Page last updated: 2024-12-06

lovastatin

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Description

Lovastatin is a statin medication used to lower cholesterol levels in the blood. It is a competitive inhibitor of the enzyme HMG-CoA reductase, which is involved in the synthesis of cholesterol in the liver. Lovastatin was first isolated from the fungus Aspergillus terreus in 1978. It is available in both generic and brand-name forms. Lovastatin is effective in lowering LDL (bad) cholesterol and triglycerides, and raising HDL (good) cholesterol. It is typically used for individuals with high cholesterol levels who are at increased risk for heart disease. Lovastatin is also being studied for its potential benefits in treating other conditions such as Alzheimer's disease and cancer.'

Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom). [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID53232
CHEMBL ID503
CHEBI ID40303
SCHEMBL ID3136
SCHEMBL ID14227102
MeSH IDM0012707

Synonyms (242)

Synonym
BIDD:GT0749
BIDD:PXR0113
AC-13961
HMS3268C03
BRD-K09416995-001-06-8
gtpl2739
(+)-mevinolin
nsc-633781
mevinolin
nsc633781
1s,7s,8s,8ar)-8-{2-[(2r,4r)-4-hydroxy-6-oxooxan-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl (2s)-2-methylbutanoate
mk-803
smr000058779
KBIO1_001032
DIVK1C_001032
liposcler
l-154803
rextat
monakolin k
(s)-2-methyl-butyric acid (1s,3r,7s,8s,8ar)-8-[2-((3r,5r)-4-hydroxy-6-oxo-tetrahydro-pyran-2-yl)-ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl ester
6-methylcompactin
butanoic acid, 2-methyl-, (1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl ester, (2s)-
(1s,3r,7s,8s,8ar)-8-{2-[(2r,4r)-4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl (2s)-2-methylbutanoate
altoprev
butanoic acid, 2-methyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl ester, (1s-(1alpha(r*),3alpha,7beta,8beta(2s*,4s*),8abeta))-
brn 3631989
BSPBIO_003346
BSPBIO_000471
PRESTWICK_819
cas-75330-75-5
ACON0_000534
ACON1_000390
BSPBIO_001265
IDI1_001032
PRESTWICK3_000516
PRESTWICK2_000516
BPBIO1_000519
SPECTRUM5_001294
lipofren
2beta,6alpha-dimethyl-8alpha-(2-methyl-1-oxobutoxy)-mevinic acid lactone
lovastin
hsdb 6534
colevix
belvas
6-alpha-methylcompactin
rodatin
lestatin
6alpha-methylcompactin
rovacor
teroltrat
tecnolip
hipovastin
hipolip
altocor
closterol
mevlor
lovastatinum [latin]
cholestra
sivlor
lovastatine [french]
lovasterol
lozutin
lipdip
lipivas
artein
(1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(2r,4r)-(tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl (s)-2-methyl-butyrate
nergadan
lovastatina [spanish]
lovalord
taucor
paschol
(2s)-2-methylbutanoic acid (1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-[(2r,4r)-tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl]ethyl]-1-naphthalenyl ester
NCGC00023509-03
lovastatin
75330-75-5
C07074
butanoic acid, 2-methyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-- oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl ester, (1s-(1alpha(r*),3alpha,7beta,8beta(2s*,4s*),8abeta))-
[(1s,3r,7s,8s,8ar)-8-[2-[(2r,4r)-4-hydroxy-6-oxo-tetrahydropyran-2-yl]ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] (2s)-2-methylbutanoate
msd 803
mevinolin from aspergillus sp., >=98% (hplc)
CHEBI:40303 ,
DB00227
1CQP
D00359
lovastatin (usp/inn)
ml-530b
mevacor (tn)
NCGC00023509-04
MLS000069585 ,
KBIO3_002848
SPECTRUM3_001873
PRESTWICK0_000516
NINDS_001032
PRESTWICK1_000516
SPBIO_002392
SPECTRUM1503977
MEGXM0_000398
NCGC00023509-06
NCGC00023509-05
NCGC00023509-07
NCGC00023509-08
6 methylcompactin
smr000673570
MLS001055358
lovastatin & primycin
HMS1990O07
HMS2093O03
HMS2089M06
L0214
c10aa02
6.alpha.-methylcompactin
nsc-758662
simvastatin impurity, lovastatin-
CHEMBL503 ,
HMS1792O07
HMS503O05
HMS1569H13
HMS1923O13
[(1s,3r,7s,8s,8ar)-8-[2-[(2r,4r)-4-hydroxy-6-oxooxan-2-yl]ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] (2s)-2-methylbutanoate
STK801953
A838030
[(1s,3r,7s,8s,8ar)-8-[2-[(2r,4r)-4-hydroxy-6-oxo-tetrahydropyran-2-yl]ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] 2-methylbutanoate
(2s)-2-methylbutanoic acid [(1s,3r,7s,8s,8ar)-8-[2-[(2r,4r)-4-hydroxy-6-oxo-2-oxanyl]ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] ester
[(1s,3r,7s,8s,8ar)-3,7-dimethyl-8-[2-[(2r,4r)-4-oxidanyl-6-oxidanylidene-oxan-2-yl]ethyl]-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] (2s)-2-methylbutanoate
74133-25-8
A838383
AKOS005267139
NCGC00023509-11
NCGC00023509-09
NCGC00023509-10
HMS2096H13
HMS3259F10
(1s,3r,7s,8s,8ar)-8-{2-[(2r,4r)-4-hydroxy-6-oxooxan-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl (2s)-2-methylbutanoate
lovastatine
EN300-52515
HMS3039N16
nsc 758662
ccris 8092
lovastatinum
lovastatin [usan:usp:inn:ban]
lovastatina
9lhu78oqfd ,
unii-9lhu78oqfd
(1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-8-(2-((4r,6r)-4-hydroxy-2-oxo-2h-pyran-6-yl)ethyl)-3,7-dimethylnaphtyl(s)-2-methylbutyrat
ec 616-212-7
tox21_201475
tox21_300268
NCGC00254157-01
NCGC00259026-01
nsc758662
pharmakon1600-01503977
lovastatin [usan]
dtxcid50784
dtxsid5020784 ,
tox21_110888
6 alpha-methylcompactin
HMS2236F07
CCG-39627
NCGC00023509-14
S2061
BBL024473
lovastatin [ep monograph]
lovastatin [inn]
lovastatin [who-dd]
lovastatin [orange book]
lovastatin [vandf]
(2s)-2-methylbutanoic acid (1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-((2r,4r)-tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl ester
lovastatin [hsdb]
lovastatin [usp monograph]
lovastatin [mart.]
lovastatin [mi]
simvastatin impurity e [ep impurity]
butanoic acid, 2-methyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl)ethyl)-1-naphthalenyl ester, (1s-(1.alpha.(r*),3.alpha.,7.beta.,8.beta.(2s*,4s*),8.alpha..beta.))-
simvastatin impurity, lovastatin- [usp impurity]
lovastatin [usp-rs]
lovastatin component of advicor
advicor component lovastatin
G226
CS-1990
HY-N0504
NC00713
SCHEMBL3136
tox21_110888_1
NCGC00023509-13
KS-1082
AB00052400-17
SCHEMBL14227102
us9353061, lovastatina
us9115116, lovastatin
bdbm34168
cid_53232
(2s)-(1s,3r,7s,8s,8ar)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-[(2r,4r)-tetrahydro-4-hydroxy-6-oxo-2h-pyran-2-yl]ethyl]-1-naphthalenyl-2-methyl butanoate
PCZOHLXUXFIOCF-BXMDZJJMSA-N
MLS006011867
HMS3403O07
AB00052400_19
AB00052400_18
OPERA_ID_1578
mfcd00072164
sr-01000000123
SR-01000000123-3
(1s,3r,7s,8s,8ar)-8-(2-((2r,4r)-4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl)ethyl)-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl (s)-2-methylbutanoate
mevinolin from aspergillus sp., powder
SR-05000001880-1
SR-05000001880-2
sr-05000001880
lovastatin (mevacor)
SBI-0051881.P002
HMS3713H13
NCGC00023509-16
lovastatin (mk-803)
(s)-((1s,3r,7s,8s,8ar)-8-(2-((2r,4r)-4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl)ethyl)-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl) 2-methylbutanoate
mk-803; lovalip; mevacor
mevinolin (lovastatin)
mevinolin from aspergillus sp.
(s)-(1s,3r,7s,8s,8ar)-8-(2-((2r,4r)-4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl)ethyl)-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2-methylbutanoate
HMS3676H19
8-[2-(4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl)ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydro-1-naphthale
lovastatin,(s)
HMS3412H19
Q417740
BRD-K09416995-001-21-7
HMS3884B03
mevacor;monacolin k;mevinolin;6-alpha-methylcompactin
nsc-779704
nsc779704
lovastatin for peak identification
BL164644
lovastatin- bio-x
HY-N0504R
CS-0694830
lovastatin (standard)
Z754931258
lovastatin (usp monograph)
(1s,3r,7s,8s,8ar)-8-(2-((2r,4r)-4-hydroxy-6-oxotetrahydro-2h-pyran-2-yl)ethyl)-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl (2s)-2-methylbutanoate
simvastatin impurity e (ep impurity)
lovastatin (ep monograph)
simvastatin impurity, lovastatin-(usp impurity)
lovastatin (usp-rs)
lovastatinum (latin)
lovastatin (mart.)
lovastatin (usan:usp:inn:ban)

Research Excerpts

Overview

Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment. Lovastatin has 5% bioavailability due to extensive first pass metabolism and poor solubility.

ExcerptReferenceRelevance
"Lovastatin (LV) is a natural compound extracted from Monascus-fermented foods and is an inhibitor of HMG-CoA reductase (HMGCR), which has been approved by the FDA for hyperlipidemia treatment."( Lovastatin enhances chemosensitivity of paclitaxel-resistant prostate cancer cells through inhibition of CYP2C8.
Chen, S; Deng, X; Fu, S; He, G; Li, Y; Wu, M; Xue, L; Zheng, C; Zhu, J, 2022
)
2.89
"Lovastatin (Lov) is a lipid-lowering agent, with 5% bioavailability (BA) due to extensive first pass metabolism and poor solubility. "( Design and Development of Solid SMEDDS and Liquisolid Formulations of Lovastatin, for Improved Drug Dissolution and In vivo Effects-a Pharmacokinetic and Pharmacodynamic Assessment.
Suram, D; Veerabrahma, K, 2022
)
2.4
"Lovastatin is a blood cholesterol-lowering agent and is produced as a secondary metabolite by "( Lovastatin production by
Babaei, A; Bizukojc, M; Jalili, H; Kargar, S; Mohseny Takloo, S; NoorMohammedi, J, 2023
)
3.8
"Lovastatin is a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor that impacts the mevalonate pathway."( Effects of Lovastatin on Brain Cancer Cells.
Amadasu, E; Borlongan, CV; Kang, R; Usmani, A,
)
1.24
"Lovastatin is a commonly prescribed drug for hypercholesterolemia and possesses remarkable antioxidant potential."( Evaluating The Protective Effects Of Lovastatin Against Doxorubicin Induced Cardiotoxicity In Balb-C Mice.
Afzal, A; Ajmal, K; Rafique, S; Sikandar, A; Tehseen, T; Zafar, A,
)
1.13
"Lovastatin is an FDA approved drug that has been used clinically for over a decade as a lipid-lowering medication."( Lovastatin inhibits Toll-like receptor 4 signaling in microglia by targeting its co-receptor myeloid differentiation protein 2 and attenuates neuropathic pain.
Chen, H; Grace, PM; Hutchinson, MR; Li, H; Peng, Y; Wang, X; Wang, Y; Watkins, LR; Yin, H; Zhang, T; Zhang, X, 2019
)
2.68
"Lovastatin (LVS) is an effective therapeutic and prophylactic agent in several cardiovascular disorders. "( Thermodynamics and solute-solvent interactions of lovastatin in an aqueous arginine solution.
Affandi, MMRMM; Majeed, ABA; Zolkiflee, NF, 2020
)
2.25
"Lovastatin is a typical drug interacting with grapefruit juice and naringin and vitamin C are main active constituents in fruit juice. "( Study on the interaction between lovastatin and three digestive enzymes and the effect of naringin and vitamin C on it by spectroscopy and docking methods.
Liu, Y; Liu, Z; Meng, X; Nan, G; Song, N; Wang, Y; Yang, G; Yang, L; Zhang, L, 2020
)
2.28
"Lovastatin is a promising therapeutic agent for the treatment of neurodegenerative disorders."( Lovastatin alters neurotrophin expression in rat hippocampus‑derived neural stem cells in vitro.
Abdanipour, A; Anarkooli, IJ; Fakheri, F; Parivar, K; Rastegar, H, 2019
)
2.68
"Lovastatin is an important medicine and it shows a significant effect against glucocorticoid-induced necrosis of the femoral head. "( Untargeted metabolomics reveals the effect of lovastatin on steroid-induced necrosis of the femoral head in rabbits.
Chen, K; Fan, W; Ren, X; Shao, Z; Wang, Z; Yu, X, 2020
)
2.26
"Lovastatin of RYP is a hypolipidemic commercial drug."( The physico-chemical alteration of lovastatin and enhanced antioxidant effect of Bacillus subtilis fermented-red yeast rice product.
Cho, MK; Gum, SI; Han, YH; Lee, JR; Nguyen, PA, 2017
)
1.45
"Lovastatin is a commercially important secondary metabolite produced by Aspergillus terreus, either by solid-state fermentation or by submerged fermentation. "( Key role of alternative oxidase in lovastatin solid-state fermentation.
Barrios-González, J; Cabrera-Orefice, A; Pérez-Sánchez, A; Uribe-Carvajal, S, 2017
)
2.17
"Lovastatin is a competitive inhibitor of the enzyme hydroxymethyl glutaryl coenzyme A reductase (HMGR) in cholesterol biosynthetic pathway and hence used in the treatment of hyperlipidemia. "( Comparative Study on Whole Genome Sequences of Aspergillus terreus (Soil Fungus) and Diaporthe ampelina (Endophytic Fungus) with Reference to Lovastatin Production.
Anil Kumar, M; Bhargavi, SD; Praveen, VK; Savitha, J, 2018
)
2.12
"Lovastatin is a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor that is clinically used for the prevention of cardiovascular diseases. "( Anti-inflammatory effect of lovastatin is mediated via the modulation of NF-κB and inhibition of HDAC1 and the PI3K/Akt/mTOR pathway in RAW264.7 macrophages.
Choi, HW; Choi, WS; Kang, MJ; Kim, GD; Kong, WS; Lee, JH; Oh, MJ; Seo, YB; Shin, PG, 2018
)
2.22
"Lovastatin is a natural competitive inhibitor of 3-hydroxy-3-methyl glutaryl coenzyme-A (HMG-CoA) reductase and inhibits specifically rate limiting step in cholesterol biosynthesis. "( Enhanced production of Lovastatin by filamentous fungi through solid state fermentation.
Akhlaq, M; Akhter, N; Akram, M; Farooq, T; Kamal, S; Khan, SG; Kiran, S; Said, F; Shah, SMA; Tahir, IM; Zaheer, J, 2018
)
2.23
"Lovastatin is a breast CSC-targeting drug. "( Transcriptome-based identification of lovastatin as a breast cancer stem cell-targeting drug.
Castro-Vázquez, SS; De La Fuente-Granada, M; González-Arenas, A; Guerrero-Rodríguez, SL; Mondragon-Peralta, A; Pérez-Tapia, SM; Vásquez-Bochm, LX; Velasco-Velázquez, MA; Velázquez-Paniagua, M, 2019
)
2.23
"Lovastatin is a potent drug for lowering blood cholesterol. "( Lovastatin-producing endophytic fungus isolated from a medicinal plant Solanum xanthocarpum.
Parthasarathy, R; Sathiyabama, M, 2015
)
3.3
"Lovastatin (LOV) is a statin, used to lower cholesterol which has been found as a hypolipidemic agent in commercial red yeast rice. "( A sensitive molecularly imprinted polymer based quartz crystal microbalance nanosensor for selective determination of lovastatin in red yeast rice.
Atar, N; Eren, T; Karimi-Maleh, H; Yola, ML, 2015
)
2.07
"Lovastatin is a proteasome inhibitor that enhances gefitinib-induced antiproliferation in non-small cell lung cancer."( Lovastatin overcomes gefitinib resistance through TNF-α signaling in human cholangiocarcinomas with different LKB1 statuses in vitro and in vivo.
Chang, VH; Chen, CC; Jiang, X; Lin, HY; Liu, YR; Wang, J; Yang, SH; Yen, Y; Zhang, K, 2015
)
2.58
"Lovastatin is a member of Statins, which are beneficial in a lot of immunologic cardiovascular diseases and T cell-mediated autoimmune diseases. "( Lovastatin blocks Kv1.3 channel in human T cells: a new mechanism to explain its immunomodulatory properties.
Cheng, X; Ding, D; Dong, Q; Du, YM; Guo, KF; Li, J; Li, S; Liao, YH; Qian, C; Wang, BB; Wu, QF; Xie, JJ; Zhao, N, 2015
)
3.3
"Lovastatin (LOV) is an antihyperlipidemic agent which exhibits low bioavailability due to its poor solubility. "( Simultaneous determination of lovastatin and its metabolite lovastatin acid in rat plasma using UPLC-MS/MS with positive/negative ion-switching electrospray ionization: Application to a pharmacokinetic study of lovastatin nanosuspension.
Fu, Q; Guo, M; He, Z; Li, M; Liu, B; Pu, X; Yang, L; Zhao, L, 2016
)
2.17
"Lovastatin is a prodrug that is hydrolysed in vivo to β-hydroxy acid lovastatin, which inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-Co-A) reductase (HMGR), thereby lowering cholesterol in humans. "( In vitro susceptibility of cultured human methanogens to lovastatin.
Armstrong, N; Demonfort Nkamga, V; Drancourt, M, 2017
)
2.14
"Lovastatin is a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor. "( Lovastatin overcomes gefitinib resistance in human non-small cell lung cancer cells with K-Ras mutations.
Han, JY; Jung, JI; Kim, JY; Park, IH, 2010
)
3.25
"Lovastatin is an effective drug for treatment of hyperlipidemia. "( Cloning and bioinformatic analysis of lovastatin biosynthesis regulatory gene lovE.
Huang, X; Li, HM, 2009
)
2.07
"Lovastatin is an inhibitor of P-glycoprotein (P-gp) and is metabolized by the cytochrome P450 (CYP) 3A4 isoenzyme. "( Pharmacokinetic interaction between oral lovastatin and verapamil in healthy subjects: role of P-glycoprotein inhibition by lovastatin.
Choi, DH; Choi, JS; Chung, JH, 2010
)
2.07
"Lovastatin is an important statin prescribed for the treatment and prevention of cardiovascular diseases. "( Crystal structure and biochemical studies of the trans-acting polyketide enoyl reductase LovC from lovastatin biosynthesis.
Ames, BD; Bruegger, J; Li, JW; Ma, S; Nguyen, C; Smith, P; Tang, Y; Tsai, SC; Vederas, JC; Wong, E; Wong, S; Xie, X; Xu, W, 2012
)
2.04
"Lovastatin is a main component of Monascus purpureus fermented red rice contributing to the lipid-lowering effect. "( Simultaneous determination of lovastatin and citrinin in red yeast rice supplements by micellar electrokinetic capillary chromatography.
Mornar, A; Nigović, B; Sertić, M, 2013
)
2.12
"Lovastatin is a competitive inhibitor of 3-hydroxy 3-methylglutaryl coenzyme A reductase, the key regulatory enzyme of cholesterol biosynthesis. "( Lovastatin alters cytoskeleton organization and inhibits experimental metastasis of mammary carcinoma cells.
Alonso, DF; Bublik, DR; Farina, HG; Gomez, DE, 2002
)
3.2
"Lovastatin is a HMC proliferation inhibitor. "( [Inhibitory effects of lovastatin on the proliferation and cell cycle phase of cultured human glomerular mesangial cells in vitro].
Duan, L; Li, CH; Li, H; Li, XW, 2002
)
2.07
"Lovastatin is a naturally occurring component of Chinese red rice and was the probable cause of his myopathy."( Chinese red rice-induced myopathy.
Olive, KE; Smith, DJ, 2003
)
1.04
"Lovastatin is a specific inhibitor of three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, used commonly for the treatment of hypercholesterolemia."( The HMG-CoA reductase inhibitor lovastatin reverses the learning and attention deficits in a mouse model of neurofibromatosis type 1.
Brown, RA; Cannon, TD; Cui, Y; Frankland, PW; Jentsch, JD; Kushner, SA; Li, W; Silva, AJ, 2005
)
1.33
"Lovastatin is a specific and potent inhibitor of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of the mevalonate pathway."( Strategies to enhance epidermal growth factor inhibition: targeting the mevalonate pathway.
Dimitroulakos, J; Goss, G; Lorimer, IA, 2006
)
1.06
"Lovastatin is a lipid-lowering agent indicated for primary hypercholesterolemia. "( Pharmacokinetics and bioequivalence study of two tablet formulations of lovastatin in healthy volunteers.
Amenta, F; Mignini, F; Streccioni, V; Tomassoni, D; Traini, E, 2008
)
2.02
"Lovastatin acts as an antioxidant by decreasing oxygen radical production by human phagocytes and may be important in abrogating the carcinogenic effect of chronic inflammation."( The antioxidant effect of lovastatin on phagocyte-induced DNA damage: implications for cancer prevention.
Weitberg, AB, 2007
)
1.36
"Lovastatin is a widely used anticholesterolemic drug which exercises its effect by inhibiting hepatic cholesterol synthesis and up-regulating low density lipoprotein (LDL) receptors. "( Effect of lovastatin on cell surface expression of Fc receptors or CD14 antigen in human monocytes.
Bigler, RD; Esfahani, M; Gressen, E, 1993
)
2.13
"Lovastatin (LST) is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a rate-limiting enzyme that regulates the biosynthesis of cholesterol. "( Metastasis of B16F10 mouse melanoma inhibited by lovastatin, an inhibitor of cholesterol biosynthesis.
Blanock, K; Gupta, V; Jani, JP; Katoh, A; Singh, SV; Specht, S; Stemmler, N, 1993
)
1.98
"Lovastatin is a prodrug lactone whose open-chain 3,5-dihydroxy acid is a potent, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme in cholesterol biosynthesis. "( Biotransformation of lovastatin. V. Species differences in in vivo metabolite profiles of mouse, rat, dog, and human.
Duggan, DE; Halpin, RA; Hunninghake, DB; Kari, PH; Till, AE; Ulm, EH; Vyas, KP,
)
1.89
"Lovastatin (monocolin K) is a competitive inhibitor of 3-hydroxy-3-methylglutaryl-CoA-reductase. "( [The effect of lovastatin on sterol synthesis and yeast resistance to polyene antibiotics].
Baranova, NA; Egorov, NS; Kreĭner, VG; Vybornykh, SN,
)
1.93
"Lovastatin is an inactive lacton prodrug which must be enzymatically or chemically transformed to the active form."( Evidence of combined therapy of dyslipoproteinemia by HMG-CoA reductase inhibitors and "essential" phospholipids.
Bondarenko, BB; Gurevich, VS; Kasennova, NI; Le Van Thach, TD; Mikhailova, IA, 1993
)
1.01
"Like lovastatin, it is an inactive hydrophobic lactone prodrug which is metabolised in vivo to several more polar, pharmacologically active compounds, most notably the corresponding hydroxy acid form, simvastatin acid."( Clinical pharmacokinetics and practical applications of simvastatin.
Mauro, VF, 1993
)
0.74
"Lovastatin is an HMG Coenzyme A reductase inhibitor which is useful in treating non-uraemic patients with hypercholesterolaemia."( Effect of lovastatin on serum lipid profile in the treatment of dyslipoproteinaemia in uraemic patients on continuous ambulatory peritoneal dialysis.
Chiu, K; Lai, KN; Lam, CW; Leung, CB; Li, PK; Lui, SF; Mak, GY; Mak, TW, 1993
)
1.41
"Lovastatin appears to be a safe and useful drug in effectively treating dyslipoproteinaemia in CAPD patients."( Effect of lovastatin on serum lipid profile in the treatment of dyslipoproteinaemia in uraemic patients on continuous ambulatory peritoneal dialysis.
Chiu, K; Lai, KN; Lam, CW; Leung, CB; Li, PK; Lui, SF; Mak, GY; Mak, TW, 1993
)
2.13
"Lovastatin (LS) is a potent HMG-CoA inhibitor used in the treatment of hypercholesterolemia. "( Experimental lovastatin myopathy.
Engel, AG; Lindal, S; Waclawik, AJ, 1993
)
2.1
"Lovastatin is a generally well-tolerated and effective drug during long-term use."( Lovastatin 5-year safety and efficacy study. Lovastatin Study Groups I through IV.
, 1993
)
3.17
"Lovastatin (LOVA) is a potent inhibitor of 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase widely used in clinical practice. "( Regulation of phenobarbital-inducible cytochrome P450 2B1/2 mRNA by lovastatin and oxysterols in primary cultures of adult rat hepatocytes.
Guzelian, PS; Kocarek, TA; Schuetz, EG, 1993
)
1.96
"Lovastatin is a cholesterol-lowering drug that can cause myopathy as a rare side effect. "( Itraconazole drastically increases plasma concentrations of lovastatin and lovastatin acid.
Jalava, KM; Neuvonen, PJ, 1996
)
1.98
"Lovastatin is a popular drug for the treatment of hypercholesterolemia. "( Rhabdomyolysis, acute renal failure and hepatopathy induced by lovastatin monotherapy.
Chen, WJ; Chiang, CW; Chu, PH; Lee, YS, 1997
)
1.98
"Lovastatin serves as a potential therapeutic approach to mesangial proliferative disease."( Lovastatin inhibits mesangial cell proliferation via p27Kip1.
Inoshita, S; Kuwahara, M; Marumo, F; Nakashima, O; Sasaki, S; Terada, Y; Yamada, T, 1998
)
2.46
"Lovastatin is an inhibitor of HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis."( Low density lipoproteins and Lovastatin modulate the organ-specific transendothelial migration of primary and metastatic human colon adenocarcinoma cell lines in vitro.
Cohen, SA; Doerr, RJ; Hordines, J; Mehta, N; Sykes, D, 1998
)
1.31
"Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis."( Lovastatin-mediated G1 arrest is through inhibition of the proteasome, independent of hydroxymethyl glutaryl-CoA reductase.
Chen, X; Herliczek, T; Keyomarsi, K; Lowe, M; Porter, DC; Rao, S, 1999
)
2.47
"Lovastatin is a potent inhibitor of protein prenylation, and it has been reported to have pleiotropic cellular effects. "( Lovastatin inhibits G1/S transition of normal human B-lymphocytes independent of apoptosis.
Blomhoff, HK; Blomhoff, R; Erikstein, B; Myklebust, J; Naderi, S; Norum, KR; Smeland, EB, 1999
)
3.19
"Lovastatin is a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor that inhibits cholesterol biosynthesis and affects the activity of some signal transduction pathways and liver transcription factors."( Lovastatin decreases mortality and improves liver functions in fulminant hepatic failure from 90% partial hepatectomy in rats.
Cai, SR; Flye, MW; Kennedy, SC; Motoyama, K; Ponder, KP; Shen, KJ, 2000
)
2.47
"Lovastatin is a lipid lowering agent that acts by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, a key regulatory enzyme in cholesterol biosynthesis. "( Proteomics to display lovastatin-induced protein and pathway regulation in rat liver.
Anderson, NL; Aponte, AM; Gatlin, CL; Lennon, JJ; Makusky, AJ; McGrath, AM; Rohrs, MC; Steiner, S, 2000
)
2.06
"Lovastatin is a secondary metabolite produced by Aspergillus terreus. "( Lovastatin biosynthesis by Aspergillus terreus in a chemically defined medium.
Duboc, P; Hajjaj, H; Niederberger, P, 2001
)
3.2
"Lovastatin is an inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the major regulatory enzyme of the mevalonate pathway. "( Blocking protein geranylgeranylation is essential for lovastatin-induced apoptosis of human acute myeloid leukemia cells.
Dimitroulakos, J; Minden, MD; Penn, LZ; Tan, MM; Wong, WW; Xia, Z, 2001
)
2
"Lovastatin is a potent inhibitor of meningioma cell proliferation which may act in part by reducing activation of MEK-1-MAPK/ERK pathway."( Lovastatin is a potent inhibitor of meningioma cell proliferation: evidence for inhibition of a mitogen associated protein kinase.
Allen, GS; Johnson, MD; Okediji, EJ; Toms, SA; Woodard, A, 2002
)
2.48
"Lovastatin is an irreversible inhibitor of HMG-CoA reductase and blocks the production of mevalonate, a critical compound in the production of cholesterol and isoprenoids. "( The cholesterol lowering drug lovastatin induces cell death in myeloma plasma cells.
Bloem, AC; Kamphuis, MM; Lokhorst, HM; van de Donk, NW, 2002
)
2.05
"Lovastatin appears to be a safe and effective treatment for pediatric cholesteryl ester storage disease."( Safety and efficacy of treatment of pediatric cholesteryl ester storage disease with lovastatin.
Glueck, CJ; Lichtenstein, P; Speirs, J; Tracy, T, 1992
)
1.23
"Lovastatin is an inhibitor of HMG-Co A reductase, a key enzyme in cholesterol biosynthesis. "( [Absence of cataractogenic effect of lovastatin (Mevinacor) so far].
Schneider, T; Ulbig, M, 1991
)
2
"Lovastatin is a new drug that has become popular for the treatment of patients with hyperlipidemias. "( Lovastatin-associated rhabdomyolysis.
Sylvain-Moore, H; Worden, JP, 1991
)
3.17
"Lovastatin, which is an inhibitor of hydroxymethygluteryl coenzyme A reductase, is a new agent for treating hypercholesterolemia and is administered in a dose of 20 to 80 mg/day."( Cholesterol-lowering effects of a 10 mg daily dose of lovastatin in patients with initial total cholesterol levels 200 to 240 mg/dl (5.18 to 6.21 mmol/liter).
Groskop, I; Lurie, Y; Rubinstein, A; Weintrob, M, 1991
)
1.25
"Lovastatin is a potent inhibitor of cholesterol synthesis in CaCo-2 cells."( Effect of lovastatin on acyl-CoA: cholesterol O-acyltransferase (ACAT) activity and the basolateral-membrane secretion of newly synthesized lipids by CaCo-2 cells.
Albright, E; Field, FJ; Kam, NT; Mathur, S, 1990
)
1.4
"Lovastatin is a pro-drug lactone whose open chain beta-hydroxy-acid (HA) is a potent inhibitor of hydroxymethylglutaryl-CoA-reductase and thus of cholesterol synthesis. "( The physiological disposition of lovastatin.
Bayne, WF; Chen, IW; Duggan, DE; Duncan, CA; Halpin, RA; Schwartz, MS; Stubbs, RJ; Vickers, S,
)
1.86
"Lovastatin (mevinolin) is a new hypolipidemic agent which blocks cholesterol synthesis by competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase."( Testicular function in type II hyperlipoproteinemic patients treated with lovastatin (mevinolin) or neomycin.
Brewer, HB; Brittain, EH; Farnsworth, WH; Hoeg, JM; Maher, M; Sherins, RJ, 1987
)
1.23
"Lovastatin is a potent competitive inhibitor of the rate-limiting enzyme of cholesterol synthesis, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (NADPH) [HMG-CoA reductase; (S)-mevalonate:NADP+ oxidoreductase (CoA-acylating), EC 1.1.1.34]. "( Lovastatin, an inhibitor of cholesterol synthesis, induces hydroxymethylglutaryl-coenzyme A reductase directly on membranes of expanded smooth endoplasmic reticulum in rat hepatocytes.
Huff, JW; Kazazis, DM; Scott, S; Singer, II, 1988
)
3.16
"Lovastatin is a potent new drug for lowering serum cholesterol through inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme for cholesterol biosynthesis. "( Lovastatin: a new cholesterol-lowering agent.
Krukemyer, JJ; Talbert, RL, 1987
)
3.16

