination-58.9
Co-Administration Ezetimibe and Atorvastatin-58.7

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Percent Change From Baseline in Apolipoprotein (Apo) B After 6 Weeks of Treatment

Serum Apo B measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination-48.7
Co-Administration Ezetimibe and Atorvastatin-48.3

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Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) After 6 Weeks of Treatment

Serum HDL-C measured at baseline and after 6 weeks of treatment in each of the 2 treatment periods. (NCT01370603)
Timeframe: Baseline and Week 6

InterventionPercentage Change (Least Squares Mean)
Ezetimibe/Atorvastatin Fixed Dose Combination2.3
Co-Administration Ezetimibe and Atorvastatin2.6

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Change From Baseline in Plasma CETP Mass

Plasma CETP mass assay was a solid-phase enzyme-linked immunosorbent assay (ELISA) designated to measure human CETP mass which employed the quantitative enzyme immunoassay principle. An increase in plasma CETP mass represented an improvement. LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline, Weeks 4, 8, and 12

,,,,,
Interventionmicrograms per milliliter (µg/mL) (Least Squares Mean)
4 weeks8 weeks12 weeks
10 mg Atorvastatin-0.28-0.21-0.19
100 mg LY24845953.143.092.96
100 mg LY2484595 + 10 mg Atorvastatin1.941.831.95
30 mg LY24845951.881.981.95
500 mg LY24845953.544.023.36
Placebo0.080.100.13

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Pharmacokinetics - Area Under the Curve (AUC) of LY2484595 and Atorvastatin

(NCT01375075)
Timeframe: Weeks 2, 4, 8, 12 (predose and postdose), and Week 16

Interventionnanograms*hours per milliliter (ng*h/mL) (Geometric Mean)
30 mg LY24845953110
100 mg LY24845958690
500 mg LY248459529400
100 mg LY2484595 + 10 mg Atorvastatin8080

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Change From Baseline to 12 Weeks in Serum Sodium

LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

Interventionmilliequivalents per liter (mEq/L) (Least Squares Mean)
30 mg LY2484595-0.18
100 mg LY2484595-0.32
500 mg LY2484595-0.07
Placebo-0.32
10 mg Atorvastatin0.35
100 mg LY2484595 + 10 mg Atorvastatin0.53

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Change From Baseline to 12 Weeks in Serum Bicarbonate

LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

Interventionmilliequivalents per liter (mEq/L) (Least Squares Mean)
30 mg LY24845950.63
100 mg LY24845950.62
500 mg LY24845950.62
Placebo0.52
10 mg Atorvastatin0.62
100 mg LY2484595 + 10 mg Atorvastatin1.23

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Change From Baseline to 12 Weeks in Plasma Renin Activity

LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

Interventionnanograms per milliliter per hour (Least Squares Mean)
30 mg LY2484595-0.32
100 mg LY24845950.01
500 mg LY2484595-0.21
Placebo-0.21
10 mg Atorvastatin-0.01
100 mg LY2484595 + 10 mg Atorvastatin-0.43

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Change From Baseline to 12 Week Endpoint in Highly-Sensitive C-Reactive Protein (hsCRP)

LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

Interventionmilligrams per deciliter (mg/dL) (Least Squares Mean)
30 mg LY2484595-0.03
100 mg LY24845950.00
500 mg LY24845950.13
Placebo-0.01
10 mg Atorvastatin-0.03
100 mg LY2484595 + 10 mg Atorvastatin0.15

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The Number and Severity of Episodes of Rashes at Any Time From Baseline Through Week 12

All rash cases were adjudicated by a central dermatologist blinded to treatment assignment according to a study-specific Clinical Events Committee (CEC) charter. Rash events were assessed according to clinical relevance (severity). Categories included high risk, low risk, not a relevant dermatosis, or insufficient documentation for determination. High risk rashes included anaphylaxis, toxic epidermal necrolysis, Stevens Johnson Syndrome, Drug Reaction with Eosinophilia and System Symptoms (DRESS), urticaria/angioedema, vasculitis, erythroderma, and lupus-like reaction. All other rashes were considered low risk or not a relevant dermatosis per the Investigator's clinical opinion. A participant could be reported in multiple categories. (NCT01375075)
Timeframe: Baseline through Week 12

,,,,,
Interventionevents (Number)
Low riskHigh riskNot a relevant dermatosisInsufficient documentation for determination
10 mg Atorvastatin0000
100 mg LY24845950000
100 mg LY2484595 + 10 mg Atorvastatin1010
30 mg LY24845950000
500 mg LY24845951100
Placebo0010

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Percent Change From Baseline to 12 Weeks in High Density Lipoprotein Cholesterol (HDL-C) and Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 and Placebo

Percent change from baseline = 100*(post-baseline assessment - baseline assessment)/baseline assessment. Higher values in the percent change from baseline represented an improvement for HDL-C and lower values in the percent change from baseline represented an improvement for LDL-C. Least Squares (LS) mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

,,,,,
Interventionpercent change (Least Squares Mean)
HDL-CLDL-C
10 mg Atorvastatin17.35-37.66
100 mg LY2484595123.35-22.13
100 mg LY2484595 + 10 mg Atorvastatin120.60-52.29
30 mg LY248459582.22-14.23
500 mg LY2484595143.56-20.95
Placebo8.001.24

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Percent Change From Baseline in Plasma Cholesteryl Ester Transfer Protein (CETP) Activity

Plasma CETP activity assay employed a fluorometric method to determine the CETP transfer activity. Percent change from baseline = 100*(post-baseline assessment - baseline assessment)/baseline assessment. An increase in the percent change from baseline represented an improvement. LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline, Weeks 4, 8, and 12

,,,,,
Interventionpercent change in CETP activity (Least Squares Mean)
4 Weeks8 Weeks12 Weeks
10 mg Atorvastatin-1.33-4.89-5.69
100 mg LY2484595-75.26-76.23-73.86
100 mg LY2484595 + 10 mg Atorvastatin-68.58-79.90-73.38
30 mg LY2484595-41.62-39.91-41.07
500 mg LY2484595-89.14-90.97-85.30
Placebo1.672.709.22

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) and Low Density Lipoprotein Cholesterol (LDL-C) With LY2484595 in Combination With Atorvastatin

Percent change from baseline = 100*(post-baseline assessment - baseline assessment)/baseline assessment. An increase in the percent change from baseline represented an improvement for HDL-C and a decrease in the percent change from baseline represents an improvement for LDL-C. LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline, Weeks 2, 4, and 8

,,,,,
Interventionpercent change (Least Squares Mean)
HDL-C, Week 2HDL-C, Week 4HDL-C, Week 8LDL-C, Week 2LDL-C, Week 4LDL-C, Week 8
10 mg Atorvastatin8.8510.8712.98-38.29-42.23-38.97
100 mg LY2484595108.21122.68130.69-27.50-24.43-23.56
100 mg LY2484595 + 10 mg Atorvastatin101.45117.04116.64-55.74-52.62-51.23
30 mg LY248459575.3077.9478.65-17.46-13.32-12.50
500 mg LY2484595122.60147.22169.05-33.19-29.25-25.48
Placebo-0.732.095.19-2.142.840.24

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Change From Baseline to 12 Weeks in Aldosterone

LS mean was adjusted for baseline value of the variable analyzed. (NCT01375075)
Timeframe: Baseline and Week 12

Interventionnanograms per deciliter (ng/dL) (Least Squares Mean)
30 mg LY2484595-0.40
100 mg LY24845950.37
500 mg LY24845950.59
Placebo0.33
10 mg Atorvastatin0.95
100 mg LY2484595 + 10 mg Atorvastatin0.62

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Number of Myopathy and Liver Injury Events

Myopathy events were considered muscle-related treatment emergent adverse events (TEAEs) and liver injury events were considered hepatic disorder-related TEAEs reported per Medical Dictionary for Regulatory Activities (MedDRA). An adverse event (AE) was any untoward medical occurrence attributed to study drug in a participant who received study drug. TEAEs were newly occurring AEs or AEs worsening after first dose. (NCT01375075)
Timeframe: Baseline through Week 12

,,,,,
Interventionevents (Number)
Blood creatine phosphokinase increasedMyalgiaHepatic function abnormalGamma-glutamyltransferase increasedAlanine aminotransferase increased
10 mg Atorvastatin11100
100 mg LY248459511010
100 mg LY2484595 + 10 mg Atorvastatin00200
30 mg LY248459500100
500 mg LY248459500100
Placebo00001

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Change From Baseline to 12 Weeks in Blood Pressure

"Blood pressure reported as systolic blood pressure (SBP) and diastolic blood pressure (DBP).~LS mean was adjusted for baseline value of the variable analyzed." (NCT01375075)
Timeframe: Baseline and Week 12

,,,,,
Interventionmillimeters of mercury (mm Hg) (Least Squares Mean)
SBPDBP
10 mg Atorvastatin2.591.49
100 mg LY24845951.440.02
100 mg LY2484595 + 10 mg Atorvastatin2.040.51
30 mg LY24845952.351.46
500 mg LY24845954.512.51
Placebo-1.390.68

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Number of Participants With SAE

Number of participants who experienced an SAE within the 6 week study period (NCT01431105)
Timeframe: At 6 weeks after initiation of study drug

InterventionParticipants (Count of Participants)
Atorvasatin4

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Percent Change From Baseline in Triglycerides at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-9.9
Atorvastatin/Atorvastatin + Glimepiride-28.7
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-10.5

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Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-15.5
Atorvastatin/Atorvastatin + Glimepiride-28.6
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-10.4

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Percent Change From Baseline in Total Cholesterol at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-1.7
Atorvastatin/Atorvastatin + Glimepiride-28.3
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-25.7

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Percent Change From Baseline in Non-high Density Lipoprotein Cholesterol (Non-HDL-C) at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-1.0
Atorvastatin/Atorvastatin + Glimepiride-34.4
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-34.6

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Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin4.9
Atorvastatin/Atorvastatin + Glimepiride-35.7
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-38.7

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-0.3
Atorvastatin/Atorvastatin + Glimepiride-5.8
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin1.5

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Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 16

Percent change from baseline was calculated as the Week 16 value minus the Week 0 value, divided by the Week 0 value ×100%. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent change (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-4.8
Atorvastatin/Atorvastatin + Glimepiride-32.9
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-29.0

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Number of Participants Who Experienced at Least One Adverse Event

An adverse event is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the investigational product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the investigational product, is also an adverse event. Data presented exclude data following the initiation of glycemic rescue therapy. (NCT01477853)
Timeframe: Up to 56 weeks (including 2-week follow-up)

InterventionParticipants (Number)
Sitagliptin/Sitagliptin + Atorvastatin10
Atorvastatin/Atorvastatin + Glimepiride13
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin13

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Number of Participants Who Discontinued Study Drug Due to an Adverse Event

An adverse event is defined as any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the investigational product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the investigational product, is also an adverse event. Data presented exclude data following the initiation of glycemic rescue therapy. (NCT01477853)
Timeframe: Up to 54 weeks

InterventionParticipants (Number)
Sitagliptin/Sitagliptin + Atorvastatin1
Atorvastatin/Atorvastatin + Glimepiride2
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin2

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Change From Baseline in Hemoglobin A1C (A1C) at Week 16

A1C is measured as percent. Thus, this change from baseline reflects the Week 16 A1C percent minus the Week 0 A1C percent. (NCT01477853)
Timeframe: Baseline and Week 16

InterventionPercent (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-1.17
Atorvastatin/Atorvastatin + Glimepiride0.04
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-1.01

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Change From Baseline in Fasting Plasma Glucose (FPG) at Week 16

Change from baseline reflects the Week 16 value minus the Week 0 value. (NCT01477853)
Timeframe: Baseline and Week 16

Interventionmg/dL (Mean)
Sitagliptin/Sitagliptin + Atorvastatin-15.7
Atorvastatin/Atorvastatin + Glimepiride22.7
Sitagliptin + Atorvastatin/Sitagliptin + Atorvastatin-26.0

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Non Relapse Mortality (NRM) at One Year

Cumulative incidence of NRM will be calculated as the time from transplant until death not related to disease, where the competing risk for NRM was death due to disease. Patients who had not died were censored at last follow up. (NCT01491958)
Timeframe: up to 12 months post transplant

Interventionpercentage of patients (Number)
Patients5.5

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Safety of Atorvastatin in Transplant Recipients in Terms of Adverse Events and Toxicities.

Adverse events and toxicities were monitored in patients using the National Cancer Institute Common Terminology Criteria for Adverse Events (CTCAE) version 4.0 criteria. (NCT01491958)
Timeframe: Patients: Baseline, weekly for 9 weeks and then on days 84, 91-100, 180 and 365. Donors: at apheresis and then 30 days later.

Interventionpatients (Number)
Grade 2 elevated liver enzymesGrade 4 elevated liver enzymes
Patients21

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Percentage of Participants With Grades II to IV aGVHD at Day +100 of Atorvastatin Administration

The incidence of grades II to IV aGVHD at day +100 of atorvastatin administration. The grading of aGVHD and cGVHD were done using the Consensus Conference criteria. (NCT01491958)
Timeframe: Up through day 100 following transplant

Interventionpercentage of patients (Number)
Patients30

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Percentage of Patients With Chronic Graft Versus Host Disease (cGVHD)

cGVHD occurring anytime after day 100 post transplant will be termed chronic GVHD, and evaluated in patients who were followed for at least 100 days without early progression or death. Grading of cGVHD was done using the National Institutes of Health Consensus Development Project Criteria (NCT01491958)
Timeframe: up 1 year post transplant

Interventionpercentage of patients (Number)
Patients43

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Time to Neutrophil and Platelet Engraftment

Neutrophil engraftment will be defined as first of three consecutive days with ANC ≥ 0.5 x 109/L post-conditioning regimen induced nadir. Similarly platelet engraftment is defined as first day of platelet count ≥ 20,000 x 109/L, without transfusion for 7 consecutive days. (NCT01491958)
Timeframe: weekly for 12 weeks, 100 days, 6 months, and 12 months

Interventiondays (Median)
Neutrophil engraftmentPlatelet engraftment
Patients1814

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Percent Change From Baseline in Total Cholesterol at Week 12

(NCT01516879)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
Placebo2.85
Evolocumab-32.30

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Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo6.47
Evolocumab-30.67

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Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo8.44
Evolocumab-41.82

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Percent Change From Baseline in Lipoprotein(a) at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo-5.37
Evolocumab-27.72

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Percent Change From Baseline in LDL-C at Week 52

Cholesterol was measured by means of ultracentrifugation. (NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo6.83
Evolocumab-50.14

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Percent Change From Baseline in LDL-C at Week 12

Cholesterol was measured by means of ultracentrifugation. (NCT01516879)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
Placebo3.17
Evolocumab-54.35

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Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo0.35
Evolocumab5.77

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo4.46
Evolocumab-41.75

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Percent Change From Baseline in Apolipoprotein B at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo2.94
Evolocumab-41.26

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Change From Baseline in LDL-C at Week 52

Cholesterol was measured by means of ultracentrifugation. (NCT01516879)
Timeframe: Baseline and Week 52

Interventionmg/dL (Least Squares Mean)
Placebo5.1
Evolocumab-52.7

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Percentage of Participants With an LDL-C Response at Week 52

An LDL-C response is defined as LDL-C level < 70 mg/dL (1.8 mmol/L) at Week 52. (NCT01516879)
Timeframe: Week 52

Interventionpercentage of participants (Number)
Placebo6.4
Evolocumab82.3

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Percent Change From Week 12 to Week 52 in LDL-C

Cholesterol was measured by means of ultracentrifugation. (NCT01516879)
Timeframe: Week 12 and Week 52

Interventionpercent change (Least Squares Mean)
Placebo2.57
Evolocumab2.44

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Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at Week 52

Cholesterol was measured by means of ultracentrifugation. (NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo31.89
Evolocumab2.74

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Percent Change From Baseline in Triglycerides at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo8.99
Evolocumab-2.55

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Percent Change From Baseline in Total Cholesterol at Week 52

(NCT01516879)
Timeframe: Baseline and Week 52

Interventionpercent change (Least Squares Mean)
Placebo5.26
Evolocumab-28.18

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Recurrent or Progressive Malignancy

Cumulative incidence rate of recurrent or progressive malignancy with death as a competing risk, assessed at 3 years in the patients/recipients. (NCT01525407)
Timeframe: Up to 3 years

Interventionprobability (Number)
Patients0.27

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Non-relapse Mortality

Cumulative incidence rate of non-relapse mortalities, assessed at day 100 in the patients/recipients. (NCT01525407)
Timeframe: At day 100

Interventionprobability (Number)
Patients0.13

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Non-relapse Mortality

Cumulative incidence rate of non-relapse mortalities, assessed at one year in the patients/recipients. (NCT01525407)
Timeframe: At 1 year after HCT

Interventionprobability (Number)
Patients0.29

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Overall Survival

Determined and presented as Kaplan-Meier estimates, assessed at 1 year in the patients/recipients. (NCT01525407)
Timeframe: 1 year after transplant

Interventionsurvival probability (Number)
Patients0.55

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Proportion of Donors Who Have to Discontinue Atorvastatin Because of Toxicity

(NCT01525407)
Timeframe: Until completion of stem cell collection (on average 14 days)

InterventionParticipants (Count of Participants)
Donors3

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Chronic Extensive GVHD

Cumulative incidence rate of chronic extensive GVHD with death as a competing risk, assessed at 2 years in the patients/recipients. (NCT01525407)
Timeframe: 2 years post transplant

Interventionprobability (Number)
Patients0.51

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Proportion of Patients Requiring Secondary Systemic Immunosuppressive Therapy

(NCT01525407)
Timeframe: First 100 days after transplant

InterventionParticipants (Count of Participants)
Patients5

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Disease-free Survival

Evaluated as Kaplan-Meier estimate in the patients/recipients. (NCT01525407)
Timeframe: 1 year after transplant

Interventiondisease free survival probability (Number)
Patients0.47

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Grade 3-4 Acute GVHD

Cumulative incidence rate of grade 3-4 acute GVHD with death as a completing risk, assessed at day 100 in the patients/recipients. (NCT01525407)
Timeframe: First 100 days after transplant

Interventionprobability (Number)
Patients0.21

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Grades II-IV Acute GVHD

Cumulative incidence rate of grades II-IV acute GVHD with death as a competing risk, assessed at 100 days in the patients/recipients. (NCT01525407)
Timeframe: First 100 days after transplant

Interventionprobability (Number)
Patients0.78

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Number of Patients Requiring Secondary Systemic Immunosuppressive Therapy

Number of patients requiring systemic immunosuppressive therapy other than those used for prophylaxis and initial therapy. (NCT01527045)
Timeframe: 1 Year post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)23
Primary - Reg B (TBI Alone)3
Adjunct4

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Number of Patients Surviving Overall

Number of patients surviving overall post-transplant (NCT01527045)
Timeframe: 1 Year post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)21
Primary - Reg B (TBI Alone)3
Adjunct9

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Number of Patients With Chronic Extensive GVHD

Number of patients who developed chronic extensive GVHD post-transplant. The diagnosis of chronic GVHD requires at least one manifestation that is distinctive for chronic GVHD as opposed to acute GVHD. In all cases, infection and others causes must be ruled out in the differential diagnosis of chronic GVHD. Patients were evaluated as described in the National Institutes of Health (NIH) consensus project guidelines. (NCT01527045)
Timeframe: 1 Year post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)8
Primary - Reg B (TBI Alone)1
Adjunct5

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Number of Patients With Grade III-IV Acute Graft-versus-host Disease (GVHD) Post-transplant

"Number of patients who developed acute GVHD post allogeneic transplant.~aGVHD Stages~Skin:~a maculopapular eruption involving < 25% BSA~a maculopapular eruption involving 25 - 50% BSA~generalized erythroderma~generalized erythroderma w/ bullous formation and often w/ desquamation~Liver:~bilirubin 2.0 - 3.0 mg/100 mL~bilirubin 3 - 5.9 mg/100 mL~bilirubin 6 - 14.9 mg/100 mL~bilirubin > 15 mg/100 mL~Gut:~Diarrhea is graded 1 - 4 in severity. Nausea and vomiting and/or anorexia caused by GVHD is assigned as 1 in severity. The severity of gut involvement is assigned to the most severe involvement noted. Patients with visible bloody diarrhea are at least stage 2 gut and grade 3 overall.~aGVHD Grades Grade II: Stage 1 - 2 skin w/ no gut/liver involvement Grade III: Stage 2 - 4 gut involvement and/or stage 2 - 4 liver involvement Grade IV: Pattern and severity of GVHD similar to grade 3 w/ extreme constitutional symptoms or death" (NCT01527045)
Timeframe: 100 days post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)2
Primary - Reg B (TBI Alone)0
Adjunct0

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Number of Patients With Recurrent or Progressive Malignancy

"CML New cytogenetic abnormality and/or development of accelerated phase or blast crisis. The criteria for accelerated phase will be defined as unexplained fever greater than 38.3°C, new clonal cytogenetic abnormalities in addition to a single Ph-positive chromosome, marrow blasts and promyelocytes >20%.~AML, ALL, MDS >5% marrow blasts by morphologic or flow cytometric, or appearance of extramedullary disease.~CLL ≥1 of: Physical exam/Imaging studies (nodes, liver, and/or spleen) ≥50% increase or new, circulating lymphocytes by morphology and/or flow cytometry ≥50% increase, and lymph node biopsy w/ Richter's transformation.~NHL >25% increase in the sum of the products of the perpendicular diameters of marker lesions, or the appearance of new lesions.~MM~≥100% increase of the serum myeloma protein from its lowest level, or reappearance of myeloma peaks that had disappeared w/ treatment; or definite increase in the size or number of plasmacytomas or lytic bone lesions." (NCT01527045)
Timeframe: 1 Year post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)7
Primary - Reg B (TBI Alone)4
Adjunct3

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Number of Patients With Grades II-IV Acute Graft-versus-host-disease (GVHD)

"Number of patients who developed acute GVHD post allogeneic transplant.~aGVHD Stages~Skin:~a maculopapular eruption involving < 25% BSA~a maculopapular eruption involving 25 - 50% BSA~generalized erythroderma~generalized erythroderma w/ bullous formation and often w/ desquamation~Liver:~bilirubin 2.0 - 3.0 mg/100 mL~bilirubin 3 - 5.9 mg/100 mL~bilirubin 6 - 14.9 mg/100 mL~bilirubin > 15 mg/100 mL~Gut:~Diarrhea is graded 1 - 4 in severity. Nausea and vomiting and/or anorexia caused by GVHD is assigned as 1 in severity. The severity of gut involvement is assigned to the most severe involvement noted. Patients with visible bloody diarrhea are at least stage 2 gut and grade 3 overall.~aGVHD Grades Grade II: Stage 1 - 2 skin w/ no gut/liver involvement Grade III: Stage 2 - 4 gut involvement and/or stage 2 - 4 liver involvement Grade IV: Pattern and severity of GVHD similar to grade 3 w/ extreme constitutional symptoms or death" (NCT01527045)
Timeframe: 100 days post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)15
Primary - Reg B (TBI Alone)2
Adjunct6

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Number of Donors Discontinuing Atorvastatin Due to Toxicity

"The number of donors who prematurely discontinue atorvastatin therapy due to toxicity. Donors will be assessed for the following events:~Musculoskeletal and connective tissue disorders: grade 2-5~Hepatobiliary disorders: grade 2-5~Other unexpected events thought related to the use of atorvastatin; grade 2-5~In cases where the NCI criteria do not apply, intensity will be defined as:~Mild: awareness of symptom or sign, but easily tolerated~Moderate: discomfort is enough to cause interference with normal activities~Severe: inability to perform normal daily activities~Life threatening: immediate risk of death from the reaction as it occurred" (NCT01527045)
Timeframe: Prior to stem cell collection

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)2
Primary - Reg B (TBI Alone)0
Adjunct1

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Number of Non-relapse Mortalities

Number of patients who died without relapsed/progressive disease. (NCT01527045)
Timeframe: 1 Year post-transplant

InterventionParticipants (Count of Participants)
Primary - Reg A (Flu/TBI)4
Primary - Reg B (TBI Alone)1
Adjunct0

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Saphenous Vein Graft Occlusion (Percentage of Vein Grafts Occluded) Based on CT Coronary Angiography at 1 Year

Vein graft patency will be assessed in a blinded fashion by CT coronary angiography 1 year after CABG (NCT01528709)
Timeframe: 1 year after CABG

InterventionVein grafts (Count of Units)
High-dose Statin Therapy14
Moderate-dose Statin Therapy16

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Vein Graft Stenosis 1 Year After CABG Based on CT Coronary Angiography

Vein graft stenosis 1 year after CABG based on CT coronary angiography (NCT01528709)
Timeframe: Within 1 year after CABG

InterventionVein grafts (Count of Units)
High-dose Statin Therapy4
Moderate-dose Statin Therapy7

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Frequency of Serious Adverse Events (SAE)

(NCT01544309)
Timeframe: Up to 12 months

InterventionNumber of patients with SAE (Number)
Atorvastatin Administration Group14
Rosuvastatin Administration Group19

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Percent Change in 1,5-AG Level

An inverse relationship exists between mean change in 1,5-AG level and the mean rate of change when the degree of standard deviation is large, wherein the mean change is negative although the mean rate of change is positive or vice versa (NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment(or at the occurrence of deterioration of diabetic treatment status)

,
InterventionPercent change (Mean)
At 3 monthsAt 6 monthsAt 12 months
Atorvastatin Administration Group-1.6-6.5-3.8
Rosuvastatin Administration Group5.52.63.5

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Number of Participants Stratified by Time to the Occurrence of Deterioration of Diabetic Treatment Status

"Deterioration of diabetic treatment status is defined as addition of new drug, increase in dosage, drug changes (therapy intensification), and deterioration in HbA1c of > 0.5%." (NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration

,
Interventionparticipants (Number)
Therapy intensification: 0-3 monthsTherapy intensification: 3-6 monthsTherapy intensification: 6-12 monthsOther: 0-3 monthsOther: 3-6 monthsOther: 6-12 monthsNo deterioration
Atorvastatin Administration Group201232658421
Rosuvastatin Administration Group14823556453

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Percent Change in Blood Glucose Level (Fasting)

(NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment(or at the occurrence of deterioration of diabetic treatment status)

,
InterventionPercent change (Mean)
At 3 monthsAt 6 monthsAt 12 months
Atorvastatin Administration Group3.37.04.6
Rosuvastatin Administration Group2.75.93.7

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Occurrence of Deterioration of Diabetic Treatment Status

"Deterioration of diabetic treatment status is defined as addition of new drug, increase in dosage, drug changes (therapy intensification), and deterioration in HbA1c of > 0.5%." (NCT01544309)
Timeframe: Baseline, 12 months after administration

,
InterventionParticipants (Number)
Therapy intensificationDeterioration in HbA1c of > 0.5%
Atorvastatin Administration Group64177
Rosuvastatin Administration Group45162

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Percent Change in Non-high-density Lipoprotein Cholesterol (HDL-C) Level

(NCT01544309)
Timeframe: Baseline, and 12 months after administration

InterventionPercent change (Mean)
Atorvastatin Administration Group-31.3
Rosuvastatin Administration Group-32.8

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Change From Baseline in Insulin Level

An inverse relationship exists between mean change in insulin level and the mean rate of change when the degree of standard deviation is large, wherein the mean change is negative although the mean rate of change is positive or vice versa (NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment (or at the occurrence of deterioration of diabetic treatment status)

,
InterventionμU/mL (Mean)
At 3 monthsAt 6 monthsAt 12 monthsBaseline Insulin level
Atorvastatin Administration Group-0.100.66-1.5010.95
Rosuvastatin Administration Group-0.54-0.44-2.9112.57

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Change in Blood Glucose Level (Fasting)

(NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment(or at the occurrence of deterioration of diabetic treatment status)

,
Interventionmg/dL (Mean)
At 3 monthsAt 6 monthsAt 12 months
Atorvastatin Administration Group2.66.83.6
Rosuvastatin Administration Group0.14.31.5

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Rate of Patients Who Have Reached the Target LDL-C Level Specified in Japan Atherosclerosis Society Guidelines (JASGL) 2007

Percentage of participants achieving the target LDL-C levels <100 mg/dL for participants with history of coronary artery diseases (CAD) and <120 mg/dL for participants without history of CAD are presented. (NCT01544309)
Timeframe: 3 months after administration, the end of starting dose and the end of study treatment

,
InterventionPercentage of participants (Number)
At 3 monthsAt the end of study treatment
Atorvastatin Administration Group89.086.3
Rosuvastatin Administration Group89.987.5

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Percent Changes in Lipids (LDL-C, HDL-C, TC, TG, Non-HDL-C/HDL-C Ratio, and FFA)

(NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration, the end of starting dose and the end of study treatment

,
InterventionPercent change (Mean)
LDL-C: at 3 monthsLDL-C: at 6 monthsLDL-C: at 12 monthsHDL-C: at 3 monthsHDL-C: at 6 monthsHDL-C: at 12 monthsTC: at 3 monthsTC: at 6 monthsTC: at 12 monthsTG at 3 monthsTG: at 6 monthsTG: at 12 monthsNon-HDL-C/HDL-C ratio: at 3 monthsNon-HDL-C/HDL-C ratio: at 6 monthsNon-HDL-C/HDL-C ratio: at 12 monthsFFA: at 3 monthsFFA: at 6 monthsFFA: at 12 months
Atorvastatin Administration Group-36.6-35.6-33.24.17.14.9-24.7-23.5-22.7-12.7-12.4-12.6-34.8-36.1-33.119.913.837.2
Rosuvastatin Administration Group-39.2-36.4-34.75.68.27.7-25.9-23.8-23.5-11.0-11.9-15.9-37.7-37.2-36.025.915.934.8

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Percent Change in Non-HDL-C Level

(NCT01544309)
Timeframe: Baseline, 3 and 6 months after administration, the end of starting dose and the end of study treatment

,
InterventionPercent change (Mean)
At 3 monthsAt 6 months
Atorvastatin Administration Group-33.8-33.2
Rosuvastatin Administration Group-35.5-33.5

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Frequency of Cardiovascular Events (Coronary Artery Disease, Heart Failure, Cerebrovascular Disease, Peripheral Artery Disease and Aortic Disease)

(NCT01544309)
Timeframe: From the start of the treatment to the end of study treatment

InterventionNumber of patients with any events (Number)
Atorvastatin Administration Group5
Rosuvastatin Administration Group9

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Change in HbA1c Level

(NCT01544309)
Timeframe: Baseline, 12 months after administration

InterventionAmount of change (%) (Mean)
Atorvastatin Administration Group0.120
Rosuvastatin Administration Group0.10

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Percent Change in Insulin Level

An inverse relationship exists between mean change in insulin level and the mean rate of change when the degree of standard deviation is large, wherein the mean change is negative although the mean rate of change is positive or vice versa. (NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment (or at the occurrence of deterioration of diabetic treatment status)

,
InterventionPercent change (Mean)
At 3 monthsAt 6 monthsAt 12 months
Atorvastatin Administration Group40.745.117.4
Rosuvastatin Administration Group31.335.513.8

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Change From Baseline in 1,5-AG Level

An inverse relationship exists between mean change in 1,5-AG level and the mean rate of change when the degree of standard deviation is large, wherein the mean change is negative although the mean rate of change is positive or vice versa (NCT01544309)
Timeframe: Baseline, 3, 6, 12 months after administration and the end of study treatment(or at the occurrence of deterioration of diabetic treatment status)

,
Interventionμg/mL (Mean)
At 3 monthsAt 6 monthsAt 12 monthsBaseline 1,5-AG level
Atorvastatin Administration Group-0.51-1.28-0.8815.40
Rosuvastatin Administration Group-0.21-0.94-1.0915.39

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Change in HbA1c Level

(NCT01544309)
Timeframe: Baseline, 3, 6 months after administration and the end of study treatment (or at the occurrence of deterioration of diabetic treatment status)

,
InterventionAmount of change (%) (Mean)
At 3 monthsAt 6 months
Atorvastatin Administration Group0.050.13
Rosuvastatin Administration Group0.000.12

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Intravascular Ultrasound (IVUS) Parameters

"Change in atheroma volume and lumen CSA on IVUS as related to change in yellow plaque index as compared from baseline to 6-8 weeks after intervention.~Data not analyzed. Data not available." (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

,
Interventionmm^2 (Mean)
Baseline Total atheroma volume6-8 weeks Total atheroma volumeBaseline Lumen CSA6-8 weeks Lumen CSA
Aggressive Lipid Therapy195.8209.62.52.5
Standard of Care Lipid Therapy193.7199.62.42.4

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LCBI4mm Max

LCBI4mm max = change in lipid-core burden index at the 4-mm maximal segment. Spectroscopic information obtained from raw spectra was transformed into a probability of lipid core that was mapped to a red-to-yellow color scale, with the low probability of lipid shown as red and the high probability of lipid shown as yellow. Yellow pixels within the analyzed segment were divided by all viable pixels to generate the lipid-core burden index (LCBI). The maximal value of LCBI for each nonculprit obstructive lesion was recorded and used for comparison. (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

,
Interventionratio (Median)
Baseline LCBI4mm maxFollow-up LCBI4mm max
Aggressive Lipid Therapy490.6336.1
Standard of Care Lipid Therapy356.7385.7

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Lipiscan - Lipid Core Burden Index (LCBI)

The regression of yellow plaque content from the atherosclerotic lipid pool after statin therapy by utilizing NIR spectroscopy as compared from baseline to 6-8 weeks after intervention. Spectroscopic information obtained from raw spectra was transformed into a probability of lipid core that was mapped to a red-to-yellow color scale, with the low probability of lipid shown as red and the high probability of lipid shown as yellow. Analyses were performed offline using the Matlab-based software, as previously published. Yellow pixels within the analyzed segment were divided by all viable pixels to generate the lipid-core burden index (LCBI). The maximal value of LCBI for each nonculprit obstructive lesion was recorded and used for comparison. (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

,
Interventionratio (Median)
Baseline LCBI, lesionFollow-up LCBI, lesion
Aggressive Lipid Therapy132.499.8
Standard of Care Lipid Therapy95.499.9

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Major Adverse Cardiac Events (MACE)

MACE defined as a combined clinical endpoint of death, MI (Q wave or non Q-wave with CK-MB >3 times above the upper normal limit (48 U/L), urgent revascularization or stroke at 30 days and 1 year. Details reported in adverse events section. (NCT01567826)
Timeframe: at 6-8 weeks after intervention

Interventionparticipants (Number)
Standard of Care Lipid Therapy2
Aggressive Lipid Therapy3

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Change in LCBI4mm Max

Change in LCBI4mm max at 6-8 weeks after intervention as compared to baseline. LCBI4mm max = change in lipid-core burden index at the 4-mm maximal segment. (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

Interventionratio (Median)
Standard of Care Lipid Therapy2.4
Aggressive Lipid Therapy-149.1

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Change in LCBI, Lesion

Change in LCBI at 6-8 weeks after intervention as compared to baseline (NCT01567826)
Timeframe: at baseline and at 6-8 weeks post intervention

Interventionratio (Median)
Standard of Care Lipid Therapy8.0
Aggressive Lipid Therapy-22.5

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Post PCI Cardiac Enzymes

Correlation of yellow plaque index with post procedure CK-MB, Troponin-I release. (NCT01567826)
Timeframe: at 6-8 weeks after intervention

,
Interventionng/mL (Mean)
CK-MBTroponin-I
Aggressive Lipid Therapy3.70.3
Standard of Care Lipid Therapy5.10.4

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Blood Chemistry - HsCRP

Correlation of yellow plaque index with changes in levels of blood HsCRP as compared from baseline to 6-8 weeks after intervention (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

,
Interventionmg/l (Median)
BaselineFollow-Up
Aggressive Lipid Therapy1.71.2
Standard of Care Lipid Therapy1.71.9

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Diameter Stenosis

Percentage stenosis of vessel diameter in the analysis segment of nontarget lesions as measured by angiography that remained >70%, after successful PCI of the target lesion. (NCT01567826)
Timeframe: Baseline and 6-8 weeks post intervention

,
Interventionpercentage of lesions (Number)
BaselineFollow-up
Aggressive Lipid Therapy79.679.4
Standard of Care Lipid Therapy79.983

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Fractional Flow Reserve (FFR) Value

Change in FFR as related to change in yellow plaque index as compared from baseline to 6-8 weeks after intervention. Fractional flow reserve (FFR), defined as the ratio of maximum flow in the presence of a stenosis to normal maximum flow, is a lesion-specific index of stenosis severity that can be calculated by simultaneous measurement of mean arterial, distal coronary, and central venous pressure. (NCT01567826)
Timeframe: at baseline and at 6-8 weeks after intervention

,
Interventionratio (Mean)
BaselineFollow-up
Aggressive Lipid Therapy0.730.75
Standard of Care Lipid Therapy0.730.73

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Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CCR2 at 12 Weeks, as a Result of Treatment.

"Whole blood drawn from participants were stained with fluorochrome tagged antibodies to the surface marker CCR2. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the change in percentage of monocytes expressing the specific marker (CCR2) at 12 wk versus 0wk within each Period.~Data in each treatment arm is shown as fold change over 12 weeks, in percent positive monocytes expressing surface marker CCR2." (NCT01600170)
Timeframe: week 0 and week 12

InterventionFold Change (Mean)
Atorvastatin1.60
Placebo0.78

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Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CD16 at 12 Weeks, as a Result of Treatment.

"Whole blood drawn from participants were stained with fluorochrome tagged antibodies to the surface markers. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the change in percentage of monocytes expressing the specific marker (CD16) at 12 wk versus 0wk within each Period.~Data is shown as fold change over 12 weeks, in percent positive monocytes expressing surface markers.~Change in primary outcome measures in each treatment arm is expressed as fold change (at week 12 versus week 0). For eg. outcome measure CD14+CD16+ in atorvastatin arm shows a mean value of 1.14. This means at 12 weeks there is an increase of 0.14 fold in the percent monocyte population expressing CD14+CD16+ marker, versus 0 week. Similarly in the placebo group. If fold change in atorvastatin group is smaller than in placebo group, then the treatment had no effect." (NCT01600170)
Timeframe: Week 0 and week 12

InterventionFold change (Mean)
Atorvastatin1.14
Placebo1.51

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Change From Week 0 in Percentage of Blood Monocytes Expressing Surface Marker CD163 at 12 Weeks, as a Result of Treatment.

"Whole blood drawn from participants were stained with fluorochrome tagged antibodies to the surface marker CD163. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the change in percentage of monocytes expressing the specific marker (CD163) at 12 wk versus 0wk within each Period.~Data in each treatment arm is shown as 'mean difference' at 12 weeks versus 0 week, in percent positive monocytes expressing surface marker CD163.~Data is expressed as the difference of the mean values at week 12 and week 0. The negative values mean that the mean values at 12 week were lower than the mean values at 0 week." (NCT01600170)
Timeframe: week 0 and week 12

InterventionPercentage of monocytes (Mean)
Atorvastatin-0.06
Placebo-5.14

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Change From Week 0 in Plasma sCD163 Levels, at Week 12 Following Treatment.

"Monocyte specific inflammatory soluble factor sCD163 was measured by ELISA in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following treatment (atorvastatin or placebo).~Data are expressed as fold change at 12 week versus week 0." (NCT01600170)
Timeframe: 0 week and 12 week

InterventionFold Change (Mean)
Atorvastatin1.08
Placebo1.02

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Change From Week 0 to Week 12 in Percentage of Blood Monocytes Expressing Surface Marker Tissue Factor (TF), Following Treatment.

"Whole blood drawn from participants were stained with fluorochrome tagged antibodies to the surface marker TF. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the change in percentage of monocytes expressing the specific marker TF at 12 wk versus 0wk within each Period.~Data are expressed as fold change." (NCT01600170)
Timeframe: 0 week and 12 week

InterventionFold change (Mean)
Atorvastatin1.18
Placebo1.52

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Change From 0 Week in Levels of Plasma Inflammatory Marker hsCRP in Chronic HIV+/ HAART+ Subjects Over 12 Weeks, Following Treatment.

"Monocyte specific inflammatory soluble factor hsCRP was measured by Quest in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following treatment (atorvastatin or placebo).~Data shown as fold change at week 12 versus week 0." (NCT01600170)
Timeframe: 0 week and 12 week

InterventionFold change (Mean)
Atorvastatin0.94
Placebo1.70

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Change From Week 0 to Week 12 in Percentage of Blood Monocytes Expressing Surface Marker CD38, Following Treatment.

"Whole blood drawn from participants were stained with fluorochrome tagged antibodies to the surface marker CD38. Stained whole blood cells were then acquired on a flow cytometer and analyzed using the Flowjo software to determine the change in percentage of monocytes expressing the specific marker CD38 at 12 wk versus 0wk within each Period.~Data are expressed as fold change at 12 week versus week 0." (NCT01600170)
Timeframe: 0 week and 12 week

InterventionFold Change (Mean)
Atorvastatin0.98
Placebo1.04

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Change From Baseline Within Each Period in Levels of Plasma Inflammatory Marker MCP-1 in Chronic HIV+/ HAART+ Subjects Over 12 Weeks.

"Monocyte specific inflammatory soluble factor MCP-1 was measured by Luminex in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following treatment (atorvastatin or placebo).~Data is shown as fold change in concentration of MCP-1 over 12wks within each treatment period." (NCT01600170)
Timeframe: Week 0 and week 12

InterventionFold change (Mean)
Atorvastatin0.96
Placebo0.87

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Change From Baseline Within Each Period in Levels of Plasma Inflammatory Marker sCD14 in Chronic HIV+/ HAART+ Subjects Over 12 Weeks.

"Monocyte specific inflammatory soluble factor sCD14 was measured by ELISA in plasma of HIV+/HAART+ subjects at baseline and at 12 weeks following treatment (atorvastatin or placebo).~Data is shown as fold change in concentration of sCD14 over 12wks within each treatment period." (NCT01600170)
Timeframe: 0 week and 12 week

InterventionFold Change (Mean)
Atorvastatin0.95
Placebo1.04

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Change in Synovitis

"MRI readings performed independently by two musculoskeletal radiologists, using a semi-quantitative scoring system based on MRI assessment of knee OASynovitis scored using axial & sagittal CE-MRI sequence, while effusion & bone marrow lesions were scored using non-CE-MRI sequences of parent study.~Synovitis defined as enhancing thickened synovium (>2 mm) & was evaluated at nine sites of joint-medial & lateral parapatellar recess, suprapateller, infrapatellar, intercondylar, medial & lateral perimeniscal, & adjacent to anterior & posterior cruciate ligaments (ACL/PCL) in all subjects. Synovial thickness was scored semi-quantitatively based on maximal thickness in any slice at each site as follows: grade 0 if <2mm, grade 1 if 2-4 mm & grade 2 if >4mm. For assessment of whole knee synovitis scores of all sites were summed and categorized: 0-4 normal or equivocal synovitis; 5-8 mild synovitis; 9-12 moderate synovitis & >/= 13 severe synovitis." (NCT01645176)
Timeframe: baseline and 16 weeks

Interventionunits on a scale (Mean)
Osteoarthritis of Knee9.8

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Changes in Major Lipid Parameters - VLDL Size

Change in levels will be measured by difference in levels at 12 weeks. Measure based on VLDL size. (NCT01660191)
Timeframe: Change from Baseline to 12 Weeks

Interventionnanometre (nm) (Mean)
Atorvastatin 20mg0.68
Pitavastatin 4mg0.81
Rosuvastatin 5 mg3.17

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Changes in Plasma CoQ10 Levels

Change in levels will be measured by taking difference between Baseline and Week 12 measures. (NCT01660191)
Timeframe: Change from Baseline to 12 Weeks

,,
Interventionμg/g (Mean)
UbiquinoneTotal CoQ10Upiquinol
Atorvastatin 20mg-96.70-721.09-624.39
Pitavastatin 4mg-110.42-464.85-354.43
Rosuvastatin 5 mg-103.91-642.43-538.52

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Changes to Glucose Metabolism - Fructosamine

Change in levels will be measured by levels at 12 weeks minus levels at baseline. Changes measured based in fructosamine. (NCT01660191)
Timeframe: Change from Baseline to 12 weeks

Interventionµmol (Mean)
Atorvastatin 20mg1.91
Pitavastatin 4mg-1.17
Rosuvastatin 5 mg-3.07

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Changes in HDL and LDL Size

Change in levels will be measured by difference in levels at 12 weeks (NCT01660191)
Timeframe: Change from Baseline to 12 Weeks

,,
Interventionnanometre (nm) (Mean)
HDL SizeLDL Size
Atorvastatin 20mg0.23-0.02
Pitavastatin 4mg0.23-0.11
Rosuvastatin 5 mg0.12-0.09

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Changes to Glucose Metabolism - HbA1c and Insulin

Change in levels will be measured by levels at 12 weeks minus levels at baseline. Changes measured based in HbA1c, and insulin. (NCT01660191)
Timeframe: Change from Baseline to 12 weeks

,,
Interventionpercentage change from baseline measure (Mean)
HbA1cInsulin
Atorvastatin 20mg0.000.16
Pitavastatin 4mg0.000.01
Rosuvastatin 5 mg0.000.17

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Changes HDL Particle Number and LDL Particle Number

Change in levels will be measured by difference in levels at 12 weeks. (NCT01660191)
Timeframe: Change from Baseline to 12 Weeks

,,
Interventionparticle number (Mean)
HDL Particle NumberLDL Particle Number
Atorvastatin 20mg0.64-873.48
Pitavastatin 4mg2.55-768.26
Rosuvastatin 5 mg2.05-626.61

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Matched Unrelated Donors Transplants Who Develop Grade II-IV Acute GVHD.

The number of subjects in the matched unrelated donor cohort who develop grade II-IV acute GVHD. Acute GVHD will be assessed by consensus criteria and graded on Bone Marrow Transplant Clinical Trials Network Manual of Procedures suggested grading sheets. Grade I is mild GVHD involving up to 25% of the subject's skin; Grade II is moderate GVHD. involving 25 to 50% of the subject's skin and can include mild changes in liver and/or mild diarrhea; Grade III is severe GVHD involving over 50% of the subject's skin. Liver involvement is likely as are stomach cramps and diarrhea; and Grade 4 is very severe GvHD. Skin may be blistered and may have broken down in places. Skin may be yellow due to liver injury. Severe diarrhea is common. Subjects in the matched related donors are not included in this analysis. (NCT01665677)
Timeframe: Day 100

InterventionParticipants (Count of Participants)
Matched Unrelated Donor12

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Matched Unrelated Donors Transplants Who Develop Grade II-IV Chronic GVHD.

The number of subjects who develop grade II-IV chronic GVHD. Chronic GVHD diagnosis and grading I to IV will be according to National Institutes of Health (NIH) Criteria rating progressively intense symptoms involving: skin (asymptomatic to deep sclerosis, impaired mobility, ulceration, or pruritus), oral cavity (asymptomatic to symptoms limiting oral intake), eyes (asymptomatic to severe dry eye, inability to work, or loss of vision due to keratoconjunctivitis), gastrointestinal tract (asymptomatic to significant weight loss [>15%] or esophageal dilation), liver (normal function to bilirubin or enzymes >5 times ULN), lungs (asymptomatic to severe shortness of breath requiring supplemental oxygen), joints and fascia (asymptomatic to contractures with reduced range of motion and limited ability to perform daily care), and genital tract (asymptomatic to strictures and severe pain). Subjects in the matched related donors are not included. (NCT01665677)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Matched Unrelated Donor15

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Phosphocreatine Recovery

Percentage change in phosphocreatine recovery from baseline to month as measured by 31PMRS is the primary outcome measure is a representative of mitochondrial oxidative capacity (NCT01702987)
Timeframe: 1 month

Interventionpercentage change from baseline (Mean)
Statin + Placebo-18.9
Statin + Ubiquinol7.7

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Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg2.8
Placebo-1.6

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Percent Change From Baseline in Apo A-1 at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg0.4
Placebo-1.9

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Percent Change From Baseline in Calculated LDL-C at Week 12 - On- Treatment Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 52 (i.e. up to 21 days after last injection) (on-treatment analysis). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-44.2
Placebo4.6

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Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent--to--Treat (ITT) Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Adjusted Least- squares (LS) means and standard errors at Week 24 were obtained from a mixed -effect model with repeated measures (MMRM) to account for missing data. All available post -baseline data from Week 4 to Week 52 regardless of status on- or off-treatment were used in the model. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-48.7
Placebo2.8

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Percent Change From Baseline in Calculated LDL-C at Week 24 - On-Treatment Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post baseline on-treatment data from Week 4 to Week 52 (i.e. up to 21 days after last injection) (on-treatment analysis). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-49.4
Placebo2.7

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Percent Change From Baseline in Calculated LDL-C at Week 52 - ITT Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Adjusted LS means and standard errors at Week 52 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off treatment (ITT analysis). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-50.3
Placebo8.4

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Percent Change From Baseline in Fasting Triglycerides at Week 12 - ITT Analysis

Adjusted means and standard errors at Week 12 from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Mean)
Alirocumab 75 mg/up to 150 mg-8.1
Placebo0.6

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Percent Change From Baseline in Apo B at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-35.4
Placebo-0.9

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Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis

Adjusted means and standard errors at Week 24 from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Mean)
Alirocumab 75 mg/up to 150 mg-10.4
Placebo0.5

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Percent Change From Baseline in HDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg6.0
Placebo-0.8

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Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg6.0
Placebo-0.8

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Percent Change From Baseline in Lipoprotein (a) at Week 24 - ITT Analysis

Adjusted means and standard errors at Week 24 from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Mean)
Alirocumab 75 mg/up to 150 mg-30.3
Placebo-10

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Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-37.9
Placebo4.1

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Percent Change From Baseline in Non-HDL-C at Week 24 - On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 52 (i.e. up to 21 days after last injection). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-43.2
Placebo3.1

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Percent Change From Baseline in Non-High -Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-42.6
Placebo3.1

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Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-30.6
Placebo2.1

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Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01709500)
Timeframe: Up to Week 52

Interventionpercentage of participants (Number)
Alirocumab 75 mg/up to 150 mg81.4
Placebo11.3

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Percent Change From Baseline in Total-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post baseline data from Week 4 to Week 52 regardless of status on- or off treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-26.6
Placebo3.4

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Percentage of Participants Reaching Calculated LDL--C <70 mg/dL (1.81 mmol/L) at Week 52 - On-Treatment Analysis

Adjusted percentages at Week 52 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 52 i.e. up to 21 days after last injection (on-treatment analysis). (NCT01709500)
Timeframe: Up to Week 52

Interventionpercentage of participants (Number)
Alirocumab 75 mg/up to 150 mg68.8
Placebo1.3

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01709500)
Timeframe: Up to Week 52

Interventionpercentage of participants (Number)
Alirocumab 75 mg/up to 150 mg68.2
Placebo1.2

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Percentage of Very High CV Risk Participants Reaching Calculated LDL--C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL--C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 52 i.e. up to 21 days after last injection (on-treatment analysis). (NCT01709500)
Timeframe: Up to week 52

Interventionpercentage of participants (Number)
Alirocumab 75 mg/up to 150 mg82.1
Placebo11.6

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Percent Change From Baseline in Lipoprotein (a) at Week 12 - ITT Analysis

Adjusted means and standard errors at Week 12 from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 52 regardless of status on-or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Mean)
Alirocumab 75 mg/up to 150 mg-24.7
Placebo-5.6

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Percent Change From Baseline in Apo B at Week 24 - On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 52 (i.e. up to 21 days after last injection). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-43.2
Placebo-3.5

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Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment. (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-42.8
Placebo-3.5

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Percent Change From Baseline in Calculated LDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 52 regardless of status on- or off-treatment (ITT analysis). (NCT01709500)
Timeframe: From Baseline to Week 52

Interventionpercent change (Least Squares Mean)
Alirocumab 75 mg/up to 150 mg-43.8
Placebo4.6

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Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or Moderate or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 24 i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first (on-treatment analysis). (NCT01709513)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe5.6
Alirocumab 75 mg/ up to 150 mg51.2

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Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or Moderate or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01709513)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe4.4
Alirocumab 75 mg/ up to 150 mg41.9

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 24 i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first (on-treatment analysis). (NCT01709513)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe0.8
Alirocumab 75 mg/ up to 150 mg39.0

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01709513)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe0.8
Alirocumab 75 mg/ up to 150 mg32.5

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Percent Change in Fasting Triglycerides From Baseline to Week 12 -- ITT Analysis

Combined Estimate for Adjusted Mean (Standard Error) at Week 24 from multiple imputation followed by robust regression including all available post-baseline data from Week 4 to Week 24 regardless of status on or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Mean)
Ezetimibe-9.4
Alirocumab 75 mg/ up to 150 mg-8.0

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Percent Change From Baseline in Total Cholesterol (Total--C) at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-10.9
Alirocumab 75 mg/ up to 150 mg-31.8

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Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe-15.8
Alirocumab 75 mg/ up to 150 mg-41.5

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Percent Change From Baseline in Non--High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 -- ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-14.6
Alirocumab 75 mg/ up to 150 mg-40.2

[back to top]

Percent Change From Baseline in Apo B at Week 12 -- ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.6
Alirocumab 75 mg/ up to 150 mg-36.1

[back to top]

Percent Change From Baseline in Total-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.6
Alirocumab 75/ up to 150-32.7

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Percent Change in HDL-C From Baseline to Week 12 -- ITT Analysis

Least-squares (LS) means and standard errors (SE) taken from MMRM (mixed-effect model with repeated measures) analysis (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe7.6
Alirocumab 75 mg/ up to 150 mg9.0

[back to top]

Percent Change From Baseline in Lipoprotein(a) at Week 24 - ITT Analysis

Combined Estimate for Adjusted Mean (Standard Error) at Week 24 from multiple imputation followed by robust regression including all available post-baseline data from Week 4 to Week 24 regardless of status on or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Ezetimibe-7.3
Alirocumab 75 mg/ up to 150 mg-25.9

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Percent Change From Baseline in Apo A--1 at Week 12 -- ITT Analysis

Least squares (LS) means and standard errors (SE) taken from MMRM (mixed effect model with repeated measures) analysis. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe3.9
Alirocumab 75 mg/ up to 150 mg5.5

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Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe2.9
Alirocumab 75 mg/ up to 150 mg4.8

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Percent Change From Baseline in Apo B at Week 24 -- On--Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first). (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-14.4
Alirocumab 75 mg/ up to 150 mg-42.6

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Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis

Combined Estimate for Adjusted Mean (Standard Error) at Week 24 from multiple imputation followed by robust regression including all available post-baseline data from Week 4 to Week 24 regardless of status on or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Ezetimibe-3.6
Alirocumab 75 mg/ up to 150 mg-9.3

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Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe6.8
Alirocumab 75 mg/ up to 150 mg7.7

[back to top]

Percent Change From Baseline in Lipoprotein(a) at Week 12 -- ITT Analysis

Combined Estimate for Adjusted Mean (Standard Error) at Week 24 from multiple imputation followed by robust regression including all available post-baseline data from Week 4 to Week 24 regardless of status on or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Mean)
Ezetimibe-4.5
Alirocumab 75 mg/ up to 150 mg-21.7

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Percent Change From Baseline in Non--HDL-C at Week 24 -- On--Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first). (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-17.1
Alirocumab 75 mg/ up to 150 mg-46.9

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Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 -- ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post--baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.2
Alirocumab 75 mg/ up to 150 mg-36.3

[back to top]

Percent Change From Baseline in Calculated LDL--C at Week 12 -- ITT Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe-15.6
Alirocumab 75 mg/ up to 150 mg-47.0

[back to top]

Percent Change From Baseline in Calculated LDL-C at Week 12 - On--Treatment Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT01709513)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe-18.0
Alirocumab 75 mg/ up to 150 mg-51.2

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Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent--To-Treat (ITT) Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted Least-squares (LS) means and standard errors at Week 24 were obtained from a mixed-effect model with repeated measures (MMRM) to account for missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were used in the model (ITT analysis). (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-14.6
Alirocumab 75 mg/ up to 150 mg-45.0

[back to top]

Percent Change From Baseline in Calculated LDL-C at Week 24 - On--Treatment Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT01709513)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-17.1
Alirocumab 75 mg/ up to 150 mg-52.2

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Percent Change From Baseline in Calculated LDL-C at Week 24 Versus Atorvastatin - Raw Data Description - Intent-To-Treat (ITT) Analysis

(NCT01709513)
Timeframe: From Baseline up to Week 24

Interventionpercent change (Mean)
Atorvastatin (Statin Rechallenge Arm)-31.9
Ezetimibe (Active Comparator)-15.2
Alirocumab 75 mg/ up to 150 mg-47.3

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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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Percent Change From Baseline in Apo B at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-6.9
Ezetimibe 10 mg + Atorvastatin 20 mg-13.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-38.4
Atorvastatin 80 mg-9.5
Rosuvastatin 40 mg-14.1
Ezetimibe 10 mg + Atorvastatin 40 mg-20.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-36.2

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Percent Change From Baseline in Apo A-1 at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg1.2
Ezetimibe 10 mg + Atorvastatin 20 mg1.0
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg7.6
Atorvastatin 80 mg2.2
Rosuvastatin 40 mg4.7
Ezetimibe 10 mg + Atorvastatin 40 mg-1.8
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg5.8

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Percent Change From Baseline in Apo A-1 at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-0.8
Ezetimibe 10 mg + Atorvastatin 20 mg1.7
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg5.4
Atorvastatin 80 mg1.6
Rosuvastatin 40 mg5.6
Ezetimibe 10 mg + Atorvastatin 40 mg1.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg9.4

[back to top]

Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 24 i.e. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first (on-treatment analysis). (NCT01730040)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Atorvastatin 40 mg37.8
Ezetimibe 10 mg + Atorvastatin 20 mg72.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg91.2
Atorvastatin 80 mg18.5
Rosuvastatin 40 mg64.0
Ezetimibe 10 mg + Atorvastatin 40 mg66.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg90.0

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Percentage of Very High CV Risk Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) or High CV Risk Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to week 24 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01730040)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Atorvastatin 40 mg34.5
Ezetimibe 10 mg + Atorvastatin 20 mg68.4
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg87.2
Atorvastatin 80 mg18.5
Rosuvastatin 40 mg62.2
Ezetimibe 10 mg + Atorvastatin 40 mg65.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg84.6

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model including available post-baseline on-treatment data from Week 4 to Week 24 i.e. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first (on-treatment analysis). (NCT01730040)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Atorvastatin 40 mg20.0
Ezetimibe 10 mg + Atorvastatin 20 mg55.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg82.3
Atorvastatin 80 mg10.5
Rosuvastatin 40 mg42.4
Ezetimibe 10 mg + Atorvastatin 40 mg55.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg83.7

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 24 - ITT Analysis

Adjusted percentages at Week 24 were obtained from a multiple imputation approach model for handling of missing data. All available post-baseline data from Week 4 to week 24 regardless of status on- or off-treatment were included in the imputation model (ITT analysis). (NCT01730040)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Atorvastatin 40 mg16.0
Ezetimibe 10 mg + Atorvastatin 20 mg50.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg79.2
Atorvastatin 80 mg10.2
Rosuvastatin 40 mg42.2
Ezetimibe 10 mg + Atorvastatin 40 mg54.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg77.2

[back to top]

Percent Change From Baseline in Total-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-6.5
Ezetimibe 10 mg + Atorvastatin 20 mg-13.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-29.0
Atorvastatin 80 mg-9.9
Rosuvastatin 40 mg-13.5
Ezetimibe 10 mg + Atorvastatin 40 mg-19.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-29.0

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Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-4.0
Ezetimibe 10 mg + Atorvastatin 20 mg-11.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-27.1
Atorvastatin 80 mg-4.8
Rosuvastatin 40 mg-11.7
Ezetimibe 10 mg + Atorvastatin 40 mg-15.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-33.6

[back to top]

Percent Change From Baseline in Non-High-density Lipoprotein Cholesterol (Non-HDL-C) at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-6.3
Ezetimibe 10 mg + Atorvastatin 20 mg-15.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-36.7
Atorvastatin 80 mg-6.5
Rosuvastatin 40 mg-17.4
Ezetimibe 10 mg + Atorvastatin 40 mg-21.0
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-47.6

[back to top]

Percent Change From Baseline in Non-HDL-C at Week 24 - On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-7.5
Ezetimibe 10 mg + Atorvastatin 20 mg-18.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-40.5
Atorvastatin 80 mg-7.0
Rosuvastatin 40 mg-18.4
Ezetimibe 10 mg + Atorvastatin 40 mg-23.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-50.5

[back to top]

Percent Change From Baseline in Non-HDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-7.1
Ezetimibe 10 mg + Atorvastatin 20 mg-17.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-40.6
Atorvastatin 80 mg-13.0
Rosuvastatin 40 mg-19.8
Ezetimibe 10 mg + Atorvastatin 40 mg-27.5
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-42.3

[back to top]

Percent Change From Baseline in Lipoprotein(a) at Week 24 - ITT Analysis

Adjusted means and standard errors at Week 24 from from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Atorvastatin 40 mg-20.2
Ezetimibe 10 mg + Atorvastatin 20 mg-10.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-23.6
Atorvastatin 80 mg-9.7
Rosuvastatin 40 mg-4.9
Ezetimibe 10 mg + Atorvastatin 40 mg0.2
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-30.8

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Percent Change From Baseline in Lipoprotein(a) at Week 12 - ITT Analysis

Adjusted means and standard errors at Week 12 from from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Atorvastatin 40 mg-11.7
Ezetimibe 10 mg + Atorvastatin 20 mg-5.4
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-24.0
Atorvastatin 80 mg-1.6
Rosuvastatin 40 mg11.5
Ezetimibe 10 mg + Atorvastatin 40 mg7.9
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-27.9

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Percent Change From Baseline in HDL-C at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg1.9
Ezetimibe 10 mg + Atorvastatin 20 mg-0.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg4.8
Atorvastatin 80 mg4.7
Rosuvastatin 40 mg5.7
Ezetimibe 10 mg + Atorvastatin 40 mg2.0
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg7.7

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Percent Change From Baseline in HDL-C at Week 12 - ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-3.2
Ezetimibe 10 mg + Atorvastatin 20 mg-1.7
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg4.1
Atorvastatin 80 mg3.0
Rosuvastatin 40 mg4.6
Ezetimibe 10 mg + Atorvastatin 40 mg4.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg8.5

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Percent Change From Baseline in Fasting Triglycerides at Week 24 - ITT Analysis

Adjusted means and standard errors at Week 24 from from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Atorvastatin 40 mg-6.7
Ezetimibe 10 mg + Atorvastatin 20 mg-3.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-12.0
Atorvastatin 80 mg-7.3
Rosuvastatin 40 mg-0.5
Ezetimibe 10 mg + Atorvastatin 40 mg-13.9
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-19.1

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Percent Change From Baseline in Fasting Triglycerides at Week 12 - ITT Analysis

Adjusted means and standard errors at Week 12 from from a multiple imputation approach model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Atorvastatin 40 mg-4.7
Ezetimibe 10 mg + Atorvastatin 20 mg0.5
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-12.4
Atorvastatin 80 mg-4.6
Rosuvastatin 40 mg-3.7
Ezetimibe 10 mg + Atorvastatin 40 mg-16.8
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-12.1

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Percent Change From Baseline in Calculated LDL-C at Week 24 - On-Treatment Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first) (on-treatment analysis). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-6.1
Ezetimibe 10 mg + Atorvastatin 20 mg-23.7
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-48.6
Atorvastatin 80 mg-5.0
Rosuvastatin 40 mg-22.9
Ezetimibe 10 mg + Atorvastatin 40 mg-24.5
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-57.8

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Percent Change From Baseline in Calculated LDL-C at Week 24 - Intent-to-treat (ITT) Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted Least-squares (LS) means and standard errors at Week 24 were obtained from a mixed-effect model with repeated measures (MMRM) to account for missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were used in the model (ITT analysis). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-5
Ezetimibe 10 mg + Atorvastatin 20 mg-20.5
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-44.1
Atorvastatin 80 mg-4.8
Rosuvastatin 40 mg-21.4
Ezetimibe 10 mg + Atorvastatin 40 mg-22.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-54

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Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first) (on-treatment analysis). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-9.2
Ezetimibe 10 mg + Atorvastatin 20 mg-27.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-53.7
Atorvastatin 80 mg-14.6
Rosuvastatin 40 mg-23.3
Ezetimibe 10 mg + Atorvastatin 40 mg-30.7
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-50.9

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Percent Change From Baseline in Calculated LDL-C at Week 12 - ITT Analysis

Calculated LDL-C values were obtained from Friedewald formula. Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment (ITT analysis). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-8.5
Ezetimibe 10 mg + Atorvastatin 20 mg-22.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-48.4
Atorvastatin 80 mg-14.5
Rosuvastatin 40 mg-23.3
Ezetimibe 10 mg + Atorvastatin 40 mg-29.7
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-50.5

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Percent Change From Baseline in Apolipoprotein (Apo) B at Week 24 - ITT Analysis

Adjusted LS means and standard errors at Week 24 from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-4.4
Ezetimibe 10 mg + Atorvastatin 20 mg-10.1
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-33.7
Atorvastatin 80 mg-3.5
Rosuvastatin 40 mg-10.9
Ezetimibe 10 mg + Atorvastatin 40 mg-14.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-41.9

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Percent Change From Baseline in Apo B at Week 24 - On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 24 (ie. up to 21 days after last injection or 3 days after the last capsule [whatever atorvastatin, rosuvastatin or ezetimibe], whichever came first). (NCT01730040)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Atorvastatin 40 mg-5.1
Ezetimibe 10 mg + Atorvastatin 20 mg-12.6
Alirocumab 75 mg/up to 150 mg + Atorvastatin 20 mg-37.7
Atorvastatin 80 mg-4.4
Rosuvastatin 40 mg-12.8
Ezetimibe 10 mg + Atorvastatin 40 mg-16.3
Alirocumab 75 mg/up to 150 mg + Atorvastatin 40 mg-42.7

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Change From Baseline to Week 6 in Renal Function

Investigators will assess the effect of atorvastatin on albuminuria by spot urine microalbuminuria/creatinine ratio measured at baseline and at 6 weeks of treatment. (NCT01732718)
Timeframe: Baseline, 6 weeks

Interventionug per mg (Median)
Atorvastatin28.8
Placebo74.9

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Change From Baseline to Week 6 in Tricuspid Regurgitant (TR) Jet.

Echocardiogram will be used to assess TR jet before and after treatment. (NCT01732718)
Timeframe: Baseline, Week 6

Interventionm/sec (Mean)
Atorvastatin0.80
Placebo-0.05

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Occurrence of Adverse Events.

Subjects will be evaluated for safety by patient self-report of adverse events and results of laboratory tests. (NCT01732718)
Timeframe: Continuously from randomization through end of study

Interventionevents (Number)
Atorvastatin9
Placebo13

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Mean Change From Baseline to Week 6 in Absolute Cell Counts

Flow cytometry will be performed to assess absolute cell counts at baseline and at 6 weeks of treatment. (NCT01732718)
Timeframe: Baseline, 6 weeks

,
Intervention10^9 cells/L (Mean)
AMCALCANC
Atorvastatin-0.070.08-0.18
Placebo0.15-0.22-0.55

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Change From Baseline to Week 6 in Plasma Markers of Endothelial Activation

Investigators will measure plasma levels of soluble vascular cell adhesion molecules (sVCAM) and soluble intracellular adhesion molecule (sICAM) at baseline and at 6 weeks of treatment. (NCT01732718)
Timeframe: Baseline, 6 weeks

Interventionng/mL (Mean)
Atorvastatin22.99
Placebo7.54

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Change From Baseline to Week 6 in Plasma Levels of Vascular Endothelial Growth Factor (VEGF)

Investigators will measure plasma levels of vascular endothelial growth factor (VEGF) at baseline and at 6 weeks of treatment. (NCT01732718)
Timeframe: Baseline, 6 weeks

Interventionpg/mL (Mean)
Atorvastatin-3.99
Placebo-10.5

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Abnormal Physical Findings.

Subjects will be evaluated by physical examination and/or measurement of vital signs at each study visit. (NCT01732718)
Timeframe: Baseline, 2, 4, and 6 weeks during treatment, and at follow-up.