Effects

Lovastatin treatment has a weaker inhibitory effect on the progression of atherosclerosis and no effect on vascular NO elaboration. Lovastatin has been shown to effectively lower both the serum total cholesterol and triglyceride levels, the most common abnormalities in these patients.

ExcerptReferenceRelevance
"Lovastatin treatment has a weaker inhibitory effect on the progression of atherosclerosis and no effect on vascular NO elaboration, which may be due to its stimulatory effect on vascular superoxide radical generation."( Dietary L-arginine reduces the progression of atherosclerosis in cholesterol-fed rabbits: comparison with lovastatin.
Bode-Böger, SM; Böger, RH; Böhme, M; Brandes, RP; Frölich, JC; Mügge, A; Nafe, R; Phivthong-ngam, L, 1997
)
1.23
"Lovastatin has been indicated to impair growth and development of Phytophthora sojae. "( Transcriptome reveals BCAAs biosynthesis pathway is influenced by lovastatin and can act as a potential control target in Phytophthora sojae.
Gao, Z; Huang, Q; Jiang, X; Liang, Y; Wu, Y; Xu, J; Yang, X; Ye, W, 2022
)
2.4
"Lovastatin has great medical and economic importance, and its production in Aspergillus terreus is positively regulated at transcriptional level, by reactive oxygen species (ROS) generated during idiophase. "( Role of AtYap1 in the reactive oxygen species regulation of lovastatin production in Aspergillus terreus.
Barrios-González, J; Mejía, A; Miranda-Labra, RU; Pérez-Sánchez, A, 2023
)
2.6
"Lovastatin also has anti-inflammatory, anti-cancer, and neuroprotective effects."( An overview on the biological activity and anti-cancer mechanism of lovastatin.
Chen, X; Ji, X; Shang, J; Wei, Y; Xie, L; Zhang, C; Zhang, Q; Zhu, G, 2021
)
1.58
"Lovastatin has been shown to protect mice from late radiation injury."( A Phase II Study to Prevent Radiation-induced Rectal Injury With Lovastatin.
Anscher, MS; Chang, MG; Grob, BM; Holdford, D; Mikkelsen, RB; Moghanaki, D; Mukhopadhyay, ND; Rosu, M; Sanyal, A; Skinner, V; Wang, A, 2018
)
1.44
"Lovastatin has been prescribed to lower total cholesterol and low-density lipoprotein cholesterol, reducing cardiovascular-related morbidity and mortality in patients with hypercholesterolemia."( Rhabdomyolysis and pancreatitis associated with coadministration of danazol 600 mg/d and lovastatin 40 mg/d.
Chen, CH; Hsieh, CY, 2008
)
1.29
"Lovastatin (LOV), which has low water solubility, was chosen as a model drug."( Uniform mesoporous carbon as a carrier for poorly water soluble drug and its cytotoxicity study.
Deng, Y; Jiang, T; Sun, C; Sun, J; Wang, L; Wang, S; Zhang, J; Zhang, Q; Zhao, P, 2012
)
1.1
"Lovastatin has also been proved to potentiate antitumor effects of both cisplatin and TNF-alpha in murine melanoma models."( Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism.
Feleszko, W; Grzela, T; Hoser, G; Jakóbisiak, M; Jalili, A; Korczak-Kowalska, G; Lasek, W; Młynarczuk, I; Olszewska, D, 2002
)
2.48
"Lovastatin has been used to treat hypercholesterolemia through blocking the mevalonate biosynthesis pathway. "( Lovastatin induces apoptosis of anaplastic thyroid cancer cells via inhibition of protein geranylgeranylation and de novo protein synthesis.
Chang, TC; Lee, WS; Wang, CY; Zhong, WB, 2003
)
3.2
"Lovastatin has been shown to decrease the production of Abeta and to promote neuronal survival."( Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling.
Amara, F; Arthur, G; Dibrov, A; He, Y; Kashour, T; Salins, P; Shawesh, S, 2007
)
2.5
"Lovastatin has been shown to effectively lower both the serum total cholesterol and triglyceride levels, the most common abnormalities in these patients."( Lipid-lowering effects of lovastatin in CAPD patients.
Jacobs, RH; Lal, SM; Nolph, KD, 1993
)
1.31
"Lovastatin has effects similar to those reported in younger subjects in previous controlled trials."( Cholesterol lowering in the elderly. Results of the Cholesterol Reduction in Seniors Program (CRISP) pilot study.
Applegate, W; Crouse, JR; Davis, CE; Eckfeldt, JH; Gordon, DJ; Grimm, R; Hunninghake, DB; Knopp, R; LaRosa, JC, 1994
)
1.01
"Lovastatin has been associated with development of subcapsular cataract in dogs given high doses. "( Lovastatin and the human lens; results of a two year study. The MSDRL Study Group.
Chylack, LT; Friend, J; Mantell, G; Rosner, B; Wolfe, JK, 1993
)
3.17
"Lovastatin treatment has a weaker inhibitory effect on the progression of atherosclerosis and no effect on vascular NO elaboration, which may be due to its stimulatory effect on vascular superoxide radical generation."( Dietary L-arginine reduces the progression of atherosclerosis in cholesterol-fed rabbits: comparison with lovastatin.
Bode-Böger, SM; Böger, RH; Böhme, M; Brandes, RP; Frölich, JC; Mügge, A; Nafe, R; Phivthong-ngam, L, 1997
)
1.23
"Lovastatin has been shown to reduce cholesterol esterification in cholesterol-loaded human macrophages. "( Differential effects of lovastatin on the trafficking of endogenous and lipoprotein-derived cholesterol in human monocyte-derived macrophages.
Assmann, G; Brennhausen, B; Cignarella, A; Cullen, P; von Eckardstein, A, 1998
)
2.05
"Lovastatin has been shown to reduce tumor cell proliferation in a dose-dependent manner."( Increased sensitivity of myeloid leukemia cell lines: potential of lovastatin as bone-marrow-purging agent.
Csipai, M; Glasmacher, A; Huhn, D; Lefterova, P; Neubauer, A; Scheffold, C; Schmidt-Wolf, IG; Schöttker, B, 2000
)
1.26
"Lovastatin has been proven to effectively lower circulating LDL cholesterol and to exert antiproliferative effects on various cell lines, the latter effect being only incompletely understood. "( Lovastatin controls signal transduction in vascular smooth muscle cells by modulating phosphorylation levels of mevalonate-independent pathways.
Breithardt, G; Buddecke, E; Schmidt, A; Sindermann, JR,
)
3.02
"Lovastatin has been used with increasing frequency over the past few years to reduce serum cholesterol. "( Lovastatin/gemfibrozil myopathy: a clinical, histochemical, and ultrastructural study.
Chucrallah, A; De Girolami, U; Federman, M; Freeman, R, 1992
)
3.17
"Lovastatin has been available in the United States since September 1987."( Clinical experience with lovastatin.
Chremos, AN; Mantell, GE; Shear, CL; Tobert, JA, 1990
)
1.3
"Lovastatin has been available for prescription use in the United States for about 20 months (as of June 1989). "( Extended clinical safety profile of lovastatin.
Burke, MT; Mantell, G; Staggers, J, 1990
)
2
"Lovastatin has been available in the United States since September 1987."( Efficacy and long-term adverse effect pattern of lovastatin.
Tobert, JA, 1988
)
1.25
"Lovastatin has been marketed in the United States for over 6 months."( HMG CoA reductase inhibitors. Current clinical experience.
Walker, JF, 1988
)
1
"Lovastatin (Mevacor) has emerged as an agent that may effectively manage this condition."( Rhabdomyolysis and renal injury with lovastatin use. Report of two cases in cardiac transplant recipients.
Corpier, CL; Jones, PH; Lederer, ED; Quinones, MA; Schmidt, SW; Suki, WN; Young, JB, 1988
)
1.27
"Lovastatin has been well tolerated and patients maintained on this drug as a single agent have shown sustained reductions in the plasma concentrations of total and low density lipoprotein cholesterol."( Long term administration of lovastatin in the treatment of hypercholesterolaemia.
Illingworth, DR, 1987
)
1.29

Actions

Lovastatin did not inhibit palmitate-induced apoptosis. The lovastatin-induced increase in regulatory T cells in the inflamed skin was dependent on expression of CCL1. Lovastatin could inhibit the proliferation of MCF-7 cells significantly.

ExcerptReferenceRelevance
"The lovastatin-induced increase in regulatory T cells in the inflamed skin was dependent on expression of CCL1, a chemokine that is locally up-regulated by statin administration."( Statins induce regulatory T cell recruitment via a CCL1 dependent pathway.
Almonacid, L; Ardavín, C; Barber, DF; Goya, I; Jiménez-Baranda, S; León, B; Mañes, S; Márquez, G; Martínez-A, C; Mira, E; Stein, JV; Zaballos, A, 2008
)
0.83
"The lovastatin-mediated increase in the cytoplasm and at the cell surface is dose-dependent and significant at lovastatin concentrations comparable to plasma levels in patients under lovastatin treatment."( Lovastatin-stimulated superinduction of E-selectin, ICAM-1 and VCAM-1 in TNF-alpha activated human vascular endothelial cells.
Buddecke, E; Feitsma, K; Goepfert, C; Schmidt, A, 2002
)
2.24
"Lovastatin did not inhibit palmitate-induced apoptosis."( Lovastatin does not accentuate but is rather additive to palmitate-induced apoptosis in cardiomyocytes.
Kong, JY; Rabkin, SW, 2002
)
2.48
"But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1."( Statin inhibits interferon-gamma-induced expression of intercellular adhesion molecule-1 (ICAM-1) in vascular endothelial and smooth muscle cells.
Chung, HK; Kang, H; Kim, DW; Kim, H; Kim, YK; Lee, IK; Park, KC; Ro, HK; Shong, M; Suh, JM, 2002
)
0.8
"Lovastatin could inhibit the proliferation of MCF-7 cells significantly and 75.80 percent of cells were inhibited after treated with 16 micromol/L lovastatin for 72 hours (P< 0.05). "( [Effects of lovastatin on proliferation and gap junctional intercellular communication of human breast cancer cell MCF-7].
Mi, MT; Zhang, QY; Zhou, Y; Zhu, JD, 2003
)
2.14
"Lovastatin was found to inhibit HMC proliferation in a dose-dependent manner. "( [Inhibitory effects of lovastatin on the proliferation and cell cycle phase of cultured human glomerular mesangial cells in vitro].
Duan, L; Li, CH; Li, H; Li, XW, 2002
)
2.07
"Lovastatin promotes osteoblast differentiation by increasing bone morphogenetic protein-2 (BMP-2) expression. "( Statin-induced Ras activation integrates the phosphatidylinositol 3-kinase signal to Akt and MAPK for bone morphogenetic protein-2 expression in osteoblast differentiation.
Choudhury, GG; Ghosh-Choudhury, N; Mandal, CC, 2007
)
1.78
"Lovastatin may also produce oxidant stress by reducing levels of an endogenous antioxidant, coenzyme Q (CoQ)."( Effects of ethanol, lovastatin and coenzyme Q10 treatment on antioxidants and TBA reactive material in liver of rats.
Anthony, M; Folkers, K; Loop, RA; Willis, RA, 1994
)
1.33
"Lovastatin did not inhibit Ca(2+)-discharge from intracellular stores."( Lovastatin inhibits receptor-stimulated Ca(2+)-influx in retinoic acid differentiated U937 and HL-60 cells.
Aepfelbacher, M; Grünberg, B; Haag, H; Siess, W; Vauti, F; Weber, C, 1994
)
2.45
"Lovastatin did not cause cell death in a leucine auxotroph of Mucor grown in YNB minimal medium, conditions which support only spherical growth during spore germination."( Lovastatin triggers an apoptosis-like cell death process in the fungus Mucor racemosus.
Linz, JE; Roze, LV, 1998
)
2.46
"Lovastatin may therefore produce favorable alterations in endothelial healing, resulting in a decreased smooth muscle cell proliferative response to injury after angioplasty."( Background and methods for the lovastatin restenosis trial after percutaneous transluminal coronary angioplasty. The Lovastatin Restenosis Trial Study Group.
Alexander, RW; Boccuzzi, SJ; Brown, CL; Cohen, CL; Hirsch, LJ; King, SB; Weintraub, WS, 1992
)
1.29
"lovastatin therapy to lower plasma cholesterol does not lead to corresponding reductions in body cholesterol pools or to a reduction in the rate of whole-body cholesterol synthesis. "( Lack of effect of lovastatin therapy on the parameters of whole-body cholesterol metabolism.
Adams, M; Dell, RB; Goldberg, IJ; Goodman, DS; Holleran, S; Palmer, RH; Ramakrishnan, R, 1990
)
2.06

Treatment

Lovastatin treatment in patients with early-stage PD was associated with a trend of less motor symptom worsening. Lovastatin did not reduce the cellular cholesterol levels in RSV-infected cells, nor did it inhibit RSV infection.

ExcerptReferenceRelevance
"Lovastatin treatment significantly influences the BCAAs biosynthesis pathway in P. "( Transcriptome reveals BCAAs biosynthesis pathway is influenced by lovastatin and can act as a potential control target in Phytophthora sojae.
Gao, Z; Huang, Q; Jiang, X; Liang, Y; Wu, Y; Xu, J; Yang, X; Ye, W, 2022
)
2.4
"Lovastatin treatment in patients with early-stage PD was associated with a trend of less motor symptom worsening and was well tolerated. "( A Double-Blind, Randomized, Controlled Trial of Lovastatin in Early-Stage Parkinson's Disease.
Chang, CH; Chao, YT; Chen, YC; Cheng, MF; Huang, TL; Lin, CH; Tai, CH; Wu, RM; Yen, RF, 2021
)
2.32
"Lovastatin treatment also inhibited the increased expressions of β-secretase 1 (BACE1) and γ-secretase in hippocampal neurons under sevoflurane exposure in vitro."( Lovastatin attenuates sevoflurane-induced cognitive disorder in aged rats via reducing Aβ accumulation.
Chu, H; Dong, Y; Jiang, Q; Tian, Y; Wang, C; Xu, Y, 2021
)
2.79
"In Lovastatin treatment groups, a single dose of agent (2 and 5mg/kg) was administered daily."( Neuroprotective effect of Lovastatin on motor deficit induced by sciatic nerve crush in the rat.
Abdolmaleki, A; Ghayour, MB; Rassouli, MB, 2017
)
1.27
"Lovastatin treatment resulted in increased levels of IL-6, IL-12p40, and IFN-γ mRNA in both PBMCs and monocytes following LPS stimulation compared with control cells."( Monocyte Production of IFN-γ Is Interleukin-12 Dependent in a Model of Mevalonate Kinase Deficiency.
English, H; Frey, T; Llewellyn, T; Monteferante, K; Swade, K; Vogt, E; Zwecker, L, 2019
)
1.24
"Lovastatin treatment did not reduce the cellular cholesterol levels in RSV-infected cells, nor did it inhibit RSV infection."( Lovastatin treatment mitigates the pro-inflammatory cytokine response in respiratory syncytial virus infected macrophage cells.
Li, L; Ravi, LI; Sugrue, RJ; Sutejo, R; Tan, BH; Wong, PS, 2013
)
2.55
"Lovastatin treatment increased the yield of purpurin and mollugin significantly. "( Effects of lovastatin, clomazone and methyl jasmonate treatment on the accumulation of purpurin and mollugin in cell suspension cultures of Rubia cordifolia.
Fan, X; Han, ZF; Hu, GS; Jia, JM; Li, N, 2013
)
2.22
"Lovastatin treatment of either mouse alveolar epithelial cells endogenously expressing RAGE or HEK cells overexpressing RAGE caused induction of RAGE shedding, but did not influence secretion of esRAGE from HEK cells overexpressing esRAGE."( Statins stimulate the production of a soluble form of the receptor for advanced glycation end products.
Baiersdörfer, M; Kanarek, AM; Kojro, E; Postina, R; Quade-Lyssy, P, 2013
)
1.11
"Lovastatin treatment upregulated KLF4 mRNA and protein levels."( Pharmacological regulation of SPARC by lovastatin in human trabecular meshwork cells.
Chatterjee, A; Oh, DJ; Oh, SS; Rhee, DJ; Villarreal, G, 2014
)
1.39
"The Lovastatin treatment group (OVx+Lov) was given a single injection of 750 µg/kg lovastatin particles."( Targeted delivery of lovastatin and tocotrienol to fracture site promotes fracture healing in osteoporosis model: micro-computed tomography and biomechanical evaluation.
Abdullah, S; Ibrahim, N'; Khamis, MF; Mod Yunoh, MF; Mohamed, N; Shuid, AN, 2014
)
1.2
"Lovastatin treatment also inhibited the antioxidative capability of wheat seedlings, and tasg1 was more sensitive to lovastatin than WT, as indicated by the MDA content, protein carbonylation, and antioxidant enzyme activity."( The stay-green phenotype of wheat mutant tasg1 is associated with altered cytokinin metabolism.
Hao, Q; Li, Q; Tian, F; Wang, W, 2016
)
1.16
"Lovastatin treatment did not increase the surface expression of P-selectin or PAC-1 binding but led to strongly reduced collagen- and thrombin-induced platelet aggregation."( Lovastatin induces platelet apoptosis.
Chen, M; Dai, K; Hu, R; Li, M; Yan, R; Zhao, L; Zhao, Q; Zhou, L, 2016
)
2.6
"Lovastatin treatment down-regulates the expression of Bcl-2 and activates apoptosis through a mitochondria-operated, ErbB2- regulated mechanism."( Statins activate a mitochondria-operated pathway of apoptosis in breast tumor cells by a mechanism regulated by ErbB2 and dependent on the prenylation of proteins.
Herrero-Martin, G; López-Rivas, A, 2008
)
1.07
"The lovastatin-treated mice received 0.15 mg activated lovastatin by daily gavage."( Modelling neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin.
Kolanczyk, M; Kornak, U; Kossler, N; Kühnisch, J; Mundlos, S; Osswald, M; Stumpp, S; Thurisch, B, 2008
)
1.06
"Lovastatin treatment normalized all of these changes."( Systemic administration of HMG-CoA reductase inhibitor protects the blood-retinal barrier and ameliorates retinal inflammation in type 2 diabetes.
Chen, D; Li, J; Ma, JX; Mott, R; Wang, JJ; Yu, Q; Zhang, SX, 2009
)
1.07
"Lovastatin-treated mice displayed significantly reduced plasma cholesterol levels and levels of oxidized cholesterol metabolites in the brain in comparison to saline-treated controls."( Lovastatin ameliorates alpha-synuclein accumulation and oxidation in transgenic mouse models of alpha-synucleinopathies.
Adame, A; Kelly, J; Koob, AO; Mante, M; Masliah, E; Paulsson, JF; Rockenstein, E; Ubhi, K, 2010
)
2.52
"Lovastatin treatment reduced the volume fraction of liver nodules by 50% and the cell proliferation within the liver nodules was reduced to one third. "( Lovastatin prevents carcinogenesis in a rat model for liver cancer. Effects of ubiquinone supplementation.
Acimovic, J; Björkhem-Bergman, L; Eriksson, LC; Parini, P; Torndal, UB, 2010
)
3.25
"Lovastatin treatment induced actin cytoskeletal disorganization and the expression of geranylgeranylated rho family proteins that regulate the actin cytoskeleton, including rhoA."( Lovastatin inhibits EGFR dimerization and AKT activation in squamous cell carcinoma cells: potential regulation by targeting rho proteins.
Bradbury, PA; Dimitroulakos, J; Ding, K; Goss, G; Le Francois, BG; Zhao, TT, 2010
)
2.52
"Lovastatin treatment enhanced the expression of ergosterol biosynthetic genes, ERG2 and ERG3 in wild-type and upc2BΔ but not in upc2AΔ cells."( Transcription factors CgUPC2A and CgUPC2B regulate ergosterol biosynthetic genes in Candida glabrata.
Aoyama, T; Bard, M; Chibana, H; Higashi, S; Kajiwara, S; Miyazaki, Y; Nagi, M; Nakayama, H; Niimi, M; Ohno, H; Okano, M; Tanabe, K; Ueno, K; Umeyama, T; Yamagoe, S, 2011
)
1.09
"Lovastatin treatment impaired mitochondrial function and also decreased cellular ADP/ATP ratios, common triggers of LKB1/AMPK activation."( Lovastatin induces multiple stress pathways including LKB1/AMPK activation that regulate its cytotoxic effects in squamous cell carcinoma cells.
Dayekh, K; Dimitroulakos, J; Gorn-Hondermann, I; Ma, L; Niknejad, N, 2012
)
2.54
"Lovastatin treatment resulted in decreased apoptosis, senescence and LDH release and in increased viability and proliferation of WJMSC-derived chondrocytes."( Lovastatin protects chondrocytes derived from Wharton's jelly of human cord against hydrogen-peroxide-induced in vitro injury.
Bhatti, FU; Khan, SN; Mehmood, A; Riazuddin, S; Wajid, N, 2013
)
2.55
"Lovastatin treatment resulted also in significant reduction of the number of experimental metastasis in doxorubicin-treated mice."( Lovastatin potentiates antitumor activity of doxorubicin in murine melanoma via an apoptosis-dependent mechanism.
Feleszko, W; Grzela, T; Hoser, G; Jakóbisiak, M; Jalili, A; Korczak-Kowalska, G; Lasek, W; Młynarczuk, I; Olszewska, D, 2002
)
2.48
"Lovastatin treatment reduced both hepatic and gallbladder bile cholesterol, altered bile acid composition, and induced a 79% total response compared to placebo."( Lovastatin alters biliary lipid composition and dissolves gallstones: a long-term study in prairie dogs.
Abedin, MZ; Kirkwood, KS; Narins, SC; Park, EH; Smith, PR, 2002
)
2.48
"Lovastatin treatment induced NO by increasing NF-kappaB translocation and its association with the CREB-binding protein (CBP/p300) via the downregulation of RhoA."( Rho A negatively regulates cytokine-mediated inducible nitric oxide synthase expression in brain-derived transformed cell lines: negative regulation of IKKalpha.
Giri, S; Rattan, R; Singh, AK; Singh, I, 2003
)
1.04
"Lovastatin (5 microm) treatment causes extensive cell death in two of the cell lines, U87 and U251; but only minimal in a third, U138."( Lovastatin-induced up-regulation of the BH3-only protein, Bim, and cell death in glioblastoma cells.
Higashikubo, R; Jiang, Z; Lytle, RA; Rich, KM; Zheng, X, 2004
)
2.49
"Lovastatin treatment (20 mg/kg/day i.p.) over 7 days, which resulted in plasma lovastatin hydroxyacid concentrations of 0.098 +/- 0.03 microM, did not induce splenocyte Th2 cytokine production but did cause a small reduction in Ag-induced T cell proliferation and a decrease in the production of IFN-gamma and IL-10."( Suppression of autoimmune retinal disease by lovastatin does not require Th2 cytokine induction.
Adamson, P; Baker, D; Calder, V; Gegg, M; Greenwood, J; Hankey, D; Harry, R; Pryce, G; Zambarakji, H, 2005
)
1.31
"In lovastatin-treated resting human umbilical vein endothelial cells (HUVECs), increased levels of mRNA and protein of PECAM-1 as well as its bio-synthesis (all approximately 2-fold) were observed by real-time PCR, Western blotting and 35S-labeled methionine incorporation assay, respectively."( Statin-inhibited endothelial permeability could be associated with its effect on PECAM-1 in endothelial cells.
Chatterjee, S; Fang, L; Song, J; Wei, H, 2005
)
0.84
"Lovastatin treatment inhibited EGF-induced EGFR autophosphorylation by 24 hours that was reversed by the coadministration of mevalonate. "( Targeting the mevalonate pathway inhibits the function of the epidermal growth factor receptor.
Dimitroulakos, J; Goss, G; Hanson, JE; Lagarde, AE; Lorimer, IA; Mantha, AJ, 2005
)
1.77
"Lovastatin treatment significantly increased the level of myelin lipids in the spinal cord of treated EAE animals, coinciding with the attenuation of disease severity and inflammatory demyelination as compared with untreated EAE animals."( HMG-CoA reductase inhibitor augments survival and differentiation of oligodendrocyte progenitors in animal model of multiple sclerosis.
Khan, M; Paintlia, AS; Paintlia, MK; Singh, AK; Singh, I; Vollmer, T, 2005
)
1.05
"Lovastatin treatment was efficacious at reducing low-density lipoprotein cholesterol by 23% to 27%, total cholesterol by 17% to 22%, and apo B by 20% to 23% at weeks 4 and 24, respectively."( Efficacy and safety of lovastatin therapy in adolescent girls with heterozygous familial hypercholesterolemia.
Cho, M; Clauss, SB; Holmes, KW; Hopkins, P; Johnson-Levonas, AO; Kwiterovich, PO; Stein, E; Tate, A, 2005
)
1.36
"Lovastatin treatment inhibited EGF-induced EGFR autophosphorylation and its downstream signaling cascades by 24 hours."( Strategies to enhance epidermal growth factor inhibition: targeting the mevalonate pathway.
Dimitroulakos, J; Goss, G; Lorimer, IA, 2006
)
1.06
"Lovastatin treatment induced an increase in TCF/LEF-chloramphenicol acetyl transferase (CAT) gene reporter activity."( Lovastatin protects human neurons against Abeta-induced toxicity and causes activation of beta-catenin-TCF/LEF signaling.
Amara, F; Arthur, G; Dibrov, A; He, Y; Kashour, T; Salins, P; Shawesh, S, 2007
)
2.5
"Lovastatin treatment significantly increased the effects of dl1520 against ATC cells."( Lovastatin enhances the replication of the oncolytic adenovirus dl1520 and its antineoplastic activity against anaplastic thyroid carcinoma cells.
Bifulco, M; Ferraro, A; Fusco, A; Iacuzzo, I; Libertini, S; Portella, G; Vitale, M, 2007
)
2.5
"Lovastatin treatments significantly attenuated both the augmented contraction and RhoA translocation to the plasma membrane."( Lovastatin inhibits bronchial hyperresponsiveness by reducing RhoA signaling in rat allergic asthma.
Arima, J; Chiba, Y; Misawa, M; Sakai, H, 2008
)
2.51
"Lovastatin treatment in rat brain neuroblasts causes a significant time- and concentration-inhibition of protein synthesis, which is partially mediated by phosphatydilinositol 3-kinase/mammalian target of rapamycin (mTOR) pathway inhibition."( Lovastatin effect in rat neuroblasts of the CNS: inhibition of cap-dependent translation.
Bragado, MJ; Garcia-Marin, LJ; Santa-Catalina, MO, 2008
)
2.51
"In lovastatin-treated cells, reductase mRNA was primarily associated with heavy polysome fractions."( Mevalonate regulates polysome distribution and blocks translation-dependent suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase mRNA: relationship to translational control.
Gayen, AK; Peffley, DM, 1995
)
0.81
"Lovastatin treatment was associated with significant reductions in total cholesterol (p < 0.001), LDL-cholesterol (p < 0.001) and apo B (p < 0.01), the reductions at 24 months being 26, 30 and 18%, respectively."( Cholesterol-lowering therapy may retard the progression of diabetic nephropathy.
Cheng, IK; Janus, ED; Lam, KS; Pang, RW, 1995
)
1.01
"Lovastatin treatment was associated with a reduction in progression of mean maximum IMT (p < 0.001)."( Results of the primary outcome measure and clinical events from the Asymptomatic Carotid Artery Progression Study.
Byington, RP; Espeland, MA; Furberg, CD; Margitic, SE; Probstfield, JL, 1995
)
1.01
"Lovastatin-treated cells also exhibited decreased adherence to substrate (p < 0.05)."( Effect of lovastatin alone and as an adjuvant chemotherapeutic agent on hepatoma tissue culture-4 cell growth.
Buchwald, H; Furcht, LL; Morris, TJ; Palm, SL, 1995
)
1.41
"Lovastatin treatment resulted in a 20% decrease in TPC as compared to untreated controls.(ABSTRACT TRUNCATED AT 250 WORDS)"( Comparative effects of HMG-CoA reductase inhibitors on apo B production in the casein-fed rabbit: atorvastatin versus lovastatin.
Auerbach, BJ; Bisgaier, CL; Krause, BR; Newton, RS, 1995
)
1.22
"Five lovastatin-treated participants suffered major cardiovascular events--coronary heart disease mortality, nonfatal myocardial infarction, or stroke--versus 14 in the lovastatin-placebo groups (P = .04)."( Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group.
Adams, HP; Applegate, WB; Byington, RP; Espeland, MA; Furberg, CD; Hartwell, T; Hunninghake, DB; Lefkowitz, DS; Probstfield, J; Riley, WA, 1994
)
1.15
"Lovastatin reduced pretreatment levels of atherogenic and triglyceride-rich lipoprotein components and slowed post-treatment increases compared with no drug therapy."( Changes in plasma lipid and apolipoprotein levels between heparin-induced extracorporeal low-density lipoprotein precipitation (HELP) treatments.
Alaupovic, P; Dudley, VS; Knight-Gibson, C; Lane, DM; Laughlin, LO, 1995
)
1.01
"Lovastatin-treated rats displayed a 30% lower hepatic triacylglycerol secretion rate compared to controls as estimated using Triton WR-1339."( Studies on rat liver phosphatidate phosphohydrolase and plasma lipids: effect of HMG-CoA reductase inhibitors.
al-Shurbaji, A; Berglund, L; Humble, E; Lund, E, 1994
)
1.01
"Lovastatin treatment (4 mg/kg day x 13 days), as compared with placebo, decreased the concentrations of fasting plasma triglyceride (1740 +/- 170 vs."( Effect of lovastatin on the secretion of very low density lipoprotein lipids and apolipoprotein B in the hypertriglyceridemic Zucker obese rat.
Almario, RU; Elovson, J; Jen, KL; Kasim, SE; Khilnani, S, 1993
)
1.41
"Lovastatin treatment increased the liver/heart ratio (15%, P < 0.01) in the patients with polygenic hypercholesterolemia and the FCR for LDL in both groups (22%, P < 0.05, for those with familial hypercholesterolemia and 37%, P < 0.01 for those with polygenic hypercholesterolemia)."( Lovastatin enhances hepatic uptake of low density lipoprotein in humans.
Heikkilä, JI; Kervinen, K; Kesäniemi, YA; Savolainen, MJ, 1993
)
2.45
"Lovastatin treatment (25 microM, 24 h) decreased protein isoprenylation and affected the distribution of several SMGs, causing a large accumulation in the cytosol and a detectable decrease in membranes."( Blockade of mevalonate production by lovastatin attenuates bombesin and vasopressin potentiation of nutrient-induced insulin secretion in HIT-T15 cells. Probable involvement of small GTP-binding proteins.
Li, G; Regazzi, R; Roche, E; Wollheim, CB, 1993
)
1.28
"Lovastatin-treated smokers had less worsening (0.07 +/- 0.15 mm) than placebo-treated smokers (P = .024)."( Effects of cigarette smoking on the angiographic evolution of coronary atherosclerosis. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. CCAIT Study Group.
Boccuzzi, SJ; Cook, T; Gladstone, P; Higginson, L; Hudgin, R; Krip, G; Lespérance, J; Waters, D, 1996
)
1.02
"The lovastatin-treated group had a lower serum cholesterol (59 +/- 3 mg/dL versus 71 +/- 2 mg/dL, P < 0.05), but serum triglyceride levels were not different between the two groups."( Renal hemodynamic effects of lovastatin in a renal ablation model.
Hafez, KS; Inman, SR; Novick, AC; Stowe, NT, 1996
)
1.07
"The lovastatin-treated group demonstrated significant reductions in mean total cholesterol (TC) (14.7%, 95% confidence interval [CI]-6.6 to -22.8, P < 0.01) and low-density lipoprotein (LDL) cholesterol (20.0%, 95% CI-7.9 to -32.1, P < 0.01) from baseline. "( The efficacy of lovastatin in lowering cholesterol in African Americans with primary hypercholesterolemia.
Fong, RL; Ward, HJ, 1997
)
1.2
"Lovastatin treatment reduced plasma cholesterol by 32% but did not improve urinary nitrate or cGMP excretion or endothelium-dependent vasodilation."( Dietary L-arginine reduces the progression of atherosclerosis in cholesterol-fed rabbits: comparison with lovastatin.
Bode-Böger, SM; Böger, RH; Böhme, M; Brandes, RP; Frölich, JC; Mügge, A; Nafe, R; Phivthong-ngam, L, 1997
)
1.23
"Lovastatin treatment has a weaker inhibitory effect on the progression of atherosclerosis and no effect on vascular NO elaboration, which may be due to its stimulatory effect on vascular superoxide radical generation."( Dietary L-arginine reduces the progression of atherosclerosis in cholesterol-fed rabbits: comparison with lovastatin.
Bode-Böger, SM; Böger, RH; Böhme, M; Brandes, RP; Frölich, JC; Mügge, A; Nafe, R; Phivthong-ngam, L, 1997
)
1.23
"The Lovastatin treatment did not results in more adverse events than the placebo treatment."( [The effect of hypolipidemia treatment on the function of kidney transplanted from cadavers].
Bill, M; Durlik, M; Gaciong, Z; Gradowska, L; Juskowa, J; Lao, M; Paczek, L; Wyzgał, J, 1997
)
0.78
"Lovastatin treatment decreased F-actin content in a time- and concentration-dependent manner."( Role of Rho protein in lovastatin-induced breakdown of actin cytoskeleton.
Aktories, K; Benz, C; Koch, G; Olenik, C; Schmidt, G, 1997
)
1.33
"Lovastatin treatment resulted in smaller efferent vessel diameters."( Renal microcirculatory effects of lovastatin in a rat model of reduced renal mass.
Glazer, AA; Inman, SR; Novick, AC; Stowe, NT, 1997
)
1.3
"Lovastatin treatment had no effect on the lipid and protein composition, the fatty acid profile, or the vitamin E content of either VLDL or LDL; likewise, lipoprotein oxidation markers (Cu-induced conjugated dienes, thiobarbituric acid reactive substances formation, and lysine residues) were similar before and after lovastatin treatment."( Lipoprotein composition and oxidative modification during therapy with gemfibrozil and lovastatin in patients with combined hyperlipidaemia.
Adzet, T; Hernández, Y; Laguna, JC; Merlos, M; Ros, E; Vázquez, M; Zambón, D, 1998
)
1.24
"Lovastatin treatment increased protein and mRNA levels of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), increased binding of p21 with Cdk2, markedly inhibited cyclin E- and Cdk2-associated phosphorylation of histone H1 or GST-retinoblastoma protein, enhanced binding of the retinoblastoma protein to the transcription factor E2F-1 in vivo, and induced the activation of a p21 promoter reporter construct."( Inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway induces p53-independent transcriptional regulation of p21(WAF1/CIP1) in human prostate carcinoma cells.
Choi, YH; Ha, MJ; Kang, WK; Kim, SJ; Lee, J; Lee, SJ; Nguyen, P; Pirnia, F; Trepel, JB; Wang, XF, 1998
)
1.02
"Lovastatin treatment (10 microM) of control 3T3 cells resulted in growth arrest at G1 accompanied by actin stress fiber disassembly, cell rounding, and decreased active RhoA from the membranous protein fraction."( Effect of cyclin E overexpression on lovastatin-induced G1 arrest and RhoA inactivation in NIH3T3 cells.
Ghosh, PM; Kreisberg, JI; Mott, GE; Moyer, ML, 1999
)
1.3
"Lovastatin treatment resulted in decreased expression of the antiapoptotic protein bcl-2 and increased the expression of the proapoptotic protein bax."( Lovastatin augments apoptosis induced by chemotherapeutic agents in colon cancer cells.
Agarwal, B; Bhendwal, S; Halmos, B; Holt, PR; Moss, SF; Ramey, WG, 1999
)
2.47
"Lovastatin treatment reduced cholesterol concentration by 35% as compared to the cholesterol group (899+/-51, p<0.05 vs."( L-arginine supplementation in hypercholesterolemic rabbits normalizes leukocyte adhesion to non-endothelial matrix.
Bode-Böger, SM; Böger, RH; Brandes, RP; Brandes, S; Mügge, A, 2000
)
1.03
"Lovastatin treatment also resulted in a significant reduction of troponin T release by cardiomyocytes in doxorubicin-treated mice."( Lovastatin potentiates antitumor activity and attenuates cardiotoxicity of doxorubicin in three tumor models in mice.
Balkowiec-Iskra, EZ; Czajka, A; Feleszko, W; Giermasz, A; Jakóbisiak, M; Mlynarczuk, I; Stoklosa, T; Switaj, T, 2000
)
2.47
"Lovastatin treatment significantly reduced the cumulative rate of cardiovascular hospitalizations and procedures (p = 0.002)."( Effect of lovastatin on cardiovascular resource utilization and costs in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS). AFCAPS/TexCAPS Research Group.