Interventionparticipants (Number)
Baseline-Atorvastatin0
Week 4-Atorvastatin2
Week 6-Atorvastatin1
Baseline-Placebo1
Week 4-Placebo0
Week 6-Placebo1

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Change From Baseline to Week 6 in Plasma Levels of Soluble Fms-like Tyrosine Kinase-1 (sFLT-1)

Investigators will measure plasma levels of soluble fms-like tyrosine kinase-1 (sFLT-1) at baseline and at 6 weeks of treatment. (NCT01732718)
Timeframe: Baseline, 6 weeks

Interventionpg/mL (Median)
Atorvastatin19.2
Placebo36.9

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Change From Baseline to Week 6 in Endothelial Function

Endothelial function will be assessed using ultrasound imaging of the brachial artery, with measurement of endothelium-dependent (flow-mediated) and endothelium-independent (nitroglycerin-mediated) dilation of the artery measured in millimeters (mm). (NCT01732718)
Timeframe: Baseline, 6 weeks

Intervention% diameter change (Median)
Atorvastatin1.44
Placebo0.69

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Change From Baseline in Brachial Artery Flow-Mediated Dilation at 6-months

(NCT01733953)
Timeframe: Baseline and 6-Months

Interventionpercentage change (Mean)
Atorvastatin-0.5
Sugar Pill (Placebo)-3.4

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Change From Baseline in Carotid Artery Compliance at 6-Months

Carotid Artery Compliance is a measure of arterial stiffness. Higher arterial stiffness places persons at higher risk for CVD. (NCT01733953)
Timeframe: Baseline and 6-Months

Interventionmm/mmHg x 10^-3 (Mean)
Atorvastatin-.34
Sugar Pill (Placebo)0.57

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Change From Baseline in Carotid Artery Distensibility at 6-Months

(NCT01733953)
Timeframe: Baseline and 6-Months

Intervention% distensibility (Mean)
Atorvastatin0.31
Sugar Pill (Placebo)0.33

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Change From Baseline in Carotid Intima-Media Thickness at 6-Months

(NCT01733953)
Timeframe: Baseline and 6-Months

Interventionmm (Mean)
Atorvastatin-.01
Sugar Pill (Placebo)0.01

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Change From Baseline in Pulse Wave Velocity at 6-Months

(NCT01733953)
Timeframe: Baseline and 6-Months

Interventionm/s (Mean)
Atorvastatin-0.52
Sugar Pill (Placebo)-0.3

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Change From Baseline in Augmentation Index at 6-Months

(NCT01733953)
Timeframe: Baseline and 6-Months

InterventionP2/P1 (Mean)
Atorvastatin-0.66
Sugar Pill (Placebo)-6.01

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Percentage of Participants Who Achieved LDL-C < 70 mg/dL at Week 12

(NCT01763866)
Timeframe: Week 12

Interventionpercentage of participants (Number)
A10 PBO Q2W2.0
A10 PBO QM5.9
A10 EZE (Q2W)22.4
A10 EZE (QM)19.2
A10 EvoMab Q2W85.4
A10 EvoMab QM84.2
A80 PBO Q2W13.0
A80 PBO QM9.8
A80 EZE (Q2W)52.0
A80 EZE (QM)55.8
A80 EvoMab Q2W93.1
A80 EvoMab QM91.0
R5 PBO Q2W7.7
R5 PBO QM5.5
R5 EvoMab Q2W85.0
R5 EvoMab QM86.5
R40 PBO Q2W39.6
R40 PBO QM28.0
R40 EvoMab Q2W92.3
R40 EvoMab QM92.3
S40 PBO Q2W1.9
S40 PBO QM6.4
S40 EvoMab Q2W94.4
S40 EvoMab QM84.8

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Percentage of Participants Who Achieved a Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL

(NCT01763866)
Timeframe: Weeks 10 and 12

Interventionpercentage of participants (Number)
A10 PBO Q2W5.7
A10 PBO QM5.6
A10 EZE (Q2W)20.0
A10 EZE (QM)16.7
A10 EvoMab Q2W88.1
A10 EvoMab QM85.8
A80 PBO Q2W13.7
A80 PBO QM9.3
A80 EZE (Q2W)50.9
A80 EZE (QM)62.3
A80 EvoMab Q2W94.4
A80 EvoMab QM92.5
R5 PBO Q2W7.0
R5 PBO QM5.3
R5 EvoMab Q2W88.7
R5 EvoMab QM89.9
R40 PBO Q2W38.9
R40 PBO QM28.8
R40 EvoMab Q2W93.5
R40 EvoMab QM94.5
S40 PBO Q2W1.9
S40 PBO QM3.9
S40 EvoMab Q2W93.6
S40 EvoMab QM88.5

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Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.07
A10 PBO QM-0.77
A10 EZE (Q2W)1.44
A10 EZE (QM)6.85
A10 EvoMab Q2W-26.01
A10 EvoMab QM-22.64
A80 PBO Q2W-3.45
A80 PBO QM1.51
A80 EZE (Q2W)8.05
A80 EZE (QM)9.96
A80 EvoMab Q2W-23.97
A80 EvoMab QM-27.46
R5 PBO Q2W11.41
R5 PBO QM3.65
R5 EvoMab Q2W-24.26
R5 EvoMab QM-23.16
R40 PBO Q2W8.59
R40 PBO QM6.26
R40 EvoMab Q2W-24.96
R40 EvoMab QM-25.93
S40 PBO Q2W-10.57
S40 PBO QM-4.99
S40 EvoMab Q2W-38.64
S40 EvoMab QM-32.16

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Percent Change From Baseline in LDL-C at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W8.54
A10 PBO QM0.35
A10 EZE (Q2W)-23.88
A10 EZE (QM)-18.98
A10 EvoMab Q2W-61.41
A10 EvoMab QM-62.47
A80 PBO Q2W13.12
A80 PBO QM9.76
A80 EZE (Q2W)-16.85
A80 EZE (QM)-21.25
A80 EvoMab Q2W-61.80
A80 EvoMab QM-65.05
R5 PBO Q2W7.55
R5 PBO QM2.79
R5 EvoMab Q2W-59.33
R5 EvoMab QM-63.79
R40 PBO Q2W6.57
R40 PBO QM-0.02
R40 EvoMab Q2W-59.08
R40 EvoMab QM-62.94
S40 PBO Q2W3.26
S40 PBO QM6.00
S40 EvoMab Q2W-66.17
S40 EvoMab QM-62.45

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Percent Change From Baseline in HDL-C at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W0.22
A10 PBO QM0.01
A10 EZE (Q2W)-1.76
A10 EZE (QM)-0.40
A10 EvoMab Q2W7.04
A10 EvoMab QM7.88
A80 PBO Q2W5.02
A80 PBO QM0.30
A80 EZE (Q2W)0.62
A80 EZE (QM)0.21
A80 EvoMab Q2W9.09
A80 EvoMab QM7.36
R5 PBO Q2W2.87
R5 PBO QM-0.16
R5 EvoMab Q2W6.07
R5 EvoMab QM7.18
R40 PBO Q2W-0.39
R40 PBO QM0.73
R40 EvoMab Q2W4.65
R40 EvoMab QM5.57
S40 PBO Q2W1.14
S40 PBO QM-2.65
S40 EvoMab Q2W10.92
S40 EvoMab QM6.41

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Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.09
A10 PBO QM2.80
A10 EZE (Q2W)-12.14
A10 EZE (QM)-9.85
A10 EvoMab Q2W-40.74
A10 EvoMab QM-40.07
A80 PBO Q2W4.31
A80 PBO QM6.18
A80 EZE (Q2W)-10.53
A80 EZE (QM)-11.06
A80 EvoMab Q2W-40.79
A80 EvoMab QM-36.25
R5 PBO Q2W4.68
R5 PBO QM6.07
R5 EvoMab Q2W-38.57
R5 EvoMab QM-39.26
R40 PBO Q2W5.96
R40 PBO QM2.69
R40 EvoMab Q2W-35.17
R40 EvoMab QM-32.30
S40 PBO Q2W-0.20
S40 PBO QM5.13
S40 EvoMab Q2W-47.24
S40 EvoMab QM-39.47

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Change From Baseline in LDL-C at at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionmg/dL (Least Squares Mean)
A10 PBO Q2W6.8
A10 PBO QM-0.4
A10 EZE (Q2W)-32.4
A10 EZE (QM)-25.1
A10 EvoMab Q2W-76.8
A10 EvoMab QM-80.1
A80 PBO Q2W11.0
A80 PBO QM5.5
A80 EZE (Q2W)-13.0
A80 EZE (QM)-21.3
A80 EvoMab Q2W-58.8
A80 EvoMab QM-60.1
R5 PBO Q2W6.5
R5 PBO QM0.1
R5 EvoMab Q2W-68.9
R5 EvoMab QM-77.8
R40 PBO Q2W3.4
R40 PBO QM-4.8
R40 EvoMab Q2W-52.3
R40 EvoMab QM-55.3
S40 PBO Q2W-5.7
S40 PBO QM1.7
S40 EvoMab Q2W-83.8
S40 EvoMab QM-78.4

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Change From Baseline in LDL-C at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionmg/dL (Least Squares Mean)
A10 PBO Q2W8.6
A10 PBO QM0.8
A10 EZE (Q2W)-30.1
A10 EZE (QM)-23.3
A10 EvoMab Q2W-77.0
A10 EvoMab QM-75.1
A80 PBO Q2W12.7
A80 PBO QM7.0
A80 EZE (Q2W)-9.9
A80 EZE (QM)-19.5
A80 EvoMab Q2W-59.0
A80 EvoMab QM-54.8
R5 PBO Q2W7.8
R5 PBO QM2.4
R5 EvoMab Q2W-69.2
R5 EvoMab QM-73.3
R40 PBO Q2W5.1
R40 PBO QM-2.0
R40 EvoMab Q2W-52.1
R40 EvoMab QM-46.7
S40 PBO Q2W-4.5
S40 PBO QM-0.6
S40 EvoMab Q2W-83.5
S40 EvoMab QM-72.5

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Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W7.55
A10 PBO QM0.81
A10 EZE (Q2W)-17.29
A10 EZE (QM)-11.43
A10 EvoMab Q2W-50.95
A10 EvoMab QM-51.44
A80 PBO Q2W10.20
A80 PBO QM5.48
A80 EZE (Q2W)-14.22
A80 EZE (QM)-13.62
A80 EvoMab Q2W-49.14
A80 EvoMab QM-53.26
R5 PBO Q2W5.07
R5 PBO QM2.54
R5 EvoMab Q2W-49.79
R5 EvoMab QM-53.59
R40 PBO Q2W3.71
R40 PBO QM1.98
R40 EvoMab Q2W-47.07
R40 EvoMab QM-52.95
S40 PBO Q2W-0.31
S40 PBO QM2.49
S40 EvoMab Q2W-55.65
S40 EvoMab QM-54.37

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Percent Change From Baseline in Apolipoprotein B at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W7.89
A10 PBO QM0.21
A10 EZE (Q2W)-15.98
A10 EZE (QM)-10.95
A10 EvoMab Q2W-50.90
A10 EvoMab QM-47.15
A80 PBO Q2W11.64
A80 PBO QM6.54
A80 EZE (Q2W)-12.31
A80 EZE (QM)-12.16
A80 EvoMab Q2W-49.77
A80 EvoMab QM-46.47
R5 PBO Q2W6.35
R5 PBO QM4.63
R5 EvoMab Q2W-50.15
R5 EvoMab QM-48.58
R40 PBO Q2W4.91
R40 PBO QM3.24
R40 EvoMab Q2W-45.61
R40 EvoMab QM-43.71
S40 PBO Q2W0.35
S40 PBO QM3.57
S40 EvoMab Q2W-55.95
S40 EvoMab QM-49.16

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Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W5.96
A10 PBO QM2.24
A10 EZE (Q2W)-14.39
A10 EZE (QM)-10.86
A10 EvoMab Q2W-40.44
A10 EvoMab QM-42.45
A80 PBO Q2W4.26
A80 PBO QM6.42
A80 EZE (Q2W)-11.92
A80 EZE (QM)-12.25
A80 EvoMab Q2W-40.22
A80 EvoMab QM-40.43
R5 PBO Q2W5.41
R5 PBO QM5.02
R5 EvoMab Q2W-39.33
R5 EvoMab QM-42.00
R40 PBO Q2W4.55
R40 PBO QM1.71
R40 EvoMab Q2W-36.04
R40 EvoMab QM-38.62
S40 PBO Q2W-0.14
S40 PBO QM5.45
S40 EvoMab Q2W-47.20
S40 EvoMab QM-43.17

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Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W-0.99
A10 PBO QM-0.45
A10 EZE (Q2W)-1.13
A10 EZE (QM)-0.92
A10 EvoMab Q2W5.54
A10 EvoMab QM7.66
A80 PBO Q2W4.48
A80 PBO QM-1.37
A80 EZE (Q2W)0.86
A80 EZE (QM)-0.59
A80 EvoMab Q2W8.44
A80 EvoMab QM7.76
R5 PBO Q2W0.87
R5 PBO QM-0.94
R5 EvoMab Q2W6.23
R5 EvoMab QM7.72
R40 PBO Q2W-0.60
R40 PBO QM-0.40
R40 EvoMab Q2W4.86
R40 EvoMab QM6.35
S40 PBO Q2W0.13
S40 PBO QM-2.14
S40 EvoMab Q2W10.35
S40 EvoMab QM6.71

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Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.49
A10 PBO QM9.17
A10 EZE (Q2W)-3.16
A10 EZE (QM)1.57
A10 EvoMab Q2W-5.61
A10 EvoMab QM-13.38
A80 PBO Q2W6.16
A80 PBO QM8.05
A80 EZE (Q2W)-8.10
A80 EZE (QM)-4.86
A80 EvoMab Q2W-9.27
A80 EvoMab QM-6.36
R5 PBO Q2W12.43
R5 PBO QM12.26
R5 EvoMab Q2W-10.28
R5 EvoMab QM-7.26
R40 PBO Q2W8.44
R40 PBO QM10.75
R40 EvoMab Q2W-9.15
R40 EvoMab QM-15.43
S40 PBO Q2W9.29
S40 PBO QM13.78
S40 EvoMab Q2W-11.67
S40 EvoMab QM-15.93

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Percent Change From Baseline in Triglycerides at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W8.27
A10 PBO QM14.35
A10 EZE (Q2W)-0.43
A10 EZE (QM)4.88
A10 EvoMab Q2W-3.79
A10 EvoMab QM-13.26
A80 PBO Q2W6.65
A80 PBO QM8.22
A80 EZE (Q2W)-7.40
A80 EZE (QM)-3.11
A80 EvoMab Q2W-10.07
A80 EvoMab QM-1.10
R5 PBO Q2W13.57
R5 PBO QM12.96
R5 EvoMab Q2W-4.46
R5 EvoMab QM-6.88
R40 PBO Q2W10.97
R40 PBO QM10.00
R40 EvoMab Q2W-5.58
R40 EvoMab QM-10.51
S40 PBO Q2W8.07
S40 PBO QM16.72
S40 EvoMab Q2W-13.71
S40 EvoMab QM-14.65

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Percent Change From Baseline in Lipoprotein(a) at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W7.34
A10 PBO QM-0.43
A10 EZE (Q2W)3.29
A10 EZE (QM)7.18
A10 EvoMab Q2W-25.87
A10 EvoMab QM-20.25
A80 PBO Q2W-2.23
A80 PBO QM3.41
A80 EZE (Q2W)8.01
A80 EZE (QM)10.20
A80 EvoMab Q2W-24.61
A80 EvoMab QM-24.68
R5 PBO Q2W11.40
R5 PBO QM4.49
R5 EvoMab Q2W-25.09
R5 EvoMab QM-20.85
R40 PBO Q2W10.38
R40 PBO QM10.21
R40 EvoMab Q2W-26.11
R40 EvoMab QM-21.97
S40 PBO Q2W-6.81
S40 PBO QM-1.06
S40 EvoMab Q2W-38.06
S40 EvoMab QM-29.23

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Percent Change From Baseline in Very Low-Density Cholesterol (VLDL-C) at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.51
A10 PBO QM9.53
A10 EZE (Q2W)-5.35
A10 EZE (QM)1.77
A10 EvoMab Q2W-6.85
A10 EvoMab QM-11.77
A80 PBO Q2W6.24
A80 PBO QM8.31
A80 EZE (Q2W)-8.52
A80 EZE (QM)-6.13
A80 EvoMab Q2W-8.96
A80 EvoMab QM-6.38
R5 PBO Q2W12.86
R5 PBO QM12.54
R5 EvoMab Q2W-12.22
R5 EvoMab QM-7.25
R40 PBO Q2W7.06
R40 PBO QM8.13
R40 EvoMab Q2W-9.09
R40 EvoMab QM-15.05
S40 PBO Q2W8.64
S40 PBO QM16.37
S40 EvoMab Q2W-14.57
S40 EvoMab QM-16.50

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Percent Change From Baseline in Very Low-Density Cholesterol (VLDL-C) at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W8.32
A10 PBO QM14.74
A10 EZE (Q2W)-4.61
A10 EZE (QM)3.45
A10 EvoMab Q2W-6.16
A10 EvoMab QM-11.73
A80 PBO Q2W6.73
A80 PBO QM8.54
A80 EZE (Q2W)-7.92
A80 EZE (QM)-6.00
A80 EvoMab Q2W-9.69
A80 EvoMab QM-1.06
R5 PBO Q2W13.79
R5 PBO QM12.47
R5 EvoMab Q2W-8.20
R5 EvoMab QM-6.28
R40 PBO Q2W10.09
R40 PBO QM8.59
R40 EvoMab Q2W-6.10
R40 EvoMab QM-9.95
S40 PBO Q2W7.63
S40 PBO QM20.97
S40 EvoMab Q2W-14.83
S40 EvoMab QM-15.86

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

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W9.86
A10 PBO QM0.97
A10 EZE (Q2W)-21.96
A10 EZE (QM)-17.08
A10 EvoMab Q2W-61.56
A10 EvoMab QM-58.19
A80 PBO Q2W14.49
A80 PBO QM11.83
A80 EZE (Q2W)-14.60
A80 EZE (QM)-19.80
A80 EvoMab Q2W-61.80
A80 EvoMab QM-58.68
R5 PBO Q2W8.12
R5 PBO QM5.10
R5 EvoMab Q2W-60.09
R5 EvoMab QM-59.40
R40 PBO Q2W9.42
R40 PBO QM2.59
R40 EvoMab Q2W-58.89
R40 EvoMab QM-52.40
S40 PBO Q2W4.70
S40 PBO QM3.40
S40 EvoMab Q2W-65.86
S40 EvoMab QM-57.02

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Percent Change From Baseline in Non-HDL-C at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W8.25
A10 PBO QM2.43
A10 EZE (Q2W)-18.27
A10 EZE (QM)-14.78
A10 EvoMab Q2W-53.39
A10 EvoMab QM-52.20
A80 PBO Q2W11.79
A80 PBO QM9.95
A80 EZE (Q2W)-14.34
A80 EZE (QM)-17.26
A80 EvoMab Q2W-54.84
A80 EvoMab QM-50.05
R5 PBO Q2W7.92
R5 PBO QM5.85
R5 EvoMab Q2W-52.04
R5 EvoMab QM-51.57
R40 PBO Q2W8.61
R40 PBO QM3.35
R40 EvoMab Q2W-50.97
R40 EvoMab QM-46.42
S40 PBO Q2W1.89
S40 PBO QM5.66
S40 EvoMab Q2W-59.02
S40 EvoMab QM-50.96

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Percent Change From Baseline in Non-High-Density Lipoprotein Cholesterol (Non-HDL-C) at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.80
A10 PBO QM1.28
A10 EZE (Q2W)-20.71
A10 EZE (QM)-16.56
A10 EvoMab Q2W-53.48
A10 EvoMab QM-56.09
A80 PBO Q2W10.74
A80 PBO QM8.45
A80 EZE (Q2W)-16.19
A80 EZE (QM)-18.79
A80 EvoMab Q2W-54.44
A80 EvoMab QM-56.31
R5 PBO Q2W7.02
R5 PBO QM3.73
R5 EvoMab Q2W-52.59
R5 EvoMab QM-55.47
R40 PBO Q2W6.19
R40 PBO QM1.58
R40 EvoMab Q2W-52.08
R40 EvoMab QM-55.72
S40 PBO Q2W0.74
S40 PBO QM6.81
S40 EvoMab Q2W-59.33
S40 EvoMab QM-56.01

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at the Mean of Weeks 10 and 12

(NCT01763866)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.41
A10 PBO QM0.78
A10 EZE (Q2W)-15.77
A10 EZE (QM)-11.47
A10 EvoMab Q2W-53.56
A10 EvoMab QM-53.33
A80 PBO Q2W4.48
A80 PBO QM5.79
A80 EZE (Q2W)-15.17
A80 EZE (QM)-12.91
A80 EvoMab Q2W-52.43
A80 EvoMab QM-56.20
R5 PBO Q2W2.82
R5 PBO QM2.58
R5 EvoMab Q2W-52.46
R5 EvoMab QM-56.66
R40 PBO Q2W2.17
R40 PBO QM2.60
R40 EvoMab Q2W-48.47
R40 EvoMab QM-54.17
S40 PBO Q2W-1.00
S40 PBO QM-1.42
S40 EvoMab Q2W-58.76
S40 EvoMab QM-57.47

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 12

(NCT01763866)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A10 PBO Q2W6.13
A10 PBO QM-1.21
A10 EZE (Q2W)-14.51
A10 EZE (QM)-12.33
A10 EvoMab Q2W-54.17
A10 EvoMab QM-49.65
A80 PBO Q2W4.19
A80 PBO QM6.50
A80 EZE (Q2W)-13.69
A80 EZE (QM)-12.19
A80 EvoMab Q2W-53.59
A80 EvoMab QM-50.76
R5 PBO Q2W1.44
R5 PBO QM4.00
R5 EvoMab Q2W-52.97
R5 EvoMab QM-52.13
R40 PBO Q2W1.64
R40 PBO QM3.16
R40 EvoMab Q2W-47.53
R40 EvoMab QM-45.65
S40 PBO Q2W-1.80
S40 PBO QM-0.52
S40 EvoMab Q2W-59.53
S40 EvoMab QM-52.56

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Percentage Change in Immune Activation Levels After 12 Weeks of Atorvastatin 80mg Daily

Immune activation was measured by co-expression of CD38 and HLADR on CD4 T-cells (CD4+CD38+HLADR+) Mean percentage change at 12 weeks was calculated (NCT01766076)
Timeframe: 12 weeks

Interventionpercentage change in activated T-cells (Median)
Atorvastatin60
Placebo21

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Mean Low Density Lipoprotein Cholesterol in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionmg/dl (Mean)
Atorvastatin70
Sugar Pill135

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Mean Myeloperoxidase in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionng/ml (Mean)
Healthy Women43.7
Metabolic Syndrome Women52.3

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Mean Myeloperoxidase in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionng/ml (Mean)
Atorvastatin52.18
Sugar Pill59.19

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Mean Plasminogen Activator Inhibitor-1 in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionng/ml (Mean)
Atorvastatin6.18
Sugar Pill6.60

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Mean Soluble Intercellular Adhesion Molecule in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionng/ml (Mean)
Atorvastatin192
Sugar Pill220

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Mean Soluble Vascular Adhesion Molecule in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionng/ml (Mean)
Atorvastatin512.9
Sugar Pill534.4

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Mean Systolic Blood Pressure

Measured with a blood pressure cuff (NCT01785615)
Timeframe: 0 weeks

Interventionmm Hg (Mean)
Healthy Women114.5
Metabolic Syndrome Women132.3

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Mean Triglycerides in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women94.6
Metabolic Syndrome Women197.4

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Mean Triglycerides in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionmg/dl (Mean)
Atorvastatin139
Sugar Pill185

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Mean Vascular Adhesion Molecule in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionng/ml (Mean)
Healthy Women614.8
Metabolic Syndrome Women525.0

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Mean Waist Circumference

Waist circumference was measured with a ruler tape. (NCT01785615)
Timeframe: 6 weeks

Interventioninches (Mean)
Atorvastatin41.29
Sugar Pill42.79

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Mean Waist Circumference

Waist circumference was measured with a ruler tape. (NCT01785615)
Timeframe: week 0

Interventioninches (Mean)
Healthy Women33.3
Metabolic Syndrome Women42.6

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Mean Systolic Blood Pressure

Measured with a blood pressure cuff (NCT01785615)
Timeframe: 6 weeks

Interventionmm Hg (Mean)
Atorvastatin130.9
Sugar Pill130.4

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Mean Fasting Plasma Glucose in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionmg/dl (Mean)
Atorvastatin90
Sugar Pill93

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Mean Plasminogen Activator Inhibitor-1 in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionng/ml (Mean)
Healthy Women4.5
Metabolic Syndrome Women6.2

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Mean Alanine Aminotransferase in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionunits/L (Mean)
Atorvastatin21.59
Sugar Pill23.75

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Mean Apolipoprotein A-1 in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women172.0
Metabolic Syndrome Women134.3

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Mean Apolipoprotein B in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women86.3
Metabolic Syndrome Women107.2

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Mean Apolipoprotein B in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionmg/dl (Mean)
Atorvastatin63
Sugar Pill110

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Mean Apolipoprotein B/ Apolipoprotein A1 Ratio in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. The ratio of Apo B to Apo A1 ratio was calculated. (NCT01785615)
Timeframe: 0 weeks

Interventionratio (Mean)
Healthy Women0.5
Metabolic Syndrome Women0.8

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Mean Apolipoprotein B/ Apolipoprotein A1 Ratio in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. The ratio of Apo B to Apo A1 ratio was calculated. (NCT01785615)
Timeframe: 6 weeks

Interventionratio (Mean)
Atorvastatin0.48
Sugar Pill0.86

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Mean Aspartate Aminotransferase in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionunits/L (Mean)
Atorvastatin20.27
Sugar Pill21.09

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Mean Diastolic Blood Pressure

Measured with a blood pressure cuff (NCT01785615)
Timeframe: 0 weeks

Interventionmm Hg (Mean)
Healthy Women74.6
Metabolic Syndrome Women82.9

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Mean Diastolic Blood Pressure

Measured with a blood pressure cuff (NCT01785615)
Timeframe: 6 weeks

Interventionmm Hg (Mean)
Atorvastatin83.16
Sugar Pill81.86

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Mean Fasting Blood Glucose in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women84.3
Metabolic Syndrome Women95.7

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Mean High Density Lipoprotein Cholesterol in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women66.6
Metabolic Syndrome Women46.3

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Mean High Density Lipoprotein Cholesterol in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionmg/dl (Mean)
Atorvastatin46.4
Sugar Pill44.2

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Mean High Sensitivity C-reactive Protein in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. The ratio of Apo B to Apo A1 ratio was calculated (NCT01785615)
Timeframe: 6 weeks

Interventionng/dl (Mean)
Atorvastatin3095
Sugar Pill4027

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Mean Hs-C Reactive Protein in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionng/ml (Mean)
Healthy Women1761.5
Metabolic Syndrome Women3586.9

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Mean Intercellular Adhesion Molecule in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionng/ml (Mean)
Healthy Women179.2
Metabolic Syndrome Women212.9

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Mean Leptin in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionpg/ml (Mean)
Healthy Women16285.3
Metabolic Syndrome Women45518.1

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Mean Leptin in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 6 weeks

Interventionpg/ml (Mean)
Atorvastatin43077
Sugar Pill46721.3

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Mean Low Density Lipoprotein Cholesterol in Blood

Approximately 30 ml of blood was collected in two serum (red top), four 3.2% (0.105M) sodium citrate (blue top) Vacutainer® tubes and a syringe at each visit. Collected samples were centrifuged within an hour of collection at 3000xG for 15 minutes at 20°C to obtain platelet-poor plasma and complete serum separation. Each sample was sent to the University of Rochester Clinical Laboratories for testing. (NCT01785615)
Timeframe: 0 weeks

Interventionmg/dl (Mean)
Healthy Women119.9
Metabolic Syndrome Women133.3

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Cmax of Rosuvastatin

"Maximum measured concentration of the analyte in plasma of rosuvastatin (Cmax). Outcome measure for the statins part of this trial, treatment sequence E_F.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of rosuvastatin on Day 1 of both periods

Interventionng/mL (Geometric Mean)
Rosuvastatin2.73
Rosuvastatin+Faldaprevir89.6

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Cmax of Atorvastatin (Statins Part)

"Maximum measured concentration of the analyte in plasma of atorvastatin (Cmax). Outcome measure for the statins part of this trial, treatment sequence C_D.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of atorvastatin on Day 1 of both periods

Interventionng/mL (Geometric Mean)
Atorvastatin0.94
Atorvastatin+Faldaprevir31.10

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AUCτ,ss (Itraconazole Part)

Area under the concentration-time curve of the analyte in plasma at steady state over the dosing interval τ (AUCτ,ss) of faldaprevir. Outcome measure for the itraconazole part (treatment sequence A_B) of this trial. The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities. (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00 h (hours) after administration of faldaprevir on Day 1 of both periods

Interventionng*h/mL (Geometric Mean)
Faldaprevir29900
Faldaprevir+Itraconazole59500

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AUC0-tz of Atorvastatin

"Area under the plasma concentration-time curve of the analyte over the time interval from 0 to the time tz of the last measurable concentration (AUC0-tz) of atorvastatin. Outcome measure for the statins part of this trial, treatment sequence C_D.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of atorvastatin on Day 1 of both periods

Interventionng*h/mL (Geometric Mean)
Atorvastatin9.5
Atorvastatin+Faldaprevir129.6

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AUC0-tz of Rosuvastatin

"Area under the plasma concentration-time curve of the analyte over the time interval from 0 to the time tz of the last measurable concentration (AUC0-tz) of rosuvastatin. Outcome measure for the statins part of this trial, treatment sequence E_F.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of rosuvastatin on Day 1 of both periods

Interventionng*h/mL (Geometric Mean)
Rosuvastatin21.5
Rosuvastatin+Faldaprevir361.0

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AUC0-∞ of Rosuvastatin (Statins Part)

"Area under the concentration-time curve of the analyte in plasma over the time interval from 0 extrapolated to infinity (AUC0-∞) of rosuvastatin after single dose administration of rosuvastatin. Outcome measure for the statins part of this trial, treatment sequence E_F.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of rosuvastatin on Day 1 of both periods

Interventionng*h/mL (Geometric Mean)
Rosuvastatin24.9
Rosuvastatin+Faldaprevir365.0

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Cmax,ss of Faldaprevir (Statins Part)

Maximum measured concentration of the analyte in plasma at steady state over the dosing interval (Cmax,ss) of faldaprevir. Outcome measure for the statins part of this trial, treatment sequences C_D and E_F. (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of rosuvastatin/atorvastatin on Day 1 of the second periods of each treatment sequence.

Interventionng/mL (Geometric Mean)
Atorvastatin+Faldaprevir12900
Rosuvastatin+Faldaprevir12200

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AUC0-∞ of Atorvastatin (Statins Part)

"Area under the concentration-time curve of the analyte in plasma over the time interval from 0 extrapolated to infinity (AUC0-∞) of atorvastatin after single dose administration. Outcome measure for the statins part of this trial, treatment sequence C_D.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of atorvastatin on Day 1 of both periods.

Interventionng*h/mL (Geometric Mean)
Atorvastatin13.7
Atorvastatin+Faldaprevir129.0

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Cmax,ss (Itraconazole Part)

"Maximum measured concentration of the analyte in plasma at steady state over the dosing interval (Cmax,ss) of faldaprevir. Outcome measure for the itraconazole part (Treatment sequence A_B) of this trial.~The measured values show inter-individual variabilities, whereas the statistical analyses show intra-individual variabilities." (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00 h after administration of faldaprevir on Day 1 of both periods.

Interventionng/mL (Geometric Mean)
Faldaprevir2780
Faldaprevir+Itraconazole5030

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AUCτ,ss of Faldaprevir (Statins Part)

Area under the concentration-time curve of the analyte in plasma at steady state over the dosing interval τ (AUCτ,ss) of faldaprevir. Outcome measure for the statins part of this trial, treatment sequences C_D and E_F. (NCT01795937)
Timeframe: -1:30, 0:30, 1:00, 1:30, 2:00, 3:00, 4:00, 6:00, 8:00, 10:00, 11:00, 12:00, 24:00, 36:00, 48:00, 60:00 h after administration of rosuvastatin/atorvastatin on Day 1 of the second periods of each treatment sequence.