Alexander, CM; Boccuzzi, SJ; Clearfield, M; Cook, JR; Gotto, AM; Meyer, GS; Roehm, JB; Weis, S; Whitney, E, 2000
)
1.43
"Lovastatin treatment was also associated with decreased prenylation of both Ras and Rho A proteins whereas Rac 1 geranylgeranylation was not affected."( Lovastatin induces apoptosis of spontaneously immortalized rat brain neuroblasts: involvement of nonsterol isoprenoid biosynthesis inhibition.
Alvarez, AM; García-Román, N; Lorenzo, MJ; Montes, A; Toro, MJ, 2001
)
2.47
"Lovastatin treatment did not significantly affect the antioxidant capacity of LDL."( Comparison of LDL trap assay to other tests of antioxidant capacity; effect of vitamin E and lovastatin treatment.
Malminiemi, K; Malminiemi, O; Palomäki, A, 2000
)
1.25
"Lovastatin treatment also led to the accumulation of nonisoprenylated Rho and Rac GTPases in cytosolic fraction."( Lovastatin-induced cytoskeletal reorganization in lens epithelial cells: role of Rho GTPases.
Maddala, RL; Rao, PV; Reddy, VN, 2001
)
2.47
"Lovastatin treatment caused down-regulation of the insulin-responsive glucose transporter 4 (Glut4) and up-regulation of Glut1 in 3T3-L1 adipocytes. "( Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes.
Chamberlain, LH, 2001
)
1.75
"Lovastatin treatment was associated with statistically significant decreases in"( Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS): efficacy and tolerability of long-term treatment with lovastatin in women.
Beere, PA; Clearfield, M; Downs, JR; Gotto, AM; Kruyer, W; Langendorfer, A; Shapiro, DR; Stein, EA; Weis, S; Whitney, EJ, 2001
)
1.24
"Lovastatin treatment resulted in a shift of Ras localization from the membrane to the cytosol that was reversed by mevalonate."( The cholesterol lowering drug lovastatin induces cell death in myeloma plasma cells.
Bloem, AC; Kamphuis, MM; Lokhorst, HM; van de Donk, NW, 2002
)
1.32
"Lovastatin treatment resulted in a significant reduction of total plasma cholesterol, LDL cholesterol and VLDL cholesterol (-41%, -44%, -68%, respectively)."( Effect of lovastatin on lipoprotein fluidity in patients with hypercholesterolaemia.
Aviram, M; Brook, GJ; Cogan, U; Klein, L; Levy, Y, 1992
)
1.41
"Lovastatin treatment also caused the accumulation of the noncomplexed form of CDC42 but not of rho proteins."( The small GTP-binding proteins in the cytosol of insulin-secreting cells are complexed to GDP dissociation inhibitor proteins.
Kikuchi, A; Regazzi, R; Takai, Y; Wollheim, CB, 1992
)
1
"Lovastatin treatment (4 mg/kg), as compared to placebo, caused a 338% reduction in plasma triglyceride (146 +/- 5 vs."( Mechanisms of triglyceride-lowering effect of an HMG-CoA reductase inhibitor in a hypertriglyceridemic animal model, the Zucker obese rat.
Dayananda, D; Jen, KL; Kasim, SE; Khilnani, S; LeBoeuf, RC; Tallapaka, L, 1992
)
1
"The lovastatin-treated low density lipoprotein (LDL) displayed 28% increased fluidity in comparison with control LDL."( Dual effect of lovastatin and simvastatin on LDL-macrophage interaction.
Aviram, M; Brook, GJ; Keidar, S, 1991
)
1.12
"Lovastatin treatment resulted in a considerable reduction in plasma cholesterol and triglyceride levels."( Toxicity of lovastatin in rats with experimentally induced nephrotic syndrome.
Camps, J; Joven, J; Masana, L; Simó, JM; Turner, PR; Vilella, E; Villabona, C, 1990
)
1.38
"Lovastatin treatment also produced shifts in the electrophoretic mobilities of the G25K isoforms on two-dimensional gels."( Isoprenoid modification of G25K (Gp), a low molecular mass GTP-binding protein distinct from p21ras.
Maltese, WA; Sheridan, KM, 1990
)
1
"Lovastatin-treated animals that were supplemented with CoQ10 had blood, heart, and liver CoQ10 concentrations that approximated or exceeded those of control animals."( Lovastatin decreases coenzyme Q levels in rats.
Folkers, K; Tamagawa, H; Tucker, JL; Willis, RA; Xia, LJ; Ye, CQ, 1990
)
2.44
"Lovastatin-treated rats had significantly lower cholesterol at day 23 and 60 than vehicle-treated rats (270.5 +/- 39.7 v 501.7 +/- 81.9 and 148.2 +/- 10.7 v 268.2 +/- 40.8 mg/dL, P less than 0.05)."( Lovastatin ameliorates the development of glomerulosclerosis and uremia in experimental nephrotic syndrome.
Harris, KP; Klahr, S; Purkerson, ML; Yates, J, 1990
)
2.44
"Lovastatin treatment decreased cholesterol synthesis more than 60% but did not increase high affinity catabolism of LDL further in the sitosterolemic cells, compared to a more than 20% rise in control mononuclear leukocytes."( Unexpected failure of bile acid malabsorption to stimulate cholesterol synthesis in sitosterolemia with xanthomatosis. Comparison with lovastatin.
Ness, G; Nguyen, L; Salen, G; Shefer, S; Shore, V; Tint, GS,
)
1.06
"Lovastatin treatment to vitamin E-deficient rats was associated with dose-dependent toxicity, resulting in 100%, 75%, and 50% mortality at concentrations of 2, 1, and 0.5 g/kg diet, respectively."( Effects of lovastatin and leupeptin on ceroidogenesis of vitamin E-deficient and -supplemented young rats.
Berra, A; Monserrat, AJ; Porta, EA; Rubio, MC, 1989
)
1.39
"Only lovastatin treatment was free of adverse effects."( Comparison of six pharmacologic regimens for hypercholesterolemia.
Bailey, KR; Brewer, HB; Hoeg, JM; Maher, MB, 1987
)
0.73
"Treatment with lovastatin, a mevalonate biosynthesis inhibitor, selectively inhibited protein prenylation and induced apoptosis in MESN cells, while having little effect in MYCNA lines."( Mesenchymal subtype neuroblastomas are addicted to TGF-βR2/HMGCR-driven protein geranylgeranylation.
Califano, A; Hirschhorn, T; Shimada, K; Small, JC; Stockwell, BR; Stokes, ME; Vasciaveo, A, 2020
)
0.9
"Pre-treatment with lovastatin potentially reversed GO-induced mitochondrial toxicity."( Lovastatin attenuates glyoxal-induced toxicity on rat liver mitochondria.
Badavi, M; Goudarzi, M; Hosseinzadeh, A; Mehrzadi, S; Nesari, A; Rezaei, M, 2021
)
2.38
"Pretreatment with lovastatin (20mg/kg s.c."( Lovastatin inhibits visceral allodynia and increased colonic permeability induced by lipopolysaccharide or repeated water avoidance stress in rats.
Kumei, S; Miyagishi, S; Nozu, R; Nozu, T; Okumura, T; Takakusaki, K, 2018
)
2.25
"For treating GC, lovastatin may be a potential drug."( Weighted gene co-expression network analysis and connectivity map identifies lovastatin as a treatment option of gastric cancer by inhibiting HDAC2.
Dong, L; Kang, W; Lu, X; Ma, S; Zhang, L; Zou, B, 2019
)
1.07
"Treatment with lovastatin decreased growth cone actin filament content by up to 24.3 %."( Inhibiting geranylgeranylation increases neurite branching and differentially activates cofilin in cell bodies and growth cones.
Hynds, DL; Kaimal, R; Mo, H; Reddy, J; Samuel, F; Segovia, V, 2014
)
0.74
"Treatment with lovastatin markedly increased the expression of the hepatic LDL receptor in rats with nephrotic syndrome, which was accompanied by significantly improved hyperlipidemia."( Effects of lovastatin on hepatic expression of the low-density lipoprotein receptor in nephrotic rats.
Chen, L; Liang, SF; Shu, GY; Wang, WM; Wei, LX; Wu, JB; Zhang, XH, 2014
)
1.13
"Co-treatment with lovastatin for 24 hours before harvesting attenuated the up-regulation of miR-21 (P = 0.013)."( Regulation of lovastatin on a key inflammation-related microRNA in myocardial cells.
Du, A; Guo, W; Li, L; Liu, H; Yang, M, 2014
)
1.09
"Pretreatment with lovastatin or imatinib prevented proliferation."( Platelet Derived Growth Factor Has a Role in Pressure Induced Bladder Smooth Muscle Cell Hyperplasia and Acts in a Paracrine Way.
Adam, RM; Dietz, HG; Herlemann, A; Kappler, R; Preis, L; Stehr, M, 2015
)
0.74
"When treated with lovastatin, both the chlorophyll content and thylakoid membrane protein stability were significantly lower in tasg1 than WT, consistent with the inhibited expression of senescence-associated genes (TaSAGs) in tasg1."( The stay-green phenotype of wheat mutant tasg1 is associated with altered cytokinin metabolism.
Hao, Q; Li, Q; Tian, F; Wang, W, 2016
)
0.76
"Co-treatment with lovastatin and enzastaurin was found to synergistically suppress HCC cell growth in vitro. "( Synergistic anti-tumor efficacy of lovastatin and protein kinase C-beta inhibitor in hepatocellular carcinoma.
Bang, YJ; Jang, IJ; Kim, JR; Kim, W; Kim, YJ; Lee, HS; Yoon, JH, 2009
)
0.96
"Treatment with lovastatin or celecoxib decreased the levels of cyclin D1, CDK2, pRb and E2F1, while the combination treatment showed more pronounced suppression."( Synergistic effects of lovastatin and celecoxib on caveolin-1 and its down-stream signaling molecules: Implications for colon cancer prevention.
Guruswamy, S; Rao, CV, 2009
)
1
"Treatment with lovastatin and simvastatin (40 mg b.i.d.) significantly reduced 24-h mean plasma mevalonate levels from baseline values."( The effects of lovastatin and simvastatin on the diurnal periodicity of plasma mevalonate concentrations in patients with heterozygous familial hypercholesterolemia.
Illingworth, DR; Pappu, AS, 2002
)
1.01
"Treatment with lovastatin for 4 weeks did inhibit the formation of pre-neoplastic mammary intraepithelial neoplasias (MIN) in vivo, but not invasive carcinomas in the C3(1)/SV40 TAg transgenic model of mammary cancer."( Comparative effects of lovastatin on mammary and prostate oncogenesis in transgenic mouse models.
Abe, H; Green, JE; Kavanaugh, C; Nguyen, P; Otsuki, Y; Shibata, E; Shibata, MA; Trepel, JB, 2003
)
0.97
"Treatment with lovastatin resulted in the induction of LPS/IFN-gamma-mediated iNOS mRNA and increased nitric oxide (NO) production."( Rho A negatively regulates cytokine-mediated inducible nitric oxide synthase expression in brain-derived transformed cell lines: negative regulation of IKKalpha.
Giri, S; Rattan, R; Singh, AK; Singh, I, 2003
)
0.66
"Pretreatment with lovastatin eliminated excessive expression of TF in the posthypoxic mild sickle mouse (approximately 16% positive) and in the more severe mouse at ambient air (approximately 21% positive)."( Endothelial cell expression of tissue factor in sickle mice is augmented by hypoxia/reoxygenation and inhibited by lovastatin.
Blazar, BR; Choong, S; Hebbel, RP; Kelm, RJ; Kollander, R; Milbauer, LC; Panoskaltsis-Mortari, A; Shet, A; Solovey, A, 2004
)
0.86
"Treatment with lovastatin may prevent bone loss in postmenopausal women with type 2 DM."( Lovastatin effects on bone mineral density in postmenopausal women with type 2 diabetes mellitus.
Amini, M; Aminorroaya, A; Janghorbani, M; Safaei, H, 2007
)
2.12
"Treatment with lovastatin for 2.2 years in the MARS study significantly reduced the mean percent diameter stenosis compared with placebo (p = 0.005) in patients with more severe stenosis, and also significantly (p = 0.002) reduced the mean global change score (indicating less progression)."( Regression or reduction in progression of atherosclerosis, and avoidance of coronary events, with lovastatin in patients with or at high risk of cardiovascular disease: a review.
Frisinghelli, A; Mafrici, A, 2007
)
0.9
"Treatment with lovastatin increased the content of the mRNA in epithelium and cortex by approximately 0.4-fold and HMGR protein content approximately 5-fold."( Role of transcription, translation, and protein turnover in controlling the distribution of 3-hydroxy-3-methylglutaryl coenzyme A reductase in the lens.
Cenedella, RJ, 1995
)
0.63
"Treatment with lovastatin results in a favorable response in terms of total and low-density lipoprotein cholesterol lowering in patients with the nephrotic syndrome; however, plasma Lp(a) levels are uniformly and significantly reduced only in nephrotic patients with elevated baseline plasma Lp(a) concentrations."( Reduction of lipoprotein(a) following treatment with lovastatin in patients with unremitting nephrotic syndrome.
Azrolan, N; Bostom, A; Brown, CD; Friedman, EA; Roberts, KG; Thomas, L; Zhao, ZH, 1995
)
0.88
"Treatment with lovastatin brought about similar hypolipidaemic responses in FH patients with either mutation type (FH Helsinki or FH North Karelia) or PvuII RFLP status (P+ or P-)."( Heterozygous familial hypercholesterolaemia: the influence of the mutation type of the low-density-lipoprotein receptor gene and PvuII polymorphism of the normal allele on serum lipid levels and response to lovastatin treatment.
Kontula, K; Ojala, JP; Sarna, S; Tikkanen, MJ; Turtola, H; Vuorio, AF, 1995
)
0.82
"The treatment with Lovastatin and Colestipol failed to change significantly the concentrations of triglycerides, HDL cholesterol and AI and AII apolipoproteins."( [Effect of combined treatment with lovastatin and colestipol on serum lipids and lipoproteins].
Kłosiewicz-Latoszek, L; Nowicka, G; Szostak, WB, 1993
)
0.88
"When treated with lovastatin, the cells were blocked in G1 and appeared to express increased levels of wild-type p53 when examined by immunostaining."( Expression of wild-type p53 during the cell cycle in normal human mammary epithelial cells.
Cowan, KH; Diella, F; Gudas, JM; Oka, M; Trepel, J, 1994
)
0.61
"Treatment with lovastatin (40 mg/d) reduced plasma cholesterol concentrations 13%, but failed to decrease plasma cholestanol or bile alcohol levels."( Comparative effects of lovastatin and chenodeoxycholic acid on plasma cholestanol levels and abnormal bile acid metabolism in cerebrotendinous xanthomatosis.
Batta, AK; Salen, G; Shefer, S; Tint, GS, 1994
)
0.94
"Treatment with lovastatin alone (L, n = 7) also reduced glomerulosclerosis and serum cholesterol compared to the controls."( Effects of delayed treatment with enalapril and/or lovastatin on the progression of glomerulosclerosis in 5/6 nephrectomized rats.
Han, DC; Hwang, SD; Jin, SY; Lee, HB; Lee, SK, 1993
)
0.88
"Treatment with lovastatin plus diet slows the rate of progression and increases the frequency of regression in coronary artery lesions (by global change score), especially in more severe lesions (by quantitative angiography). "( Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS).
Alaupovic, P; Azen, SP; Blankenhorn, DH; Cashin-Hemphill, L; DeBoer, LW; Hirsch, LJ; Hodis, HN; Kramsch, DM; Mack, WJ; Mahrer, PR; Masteller, MJ; Vailas, LI, 1993
)
0.92
"Treatment with lovastatin (1-30 microM) for 24 h decreased the level of activation of MAP kinase by insulin by as much as 60%."( Lovastatin inhibits the stimulation of mitogen-activated protein kinase by insulin in HIRcB fibroblasts.
Blaskovich, MA; McGuire, TF; Romero, G; Sebti, SM; Xu, XQ, 1996
)
2.08
"Treatment with lovastatin increased delta 5 and delta 9 desaturation in tumor microsomes, whereas delta 6 desaturation did not change in tumors of treated mice."( Effects of lovastatin on the fatty acid desaturation in a human lung mucoepidermoid carcinoma grown in nude mice.
de Bravo, MG; Polo, M; Schinella, G; Tournier, H, 1996
)
1.02
"Treatment with lovastatin decreased total cholesterol by 19% (P < 0.001), primarily by an effect on LDL cholesterol."( Post-transplant hyperlipidaemia: low-dose lovastatin lowers atherogenic lipids without plasma accumulation of lovastatin.
Berg, KJ; Cheng, H; Forfang, K; Geiran, O; Gullestad, L; Høstmark, A; Ihlen, H; Nordal, KP; Schwartz, MS; Simonsen, S, 1997
)
0.9
"Treatment with lovastatin revealed the increment of both CDK2- and CDK4-bound-p27Kip1."( Lovastatin inhibits mesangial cell proliferation via p27Kip1.
Inoshita, S; Kuwahara, M; Marumo, F; Nakashima, O; Sasaki, S; Terada, Y; Yamada, T, 1998
)
2.08
"Pretreatment with lovastatin significantly increased apoptosis induced by 5-fluorouracil (5-FU) or cisplatin in all four cell lines."( Lovastatin augments apoptosis induced by chemotherapeutic agents in colon cancer cells.
Agarwal, B; Bhendwal, S; Halmos, B; Holt, PR; Moss, SF; Ramey, WG, 1999
)
2.07
"Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression despite high blood glucose levels."( Lovastatin inhibits transforming growth factor-beta1 expression in diabetic rat glomeruli and cultured rat mesangial cells.
Han, DC; Kim, SI; Lee, HB, 2000
)
2.09
"Treatment with lovastatin (20 to 40 mg/d) resulted in a 25% reduction in LDL-C and a 6% increase in HDL-C, as well as a 37% reduction in risk for first acute major coronary event (AMCE), defined as fatal or nonfatal myocardial infarction, unstable angina, or sudden cardiac death."( Relation between baseline and on-treatment lipid parameters and first acute major coronary events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS).
Beere, PA; Clearfield, M; de Cani, JS; Downs, JR; Gotto, AM; Jou, JY; Langendörfer, A; Shapiro, DR; Stein, EA; Watson, DJ; Weis, S; Whitney, E, 2000
)
0.65
"Treatment of lovastatin caused a rapid release of mitochondrial cytochrome c into cytosol and subsequent induction of caspase-3, but not caspase-1 activity."( Induction of apoptosis by lovastatin through activation of caspase-3 and DNase II in leukaemia HL-60 cells.
Lin, JK; Lin-Shiau, SY; Wang, IK, 2000
)
0.96
"Treatment with lovastatin caused statistically significant reductions in I(p), myocardial and skeletal muscle K-dependent p-NPPase activity and 3H-ouabain binding in the myocardium and skeletal muscle. "( HMG CoA reductase inhibition reduces sarcolemmal Na(+)-K(+) pump density.
Buhagiar, KA; Bundgaard, H; Gray, DF; Hansen, PS; Jessup, W; Kjeldsen, K; Mihailidou, AS; Rasmussen, HH, 2000
)
0.66
"Treatment with lovastatin reduces Na(+)-K(+) pump activity and abundance in rabbit and rat sarcolemma."( HMG CoA reductase inhibition reduces sarcolemmal Na(+)-K(+) pump density.
Buhagiar, KA; Bundgaard, H; Gray, DF; Hansen, PS; Jessup, W; Kjeldsen, K; Mihailidou, AS; Rasmussen, HH, 2000
)
0.66
"Treatment with lovastatin, however, did not correct the accumulation of VLCFA in the plasma or tissues, including the brain and spinal cord."( Lovastatin does not correct the accumulation of very long-chain fatty acids in tissues of adrenoleukodystrophy protein-deficient mice.
Asahara, H; Kira, J; Ohyagi, Y; Shinnoh, N; Taniwaki, T; Yamada, T, 2000
)
2.09
"Treatment with lovastatin 20 to 40 mg daily for primary prevention of coronary heart disease was well tolerated and reduced the risk of first acute coronary events without increasing the risk of either noncardiovascular mortality or cancer."( Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TEXCAPS): additional perspectives on tolerability of long-term treatment with lovastatin.
Beere, PA; Clearfield, M; Downs, JR; Gotto, AM; Kruyer, W; Langendorfer, A; Shapiro, DR; Tyroler, HA; Weis, S; Whitney, EJ; Zagrebelsky, V, 2001
)
0.85
"Treatment with lovastatin led to a dose-dependent reduction in serum total cholesterol levels without affecting the enzyme activity."( Effect of lovastatin on hypercholesterolemia in chronic renal failure.
Gagnon, RF; Stewart-Phillips, JL; Subang, MC, 1992
)
1.03
"Treatment with lovastatin resulted in decreases in LDL cholesterol concentrations from 274 mg/dl at baseline to 211, 192 and 178 mg/dl, respectively, on doses of 20, 40 and 80 mg/day."( Comparative hypolipidemic effects of lovastatin and simvastatin in patients with heterozygous familial hypercholesterolemia.
Bacon, S; Illingworth, DR; Pappu, AS; Sexton, GJ, 1992
)
0.9
"Treatment with lovastatin was associated with a significant improvement in whole blood filtration time and a tendency toward normalization in red blood cell morphology."( Lovastatin therapy in hypercholesterolemia: effect on fibrinogen, hemorrheologic parameters, platelet activity, and red blood cell morphology.
Beigel, Y; Djaldetti, M; Fuchs, J; Green, P; Lurie, Y; Snir, M, 1991
)
2.06
"Treatment with lovastatin at concentrations ranging from 5 to 15 microM for up to 96 h resulted in a time- and dose-dependent inhibition of cell growth in all lines tested."( Inhibition of cell growth by lovastatin is independent of ras function.
DeClue, JE; Lowy, DR; Papageorge, AG; Vass, WC; Willumsen, BM, 1991
)
0.91
"Treatment with lovastatin (an HMG-CoA reductase inhibitor) was then started at a dosage of 20 mg daily."( [Cholestatic jaundice during lovastatin medication].
Haacke, H; Kirchhoff, R; Spreckelsen, U, 1991
)
0.91
"Treatment with lovastatin did not significantly alter VLDL apoB conversion to LDL apoB or LDL apoB fractional catabolic rate (FCR) in CHL patients."( Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production.
Arad, Y; Ginsberg, HN; Ramakrishnan, R, 1990
)
2.06
"Treatment with lovastatin decreased the secretion of all plasma VLDL lipids, the average decrease after 2 h for VLDL triacylglycerol, phospholipid, cholesterol and cholesteryl ester being 45%."( Cholesterol is required for the secretion of the very-low-density lipoprotein: in vivo studies.
Fungwe, TV; Heimberg, M; Khan, BV; Wilcox, HG, 1990
)
0.62
"Treatment with lovastatin and cholestyramine can inhibit the direct synthesis pathway in this species, thereby lowering LDL apo B concentrations."( Regulation of low density lipoprotein apoprotein B metabolism by lovastatin and cholestyramine in miniature pigs: effects on LDL composition and synthesis of LDL subfractions.
Huff, MW; Telford, DE, 1989
)
0.85
"Treatment with lovastatin (mevinolin) one year after transplantation produced a marked improvement in the patient's lipoprotein profile."( Normal cholesterol levels with lovastatin (mevinolin) therapy in a child with homozygous familial hypercholesterolemia following liver transplantation.
Bilheimer, DW; East, C; Grundy, SM, 1986
)
0.9
"Treatment with lovastatin, a competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase, resulted in significant reductions in TC (196.8 +/- 7.9 mg/dl), TG (100.8 +/- 20.6 mg/dl), and LDL cholesterol (102.0 +/- 10.9 mg/dl)."( Suppression of apolipoprotein B production during treatment of cholesteryl ester storage disease with lovastatin. Implications for regulation of apolipoprotein B synthesis.
Desnick, RJ; Ginsberg, HN; Le, NA; Ramakrishnan, R; Short, MP, 1987
)
0.83