Interventionng*h/mL (Geometric Mean)
Atorvastatin+Faldaprevir145000
Rosuvastatin+Faldaprevir136000

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Percent Change From Baseline in Fasting Triglycerides and Lipoprotein (a) at Week 12 - On-Treatment Analysis

Since the assumptions of normal distribution and equality of variances were not verified for the lipid parameters, percent changes were expressed as median (inter-quartile range). (NCT01812707)
Timeframe: Baseline to Week 12 (LOCF)

,,,
Interventionpercent change (Median)
Fasting TriglyceridesLipoprotein (a)
Alirocumab 150 mg Q2W-15.0-43.3
Alirocumab 50 mg Q2W-21.1-35.6
Alirocumab 75 mg Q2W-10.7-40.2
Placebo1.3-3.7

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Percent Change From Baseline in Total Cholesterol, High-Density Lipoprotein Cholesterol (HDL-C), Non-HDL-C, and Apolipoprotein B (Apo-B) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01812707)
Timeframe: Baseline to Week 12 (LOCF)

,,,
Interventionpercent change (Least Squares Mean)
Total CholesterolHDL-CNon-HDL-CApo-B
Alirocumab 150 mg Q2W-41.43.2-62.2-60.0
Alirocumab 50 mg Q2W-31.95.1-46.3-43.5
Alirocumab 75 mg Q2W-36.35.0-53.1-48.6
Placebo-1.2-0.2-0.9-2.3

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Percentage of Participants Achieving Calculated LDL-C <100 mg/dL (2.59 mmol/L) and < 70 mg/dL (1.81 mmol/L) at Week 12 - On-Treatment Analysis

(NCT01812707)
Timeframe: Week 12 (LOCF)

,,,
Interventionpercentage of participants (Number)
LDL-C <100 mg/dL (2.59 mmol/L)LDL-C < 70 mg/dL (1.81 mmol/L)
Alirocumab 150 mg Q2W100.088.0
Alirocumab 50 mg Q2W100.084.0
Alirocumab 75 mg Q2W100.084.0
Placebo8.00.0

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Percent Change From Baseline in Calculated LDL-C at Week 12 - On-Treatment Analysis

Calculated LDL-C values were obtained using the Friedewald formula. Baseline adjusted least squares (LS) means and standard errors were estimated using an analysis of covariance (ANCOVA) model including available post-baseline data on treatment from first investigational product (IP) injection up to 21 days after last IP injection (on-treatment analysis). Missing Week 12 data were imputed by last observation carried forward [LOCF] method. (NCT01812707)
Timeframe: Baseline to Week 12 (LOCF)

Interventionpercent change (Least Squares Mean)
Placebo-2.7
Alirocumab 50 mg Q2W-54.8
Alirocumab 75 mg Q2W-62.3
Alirocumab 150 mg Q2W-71.7

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Absolute Change From Baseline in Calculated LDL-C (mmol/L) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01812707)
Timeframe: Baseline to Week 12 (LOCF)

Interventionmmol/L (Least Squares Mean)
Placebo-0.1
Alirocumab 50 mg Q2W-1.7
Alirocumab 75 mg Q2W-1.9
Alirocumab 150 mg Q2W-2.2

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Absolute Change From Baseline in Calculated LDL-C (mg/dL) at Week 12 - On-Treatment Analysis

Adjusted LS means and standard errors were estimated using the same ANCOVA model as for primary endpoint. (NCT01812707)
Timeframe: Baseline to Week 12 (LOCF)

Interventionmg/dL (Least Squares Mean)
Placebo-5.0
Alirocumab 50 mg Q2W-67.1
Alirocumab 75 mg Q2W-74.6
Alirocumab 150 mg Q2W-85.8

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Absolute Change From Baseline in Apolipoprotein B/Apolipoprotein A-1 (ApoB/ApoA-1) Ratio at Week 12 - On-Treatment Analysis

Adjusted LS mean and standard errors were estimated using the same ANCOVA as for primary endpoint. (NCT01812707)
Timeframe: From Baseline to Week 12 (LOCF)

Interventionratio (Least Squares Mean)
Placebo0.02
Alirocumab 50 mg Q2W-0.30
Alirocumab 75 mg Q2W-0.32
Alirocumab 150 mg Q2W-0.38

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Number of Partipants That Experienced Death, Myocardial Infarction, Stroke, Transient Ischemic Attack, Myocardial Necrosis, or Venous Thromboembolism

(NCT01837069)
Timeframe: 30 days

Interventionparticipants (Number)
Treatment10
Control2

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Length of Stay

(NCT01837069)
Timeframe: Hospital stay, ~7 days

Interventiondays (Median)
Treatment3
Control3

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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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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 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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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 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 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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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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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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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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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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Change in Bleeding on Probing Index (BOP)

"The bleeding on probing index (BOP) will be determined by assigning + to the presence of bleeding on vestibular / palatine probing of the tooth examined and with a sign - the abscence. Later the + signs will be summed and divided by the number of sites examined.~Change in BOP: baseline measure minus 1 month later measure." (NCT01929135)
Timeframe: baseline and 1 month after intervention

Interventionpercentage of BOP (Mean)
Atorvastatin Toothpaste64.42
Non Medicated Gel Toothpaste28.56

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Change in Periodontal Inflammation Surface Area (PISA)

"PISA will be computed through an Excel spreadsheet, using data of clinical attachment level, gingival recession and bleeding on probing.~Change in PISA: baseline measure minus 1 month later measure." (NCT01929135)
Timeframe: baseline and 1 month later of intervention

Interventionsquare millimeters (Mean)
Atorvastatin Toothpaste638.16
Non Medicated Gel Toothpaste288.72

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Change in Mean Pocket Depth (PD)

"The PD will be defined as the distance from the free gingival margin to the bottom of the pocket. For each tooth will be conducted periodontal probing at 6 sites (mesiobuccal, mediobuccal, distobuccal, mesiolingual / palatal, mediolingual / palatal, distolingual/ palatal).~Change in mean PD: baseline measure minus 1 month later measure." (NCT01929135)
Timeframe: baseline and 1 month later

Interventionmillimeters (Mean)
Atorvastatin Toothpaste1.29
Non Medicated Gel Toothpaste0.70

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Change in Gingival Index

"Determined as score assigned to each site evaluated respect to clinical criteria as followed:~Score Criteria:~0. No inflammation~Mild inflammation, slight change in color, slight edema, no bleeding on probing.~Moderate inflammation, moderate glazing, redness, bleeding on probing.~Severe inflammation, marked redness and hypertrophy, ulceration, tendency to spontaneous bleeding.~Then was calculated a score for each sextant summed the score and divided by the number of examined sites. Later was summed each sextant score and divided by sextant evaluated.~The change was calculated as baseline measure minus 1 month later measure." (NCT01929135)
Timeframe: baseline and 1 month after intervention

Interventionscore on a scale (Mean)
Atorvastatin Group1.04
Placebo Group0.54

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Change in Clinical Attachment Level (CAL)

"The Clinical Attachment Level (CAL) is defined as the distance from the cement-enamel junction to the fornix of the pocket. For each tooth will be performed periodontal probing at 6 sites (mesiobuccal, mediobuccal, distobuccal mesiolingual / palatal mediolingual / distolingual palatal / lingual).~Change in CAL: baseline measure minus 1 month later measure." (NCT01929135)
Timeframe: baseline and 1 month after intervention

Interventionmillimeters (Mean)
Atorvastatin Toothpaste0.89
Non Medicated Gel Toothpaste0.49

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Percent Change From Baseline in the Apolipoprotein B/Apolipoprotein A-1 Ratio at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W0.71
A5 Placebo QM4.08
A5 Evolocumab Q2W-67.59
A5 Evolocumab QM-58.45
A20 Placebo Q2W-1.15
A20 Placebo QM0.06
A20 Evolocumab Q2W-65.11
A20 Evolocumab QM-60.56

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Percent Change From Baseline in Non-HDL-C at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W1.12
A5 Placebo QM5.55
A5 Evolocumab Q2W-67.81
A5 Evolocumab QM-58.03
A20 Placebo Q2W-0.07
A20 Placebo QM-2.38
A20 Evolocumab Q2W-68.89
A20 Evolocumab QM-63.27

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Percent Change From Baseline in Non-HDL-C at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W0.18
A5 Placebo QM4.26
A5 Evolocumab Q2W-68.48
A5 Evolocumab QM-61.69
A20 Placebo Q2W-1.57
A20 Placebo QM-1.79
A20 Evolocumab Q2W-69.72
A20 Evolocumab QM-69.07

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

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W1.28
A5 Placebo QM5.29
A5 Evolocumab Q2W-73.57
A5 Evolocumab QM-64.62
A20 Placebo Q2W1.39
A20 Placebo QM-3.49
A20 Evolocumab Q2W-74.46
A20 Evolocumab QM-70.36

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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W0.27
A5 Placebo QM3.91
A5 Evolocumab Q2W-73.70
A5 Evolocumab QM-69.98
A20 Placebo Q2W-0.42
A20 Placebo QM-2.67
A20 Evolocumab Q2W-74.82
A20 Evolocumab QM-76.93

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Percent Change From Baseline in Lipoprotein(a) at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W4.35
A5 Placebo QM7.03
A5 Evolocumab Q2W-45.72
A5 Evolocumab QM-41.74
A20 Placebo Q2W10.75
A20 Placebo QM-5.73
A20 Evolocumab Q2W-41.93
A20 Evolocumab QM-45.70

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Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W5.23
A5 Placebo QM4.07
A5 Evolocumab Q2W-45.97
A5 Evolocumab QM-45.01
A20 Placebo Q2W6.52
A20 Placebo QM-5.62
A20 Evolocumab Q2W-43.03
A20 Evolocumab QM-49.55

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Percent Change From Baseline in HDL-C at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W-4.59
A5 Placebo QM-0.40
A5 Evolocumab Q2W8.88
A5 Evolocumab QM14.80
A20 Placebo Q2W-3.57
A20 Placebo QM-2.36
A20 Evolocumab Q2W13.28
A20 Evolocumab QM7.84

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Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W-4.83
A5 Placebo QM-1.57
A5 Evolocumab Q2W7.50
A5 Evolocumab QM13.05
A20 Placebo Q2W-4.03
A20 Placebo QM-3.06
A20 Evolocumab Q2W11.34
A20 Evolocumab QM6.09

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A-1 Ratio at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W0.06
A5 Placebo QM2.79
A5 Evolocumab Q2W-66.41
A5 Evolocumab QM-61.55
A20 Placebo Q2W-1.92
A20 Placebo QM1.54
A20 Evolocumab Q2W-65.97
A20 Evolocumab QM-65.72

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Percent Change From Baseline in Apolipoprotein B at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W0.74
A5 Placebo QM2.42
A5 Evolocumab Q2W-64.83
A5 Evolocumab QM-54.80
A20 Placebo Q2W-2.47
A20 Placebo QM-1.89
A20 Evolocumab Q2W-62.83
A20 Evolocumab QM-58.04

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Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W-0.32
A5 Placebo QM0.76
A5 Evolocumab Q2W-64.76
A5 Evolocumab QM-58.47
A20 Placebo Q2W-4.32
A20 Placebo QM-0.85
A20 Evolocumab Q2W-64.38
A20 Evolocumab QM-64.24

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Change From Baseline in LDL-C at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionmg/dL (Least Squares Mean)
A5 Placebo Q2W-13.7
A5 Placebo QM-0.4
A5 Evolocumab Q2W-104.5
A5 Evolocumab QM-84.0
A20 Placebo Q2W-7.7
A20 Placebo QM-6.2
A20 Evolocumab Q2W-77.2
A20 Evolocumab QM-71.7

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Change From Baseline in LDL-C at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionmg/dL (Least Squares Mean)
A5 Placebo Q2W-14.8
A5 Placebo QM-2.6
A5 Evolocumab Q2W-104.1
A5 Evolocumab QM-88.9
A20 Placebo Q2W-8.9
A20 Placebo QM-5.7
A20 Evolocumab Q2W-77.6
A20 Evolocumab QM-77.7

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Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W4.69
A5 Placebo QM4.54
A5 Evolocumab Q2W-23.23
A5 Evolocumab QM-17.41
A20 Placebo Q2W-2.11
A20 Placebo QM8.06
A20 Evolocumab Q2W-22.12
A20 Evolocumab QM-12.66

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Percentage of Participants Who Achieved LDL-C < 70 mg/dL at Week 12

(NCT01953328)
Timeframe: Week 12

Interventionpercentage of participants (Number)
A5 Placebo Q2W0.0
A5 Placebo QM4.2
A5 Evolocumab Q2W98.0
A5 Evolocumab QM96.0
A20 Placebo Q2W20.4
A20 Placebo QM20.0
A20 Evolocumab Q2W96.0
A20 Evolocumab QM98.0

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Percentage of Participants Who Achieved a Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL

(NCT01953328)
Timeframe: Weeks 10 and 12

Interventionpercentage of participants (Number)
A5 Placebo Q2W0.0
A5 Placebo QM0.0
A5 Evolocumab Q2W98.0
A5 Evolocumab QM96.0
A20 Placebo Q2W22.4
A20 Placebo QM15.7
A20 Evolocumab Q2W96.0
A20 Evolocumab QM98.0

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Percent Change From Baseline in VLDL-C at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W4.09
A5 Placebo QM2.92
A5 Evolocumab Q2W-24.33
A5 Evolocumab QM-17.89
A20 Placebo Q2W-3.03
A20 Placebo QM9.17
A20 Evolocumab Q2W-18.08
A20 Evolocumab QM-15.18

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Percent Change From Baseline in VLDL-C at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W2.57
A5 Placebo QM3.10
A5 Evolocumab Q2W-25.29
A5 Evolocumab QM-19.55
A20 Placebo Q2W-1.32
A20 Placebo QM9.96
A20 Evolocumab Q2W-19.41
A20 Evolocumab QM-17.20

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Percent Change From Baseline in Triglycerides at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W7.84
A5 Placebo QM4.34
A5 Evolocumab Q2W-19.73
A5 Evolocumab QM-15.63
A20 Placebo Q2W-3.88
A20 Placebo QM7.30
A20 Evolocumab Q2W-21.05
A20 Evolocumab QM-9.63

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Percent Change From Baseline in Total Cholesterol at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W-1.70
A5 Placebo QM2.29
A5 Evolocumab Q2W-47.14
A5 Evolocumab QM-39.06
A20 Placebo Q2W-3.08
A20 Placebo QM-2.44
A20 Evolocumab Q2W-44.04
A20 Evolocumab QM-40.88

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Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W-2.49
A5 Placebo QM1.09
A5 Evolocumab Q2W-48.03
A5 Evolocumab QM-42.34
A20 Placebo Q2W-4.21
A20 Placebo QM-2.35
A20 Evolocumab Q2W-45.19
A20 Evolocumab QM-45.49

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Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at Week 12

(NCT01953328)
Timeframe: Baseline and Week 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W4.73
A5 Placebo QM4.33
A5 Evolocumab Q2W-50.72
A5 Evolocumab QM-46.62
A20 Placebo Q2W1.84
A20 Placebo QM0.83
A20 Evolocumab Q2W-49.52
A20 Evolocumab QM-44.61

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Percent Change From Baseline in the Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12

(NCT01953328)
Timeframe: Baseline and Weeks 10 and 12

Interventionpercent change (Least Squares Mean)
A5 Placebo Q2W3.77
A5 Placebo QM3.94
A5 Evolocumab Q2W-51.00
A5 Evolocumab QM-48.71
A20 Placebo Q2W1.04
A20 Placebo QM1.58
A20 Evolocumab Q2W-49.79
A20 Evolocumab QM-48.11

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Percentage of Participants Who Complied With the Direction to Check Their Low-density Lipoprotein Cholesterol (LDL-C) Level

Percentage of participants whose behavior was either correct or acceptable were considered to be compliant. The behavior was considered correct if participants had their LDL-C checked between Weeks 4 and 12. The behavior was considered acceptable if participants had their LDL-C checked between Weeks 2 and 3 (before Week 4) or between Weeks 13 (after Week 12) and 26 or if participants were instructed by a physician that an LDL-C test was not needed. (NCT01964326)
Timeframe: Day 1 up to Week 26

InterventionPercentage of participants (Number)
Atorvastatin49.7

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"Percentage of Participants Taking an Ask a Doctor or Pharmacist Before Use Medication Who Followed the Labeling and Contacted a Doctor or Pharmacist Before Using Study Medication"

Percentage of participants whose behavior was either correct or acceptable were considered to be compliant. 'Ask a doctor or pharmacist before use' medication included human immunodeficiency virus (HIV) medicine, digoxin, telaprevir, rifampin, colchicine, or oral contraceptives. The behavior of the participants was considered correct if participants asked a doctor or pharmacist before use. The behavior was considered acceptable if participants contacted a doctor or pharmacist within 7 days of initiating therapy. (NCT01964326)
Timeframe: Day 1 up to Week 26

InterventionPercentage of participants (Number)
Atorvastatin29.2

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"Percentage of Participants Who Stopped Study Medication Use and Asked a Doctor if They Experienced Any of the Labeled Stop Use and Ask a Doctor Symptoms"

"Percentage of participants whose behavior was either correct or acceptable were considered to be compliant. The Stop use and ask a doctor symptoms included: (a) unexplained muscle pain or weakness or tenderness, (b) unusual fatigue, (c) loss of appetite (d) upper belly pain (e) dark-colored urine or (f) yellowing of the whites of eyes or skin. The behavior of the participants was considered correct if participants stopped use and contacted a doctor within 7 days after the event (symptom development).The behavior was considered acceptable if participants either stopped use or contacted a doctor (but did not do both) within the 7 days' timeframe." (NCT01964326)
Timeframe: Day 1 up to Week 26

InterventionPercentage of participants (Number)
Atorvastatin10.2

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Percentage of Participants Who Took Appropriate Action Based on Their LDL-C Results

Percentage of participants whose behavior was either correct or acceptable were considered to be compliant. The behavior was considered correct if participants self-reported an LDL-C level below 130 milligram per deciliter (mg/dL) or normal, or low and decided to continue with atorvastatin OTC or if participants self-reported an LDL-C below 130 mg/dL, or normal, or low but stopped the use because of new conditions preventing them from continuing use. The behavior was considered acceptable if participants self-report LDL-C level between 130 and 135 mg/dL and continued to use atorvastatin OTC without contacting a physician or other health care practitioner or if participants self-reported LDL-C greater than or equal to (>=) 130 mg/dL('borderline high' or 'high' LDL-C), and contacted a physician after getting the LDL-C test results. (NCT01964326)
Timeframe: Day 1 up to Week 26

InterventionPercentage of participants (Number)
Atorvastatin52.6

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Change From Baseline in LDL-C at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionmg/dL (Least Squares Mean)
Ezetimibe-31.2
Evolocumab-102.9

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Change From Baseline in LDL-C at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baselie and weeks 22 and 24

Interventionmg/dL (Least Squares Mean)
Ezetimibe-31.0
Evolocumab-106.8

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Percent Change From Baseline in Very Low-density Lipoprotein Cholesterol (VLDL-C) at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-2.15
Evolocumab-6.81

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Percent Change From Baseline in VLDL-C at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-2.66
Evolocumab-3.90

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Percentage of Participants Who Achieved a Mean LDL-C at Weeks 22 and 24 of Less Than 70 mg/dL

(NCT01984424)
Timeframe: Weeks 22 and 24

Interventionpercentage of participants (Number)
Ezetimibe1.4
Evolocumab29.9

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Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.48
Evolocumab-41.39

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Percentage of Participants Who Achieved LDL-C at Week 24 of Less Than 70 mg/dL

(NCT01984424)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Ezetimibe0.0
Evolocumab27.4

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Percent Change From Baseline in Apolipoprotein B at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.42
Evolocumab-45.28

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Percent Change From Baseline in Triglycerides at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-0.95
Evolocumab-5.39

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Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-12.84
Evolocumab-40.04

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Percent Change From Baseline in Triglycerides at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-1.07
Evolocumab-2.88

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-12.62
Evolocumab-44.60

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Percent Change From Baseline in HDL-C at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe2.90
Evolocumab7.40

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Percent Change From Baseline in High-density Lipoprotein Cholesterol (HDL-C) at Week 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe1.66
Evolocumab7.85

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Percent Change From Baseline in LDL-C at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-16.70
Evolocumab-54.50

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Percent Change From Baseline in LDL-C at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-16.69
Evolocumab-52.76

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Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and Weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-1.63
Evolocumab-22.71

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Percent Change From Baseline in Lipoprotein(a) at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe0.17
Evolocumab-21.06

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Percent Change From Baseline in Non-HDL-C at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-14.62
Evolocumab-45.72

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Percent Change From Baseline in Non-high-density Lipoprotein Cholesterol (Non-HDL-C) at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-14.38
Evolocumab-47.44

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Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.43
Evolocumab-38.04

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Percent Change From Baseline in Total Cholesterol at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.57
Evolocumab-36.64

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Percent Change From Baseline in Apolipoprotein B at Week 24

(NCT01984424)
Timeframe: Baseline and week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.74
Evolocumab-43.50

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Percent Change From Baseline in Apolipoprotein B/Apolipoprotein A1 Ratio at the Mean of Weeks 22 and 24

(NCT01984424)
Timeframe: Baseline and Weeks 22 and 24

Interventionpercent change (Least Squares Mean)
Ezetimibe-11.86
Evolocumab-45.99

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Patient-reported Outcomes Measurement (PROMIS) Questionnaire - Fatigue Short Form 41

Patient reported quality of life outcomes obtained from patient-reported outcomes measurement (PROMIS) questionnaire - Fatigue Short Form 41. Scores range from 4-20 and then adjusted by t-scores ranging from 33.7-75.8. Higher scores reflect worse fatigue. Linear models include baseline assessment and group and multiple imputation was utilized. (NCT01988571)
Timeframe: 24 months

Interventiont-score (Least Squares Mean)
Arm 1 - Atorvastatin48.17
Arm 2 - Placebo49.29

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Left Ventricular Ejection Fraction (LVEF)

24 month estimated values of clinical measurements obtained from Cardiac MRI left ventricular ejection fraction by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventionpercent ejected from LV per heartbeat (Least Squares Mean)
Arm 1 - Atorvastatin58.1
Arm 2 - Placebo57.9

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Stroke Volume

24 month estimated values of clinical measurements obtained from Cardiac MRI Stroke Volume by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventionmilliliters per minute (Least Squares Mean)
Arm 1 - Atorvastatin71
Arm 2 - Placebo72.2

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Pulse Wave Velocity

24 month estimated values of clinical measurements obtained from Cardiac MRI pulse wave velocity by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventionm/s (Least Squares Mean)
Arm 1 - Atorvastatin5.73
Arm 2 - Placebo5.51

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Patient-reported Outcomes Measurement (PROMIS) Questionnaire - Applied Cognition - General Concerns - Short Form 4a

Patient reported quality of life outcomes obtained from patient-reported outcomes measurement (PROMIS) questionnaire - Applied Cognition - General Concerns - Short Form 4a . Scores range from 4-20 and then adjusted by t-scores ranging from 30.1-63.8. Higher scores reflect better cognition. Linear models include baseline assessment and group and multiple imputation was utilized. (NCT01988571)
Timeframe: 24 months

Interventiont-score (Least Squares Mean)
Arm 1 - Atorvastatin45.57
Arm 2 - Placebo46.55

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Left Ventricular (LV) Mass

24 month estimated values of clinical measurements obtained from Cardiac MRI left ventricular mass by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventiongram per meter squared (Least Squares Mean)
Arm 1 - Atorvastatin88.4
Arm 2 - Placebo87.5

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Hopkins Verbal Learning Test (HVLT) Total Recall

24 month estimated values Hopkins Verbal Learning test (HVLT) total recall by group. Linear model adjusts for baseline value and group assignment. No missing imputation performed. Ranges from 0 to 36 and higher numbers reflect better recall. (NCT01988571)
Timeframe: 24 months

Interventionscore on a scale (Least Squares Mean)
Arm 1 - Atorvastatin28.5
Arm 2 - Placebo27.5

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End Systolic Volume

24 month estimated values of clinical measurements obtained from Cardiac MRI End Systolic Volume by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventionmilliliters of blood (Least Squares Mean)
Arm 1 - Atorvastatin51.8
Arm 2 - Placebo52.9

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End Diastolic Volume

24 month estimated values of clinical measurements obtained from Cardiac MRI End Diastolic Volume by group. Linear model adjusts for baseline value and group assignment and multiple imputation was utilized for missing data. (NCT01988571)
Timeframe: 24 months

Interventionmilliliters of blood (Least Squares Mean)
Arm 1 - Atorvastatin123
Arm 2 - Placebo125

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Controlled Oral Word Association (COWA)

24 month estimated values Controlled Oral Word Association (COWA) by group. Linear model adjusts for baseline value and group assignment. No missing imputation performed. The COWA uses the three letter set of C, F, and L to assess phonemic fluency. Individuals are given 1 min to name as many words as possible beginning with one of the letters. The procedure is then repeated for the remaining two letters. Ranges from 0 to the total number of correct words that begin with one of the letters in the set. There is no ceiling of a maximum score. Higher numbers reflect better verbal fluency. (NCT01988571)
Timeframe: 24 months

Interventionscore on a scale (Least Squares Mean)
Arm 1 - Atorvastatin41.6
Arm 2 - Placebo44.7

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Change in Inflammatory Markers From Time Zero to 72 Hours

The primary IL- 6 measurements were at time zero and at 72 hours. Analysis was performed using a linear mixed effects model to make use of all biomarker timepoints as hospitalized patients had biomarkers measured at additional timepoints. (NCT02056340)
Timeframe: Baseline to 72 hours

,
Interventionpg/ml (Median)
Baseline72 hours
Atorvastatin2.40.91
Placebo3.460.57

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Severity of Illness Score Baseline to 72 Hours

Composite score for 5 major symptoms (fever, cough, sore throat, headache, myalgia) ranked from 0 to 3 (none, mild, moderate, severe) for a score ranging from 0 to 15. Higher scores reflect more severe symptoms. (NCT02056340)
Timeframe: Baseline and 72 hours

,
Interventionscore on a scale (Median)
Baseline72 hours
Atorvastatin82
Placebo83

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AUC0-t

Area under the concentration-time curve from zero to the last quantifiable concentration of lomitapide and its 2 primary metabolites (M1 & M3), following administration of lomitapide alone and coadministered with atorvastatin simultaneously (Arm 1) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng*hr/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)36.4
PK of Lomitapide (Coadministered Simultaneously)71.5
PK of M1 (Lomitapide Alone)76.8
PK of M1 (Coadministered Simultaneously)76.3
PK of M3 (Lomitapide Alone)434
PK of M3 (Coadministered Simultaneously)475

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AUC0-∞

Area under the concentration-time curve from zero to infinity of lomitapide and its 2 primary metabolites (M1 & M3) following administration of lomitapide alone and coadministered with atorvastatin 12 hours apart (Arm 2) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng*hr/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)42.8
PK of Lomitapide (Coadminister 12 Hours Apart)55.8
PK of M1 (Lomitapide Alone)70.0
PK of M1 (Coadministered 12 Hours Apart)79.2
PK of M3 (Lomitapide Alone)406
PK of M3 (Coadministered 12 Hours Apart)553

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AUC0-∞

Area under the concentration-time curve from zero to infinity of lomitapide and its 2 primary metabolites (M1 & M3), following administration of lomitapide alone and coadministered with atorvastatin simultaneously (Arm 1) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng*hr/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)40.4
PK of Lomitapide (Coadministered Simultaneously)76.7
PK of M1 (Lomitapide Alone)79.1
PK of M1 (Coadministered Simultaneously)78.7
PK of M3 (Lomitapide Alone)469
PK of M3 (Coadministered Simultaneously)487

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AUC0-t

Area under the concentration-time curve from zero to the last quantifiable concentration of lomitapide and its 2 primary metabolites (M1 & M3) following administration of lomitapide alone and coadministered with atorvastatin 12 hours apart (Arm 2) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng*hr/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)38.8
PK of Lomitapide (Coadministered 12 Hours Apart)50.5
PK of M1 (Lomitapide Alone)68.3
PK of M1 (Coadministered 12 Hours Apart)77.6
PK of M3 (Lomitapide Alone)410
PK of M3 (Coadministered 12 Hours Apart)542

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Cmax

Maximum observed plasma concentration of lomitapide and its 2 primary metabolites (M1 & M3) following administration of lomitapide alone and coadministered with atorvastatin 12 hours apart (Arm 2) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)1.09
PK of Lomitapide (Coadministered 12 Hours Apart)1.39
PK of M1 (Lomitapide Alone)2.38
PK of M1 (Coadministered 12 Hours Apart)2.66
PK of M3 (Lomitapide Alone)28.5
PK of M3 (Coadministered 12 Hours Apart)35.9

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Tmax

Time to reach maximum observed plasma concentration of lomitapide and its 2 primary metabolites (M1 & M3), following administration of lomitapide alone and coadministered with atorvastatin simultaneously (Arm 1) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionhr (Median)
PK of Lomitapide (Lomitapide Alone)6.00
PK of Lomitapide (Coadministered Simultaneously)10.0
PK of M1 (Lomitapide Alone)6.02
PK of M1 (Coadministered Simultaneously)10.0
PK of M3 (Lomitapide Alone)4.00
PK of M3 (Coadministered Simultaneously)6.00

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Cmax

Maximum observed plasma concentration of lomitapide and its 2 primary metabolites (M1 & M3), following administration of lomitapide alone and coadministered with atorvastatin simultaneously (Arm 1) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionng/mL (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)0.940
PK of Lomitapide (Coadministered Simultaneously)2.00
PK of M1 (Lomitapide Alone)2.24
PK of M1 (Coadministered Simultaneously)2.11
PK of M3 (Lomitapide Alone)32.3
PK of M3 (Coadministered Simultaneously)27.2

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t1/2

Apparent terminal elimination half-life of lomitapide and its 2 primary metabolites (M1 & M3) following administration of lomitapide alone and coadministered with atorvastatin 12 hours apart (Arm 2) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionhr (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)52.0
PK of Lomitapide (Coadministered 12 Hours Apart)54.7
PK of M1 (Lomitapide Alone)31.2
PK of M1 (Coadministered 12 Hours Apart)32.3
PK of M3 (Lomitapide Alone)48.0
PK of M3 (Coadministered 12 Hours Apart)49.7

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t1/2

Apparent terminal elimination half-life of lomitapide and its 2 primary metabolites (M1 & M3), following administration of lomitapide alone and coadministered with atorvastatin simultaneously (Arm 1) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionhr (Geometric Mean)
PK of Lomitapide (Lomitapide Alone)50.7
PK of Lomitapide (Coadministered Simultaneously)50.4
PK of M1 (Lomitapide Alone)34.0
PK of M1 (Coadministered Simultaneously)35.2
PK of M3 (Lomitapide Alone)50.2
PK of M3 (Coadministered Simultaneously)43.2

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Tmax

Time to reach maximum observed plasma concentration of lomitapide and its 2 primary metabolites (M1 & M3) following administration of lomitapide alone and coadministered with atorvastatin 12 hours apart (Arm 2) (NCT02080455)
Timeframe: Predose and at 1, 2, 3, 4, 5, 6, 8, 10, 12, 18, 24, 48, 72, 96, 120, 144, and 168 hours after dosing

Interventionhr (Median)
PK of Lomitapide (Lomitapide Alone)8.02
PK of Lomitapide (Coadministered 12 Hours Apart)8.00
PK of M1 (Lomitapide Alone)8.00
PK of M1 (Coadministered 12 Hours Apart)8.00
PK of M3 (Lomitapide Alone)6.00
PK of M3 (Coadministered 12 Hours Apart)5.00

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Changes in sCD14 After 9 Months of Treatment With Aspirin or Atorvastatin

sCD14 change between baseline (average of month 0 and month 3 in the study) and month 12 (NCT02081638)
Timeframe: Month 12

Interventionpg/mL (Median)
Daily Aspirin-0.131
Daily Atorvastatin-0.09

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Changes in sCD14 in EC and ART <50 Groups Treated With Aspirin or Atorvastatin.

sCD14 change between baseline (average of month 0 and month 3 in the study) and month 12 (NCT02081638)
Timeframe: Month 12

Interventionpg/mL (Median)
Daily Aspirin on ART-0.1249
Daily Aspirin Not on ART-0.1353
Daily Atorvastatin on ART-0.3242
Daily Atorvastatin Not on ART0.1758

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Atrial Fibrillation Incidence After Open Cardiac Valve Repair

(NCT02084069)
Timeframe: Within 5 days after open cardiac valve repair

Interventionparticipants (Number)
Treatment6
Control13

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Terminal Disposition Half-life (t1/2) of TAK-385

Terminal disposition half-life (T1/2) is the time required for half of the drug to be eliminated from the plasma. (NCT02093390)
Timeframe: Days 1 and 10 (Predose and multiple time points up to 120 hours postdose)

,
Interventionhours (Mean)
Day 1 (n=20, 19)Day 10 (n=19, 19)
TAK-385 + Atorvastatin36.541.1
TAK-385 + Fluconazole34.839.2

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Tmax: Time to Reach the Maximum Plasma Concentration of TAK-385

Tmax is the time to reach the maximum concentrations (Cmax), equal to time (hours) to Cmax. (NCT02093390)
Timeframe: Days 1 and 10 (Predose and multiple time points up to 120 hours postdose)

,
Interventionhours (Median)
Day 1 (n=20, 20)Day 10 (n=19, 19)
TAK-385 + Atorvastatin1.001.01
TAK-385 + Fluconazole1.001.00

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AUC(0-inf): Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity of TAK-385 on Day 1

Area under the plasma concentration-time curve from time 0 to infinity. (NCT02093390)
Timeframe: Day 1 (Predose and multiple time points up to 120 hours postdose)

Interventionng*hr/mL (Mean)
TAK-385 + Fluconazole92.6
TAK-385 + Atorvastatin123.0

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AUC(0-tlast): Area Under the Plasma Concentration Curve From Time Zero to the Time of the Last Quantifiable Concentration of TAK-385 on Day 10

Area under the plasma concentration versus time curve from zero to the time of the last quantifiable concentration. (NCT02093390)
Timeframe: Day 10 (Predose and multiple time points up to 120 hours postdose)

Interventionng*hr/mL (Mean)
TAK-385 + Fluconazole104.0
TAK-385 + Atorvastatin99.8

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Cmax: Maximum Observed Plasma Concentration of TAK-385 on Day 1

Cmax is the peak concentration of a drug after administration, obtained directly from the plasma concentration-time curve. (NCT02093390)
Timeframe: Day 1 (Predose and multiple time points up to 120 hours postdose)

Interventionng/mL (Mean)
TAK-385 + Fluconazole10.9
TAK-385 + Atorvastatin20.1

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Cmax: Maximum Observed Plasma Concentration of TAK-385 on Day 10

Cmax is the peak concentration of a drug after administration, obtained directly from the plasma concentration-time curve. (NCT02093390)
Timeframe: Day 10 (Predose and multiple time points up to 120 hours postdose)

Interventionng/mL (Mean)
TAK-385 + Fluconazole14.4
TAK-385 + Atorvastatin14.1

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AUC(0-inf): Area Under the Plasma Concentration-Time Curve From Time 0 to Infinity of TAK-385 on Day 10

Area under the plasma concentration-time curve from time 0 to infinity. (NCT02093390)
Timeframe: Day 10 (Predose and multiple time points up to 120 hours postdose)

Interventionng*hr/mL (Mean)
TAK-385 + Fluconazole112.0
TAK-385 + Atorvastatin108.0

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Number of Participants With at Least 1 Treatment Emergent Adverse Event (AE)

An Adverse Event (AE) is defined as any untoward medical occurrence in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (eg, a clinically significant abnormal laboratory finding), symptom, or disease temporally associated with the use of a drug, whether or not it is considered related to the drug. A treatment-emergent adverse event (TEAE) is defined as an adverse event with an onset that occurs after receiving study drug. (NCT02093390)
Timeframe: First dose of study drug through the end of the study (22 days ± 3 days)

Interventionparticipants (Number)
TAK-385 + Fluconazole5
TAK-385 + Atorvastatin6

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Number of Participants With Clinical Significant Changes in Electrocardiogram (ECG) Findings

A 12-lead ECG was administered on Days 1,9,10,11,15. (NCT02093390)
Timeframe: Baseline and First dose of study drug through Day 15

Interventionparticipants (Number)
TAK-385 + Fluconazole0
TAK-385 + Atorvastatin0

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Number of Participants With Clinical Significant Changes in Laboratory Tests

Blood samples were collected for analysis of clinical chemistry and hematological parameters and urine samples were obtained for urinalysis. Clinical laboratory evaluations were performed at central and /local laboratories. (NCT02093390)
Timeframe: Baseline and First dose of study drug through the end of the study (22 days ± 3 days)

Interventionparticipants (Number)
TAK-385 + Fluconazole0
TAK-385 + Atorvastatin0

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Number of Participants With Clinical Significant Changes in Vital Signs

Vital sign measurements included oral temperature, heart rate, supine (after 3 to 5 minutes in this position) and standing (after 3 to 5 minutes in this position) measurements of diastolic and systolic blood pressure. (NCT02093390)
Timeframe: Baseline and First dose of study drug through the end of the study (22 days ± 3 days)

Interventionparticipants (Number)
TAK-385 + Fluconazole0
TAK-385 + Atorvastatin0

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AUC(0-tlast): Area Under the Plasma Concentration Curve From Time Zero to the Time of the Last Quantifiable Concentration of TAK-385 on Day 1

Area under the plasma concentration versus time curve from zero to the time of the last quantifiable concentration. (NCT02093390)
Timeframe: Day 1 (Predose and multiple time points up to 120 hours postdose)

Interventionng*hr/mL (Mean)
TAK-385 + Fluconazole87.4
TAK-385 + Atorvastatin116.0

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Apparent Total Body Clearance (CL/F) of TAK-385

(NCT02093390)
Timeframe: Days 1 and 10 (Predose and multiple time points up to 120 hours postdose)

,
Interventionliters/hour (Mean)
Day 1 (n=20, 19)Day 10 (n=19, 19)
TAK-385 + Atorvastatin420406
TAK-385 + Fluconazole502421

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AUC (0-120): Area Under the Plasma Concentration-Time Curve From Time 0 to 120 Hours of TAK-385

Area under the plasma concentration versus time curve from 0 to 120 hours after study drug administration. (NCT02093390)
Timeframe: Days 1 and 10 (Predose and multiple time points up to 120 hours postdose)

,
Interventionng*hr/mL (Mean)
Day 1 (n=20,19)Day 10 (n=19,19)
TAK-385 + Atorvastatin116.099.8
TAK-385 + Fluconazole87.4104.0

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Fraction Excreted Unchanged (Fe) of TAK-385

Fraction of TAK-385 excreted in the urine unchanged. (NCT02093390)
Timeframe: Days 1 and 10 (Predose and multiple time points up to 120 hours postdose)

,
Interventionpercent of TAK-385 (Mean)
Day 1 (n=20, 19)Day 10 (n=20, 19)
TAK-385 + Atorvastatin1.991.40
TAK-385 + Fluconazole1.561.61

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Plasma Trough Concentrations for Atorvastatin

Blood samples for atorvastatin trough levels were collected predose (before dosing with atorvastatin and before breakfast) on Days 8 through 12. (NCT02093390)
Timeframe: Days 8 to 12 Predose

Interventionng/mL (Mean)
Day 8Day 9Day 10Day 11Day 12
TAK-385 + Atorvastatin0.7420.7530.7020.5590.536

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Plasma Trough Concentrations for Fluconazole

Blood samples for fluconazole trough levels were collected predose (before dosing with fluconazole and before breakfast) on Days 8 through 12. (NCT02093390)
Timeframe: Days 8 to 12 Predose

Interventionng/mL (Mean)
Day 8Day 9Day 10Day 11Day 12
TAK-385 + Fluconazole63306540703070307200

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Absolute Change From Baseline in Lipoprotein (A) (Lp[A]) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmg/dL (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo31.71.9
PF-04950615 150 Milligram (mg) + Placebo27.1-5.8
Placebo32.00.7

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Anti-drug Antibody (ADA) and Neutralizing Anti-body (nAb) Titer Level in Participants Who Tested Positive for ADA and nAb Respectively

Titer levels of participants who tested positive for ADA and nAb are reported. Titers are expressed as log2 reciprocal dilution at assay cutpoint. (NCT02135029)
Timeframe: Week 4, 12, 24 and 30 (Follow-up)