Toxicity

Lovastatin and gemfibrozil are both safe and efficacious in transplant patients. The drugs have no undesirable toxic effects on the lens and other ocular tissues.

ExcerptReferenceRelevance
" The frequency of clinical adverse experiences was low and similar among treatment groups, the frequency of laboratory adverse experiences was higher in the Lovastatin group."( Efficacy, safety and tolerability of lovastatin and bezafibrate retard in patients with hypercholesterolemia.
Breier, C; Eber, B; Gaul, G; Klein, W; Schmidt, P; Schumacher, M; Silberbauer, K; Stühlinger, W, 1992
)
0.75
" Lovastatin was well tolerated without overt side effects or complications and without adverse changes in liver function tests or creatine phosphokinase."( Safety and efficacy of treatment of pediatric cholesteryl ester storage disease with lovastatin.
Glueck, CJ; Lichtenstein, P; Speirs, J; Tracy, T, 1992
)
1.42
"to investigate the symptomatic and biochemical side effect profile of simvastatin (a new cholesterol lowering drug) following routine use in a specialist hospital outpatient clinic."( Simvastatin and side effects.
Lintott, CJ; Scott, RS; Wilson, MJ, 1991
)
0.28
" It is concluded that simvastatin is a safe and efficient cholesterol-lowering drug for long-term therapy, both as a single drug and in combination with cholestyramine."( Long-term efficacy and safety of simvastatin alone and in combination therapy in treatment of hypercholesterolaemia.
Lundh, BL; Mölgaard, J; Olsson, AG; von Schenck, H, 1991
)
0.28
" The most frequently reported drug-related clinical adverse experiences were constipation (2."( Long-term safety and efficacy profile of simvastatin.
Bocanegra, TS; Boccuzzi, SJ; Keegan, ME; Shapiro, DR; Walker, JF, 1991
)
0.28
" The adverse effects of many of the principal drugs in this category are discussed."( A comparative review of the adverse effects of treatments for hyperlipidaemia.
Steiner, A; Vetter, W; Weisser, B,
)
0.13
" The most serious side-effect in our study was myolysis which occurred in two patients with a marked increase in creatine phosphokinase."( Efficacy and safety of simvastatin (alone or in association with cholestyramine). A 1-year study in 66 patients with type II hyperlipoproteinaemia.
Aubert, I; Bauduceau, B; Chanu, B; Dachet, C; Emmerich, J; Erlich, D; Gautier, D; Jacotot, B; Rouffy, J, 1990
)
0.28
" There are new data from a recently completed 1 year, placebo-controlled trial in 8,245 patients (Expanded Clinical Evaluation of Lovastatin study) and 20 months of health professionals' reports on spontaneous adverse events associated with large prescription usage."( Extended clinical safety profile of lovastatin.
Burke, MT; Mantell, G; Staggers, J, 1990
)
0.76
" To determine whether lower doses of lovastatin would be effective and safe for lowering cholesterol after cardiac transplantation, 44 patients with blood cholesterol greater than 200 mg/dl at least 6 months after cardiac transplantation received 10-20 mg lovastatin daily."( Low-dose lovastatin safely lowers cholesterol after cardiac transplantation.
Brownfield, E; Chuck, C; Kamjoo, P; Kawata, N; Kobashigawa, JA; Leonard, L; Moriguchi, JD; Murphy, FL; Stevenson, LW; Wilmarth, J, 1990
)
0.97
" No consistent adverse clinical or biochemical effects were observed during the three-year therapy."( [Evaluation of tolerance, efficacy and safety of 3-year simvastatin use in the treatment of primary hypercholesterolemia].
Bercher, L; Bovet, P; Brunner, HR; Darioli, R, 1990
)
0.28
" The serious reported adverse effects of lovastatin are myopathy (0."( Efficacy and long-term adverse effect pattern of lovastatin.
Tobert, JA, 1988
)
0.8
" Our observations provide good evidence that lovastatin and simvastatin have no undesirable toxic effects on the lens and other ocular tissues, compared with fenofibrate."( Ocular drug safety and HMG-CoA-reductase inhibitors.
Hockwin, O; Paulus, U; Schmidt, J; Schmitt, C; von Bergmann, K, 1994
)
0.55
" No adverse effects requiring treatment discontinuation were observed for both drugs."( [Randomized, double-blind comparative study between pravastatin and lovastatin. Evaluation of efficacy and safety].
Bertolami, MC; Diament, J; Faludi, AA; Forti, N; Giannini, SD; Schölz, J, 1994
)
0.52
""Is there any safe and optimal treatment of hyperlipidemia following heart transplantation?" The problem of hypercholesterolemia following heart transplantation if often underestimated."( [Can hyperlipidemia after heart transplantation be optimally and safely treated?].
Arndtz, N; Reichart, B; Seidel, D; Thiery, J; Wenke, K, 1994
)
0.29
" There were no differences between the treatment groups in the numbers of reports of 'possible adverse effects' of treatment or of a range of different symptoms or conditions (including those related to sleep or mood) recorded at regular clinic follow-up."( Three-year follow-up of the Oxford Cholesterol Study: assessment of the efficacy and safety of simvastatin in preparation for a large mortality study.
Armitage, J; Collins, R; Fatemian, M; Kearney, E; Keech, A; Lawson, A; Lyon, V; MacMahon, S; Mindell, J; Wallendszus, K, 1994
)
0.29
" This short-term study showed few adverse effects for both drugs."( Comparative efficacy and safety of micronized fenofibrate and simvastatin in patients with primary type IIa or IIb hyperlipidemia.
Bonnefous, F; Debbas, N; Farnier, M; Irvine, A, 1994
)
0.29
" Adverse experiences were mild and did not differ between treatment groups; in each group, one subject discontinued medication because of complaints of dizziness."( Treatment of primary hypercholesterolaemia. Short-term efficacy and safety of increasing doses of simvastatin and pravastatin: a double-blind comparative study.
De Haan, AF; Kastelein, JJ; Kortmann, B; Kroon, AA; Lansberg, PJ; Stalenhoef, AF; Stuyt, PM, 1993
)
0.29
" Compliance with prescribed medication was very good and the drug was well tolerated; only 3% of patients manifested a clinical adverse experience requiring discontinuation or a clinical adverse experience described as serious (associated with hospitalization or serious disability)."( Simvastatin in severe primary hypercholesterolemia: efficacy, safety, and tolerability in 595 patients over 18 weeks. The Principal Investigators.
Simons, LA, 1993
)
0.29
" Eighty percent of patients completed the study, 13% were unavailable for follow-up, 4% were discontinued due to adverse events unlikely to be related to lovastatin, and 3% (21) were discontinued because of drug-attributable adverse events: marked but asymptomatic increase in aminotransferase values (10 patients), gastrointestinal disturbance (three patients), rash (two patients), myalgia (one patient), myopathy (two patients), arthralgia (one patient), insomnia (one patient), and weight gain (one patient)."( Lovastatin 5-year safety and efficacy study. Lovastatin Study Groups I through IV.
, 1993
)
1.93
"Between December 1989 and December 1992, the Netherlands Centre for Monitoring of Adverse Reactions to Drugs received 142 reports of suspected adverse reactions to simvastatin or pravastatin."( [Side effects of cholesterol synthesis inhibitors].
Stricker, BH; Wolterbeek, R, 1993
)
0.29
" There was no significant difference between groups in the frequency of drug-related adverse experiences."( Comparison of the efficacy, safety and tolerability of simvastatin and pravastatin for hypercholesterolemia. The Simvastatin Pravastatin Study Group.
, 1993
)
0.29
" Relevant data on the incidence of adverse effects are presented."( Comparative evaluation of the safety and efficacy of HMG-CoA reductase inhibitor monotherapy in the treatment of primary hypercholesterolemia.
Hsu, I; Johnson, NE; Spinler, SA,
)
0.13
"Oxidized low density lipoprotein (oxLDL) is known to be toxic to a variety of cell types, but relatively little is known about the toxic effects of oxLDL on vascular smooth muscle cells (SMC)."( Toxicity of oxidized low density lipoproteins for vascular smooth muscle cells and partial protection by antioxidants.
Guyton, JR; Hughes, H; Karsan, D; Lenz, ML; Mathews, B; Selinger, E; Smith, CV, 1995
)
0.29
"We sought to identify differences in the description of adverse drug experiences in reports of randomized clinical trials (RCTs) from the United States and Japan, using diclofenac and simvastatin as test drugs."( Japanese and American reports of randomized trials: differences in the reporting of adverse effects.
Hayashi, K; Walker, AM, 1996
)
0.29
"Oxidized low density lipoproteins (OxLDL) are toxic to cells of the arterial wall and trigger the expression of the inducible form of hsp 70 in cultured endothelial cells (EAhy-926) and smooth muscle cells (HUVSMC)."( Simvastatin modulates the heat shock response and cytotoxicity mediated by oxidized LDL in cultured human endothelial smooth muscle cells.
Catapano, AL; Jacoviello, C; Longoni, C; Pirillo, A; Radaelli, A, 1997
)
0.3
" 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
)
0.53
" 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
)
0.3
" Results of this study confirmed that a low dose (10 mg) of simvastatin daily is a safe and effective method of reducing plasma levels of total and low-density lipoprotein cholesterol in hypercholesterolemic, hypertensive elderly patients receiving concurrent antihypertensive drug therapy, and that it has the additional potential benefit of reducing plasma levels of insulin."( Short-term safety and efficacy of low-dose simvastatin in elderly patients with hypertensive hypercholesterolemia and fasting hyperinsulinemia.
Chan, P; Huang, TY; Lee, C; Lee, YS; Tomlinson, B, 1997
)
0.3
" Physical and laboratory investigations for adverse effects were performed every month for the first 3 months and every 3 months thereafter."( Safety and efficacy of long-term statin-fibrate combinations in patients with refractory familial combined hyperlipidemia.
Athyros, VG; Carina, MV; Didangelos, TP; Hatzikonstandinou, HA; Kontopoulos, AG; Kranitsas, DF; Papageorgiou, AA, 1997
)
0.3
" There was no significant difference between the incidence of adverse effects with cerivastatin and comparator statins or between cerivastatin and other statins with respect to clinically significant increases in either hepatic enzymes or creatine phosphokinase."( Clinical efficacy and safety of cerivastatin: summary of pivotal phase IIb/III studies.
Davignon, J; Hanefeld, M; Hunninghake, DB; Insull, W; Nakaya, N; Ose, L, 1998
)
0.3
" The most important and commonly observed adverse effects in the fenofibrate group were dermatological events (three patients), myalgia (two patients) and asymptomatic increase in aminotransferase values (nine patients), while in the lovastatin group cardiovascular events (five patients) were the most common."( Comparison of the efficacy and safety of fenofibrate and lovastatin in patients with primary type IIa or IIb hyperlipidaemia.
Gholami, K; Maleki, M; Shafiee, A; Tavakoli, N, 1998
)
0.73
" These results suggest that lovastatin and gemfibrozil are both safe and efficacious in transplant patients."( A crossover comparison of the efficacy and safety of lovastatin and gemfibrozil in the treatment of hyperlipidemic organ transplant recipients.
Behrens, MT; Hanes, DS; Hooper, FL; Nicholson, PG; Raval, DD; Weir, MR,
)
0.67
" The frequency of treatment-associated adverse events (AEs) in the atorvastatin LDL-C < or =80 mg/dl (2."( Safety profile of atorvastatin-treated patients with low LDL-cholesterol levels.
Bakker-Arkema, RG; Black, DM; Nawrocki, JW, 2000
)
0.31
" Lovastatin ER was well tolerated, with no discontinuations due to adverse events."( A multiple-dose pharmacodynamic, safety, and pharmacokinetic comparison of extended- and immediate-release formulations of lovastatin.
Davidson, MH; Friedhoff, L; Lukacsko, P; Niecestro, R; Phillips, G; Sterman, A; Sun, JX; Walters, E, 2002
)
1.43
" The most common adverse event was flushing, which caused 10% of patients to withdraw."( Long-term safety and efficacy of a once-daily niacin/lovastatin formulation for patients with dyslipidemia.
Bays, HE; Berra, K; Favrot, LK; Guyton, JR; Harper, WL; Kashyap, ML; Kerzner, B; Kwiterovich, PO; McGovern, ME; Nash, SD; Simmons, PD; Toth, PD, 2002
)
0.56
" However, policosanol, a mixture of long-chain aliphatic alcohols extractable from sugar cane wax, has shown cholesterol-lowering potency comparable to that of statins, and yet appears to be devoid of toxic risk."( Policosanol safely down-regulates HMG-CoA reductase - potential as a component of the Esselstyn regimen.
McCarty, MF, 2002
)
0.31
"Cell degeneration in Alzheimer's disease is mediated by a toxic mechanism that involves interaction of the AbetaP peptide with the plasma membrane of the target cell."( Plasma membrane cholesterol controls the cytotoxicity of Alzheimer's disease AbetaP (1-40) and (1-42) peptides.
Arispe, N; Doh, M, 2002
)
0.31
" We show that mevastatin kills certain AML cell lines and is more toxic to a majority of primary AML cell samples than to myeloid cells in bone marrow (BM) samples from normal donors, and that mevastatin can produce more than additive kill with standard chemotherapeutics."( Mevastatin can increase toxicity in primary AMLs exposed to standard therapeutic agents, but statin efficacy is not simply associated with ras hotspot mutations or overexpression.
Appelbaum, FR; Banker, DE; Stirewalt, DL; Willman, CL; Zager, RA, 2003
)
0.32
" Abeta peptides were also toxic to vascular smooth muscle cells."( Cholesterol is necessary both for the toxic effect of Abeta peptides on vascular smooth muscle cells and for Abeta binding to vascular smooth muscle cell membranes.
Aguilar, MI; Barrow, CJ; Mok, SS; Small, DH; Subasinghe, S; Unabia, S, 2003
)
0.32
" Data included medication use, clinic visits, adverse events, LDL-C and other laboratory measures."( An economic analysis of the Atorvastatin Comparative Cholesterol Efficacy and Safety Study (ACCESS).
McBurney, CR; Smith, DG, 2003
)
0.32
" Some lovastatin-related adverse effects have been reported, and preclinical assessment has shown that the rabbit is the most sensitive species to lovastatin toxicity."( Comparison of the cholesterol-lowering effects and toxicity of D-003 and lovastatin in normocholesterolaemic rabbits.
Arruzazabala, L; Carbajal, D; Castaño, G; Gámez, R; Goicochea, E; Mas, R; Mendoza, N; Mendoza, S; Mesa, M; Noa, M, 2003
)
1.03
" Patients in the southeast and those enrolled by endocrinologists had the lowest compliance and highest adverse event rates."( Safety and compliance with once-daily niacin extended-release/lovastatin as initial therapy in the Impact of Medical Subspecialty on Patient Compliance to Treatment (IMPACT) study.
Rubenfire, M, 2004
)
0.56
" Finally, a series of toxicokinetic studies assessed whether the 2 different developmental toxicity profiles were due to differences in drug exposure between the developmentally toxic and non-toxic dosing regimes."( The role of maternal toxicity in lovastatin-induced developmental toxicity.
Cukierski, MA; Lankas, GR; Wise, LD, 2004
)
0.6
" Lovastatin was generally safe and well tolerated."( Efficacy and safety of lovastatin therapy in adolescent girls with heterozygous familial hypercholesterolemia.
Cho, M; Clauss, SB; Holmes, KW; Hopkins, P; Johnson-Levonas, AO; Kwiterovich, PO; Stein, E; Tate, A, 2005
)
1.55
"58% w/v), which is known to cause toxic release of proteins from cell."( Absorption enhancement, mechanistic and toxicity studies of medium chain fatty acids, cyclodextrins and bile salts as peroral absorption enhancers.
Chawla, HP; Panchagnula, R; Sharma, P; Varma, MV,
)
0.13
"Although statin drugs can have adverse effects on muscles and the liver, these effects are uncommon."( Safety of statins: effects on muscle and the liver.
Hamirani, YS; Jones, PH; Vasudevan, AR, 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
" 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
)
0.74
" Thirteen patients (10%) were lost to follow-up and 4 (3%) withdrew because of dermatological adverse effects: flushing, pruritus, and rash."( Evaluation of efficacy and safety of fixed dose lovastatin and niacin(ER) combination in asian Indian dyslipidemic patients: a multicentric study.
Gupta, R; Hira, HS; Kumar, N; Mohan, B; Panwar, RB; Sharma, DR; Sharma, M; Sharma, SK; Singh, V, 2006
)
0.59
" purpureus did not cause any toxic effects in albino rats."( Safety evaluation of Monascus purpureus red mould rice in albino rats.
Kumari, HP; Naidu, KA; Narasimhamurthy, K; Vijayalakshmi, G; Vishwanatha, S, 2009
)
0.35
"The 3-hydroxy-3-methylglutaryl (HMG)-coenzyme A reductase inhibitor, lovastatin (lova), has been reported to both sensitize to, and protect against, the toxic effects of the antitumor anthracycline doxorubicin (dox) in cellular and in vivo systems."( Lovastatin enhances the genotoxicity of doxorubicin in Chinese hamster V79 cells via noncovalent DNA binding.
Snyder, RD, 2009
)
2.03
" As a consequence, statins impair mitochondrial metabolism and the activation of small monomeric GTPases (such as Rho and Ras), causing toxic effects."( Geranylgeraniol prevents the cytotoxic effects of mevastatin in THP-1 cells, without decreasing the beneficial effects on cholesterol synthesis.
Bosia, A; Campia, I; Ghigo, D; Lussiana, C; Pescarmona, G; Riganti, C, 2009
)
0.35
" However, the side effect of flushing can challenge patient adherence to treatment."( Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis.
Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011
)
0.37
"Data were pooled from eight NER studies (administered as NER with a maximum dosage of 1000, 1500, and 2000 mg/day, either as monotherapy or in combination with simvastatin 20 or 40 mg/day [NER/S], or lovastatin 20 or 40 mg/day [NER/L]) to evaluate rates of study discontinuation due to flushing or any treatment-related adverse events."( Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis.
Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011
)
0.56
" Of the total number of patients treated with NER (n = 307), NER/S (n = 912), or NER/L (n = 928), 34 (11%), 105 (11%), and 127 (14%) patients discontinued due to any treatment-related adverse event, respectively, while 14 (5%), 43 (5%), and 55 (6%) discontinued due to flushing."( Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis.
Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011
)
0.37
" For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity."( Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity.
Fritz, G; Henninger, C; Huelsenbeck, J; Kaina, B; Lackner, KJ; Schad, A, 2011
)
0.65
" 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
" Rhabdomyolysis is a potentially dangerous side effect of statin drugs."( Red mold dioscorea: a potentially safe traditional function food for the treatment of hyperlipidemia.
Chen, CL; Pan, TM, 2012
)
0.38
" Monacolin K also serves as a well-known hypolipidemic medication, but its side effect myopathy is a concern."( Monascin and ankaflavin have more anti-atherosclerosis effect and less side effect involving increasing creatinine phosphokinase activity than monacolin K under the same dosages.
Hsu, YW; Hung, YP; Lee, CL; Pan, TM, 2013
)
0.39
" 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
"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
" Outcome measures were the effect of RYR on LDL cholesterol and incidence of adverse reactions with emphasis on liver and kidney injury and muscle symptoms."( Traditional Chinese lipid-lowering agent red yeast rice results in significant LDL reduction but safety is uncertain - a systematic review and meta-analysis.
Gerards, MC; Gerdes, VE; Koks, CH; Terlou, RJ; Yu, H, 2015
)
0.42
" Only when the mild profile of adverse reactions can be affirmed in studies with adequate methodology for safety assessment, RYR might be a safe and effective treatment option for dyslipidemia and cardiovascular risk reduction in statin intolerant patients."( Traditional Chinese lipid-lowering agent red yeast rice results in significant LDL reduction but safety is uncertain - a systematic review and meta-analysis.
Gerards, MC; Gerdes, VE; Koks, CH; Terlou, RJ; Yu, H, 2015
)
0.42
" Safety outcomes were evaluated by the risk of adverse events (AE)."( Efficacy and safety of long-term treatment with statins for coronary heart disease: A Bayesian network meta-analysis.
Bai, Y; Chan, C; Chang, X; Cheng, N; Cheng, Z; Lu, Y; Zhao, Y, 2016
)
0.43
" In this work, we report on a strategy to rational design of lovastatin (LOV)-loaded spherical rHDL (LOV-s-rHDL) for efficient and safe anti-atherosclerotic therapy."( Rational Design of Lovastatin-Loaded Spherical Reconstituted High Density Lipoprotein for Efficient and Safe Anti-Atherosclerotic Therapy.
Jia, H; Jiang, C; Li, Z; Liu, J; Qi, Z; Tang, Y; Zhang, W, 2019
)
1.08
" 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
" No severe adverse events occurred during the study."( Effectiveness and safety of red yeast rice predominated by monacolin K β-hydroxy acid form for hyperlipidemia treatment and management.
Benjian, C; Danping, XU; Huanlin, WU; Huiting, P; Xiaodan, H; Yishi, LI; Yongtao, C, 2022
)
0.72
" Secondary efficacy measures included patient-reported outcomes, application frequency, and adverse events (AEs)."( Safety and Efficacy of Topical Lovastatin Plus Cholesterol Cream vs Topical Lovastatin Cream Alone for the Treatment of Disseminated Superficial Actinic Porokeratosis: A Randomized Clinical Trial.
Barton, V; Drohan, A; Elston, DM; Gregoski, MJ; Lateef, A; Santa Lucia, G; Snyder, A, 2023
)
1.2
" Adverse events reported included myalgia (n = 2), elevation in the creatine kinase level (n = 1), application discomfort (n = 4), and rash (n = 1)."( Safety and Efficacy of Topical Lovastatin Plus Cholesterol Cream vs Topical Lovastatin Cream Alone for the Treatment of Disseminated Superficial Actinic Porokeratosis: A Randomized Clinical Trial.
Barton, V; Drohan, A; Elston, DM; Gregoski, MJ; Lateef, A; Santa Lucia, G; Snyder, A, 2023
)
1.2
"In doxorubicin-based regimens, pretreatment for at least seven days with an easily available and safe statin can effectively prevent its potentially life threatening cardiotoxicity."( Evaluating The Protective Effects Of Lovastatin Against Doxorubicin Induced Cardiotoxicity In Balb-C Mice.
Afzal, A; Ajmal, K; Rafique, S; Sikandar, A; Tehseen, T; Zafar, A,
)
0.4

Pharmacokinetics

Plasma concentrations of lovastatin (lactone and acid) were determined using high-performance liquid chromatography. Co-administration of ezetimibe and Lovastatin is unlikely to cause a clinically significant pharmacokinetic drug interaction.

ExcerptReferenceRelevance
" Current ongoing clinical studies in patients with renal dysfunction will allow better assessment of the pharmacodynamic meaning of our observations."( Single-dose pharmacokinetics of 14C-lovastatin in chronic renal failure.
Cusson, JR; Grégoire, S; Lambert, R; Larochelle, P; Quérin, S; Stubbs, RJ; Sweany, AE; Vickers, S, 1991
)
0.56
" We also assessed the potential pharmacokinetic interaction between simvastatin and cyclosporine by comparing mean plasma concentrations of simvastatin beta-hydroxy acid, the major metabolite of the drug, in a group of heart transplant patients treated with cyclosporine and in a control group of patients who had not received heart transplants."( Efficacy and pharmacokinetics of simvastatin in heart transplant recipients.
Campana, C; Gavazzi, A; Iacona, I; Montemartini, C; Perani, G; Raddato, V; Regazzi, MB; Viganò, M, 1995
)
0.29
"The Division of Cardiology and the First Medical Clinic for the clinical study, as well as the Department of Pharmacology for the pharmacokinetic analysis."( Efficacy and pharmacokinetics of simvastatin in heart transplant recipients.
Campana, C; Gavazzi, A; Iacona, I; Montemartini, C; Perani, G; Raddato, V; Regazzi, MB; Viganò, M, 1995
)
0.29
"We have examined the pharmacokinetic interaction between isradipine and lovastatin in six male and six female, healthy, normotensive, human subjects after a single dose and after treatment for 5 days."( Pharmacokinetic interaction between isradipine and lovastatin in normal, female and male volunteers.
Finley, DK; Hassell, AE; Holtzman, JL; Zhou, LX, 1995
)
0.78
" In addition, a pharmacodynamic assay has been developed that measures HMG-CoA reductase inhibitory activity."( Clinical pharmacokinetics and practical applications of simvastatin.
Mauro, VF, 1993
)
0.29
" There are no simple methods to investigate the concentration-dependent inhibition of HMG-CoA reductase in human pharmacodynamic studies."( Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences.
Fager, G; Lennernäs, H, 1997
)
0.3
"The effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin, two inhibitors of HMG-CoA reductase with different pharmacokinetic properties, were studied."( Different effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin.
Kantola, T; Kivistö, KT; Neuvonen, PJ, 1998
)
0.76
" Pharmacodynamic parameters (LDL-C, high-density lipoprotein cholesterol, total cholesterol, and triglyceride levels) were evaluated by combining data from weeks 3 and 4 of treatment."( A multiple-dose pharmacodynamic, safety, and pharmacokinetic comparison of extended- and immediate-release formulations of lovastatin.
Davidson, MH; Friedhoff, L; Lukacsko, P; Niecestro, R; Phillips, G; Sterman, A; Sun, JX; Walters, E, 2002
)
0.52
"2 years) were randomized to receive active treatment and 24 were included in the efficacy analysis; 13 patients were included in the pharmacokinetic substudy, 12 of whom had complete pharmacokinetic data."( A multiple-dose pharmacodynamic, safety, and pharmacokinetic comparison of extended- and immediate-release formulations of lovastatin.
Davidson, MH; Friedhoff, L; Lukacsko, P; Niecestro, R; Phillips, G; Sterman, A; Sun, JX; Walters, E, 2002
)
0.52
" Plasma concentrations of lovastatin (lactone and acid) were determined using high-performance liquid chromatography, and the pharmacokinetic parameters were estimated."( Effect of roxithromycin on the pharmacokinetics of lovastatin in volunteers.
Bucher, M; Kees, F; Mair, G, 2002
)
0.87
" A split-dosing regimen resulted in alterations in pharmacokinetic parameters for lovastatin and lovastatin hydroxyacid that are likely due to known differences in the pharmacokinetics of lovastatin when administered to patients with meals or in a fasting state."( Effect of colesevelam on lovastatin pharmacokinetics.
Burke, SK; Donovan, JM; Kisicki, JC; Stiles, MR; Tracewell, WG, 2002
)
0.84
" This study investigated the potential for pharmacodynamic and/or pharmacokinetic interactions between ezetimibe and lovastatin."( Effects of ezetimibe on the pharmacodynamics and pharmacokinetics of lovastatin.
Cutler, DL; Kosoglou, T; Maxwell, SE; Meyer, I; Musiol, B; Statkevich, P; Veltri, EP; Yang, B; Zhu, Y, 2004
)
0.77
" Pharmacokinetic findings were compared among three preparation(lovastatin sustained-release tablet, Tp; sustained-release capsule, TJ and conventional capsule)."( Pharmacokinetic study on lovastatin sustained-release tablet and sustained-release capsule in Beagal dogs.
Dai, Z; Fu, L; Hou, S; Wan, Y, 2004
)
0.87
" In a separate pilot study, co-administration of ezetimibe and lovastatin resulted in a significant pharmacodynamic interaction, leading to an additive reduction in LDL-C."( Pharmacokinetic interaction between ezetimibe and lovastatin in healthy volunteers.
Boutros, T; Kosoglou, T; Reyderman, L; Seiberling, M; Statkevich, P, 2004
)
0.82
" The point estimates based on the log-transformed Cmax and AUC values for lovastatin and beta-hydroxylovastatin were 113% and 119%, respectively, for co-administration of ezetimibe with lovastatin vs."( Pharmacokinetic interaction between ezetimibe and lovastatin in healthy volunteers.
Boutros, T; Kosoglou, T; Reyderman, L; Seiberling, M; Statkevich, P, 2004
)
0.81
" Co-administration of ezetimibe and lovastatin is unlikely to cause a clinically significant pharmacokinetic drug interaction."( Pharmacokinetic interaction between ezetimibe and lovastatin in healthy volunteers.
Boutros, T; Kosoglou, T; Reyderman, L; Seiberling, M; Statkevich, P, 2004
)
0.85
"Four separate studies investigated the pharmacokinetic interaction between single oral doses of aliskiren and lovastatin, atenolol, celecoxib or cimetidine, respectively."( Pharmacokinetic interactions of the oral renin inhibitor aliskiren with lovastatin, atenolol, celecoxib and cimetidine.
Corynen, S; Dieterle, W; Mann, J; Vaidyanathan, S, 2005
)
0.77
" Aliskiren mean Cmax was not affected by either lovastatin or atenolol, although a non-significant 36% increase was observed with celecoxib."( Pharmacokinetic interactions of the oral renin inhibitor aliskiren with lovastatin, atenolol, celecoxib and cimetidine.
Corynen, S; Dieterle, W; Mann, J; Vaidyanathan, S, 2005
)
0.82
"Overall, single doses of aliskiren showed no evidence of clinically important pharmacokinetic interactions with lovastatin, atenolol, celecoxib or cimetidine."( Pharmacokinetic interactions of the oral renin inhibitor aliskiren with lovastatin, atenolol, celecoxib and cimetidine.
Corynen, S; Dieterle, W; Mann, J; Vaidyanathan, S, 2005
)
0.77
"The Cmax and area under the curve (AUC) of lovastatin were 22."( Plasma clearance of lovastatin versus chinese red yeast rice in healthy volunteers.
Heber, D; Lee, R; Li, Z; Minutti, C; Seeram, NP; Thames, G; Wang, HJ, 2005
)
0.91
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.63
" Lovastatin, a blood cholesterol-lowering drug with a short elimination half-life in humans, was used to assess the influence of two different dosing methods on the drug pharmacokinetics and pharmacodynamics."( Comparing pharmacokinetic and pharmacodynamic profiles in female rats orally exposed to lovastatin by gavage versus diet.
Chen, Y; Kapetanovic, IM; Lindeblad, M; Lyubimov, A; Martín-Jiménez, T, 2008
)
1.48
"A selective, rapid and sensitive ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was developed for the quantitative determination of lovastatin in human plasma and its application in a pharmacokinetic study."( Determination of lovastatin in human plasma by ultra-performance liquid chromatography-electrospray ionization tandem mass spectrometry and its application in a pharmacokinetic study.
Li, H; Peng, W; Tu, J; Wang, F; Yuan, H, 2008
)
0.88
" The pharmacokinetic parameters, area under the curve total (AUC(t)) and to infinity (AUC(inf)), peak plasma concentration (C(max)), time to attain peak (t(max)), and elimination half-life (t(1/2)) were determined and analyzed statistically."( Pharmacokinetics and bioequivalence study of two tablet formulations of lovastatin in healthy volunteers.
Amenta, F; Mignini, F; Streccioni, V; Tomassoni, D; Traini, E, 2008
)
0.58
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
Lombardo, F; Obach, RS; Waters, NJ, 2008
)
0.35
" In addition, the pharmacokinetic parameters and absolute bioavailability suggested that the absorption and elimination of lovastatin in Bama miniature pigs were similar to those in humans."( Bama miniature pigs (Sus scrofa domestica) as a model for drug evaluation for humans: comparison of in vitro metabolism and in vivo pharmacokinetics of lovastatin.
Cen, YY; Liu, Y; Shang, HT; Wei, H; Zeng, BH, 2008
)
0.75
" The pharmacokinetic parameters of verapamil and norverapamil in rats were measured after the oral administration of verapamil (9 mg/kg) in the presence or absence of lovastatin (0."( Effects of lovastatin on the pharmacokinetics of verapamil and its active metabolite, norverapamil in rats: possible role of P-glycoprotein inhibition by lovastatin.
Chang, KS; Choi, DH; Choi, JS; Hong, SP; Koh, YY, 2009
)
0.94
"The pharmacokinetic parameters of verapamil and one of its metabolites, norverapamil, were compared in 14 healthy male Korean volunteers (age range 22-28 years) who had been administered verapamil (60 mg) orally in the presence or absence of oral lovastatin (20 mg)."( Pharmacokinetic interaction between oral lovastatin and verapamil in healthy subjects: role of P-glycoprotein inhibition by lovastatin.
Choi, DH; Choi, JS; Chung, JH, 2010
)
0.81
"The pharmacokinetic parameters of verapamil were significantly altered by the co-administration of lovastatin compared to the control."( Pharmacokinetic interaction between oral lovastatin and verapamil in healthy subjects: role of P-glycoprotein inhibition by lovastatin.
Choi, DH; Choi, JS; Chung, JH, 2010
)
0.84
"The pharmacokinetic parameters of diltiazem and desacetyldiltiazem were determined after orally administering diltiazem (12 mg/kg) to rats in the presence and absence of lovastatin (0."( Effects of lovastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats: possible role of cytochrome P450 3A4 and P-glycoprotein inhibition by lovastatin.
Chang, KS; Choi, DH; Chung, JW; Ha, SI; Han, JY; Hong, SP; Koh, YY; Yang, JS, 2011
)
0.95
" Compared with the control (given diltiazem alone), the presence of lovastatin significantly altered the pharmacokinetic parameters of diltiazem."( Effects of lovastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats: possible role of cytochrome P450 3A4 and P-glycoprotein inhibition by lovastatin.
Chang, KS; Choi, DH; Chung, JW; Ha, SI; Han, JY; Hong, SP; Koh, YY; Yang, JS, 2011
)
0.99
" Pharmacokinetic parameters of losartan and EXP-3174 in rats were determined after oral and intravenous administration of losartan (9 mg/kg) without and with HMG-CoA reductase inhibitors (1 mg/kg)."( Effects of HMG-CoA reductase inhibitors on the pharmacokinetics of losartan and its main metabolite EXP-3174 in rats: possible role of CYP3A4 and P-gp inhibition by HMG-CoA reductase inhibitors.
Choi, DH; Choi, JS; Yang, SH, 2011
)
0.37
"A single-dose pharmacokinetic study was performed with lovastatin in 23 Chinese healthy male subjects."( Impact of CYP2D6 polymorphisms on the pharmacokinetics of lovastatin in Chinese subjects.
Chow, MS; Fok, BS; Hu, M; Mak, VW; Tomlinson, B; Yin, OQ, 2012
)
0.87
"In the SLCO1B1*5/*15 or *15/*15 genotype group, the geometric mean Cmax and AUC0-24 of lovastatin acid were 340 and 286% of the corresponding values in the SLCO1B1*1A/*1A (reference) genotype group (P<0."( SLCO1B1 polymorphism markedly affects the pharmacokinetics of lovastatin acid.
Backman, JT; Neuvonen, M; Neuvonen, PJ; Niemi, M; Tornio, A; Vakkilainen, J, 2015
)
0.88
" SD male rats were random divided into lovastatin group and berberine induced prior to lovastatin group for the in vivo pharmacokinetic studies."( In Vivo and in Vitro Study on Drug-Drug Interaction of Lovastatin and Berberine from Pharmacokinetic and HepG2 Cell Metabolism Studies.
Cui, H; Dang, M; Dong, Y; Liu, H; Tong, X; Wang, J; Wu, J; Yang, F; Zhang, L; Zhang, Q, 2016
)
0.95
" Finally, this method has been successfully applied to a pharmacokinetic study in rats following a single oral dose of 10mg/kg LOV-NS."( Simultaneous determination of lovastatin and its metabolite lovastatin acid in rat plasma using UPLC-MS/MS with positive/negative ion-switching electrospray ionization: Application to a pharmacokinetic study of lovastatin nanosuspension.
Fu, Q; Guo, M; He, Z; Li, M; Liu, B; Pu, X; Yang, L; Zhao, L, 2016
)
0.72
" However, the pharmacokinetic mechanisms contributing to its distinct efficacy and low side effects are unclear."( Isoflavones enhance pharmacokinetic exposure of active lovastatin acid via the upregulation of carboxylesterase in high-fat diet mice after oral administration of Xuezhikang capsules.
Aa, JY; Feng, D; Ge, C; Sun, JG; Tan, ZY; Wang, GJ; Xie, Y; Yan, CX; Yao, L, 2018
)
0.73
" This study was to investigate whether and how CV drugs affect the pharmacokinetic profile of sinomenine."( Co-administration with simvastatin or lovastatin alters the pharmacokinetic profile of sinomenine in rats through cytochrome P450-mediated pathways.
Dai, Y; Jin, Y; Wang, M; Wang, Y; Xia, Y; Yun, X, 2018
)
0.75