Interventiontiter (Mean)
ADA Titer: Week 4ADA Titer: Week 12ADA Titer: Week 24ADA Titer: Week 30nAb Titer: Week 12nAb Titer: Week 24nAb Titer: Week 30
PF-04950615 150 Milligram (mg) + Placebo9.949.499.4610.126.055.286.09

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Number of Participants With Positive Anti-drug Antibodies (ADA) and Neutralizing Antibodies (nAb)

Participants with at least one positive ADA titer greater than or equal to (>=) 6.23 or positive nAb titer >=4.32 were reported. Titers are expressed as log2 reciprocal dilution at assay cutpoint. (NCT02135029)
Timeframe: Baseline up to Week 30

Interventionparticipants (Number)
ADAnAb
PF-04950615 150 Milligram (mg) + Placebo3521

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Percent Change From Baseline in Fasting Apolipoprotein A-I (ApoA-I) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-2.8-2.2
PF-04950615 150 Milligram (mg) + Placebo8.08.0
Placebo1.92.3

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Percent Change From Baseline in Fasting Apolipoprotein A-II (ApoA-II) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-3.2-0.6
PF-04950615 150 Milligram (mg) + Placebo4.13.9
Placebo-0.4-2.2

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Percent Change From Baseline in Fasting Apolipoprotein B (ApoB) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-27.2-28.1
PF-04950615 150 Milligram (mg) + Placebo-46.0-39.1
Placebo0.90.1

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Percent Change From Baseline in Fasting High Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo0.40.2
PF-04950615 150 Milligram (mg) + Placebo13.211.5
Placebo0.4-0.3

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Percent Change From Baseline in Fasting Lipoprotein (a) (Lp[a]) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo5.14.1
PF-04950615 150 Milligram (mg) + Placebo-21.5-16.6
Placebo2.00.8

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Percent Change From Baseline in Fasting Non High Density Lipoprotein Cholesterol (Non HDL-C) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-32.5-34.0
PF-04950615 150 Milligram (mg) + Placebo-50.0-41.9
Placebo1.1-0.3

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Percent Change From Baseline in Fasting Total Cholesterol (TC) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-25.7-26.8
PF-04950615 150 Milligram (mg) + Placebo-37.0-31.2
Placebo1.3-0.5

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Percent Change From Baseline in Fasting Triglycerides (TG) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-20.7-21.9
PF-04950615 150 Milligram (mg) + Placebo-12.5-13.6
Placebo2.2-3.3

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Percent Change From Baseline in Fasting Very Low Density Lipoprotein Cholesterol (VLDL-C) at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionpercent change (Mean)
Percent change at Week 12Percent change at Week 24
Atorvastatin 40 mg + Placebo-20.7-21.9
PF-04950615 150 Milligram (mg) + Placebo-12.5-13.6
Placebo2.2-3.3

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Percentage of Participants Achieving Fasting Low Density Lipoprotein Cholesterol (LDL-C) Less Than or Equal to (<=) 100 Milligram Per Deciliter (mg/dL) at Weeks 12 and 24

(NCT02135029)
Timeframe: Week 12, 24

,,
Interventionpercentage of participants (Number)
Week 12Week 24
Atorvastatin 40 mg + Placebo42.945.5
PF-04950615 150 Milligram (mg) + Placebo71.861.4
Placebo1.40

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Absolute Change From Baseline in Fasting Low Density Lipoprotein Cholesterol (LDL-C) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmilligrams per deciliter (mg/dL) (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo169.9-56.5
PF-04950615 150 Milligram (mg) + Placebo168.8-88.0
Placebo182.13.1

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Absolute Change From Baseline in Fasting Non High Density Lipoprotein Cholesterol (Non HDL-C) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmg/dL (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo200.5-67.1
PF-04950615 150 Milligram (mg) + Placebo199.2-99.8
Placebo210.72.2

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Absolute Change From Baseline in Fasting Total Cholesterol (TC) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmg/dL (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo256.2-67.7
PF-04950615 150 Milligram (mg) + Placebo250.1-93.8
Placebo262.33.2

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Absolute Change From Baseline in Fasting Total Cholesterol (TC)/ High Density Lipoprotein Cholesterol (HDL-C) Ratio at Weeks 12 and 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionratio (Mean)
BaselineAbsolute change at Week 12Absolute change at Week 24
Atorvastatin 40 mg + Placebo4.8-1.3-1.3
PF-04950615 150 Milligram (mg) + Placebo5.2-2.3-2.0
Placebo5.40.10.0

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Percentage of Participants Discontinued Due to Myalgia, Myopathy, Creatinine Kinase (CK) and Liver Function Tests (LFT) Elevations

(NCT02135029)
Timeframe: Baseline (Day 1) up to Week 30

,,
Interventionpercentage of participants (Number)
MyalgiaMyopathyCK ElevationsLFT Elevations
Atorvastatin 40 mg + Placebo16.7000
PF-04950615 150 Milligram (mg) + Placebo10.8000
Placebo9.6000

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Plasma PF-04950615 Concentrations at Weeks 12 and 24

Concentration versus time summary was calculated by setting concentration values below the lower limit of quantification (LLOQ =0.4 micrograms per milliliter [mcg/mL]) to zero. Participants who received PF-04950615 150 mg were evaluable for this outcome measure. (NCT02135029)
Timeframe: Week 12 and 24

Interventionmcg/mL (Mean)
Week 12Week 24
PF-04950615 150 Milligram (mg) + Placebo10.217.38

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Percentage of Participants Achieving Fasting Low Density Lipoprotein Cholesterol (LDL-C) Less Than or Equal to (<=) 70 Milligram Per Deciliter (mg/dL) at Weeks 12 and 24

(NCT02135029)
Timeframe: Week 12, 24

,,
Interventionpercentage of participants (Number)
Week 12Week 24
Atorvastatin 40 mg + Placebo14.315.2
PF-04950615 150 Milligram (mg) + Placebo45.141.4
Placebo00

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

(NCT02135029)
Timeframe: Baseline, Week 12

Interventionpercent (%) change (Mean)
Placebo2.4
PF-04950615 150 Milligram (mg) + Placebo-52.0
Atorvastatin 40 mg + Placebo-32.6

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Percent Change From Baseline in Fasting Low Density Lipoprotein Cholesterol (LDL-C) at Week 24

(NCT02135029)
Timeframe: Baseline, Week 24

Interventionpercent change (Mean)
Placebo1.6
PF-04950615 150 Milligram (mg) + Placebo-42.7
Atorvastatin 40 mg + Placebo-33.3

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Absolute Change From Baseline in Apolipoprotein B (ApoB) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmg/dL (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo124.6-35.3
PF-04950615 150 Milligram (mg) + Placebo125.8-57.5
Placebo133.31.1

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Absolute Change From Baseline in Fasting Apolipoprotein B (ApoB)/Apolipoprotein A-I (ApoA-I) Ratio at Weeks 12 And 24

(NCT02135029)
Timeframe: Baseline, Week 12, 24

,,
Interventionratio (Mean)
BaselineAbsolute change at Week 12Absolute change at Week 24
Atorvastatin 40 mg + Placebo0.8-0.2-0.2
PF-04950615 150 Milligram (mg) + Placebo0.9-0.4-0.4
Placebo0.9-0.0-0.0

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Absolute Change From Baseline in Fasting High Density Lipoprotein Cholesterol (HDL-C) at Week 12

(NCT02135029)
Timeframe: Baseline, Week 12

,,
Interventionmg/dL (Mean)
BaselineChange at Week 12
Atorvastatin 40 mg + Placebo55.7-0.5
PF-04950615 150 Milligram (mg) + Placebo51.16.0
Placebo51.60.1

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Effect of Evacetrapib Single and Multiple Doses on High Density Lipoprotein Cholesterol (HDL-C), Low Density Lipoprotein Cholesterol (LDL-C), and Triglycerides (TG)

(NCT02156492)
Timeframe: Single Dose Day 2 and Multiple Dose Day 22

,
Interventionmillimoles per liter (mmol/L) (Mean)
HDL-CLDL-CTG
Evacetrapib Multiple Dose Day 222.6761.2411.221
Evacetrapib Single Dose Day 21.6412.2890.984

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Pharmacokinetics (PK): Area Under Curve (AUC 0-inf) of Evacetrapib

Pharmacokinetic (PK) parameter estimates from evacetrapib concentrations following single dose and daily dose of 130 mg evacetrapib. (NCT02156492)
Timeframe: Part 1: Day 1 Predose 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 24, 48, 72, 96, 144, and 168 hours Postdose; Part 2 Day 14 Predose 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 24 hours Postdose

Interventionnanogram * hour per milliliter (ng*h/mL) (Geometric Mean)
Day 1Day 14
Evacetrapib Single and Multiple Dose770023600

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PK: AUC of Evacetrapib Alone and With Simvastatin or Atorvastatin

Pharmacokinetic parameter estimates of evacetrapib following 130 mg evacetrapib daily alone or with 40 mg simvastatin or 20 mg atorvastatin daily AUC (0-24). (NCT02156492)
Timeframe: Part 2: Day 14 and 22 Predose, 0.5, 1, 2, 3, 4, 6, 8, 12, and 24 hours Postdose

,
Interventionng*h/mL (Geometric Mean)
Days 5-14Days 15-22
Evacetrapib Daily and Atorvastatin106009480
Evacetrapib Daily and Simvastatin107009640

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PK: Cmax of Evacetrapib Alone and With Simvastatin or Atorvastatin

Pharmacokinetic parameter estimates of evacetrapib following 130 mg evacetrapib daily alone or with 40 mg simvastatin or 20 mg atorvastatin daily. (NCT02156492)
Timeframe: Part 2: Day 14 and 22 Predose, 0.5, 1, 2, 3, 4, 6, 8, 12, and 24 hours Postdose.

,
Interventionng/mL (Geometric Mean)
Days 5-14Days 15- 22
Evacetrapib Daily and Simvastatin11801020
Evactrapib Daily and Atorvastatin11201000

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PK: Maximum Concentration (Cmax) of Evacetrapib

Pharmacokinetic parameter estimates from evacetrapib following single dose and daily doses of 130 mg. (NCT02156492)
Timeframe: Part 1: Day 1 and Day 14 Predose 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 24, 48, 72, 96, 144, and 168 hours Postdose; Part 2 Day 14: Predose 0.5, 1, 2, 3, 4, 6, 8, 10, 12, and 24 hours Postdose

Interventionng/mL (Geometric Mean)
Single Dose Day 1Multiple Dose Day 14
Evacetrapib Single and Multiple Dose418954

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PK: Time to Maximum Concentration (Tmax) of Evacetrapib

Pharmacokinetic parameter estimates of evacetrapib following single and daily doses of 130 mg evacetrapib. (NCT02156492)
Timeframe: Part 1: Day 1 Predose on Day 1 or Day 14 and at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, 24, 48, 72, 96, 144, and 168 hours postdose. Part 2: Predose on Day 14 at 0.5, 1, 2, 3, 4, 6, 8, 10, 12, and 24 hours post dose.

Interventionhours (h) (Median)
Single Dose Day 1Daily Dose Day 14
Evacetrapib Single and Multiple Dose3.003.00

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PK: Tmax of Evacetrapib Alone and With Simvastatin or Atorvastatin

Pharmacokinetic parameter estimates of Tmax of evacetrapib following 130 mg daily dose alone or with 40 mg Simvastatin or 20 mg Atorvastatin. Tmax of simvastatin and atorvastatin. (NCT02156492)
Timeframe: Part 2: Predose on Day 14 and 22 and at 0.5, 1, 2, 3, 4, 6, 8, 12, and 24 hours postdose.

,
Interventionh (Median)
Days 5-14Days 15- 22
Evacetrapib Daily and Atrovastatin3.003.00
Evacetrapib Daily and Simvastatin3.003.00

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Percent Change From Baseline in Low-density Lipoprotein (LDL) Apolipoprotein B-100 Fractional Catabolic Rate (FCR)

The fractional catabolic rate (the percentage of apolipoprotein B-100 in LDL which is replaced, transferred or lost per unit of time) was measured at Baseline and Day 50 over 5 consecutive days using the stable isotope tracer, D3-leucine. LDL particles were isolated from plasma by sequential ultracentrifugation, and isotopic enrichment was determined using gas chromatography-mass spectrometry. Mathematical modelling of the protein enrichment data was used to estimate protein catabolism. (NCT02189837)
Timeframe: Baseline (5 days prior to Day 1) and Day 50; plasma samples for fasting lipids were obtained at 0, 5, 10, 20, 30, 40, and 60 min, as well as at 1.5, 2, 2.5, 3, 4, 5, 6, 8, and 10 hours, and 2, 3, 4 and 5 days after D3-leucine administration.

Interventionpercent change (Least Squares Mean)
Placebo-5.07
Atorvastatin74.13
Evolocumab83.70
Evolocumab and Atorvastatin310.48

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Percent Change From Baseline in LDL-C at Day 50

LDL-C was measured using ultrcentrifugation. (NCT02189837)
Timeframe: Baseline and Day 50

Interventionpercent change (Least Squares Mean)
Placebo-0.65
Atorvastatin-45.25
Evolocumab-57.79
Evolocumab and Atorvastatin-83.19

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Percent Change From Baseline in LDL Apolipoprotein B-100 Production Rate (PR)

The production rate of apolipoprotein B-100 in LDL was measured at Baseline and Day 50 over 5 consecutive days using the stable isotope tracer, D3-leucine. LDL particles were isolated from plasma by sequential ultracentrifugation and isotopic enrichment was determined using gas chromatography-mass spectrometry. Mathematical modelling of the protein enrichment data was used to estimate the production rate. (NCT02189837)
Timeframe: Baseline and Day 50

Interventionpercent change (Least Squares Mean)
Placebo-3.80
Atorvastatin-3.27
Evolocumab-20.45
Evolocumab and Atorvastatin-35.93

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Percent Change From Baseline in Lipoprotein (a) Fractional Catabolic Rate (FCR)

The fractional catabolic rate (the percentage of lipoprotein(a) (Lp[a]) which is replaced, transferred or lost per unit of time) was measured at Baseline and Day 50 over 5 consecutive days using the stable isotope tracer, D3-leucine. Lp(a) was isolated from plasma using an immunoprecipitation method employing immunomagnetic beads and polyacrylamide gel electrophoresis. Isotopic enrichment was determined using gas chromatography-mass spectrometry. Mathematical modelling of the protein enrichment data was used to estimate protein catabolism. (NCT02189837)
Timeframe: Baseline (5 days prior to Day 1) and Day 50; plasma samples for fasting lipids were obtained at 0, 5, 10, 20, 30, 40, and 60 min, as well as at 1.5, 2, 2.5, 3, 4, 5, 6, 8, and 10 hours, and 2, 3, 4 and 5 days after D3-leucine administration.

Interventionpercent change (Least Squares Mean)
Placebo7.49
Atorvastatin25.52
Evolocumab5.37
Evolocumab and Atorvastatin64.57

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Percent Change From Baseline in Lipoprotein(a) Production Rate (PR)

The production rate of lipoprotein(a) was measured at Baseline and Day 50 over 5 consecutive days using the stable isotope tracer, D3-leucine. Lp(a) was isolated from plasma using an immunoprecipitation method employing immunomagnetic beads and polyacrylamide gel electrophoresis. Isotopic enrichment was determined using gas chromatography-mass spectrometry. Mathematical modelling of the protein enrichment data was used to estimate protein catabolism. (NCT02189837)
Timeframe: Baseline and Day 50

Interventionpercent change (Least Squares Mean)
Placebo3.52
Atorvastatin-6.88
Evolocumab-35.91
Evolocumab and Atorvastatin16.40

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Peri-operative Rise in Interleukin-6 (IL-6) Levels

The change in the level of IL-6 from baseline to POD2 in 16 arthroplasty patients randomized (1:1) to atorvastatin 40mg versus placebo. (NCT02197065)
Timeframe: Change from preoperative to postoperative day 2

Interventionpg/mL (Median)
Atorvastatin1.28
Sugar Pill0.98

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Peri-operative Rise in High Sensitivity C-reactive Protein (Hs-CRP)

The change in the level of hs-CRP from baseline to POD2 in 20 orthopedic patients randomized (1:1) to atorvastatin 40mg versus placebo. (NCT02197065)
Timeframe: Change from preoperative to post-operative day 2

Interventionmg/L (Median)
Atorvastatin98.95
Sugar Pill85.95

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Percentage of All Enrolled Patients With a Peri-operative Rise in High-sensitivity Cardiac Troponin I

The percentage of orthopedic patients with a ≥ 10 pg/mL rise in high-sensitivity cardiac troponin I (hs-cTnI) from baseline pre-operatively to post-operative day (POD)2 (NCT02197065)
Timeframe: change from preoperative to postoperative day 2

Interventionpercentage of patients (Number)
All Patients20

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Percent Change From Baseline to 3 Months in Non-HDL-C

Change in Non-HDL-C levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. LS medians and median differences were analyzed in log units and converted to standard units. Statistics are from mixed model repeated measures analysis with log baseline measurement, treatment, visit, and treatment by visit interaction included in the model. Log percent change from baseline response is the dependent variable. Within-participant repeated measures at multiple visits are modeled by a compound symmetry covariance structure. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib-31.42
Atorvastatin 40 mg-4.95
Atorvastatin 80 mg-9.40
Atorvastatin + Ezetimibe-24.37

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Percent Change From Baseline to 3 Months in Apolipoprotein AI (apoAI)

Change in apoAI levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. Statistics are from analysis of covariance with log baseline measurement and treatment is included in the model. LS means and median differences were analyzed in log units and converted to standard units. Log Percent change from baseline response is the dependent variable. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib46.08
Atorvastatin 40 mg-0.27
Atorvastatin 80 mg-6.14
Atorvastatin + Ezetimibe-2.36

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Percent Change From Baseline to 3 Months in Apolipoprotein B (apoB)

Change in apoB levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. Statistics are from analysis of covariance with log baseline measurement and treatment is included in the model. LS means and median differences were analyzed in log units and converted to standard units. Log Percent change from baseline response is the dependent variable. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib-22.96
Atorvastatin 40 mg0.21
Atorvastatin 80 mg-6.54
Atorvastatin + Ezetimibe-18.84

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Percent Change From Baseline to 3 Months in Cholesterol Efflux Capacity

Change in cholesterol efflux capacity from baseline to the 3-month visit expressed as a percentage of the baseline levels. Statistics are from analysis of covariance with log baseline measurement and treatment is included in the model. LS means and median differences were analyzed in log units and converted to standard units. Log Percent change from baseline response is the dependent variable. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib35.09
Atorvastatin 40 mg-2.96
Atorvastatin + Ezetimibe-7.03
Atorvastatin 80 mg-4.55

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Percent Change From Baseline to 3 Months in High-Density Lipoprotein Cholesterol (HDL-C)

Change in HDL-C levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. LS medians and median differences were analyzed in log units and converted to standard units. Statistics are from mixed model repeated measures analysis with log baseline measurement, treatment, visit, and treatment by visit interaction included in the model. Log percent change from baseline response is the dependent variable. Within-participant repeated measures at multiple visits are modeled by a compound symmetry covariance structure. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib125.39
Atorvastatin 40 mg0.11
Atorvastatin 80 mg-6.10
Atorvastatin + Ezetimibe-2.18

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Percent Change From Baseline to 3 Months in Lipoprotein(a) (Lp[a])

Change in Lp(a) levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. Statistics are from analysis of covariance with log baseline measurement and treatment is included in the model. LS means and median differences were analyzed in log units and converted to standard units. Log Percent change from baseline response is the dependent variable. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib-28.73
Atorvastatin 40 mg4.45
Atorvastatin 80 mg3.90
Atorvastatin + Ezetimibe13.42

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Percent Change From Baseline to 3 Months in Low-Density Lipoprotein Cholesterol (LDL-C)

Change in LDL-C levels from baseline to the 3-month visit expressed as a percentage of the baseline levels. LDL-C was measured by beta quantification. Statistics are from analysis of covariance with log baseline measurement and treatment is included in the model. Least Square Means (LS means) and median differences were analyzed in log units and converted to standard units. Log Percent change from baseline response is the dependent variable. (NCT02227784)
Timeframe: Baseline, 3 Months

Interventionpercent (Median)
Atorvastatin + Evacetrapib-33.44
Atorvastatin 40 mg0.04
Atorvastatin 80 mg-6.19
Atorvastatin + Ezetimibe-27.30

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Percent Change From Baseline to Week 12 in Apolipoprotein B

The ANCOVA model using last observation carried forward (LOCF) was applied to analyze percent changes from baseline. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in Apolipoprotien B (Least Squares Mean)
Evacetrapib-20.4
Placebo-3.0
Ezetimibe-20.4

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Percent Change From Baseline to Week 12 in High-Density Lipoprotein Cholesterol (HDL-C)

The MMRM was used for the LS Mean estimates at Week 12 for HDL-C adjusting for baseline as response variables, baseline measurement as a covariate, treatment, visit, and treatment-by-visit interaction as fixed effects, and participant as a random effect, and treatment-by-visit interaction as fixed effects, and participant as a random effect. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in HDL-C (Least Squares Mean)
Evacetrapib108.96
Placebo-0.90
Ezetimibe-3.12

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Percent Change From Baseline to Week 12 in LDL-C (Direct)

The MMRM was used for the LS Mean estimates at Week 12 for LDL-C (direct) adjusting for baseline as response variables, baseline measurement as a covariate, treatment, visit, and treatment-by-visit interaction as fixed effects, and participant as a random effect. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in LDL-C (Direct) (Least Squares Mean)
Evacetrapib-27.17
Placebo-3.40
Ezetimibe-28.96

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Percent Change From Baseline to Week 12 in Lipoprotein-a

The analysis of covariance (ANCOVA) model using last observation carried forward (LOCF) was applied to analyze percent changes from baseline. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in Lipoprotein-a (Least Squares Mean)
Evacetrapib-33.17
Placebo7.78
Ezetimibe0.68

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Percent Change From Baseline to Week 12 in Low-Density Lipoprotein Cholesterol (LDL-C) Measured by Beta Quantification

The mixed-effects model for repeated measures (MMRM) was used for the Least Squares Mean (LS Mean) estimates at Week 12 for LDL-C adjusting for baseline as response variables, baseline measurement as a covariate, treatment, Visit (4,5,6, or 7), and treatment-by-visit interaction as fixed effects, and participant as a random effect. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in LDL-C (Least Squares Mean)
Evacetrapib-26.37
Placebo-3.75
Ezetimibe-27.31

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Percent Change From Baseline to Week 12 in Non HDL-C

The MMRM was used for the LS Mean estimates at Week 12 for Non HDL-C adjusting for baseline as response variables, baseline measurement as a covariate, treatment, visit, and treatment-by-visit interaction as fixed effects, and participant as a random effect. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in non HDL-C (Least Squares Mean)
Evacetrapib-22.01
Placebo-6.42
Ezetimibe-27.35

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Percent Change From Baseline to Week 12 in Apolipoprotein A-I

The ANCOVA model using last observation carried forward (LOCF) was applied to analyze percent changes from baseline. (NCT02260648)
Timeframe: Baseline, Week 12

Interventionpercent change in Apolipoprotein A-I (Least Squares Mean)
Evacetrapib42.8
Placebo0.6
Ezetimibe-0.6

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Medication Adherence-Percentage of Pills Taken

polypill arm-evaluation via pill counts. (NCT02278471)
Timeframe: 12 months

Interventionpercentage of pills taken (Median)
Polypill86

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Systolic Blood Pressure

polypill versus usual care (NCT02278471)
Timeframe: 2 months

Interventionmm Hg (Mean)
Usual Care133
Polypill128

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Systolic Blood Pressure

polypill versus usual care (NCT02278471)
Timeframe: 12 months

Interventionmm Hg (Mean)
Usual Care138
Polypill131

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Medication Adherence

polypill-percentage of pills taken, evaluated via pill counts (NCT02278471)
Timeframe: 2 months

Interventionpercentage of pills taken (Median)
Polypill98

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LDL Cholesterol

polypill versus usual care (NCT02278471)
Timeframe: 2 months

Interventionmg/dL (Mean)
Usual Care108
Polypill90

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LDL Cholesterol

Polypill versus usual care (NCT02278471)
Timeframe: 12 months

Interventionmg/dL (Mean)
Usual Care109
Polypill98

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The Reduction of Peak Thrombin Concentration

"Determine the reduction of thrombin peak concentration measured by Thrombin Generation Assay (TGA) at 3 months in the anticoagulation +atorvastatin arm as compared to the anticoagulation arm." (NCT02331095)
Timeframe: 3 Months

,
InterventionnM (Median)
Enrollment3 Months
Anticoagulation3754
Atorvastatin + Anticoagulation6748

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The Rate of Major, Non-major, and All Hemorrhages Defined by the International Society on Thrombosis and Haemostasis (ISTH) Criteria

Major bleeding events were defined by the International Society on Thrombosis and Haemostasis (ISTH) criteria, with overt bleeding in critical organs (e.g. central nervous system, retroperitoneum), a >2 gram/dL drop in hemoglobin from baseline, or requiring at least two units of packed red blood cell transfusion meeting the criteria for major bleeding. Clinically relevant, non-major bleeding (CRNMB) events were defined as any other bleeding events reported by patients but not otherwise meeting the above listed criteria for major bleeding. (NCT02331095)
Timeframe: 3 months and 9 months

,
InterventionParticipants (Count of Participants)
3 Months9 Months
Anticoagulation00
Atorvastatin + Anticoagulation00

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The Reduction of Endogenous Thrombin Potential

"Determine the reduction of endogenous thrombin potential measured by Thrombin Generation Assay (TGA) at 3 months in the anticoagulation +atorvastatin arm as compared to the anticoagulation arm." (NCT02331095)
Timeframe: 3 Months

,
InterventionnM*min (Median)
Enrollment3 Months
Anticoagulation11551275
Atorvastatin + Anticoagulation14401143

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The Reduction of Clinical Post-thrombotic Syndrome (PTS), as Objectively Evaluated With Villalta Scoring System

The Villata score for Post-Thrombotic Syndrome (PTS) stratifies the severity of post-thrombotic syndrome in lower extremity DVT. The score contains a combination of 5 subjective symptoms as reported by the patient (cramps, itching, pins and needles, heaviness, and pain) and 6 objective signs measured by a provider (edema, skin induration, hyperpigmentation, prominent veins on legs, redness, and tenderness on calf compression). Each sign is scaled from 0 (no or minimal) to 3 (severe) with a total score ranged from 0 to 33. Higher scores represent more severe disease. (NCT02331095)
Timeframe: 3 Months

,
Interventionscores on a scale (Median)
Enrollment3 Months
Anticoagulation76
Atorvastatin + Anticoagulation4.53.5

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The Rate of Arterial Thrombotic Events

Arterial thromboembolism was defined a new myocardial infarction (based on typical electrocardiographic findings and/or elevation of cardiac enzymes) or cerebral vascular accident (based on clinical syndrome of development of focal or global loss of brain function thought to be vascular in origin, confirmed by appropriate standard imaging studies). (NCT02331095)
Timeframe: 3 months and 9 months

,
InterventionParticipants (Count of Participants)
3 Months9 Months
Anticoagulation00
Atorvastatin + Anticoagulation00

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Change in Triglyceride Levels at 3 Months

(NCT02331095)
Timeframe: 3 Months

,
Interventionmg/dL (Mean)
Enrollment3 Months
Anticoagulation130.5127.4
Atorvastatin + Anticoagulation157.9135.3

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Change in the Levels of D-Dimer at 3 Months

(NCT02331095)
Timeframe: 3 Months

,
Interventionmcg/mL FEU (Median)
Enrollment3 Months
Anticoagulation2.120.36
Atorvastatin + Anticoagulation2.20.59

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Change in the Levels of C-Reactive Protein at 3 Months

C-Reactive (CRP) was measured using high sensitivity. (NCT02331095)
Timeframe: 3 Months

,
Interventionmg/L (Median)
Enrollment3 Months
Anticoagulation5.53.9
Atorvastatin + Anticoagulation7.05.1

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Change in Low-Density Lipoproteins (LDL) at 3 Months

(NCT02331095)
Timeframe: 3 Months

,
Interventionmg/dL (Mean)
Enrollment3 Months
Anticoagulation123.8115.9
Atorvastatin + Anticoagulation116.976.1

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The Rate of Residual (Chronic) Vein Obstruction by Doppler Ultrasound

Residual venous obstruction was assed by Doppler Ultrasonography. Residual chronic DVT (to any degree) was reported. (NCT02331095)
Timeframe: 3 Months

InterventionParticipants (Count of Participants)
Anticoagulation8
Atorvastatin + Anticoagulation8

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Change in Circulating Levels of Osteoprogenitor Cells (CD34+/OCN+/BAP+ Cells)

Circulating levels of osteoprogenitor cells (CD34+/OCN+/BAP+ cells) will be measured by FACS analysis in each patient at baseline and after three months of treatment with Atorvastatin. (NCT02342015)
Timeframe: 3 months

Interventioncells/million events (Mean)
Atorvastatin59.1

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Relative Change in OPG/RANK/RANKL mRNA Expression in Isolated T Cells and Monocytes

Isolated T cells and monocytes will be obtained at baseline and at the end of the treatment period. Gene expression analysis will be performed in each cell type to assess the expression level of OPG, RANK, and RANKL at baseline and after three months of treatment. (NCT02342015)
Timeframe: 3 months

Interventionrelative fold change (Mean)
Atorvastatin0.76

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Endothelial Progenitor Cell Colony Forming Units/ml of Peripheral Blood Across Time

The cell culture assay and quantification of circulating EPC-CFU were performed for patients recruited at the Dallas VA center only. The assay were done at 4 time points (pre-PCI, post-PCI, 30-day follow-up, and 90-day follow-up). (NCT02347098)
Timeframe: 12 weeks

,
Interventioncolonies/ml (Mean)
baseline pre-PCIbaseline post-PCI30-day90-day
Intensive LDL-lowering Therapy (ILLT)11.8515.3021.6016.32
Standard Statin Monotherapy (SMT)11.9917.8920.4015.06

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Change in % Necrotic Core Component of Atheroma

The %NC component of atheroma were obtained via IVUS-VH at 2 time points (baseline during index PCI and 90-day follow-up). (NCT02347098)
Timeframe: 12 weeks

Interventionpercentage of atheroma component (Mean)
Intensive LDL-lowering Therapy (ILLT)0.44
Standard Statin Monotherapy (SMT)0.94

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Major Adverse CV Events

The number of patients who experienced major adverse cardiovascular endpoints (MACE) including death, myocardial infarction, coronary revascularization, and stroke during the follow-up periods. (NCT02347098)
Timeframe: 6 months

InterventionParticipants (Count of Participants)
Intensive LDL-lowering Therapy (ILLT)5
Standard Statin Monotherapy (SMT)2

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Change in the Total Atheroma Volume From Baseline to 12 Weeks

The primary effectiveness outcome measure was the change in the total atheroma volume within a ≥ 20 mm long segment of the target coronary artery from baseline to 12 weeks post-PCI. The measurement was done via IVUS-VH at 2 time points (baseline during index PCI and 90-day follow-up). (NCT02347098)
Timeframe: 12 weeks

Interventionmm^3 (Mean)
Intensive LDL-lowering Therapy (ILLT)-7.63
Standard Statin Monotherapy (SMT)-3.10

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% of Patients Who Improved Their Brachial Flow-mediation Dilation (%FMD) at 16 Weeks

"%FMD = change in brachial artery flow-mediation dilation between pre and post-ischemia. Baseline (pre-ischemia) is the reference to which percentage change is calculated.~Result is expressed as the % of patients who had an improvement in their %FMD at 16 weeks compared to baseline." (NCT02370784)
Timeframe: baseline to 16 weeks

InterventionParticipants (Count of Participants)
Atorvastatin 40 mg Daily5
Placebo5

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Change in the Raynaud Condition Score (RCS) at 16 Weeks (End-of-study) From Baseline

The Raynaud Condition Score is a patient-reported outcome of a single question regarding Raynaud severity. It is a visual analog scale with a results range of 0-100. A score of 0 us is no symptoms, and 100 severe symptoms. It is recommended by OMERACT for assessment of Raynaud phenomenon. (NCT02370784)
Timeframe: change in RCS from baseline to week 16

Interventionscore on a scale (Median)
Active Drug-2.0
Placebo Control0

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Proportion of Patients Improving Their EndoPAT Reactive Hyperemia Index (RHI) at the End-of-study (16 Weeks)

"EndoPAT is a proprietary device that assesses digital (microvascular) endothelial function during reactive hyperemia. A probe is placed on both index fingers. After 5 minutes of baseline observation, one arm is occluded for 5 minutes, while the other is not and serves as control. Output is the reactive hyperemia index (RHI), calculated as the post-to-pre occlusion signal ratio in the occluded side, normalized to the control side and further corrected for baseline vascular tone per Itamar Medical. There are no units. RHI ≤ 1.67 is abnormal and indicates endothelial dysfunction." (NCT02370784)
Timeframe: Change in RHI from baseline to 16 weeks expressed as the percentage of patients who improve (respond).

InterventionParticipants (Count of Participants)
Active Drug6
Placebo Control4

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The Median Change in the Raynaud Phenomenon Visual Analog Scale (RP-VAS) Score at 16 Weeks (End-of-study) Compared to Baseline in the Atorvastatin and Placebo Groups.