Compound-Compound Interactions

Lovastatin is a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Compound 5 prevented lovastatin-induced FPP depletion and impairment of protein farnesylation.

ExcerptReferenceRelevance
"We have determined the effect of lovastatin alone or in combination with cholestyramine on lipoprotein (a) [Lp(a)] levels in 59 heterozygotes for familial hypercholesterolemia (FH) treated for 33."( Long-term effect of lovastatin alone and in combination with cholestyramine on lipoprotein (a) level in familial hypercholesterolemic subjects.
Berg, K; Foss, OP; Hjermann, I; Leren, P; Leren, TP, 1992
)
0.89
"The aim of the investigation was twofold: to study the effect of lovastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, alone and in combination with other lipid lowering drugs in an open 48 week single centre study, and to study if lipid lowering drugs influence adherence to diet in adult patients with familial hypercholesterolemia."( [Familial hypercholesterolemia--intensive diet therapy combined with drug therapy].
Lund, H; Norseth, J; Ose, L; Stugaard, M; Wiig, I, 1992
)
0.52
"Nineteen adult patients with type III hyperlipoproteinemia (HLP) and homozygosity for apolipoprotein (apo) E2 were treated with the 3-hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase inhibitor simvastatin (20 or 40 mg per day) alone or in combination with the fibrate derivative gemfibrozil (450 mg per day) during a 30-week outpatient study."( The influence of simvastatin alone or in combination with gemfibrozil on plasma lipids and lipoproteins in patients with type III hyperlipoproteinemia.
Eichinger, M; Feussner, G; Ziegler, R, 1992
)
0.28
"We have studied the effect of simvastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis, alone and in combination with cholestyramine in 48 patients."( [HMG-CoA reductase inhibitors in familial hypercholesterolemia. Therapy with simvastatin alone and in combination with cholestyramine in low dosage; a report of 2 years experiences].
Burrichter, H; Geisel, J; Oette, K, 1990
)
0.28
" The use of Simvastatin in combination with HELP significantly augments the reduction in LDL cholesterol to a level where regression of atherosclerotic lesions might be expected."( Long-term clinical experience with HELP-LDL-apheresis in combination with HMG-CoA-reductase inhibitors for maximum treatment of coronary heart disease associated with severe hypercholesterolemia.
Armstrong, VW; Eisenhauer, T; Scheler, F; Schuff-Werner, P; Schütz, E; Seidel, D; Thiery, J,
)
0.13
"Recent trials have investigated the usefulness of fenofibrate, alone and in combination with other lipid-lowering therapies, in the treatment of hyperlipidemia."( Review of clinical studies of fenofibrate in combination with currently approved lipid-lowering drugs.
Brown, WV, 1989
)
0.28
"We have studied the effect of lovastatin, an inhibitor of the rate-limiting enzyme in cholesterol biosynthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase), alone and in combination with the bile acid sequestrant cholestyramine on lipid parameters in 30 heterozygous patients with familial hypercholesterolemia (FH) during a 20-week open trial."( Effects of lovastatin alone and in combination with cholestyramine on serum lipids and apolipoproteins in heterozygotes for familial hypercholesterolemia.
Berg, K; Foss, OP; Hjermann, I; Leren, P; Leren, TP; Viksmoen, L, 1988
)
0.95
"The effects of the two HMG CoA reductase inhibitors lovastatin and pravastatin in combination with 12-16 g cholestyramine on serum lipids were studied in 18 patients with severe primary hypercholesterolemia."( Long-term treatment (2 years) with the HMG CoA reductase inhibitors lovastatin or pravastatin in combination with cholestyramine in patients with severe primary hypercholesterolemia.
Jacob, BG; Richter, WO; Schwandt, P, 1993
)
0.77
" Following an 8-week dietary phase, participants were randomized to treatment with 20 mg of lovastatin combined with 5 g or with 10 g of colestipol, or to matching placebo."( Effectiveness of low-dose lovastatin combined with low-dose colestipol in moderate to severe primary hypercholesterolaemia.
de Koning Gans, HJ; Gørbitz, C; Harrison, EM; Ose, L; Tonstad, S, 1993
)
0.81
" Judging from these results, SV was considered to interact with CT by the following procedure: SV underwent hydrolysis to SVH in aqueous solution, then CT activated the hydrolysis by binding the formed SVH, resulting in a significant reduction in concentration of SV."( Drug interaction between simvastatin and cholestyramine in vitro and in vivo.
Ichikawa, M; Matsuyama, K; Nakai, A; Nishikata, M, 1996
)
0.29
" These findings provide a molecular explanation for the ability of disparate chemicals to induce CYP3A4 levels and, furthermore, provide a basis for developing in vitro assays to aid in predicting whether drugs will interact in humans."( The human orphan nuclear receptor PXR is activated by compounds that regulate CYP3A4 gene expression and cause drug interactions.
Kliewer, SA; Lehmann, JM; McKee, DD; Moore, JT; Watson, MA; Willson, TM, 1998
)
0.3
"The objectives of this review are to discuss the role of cytochrome P450 (CYP450) isoforms in drug metabolism, to explain differences in metabolism among the HMG-CoA reductase inhibitors (HMGs, statins), to review drug-drug and drug-food interaction studies dealing with the HMGs, to present case reports dealing with HMG-related myopathy, to discuss major clinical implications of these case reports and to express an opinion of use of HMGs in clinical practice."( The role of cytochrome P450-mediated drug-drug interactions in determining the safety of statins.
Bottorff, M; Worz, CR, 2001
)
0.31
" Therefore, we determined the effect of SCH 48461 and ezetimibe in combination with 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors in chow-fed dogs."( The synergistic hypocholesterolemic activity of the potent cholesterol absorption inhibitor, ezetimibe, in combination with 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors in dogs.
Alton, KB; Burrier, RE; Davis, HR; Pula, KK; Watkins, RW, 2001
)
0.31
"We assessed the short and long-term efficacy and safety of the lipid lowering drugs, nicotinic acid, and the HMG-CoA reductase inhibitor, lovastatin, in combination with cholestyramine in four renal transplant patients."( Effects of nicotinic acid and lovastatin in combination with cholestyramine in renal transplant patients.
Katyal, A; Lal, SM,
)
0.62
"This multicenter, randomized, double-blind, placebo-controlled clinical study assessed the efficacy and safety of ezetimibe administered with lovastatin in primary hypercholesterolemia."( Efficacy and safety of ezetimibe coadministered with lovastatin in primary hypercholesterolemia.
Corbelli, J; Kerzner, B; LeBeaut, A; Lipka, LJ; Melani, L; Mukhopadhyay, P; Sharp, S; Suresh, R; Veltri, EP, 2003
)
0.77
"To investigate the effects of lovastatin combined with cyclosporine A (CsA) on cultured human peripheral blood mononuclear cells (PBMC) proliferation, cytokines expression and cytotoxicity in vitro."( [Effects of lovastatin combined with cyclosporine A on cultured human peripheral blood mononuclear cells proliferation, cytokines expression and cytotoxicity].
Duan, L; Li, CH; Li, H; Li, XW, 2001
)
0.98
" The effects of lovastatin combined with CsA on cultured PBMC proliferation and cytotoxicity were observed in 3H-TdR incorporation assay."( [Effects of lovastatin combined with cyclosporine A on cultured human peripheral blood mononuclear cells proliferation, cytokines expression and cytotoxicity].
Duan, L; Li, CH; Li, H; Li, XW, 2001
)
1.04
"Statins combined with cyclosporine A have a synergic effect and can delay the incidence and development of allograft rejection and prolong the graft life-span in animal models and clinical trials."( [Effects of lovastatin combined with cyclosporine A on cultured human peripheral blood mononuclear cells proliferation, cytokines expression and cytotoxicity].
Duan, L; Li, CH; Li, H; Li, XW, 2001
)
0.69
" Herein, we investigated in human monocytes the effect of statins alone, and in combination with PPAR-gamma ligands on CD36 expression, as well as the molecular mechanisms underlying the regulatory action of statins."( Statins upregulate CD36 expression in human monocytes, an effect strengthened when combined with PPAR-gamma ligands Putative contribution of Rho GTPases in statin-induced CD36 expression.
Domínguez, A; Ruiz-Velasco, N; Vega, MA, 2004
)
0.32
"To evaluate the effect of lovastatin alone or combined with radiation on U87MG and FaDu cells in vitro and U87MG tumors in vivo."( Effects of lovastatin alone or combined with irradiation on tumor cells in vitro and in vivo.
Baumann, M; Dörfler, A; Gabryś, D; Hessel, F; Krause, M; Oertel, R; Yaromina, A, 2008
)
1.04
" The proportion of cells in G0/G1 phase, apoptosis and p21 protein expression increased after lovastatin alone or combined with 4-Gy irradiation in both cell lines."( Effects of lovastatin alone or combined with irradiation on tumor cells in vitro and in vivo.
Baumann, M; Dörfler, A; Gabryś, D; Hessel, F; Krause, M; Oertel, R; Yaromina, A, 2008
)
0.95
" The frequency of drug-drug interactions involving lovastatin or simvastatin was studied."( Frequency and clinical relevance of drug interactions with lovastatin and simvastatin: an observational database study.
Huupponen, R; Irjala, K; Klaukka, T; Laine, K; Ryynänen, A; Tirkkonen, T; Vahlberg, T, 2008
)
0.84
" In this study, we have developed a nonpeptidomimetic GGTI, termed GGTI-2Z [(5-nitrofuran-2-yl)methyl-(2Z,6E,10E)-3,7,11,15-tetramethylhexadeca-2,6,10,14-tetraenyl 4-chlorobutyl(methyl)phosphoramidate], which in combination with lovastatin inhibits geranylgeranyl transferase I (GGTase I) and GGTase II/RabGGTase, without affecting farnesylation."( A novel geranylgeranyl transferase inhibitor in combination with lovastatin inhibits proliferation and induces autophagy in STS-26T MPNST cells.
Borch, RF; Dean, IS; Fouad, F; Gibbs, RA; Lalonde, DT; Mattingly, RR; Mynderse, M; Reiners, JJ; Sane, KM; Wojtkowiak, JW, 2010
)
0.78
" When combined with lovastatin, compound 5 prevented lovastatin-induced FPP depletion and impairment of protein farnesylation."( A novel bisphosphonate inhibitor of squalene synthase combined with a statin or a nitrogenous bisphosphonate in vitro.
Hohl, RJ; Shull, LW; Smits, JP; Wasko, BM; Wiemer, DF, 2011
)
0.69
"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
" Salubrinal, an agent that can sustain the activity of a key regulator of the ISR eIF2α, further increased the expression of ATF3 and demonstrated synergistic cytotoxicity in combination with lovastatin in SCC cells."( Lovastatin-induced apoptosis is mediated by activating transcription factor 3 and enhanced in combination with salubrinal.
Corsten, M; Dimitroulakos, J; Gorn-Hondermann, I; Johnson-Obeseki, S; Ma, L; Niknejad, N; Zahr, S, 2014
)
2.03
" This observed discrepancy between in vitro risk assessment and in vivo drug-drug interaction (DDI) profile was rationalized by time-varying dynamic pharmacokinetic models that incorporated circulating concentrations of fluoxetine and norfluoxetine enantiomers, mutual inhibitor-inhibitor interactions, and CYP3A4 induction."( Fluoxetine- and norfluoxetine-mediated complex drug-drug interactions: in vitro to in vivo correlation of effects on CYP2D6, CYP2C19, and CYP3A4.
Davis, C; Foti, RS; Isoherranen, N; Kunze, KL; Lutz, JD; Sager, JE, 2014
)
0.4
"A dispersive liquid-liquid microextraction method based on solidification of floating organic drop combined with HPLC was developed for the determination of lovastatin and simvastatin in rat urine for the first time."( A dispersive liquid-liquid microextraction method based on the solidification of a floating organic drop combined with HPLC for the determination of lovastatin and simvastatin in rat urine.
Hou, X; Li, F; Ma, X; Wang, L; Zhao, L; Zhao, P, 2014
)
0.8
", antibiotics) may lead to drug-drug interactions (DDI)."( Gut microbiota-mediated drug interactions between lovastatin and antibiotics.
Jung, IH; Kim, DH; Kim, IS; Van Le, TK; Yoo, DH; Yoo, HH, 2014
)
0.66
"An UPLC-MS/MS method was developed and validated for the pharmacokinetics tudy of lovastatin to investigate the in vivo drug-drug interactions between lovastatin and berberine."( In Vivo and in Vitro Study on Drug-Drug Interaction of Lovastatin and Berberine from Pharmacokinetic and HepG2 Cell Metabolism Studies.
Cui, H; Dang, M; Dong, Y; Liu, H; Tong, X; Wang, J; Wu, J; Yang, F; Zhang, L; Zhang, Q, 2016
)
0.91
" The drug-drug interaction assay also showed that the concomitant use of kinsenoside has a non-significant effect on the concentration of lovastatin or amlodipine, and their major metabolites."( In Vitro Assessment of CYP-Mediated Drug Interactions for Kinsenoside, an Antihyperlipidemic Candidate.
Choi, MS; Kim, IS; Luo, Z; Rehman, SU; Xue, Y; Yao, G; Yoo, HH; Zhang, Y, 2016
)
0.64
"The purpose of this study was to conduct a 20-week controlled trial of lovastatin (10 to 40 mg/day) in youth with fragile X syndrome (FXS) ages 10 to 17 years, combined with an open-label treatment of a parent-implemented language intervention (PILI), delivered via distance video teleconferencing to both treatment groups, lovastatin and placebo."( Controlled trial of lovastatin combined with an open-label treatment of a parent-implemented language intervention in youth with fragile X syndrome.
Abbeduto, L; Banasik, A; Bullard, L; Hagerman, R; Kim, K; McDuffie, A; Nguyen, V; Potter, LA; Potter, SN; Tassone, F; Thurman, AJ, 2020
)
1.11
" However, the traditional drug combination approaches are restricted with high-cost apparatus, complex and numerous unit operations."( Enabling the drug combination of celecoxib through a spherical co-agglomeration strategy with controllable and stable drug content and good powder properties.
Chen, M; Feng, S; Gao, Y; Gong, J; Guo, S; Han, D; Li, K; Li, T; Tong, L; Wei, J; Yu, C; Zhao, P, 2022
)
0.72

Bioavailability

Lovastatin solid lipid nanoparticles (SLN) duodenally to rats. Following single oral administration of the selected formulation (F9), a relative bioavailability of 162% was achieved compared to pure lovastatin.