The RP-VAS scale measure ranges from 0-100, with 0 being no symptoms and 100 severe symptoms. Reported is the median and interquartile range of change between baseline and week 16 (end-of-study). (NCT02370784)
Timeframe: baseline to 16 weeks

Interventionscore on a scale (Median)
Active Drug0.5
Placebo Control0.0

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Mean Change in hsCRP Levels

(NCT02432040)
Timeframe: 6 months

Interventionnmol/L (Mean)
Atorvastatin-7.58
Placebo-5.14

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Adverse Events

(NCT02432040)
Timeframe: 6 months

Interventionparticipants (Number)
Atorvastatin2
Placebo0

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Percentage of Patients Achieving PASI-50 at the End of 3 Months

PASI-50 means at least a 50% reduction from baseline PASI score (NCT02432040)
Timeframe: 3 months

Interventionpercentage of participants (Number)
Atorvastatin36.4
Placebo18.2

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Mean Gross Change in Psoriasis Area and Severity Index (PASI) Scores From Baseline to the End of 6 Months

Psoriasis Area and Severity Index involves grading psoriatic plaques based on erythema (E), infiltration (I), desquamation (D). Severity is graded from 0-4 for each criteria (0 - none, 1 - slight, 2 - moderate, 3 - severe, and 4 - very severe). The body is divided into 4 regions, head, upper extremities, trunk, and lower extremities, and for each region, the surface area involvement is graded on a 0-6 scale (0 - 0% involvement, 1 - <10%, 2 - 10-<30%, 3 - 30-<50%, 4 - 50-<70%, 5 - 70-<90%, 6 - 90-100%).The highest potential PASI score is 72, with higher PASI scores indicating worse psoriasis. (NCT02432040)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Atorvastatin-2.15
Placebo-1.69

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Mean Change in Lipid Profile Levels

(NCT02432040)
Timeframe: 6 months

,
Interventionmg/dL (Mean)
Total cholesterolTriglyceridesLDL CholesterolHDL Cholesterol
Atorvastatin-35.39-17.55-45.183.15
Placebo-38.32-5.12-13.48-0.69

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Monthly Mean Changes in PASI Scores

PASI scores were measured monthly and mean changes from baseline for each month for the whole 6-month duration of the study recorded. (NCT02432040)
Timeframe: Monthly from baseline to 6 months

,
Interventionunits on a scale (Mean)
Mean change for the first monthMean change for the second monthMean change for the third monthMean change for the fourth monthMean change for the fifth monthMean change for the sixth month
Atorvastatin-0.72-1.67-2.19-2.10-2.15-2.15
Placebo-0.71-0.69-1.16-1.13-1.43-1.69

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Mean Change in Dermatology Life Quality Index (DLQI) Scores After 6 Months

(NCT02432040)
Timeframe: 6 months

Interventionunits on a scale (Mean)
Atorvastatin-6.5
Placebo-2.13

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Percentage of Patients Achieving PASI-50 in Each Arm at the End of 6 Months

Percentage of patients in each arm who will achieve 50% reduction in PASI scores at the end of 6 months will be compared (NCT02432040)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Atorvastatin27.3
Placebo45.5

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OGTT Insulin AUC

Insulin area under the curve (AUC) (mU/L x 2h) measured during a 75-gram oral glucose tolerance test (OGTT). (NCT02437084)
Timeframe: baseline, week 8

InterventionmU/L x 2 h (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy127133

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Steady-state Plasma Glucose (SSPG)

Insulin sensitivity measured by SSPG concentration (mg/dL) during the insulin suppression test. (NCT02437084)
Timeframe: baseline, week 9 or 10

Interventionmg/dL (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy130139

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Fasting Plasma Insulin

Baseline and end-of-treatment fasting plasma insulin (mU/L) values represent average of up to 3 measurements for each value (obtained at baseline weeks -2, -1, and 0 and at the end of study at weeks 8, 9, and 10). (NCT02437084)
Timeframe: 10 weeks

InterventionmU/L (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy10.110.6

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Fasting Plasma Glucose

Baseline and end-of-treatment fasting plasma glucose (mg/dL) values represent average of up to 3 measurements for each value (obtained at baseline weeks -2, -1, and 0 and at the end of study at weeks 8, 9, and 10). (NCT02437084)
Timeframe: 10 weeks

Interventionmg/dL (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy99100

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Insulin Secretion Rate Area Under the Curve (ISR-AUC)

Insulin secretion measured by ISR-AUC (pmol/min x 4 h) during the graded glucose infusion test. (NCT02437084)
Timeframe: baseline, week 9 or 10

Interventionpmol/min x 4 h (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy18241942

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OGTT Glucose AUC

Glucose area under the curve (AUC) (mg/dL x 2 h) measured during a 75-gram oral glucose tolerance test (OGTT). (NCT02437084)
Timeframe: baseline, week 8

Interventionmg/dL x 2 h (Median)
BaselineEnd of Study
Individuals Without Diabetes Eligible to Receive Statin Therapy295299

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Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12

Baseline value was defined as the last observation before the first dose of the treatment. (NCT02476006)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
Alirocumab4.37

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12

Baseline value was defined as the last observation before the first dose of the treatment. (NCT02476006)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
Alirocumab-45.89

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Percentage of Participants Reaching Calculated LDL-C <100 mg/dL (2.59 mmol/L) at Week 12

LDL-Cholesterol was calculated using the Friedewald formula. Percentage of participants who reached calculated LDL-C <100 mg/dL (2.59 mmol/L) at week 12 were reported. (NCT02476006)
Timeframe: At Week 12

Interventionpercentage of participants (Number)
Alirocumab74.6

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Percentage of Participants With Treatment Emergent Adverse Events (TEAEs)

Adverse Event (AE) was defined as any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product and which does not necessarily have to have a causal relationship with this treatment. Treatment-emergent AEs (TEAEs) were defined as AEs that that developed or worsened or became serious during the TEAE period (time from the first injection of study drug up to the day of the last injection of study drug + 14 days). A Serious Adverse Event (SAE) was any untoward medical occurrence that at any dose: resulted in death, was life-threatening, required inpatient hospitalization or prolongation of existing hospitalization, resulted in persistent or significant disability/incapacity, was a congenital anomaly/birth defect, was a medically important event. (NCT02476006)
Timeframe: From first injection of investigational medicinal product (IMP) up to 2 weeks after last dose of study drug (Week 120)

Interventionpercentage of participants (Number)
Any TEAEAny treatment emergent SAEAny TEAE leading to deathAny TEAE leading to treatment discontinuation
Alirocumab71.616.20.24.5

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Assessment of Participant's Acceptability of Self-Injection Using Self Injection Assessment Questionnaire (SIAQ): Self Image, Injection-Site Reactions, Ease of Use

SIAQ: contained 2 modules: Pre-SIAQ and Post-SIAQ. Post-SIAQ: self-completed after self-injection. Post-SIAQ consisted of 21 items grouped into 6 domains: feelings about injections, self-image, self-confidence, injection-site reactions, ease of use & satisfaction with self-injection. Participants rated each item on 5-point (or 6-point) semantic Likert-type scale, where lower numbers indicated a worse experience. Item scores were transformed to obtain a score ranging from 0 (worst experience) to 10 (best experience) for each item. Transformed scores for items contributing to a domain were then averaged into a domain score. Each domain score ranges from 0 (worst experience) to 10 (best experience), higher score=better acceptability. Domain scores which are not in common with Pre-SIAQ were analyzed on the Post-SIAQ population and are reported here. (NCT02476006)
Timeframe: Week 4, Week 8, Week 12, Week 24, Week 48, Week 72, Week 96

Interventionunits on a scale (Mean)
Self Image: Week 4Self Image: Week 8Self Image: Week 12Self Image: Week 24Self Image: Week 48Self Image: Week 72Self Image: Week 96Injection-site reactions: Week 4Injection-site reactions: Week 8Injection-site reactions: Week 12Injection-site reactions: Week 24Injection-site reactions: Week 48Injection-site reactions: Week 72Injection-site reactions: Week 96Ease of use: Week 4Ease of use: Week 8Ease of use: Week 12Ease of use: Week 24Ease of use: Week 48Ease of use: Week 72Ease of use: Week 96
Alirocumab9.49.49.49.39.49.39.49.69.69.69.59.59.59.58.78.78.88.88.99.09.0

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Assessment of Participant's Acceptability of Self-Injection Using Self Injection Assessment Questionnaire (SIAQ): Feeling About Injections, Self Confidence, Satisfaction With Self-Injections

Pre-SIAQ: self-completed before first self-injection & Post-SIAQ: self-completed after self-injection. Pre-SIAQ consisted of 7 items grouped into 3 domains:feelings about injections,self-confidence & satisfaction with self-injection. Post-SIAQ consisted of 21 items grouped into 6 domains:feelings about injections,self-image,self-confidence,injection-site reactions,ease of use & satisfaction with self-injection. Participants rated each item on 5-point (or 6-point) semantic Likert-type scale, where lower numbers indicate a worse experience. Item scores were transformed to obtain a score ranging from 0 (worst experience) to 10 (best experience). Transformed scores for items contributing to a domain were then averaged into a domain score. Each domain score ranges from 0 (worst experience) to 10 (best experience), higher score=better acceptability. Domain scores common to the Pre & Post SIAQ were analyzed on participants belonging to Pre & Post-SIAQ population and are reported. (NCT02476006)
Timeframe: Baseline (Pre-SIAQ), Week 4, Week 8, Week 12, Week 24, Week 48, Week 72, Week 96

Interventionunits on a scale (Mean)
Feelings about injections: BaselineFeeling about injections: Week 4Feeling about injections: Week 8Feeling about injections: Week 12Feeling about injections: Week 24Feeling about injections: Week 48Feeling about injections: Week 72Feeling about injections: Week 96Self confidence: BaselineSelf Confidence: Week 4Self Confidence: Week 8Self Confidence: Week 12Self Confidence: Week 24Self Confidence: Week 48Self Confidence: Week 72Self Confidence: Week 96Satisfaction with self injection: BaselineSatisfaction with self-injections: Week 4Satisfaction with self-injections: Week 8Satisfaction with self-injections: Week 12Satisfaction with self-injections: Week 24Satisfaction with self-injections: Week 48Satisfaction with self-injections: Week 72Satisfaction with self-injections: Week 96
Alirocumab8.69.19.19.29.29.29.29.36.98.08.18.18.08.18.38.47.28.58.78.78.68.78.88.8

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) and/or >=50% Reduction From Baseline in LDL-C at Week 12

LDL-Cholesterol was calculated using the Friedewald formula. Percentage of participants who reached LDL-C <70 mg/dL at Week 12 and/or >=50% reduction from baseline in LDL-C at Week 12 are reported. (NCT02476006)
Timeframe: At Week 12

Interventionpercentage of participants (Number)
Alirocumab69.1

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Percent Change From Baseline in Total Cholesterol (Total-C) at Week 12

Baseline value was defined as the last observation before the first dose of the treatment. (NCT02476006)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
Alirocumab-38.28

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Percentage of Participants Reaching Calculated LDL-C <70 mg/dL (1.81 mmol/L) at Week 12

LDL-Cholesterol was calculated using the Friedewald formula. Percentage of participants who reached calculated LDL-C <70 mg/dL (1.81 mmol/L) at week 12 were reported. (NCT02476006)
Timeframe: At Week 12

Interventionpercentage of participants (Number)
Alirocumab50.2

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

Calculated LDL-C values were obtained using the Friedewald formula. Calculated LDL-C in mg/dL from Friedewald formula (LDL cholesterol = Total cholesterol - HDL cholesterol - [Triglyceride/5]). Baseline value was defined as the last observation before the first dose of the treatment. (NCT02476006)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
Alirocumab-54.84

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Percent Change From Baseline in Triglycerides at Week 12

Baseline value was defined as the last observation before the first dose of the treatment. (NCT02476006)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
Alirocumab-8.28

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Immunoassay Cortisole in Blood

Immunoassay Cortisole in the blood (nmole/L) was measured (NCT02503865)
Timeframe: up to 12 weeks

Interventionnmol/L (Mean)
Conventional Patient Group743.8
"Analimentary Detoxication"751.2
Healthy People445.3

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Systolic/ Diastolic Blood Pressures (mm Hg)

Systolic and Diastolic Blood Pressures (mm Hg) was measured by manual/automatic tonometery (NCT02503865)
Timeframe: up to 12 weeks

,,
Interventionmm Hg (Mean)
Systolic Blood PressuresDiastolic Blood Pressures
"Analimentary Detoxication Weight Loss"152.196.9
Conventional Patient Group151.294.1
Healthy People121.179.9

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Lipid Profile

Blood sample for lipid profile (Cholesterol in mmole/L, High-density Lipoproteids in mmole/L, Triglycerides in mmole/L) was measured (NCT02503865)
Timeframe: up to 12 weeks

,,
Interventionmmole/L (Mean)
CholesterolHigh-density LipoproteidsTriglycerides
"Analimentary Detoxication Weight Loss"5.350.752.2
Conventional Patient Group5.220.762.1
Healthy People4.91.221.4

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Blood Glucose Level

Fasting blood glucose (FBG) (mmole/L) and Two-hour postprandial glucose (THPG) (mmole/L) were measured. (NCT02503865)
Timeframe: up to 12 weeks

,,
Interventionmmole/L (Mean)
Fasting blood glucose levelTwo-hour postprandial glucose
"Analimentary Detoxication Weight Loss"6.4314.6
Conventional Patient Group6.0514.5
Healthy People4.585.3

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Immunoassay Hormones in Blood

Immunoassay Insulin in the blood (in nU/L) was investigated (NCT02503865)
Timeframe: up to 12 weeks

InterventionnU/L (Mean)
Conventional Patient Group22.9
"Analimentary Detoxication"23.2
Healthy People6.5

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Percentage of Participants Who Experience 1 or More Allergic Reaction or Rash AEs

Allergic Reaction or Rash AEs included Allergy to Arthropod Sting, Anaphylactoid Reaction, Anaphylactic Reaction, Anaphylatic Shock, Anaphylactoid Shock, Angioedema, Conjunctivitis Allergic, Contrast Media Reaction, Dermatitis, Dermatitis Allergic, Dermatitis Atopic, Dermatitis Bullous, Dermatitis Contact, Dermatitis Psoriasiform, Drug Hypersensitivity, Eczema, Eosinophila, Erythema, Eye Allergy, Face Oedema, Hypersensitivity, Mechanical Urticaria, Palmar Erythema, Periorbital Oedema, Photodermatosis, Photosensitivity Allergic reaction, Photosensitivity Reaction, Pigmentation Disorder, Pruritus, Pruritus Generalised, Rash, Rash Erythematous, Rash Follicular, Rash Generalised, Rash Maculo-Papular, Rash Papulosquamous, Rash Pruritic, Rash Pustular, Rash Vesicular, Rhinitis, Rhinitis Allergic, Rosacea, Skin Exfoliation, Skin Disorder, Skin Hyperpigmentation, Skin Lesion, Skin Mass, Skin Ulcer, Subcutaneous Nodule, Swelling Face, Systemic Lupus Erythematosus Rash, Urticaria. (NCT02550288)
Timeframe: up to 14 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg2.9
Atorvastatin 20 mg2.9
Ezetimibe 10 mg + Atorvastatin 10 mg0.0
Ezetimibe 10 mg + Atorvastatin 20 mg1.4

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) at Week 12

Participants had LDL-C levels assessed at baseline and after 12 weeks of study drug administration. The change from baseline was calculated. (NCT02550288)
Timeframe: Baseline and Week 12

InterventionPercentage Change (Least Squares Mean)
Ezetimibe 10 mg-19.3
Atorvastatin 10 mg-44.0
Atorvastatin 20 mg-49.1
Ezetimibe 10 mg + Atorvastatin 10 mg-55.6
Ezetimibe 10 mg + Atorvastatin 20 mg-59.2

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Percentage of Participants Who Experience Consecutive Elevations in AST ≥10 Times ULN

Participants had AST levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of AST that were 10x ULN or greater were recorded. The AST ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in Alanine Aminotransferase (ALT) ≥3 Times Upper Limit of Normal (ULN)

Participants had ALT levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of ALT that were 3 x ULN or greater were recorded. The ALT ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in ALT and/or AST ≥3 Times ULN

Participants had ALT and AST levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of ALT and/or AST that were 3 x ULN or greater were recorded. The ALT and AST ULNs were 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants With Potential Hy's Law Condition

Percentage of Participants with Potential Hy's Law Condition (defined as serum ALT or serum AST elevations >3xULN, with serum alkaline phosphatase <2xULN and total bilirubin (TBL) ≥2xULN) was summarized. The ALT and AST ULNs were 40 U/L. The ULN for alkaline phosphatase was 359 IU/L and the ULN for total bilirubin was 1.2 mg/dL. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg0.0
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in Aspartate Aminotransferase (AST) ≥3 Times ULN

Participants had AST levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of AST that were 3 x ULN or greater were recorded. The AST ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in AST ≥5 Times ULN

Participants had AST levels assessed throughout the 12 week treatment period. Participants who had an assessment of AST that was 5x ULN or greater were recorded. AST ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Have Consecutive Elevations in ALT and/or AST ≥10 Times ULN

Participants had ALT and AST levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of ALT and/or AST that were 10x ULN or greater were recorded. The ALT and AST ULNs were 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Have Consecutive Elevations in ALT and/or AST ≥5 Times ULN

Participants had ALT and AST levels assessed throughout the 12 week treatment period. Participants who had 2 consecutive assessments of ALT and/or AST that were 5 x ULN or greater were recorded. The ALT and AST ULNs were 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Have Elevations in CK ≥10xULN With Muscle Symptoms

Participants had CK levels assessed throughout the 12 week treatment period. Participants who had any CK level that was ≥10 x ULN and had associated muscle symptoms present within +/- 7 days were recorded. The CK ULNs for males and females were 287 IU/L and 163 IU/L, respectively. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg0.0
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Have Elevations in Creatine Kinase (CK) ≥10xULN

Participants had creatine phosphokinase (CK) levels assessed throughout the 12 week treatment period. Participants who had any CK level that was ≥10 x ULN were recorded. The CK ULNs for males and females were 287 IU/L and 163 IU/L, respectively. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg1.4
Ezetimibe 10 mg + Atorvastatin 10 mg0.0
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in ALT ≥5 Times ULN

Participants had ALT levels assessed throughout the 12 week treatment period. Participants who had an assessment of ALT that was 5x ULN or greater were recorded. The ALT ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg1.5
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Percentage of Participants Who Experience Consecutive Elevations in ALT ≥10 Times ULN

Participants had ALT levels assessed throughout the 12 week treatment period. Participants who had an assessment of ALT that was 10x ULN or greater were recorded. The ALT ULN was 40 U/L. (NCT02550288)
Timeframe: up to 12 weeks

InterventionPercentage of Participants (Number)
Ezetimibe 10 mg0.0
Atorvastatin 10 mg0.0
Atorvastatin 20 mg0.0
Ezetimibe 10 mg + Atorvastatin 10 mg0.0
Ezetimibe 10 mg + Atorvastatin 20 mg0.0

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Changes in the Inflammatory Marker IL-6

Switching the PI by raltegravir, plus Kivexa or Truvada for 24 weeks. After that, atorvastatin, 20mg/day has been added for 48 weeks. (intergroup and intragroup) (NCT02577042)
Timeframe: baseline, wk24 and wk72

,
Interventionpg/mL (Mean)
Baselineweek 24week 72
PI-based Regimen + Atorvastatin40.041.141.7
Raltegravir + Atorvastatin42.539.343.2

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Changes in Plasma Soluble Markers (D-dimer)

Changes in plasma soluble markers (D-dimer) (NCT02577042)
Timeframe: baseline, wk24 and wk72

,
Interventionng/mL (Median)
Baselinewk24wk72
PI-based Regimen + Atorvastatin199019171868
Raltegravir + Atorvastatin174318442051

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Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W6.8
Alirocumab 150 mg Q2W9.1
Placebo Q2W2.9

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Percent Change From Baseline in Apolipoprotein B (Apo-B) at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-32.2
Alirocumab 150 mg Q2W-57.9
Placebo Q2W-6.0

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Percent Change From Baseline in Calculated LDL-C at Week 12- Intent to Treat (ITT) Analysis

Adjusted Least-squares (LS) means and standard errors at Week 12 were obtained from a mixed-effect model with repeated measures (MMRM) to account for missing data. All available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment were used in the model (ITT analysis). (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-43.8
Alirocumab 150 mg Q2W-70.1
Placebo Q2W-4.3

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Percent Change From Baseline in Calculated LDL-C at Week 12- On-Treatment Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 12 (i.e. up to 21 days after last double-blind injection). (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-43.4
Alirocumab 150 mg Q2W-70.1
Placebo Q2W-2.8

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Percent Change From Baseline in Calculated LDL-C to Averaged Week 10 to 12- On-Treatment Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 12 (i.e. up to 21 days after last double-blind injection) and assigning a weight of 0.5 for Week 10 and 12 time points. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-54.0
Alirocumab 150 mg Q2W-69.9
Placebo Q2W-2.6

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Percent Change From Baseline in Calculated LDL-C to Averaged Week 10 to 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment and assigning a weight of 0.5 for Week 10 and 12 time points. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-54.2
Alirocumab 150 mg Q2W-69.9
Placebo Q2W-3.7

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Percent Change From Baseline in Fasting Triglycerides (TGs) at Week 12: ITT Analysis

Adjusted means and standard errors at Week 12 from multiple imputation approach followed by robust regression model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Mean)
Alirocumab 150 mg Q4W-0.6
Alirocumab 150 mg Q2W-18.0
Placebo Q2W-6.4

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Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Analysis

Adjusted means and standard errors at Week 12 were obtained from multiple imputation approach followed by robust regression model for handling of missing data. All available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment were included in the imputation model. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Mean)
Alirocumab 150 mg Q4W-31.7
Alirocumab 150 mg Q2W-49.6
Placebo Q2W1.3

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-36.2
Alirocumab 150 mg Q2W-61.1
Placebo Q2W-4.9

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Percent Change From Baseline in Total Cholesterol (Total-C) at Week 12- ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-25.8
Alirocumab 150 mg Q2W-44.7
Placebo Q2W-3.3

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Percentage of Participants Reaching Calculated LDL-C Goal at Week 12- ITT Analysis

Calculated LDL-C goal was defined as calculated LDL-C <100 mg/dL (2.59 mmol/L) for heterozygous familiar hypercholesterolemia (heFH) participants or non-familial hypercholesterolemia (non-FH) participants who had a history of documented CHD, or <120 mg/dL (3.10 mmol/L) for non-FH participants who had a history of documented diseases or other risk factors as defined in JAS Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases 2012. Adjusted percentages at Week 12 were obtained from multiple imputation approach for handling of missing data. All available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment were included in the imputation model. (NCT02584504)
Timeframe: Up to Week 12

Interventionpercentage of participants (Number)
Alirocumab 150 mg Q4W85.2
Alirocumab 150 mg Q2W96.2
Placebo Q2W14.3

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Percentage of Participants Reaching Calculated LDL-C Goal at Week 12- On-Treatment Analysis

Calculated LDL-C goal was defined as calculated LDL-C <100 mg/dL (2.59 mmol/L) for heFH participants or non-FH participants who had a history of documented CHD, or <120 mg/dL (3.10 mmol/L) for non-FH participants who had a history of documented diseases or other risk factors as defined in JAS Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases 2012. Adjusted percentages at Week 12 from multiple imputation approach including available post-baseline on-treatment data from Week 4 to Week 12 (i.e. up to 21 days after last double-blind injection). (NCT02584504)
Timeframe: Up to Week 12

Interventionpercentage of participants (Number)
Alirocumab 150 mg Q4W85.2
Alirocumab 150 mg Q2W96.2
Placebo Q2W10.8

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Percent Change From Baseline in Calculated LDL-C at Week 20, 24, 36, 48 and 64 -OLTP Analysis

(NCT02584504)
Timeframe: Baseline, Weeks 20, 24, 36, 48 and 64

,,
InterventionPercent change (Mean)
Week 20Week 24Week 36Week 48Week 64
Alirocumab 150mg Q4W/Up Q2W (After Placebo Q2W in DBTP)-45.5-47.8-56.2-57.8-58.1
Alirocumab 150mgQ4W/Up Q2W(After Alirocumab 150mgQ2W in DBTP)-47.8-46.0-51.5-53.9-55.2
Alirocumab 150mgQ4W/Up Q2W(After Alirocumab 150mgQ4W in DBTP)-42.1-39.7-49.2-48.6-44.3

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Percent Change From Baseline in Apo-B at Week 12- On-Treatment Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data at from Week 4 to Week 12 (i.e. up to 21 days after last double-blind injection). (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-31.8
Alirocumab 150 mg Q2W-58.0
Placebo Q2W-4.6

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Percent Change From Baseline in Non-HDL-C at Week 12- On-treatment Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including available post-baseline on-treatment data from Week 4 to Week 12 (i.e. up to 21 days after last double-blind injection). (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W-35.9
Alirocumab 150 mg Q2W-61.1
Placebo Q2W-3.5

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Week 12- ITT Analysis

Adjusted LS means and standard errors at Week 12 from MMRM model including all available post-baseline data from Week 4 to Week 12 regardless of status on- or off-treatment. (NCT02584504)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab 150 mg Q4W7.7
Alirocumab 150 mg Q2W9.9
Placebo Q2W2.0

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Change in Glucose From Baseline Over Time Between and Within Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmmol/L (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 (Week 76)Visit 18 (Week 100)LVTFollow-up
High-Intensity Statin Therapy+Placebo7.3857.8357.8007.8407.8907.7957.595
High-Intensity Statin Therapy+RVX0002227.5907.9257.9007.9208.0108.1007.650

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Change in Estimated Glomerular Filtration Rate (eGFR) From Baseline Over Time Within and Between Treatment Groups for Subjects With Impaired Renal Function at Baseline (eGFR <60 mL/Min/1.7m2)

(NCT02586155)
Timeframe: 120 weeks

,
Interventionml/min (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 (Week 76)Visit 18 (Week 100)LVT
High-Intensity Statin Therapy+Placebo48.953.352.554.856.753.9
High-Intensity Statin Therapy+RVX00022251.453.052.450.846.552.5

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Incidence of All-cause Mortality

(NCT02586155)
Timeframe: 120 weeks

InterventionParticipants (Count of Participants)
High-Intensity Statin Therapy+RVX00022261
High-Intensity Statin Therapy+Placebo72

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Change in Apolipoprotein A1 (ApoA-I) Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmg/dL (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 (Week 76)Visit 18 (Week 100)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo117.5125.0124.0125.0125.0129.0127.0
High-Intensity Statin Therapy+RVX000222119.0128.0129.0132.0131.0132.5131.0

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Incidence of First Occurrence of Adjudication-Confirmed Four-Point MACE

First occurrence of four-point MACE defined as a single composite endpoint of cardiovascular (CV) death (including undetermined cause of death) or non-fatal myocardial infarction (MI), stroke or hospital admission for congestive heart failure. (NCT02586155)
Timeframe: 120 weeks

,
Interventionevents (Number)
CV Death (CVD)Non-fatal MIStrokeFirst Hospitalization for CHF
High-Intensity Statin Therapy+Placebo55941748
High-Intensity Statin Therapy+RVX00022245771729

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Incidence of Hospitalization for Congestive Heart Failure (CHF)

(NCT02586155)
Timeframe: 120 weeks

Interventionevents (Number)
High-Intensity Statin Therapy+RVX00022229
High-Intensity Statin Therapy+Placebo48

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Change in C Reactive Protein (CRP) Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 52 weeks

,
Interventionmg/dL (Median)
BaselineVisit 8 (Week 12)Visit 14 (Week 52)
High-Intensity Statin Therapy+Placebo2.7401.8051.580
High-Intensity Statin Therapy+RVX0002222.8751.7551.710

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Incidence of First Occurrence of Adjudication-confirmed Narrowly Defined MACE

Incidence of first occurrence of MACE narrowly defined as a single composite endpoint of Cardiovascular (CV) Death (including undetermined cause of death) or Non-fatal Myocardial Infarction (MI) or Stroke. If a subject has multiple events, only the first event contributing to the composite endpoint is counted. (NCT02586155)
Timeframe: 120 weeks

,
Interventionevents (Number)
CV DeathNon-fatal MIStroke
High-Intensity Statin Therapy+Placebo429215
High-Intensity Statin Therapy+RVX000222347615

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Incidence of First Occurrence of Adjudication-confirmed Broadly Defined MACE

First occurrence of MACE broadly defined as a single composite endpoint of Cardiovascular Death (CVD) (including undetermined cause of death) or Non-fatal Myocardial Infarction (MI), Stroke, or Hospitalization for CVD events (including unstable angina and evidence of new or presumed new progressive obstructive coronary disease or emergency revascularization procedures at any time and urgent revascularization procedures ≥30 days after the index event as defined by Hicks et al., 2014) . If a subject has multiple events, only the first event contributing to the composite endpoint is counted. (NCT02586155)
Timeframe: 120 weeks

,
Interventionevents (Number)
CV DeathNon-fatal MIHospitalization for CVD eventsStroke
High-Intensity Statin Therapy+Placebo42911815
High-Intensity Statin Therapy+RVX00022233742215

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Change in Alkaline Phosphatase (ALP) From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 172 weeks

,
InterventionU/L (Median)
BaselineVisit 3 (Week 2)Visit 4 (Week 4)Visit 5 (Week 6)Visit 6 (Week 8)Visit 7 (Week 10)Visit 8 (Week 12)Visit 9 (Week 16)Visit 10 (Week 20)Visit 11 (Week 24)Visit 12 (Week 28)Visit 13 (Week 40)Visit 14 (Week 52)Visit 15 (Week 64)Visit 16 (Week 76)Visit 17 (Week 88)Visit 18 (Week 100)Visit 19 (Week 112)Visit 20 (Week 124)Visit 21 (Week 136)Visit 22 (Week 148)Visit 23 (Week 160)Visit 24 (Week 172)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo77.076.075.075.076.075.075.075.074.075.074.074.076.074.576.076.075.075.077.077.076.078.083.077.076.0
High-Intensity Statin Therapy+RVX00022278.071.070.070.069.069.069.068.068.068.069.069.071.071.070.072.072.071.071.069.569.068.075.572.076.0

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Change in Triglyceride (TG) Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmmol/L (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 Week 76)Visit 18 Week 100)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo1.6901.6701.7001.6701.6101.6501.720
High-Intensity Statin Therapy+RVX0002221.6301.6601.7351.7301.7551.7001.650

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Change in LDL-C Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmmol/L (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 Week 76)Visit 18 Week 100)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo1.6901.5301.6551.6601.7251.7451.680
High-Intensity Statin Therapy+RVX0002221.6901.5301.5901.6001.6601.7001.650

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Change in Hemoglobin (Hb) A1c From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Intervention% of hemoglobin (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 (Week 76)Visit 18 (Week 100)LVTFollow-up
High-Intensity Statin Therapy+Placebo7.307.207.307.407.307.307.20
High-Intensity Statin Therapy+RVX0002227.407.207.307.307.307.407.30

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Change in HDL-C Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmmol/L (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 Week 76)Visit 18 Week 100)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo0.8600.9400.9300.9200.9100.9600.950
High-Intensity Statin Therapy+RVX0002220.8700.9700.9700.9600.9700.9901.010

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Change in Apolipoprotein B (apoB) Concentration From Baseline Over Time Within and Between Treatment Groups

(NCT02586155)
Timeframe: 120 weeks

,
Interventionmg/dL (Median)
BaselineVisit 11 (Week 24)Visit 14 (Week 52)Visit 16 (Week 76)Visit 18 (Week 100)Last Visit on Treatment (LVT)Follow-up
High-Intensity Statin Therapy+Placebo66.068.068.069.072.072.071.0
High-Intensity Statin Therapy+RVX00022266.068.570.070.570.568.070.0

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The Effect of Obeticholic Acid on LDL Particle Concentration (Total) (Least Squares Mean Change From Baseline at Week 16)

The effect of Obeticholic Acid on LDL metabolism in subjects with biopsy confirmed nonalcoholic NASH and the ability of atorvastatin to modulate this effect as measured by change (least squares mean) from baseline at week 16 in LDL particle concentration (total) (NCT02633956)
Timeframe: Baseline and Week 16

Interventionnmol/L (Least Squares Mean)
5 mg Obeticholic Acid-224.79
10 mg Obeticholic Acid-325.04
25 mg Obeticholic Acid-336.22
Placebo-439.84

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The Effect of Obeticholic Acid on LDL Particle Size (Least Squares Mean Change From Baseline at Week 16)

The effect of Obeticholic Acid on LDL metabolism in subjects with biopsy confirmed NASH and the ability of atorvastatin to modulate this effect as measured by change from baseline (least squares mean) at week 16 in LDL particle size. It is LDL particle diameter size (nm) that is reported. (NCT02633956)
Timeframe: Baseline and Week 16

Interventionnm (Least Squares Mean)
5 mg Obeticholic Acid0.02
10 mg Obeticholic Acid-0.41
25 mg Obeticholic Acid-0.09
Placebo-0.49

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The Effect of Obeticholic Acid on Low-density Lipoprotein (LDL) Concentration (Least Squares Mean Change From Baseline at Week 16)

The effect of Obeticholic Acid on LDL metabolism in subjects with biopsy confirmed nonalcoholic steatohepatitis (NASH) and the ability of atorvastatin to modulate this effect as measured by change (least squares mean) from baseline at week 16 in LDL concentration (NCT02633956)
Timeframe: Baseline and Week 16

Interventionmg/dL (Least Squares Mean)
5 mg Obeticholic Acid-33.2
10 mg Obeticholic Acid-44.27
25 mg Obeticholic Acid-39.54
Placebo-53.33

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Percent Change From Baseline in LDL-C at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W4.94
Placebo QM0.99
Evolocumab Q2W-65.35
Evolocumab QM-69.05

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Percentage of Participants With LDL-C Less Than 70 mg/dL (1.8 mmol/L) at Week 12

(NCT02662569)
Timeframe: Week 12

Interventionpercentage of participants (Number)
Placebo Q2W20.9
Placebo QM21.3
Evolocumab Q2W88.2
Evolocumab QM90.2

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Percent Change From Baseline in HDL-C at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W2.57
Placebo QM6.04
Evolocumab Q2W8.45
Evolocumab QM14.18

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Percent Change From Baseline in Apolipoprotein B100 at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W3.17
Placebo QM-0.26
Evolocumab Q2W-53.90
Evolocumab QM-49.68

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Percent Change From Baseline in Apolipoprotein B100 at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W1.97
Placebo QM-1.52
Evolocumab Q2W-54.96
Evolocumab QM-56.37

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Percent Change From Baseline in Total Cholesterol at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W2.89
Placebo QM-0.25
Evolocumab Q2W-38.64
Evolocumab QM-39.74

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Percent Change From Baseline in Total Cholesterol at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W4.40
Placebo QM0.67
Evolocumab Q2W-37.82
Evolocumab QM-35.22

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Percent Change From Baseline in HDL-C at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W1.25
Placebo QM5.88
Evolocumab Q2W7.59
Evolocumab QM13.75

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Percent Change From Baseline in LDL-C at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W7.10
Placebo QM2.63
Evolocumab Q2W-64.66
Evolocumab QM-62.30

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Percent Change From Baseline in Apolipoprotein B100/Apolipoprotein A1 Ratio at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W3.23
Placebo QM-0.10
Evolocumab Q2W-54.98
Evolocumab QM-51.80

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Percent Change From Baseline in Apolipoprotein B100/Apolipoprotein A1 Ratio at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W2.60
Placebo QM-1.02
Evolocumab Q2W-55.60
Evolocumab QM-57.75

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Percent Change From Baseline in Non-HDL-C at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W5.87
Placebo QM1.30
Evolocumab Q2W-55.76
Evolocumab QM-52.92

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Percent Change From Baseline in Non-HDL-C at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W4.33
Placebo QM0.33
Evolocumab Q2W-56.57
Evolocumab QM-59.08

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Percent Change From Baseline in Lipoprotein(a) at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W26.53
Placebo QM7.47
Evolocumab Q2W-35.93
Evolocumab QM-37.85

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Percent Change From Baseline in Lipoprotein(a) at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W16.89
Placebo QM8.48
Evolocumab Q2W-38.63
Evolocumab QM-42.29

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Percentage of Participants With Mean LDL-C at Weeks 10 and 12 of Less Than 70 mg/dL (1.8 mmol/L)

(NCT02662569)
Timeframe: Weeks 10 and 12

Interventionpercentage of participants (Number)
Placebo Q2W21.7
Placebo QM19.4
Evolocumab Q2W90.1
Evolocumab QM91.3

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Change From Baseline in LDL-C at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionmg/dL (Least Squares Mean)
Placebo Q2W-0.3
Placebo QM-7.3
Evolocumab Q2W-63.9
Evolocumab QM-66.1

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Percent Change From Baseline in VLDL-C at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W9.63
Placebo QM7.92
Evolocumab Q2W-17.55
Evolocumab QM-16.09

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Percent Change From Baseline in Triglycerides at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W10.50
Placebo QM8.07
Evolocumab Q2W-5.91
Evolocumab QM-4.24

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Change From Baseline in LDL-C at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionmg/dL (Least Squares Mean)
Placebo Q2W-2.1
Placebo QM-8.8
Evolocumab Q2W-64.6
Evolocumab QM-71.9

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Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W3.03
Placebo QM-2.03
Evolocumab Q2W-41.06
Evolocumab QM-45.70

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Percent Change From Baseline in Triglycerides at the Mean of Weeks 10 and 12

(NCT02662569)
Timeframe: Baseline and weeks 10 and 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W11.54
Placebo QM8.48
Evolocumab Q2W-6.48
Evolocumab QM-7.15

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Percent Change From Baseline in Total Cholesterol/HDL-C Ratio at Week 12

(NCT02662569)
Timeframe: Baseline and week 12

Interventionpercent change (Least Squares Mean)
Placebo Q2W3.22
Placebo QM-1.22
Evolocumab Q2W-40.72
Evolocumab QM-41.78

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Pharmacokinetics (PK): Maximum Plasma Concentration (Cmax) of LY3202328 (LY) in Part A After a Single Dose

Pharmacokinetics (PK) is the maximum plasma concentration (Cmax) of LY3202328 Part A after a single dose. (NCT02714569)
Timeframe: Predose, 0.5, 1, 2, 3, 4, 6, 8, 12, 24, 48, 96 hours Postdose

Interventionnanogram/milliliter (ng/mL) (Geometric Mean)
Part A: 1 mg LY48.258
Part A: 3 mg LY105.023
Part A: 10 mg LY340.829
Part A: 30 mg LY581.782
Part A: 100 mg LY1600.953
Part A: 300 mg LY1632.595
Part A: 600 mg LY2866.855
Part A: 30 mg LY Fed1105.999

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PD: Change From Baseline to Last Day of Dosing in Fasting Total Triglycerides in Part B

PD is the change from baseline to last day of dosing in fasting total triglycerides in Part B. (NCT02714569)
Timeframe: Predose, Days 7, 14, 21, and 28 Postdose

Interventionmmol/L (Mean)
Part B: Placebo0.205
Part B: 5 mg LY-0.131
Part B: 20 mg LY-0.231
Part B: 100 mg LY0.020
Part B: 300 mg LY-0.480

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PD: Change From Baseline to Last Day of Dosing in Fasting Total Cholesterol in Part B

PD is the change from baseline to last day of dosing in fasting total cholesterol in Part B. (NCT02714569)
Timeframe: Predose, Days 7, 14, 21, and 28 Postdose

Interventionmmol/L (Mean)
Part B: Placebo0.206
Part B: 5 mg LY0.118
Part B: 20 mg LY0.183
Part B: 100 mg LY0.174
Part B: 300 mg LY-0.190

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PD: Change From Baseline to Last Day of Dosing in Fasting LDL-c in Part B

PD is the change from baseline to last day of dosing in fasting LDL-c in Part B. (NCT02714569)
Timeframe: Predose, Days 7, 14, 21, and 28 Postdose

Interventionmmol/L (Mean)
Part B: Placebo0.103
Part B: 5 mg LY0.184
Part B: 20 mg LY0.388
Part B: 100 mg LY0.227
Part B: 300 mg LY0.131

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PD: Change From Baseline to Last Day of Dosing in Fasting HDL-c in Part B

PD is the change from baseline to last day of dosing in fasting HDL-c in Part B. (NCT02714569)
Timeframe: Predose, Days 7, 14, 21, and 28 Postdose

Interventionmmol/L (Mean)
Part B: Placebo0.008
Part B: 5 mg LY-0.010
Part B: 20 mg LY-0.101
Part B: 100 mg LY-0.107
Part B: 300 mg LY-0.101

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PD: Change From Baseline to in Fasting Total Cholesterol in Part A

PD is the change from baseline in fasting total cholesterol in Part A. (NCT02714569)
Timeframe: Predose, 24, 28, 96 Hours Postdose

,,,,,,,
Interventionmmol/L (Mean)
24 Hours48 Hours96 Hours
Part A: 1 mg LY-0.186-0.436-0.527
Part A: 10 mg LY-0.203-0.376-0.609
Part A: 100 mg LY0.2850.091-0.317
Part A: 3 mg LY-0.013-0.030-0.207
Part A: 30 mg LY0.073-0.013-0.199
Part A: 300 mg LY0.2030.134-0.155
Part A: 600 mg LY0.093-0.026-0.041
Part A: Placebo0.085-0.085-0.318

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PK: Steady State Tmax of LY3202328 (LY) in Part B

PK is the Tmax of LY3202328 at steady state in Part B. (NCT02714569)
Timeframe: Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

Interventionhr (Median)
Part B: 5 mg LY2.00
Part B: 20 mg LY4.20
Part B: 100 mg LY3.00
Part B: 300 mg LY3.04

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PK: Steady State Maximum Plasma Concentration (Cmax) of LY3202328 (LY) in Part B

PK is the maximum plasma concentration of LY3202328 (Cmax) at steady state in Part B. (NCT02714569)
Timeframe: Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

Interventionng/ml (Geometric Mean)
Part B: 5 mg LY445.858
Part B: 20 mg LY882.125
Part B: 100 mg LY3687.167
Part B: 300 mg LY3209.396

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PK: Cmax of Atorvastatin With/Without LY3202328 (LY) in Part B

PK: Cmax of Atorvastatin with/without LY3202328 (LY) Co-administration in Part B. (NCT02714569)
Timeframe: Day -7 and Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

,
Interventionng/mL (Geometric Mean)
Placebo5 mg LY20 mg LY100 mg LY300 mg LY
Atorvastatin Alone (Reference)3.5753.6211.2863.1051.376
Atorvastatin With LY (Test)3.4792.8401.2382.5111.489

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PK: AUC (0-t) of Atorvastatin With/Without LY3202328 (LY) in Part B

PK: AUC (0-t) of Atorvastatin with/without LY3202328 (LY) Co-administration in Part B. AUC from time 0 to time t, where t is the time of last quantifiable plasma concentration. (NCT02714569)
Timeframe: Day -7 and Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

,
Interventionhr*ng/ml (Geometric Mean)
Placebo5 mg LY20 mg LY100 mg LY300 mg LY
Atorvastatin Alone (Reference)16.51814.9137.95213.2079.111
Atorvastatin With LY (Test)15.87417.3117.92111.9837.748

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PK: Area Under Concentration Curve From Zero to Time (AUC [0-t]) of Simvastatin With/Without LY3202328 (LY) in Part B

PK: Area Under Concentration Curve From Zero to Time (AUC [0-t]) of Simvastatin with/without LY3202328 (LY) Co-administration in Part B. AUC from time 0 to time t, where t is the time of last quantifiable plasma concentration. (NCT02714569)
Timeframe: Day -7 and Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

,
Interventionhr*ng/ml (Geometric Mean)
Placebo5 mg LY20 mg LY100 mg LY300 mg LY
Simvastatin Alone (Reference)6.2509.2877.96010.4348.951
Simvastatin With LY (Test)9.6486.6689.69714.26911.908

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Pharmacodynamics (PD): Change From Baseline in Fasting High-Density Lipoprotein Cholesterol (HDL-c) in Part A

Pharmacodynamics (PD) is the change from Baseline in Fasting High-Density Lipoprotein Cholesterol (HDL-c) in Part A. (NCT02714569)
Timeframe: Predose, 24, 48, 96 Hours Postdose

,,,,,,,
Interventionmillimole/Liter (mmol/L) (Mean)
24 Hours48 Hours96 Hours
Part A: 1 mg LY-0.030-0.039-0.073
Part A: 10 mg LY-0.047-0.043-0.134
Part A: 100 mg LY0.0520.019-0.091
Part A: 3 mg LY-0.0430.009-0.086
Part A: 30 mg LY-0.026-0.026-0.030
Part A: 300 mg LY-0.004-0.009-0.082
Part A: 600 mg LY0.010-0.052-0.005
Part A: Placebo-0.003-0.037-0.074

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PK: Cmax of Simvastatin With/Without LY3202328 (LY) in Part B

PK: Cmax of Simvastatin with/without LY3202328 (LY) Co-administration in Part B. (NCT02714569)
Timeframe: Day -7 and Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

,
Interventionng/ml (Geometric Mean)
Placebo5 mg LY20 mg LY100 mg LY300 mg LY
Simvastatin Alone (Reference)2.0613.3743.2744.3031.979
Simvastatin With LY (Test)2.9062.3883.5764.6344.221

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PD: Change From Baseline in Fasting Low-Density Lipoprotein Cholesterol (LDL-c) in Part A

PD is the change from baseline in fasting low-density lipoprotein cholesterol (LDL-c) Part A. (NCT02714569)
Timeframe: Predose, 24, 48, 96 Hours Postdose

,,,,,,,
Interventionmmol/L (Mean)
24 Hours48 Hours96 Hours
Part A: 1 mg LY0.025-0.275-0.358
Part A: 10 mg LY0.020-0.214-0.481
Part A: 100 mg LY0.4710.419-0.020
Part A: 3 mg LY0.1170.013-0.061
Part A: 30 mg LY0.2410.203-0.018
Part A: 300 mg LY0.2360.2450.075
Part A: 600 mg LY0.163-0.0010.038
Part A: Placebo0.2310.111-0.109

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PK: Time to Maximum Concentration (Tmax) of LY3202328 (LY) in Part A

PK is the time to maximum concentration (Tmax) of LY3202328 in Part A (NCT02714569)
Timeframe: Day 1: Predose, 0.5, 1, 2, 3, 4, 6, 8, 12, 24, 48, 96 hours Postdose

Interventionhour (hr) (Median)
Part A: 1 mg LY2.02
Part A: 3 mg LY3.52
Part A: 10 mg LY4.0
Part A: 30 mg LY4.00
Part A: 100 mg LY6.00
Part A: 300 mg LY4.02
Part A: 600 mg LY4.00
Part A: 30 mg LY Fed5.00

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PK: Steady State Area Under the Serum Concentration-Time Curve During the Dosing Interval (AUCτ) of LY3202328 (LY) in Part B

PK is the area under the serum concentration-time curve (AUCτ) of LY3202328 at steady state during the dosing interval in Part B. (NCT02714569)
Timeframe: Day 28: Predose, 0.5, 1, 2, 4, 4.5, 5, 6, 8, 12, 24 hours Postdose

Interventionhour*nanogram/milliliter(hr*ng/ml) (Geometric Mean)
Part B: 5 mg LY7587.24
Part B: 20 mg LY13362.44
Part B: 100 mg LY67499.80
Part B: 300 mg LY50774.85

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PK: Area Under the Serum Concentration Time Curve From Zero to Infinity (AUC[0-∞]) of LY3202328 (LY) in Part A After a Single Dose

PK is the area under the serum concentration time curve from zero to Infinity (AUC[0-∞]) of LY3202328 in Part A after a single dose. (NCT02714569)
Timeframe: Day 1: Predose, 0.5, 1, 2, 3, 4, 6, 8, 12, 24, 48, 96 hours Postdose

Interventionng/mL (Geometric Mean)
Part A: 1 mg LYNA
Part A: 3 mg of LYNA
Part A: 10 mg LY7726.17
Part A: 30 mg LY17018.43
Part A: 100 mg of LY55406.24
Part A: 300 mg LY66185.70
Part A: 600 mg LYNA
Part A: 30 mg LY Fed28415.22

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PD: Change From Baseline in Fasting Total Triglycerides Part A

PD is the change from baseline in fasting total triglycerides in Part A. (NCT02714569)
Timeframe: Predose, 24, 48, 96 Hours Postdose

,,,,,,,
Interventionmmol/L (Mean)
24 Hours48 Hours96 Hours
Part A: 1 mg LY-0.397-0.269-0.209
Part A: 10 mg LY-0.386-0.2600.013
Part A: 100 mg LY-0.523-0.766-0.455
Part A: 3 mg LY-0.190-0.115-0.132
Part A: 30 mg LY-0.311-0.418-0.331
Part A: 300 mg LY-0.064-0.226-0.326
Part A: 600 mg LY-0.302-0.1980.158
Part A: Placebo-0.276-0.320-0.239

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Percentage of Participants Reaching Calculated Low Density Lipoprotein Cholesterol <70 mg/dL (1.81 mmol/L) at Week 24: On-Treatment Analysis

Adjusted percentages at Week 24 were obtained from multiple imputation approach including all available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT02715726)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe 10 mg42.1
Alirocumab 75 mg Q2W/up to 150 mg Q2W87.0

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Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline data from Week 4 up to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-13.8
Alirocumab 75 mg Q2W/up to 150 mg Q2W-33.9

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 24: On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-20.4
Alirocumab 75 mg Q2W/up to 150 mg Q2W-49.1

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-20.7
Alirocumab 75 mg Q2W/up to 150 mg Q2W-47.4

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Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 24: On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg-21.3
Alirocumab 75 mg Q2W/up to 150 mg Q2W-58.7

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24: ITT Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-19.4
Alirocumab 75 mg Q2W/up to 150 mg Q2W-47.0

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Percent Change From Baseline in Fasting Triglycerides at Week 12: ITT Analysis

Adjusted means and standard errors at Week 12 were obtained by using multiple imputation approach followed by a robust regression model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent change (Mean)
Ezetimibe 10 mg-13.585
Alirocumab 75 mg Q2W/up to 150 mg Q2W-9.965

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Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Analysis

Adjusted means and standard errors at Week 12 were obtained from multiple imputation approach followed by robust regression model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent Change (Mean)
Ezetimibe 10 mg6.313
Alirocumab 75 mg Q2W/up to 150 mg Q2W-30.064

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Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 24: ITT Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg6.5
Alirocumab 75 mg Q2W/up to 150 mg Q2W8.3

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Percent Change From Baseline in High Density Lipoprotein Cholesterol at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg6.1
Alirocumab 75 mg Q2W/up to 150 mg Q2W7.3

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Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 12: On-Treatment Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg-22.7
Alirocumab 75 mg Q2W/up to 150 mg Q2W-58.1

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Percent Change From Baseline in Apolipoprotein B at Week 24: On-Treatment Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline on-treatment data from Week 4 to Week 24 (i.e. up to 21 days after last injection or 3 days after the last capsule, whichever came first) (on-treatment analysis). (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-17.4
Alirocumab 75 mg Q2W/up to 150 mg Q2W-45.2

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Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-16.5
Alirocumab 75 mg Q2W/up to 150 mg Q2W-43.0

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Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Analysis

Adjusted means and standard errors at Week 24 were obtained by using multiple imputation approach followed by robust regression model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent change (Mean)
Ezetimibe 10 mg-14.409
Alirocumab 75 mg Q2W/up to 150 mg Q2W-14.462

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Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-16.2
Alirocumab 75 mg Q2W/up to 150 mg Q2W-43.5

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Percent Change From Baseline in Apolipoprotein A-1 at Week 12 : ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg1.1
Alirocumab 75 mg Q2W/up to 150 mg Q2W3.7

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Percent Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 24: ITT Analysis

Adjusted LS means and standard errors at Week 24 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg-0.2
Alirocumab 75 mg Q2W/up to 150 mg Q2W3.2

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Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 24: Intent-to-treat (ITT) Analysis

Adjusted least square (LS) means and standard errors at Week 24 were obtained from mixed models analysis with repeated measures (MMRM) to account for missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were used in the model (ITT analysis). (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg-20.3
Alirocumab 75 mg Q2W/up to 150 mg Q2W-56.0

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Percent Change From Baseline in Lipoprotein (a) (Lp[a]) at Week 24: ITT Analysis

Adjusted means and standard errors at Week 24 were obtained from multiple imputation approach followed by robust regression model for handling missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were included in the imputation model. (NCT02715726)
Timeframe: From Baseline to Week 24

Interventionpercent Change (Mean)
Ezetimibe 10 mg3.956
Alirocumab 75 mg Q2W/up to 150 mg Q2W-30.317

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Percent Change From Baseline in Calculated Low Density Lipoprotein Cholesterol at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Ezetimibe 10 mg-22.2
Alirocumab 75 mg Q2W/up to 150 mg Q2W-57.1

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Percent Change From Baseline in Total Cholesterol at Week 12: ITT Analysis

Adjusted LS means and standard errors at Week 12 were obtained from MMRM model including all available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment. (NCT02715726)
Timeframe: From Baseline to Week 12

Interventionpercent Change (Least Squares Mean)
Ezetimibe 10 mg-14.9
Alirocumab 75 mg Q2W/up to 150 mg Q2W-34.2

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Percentage of Participants Reaching Calculated Low Density Lipoprotein Cholesterol <70 mg/dL (1.81 mmol/L) at Week 24: ITT Analysis

Adjusted percentages at Week 24 were obtained from multiple imputation approach for handling of missing data. All available post-baseline data from Week 4 to Week 24 regardless of status on- or off-treatment were included in the imputation model. (NCT02715726)
Timeframe: Up to Week 24

Interventionpercentage of participants (Number)
Ezetimibe 10 mg40.5
Alirocumab 75 mg Q2W/up to 150 mg Q2W85.1

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The Percentage of Participants in Each Group With New Onset Heart Failure.

To determine whether statins reduce the percentage of participants in each group with new onset heart failure after anthracyclines. (NCT02943590)
Timeframe: 2 years

InterventionParticipants (Count of Participants)
Placebo6
Atorvastatin3

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The Percentage of Individuals in Each Group With a Significant Decline in the LVEF.

To determine if the administration of statins is associated with a lower percentage of individuals who experience a significant decline in the LVEF at 12 months. The primary outcome was the percentage of participants with an absolute decline in left ventricular ejection fraction (LVEF) of>10% from prior to chemotherapy to a final value of <55% over 12 months. (NCT02943590)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Placebo22
Atorvastatin9

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Absolute Change From Baseline in Lumen Volume at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and the baseline lumen volume value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmm^3 (Mean)
Standard of Care-1.25
Alirocumab-0.93

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Absolute Change From Baseline in Lipoprotein (a) (Lp[a]) at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effect, and baseline Lp(a) value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Mean)
Standard of Care-10.3
Alirocumab-15.5

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Absolute Change From Baseline in High-density Lipoprotein Cholesterol at Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline HDL-C value and baseline HDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Least Squares Mean)
Standard of Care4.7
Alirocumab8.1

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Absolute Change From Baseline in Fasting Triglycerides (TGs) at Week 36

Adjusted mean and SE were obtained from multiple imputation approach followed by robust regression model including fixed categorical effect of treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) and the continuous fixed covariate of baseline fasting TGs value. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Mean)
Standard of Care-26.2
Alirocumab-35.3

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Absolute Change From Baseline in External Elastic Membrane (EEM) Volume at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model with treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]), as fixed categorical effects, and the baseline EEM volume value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmm^3 (Mean)
Standard of Care-8.23
Alirocumab-10.01

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Absolute Change From Baseline in Apolipoprotein B (Apo B) at Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and baseline Apo B value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Least Squares Mean)
Standard of Care-16.8
Alirocumab-51.0

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Absolute Change From Baseline in Apolipoprotein A-1 (Apo A-1) at Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and baseline Apo A-1 value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Least Squares Mean)
Standard of Care3.8
Alirocumab12.0

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Percent Change From Baseline in Lumen Volume at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effect, and the baseline lumen volume value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Mean)
Standard of Care1.20
Alirocumab-0.86

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Percent Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36

Adjusted LS mean and SE at Week 12 and Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated LDL-C value and baseline calculated LDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 12, Week 36

,
Interventionpercent change (Least Squares Mean)
Week 12Week 36
Alirocumab-64.53-63.94
Standard of Care-7.57-13.40

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Number of Participants With Cardiovascular (CV) Adverse Events

The suspected or confirmed CV events that occurred from randomization until end of the study visit were collected and reported. The various CV events included CV death, myocardial infarction, ischemic stroke, unstable angina requiring hospitalization , congestive heart failure requiring hospitalization, congestive heart failure requiring hospitalization, ischemia-driven coronary revascularization procedure. (NCT02984982)
Timeframe: Up to 36 weeks

,
InterventionParticipants (Count of Participants)
Cardiovascular deathMyocardial infarctionIschemic strokeUnstable angina requiring hospitalizationCongestive heart failure requiring hospitalizationIschemia led coronary revascularization procedure
Alirocumab022004
Standard of Care030002

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Absolute Change From Baseline in Calculated Low-density Lipoprotein Cholesterol at Week 12 and Week 36

Adjusted LS mean and SE at Week 12 and Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated LDL-C value and baseline calculated LDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 12, Week 36

,
Interventionmg/dL (Least Squares Mean)
Week 12Week 36
Alirocumab-62.4-63.2
Standard of Care-9.6-15.5

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Percent Change From Baseline in Total Cholesterol at Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline TC value and baseline TC value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care-7.59
Alirocumab-35.43

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Percent Change From Baseline in Normalized Total Atheroma Volume (TAV) at Week 36

Least-squares (LS) means and standard errors (SE) at Week 36 were obtained from analysis of covariance (ANCOVA) model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and the baseline normalized TAV as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care-3.14
Alirocumab-4.79

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Percent Change From Baseline in Non-High-density Lipoprotein Cholesterol at Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated non-HDL-C value and baseline calculated non-HDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care-14.06
Alirocumab-54.50

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Percent Change From Baseline in Lipoprotein (a) at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effect, and baseline Lp(a) value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Mean)
Standard of Care-17.23
Alirocumab-55.76

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Percent Change From Baseline in High-density Lipoprotein Cholesterol at Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline HDL-C value and baseline HDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care12.19
Alirocumab21.04

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Percent Change From Baseline in Fasting Triglycerides at Week 36

Adjusted mean and SE were obtained by multiple imputation approach followed by robust regression model included fixed categorical effect of treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) and the continuous fixed covariate of baseline fasting TGs value. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Mean)
Standard of Care-8.85
Alirocumab-18.37

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Percent Change From Baseline in External Elastic Membrane Volume at Week 36

Adjusted mean and SE at Week 36 were obtained from robust regression model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and the baseline EEM volume value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Mean)
Standard of Care-0.86
Alirocumab-3.18

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Percent Change From Baseline in Apolipoprotein B at Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and baseline Apo B value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care-16.61
Alirocumab-55.13

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Percent Change From Baseline in Apolipoprotein A-1 at Week 36

Adjusted LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and baseline Apo A-1 value as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent change (Least Squares Mean)
Standard of Care4.61
Alirocumab11.75

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Absolute Change From Baseline in Total Cholesterol (TC) at Week 36

LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated TC value and baseline calculated TC value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Least Squares Mean)
Standard of Care-15.2
Alirocumab-61.7

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Absolute Change From Baseline in Percent Atheroma Volume (PAV) at Week 36

LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and the baseline PAV as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionpercent atheroma volume (Least Squares Mean)
Standard of Care-1.28
Alirocumab-1.42

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Absolute Change From Baseline in Non-High-density Lipoprotein Cholesterol (Non-HDL-C) at Week 36

Adjusted LS mean and SE at Week 36 were obtained from mixed-effect model including all available post-baseline data from Week 4 to Week 36. Model included treatment arm (SoC arm, alirocumab arm), randomization strata (statin at ACS onset [Yes / No]), time point, treatment-by-time point and randomization strata-by-time point interaction as fixed categorical effects, and baseline calculated non-HDL-C value and baseline calculated non-HDL-C value-by-time point interaction as continuous fixed covariates. (NCT02984982)
Timeframe: Baseline, Week 36

Interventionmg/dL (Least Squares Mean)
Standard of Care-20.3
Alirocumab-69.2

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Absolute Change From Baseline in Normalized Total Atheroma Volume at Week 36

LS mean and SE at Week 36 were obtained from ANCOVA model including treatment arm (SoC arm, alirocumab arm) and randomization strata (statin at ACS onset [Yes / No]) as fixed categorical effects, and the baseline normalized TAV as continuous fixed covariate. (NCT02984982)
Timeframe: Baseline, Week 36

Interventioncubic millimeter (mm^3) (Least Squares Mean)
Standard of Care-4.73
Alirocumab-5.77

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Percent Change From Baseline in High-sensitivity C-reactive Protein (Hs-CRP) at Week 6

Percent change is calculated as the ([post-Baseline value minus the Baseline value] divided by the Baseline value ) x 100. Baseline is defined as the predose Day 1/Week 0 (Treatment Visit 1) value. If only one value is available either at Week -1 (Screening Visit 2) or Week 0 (Treatment Visit 1), then that value is used as Baseline. Missing values were imputed using LOCF, with only post-Baseline values carried forward. (NCT03051100)
Timeframe: Baseline; Week 6

Interventionpercent change (Median)
Placebo-2.7
Triplet Therapy-47.7

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Percent Change From Baseline in Low-density Lipoprotein Cholesterol (LDL-C) at Week 6

Percent change from Baseline is calculated as the ([post-Baseline value minus the Baseline value] divided by the Baseline value ) x 100. Baseline is defined as the mean of the values from Week -1 (Screening Visit 2) and predose Day 1/Week 0 (Treatment Visit 1). Percent change from Baseline in LDL-C was analyzed using analysis of covariance (ANCOVA) with treatment group as a factor and Baseline value as a covariate. Missing LDL-C values were imputed using last observation carried forward (LOCF), with only post-Baseline values carried forward. If LDL-C was measured (i.e., if TG was >400 mg/dL or LDL-C was <50 mg/dL), the measured values were used in the analysis. (NCT03051100)
Timeframe: Baseline; Week 6

Interventionpercent change (Least Squares Mean)
Placebo-3.1
Triplet Therapy-63.6

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Percent Change From Baseline in Lipid Profile Parameters at Week 6

Percent change from Baseline is calculated as the ([post-Baseline value minus the Baseline value] divided by the Baseline value ) x 100. Baseline is defined as the mean of the values from Week -1 (Screening Visit 2) and predose Day 1/Week 0 (Treatment Visit 1). Baseline apolipoprotein B (apoB) was measured only at predose/Day 1. Percent change from Baseline was analyzed using analysis of covariance (ANCOVA) with treatment group as a factor and Baseline value as a covariate. Missing values were imputed using LOCF, with only post-Baseline values carried forward. non-HDL-C, non-high-density lipoprotein cholesterol; TC, total cholesterol; TG, triglycerides; HDL-C, high-density lipoprotein cholesterol. (NCT03051100)
Timeframe: Baseline; Week 6

,
Interventionpercent change (Least Squares Mean)
non-HDL-CTCapoBTGHDL-C
Placebo-1.3-1.10.68.90.4
Triplet Therapy-60.0-47.1-53.5-27.4-1.1

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Number of Participants With LDL-C <70 mg/dL at Week 6

Analysis was based on LOCF values. If LDL-C was measured (i.e., if TG was >400 mg/dL or LDL-C was <50 mg/dL), the measured values were used in the analysis. (NCT03051100)
Timeframe: Week 6

InterventionParticipants (Count of Participants)
Placebo0
Triplet Therapy37

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Number of Participants With LDL-C Reduction ≥50% From Baseline at Week 6

If LDL-C was measured (i.e., if TG was >400 mg/dL or LDL-C was <50 mg/dL), the measured values were used in the analysis. (NCT03051100)
Timeframe: Baseline; Week 6

InterventionParticipants (Count of Participants)
Placebo0
Triplet Therapy39

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Fold Change in Composite Endothelial Inflammation

Endothelial inflammation will be monitored after 2- weeks of 40mg of atorvastatin therapy. (NCT03228017)
Timeframe: Baseline (pre-Atorvastatin), 2 weeks (post-Atorvastatin)

InterventionFold Change (Mean)
Psoriatic Disease Patients-0.1
Healthy Control0.1

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Mean Fold Change in Brachial Vein Endothelial Inflammatory Transcript

Endothelial sampling coupled to real-time PCR analysis will be used to monitor brachial vein endothelial inflammation (NCT03228017)
Timeframe: Baseline, 5 Months

InterventionFold Change (Mean)
Psoriatic Disease Patients8.6
Healthy Control2.8

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Fold Change Change in Composite Endothelial Inflammation

Endothelial inflammation will be monitored after 2 weeks of aspirin 81mg therapy (NCT03228017)
Timeframe: Baseline (pre-Aspirin), 2 weeks (post-Aspirin)

InterventionFold Change (Mean)
Psoriatic Disease Patients-0.28
Healthy Control-0.04

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Change in Levels of Circulating Thromboxane B2

Platelet activation is measured by levels of circulating thromboxane b2, which will be measured after 2- weeks of aspirin 81mg therapy (NCT03228017)
Timeframe: Baseline (pre-Aspirin), 2 weeks (post-Aspirin)

Interventionng/ml (Median)
Psoriatic Disease Patients1
Healthy Control4.05

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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 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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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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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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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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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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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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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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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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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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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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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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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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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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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 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 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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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 4: Parallel-Arm Period

Adjusted least square means and standard errors at Week 4 were calculated from analyses of covariance (ANCOVA) model with the fixed categorical effect of treatment group (SYDNEY, AI), as well as the continuous fixed covariate of baseline LDL-C value. (NCT03415178)
Timeframe: From Baseline to Week 4

Interventionpercent change (Least Squares Mean)
Auto-Injector Device (AI)-51.2
New Auto-Injector Device (SYDNEY)-66.2

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Area Under the Curve-During the Dosing Interval Tau (AUC [0-tau]) : Parallel-Arm Period

AUC0-tau: area under the serum concentration versus time curve calculated using the trapezoidal method during a dosage interval tau, where dosing interval was 4 weeks. (NCT03415178)
Timeframe: Pre-dose (Week 0) and on Day 7, 14 and 21

Interventionng*day/mL (Mean)
Auto-Injector Device (AI)381000
New Auto-Injector Device (SYDNEY)414000

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Area Under the Curve-During the Dosing Interval Tau (AUC [0-tau]) : Single-Arm Period

AUC0-tau: area under the serum concentration versus time curve calculated using the trapezoidal method during a dosage interval tau, where dosing interval was 4 weeks. (NCT03415178)
Timeframe: Pre-dose (Week 4, Week 8 and Week 12) and on Day 7, 14, 21 and 28 days following the last injection

Interventionng*day/mL (Mean)
New Auto-Injector Device (SYDNEY)509000

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Free Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Parallel-Arm Period

Free PCSK9 concentrations below the lower limit of quantification (LLOQ) were set to zero. (NCT03415178)
Timeframe: Week 4

Interventionng/mL (Mean)
Auto-Injector Device (AI)90.1
New Auto-Injector Device (SYDNEY)78.3

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Free Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Single-Arm Period

Free PCSK9 concentrations below the LLOQ were set to zero. (NCT03415178)
Timeframe: Week 16

Interventionng/mL (Mean)
New Auto-Injector Device (SYDNEY)88.9

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Injection Experience Questionnaire at Initial Supervised Injection: Overall Ease of Use Scores: Parallel-Arm Period

Participants were given an injection experience questionnaire to complete after the self-injection they administered using SYDNEY device or current AI device on Day 1, for assessment of user experience and overall ease-of-use. The questionnaire included 9 questions about specific aspects of using the device. Overall ease of use was the 9th question, response of which ranged from 1 (very difficult) to 10 (very easy), with higher score indicated more ease of use. (NCT03415178)
Timeframe: Week 0 (Day 1)

Interventionscore on a scale (Mean)
Auto-Injector Device (AI)9.9
New Auto-injector Device (SYDNEY)9.8

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Injection-Treatment Acceptance Questionnaire (I-TAQ©) After Last Injection (at Week 12) - Overall Acceptance Scores: Single-Arm Period

The I-TAQ© was a well-established and validated questionnaire to measure participant satisfaction with SC auto-injector devices. The I-TAQ© (completed by the participant after the last injection) was self-administered questionnaire administered to participants in order to measure their acceptance of the injection. The overall acceptance is one of the five domain scores. The overall acceptance score ranged from 0 to 100, with 0 indicating low acceptance and 100 indicating high acceptance. (NCT03415178)
Timeframe: At Week 12

Interventionscore on a scale (Mean)
New Auto-Injector Device (SYDNEY)93.08

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Maximum Serum Alirocumab Concentration Observed - Cmax : Parallel-Arm Period

Cmax: Maximum serum concentration observed. (NCT03415178)
Timeframe: Pre-dose (Week 0) and on Day 7, 14 and 21

Interventionnanogram per milliliter (ng/mL) (Mean)
Auto-Injector Device (AI)25800
New Auto-Injector Device (SYDNEY)26800

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Maximum Serum Alirocumab Concentration Observed - Cmax : Single-Arm Period

Cmax: maximum serum concentration observed. (NCT03415178)
Timeframe: Pre-dose (Week 4, Week 8 and Week 12) and on Day 7, 14, 21 and 28 days following the last injection

Interventionng/mL (Mean)
New Auto-injector Device (SYDNEY)31900

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Number of Participants With Treatment-Emergent Anti-Alirocumab Antibodies (ADA) Positive Response: Parallel-Arm Period

Anti-drug (alirocumab) antibodies samples were analyzed using a validated electrochemiluminescence assay. Number of participants with positive ADA during treatment emergent adverse event (TEAE) period (time from the first IMP injection to the day before the second IMP injection for participants entered into the single arm period or to 70 days after the first IMP injection, whichever comes first) was determined. Treatment-emergent positive ADA response defined as 1) participants with no ADA positive response at baseline but with any positive response in the post-baseline period or 2) participants with a positive ADA response at baseline and at least a 4- fold increase in titer in the post-baseline period. (NCT03415178)
Timeframe: Up to Week 4

InterventionParticipants (Count of Participants)
Auto-Injector Device (AI)2
New Auto-Injector Device (SYDNEY)1

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Percentage of SYDNEY-Associated Product Technical Complaints (PTCs) (Overall) at the Unsupervised Injections: Single-Arm Period

SYDNEY-associated PTC was defined as any complaint reported on the participant complaint form that triggered an investigation by the device department and was categorized as either device-related, participant-related, or undetermined whether or not associated with an adverse event (AE). Overall category included total of all 3 types of PTCs. The percentage of SYDNEY-associated PTCs was calculated as: Number of PTCs / Number of unsupervised injections*100. The confidence interval (CI) was calculated using the Wilson score method. (NCT03415178)
Timeframe: From Week 4 up to Week 12

Interventionpercentage of PTCs (Number)
New Auto-Injector Device (SYDNEY)0.5

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Time to Reach Maximum Observed Plasma Concentration (Tmax) of Alirocumab : Parallel-Arm Period

Tmax: Time to reach Cmax. (NCT03415178)
Timeframe: Pre-dose (Week 0) and on Day 7, 14 and 21

Interventiondays (Median)
Auto-Injector Device (AI)7.00
New Auto-Injector Device (SYDNEY)7.00

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Time to Reach Maximum Observed Plasma Concentration (Tmax) of Alirocumab: Single-Arm Period

Tmax: Time to reach Cmax. (NCT03415178)
Timeframe: Pre-dose (Week 4, Week 8 and Week 12) and on Day 7, 14, 21 and 28 days following the last injection

Interventiondays (Median)
New Auto-injector Device (SYDNEY)7.00

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Total Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Parallel-Arm Period

Total PCSK9 concentrations below the LLOQ were set to zero. (NCT03415178)
Timeframe: Week 4

Interventionng/mL (Mean)
Auto-Injector Device (AI)3329.7
New Auto-Injector Device (SYDNEY)3370.0

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Total Proprotein Convertase Subtilisin Kexin Type 9 (PCSK9) Concentrations : Single-Arm Period

Total PCSK9 concentrations below the LLOQ were set to zero. (NCT03415178)
Timeframe: Week 16

Interventionng/mL (Mean)
New Auto-Injector Device (SYDNEY)3481.4

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Percentage of Participants With SYDNEY-Associated Product Technical Complaint (PTCs) (Overall and by Type) at the Unsupervised Injections : Single-Arm Period