ExcerptReferenceRelevance
" SV is well absorbed by rats, dogs, and humans."( Metabolic disposition studies on simvastatin, a cholesterol-lowering prodrug.
Chen, IW; Duggan, DE; Duncan, CA; Rosegay, A; Vickers, S,
)
0.13
"The oral bioavailability of two HMG-CoA reductase inhibitors, pravastatin and lovastatin, was investigated in this randomized, two-way crossover study."( Comparative pharmacokinetics and pharmacodynamics of pravastatin and lovastatin.
DeVault, AR; Ivashkiv, E; Pan, HY; Sugerman, AA; Swanson, BN; Wang-Iverson, D, 1990
)
0.74
" In animals, lovastatin is not as well absorbed as HA given per se, but that fraction that is absorbed reaches the portal circulation largely unchanged and is more efficiently extracted by the liver, after which it is reversibly biotransformed to HA and irreversibly to other enzymatically active products."( The physiological disposition of lovastatin.
Bayne, WF; Chen, IW; Duggan, DE; Duncan, CA; Halpin, RA; Schwartz, MS; Stubbs, RJ; Vickers, S,
)
0.78
" The results imply a decreased bioavailability of SLS in the statin-treated group, while no evidence for an altered permeability barrier to water was found."( Effect of systemic treatment with cholesterol-lowering drugs on the skin barrier function in humans.
Agner, E; Agner, T; Malinowski, J; Meibom, J; Ramsing, D, 1995
)
0.29
" Simvastatin is well absorbed from the gastrointestinal tract but is highly extracted by the liver and only 7% of the dose reaches the general circulation intact."( Clinical pharmacokinetics and practical applications of simvastatin.
Mauro, VF, 1993
)
0.29
" Alternatively, they may have been due to enhanced bioavailability of lovastatin when administered with a high-fat diet."( The effect of supplemental dietary fat on plasma cholesterol levels in lovastatin-treated hypercholesterolemic patients.
Coaker, JS; Elswick, RK; Kolinski, RJ; McKenney, JM; Proctor, JD; Wright, JT,
)
0.6
"Grapefruit juice increases the bioavailability of several drugs known to be metabolized by CYP3A4."( Grapefruit juice greatly increases serum concentrations of lovastatin and lovastatin acid.
Kantola, T; Kivistö, KT; Neuvonen, PJ, 1998
)
0.54
" These differences may be due to interactions between genetic and environmental factors that effect drug bioavailability or the capacity of the lipid-regulating enzyme and receptor targets to be affected."( Lack of interaction of apolipoprotein E phenotype with the lipoprotein response to lovastatin or gemfibrozil in patients with primary hypercholesterolemia.
Ballesta, AM; Casals, E; Ojuel, J; Rodriguez-Villar, C; Ros, E; Sanllehy, C; Zambón, D, 1998
)
0.53
" Compared with lovastatin, the cytochrome P-450-dependent intestinal intrinsic clearance of pravastatin was >5000-fold lower and cannot be expected to significantly affect its oral bioavailability or to be a significant site of drug interactions."( Small intestinal metabolism of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor lovastatin and comparison with pravastatin.
Baner, K; Benet, LZ; Christians, U; Deters, M; Hackbarth, I; Hallensleben, K; Jacobsen, W; Kirchner, G; Mancinelli, L; Sewing, KF, 1999
)
0.88
"The quantitative structure-bioavailability relationship of 232 structurally diverse drugs was studied to evaluate the feasibility of constructing a predictive model for the human oral bioavailability of prospective new medicinal agents."( QSAR model for drug human oral bioavailability.
Topliss, JG; Yoshida, F, 2000
)
0.31
" 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,
)
1.04
" An even greater increase in the bioavailability of lovastatin (261%) and lovastatin acid (231%) was observed when the lovastatin ER tablets were administered under fasting conditions."( Comparative pharmacokinetics of lovastatin extended-release tablets and lovastatin immediate-release tablets in humans.
Friedhoff, L; Lukacsko, P; Niecestro, R; Phillips, G; Shen, J; Sun, JX, 2002
)
0.85
" Mean bioavailability of lovastatin lactone was lower and that of lovastatin acid was higher with concomitant treatment."( Effect of roxithromycin on the pharmacokinetics of lovastatin in volunteers.
Bucher, M; Kees, F; Mair, G, 2002
)
0.87
" 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
" Relative bioavailability was 111."( Pharmacokinetic study on lovastatin sustained-release tablet and sustained-release capsule in Beagal dogs.
Dai, Z; Fu, L; Hou, S; Wan, Y, 2004
)
0.63
" 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
"Cyclodextrins (CDs) are cyclic oligosaccharides, capable of forming inclusion complexes with hydrophobic molecules in aqueous solution and therefore, of improving the bioavailability of many drugs."( [Interactions in solution between cyclodextrins and statins].
Csempesz, F; Süle, A; Szente, L, 2005
)
0.33
" Exenatide slows gastric emptying, which may alter the absorption rate of co-administered oral medications."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.34
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.63
"The purpose of this research was to study whether the bioavailability of lovastatin could be improved by administering lovastatin solid lipid nanoparticles (SLN) duodenally to rats."( Preparation, characterization, and in vitro and in vivo evaluation of lovastatin solid lipid nanoparticles.
Manjunath, K; Satyanarayana, V; Suresh, G; Venkateswarlu, V, 2007
)
0.81
" Since both drugs are extensively metabolized, this study investigated the bioavailability and pharmacokinetics of their co-administration following single-dose administration."( The comparative bioavailability of an extended-release niacin and lovastatin fixed dose combination tablet versus extended-release niacin tablet, lovastatin tablet and a combination of extended-release niacin tablet and lovastatin tablet.
Cefali, E; Menon, R; Tolbert, D, 2007
)
0.58
" 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
" The bioavailability in SD rats was evaluated simultaneously."( Redispersible, dry emulsion of lovastatin protects against intestinal metabolism and improves bioavailability.
Gan, L; Gan, Y; Ge, Z; Zhang, XX, 2008
)
0.63
" In conclusion, MLBG could be used as a potential carrier in enhancing the dissolution rate and bioavailability of LS."( Solubility enhancement of lovastatin by modified locust bean gum using solid dispersion techniques.
Gattani, S; Patel, M; Surana, S; Tekade, A, 2008
)
0.65
" In addition, the pharmacokinetic parameters and absolute bioavailability suggested that the absorption and elimination of lovastatin in Bama miniature pigs were similar to those in humans."( Bama miniature pigs (Sus scrofa domestica) as a model for drug evaluation for humans: comparison of in vitro metabolism and in vivo pharmacokinetics of lovastatin.
Cen, YY; Liu, Y; Shang, HT; Wei, H; Zeng, BH, 2008
)
0.75
"This study was to investigate the effect of lovastatin on the bioavailability or pharmacokinetics of verapamil and its major metabolite, norverapamil, in rats."( Effects of lovastatin on the pharmacokinetics of verapamil and its active metabolite, norverapamil in rats: possible role of P-glycoprotein inhibition by lovastatin.
Chang, KS; Choi, DH; Choi, JS; Hong, SP; Koh, YY, 2009
)
1
" Consequently, the relative bioavailability of verapamil was also significantly increased (by 76."( Pharmacokinetic interaction between oral lovastatin and verapamil in healthy subjects: role of P-glycoprotein inhibition by lovastatin.
Choi, DH; Choi, JS; Chung, JH, 2010
)
0.63
"Nanostructured lipid carriers (NLCs) made from mixtures of Precirol and squalene were prepared to investigate whether the bioavailability of lovastatin can be improved by oral delivery."( Effects of lipophilic emulsifiers on the oral administration of lovastatin from nanostructured lipid carriers: physicochemical characterization and pharmacokinetics.
Chen, CC; Fang, JY; Huang, ZR; Tsai, TH, 2010
)
0.8
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010
)
0.36
" The content of cellular triglyceride and the absorption rate of free fatty acid were determined."( [Establishment of a model for evaluating hypolipidemic effect in HepG2 cells].
Li, Y; Lü, N; Niu, Y; Sun, C; Zhao, D, 2010
)
0.36
"4%), and the extent of absolute oral bioavailability (F) of nicardipine was increased (by 38."( Effects of lovastatin on the pharmacokinetics of nicardipine in rats.
Choi, JS; Chung, JW; Yang, SH, 2010
)
0.75
"A biodegradable porous starch foam (BPSF) was developed for the first time as a carrier in order to improve the dissolution and enhance the oral bioavailability of lovastatin - defined as a model poorly water soluble BCS type II drug."( Development of biodegradable porous starch foam for improving oral delivery of poorly water soluble drugs.
Jiang, T; Wang, S; Wang, Z; Wu, C; Zhang, J; Zhi, Z, 2011
)
0.56
" Our results suggest that there is an increase in lovastatin bioavailability when the formulation is administered after the high-fat meal."( Novel extended-release formulation of lovastatin by one-step melt granulation: in vitro and in vivo evaluation.
Gascón, AR; Hernández, RM; Igartua, M; Ochoa, L; Pedraz, JL; Solinis, MA, 2011
)
0.89
" Consequently, the absolute bioavailability values of diltiazem in the presence of lovastatin (11."( Effects of lovastatin on the pharmacokinetics of diltiazem and its main metabolite, desacetyldiltiazem, in rats: possible role of cytochrome P450 3A4 and P-glycoprotein inhibition by lovastatin.
Chang, KS; Choi, DH; Chung, JW; Ha, SI; Han, JY; Hong, SP; Koh, YY; Yang, JS, 2011
)
0.98
"The extents to which small intestinal (SI) cytochrome P450 (P450) enzymes control the bioavailability of oral drugs are not well defined, particularly for drugs that are substrates for both P450 and the P-glycoprotein (P-gp)."( Role of intestinal cytochrome P450 (P450) in modulating the bioavailability of oral lovastatin: insights from studies on the intestinal epithelium-specific P450 reductase knockout mouse.
D'Agostino, J; Zhang, QY; Zhu, Y, 2011
)
0.59
" Consequently, the absolute bioavailability (F) of losartan after oral administration with simvastatin was significantly increased by 59."( Effects of HMG-CoA reductase inhibitors on the pharmacokinetics of losartan and its main metabolite EXP-3174 in rats: possible role of CYP3A4 and P-gp inhibition by HMG-CoA reductase inhibitors.
Choi, DH; Choi, JS; Yang, SH, 2011
)
0.37
"To improve its bioavailability and pharmacological effects in humans, red ginseng was fermented with a newly isolated fungus, Monascus pilosus KMU103."( Simultaneous enrichment of deglycosylated ginsenosides and monacolin K in red ginseng by fermentation with Monascus pilosus.
Hong, SY; Lee, I; Oh, JH, 2011
)
0.37
" Moreover, StAR overexpression attenuated the PA-induced reduction of nitric oxide bioavailability by protecting the bioactivity of pAkt/peNOS/NO pathway."( Overexpression of steroidogenic acute regulatory protein in rat aortic endothelial cells attenuates palmitic acid-induced inflammation and reduction in nitric oxide bioavailability.
Li, X; Ning, Y; Qiu, Y; Tian, D; Wang, X; Yin, L; Zhan, Y; Zhi, X, 2012
)
0.38
"Our results showed that StAR attenuated lipid synthesis and uptake as well as PA-induced inflammation and reduction in NO bioavailability in aortic endothelial cells."( Overexpression of steroidogenic acute regulatory protein in rat aortic endothelial cells attenuates palmitic acid-induced inflammation and reduction in nitric oxide bioavailability.
Li, X; Ning, Y; Qiu, Y; Tian, D; Wang, X; Yin, L; Zhan, Y; Zhi, X, 2012
)
0.38
" The aim of this study was to compare the dissolution rate, physical state, and oral bioavailability of lovastatin in three RYR products (LipoCol Forte, Cholestin, or Xuezhikang) to those of two lovastatin tablets (Mevacor or Lovasta)."( Improved dissolution rate and oral bioavailability of lovastatin in red yeast rice products.
Chen, CH; Lin, CJ; Uang, YS; Yang, JC, 2013
)
0.85
" Following single oral administration of the selected formulation (F9), a relative bioavailability of 162% was achieved compared to pure lovastatin."( Proliposomes as a drug delivery system to decrease the hepatic first-pass metabolism: case study using a model drug.
Betageri, GV; Issar, M; Kadajji, VG; Venkatesan, N; Wang, Z; Yanamandra, S, 2014
)
0.61
"This research proved that poly(lactic acid) microspheres can significantly prolong the drug circulation time in vivo and can also significantly increase the relative bioavailability of the drug."( Development of lovastatin-loaded poly(lactic acid) microspheres for sustained oral delivery: in vitro and ex vivo evaluation.
Chen, W; Guan, Q; Hu, X, 2015
)
0.77
" Furthermore, the pharmacokinetics and relative bioavailability of the LOV-loaded MN-SLB formulation was studied in beagle dogs after oral administration and using a commercially available immediate release formulation (Sandoz Lovastatin®) as a reference."( Development of novel mesoporous nanomatrix-supported lipid bilayers for oral sustained delivery of the water-insoluble drug, lovastatin.
Che, E; Gao, C; Han, J; Wang, S; Yang, Y; Zhang, H; Zhang, L; Zhang, M; Zhang, Y, 2015
)
0.81
" More importantly, the oral bioavailability of LOV-RNs was higher than LOV-SNs (p>0."( Rod shaped nanocrystals exhibit superior in vitro dissolution and in vivo bioavailability over spherical like nanocrystals: a case study of lovastatin.
Fu, Q; Guo, M; Guo, Z; He, Z; Li, M; Sun, J; Wu, C; Yang, L, 2015
)
0.62
"Nanostructured lipid carriers (NLCs) have been one of the systems of choice for improving the oral bioavailability of drugs with poor water solubility."( Improvement of oral bioavailability of lovastatin by using nanostructured lipid carriers.
Zhou, D; Zhou, J, 2015
)
0.69
"Lovastatin (LOV) is an antihyperlipidemic agent which exhibits low bioavailability due to its poor solubility."( Simultaneous determination of lovastatin and its metabolite lovastatin acid in rat plasma using UPLC-MS/MS with positive/negative ion-switching electrospray ionization: Application to a pharmacokinetic study of lovastatin nanosuspension.
Fu, Q; Guo, M; He, Z; Li, M; Liu, B; Pu, X; Yang, L; Zhao, L, 2016
)
2.17
"Lovastatin (LOV), an antihyperlipidimic agent, is characterized by low solubility/poor dissolution and, thus, low bioavailability (<5%)."( Stabilization and Amorphization of Lovastatin Using Different Types of Silica.
Al-Nimry, S; Khanfar, M, 2017
)
2.17
"Lovastatin (LSN), a potent anti-hyperlipidemic drug, possesses poor bioavailability due to its very low aqueous solubility."( An assessment of bioavailability of acrylate based pH-sensitive complexes of lovastatin.
Asghar, S; Ashfaq, R; Chaudhry, MA; Faran, SA; Hassan, W; Khalid, SH; Khan, IU; Mehmood, HQ, 2019
)
2.19
"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
" In addition, the in vivo bioavailability of the optimum formula was studied in comparison to a marketed product in white master rats."( Nanoparticles of Lovastatin: Design, Optimization and in vivo Evaluation.
Gaber, DA, 2020
)
0.9
"Nanoparticle prepared by ultrasonication-assisted precipitation method is a promising formula for enhancing the solubility and hence the bioavailability of Lovastatin."( Nanoparticles of Lovastatin: Design, Optimization and in vivo Evaluation.
Gaber, DA, 2020
)
1.1
" We also report that the bioavailability of lovastatin particles can be improved by coating with the biopolymer layers."( Characterization and Drug Release Control Ability of Chitosan/Lovastatin Particles Coated by Alginate.
Chinh, NT; Dung, HT; Giang, BL; Hoang, T; Sathish, CI; Thang, DX; Vinu, A, 2020
)
1.06
" The LMH system is a promising novel oral delivery approach for enhancing bioavailability of poorly water-soluble drugs, especially those presenting P-gp effluxes limited absorption."( A liposome-micelle-hybrid (LMH) oral delivery system for poorly water-soluble drugs: Enhancing solubilisation and intestinal transport.
Barnes, TJ; Bremmell, KE; Garrastazu Pereira, G; Hassan, MM; Mason, AF; Prestidge, CA; Romana, B; Sonvico, F; Thordarson, P, 2020
)
0.56
"Lovastatin (Lov) is a lipid-lowering agent, with 5% bioavailability (BA) due to extensive first pass metabolism and poor solubility."( Design and Development of Solid SMEDDS and Liquisolid Formulations of Lovastatin, for Improved Drug Dissolution and In vivo Effects-a Pharmacokinetic and Pharmacodynamic Assessment.
Suram, D; Veerabrahma, K, 2022
)
2.4
" 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
)
0.72

Dosage Studied

A micellar electrokinetic chromatographic (MEKC) method was developed for the quantification of lovastatin and simvastatin, cholesterol lowering agents. The desired release profile was achieved by developing an oral dosage form with a pH-dependent "dual pulse" drug release.