"A PTC was defined as any complaint reported on the participant complaint form that triggered an investigation by the device department and was categorized as either device-related, participant-related, or undetermined, whether or not associated with an AE. Percentage of Participants With a SYDNEY-associated PTC (for the reporting arm Alirocumab from new auto-injector device [SYDNEY]) are reported." (NCT03415178)
Timeframe: From Week 4 up to Week 12

Interventionpercentage of participants (Number)
OverallType: Device-relatedType: Participant-relatedType: Undetermined
New Auto-Injector Device (SYDNEY)1.501.50

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Percentage of Participants With a SYDNEY or Current Auto-Injector (AI)-Associated Product Technical Complaint (PTCs) (Overall and by Type) at the Supervised Injections on Week 0 (Day 1): Parallel-Arm Period

"A PTC was defined as any complaint reported on the participant complaint form that triggered an investigation by the device department and was categorized as either device-related, participant-related, or undetermined, whether or not associated with an AE. Percentage of participants With a SYDNEY-associated PTC (for the reporting arm Alirocumab from new auto-injector device) or Current AI-Associated PTCs (for the reporting arm alirocumab from AI device) are reported." (NCT03415178)
Timeframe: Week 0 (Day 1)

,
Interventionpercentage of participants (Number)
OverallType: Device-relatedType: Participant-relatedType: Undetermined
Auto-Injector Device (AI)0000
New Auto-Injector Device (SYDNEY)0000

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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 8, 12, 16: Single-Arm Period

(NCT03415178)
Timeframe: From Baseline to Weeks 8, 12, and 16

Interventionpercent change (Mean)
Week 8Week 12Week 16
New Auto-Injector Device (SYDNEY)-53.737-58.610-56.991

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Patient Perspective Questionnaire After the Last Injection (at Week 12): Single-Arm Period

The aim of the patient perspective questionnaire (completed by the participant after the last injection) was to generate data to support an understanding of the participant experience and satisfaction associated with use of the large volume SYDNEY to administer the 300 mg dose. The questionnaire consisted of 6 questions about level of satisfaction with various aspects of the SYDNEY; with response to each question ranging from 1 (very dissatisfied) to 10 (very satisfied), with higher scores indicated more satisfaction. An additional question (confidence that Sydney device was used correctly) regarding confidence of use of SYDNEY device in the study was evaluated on a scale of 10; where 1 being not at all confident, to 10 being very confident, higher scores indicated more confidence. (NCT03415178)
Timeframe: At Week 12

Interventionscore on a scale (Mean)
Size of the auto-injectorEase of holding the auto-injector in hand2-step operation:remove cap, press AI against skinLength of time it took to complete the injectionFact that needle is hidden prior & after injectionOnce monthly injectionConfidence that Sydney device was used correctly
New Auto-Injector Device (SYDNEY)9.79.89.99.910.010.09.9

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Percentage of SYDNEY-Associated Product Technical Complaints (PTCs) (by Type) at the Unsupervised Injections: Single-Arm Period

SYDNEY-associated PTC was defined as any complaint reported on the participant complaint form that triggered an investigation by the device department and was categorized as either device-related, participant-related, or undetermined whether or not associated with an AE. (NCT03415178)
Timeframe: From Week 4 up to Week 12

Interventionpercentage of PTCs (Number)
Device-relatedParticipant-relatedUndetermined
New Auto-Injector Device (SYDNEY)00.50

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Number of Participants With Treatment-Emergent Anti-Alirocumab Antibodies (ADA) Positive Response According to ADA Status During Parallel-Arm Period: Single Arm Period

Number of participants with positive ADA during the TEAE period (time from the second IMP injection up to the day of last IMP injection + 70 days) were determined. Treatment-emergent positive ADA response in Single-arm period defined as 1) participants with no ADA positive response in the Parallel-arm period but with any positive response in the Single-arm period or 2) participants with a positive ADA response at baseline, with less than 4-fold increase in titer in the Parallel-arm period (Pre-existing ADA in Parallel-arm period) and at least a 4- fold increase in titer in the Single-arm period. (NCT03415178)
Timeframe: Week 16

InterventionParticipants (Count of Participants)
Pre-existing ADANegative ADA statusTreatment-emergent ADA positive
New Auto-Injector Device (SYDNEY)020

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Number of Participants With Tanner Staging at Baseline, Weeks 12, 24 and 48

Tanner stage defines physical measurements of development in children and adolescent based on external primary and secondary sex characteristics. Participants were evaluated for pubic hair distribution, breast development (only females) and genital development (only males), and classified in 3 categories as: Prepubescent (defined as a person just before start of the development of adult sexual characteristics), Pubescent (defined as a person at or approaching the age of puberty), Postpubescent (sexually mature or a person who has completed puberty). (NCT03510715)
Timeframe: Baseline, Weeks 12, 24 and 48

,
InterventionParticipants (Count of Participants)
Baseline: PrepubescentBaseline: PubescentBaseline: Post-pubescentWeek 12: PrepubescentWeek 12: PubescentWeek 12: Post-pubescentWeek 24: PrepubescentWeek 24: PubescentWeek 24: Post-pubescentWeek 48: PrepubescentWeek 48: PubescentWeek 48: Post-pubescent
Alirocumab 150 mg Q2W090081081072
Alirocumab 75 mg Q2W/up to 150 mg Q2W360360260170

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Percent Change From Baseline in Apolipoprotein (Apo) B at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab-4.2-11.80.9

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Percent Change From Baseline in Total Cholesterol (Total-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Weeks 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab-1.9-6.35.5

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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Weeks 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 24 and 48

Interventionpercent change (Least Squares Mean)
Week 24Week 48
Alirocumab-10.14.2

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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol at Week 12: On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline on-treatment data from Week 4 to Week 48 (on-treatment Analysis). (NCT03510715)
Timeframe: Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab-4.1

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Percentage of Participants Reporting >=15 Percent (%) Reduction in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted Percentage were obtained from a multiple imputation approach for handling of missing data including all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercentage of participants (Number)
Week 12Week 24Week 48
Alirocumab50.050.039.0

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Absolute Change From Baseline in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionmg/dL (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab-33.4-43.0-15.0

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Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Week 4 to 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab11.314.611.3

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Percent Change From Baseline in Fasting Triglycerides (TG) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Mean)
Week 12Week 24Week 48
Alirocumab2.85.210.0

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Percent Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Weeks 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab13.08.910.1

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Percent Change From Baseline in Lipoprotein a (Lp) (a) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data from Week 4 to Week 48 regardless of status on-or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Mean)
Week 12Week 24Week 48
Alirocumab7.4-5.2-6.4

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Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Weeks 12, 24 and 48 - ITT Analysis/On-treatment Analysis

Adjusted LS means and standard errors were obtained from the MMRM model to account for missing data using all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). Although separate analyses of all available data (ITT analysis) and only data collected within a defined time window (On-treatment analysis) were planned, if all values used in the ITT approach were within the on-treatment time window, the on-treatment analysis would be identical to the ITT analysis, thus the results would be identical and a single outcome measure presenting the results for both types of analysis would be provided. (NCT03510715)
Timeframe: Baseline to Weeks 12, 24 and 48

Interventionpercent change (Least Squares Mean)
Week 12Week 24Week 48
Alirocumab-3.9-9.25.7

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Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12: Intent-to-Treat (ITT) Analysis

Adjusted least square (LS) means and standard errors were obtained from the mixed model analysis with repeated measures (MMRM) to account for missing data using all available post-baseline data from Week 4 to Week 48 regardless of status on- or off-treatment used in the model (ITT analysis). (NCT03510715)
Timeframe: Baseline to Week 12

Interventionpercent change (Least Squares Mean)
Alirocumab-4.1

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DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 130 mg/dL (3.37 mmol/L) at Weeks 12 and 24: On-treatment Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. (NCT03510884)
Timeframe: Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week 12Week 24
DB Period: Alirocumab Q2W70.673.3
DB Period: Alirocumab Q4W72.676.3
DB Period: Placebo Q2W16.48.0
Db Period: Placebo Q4W12.922.2

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Number of Participants With Tanner Staging at Baseline and Weeks 24, 68 and 104

Tanner stage defines physical measurements of development in children and adolescent based on external primary and secondary sex characteristics. Participants were evaluated for pubic hair distribution, breast development (only females) and genital development (only males) and classified in 3 categories as: Prepubescent (defined as a person just before start of the development of adult sexual characteristics), Pubescent (defined as a person at or approaching the age of puberty), Postpubescent (sexually mature or a person who has completed puberty). (NCT03510884)
Timeframe: Baseline, Weeks 24, 68 and 104

,,,
InterventionParticipants (Count of Participants)
Baseline: Boys - PrepubescentBaseline: Boys - PubescentBaseline: Boys - PostpubescentBaseline: Girls - PrepubescentBaseline: Girls - PubescentBaseline: Girls - PostpubescentWeek 24: Boys - PrepubescentWeek 24: Boys - PubescentWeek 24: Boys - PostpubescentWeek 24: Girls - PrepubescentWeek 24: Girls - PubescentWeek 24: Girls - PostpubescentWeek 68: Boys - PrepubescentWeek 68: Boys - PubescentWeek 68: Boys - PostpubescentWeek 68: Girls - PrepubescentWeek 68: Girls - PubescentWeek 68: Girls - PostpubescentWeek 104: Boys - PrepubescentWeek 104: Boys - PubescentWeek 104: Boys - PostpubescentWeek 104: Girls - PrepubescentWeek 104: Girls - PubescentWeek 104: Girls - Postpubescent
Alirocumab Q2W41324161031134159196314918601011
Alirocumab Q4W01447131401252169096116908711711
Placebo/Alirocumab Q2W11331610134152074061067042
Placebo/Alirocumab Q4W543186173165153155152155

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DB Period: Percent Change From Baseline in Apolipoprotein A1 (Apo A1) at Week 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W-0.1
DB Period: Alirocumab Q2W1.0
DB Period: Placebo Q4W-4.5
DB Period: Alirocumab Q4W4.4

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DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 12: ITT Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data up to Week 12. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
DB Period: Placebo Q2W-7.1
DB Period: Alirocumab Q2W-12.7
DB Period: Placebo Q4W-2.5
DB Period: Alirocumab Q4W-16.0

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DB Period: Percent Change From Baseline in Apolipoprotein A1 at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W-0.1
DB Period: Alirocumab Q2W-1.7
DB Period: Placebo Q4W-0.7
DB Period: Alirocumab Q4W5.0

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DB Period: Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W8.9
DB Period: Alirocumab Q2W-30.0
DB Period: Placebo Q4W1.1
DB Period: Alirocumab Q4W-31.7

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DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 12: ITT Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data up to Week 12. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Mean)
DB Period: Placebo Q2W6.5
DB Period: Alirocumab Q2W-2.2
DB Period: Placebo Q4W7.8
Db Period: Alirocumab Q4W-0.3

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DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data up to Week 24. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Mean)
DB Period: Placebo Q2W7.7
DB Period: Alirocumab Q2W11.9
DB Period: Placebo Q4W12.2
DB Period: Alirocumab Q4W-6.8

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DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W-0.8
DB Period: Alirocumab Q2W5.6
DB Period: Placebo Q4W-1.1
DB Period: Alirocumab Q4W3.4

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DB Period: Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W10.4
DB Period: Alirocumab Q2W-27.4
DB Period: Placebo Q4W-3.6
DB Period: Alirocumab Q4W-34.3

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DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 day otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12, and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W3.55.6
DB Period: Alirocumab Q4W4.03.4
DB Period: Placebo Q2W-2.2-0.8
DB Period: Placebo Q4W-3.5-1.1

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DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W-2.2
DB Period: Alirocumab Q2W3.5
DB Period: Placebo Q4W-3.5
DB Period: Alirocumab Q4W4.0

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DB Period: Percent Change From Baseline in Lipoprotein (a) at Weeks 12 and 24: On-treatment Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline on-treatment data up to Week 12 and Week 24, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Weeks 12 and 24

,,,
Interventionpercent change (Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-12.746-14.748
DB Period: Alirocumab Q4W-16.042-22.418
DB Period: Placebo Q2W-7.0990.492
DB Period: Placebo Q4W-2.5452.468

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DB Period: Percent Change From Baseline in Lipoprotein (a) at Week 24: ITT Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline data up to Week 24. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Mean)
DB Period: Placebo Q2W0.5
DB Period: Alirocumab Q2W-14.7
DB Period: Placebo Q4W2.5
DB Period: Alirocumab Q4W-22.4

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DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol (LDL-C) at Week 24: Intent-to-treat (ITT) Estimand

Adjusted least square (LS) means and standard errors (SE) were obtained from mixed-effect model with repeated measures (MMRM) model. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W9.7
DB Period: Alirocumab Q2W-33.6
DB Period: Placebo Q4W-4.4
DB Period: Alirocumab Q4W-38.2

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DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W10.7
DB Period: Alirocumab Q2W-34.8
DB Period: Placebo Q4W2.3
DB Period: Alirocumab Q4W-39.2

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DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol (Non-HDL-C) at Week 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W9.7
DB Period: Alirocumab Q2W-31.0
DB Period: Placebo Q4W-3.7
DB Period: Alirocumab Q4W-35.6

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DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Weeks 12, and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st investigational medicinal product (IMP) injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12, and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-34.8-33.6
DB Period: Alirocumab Q4W-39.2-38.2
DB Period: Placebo Q2W10.79.7
DB Period: Placebo Q4W2.3-4.4

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DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-33.0-31.0
Db Period: Alirocumab Q4W-34.7-35.6
DB Period: Placebo Q2W9.89.7
DB Period: Placebo Q4W2.8-3.7

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DB Period: Percent Change From Baseline in Total Cholesterol at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-25.3-23.4
DB Period: Alirocumab Q4W-27.0-27.7
DB Period: Placebo Q2W7.57.4
DB Period: Placebo Q4W0.9-4.4

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DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 8, Week 12 and Week 24 were used and missing data were accounted for by the MMRM model. (NCT03510884)
Timeframe: Baseline to Weeks 8, 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 8Week 12Week 24
DB Period: Alirocumab Q2W-35.4-34.8-33.6
DB Period: Alirocumab Q4W-42.0-39.2-38.2
DB Period: Placebo Q2W7.110.79.7
DB Period: Placebo Q4W-3.82.3-4.4

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DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W9.8
DB Period: Alirocumab Q2W-33.0
DB Period: Placebo Q4W2.8
DB Period: Alirocumab Q4W-34.7

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DB Period: Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 24

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W7.4
DB Period: Alirocumab Q2W-23.4
DB Period: Placebo Q4W-4.4
DB Period: Alirocumab Q4W-27.7

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DB Period: Percent Change From Baseline in Total Cholesterol at Week 12: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model including all available post-baseline data. All post-baseline data available up to Week 12 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Week 12

Interventionpercent change (Least Squares Mean)
DB Period: Placebo Q2W7.5
DB Period: Alirocumab Q2W-25.3
DB Period: Placebo Q4W0.9
DB Period: Alirocumab Q4W-27.0

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DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 12: ITT Estimand

Adjusted percentages at Week 12 were obtained from multiple imputation approach for handling of missing data for Q4W. All available post-baseline data up to Week 12 were included in the imputation model. For Q2W, adjusted percentages at Week 12 were obtained from last observation carried forward approach (LOCF) to handle missing on-treatment LDL-C values as well as missing post-treatment LDL-C values in participants who discontinued treatment due to the coronavirus disease-2019 pandemic. Other post-treatment missing values were considered as failure. (NCT03510884)
Timeframe: At Week 12

Interventionpercentage of participants (Number)
DB Period: Placebo Q2W0.0
DB Period: Alirocumab Q2W61.2
DB Period: Placebo Q4W4.3
DB Period: Alirocumab Q4W57.0

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DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 24: ITT Estimand

Adjusted percentages at Week 24 were obtained from multiple imputation approach for handling of missing data. All available post-baseline data up to Week 24 were included in the imputation model. (NCT03510884)
Timeframe: At Week 24

Interventionpercentage of participants (Number)
DB Period: Placebo Q2W4.0
DB Period: Alirocumab Q2W57.2
DB Period: Placebo Q4W9.0
DB Period: Alirocumab Q4W67.2

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DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level <130 mg/dL (3.37 mmol/L) at Week 12: ITT Estimand

Adjusted percentages at Week 12 were obtained from multiple imputation approach for handling of missing data. All available post-baseline data up to Week 12 were included in the imputation model. (NCT03510884)
Timeframe: At Week 12

Interventionpercentage of participants (Number)
DB Period: Placebo Q2W16.4
DB Period: Alirocumab Q2W70.6
DB Period: Placebo Q4W12.9
DB Period: Alirocumab Q4W72.6

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DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level Lower Than (<) 130 mg/dL (3.37 mmol/L) at Week 24: ITT Estimand

Adjusted percentages at Week 24 were obtained from multiple imputation approach for handling of missing data. All available post-baseline data up to Week 24 were included in the imputation model. (NCT03510884)
Timeframe: At Week 24

Interventionpercentage of participants (Number)
DB Period: Placebo Q2W8.0
DB Period: Alirocumab Q2W73.3
DB Period: Placebo Q4W22.2
DB Period: Alirocumab Q4W76.3

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OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: On-treatment Estimand

Percent Change in LDL-C from Baseline to Week 104 was reported in this outcome measure. (NCT03510884)
Timeframe: Baseline, Week 104

Interventionpercent change (Least Squares Mean)
OL Period: Placebo/Alirocumab Q2W-22.8
OL Period: Alirocumab Q2W-25.8
OL Period: Placebo/Alirocumab Q4W-27.6
OL Period: Alirocumab Q4W-23.4

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Change From Baseline in Cogstate Battery Test - Overall Composite Score at Weeks 24, 68 and 104

Cogstate battery test (cognitive testing system) consisted of detection test (DET), identification test (IDN), one card learning test (OCL) and Groton maze learning test (GML) to assess processing speed, attention, visual learning and executive functioning, respectively. For each test, Z-scores were computed based on participant's age at Baseline and Weeks 24, 68 and 104. Composite score: calculated as mean of Z-scores equally weighted, provided that at least 3 of 4 tests were available and if all of these domains were covered as: attention, through either DET or IDN, visual learning, through OCL and executive function, through GML. There is not minimum/maximum since values were reported as z-score but z-score of 0 means result equals to mean with negative numbers indicating values lower than mean and positive values higher. Positive change in z-score = an improvement in cognition, i.e., a better outcome; and negative change in z-score = worsening in cognition, i.e., a worse outcome. (NCT03510884)
Timeframe: Baseline, Weeks 24, 68 and 104

,,,
InterventionZ-score (Mean)
Week 24Week 68Week 104
Alirocumab Q2W-0.313-0.334-0.439
Alirocumab Q4W-0.136-0.263-0.638
Placebo/Alirocumab Q2W-0.403-0.421-0.601
Placebo/Alirocumab Q4W-0.218-0.272-0.393

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DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: ITT Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline data available up to Week 12 and Week 24 were used and missing data were accounted for by the MMRM model. MMRM model was run on participants with a Baseline value and a post-baseline value for at least one timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12, and 24

,,,
Interventionratio (Apo B/Apo A-1) (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-0.2-0.2
DB Period: Alirocumab Q4W-0.3-0.3
DB Period: Placebo Q2W0.10.1
DB Period: Placebo Q4W0.00.0

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DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12, and 24

,,,
Interventionratio (Apo B/Apo A-1) (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-0.2-0.2
DB Period: Alirocumab Q4W-0.3-0.3
DB Period: Placebo Q2W0.10.1
DB Period: Placebo Q4W0.00.0

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DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response

Anti-drug (alirocumab) antibodies samples were analyzed using a validated non-quantitative, titer-based bridging immunoassay. Number of participants with positive ADA during 24-week treatment period is reported. Treatment-emergent positive ADA response was defined as 1) participants with no ADA positive response at baseline but with any positive response in the post-baseline period or 2) participants with a positive ADA response at baseline and at least a 4- fold increase in titer in the post-baseline period. A persistent positive response was defined as a TE ADA positive response detected in at least 2 consecutive post-baseline samples separated by at least a 12-week period. Persistent positive response was only analyzed for participants with positive TE ADA response. (NCT03510884)
Timeframe: Up to 24 weeks

,,
InterventionParticipants (Count of Participants)
TE ADA positive response
DB Period: Alirocumab Q4W0
DB Period: Placebo Q2W0
DB Period: Placebo Q4W0

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DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response

Anti-drug (alirocumab) antibodies samples were analyzed using a validated non-quantitative, titer-based bridging immunoassay. Number of participants with positive ADA during 24-week treatment period is reported. Treatment-emergent positive ADA response was defined as 1) participants with no ADA positive response at baseline but with any positive response in the post-baseline period or 2) participants with a positive ADA response at baseline and at least a 4- fold increase in titer in the post-baseline period. A persistent positive response was defined as a TE ADA positive response detected in at least 2 consecutive post-baseline samples separated by at least a 12-week period. Persistent positive response was only analyzed for participants with positive TE ADA response. (NCT03510884)
Timeframe: Up to 24 weeks

InterventionParticipants (Count of Participants)
TE ADA positive responsePersistent positive response
DB Period: Alirocumab Q2W30

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DB Period: Percent Change From Baseline in Apolipoprotein A1 at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM mode, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-1.71.0
DB Period: Alirocumab Q4W5.04.4
DB Period: Placebo Q2W-0.1-0.1
DB Period: Placebo Q4W-0.7-4.5

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DB Period: Percent Change From Baseline in Apolipoprotein B at Weeks 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. MMRM model was run on participants with a Baseline value and at one on-treatment post-baseline value for a timepoint used in the model. (NCT03510884)
Timeframe: Baseline, Weeks 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-30.0-27.4
DB Period: Alirocumab Q4W-31.7-34.3
DB Period: Placebo Q2W8.910.4
DB Period: Placebo Q4W1.1-3.6

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DB Period: Percent Change From Baseline in Fasting Triglycerides at Weeks 12 and 24: On-treatment Estimand

Adjusted means and standard errors were obtained from a multiple imputation approach followed by a robust regression model including all available post-baseline on-treatment data up to Week 12 and Week 24, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. Combined estimates and SE were obtained by combining adjusted means and SE from robust regression model analyses of the different imputed data sets. (NCT03510884)
Timeframe: Baseline, Weeks 12, and 24

,,,
Interventionpercent change (Mean)
Week 12Week 24
DB Period: Alirocumab Q2W-2.211.9
DB Period: Alirocumab Q4W-0.3-6.8
DB Period: Placebo Q2W6.57.7
DB Period: Placebo Q4W7.812.2

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DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: On-treatment Estimand

Adjusted LS means and SE were obtained from MMRM model. All post-baseline on-treatment data available up to Week 8, Week 12 and Week 24 were used for the MMRM model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for who stopped IMP before switch to Q2W regimen, + 21 days otherwise. (NCT03510884)
Timeframe: Baseline to Weeks 8, 12 and 24

,,,
Interventionpercent change (Least Squares Mean)
Week 8Week 12Week 24
DB Period: Alirocumab Q2W-35.4-34.8-33.6
DB Period: Alirocumab Q4W-42.0-39.2-38.2
DB Period: Placebo Q2W7.110.79.7
DB Period: Placebo Q4W-3.82.3-4.4

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DB Period: Percentage of Participants Achieved at Least 30% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. (NCT03510884)
Timeframe: At Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week 12Week 24
DB Period: Alirocumab Q2W65.866.7
DB Period: Alirocumab Q4W70.872.5
DB Period: Placebo Q2W0.84.0
DB Period: Placebo Q4W4.218.5

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DB Period: Percentage of Participants Who Achieved at Least 30 Percent (%) Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model. (NCT03510884)
Timeframe: At Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week12Week 24
DB Period: Alirocumab Q2W65.866.7
DB Period: Alirocumab Q4W70.872.5
DB Period: Placebo Q2W0.84.0
DB Period: Placebo Q4W4.218.5

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DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model. (NCT03510884)
Timeframe: At Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week 12Week 24
DB Period: Alirocumab Q2W25.221.6
DB Period: Alirocumab Q4W31.932.4
DB Period: Placebo Q2W0.00.0
DB Period: Placebo Q4W0.19.1

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DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. (NCT03510884)
Timeframe: At Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week 12Week 24
DB Period: Alirocumab Q2W25.221.6
DB Period: Alirocumab Q4W31.932.4
DB Period: Placebo Q2W0.00.0
DB Period: Placebo Q4W0.19.1

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DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 110 mg/dL (2.84 mmol/L) at Weeks 12 and 24: On-treatment Estimand

Adjusted percentages at Weeks 12 and 24 were obtained from multiple imputation approach for handling of missing data followed by logistic regression model. All available post-baseline on-treatment data up to Week 12 and Week 24 were included in the imputation model, i.e., for Q2W data: from 1st IMP injection up to last IMP injection + 21 days and for Q4W data: from 1st IMP injection up to last IMP injection + 35 days for those who stopped IMP before switch to Q2W regimen, + 21 days otherwise. (NCT03510884)
Timeframe: Weeks 12 and 24

,,,
Interventionpercentage of participants (Number)
Week 12Week 24
DB Period: Alirocumab Q2W61.757.2
DB Period: Alirocumab Q4W57.067.2
DB Period: Placebo Q2W0.14.0
DB Period: Placebo Q4W4.39.0

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OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: ITT Estimand

Percent Change in LDL-C from Baseline to Week 104 was reported in this outcome measure. (NCT03510884)
Timeframe: Baseline, Week 104

Interventionpercent change (Least Squares Mean)
OL Period: Placebo/Alirocumab Q2W-23.3
OL Period: Alirocumab Q2W-22.2
OL Period: Placebo/Alirocumab Q4W-27.1
OL Period: Alirocumab Q4W-23.7

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Efficacy, Number of Participants With Day 15 HDL-C More Than or Equal to 75% Baseline HDL-C

HDL-C levels were measured prior to and at the end of the 15 day treatment period to quantify the percent baseline HDL-C at 15 days. Efficacy is defined as eleven or more subjects in a dosing cohort with a Day 15 HDL-C not less than 75% of their baseline. (NCT03611010)
Timeframe: Baseline, 15 Days

InterventionParticipants (Count of Participants)
Cohort 111
Cohort 213
Cohort 31
Cohort 49

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Change in Baseline LDL-C Concentration

Mean change in LDL-C (mg/dL) from baseline at Day 15 (NCT03611010)
Timeframe: Baseline, 15 days

Interventionmg/dL (Mean)
Cohort 112.36
Cohort 22.62
Cohort 327.50
Cohort 411.22

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AUC Inf

The AUCinf of atorvastatin following an intravenous injection to a patient at steady-state. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

Interventionng*hr/mL (Mean)
Cohort 172.19
Cohort 2167.32
Cohort 3217.00

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t 1/2

The half-life of atorvastatin following an intravenous injection to a patient at a steady state. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

Interventionhours (Mean)
Cohort 14.79
Cohort 26.22
Cohort 36.38

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VDss

The volume of distribution at steady state of atorvastatin following an intravenous injection to a patient. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

Interventionliter (Mean)
Cohort 171.86
Cohort 2135.53
Cohort 3182.85

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Efficacy, Number of Participants With Day 15 LDL-C Less Than or Equal to 125% of Baseline LDL-C

LDL-C levels were measured prior to and at the end of the 15 day treatment period to quantify the percent baseline LDL-C at 15 days. Efficacy is defined as eleven or more subjects in a dosing cohort with a Day 15 LDL-C not more than 125% of their baseline. (NCT03611010)
Timeframe: Baseline, 15 Days

InterventionParticipants (Count of Participants)
Cohort 19
Cohort 29
Cohort 31
Cohort 47

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AUC 0-24

The AUC 0-24 of atorvastatin and the 2- and 4-hydroxy active metabolites following an intravenous injection to a patient at steady-state. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

,,
Interventionng*hr/mL (Mean)
Atorvastatin2-Hydroxy Atorvastatin4-Hydroxy Atorvastatin
Cohort 172.123.35NA
Cohort 2137.0416.765.45
Cohort 3212.0049.2012.65

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Cmax IV

The maximum serum concentration of atorvastatin and the 2- and 4-hydroxy active metabolites following an intravenous injection to a patient at steady-state. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

,,
Interventionmg/mL (Mean)
Atorvastatin2-Hydroxy Atorvastatin4-Hydroxy Atorvastatin
Cohort 1284.330.400.24
Cohort 2830.341.230.30
Cohort 3507.503.230.75

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Tmax IV

The time to maximum concentration of atorvastatin and the 2- and 4-hydroxy active metabolites following an intravenous injection to a patient at steady-state. (NCT03611010)
Timeframe: 3 to 7 minutes, 0.5h, 1h 2h, 4h, 6h, 8h, 24h post-dose

,,
Interventionhours (Median)
Atorvastatin2-Hydroxy Atorvastatin4-Hydroxy Atorvastatin
Cohort 10.086.000.08
Cohort 20.086.06.0
Cohort 30.155.008.0

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Number of Participants Who Discontinued From Study Treatment

The number of participants who discontinued treatment over the 12-week treatment period was assessed. (NCT03768427)
Timeframe: Up to approximately 15 weeks

InterventionNumber of Participants (Number)
Atorvastatin 10 mg - Ezetimibe 10 mg/Ator 10 mg9
Atorvastatin 10mg - Atorvastatin 20 mg5
Atorvastatin 20 mg - EZ 10 mg/Ator 20 mg13
Atorvastatin 20 mg - Atorvastatin 40 mg15

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Percent Change From Baseline in LDL-C at Week 12

Participants had LDL-C levels assessed at baseline and after 12 weeks of study drug administration. The change from baseline was calculated. (NCT03768427)
Timeframe: Baseline (Day 1) and Week 12

InterventionPercent change (Mean)
Atorvastatin 10 mg - Ezetimibe 10 mg/Ator 10 mg-24.7
Atorvastatin 10mg - Atorvastatin 20 mg-5.3
Atorvastatin 20 mg - EZ 10 mg/Ator 20 mg-23.3
Atorvastatin 20 mg - Atorvastatin 40 mg-9.1

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Percentage of Participants With An Adverse Event (AE)

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of study intervention, whether or not considered related to the study intervention. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a study intervention. (NCT03768427)
Timeframe: Up to approximately 17 weeks

InterventionPercentage of Participants (Number)
Atorvastatin 10 mg - Ezetimibe 10 mg/Ator 10 mg31.8
Atorvastatin 10mg - Atorvastatin 20 mg34.8
Atorvastatin 20 mg - EZ 10 mg/Ator 20 mg55.5
Atorvastatin 20 mg - Atorvastatin 40 mg47.9

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Change in International Index of Erectile Function (IIEF) Scores

To estimate the proportion of participants who achieve a clinically significant improvement in erectile dysfunction (ED) when treated with a combination of Atorvastatin or participant's currently prescribed statin, Vitamin E, and Pentoxifylline (PAVE) (NCT03830164)
Timeframe: 12 months

InterventionParticipants (Count of Participants)
Cohort 10
Cohort 20
Cohort 30

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Number of Participants With Incidence of Adverse Events (AEs)

The safety profile of the pentoxifylline, atorvastatin and vitamin E (PAVE) combination will be reported for each cohort, with adverse events summarized by grade and time to onset to first grade 3 adverse event. (NCT03830164)
Timeframe: Up to 12 months

,,
InterventionParticipants (Count of Participants)
Serious Adverse EventAdverse Event
Cohort 100
Cohort 202
Cohort 300

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Choosing Other Erectile Dysfunction (ED) Treatments After Pentoxifylline, Atorvastatin and Vitamin E (PAVE)

To report the rate of choosing other ED treatments after PAVE. (NCT03830164)
Timeframe: Up to 12 months

InterventionParticipants (Count of Participants)
Cohort 11
Cohort 20
Cohort 30

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PK Parameter: AUCinf of ATV, PRA, and ROS

AUCinf is defined as the concentration of drug extrapolated to infinite time. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionh*ng/mL (Mean)
PRAROS
Filgotinib + Pravastatin + Rosuvastatin234.892.3
Pravastatin + Rosuvastatin201.366.0

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PK Parameter: Cmax of ATV, PRA, and ROS

Cmax is defined as the maximum observed concentration of drug. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionng/mL (Mean)
ATV
Atorvastatin19.7
Filgotinib + Atorvastatin15.0

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PK Parameter: Cmax of ATV, PRA, and ROS

Cmax is defined as the maximum observed concentration of drug. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionng/mL (Mean)
PRAROS
Filgotinib + Pravastatin + Rosuvastatin99.212.3
Pravastatin + Rosuvastatin84.27.5

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Percentage of Participants Experiencing Treatment Emergent Adverse Events (TEAEs)

An adverse event (AE) was any untoward medical occurrence in a participant administered a study drug, which did not necessarily have a causal relationship with the treatment. AE was therefore any unfavorable and/or unintended sign, symptom, or disease temporally associated with the use of the study drug, whether or not considered related to the study drug. TEAEs: AE with an onset date on or after the study drug start date and no later than 30 days after study drug stop date; or any AE leading to study drug discontinuation. (NCT04608344)
Timeframe: Sequence AB: First dose up to 47 days, Sequence BA: First dose up to 50 days

Interventionpercentage of participants (Number)
Atorvastatin19.2
Pravastatin + Rosuvastatin24.0
Filgotinib65.4
Filgotinib + Atorvastatin7.7
Filgotinib + Pravastatin + Rosuvastatin11.5

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Percentage of Participants With Severity Grade 3 or Above Treatment-Emergent Laboratory Abnormalities

Treatment-emergent laboratory abnormalities were graded using Common Terminology Criteria for Adverse Events (CTCAE) Version 5.0 of Adverse Events and Laboratory abnormalities. Laboratory abnormalities were graded as Grade 1 (mild), Grade 2 (moderate), Grade 3 (severe), Grade 4 (Life-threatening), Grade 5 (Death). Percentage of participants with Grade 3 or higher treatment-emergent laboratory abnormalities were reported. (NCT04608344)
Timeframe: Sequence AB: First dose up to 47 days, Sequence BA: First dose up to 50 days

Interventionpercentage of participants (Number)
Atorvastatin0
Pravastatin + Rosuvastatin0
Filgotinib3.8
Filgotinib + Atorvastatin0
Filgotinib + Pravastatin + Rosuvastatin0

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Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS

AUClast is defined as the concentration of drug from time zero to the last observable concentration. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionh*ng/mL (Mean)
ATV
Atorvastatin78.8
Filgotinib + Atorvastatin70.2

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Pharmacokinetic (PK) Parameter: AUClast of ATV, PRA, and ROS

AUClast is defined as the concentration of drug from time zero to the last observable concentration. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionh*ng/mL (Mean)
PRAROS
Filgotinib + Pravastatin + Rosuvastatin232.589.3
Pravastatin + Rosuvastatin199.562.6

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PK Parameter: AUCinf of ATV, PRA, and ROS

AUCinf is defined as the concentration of drug extrapolated to infinite time. (NCT04608344)
Timeframe: AB (Days 1,3,12,14) and BA (Days 6,8,18,20): Predose, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 16, 24, 48 postdose; AB (Days 1,12) and BA (Days 6,18): 5,10,36 hours post dose; AB (Days 3,14) and BA (Days 8,20): 72 hours postdose

,
Interventionh*ng/mL (Mean)
ATV
Atorvastatin80.8
Filgotinib + Atorvastatin71.8

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