ExcerptRelevanceReference
" The lovastatin dosage varied from 20-80 mg daily."( [Influence of lovastatin on serum lipids in patients with primary hyperlipidemia phenotype IIa and IIb. I. Efficacy of lovastatin in the treatment of hyperlipoproteinemia].
Idzior-Waluś, B, 1992
)
1.16
" Lovastatin dosage varied from 20-80 mg daily."( [Examination of cortisol and insulin levels in serum of patients with primary hyperlipoproteinemia and phenotype IIa and IIb during lovastatin treatment].
Idzior-Waluś, B, 1992
)
1.4
"Subjects were randomly assigned to receive either colestipol placebo or colestipol 5 g or 10 g each morning in fixed dosage for 18 weeks."( Successful management of primary hypercholesterolaemia with simvastatin and low-dose colestipol.
Parfitt, A; Simons, J; Simons, LA, 1992
)
0.28
" Such combination therapy offers the possibility of improved cholesterol lowering without the need for full dosage of either drug."( Successful management of primary hypercholesterolaemia with simvastatin and low-dose colestipol.
Parfitt, A; Simons, J; Simons, LA, 1992
)
0.28
" Various dosing regimens of 10, 20, and 40 mg/day were employed."( Efficacy and tolerability of medium-term treatment with simvastatin in primary hypercholesterolaemia.
Cattaneo, R; Colombo, F; Geroli, L; Marnini, P; Venco, A, 1992
)
0.28
" Lovastatin was administered at a dosage of 40-80 mg for 20 weeks and was discontinued for 5 weeks thereafter."( Reduction of plasma cholesterol by lovastatin normalizes erythrocyte membrane fluidity in patients with severe hypercholesterolaemia.
Aviram, M; Brook, JG; Cogan, U; Leibowitz, R; Levy, Y, 1992
)
1.47
"The effects of age and of gender on the plasma profiles of HMG-CoA reductase inhibitors following separate once-a-day dosage regimens (17 days) of lovastatin (80 mg/day) and simvastatin (40 mg/day) were studied in hypercholesterolemic patients."( Influence of age and gender on the plasma profiles of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitory activity following multiple doses of lovastatin and simvastatin.
Amin, RD; Cheng, H; Dobrinska, MR; Quan, H; Rogers, JD; Stein, EA; Sweany, AE; Tate, AC, 1992
)
0.68
" The mean dosage of the simvastatin at fourth month was of 25 mg/die."( [Mid-term clinical study of the effectiveness of and tolerability to simvastatin ++ in dyslipidemic patients].
Aiello, C; De Lucia, R; Dragonetti, C; Irace, L; Papa, A; Petraglia, L; Sannino, A, 1992
)
0.28
" This retrospective data analysis suggests that the combination of gemfibrozil and lovastatin may be safe in patients with normal renal function when the dosage of lovastatin is limited and when CK and ALT levels are monitored carefully."( A retrospective review of the use of lipid-lowering agents in combination, specifically, gemfibrozil and lovastatin.
McIntyre, TH; Shapiro, ML; Whitney, EJ; Wirebaugh, SR, 1992
)
0.72
" The subjects selected for the study were suffering from uremia either complied with dosage prescribed or not."( [Dyslipidemia in the uremic patient: the therapeutic role played by simvastatin].
Angelé, B; Bellinghieri, G; Savica, V, 1992
)
0.28
" Lovastatin in the above dosage brought about a 66 mg/dl (from 320 +/- 12."( Effects of long-term treatment with lovastatin on the clotting system and blood platelets.
Brauer, P; Eller, T; Keller, F; Kochsiek, K; Mayer, J; Schäfer, RM; Solleder, EM, 1992
)
1.47
"This randomized, double-blind, multicenter, diet-and-placebo-controlled study was designed to clarify the dose-response relationship of lovastatin therapy to lipid-modifying efficacy and drug-related adverse events."( Expanded clinical evaluation of lovastatin (EXCEL) study results: IV. Additional perspectives on the tolerability of lovastatin.
Bradford, RH; Chremos, AN; Downton, M; Dujovne, CA; Franklin, FA; Higgins, J; Nash, DT; Pool, JL; Schnaper, H; Shear, CL, 1991
)
0.77
" This original design allowed to define the most appropriate individual cholesterol-lowering drug dosage in FH patients."( Lecithin: cholesterol acyltransferase activity in familial hypercholesterolemia treated with simvastatin and simvastatin plus low-dose colestipol.
Desager, JP; Harvengt, C; Horsmans, Y, 1991
)
0.28
" Adequate precision was obtained to reliably verify drug dosage levels."( Rapid verification of identity and content of drug formulations using mid-infrared spectroscopy.
Brooks, MA; Compton, DA; Compton, SV; Ryan, JA, 1991
)
0.28
"The effects of long-term dosing with inhibitors of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase on the rate of cholesterol biosynthesis were examined in the lens and liver of rats and hamsters."( Effects of long-term administration of HMG-CoA reductase inhibitors on cholesterol synthesis in lens.
Kalinowski, SS; Mosley, ST; Tanaka, RD, 1991
)
0.28
"An extended-release osmotic dosage form was designed for gastrointestinal delivery of the water-soluble tromethamine salt of the beta-hydroxyacid form of simvastatin, a potent HMG-CoA reductase inhibitor and cholesterol lowering agent."( Enhancement of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor efficacy through administration of a controlled-porosity osmotic pump dosage form.
Fix, JA; McClelland, GA; Pogany, SA; Stubbs, RJ; Zentner, GM, 1991
)
0.28
" The pentanoic acid derivative of lovastatin, formed by beta-oxidation of the heptanoic acid moiety, was a major metabolite in livers of mice dosed with the hydroxy acid form of lovastatin."( Biotransformation of lovastatin. I. Structure elucidation of in vitro and in vivo metabolites in the rat and mouse.
Arison, B; Halpin, RA; Hoffman, WF; Kari, PH; Murphy, JS; Pitzenberger, SM; Ramjit, HG; Schwartz, MS; Ulm, EH; Vyas, KP,
)
0.73
" Patients were randomly assigned to receive placebo or lovastatin at a dosage of 20 mg once daily, 40 mg once daily, 20 mg twice daily, or 40 mg twice daily for 48 weeks."( Expanded Clinical Evaluation of Lovastatin (EXCEL) study results. I. Efficacy in modifying plasma lipoproteins and adverse event profile in 8245 patients with moderate hypercholesterolemia.
Bradford, RH; Chremos, AN; Downton, M; Dujovne, C; Franklin, FA; Gould, AL; Hesney, M; Higgins, J; Hurley, DP; Shear, CL, 1991
)
0.81
" Twenty-seven Japanese white rabbits were divided according to dosage of simvastatin into four groups as follows, group P (placebo, 5 rabbits), group MK 1 (simvastatin 1mg/kg, 5 rabbits), group MK 3 (simvastatin 3mg/kg, 6 rabbits) and group MK 5 (simvastatin 5mg/kg, 5 rabbits)."( [Preventive effect of simvastatin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on coronary atherosclerosis in cholesterol-fed rabbits].
Oogushi, K, 1991
)
0.28
" Treatment with lovastatin (an HMG-CoA reductase inhibitor) was then started at a dosage of 20 mg daily."( [Cholestatic jaundice during lovastatin medication].
Haacke, H; Kirchhoff, R; Spreckelsen, U, 1991
)
0.92
" At the dosage used this may have some implications in its therapeutic use in certain conditions."( Toxicity of lovastatin in rats with experimentally induced nephrotic syndrome.
Camps, J; Joven, J; Masana, L; Simó, JM; Turner, PR; Vilella, E; Villabona, C, 1990
)
0.66
" Patients were treated with progressively increasing doses of simvastatin (20, 40, and 80 mg day-1) taken in a twice-daily dosage for a period of 6 weeks on each dose."( The effects of simvastatin on plasma lipoproteins and cholesterol homeostasis in patients with heterozygous familial hypercholesterolaemia.
Hagemenas, FC; Illingworth, DR; Pappu, AS, 1990
)
0.28
" Bezafibrate was administered as a 200 mg dose 3 times daily, while simvastatin dosage ranged from 10 mg to 40 mg once daily at night."( Bezafibrate and simvastatin (MK-733) in the treatment of primary hypercholesterolaemia.
Jankelow, D; Myburgh, DP; Neutel, JM; Smith, DH, 1990
)
0.28
"A multicenter study was undertaken to compare the effects of lovastatin (given in 4 different dosage regimens) and probucol in patients with severe primary hypercholesterolemia."( A multicenter comparison of lovastatin and probucol for treatment of severe primary hypercholesterolemia. The Lovastatin Study Group IV.
, 1990
)
0.81
"The randomized, double-blind, placebo-controlled trial described in this report was undertaken to clarify the dose-response relation of lovastatin therapy to lipid-modifying efficacy (lipid/lipoprotein modification) and drug-related adverse events in a population with moderately elevated fasting plasma total cholesterol (240 to 300 mg/dl) and low-density lipoprotein cholesterol (greater than or equal to 160 mg/dl)."( Expanded clinical evaluation of lovastatin (EXCEL) study: design and patient characteristics of a double-blind, placebo-controlled study in patients with moderate hypercholesterolemia.
Bradford, RH; Chremos, AN; Dujovne, C; Franklin, FA; Hesney, M; Higgins, J; Langendörfer, A; Pool, JL; Schnaper, H; Shear, CL, 1990
)
0.77
" The initial dosage of simvastatin was 10 mg/day; dosage was titrated up to 10 mg/day or to a minimum of 5 mg/day in intervals of at least 4 weeks, in order to maintain LDL-cholesterol below 140 mg/dl."( [Simvastatin (MK-733), a new HMG-CoA reductase inhibitor, in the treatment of hypercholesterolemia in elderly patients with atherosclerosis].
de Góes, JM; Dereviack, BE; Diament, J; Forti, N; Giannini, SD; Machado, C, 1990
)
0.28
" During the treatment period lovastatin dosage was adjusted from 20 mg/day to 40 or 80 mg/day, if the TC value was greater than 200 mg/dL, with the resulting mean daily increasing doses of 28 mg (weeks 0-4), 37 mg (weeks 4-8), and 55 mg (weeks 8-12)."( [Lovastatin: short-term treatment of hypercholesterolemia; multicenter clinical trial].
Brusco, OJ, 1990
)
1.48
" Analysis of lenses from dogs chronically dosed with various HMG-CoA reductase inhibitors revealed the presence of low drug levels in the lens (less than 500 ng equivalents g-1), but no correlation was observed between the amount of drug associated with the lens after chronic treatment and cataract development."( On the etiology of subcapsular lenticular opacities produced in dogs receiving HMG-CoA reductase inhibitors.
Alberts, AW; Bokelman, DL; Chen, J; Gerson, RJ; Greenspan, MD; MacDonald, JS; Rubin, LF; Yudkovitz, JB, 1990
)
0.28
" Our phase I results were commensurate with those reported for the entire international cohort of 272 patients, indicating a clear dose-response relationship, with approximately 75% of the maximum reduction in LDL-C levels being achieved with 20 mg/day and over 90% of the maximum being achieved with 40 mg of simvastatin per day."( Treatment of hypercholesterolemia with the HMG CoA reductase inhibitor, simvastatin.
Baker, SG; Berger, GM; Joffe, BI; Marais, AD; Mendelsohn, D; Seftel, HC; Welsh, NH, 1989
)
0.28
" In rat liver slices, the dose-response curves for inhibition of [14C]acetate incorporation into cholesterol were similar for the active acid forms of lovastatin, simvastatin, and pravastatin."( Tissue-selective acute effects of inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase on cholesterol biosynthesis in lens.
Kalinowski, SS; Mosley, ST; Schafer, BL; Tanaka, RD, 1989
)
0.48
" While maintaining intensive dietary therapy, administration of lovastatin was instituted at a dosage of 20 mg/day, which was increased by 20-mg increments monthly, as necessary, to a maximum of 80 mg/day."( Effect of lovastatin on serum lipids in patients with nonfamilial primary hypercholesterolemia.
De Gaetano, C; Flamenbaum, W; Itskovitz, HD; Pritchard, KA; Stemerman, MB,
)
0.77
" The initial dosage of simvastatin was a tablet of 10 mg/day, increased after a month to 20 mg and then to 40 mg/die."( [Effect of a long-term treatment with simvastatin, an inhibitor of HMG-CoA reductase, in dyslipidemic patients at high risk].
Abrignani, MG; Alaimo, G; Averna, MR; Barbagallo, CM; Davì, G; Marino, G; Notarbartolo, A; Novo, S; Strano, A, 1989
)
0.28
" Lovastatin, at an initial dosage of 20 mg/day, was administered for a period of 1 year."( Lovastatin therapy for hypercholesterolemia in cardiac transplant recipients.
DiSesa, VJ; Gordon, J; Kirshenbaum, JM; Kuo, PC; Laffel, G; Mudge, GH; Vaughan, DE; Young, P, 1989
)
2.63
" Many of the toxicities produced by high dosage levels of simvastatin in animals are directly related to the drug's biochemical mechanism of action and are the result of a profound, sustained inhibition of the target enzyme that is not anticipated at clinical dosages."( Animal safety and toxicology of simvastatin and related hydroxy-methylglutaryl-coenzyme A reductase inhibitors.
Alberts, AW; Bokelman, DL; Gerson, RJ; Kornbrust, DJ; MacDonald, JS; Majka, JA; Stubbs, RJ, 1989
)
0.28
" Gemfibrozil was given in a constant dosage of 600 mg twice daily in both strata."( Comparison of low-dose simvastatin and gemfibrozil in the treatment of elevated plasma cholesterol. A multicenter study. The Simvastatin Study Group.
Bocanegra, TS; Cook, T; Tikkanen, MJ; Walker, JF, 1989
)
0.28
" Simvastatin at the dosage of 10 mg appeared to be at least as efficient as 12 g of cholestyramine and generally better tolerated."( Comparison between low-dose simvastatin and cholestyramine in moderately severe hypercholesterolemia.
Deslypere, JP, 1989
)
0.28
" Drug dosage varied from 20 to 40 mg/d in a single dose on a 12 weeks treatment period."( [Effects of lovastatin in primary hypercholesterolemia].
Carré, JM; Garcia, RC; Nakandakare, ER; Oliveira, HC; Quintão, EC; Zerbinatti, CV, 1989
)
0.66
" The once daily dosage of these drugs, their effectiveness in low doses and the low incidence of side effects facilitate the patient's compliance."( [Treatment of hyperlipidemia with HMG-CoA reductase inhibitors].
Prager, R, 1989
)
0.28
" In the range of dosage from 10 to 40 mg once daily, therapy is associated with reductions of up to 30 percent in total cholesterol and 40 percent in low-density lipoprotein cholesterol levels, as well as with increases of approximately 10 percent in high-density lipoprotein cholesterol levels."( Simvastatin: the clinical profile.
Walker, JF, 1989
)
0.28
" With higher dosages, twice-daily dosing is preferred, particularly when the dosage reaches the maximum recommended 80 mg/d."( Lovastatin for hypercholesterolemia.
Uvodich, KC; Zeller, FP,
)
1.57
"Administration of lovastatin to animals at high dosage levels produces a broad spectrum of toxicity."( Preclinical evaluation of lovastatin.
Alberts, AW; Berry, PH; Bokelman, DL; Gerson, RJ; Kloss, MW; Kornbrust, DJ; MacDonald, JS; Prahalada, S, 1988
)
0.91
"The chemistry, pharmacology, pharmacokinetics, clinical efficacy, dosage and administration, and adverse effects of lovastatin are reviewed."( Lovastatin: a new cholesterol-lowering agent.
McKenney, JM, 1988
)
1.93
" Optimal dosing appears to be 20 mg given twice a day."( Lovastatin: a new cholesterol-lowering agent.
Krukemyer, JJ; Talbert, RL, 1987
)
1.72
" Clinical evidence of neurotoxicity occurred in up to 37% of animals given 180 mg/kg/day lovastatin for 11 or more days, especially in one laboratory where the dosing regime resulted in higher concentrations of plasma drug levels."( Brain and optic system pathology in hypocholesterolemic dogs treated with a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase.
Alberts, AW; Allen, H; Berry, PH; Chen, JS; Durand-Cavagna, G; Greenspan, MD; Jensen, R; Lo, CY; MacDonald, JS; Molon-Noblot, S, 1988
)
0.5
" The present study compares the hypocholesterolemic effects of mevinolin given in a twice-daily dosage regimen with the same total dosage given either once in the morning or once in the evening in 12 patients with heterozygous familial hypercholesterolemia."( Comparative efficacy of once versus twice daily mevinolin in the therapy of familial hypercholesterolemia.
Illingworth, DR, 1986
)
0.27
" The dose-response relationship between the abilities of HDLs to support proliferation and to induce HMG CoA reductase activity are similar."( Stimulation of the proliferation of the Madin-Darby canine kidney (MDCK) epithelial cell line by high-density lipoproteins and their induction of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity.
Cohen, DC; Gospodarowicz, D; Massoglia, SL, 1983
)
0.27
" With a single drug regimen, compactin at a dosage of 15 mg/day produced a cholesterol reduction of 23% (70 mg/dl) in cases of combined hyperlipidemia, while twice the dosage (30 mg/day) was needed to produce a comparable effect with heterozygous familial hypercholesterolemia."( Combined drug therapy--cholestyramine and compactin--for familial hypercholesterolemia.
Matsuzawa, Y; Sudo, H; Yamamoto, A; Yamamura, T; Yokoyama, S, 1984
)
0.27
" The effects of cholestyramine rapidly disappeared when it was withdrawn from the diet, while the effects of gemfibrozil persisted after dosage was stopped."( Some comparative effects of gemfibrozil, clofibrate, bezafibrate, cholestyramine and compactin on sterol metabolism in rats.
Maxwell, RE; Nawrocki, JW; Uhlendorf, PD, 1983
)
0.27
" This difference is consistent throughout the dosage range."( Pharmaco-economic assessment of the HMG-CoA reductase inhibitors.
Smart, AJ; Walters, L, 1994
)
0.29
"8% higher than an equivalent milligram dose of pravastatin, depending on the dosage used."( Pharmaco-economic assessment of the HMG-CoA reductase inhibitors.
Smart, AJ; Walters, L, 1994
)
0.29
" Severe renal insufficiency may necessitate dosage modification in lovastatin recipients."( Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors.
Garnett, WR, 1995
)
0.53
" This is possible, but such a strategy is preferable only in a subgroup of patients who cannot bear the economic burden of increasing the dosage of statins."( Escape phenomenon of low-density lipoprotein cholesterol during lovastatin treatment.
Rubinstein, A; Weintraub, M, 1995
)
0.53
" Female albino rats were dosed orally with 357 micrograms Mn/kg body weight for 15 or 30 days."( Reversibility of manganese-induced learning defect in rats.
Oner, G; Sentürk, UK, 1995
)
0.29
" Dose-response curves for serotonin-induced vasodilatation, an index of nitric oxide-dependent vasodilatation, showed a comparable and significant rightward shift after a medication-free period of 2 and 6 weeks compared with control subjects, indicating endothelial dysfunction, which was already maximum after 2 weeks."( Vascular function in the forearm of hypercholesterolaemic patients off and on lipid-lowering medication.
de Bruin, TW; Koomans, HA; Rabelink, TJ; Stroes, ES, 1995
)
0.29
" The drug acquisition cost per year of therapy was calculated for each patient's most recent dosage of lovastatin and pravastatin as of April 1993."( Replacing lovastatin with pravastatin: effect on serum lipids and costs.
Borysiuk, L; Korman, L, 1995
)
0.91
" The drugs were administered in dosages of 10 mg/kg from the fourth to seventh weeks; at the end of the seventh week, plasma cholesterol was determined, and the Pravastatin dosage adjusted to 15 mg/kg to obtain similar levels of plasma cholesterol for the two experimental groups."( Effects of simvastatin and pravastatin on endothelium-dependent relaxation in hypercholesterolemic rabbits.
Jorge, PA; Metze, K; Ozaki, MR, 1994
)
0.29
" Micronized fenofibrate, a new formulation chemically identical to the parent compound, has improved pharmacokinetic parameters which increase absorption, provide more stable plasma levels, and thus dosage can be decreased."( The fibrates in clinical practice: focus on micronised fenofibrate.
Shepherd, J, 1994
)
0.29
" Fourteen subjects were given simvastatin, and 12 were given pravastatin, both at the maximum therapeutic dosage of 40 mg/day."( Sustained therapy with 3-hydroxy-3-methylglutaryl-coenzyme-A reductase inhibitors does not impair steroidogenesis by adrenals and gonads.
Faccini, G; Moghetti, P; Muggeo, M; Negri, C; Tosi, F; Travia, D, 1995
)
0.29
" Preliminary in vivo experiments showed an inhibition of hepatic cholesterol biosynthesis after oral dosage only with prodrugs such as S 3554, whereas the hybrid molecules were inactive after oral application."( Bile acid derived HMG-CoA reductase inhibitors.
Bock, K; Enhsen, A; Falk, E; Gantz, D; Hoffmann, A; Kramer, W; Neckermann, G; Nickau, L; Schulz, S; Wess, G, 1994
)
0.29
" To date, however, no studies have directly compared the lipoprotein-modifying effects and safety of lovastatin and niacin across their usual dosage range in patients with primary hypercholesterolemia."( Comparative effects of lovastatin and niacin in primary hypercholesterolemia. A prospective trial.
Dujovne, CA; Frost, PH; Greguski, RA; Illingworth, DR; Knopp, RH; Mitchel, YB; Stein, EA; Tun, P; Zupkis, RV, 1994
)
0.81
"In the two patient groups, 66% of patients treated with lovastatin and 54% of patients treated with niacin underwent full dosage titration."( Comparative effects of lovastatin and niacin in primary hypercholesterolemia. A prospective trial.
Dujovne, CA; Frost, PH; Greguski, RA; Illingworth, DR; Knopp, RH; Mitchel, YB; Stein, EA; Tun, P; Zupkis, RV, 1994
)
0.85
" The dosage of lovastatin was 20 mg/day for the first month of therapy and could subsequently be adjusted to response, up to a maximum of 80 mg/day."( Efficacy and tolerability of lovastatin in hypercholesterolemia in patients with systemic hypertension.
D'Agostino, LC; D'Agostino, RB; Kannel, WB; Stepanians, MN, 1993
)
0.93
"Full dose-response curves were constructed in 13 hypercholesterolemic and 12 normocholesterolemic subjects by infusing bradykinin (0."( Responsiveness to bradykinin in veins of hypercholesterolemic humans.
Bedarida, GV; Blaschke, TF; Bushell, E; Haefeli, WE; Hoffman, BB, 1993
)
0.29
" Two compliance parameters were evaluated, consumption, defined as percentage of prescribed doses taken, and time compliance, the percentage of total dosing events recorded within defined intervals (6."( Actual versus prescribed timing of lovastatin doses assessed by electronic compliance monitoring.
Kruse, W; Nikolaus, T; Rampmaier, J; Schlierf, G; Weber, E, 1993
)
0.56
" During the study, 28 patients (SG0) received S 10mg; in 14 patients (SG1) dosage was titrated to 20mg and in 18 cases (SG2) to 40mg."( [Reductions in lipid fraction plasma levels induced by simvastatin and bezafibrate. Brazilian multicenter study].
Forti, N, 1993
)
0.29
" Simvastatin should be administered in a reduced dosage to CS patients."( Plasma concentration profiles of simvastatin 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitory activity in kidney transplant recipients with and without ciclosporin.
Arnadottir, M; Eriksson, LO; Karkas, JD; Thysell, H, 1993
)
0.29
"Seven sustained/controlled-release dosage forms were designed for gastrointestinal delivery of lovastatin or simvastatin, two potent HMG-CoA reductase inhibitors for the treatment of hypercholesterolemia."( Evaluation of sustained/controlled-release dosage forms of 3-hydroxy-3-methylglutaryl-coenzyme a (HMG-CoA) reductase inhibitors in dogs and humans.
Amin, RD; Cheng, H; Grasing, K; Mitchel, YB; Pipkin, JD; Rogers, JD; Schwartz, JI; Schwartz, MS; Sutton, SC; Zentner, GM, 1993
)
0.5
"Using various concentrations of the drugs, a dose-response curve was constructed for the inhibition of the cholesterol synthesis."( Pravastatin and simvastatin differently inhibit cholesterol biosynthesis in human lens.
Bloemendal, H; Cohen, LH; de Vries, AC; Vermeer, MA, 1993
)
0.29
"A randomized, controlled, double-blind trial in 672 hypercholesterolemic patients evaluated the efficacy and safety profile of lovastatin and pravastatin across their usually recommended dosage ranges (lovastatin 20 to 80 mg/day and pravastatin 10 to 40 mg/day)."( A multicenter comparative trial of lovastatin and pravastatin in the treatment of hypercholesterolemia. The Lovastatin Pravastatin Study Group.
, 1993
)
0.77
" Using various concentrations of the drugs, a dose-response curve was composed for the inhibition of the cholesterol synthesis."( Different effects of the hypolipidemic drugs pravastatin and lovastatin on the cholesterol biosynthesis of the human ocular lens in organ culture and on the cholesterol content of the rat lens in vivo.
Cohen, LH; de Vries, AC, 1993
)
0.53
"The efficacy and safety profile of simvastatin and pravastatin across their most commonly recommended dosage ranges were compared in a double-blind, parallel, multicenter study in 550 patients with primary hypercholesterolemia."( Comparison of the efficacy, safety and tolerability of simvastatin and pravastatin for hypercholesterolemia. The Simvastatin Pravastatin Study Group.
, 1993
)
0.29
" Lovastatin 20 mg/day was added to the bezafibrate 600 mg/day regimen for 6 weeks; the lovastatin dosage was then doubled to 40 mg/day for an additional 6 weeks."( Treatment of severe, resistant familial combined hyperlipidemia with a bezafibrate-lovastatin combination.
Abukarshin, R; Elias, N; Lanir, A; Naschitz, JE; Yeshurun, D,
)
1.27
" In posttransplant patients receiving cyclosporine, safety has been documented for low doses of lovastatin and simvastatin, but when a higher dosage of an HMG-CoA reductase inhibitor is warranted, pravastatin should be considered the drug of choice because of a lower incidence of myopathy."( Comparative evaluation of the safety and efficacy of HMG-CoA reductase inhibitor monotherapy in the treatment of primary hypercholesterolemia.
Hsu, I; Johnson, NE; Spinler, SA,
)
0.35
" Reductions in serum levels of total cholesterol and LDL-cholesterol were similar between agents only when lovastatin or pravastatin were administered at a total daily dosage twice that of simvastatin and when fluvastatin was administered at a total daily dosage approximately 8 times that of simvastatin."( Simvastatin. A reappraisal of its pharmacology and therapeutic efficacy in hypercholesterolaemia.
McTavish, D; Plosker, GL, 1995
)
0.5
" Therefore, our objectives were to determine the efficacy, safety, and tolerance of the short-term use of lovastatin, a 3-hydroxy 3-methylglutaryl coenzyme A reductase inhibitor, in the control of severe FH in a male pediatric population and to evaluate the dose-response relationship."( Treatment of familial hypercholesterolemia in children and adolescents: effect of lovastatin. Canadian Lovastatin in Children Study Group.
Blaichman, S; Clarke, JT; Clarson, C; Gagné, C; Hayden, M; Lambert, J; Lambert, M; Langlois, S; Lévy, E; Lupien, PJ; Parsons, H; Potvin, D; Rose, V; Stephure, DK; Wolfe, BM, 1996
)
0.73
" A dose-response relationship was seen, and between-group comparisons showed that results were significantly improved up to a dose of 30 mg/d."( Treatment of familial hypercholesterolemia in children and adolescents: effect of lovastatin. Canadian Lovastatin in Children Study Group.
Blaichman, S; Clarke, JT; Clarson, C; Gagné, C; Hayden, M; Lambert, J; Lambert, M; Langlois, S; Lévy, E; Lupien, PJ; Parsons, H; Potvin, D; Rose, V; Stephure, DK; Wolfe, BM, 1996
)
0.52
" Only 2 of the 90 patients were on maximal dosage regimens."( Inadequate treatment with HMG-CoA reductase inhibitors by health care providers.
Feingold, KR; Marcelino, JJ, 1996
)
0.29
" It is likely that the magnitude of risk reduction produced by lipid-lowering therapy is proportional to the degree of cholesterol lowering achieved, which is an important consideration when selecting an agent and deciding the dosage to use."( Benefits and risks of HMG-CoA reductase inhibitors in the prevention of coronary heart disease: a reappraisal.
Pedersen, TR; Tobert, JA, 1996
)
0.29
" In a second 4-week period, patients on lovastatin continued on the initial dosage while patients receiving fluvastatin had their daily dosage increased to 40 mg at bedtime to evaluate the range of efficacy from 20-40 mg/day."( Meeting national cholesterol education goals in clinical practice--a comparison of lovastatin and fluvastatin in primary prevention.
Nash, DT, 1996
)
0.79
" A metaanalysis of ten trials has shown a 25% decrease in vascular events in the long-term, irrespective of age, gender, blood pressure blood glucose level, and dosage whether low (75 to 160 mg) or moderate (160 to 325 mg/day)."( [Secondary prevention after myocardial infarction; rôle of platelet antiaggregants and hypolipemic agents].
Aumont, MC; Seknadji, P, 1996
)
0.29
" To evaluate the effectiveness of extending the dosage range, 156 subjects with LDL cholesterol >160 mg/dl and triglycerides (TG) <350 mg/dl were randomized to simvastatin at doses of 40, 80, and 160 mg/day in a 26 week, double-blind, 3-period, complete block crossover study."( The efficacy and six-week tolerability of simvastatin 80 and 160 mg/day.
Amin, RD; Davidson, MH; Dobrinska, MR; Dujovne, CA; Hunninghake, DB; Illingworth, DR; Knopp, RH; Melino, MR; Mitchel, YB; Stein, EA; Tobert, JA; Weiss, SR; Zupkis, RV, 1997
)
0.3
" Participants in the 4S were randomly assigned to double-blind treatment with simvastatin, 20 mg daily, with blinded dosage titration up to 40 mg daily, according to cholesterol response during the first 6-18 weeks, or placebo."( Cholesterol lowering with simvastatin improves prognosis of diabetic patients with coronary heart disease. A subgroup analysis of the Scandinavian Simvastatin Survival Study (4S)
Faergeman, O; Kjekshus, J; Olsson, AG; Pedersen, TR; Pyŏrälä, K; Thorgeirsson, G, 1997
)
0.3
"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
)
0.3
" The dosage consisted of 10 mg simvastatin daily during the 3-month trial."( Short-term safety and efficacy of low-dose simvastatin in elderly patients with hypertensive hypercholesterolemia and fasting hyperinsulinemia.
Chan, P; Huang, TY; Lee, C; Lee, YS; Tomlinson, B, 1997
)
0.3
" Plasma concentration of lovastatin was significantly higher in transplant recipients compared with controls, but there was no accumulation during incremental dosing of lovastatin."( Post-transplant hyperlipidaemia: low-dose lovastatin lowers atherogenic lipids without plasma accumulation of lovastatin.
Berg, KJ; Cheng, H; Forfang, K; Geiran, O; Gullestad, L; Høstmark, A; Ihlen, H; Nordal, KP; Schwartz, MS; Simonsen, S, 1997
)
0.86
"Itraconazole, even at a small dosage of 100 mg daily, greatly elevated plasma concentrations of lovastatin and its active metabolite, lovastatin acid."( Different effects of itraconazole on the pharmacokinetics of fluvastatin and lovastatin.
Kantola, T; Kivistö, KT; Neuvonen, PJ, 1998
)
0.75
" Cerivastatin has an uncomplicated pharmacokinetic profile; it can be administered to both young and elderly patients, male and female, without the need for dosage adjustments."( Preclinical and clinical pharmacology of cerivastatin.
Bischoff, H; Heller, AH, 1998
)
0.3
"Phase IIa clinical studies with cerivastatin--including 2 pilot US and European dose-ranging studies, and 1 US dose-scheduling study--were conducted to establish a dosage regimen and effective therapeutic doses of cerivastatin in the treatment of hypercholesterolemia."( Clinical efficacy of cerivastatin: phase IIa dose-ranging and dose-scheduling studies.
Hunninghake, DB, 1998
)
0.3
" at a level corresponding to the human dosage of 1-2 mg/kg/day."( Reduction of mouse mammary tumor formation and metastasis by lovastatin, an inhibitor of the mevalonate pathway of cholesterol synthesis.
Alonso, DF; De Lorenzo, MS; Farina, HG; Gabri, MR; Gomez, DE; Skilton, G, 1998
)
0.54
" To improve on the transient inhibitory activity of this dosing regimen on the mevalonate pathway, alternative schedules based on uninterrupted administration of lovastatin should also be studied."( Phase I study of lovastatin, an inhibitor of the mevalonate pathway, in patients with cancer.
Cooper, MR; Figg, WD; Hohl, RJ; Liang, B; Myers, CE; Patronas, N; Reed, E; Samid, D; Thibault, A; Tompkins, AC; Trepel, J; Venzon, DJ, 1996
)
0.83
" In the first period (24 weeks), lovastatin was increased at 8 and 16 weeks and the dosage remained stable during the second period (24 weeks)."( Efficacy and safety of lovastatin in adolescent males with heterozygous familial hypercholesterolemia: a randomized controlled trial.
Ames, S; Arensman, F; Brewster, TG; Davidson, M; DuJovne, C; Gormley, GJ; Graham, K; Hopkins, P; Illingworth, DR; Isaacsohn, JL; Jacobsen, CA; Jacobson, MS; Knopp, RH; Kwiterovich, PO; Laskarzewski, PM; Liacouras, CA; Siimes, MA; Stein, EA; Williams, CL, 1999
)
0.9
" The incidence of side effects with these agents increases as the dose increases within the recommended dosage range."( Comparative efficacy and tolerability of low-dose pravastatin versus lovastatin in patients with hypercholesterolemia.
Gaziano, JM; Lapsley, D; Strauss, WE, 1999
)
0.54
" In this model, there is a dose-response for cholesterol lowering with an approximate ED50 value of 40 mg/kg/day and an inverse relationship between serum cholesterol and serum LY295427 levels."( Effects of LY295427, a low-density lipoprotein (LDL) receptor up-regulator, on LDL receptor gene transcription and cholesterol metabolism in normal and hypercholesterolemic hamsters.
Archer, RA; Bean, JS; Beavers, LS; Bensch, WR; Breau, AP; Eacho, PI; Gadski, RA; Kauffman, RF; McClure, DB; Murphy, AT; Perry, DN; Schmidt, RJ, 1999
)
0.3
" We conclude that: (1) lovastatin is effective in lowering total and LDL-cholesterol in practice, but is often used in dosage insufficient to lower LDL-cholesterol to goal levels; (2) patients are not being adequately educated on dosing schedules; (3) toxicity may be underestimated by infrequent and inconsistent surveillance; and (4) nonpharmacologic therapy is underutilized."( Postmarketing analysis of lovastatin use in the VA Northern California System of Clinics: a retrospective, computer-based study.
Cogburn, D; Fann, KY; Khuu, DT; Lin, K; Noth, RH; Swislocki, AL, 1997
)
0.91
" Maximum steady-state plasma drug concentration (Cssmax) and AUC during a dosage interval (AUC tau) for cilostazol 100 mg twice daily decreased 14 and 15%, respectively, upon lovastatin coadministration."( Effect of multiple cilostazol doses on single dose lovastatin pharmacokinetics in healthy volunteers.
Bramer, SL; Brisson, J; Corey, AE; Mallikaarjun, S, 1999
)
0.75
" No dosage adjustments are necessary for cilostazol when coadministered with lovastatin, whereas lovastatin dose reductions may be needed when the 2 drugs are given together."( Effect of multiple cilostazol doses on single dose lovastatin pharmacokinetics in healthy volunteers.
Bramer, SL; Brisson, J; Corey, AE; Mallikaarjun, S, 1999
)
0.78
" The dosage of lovastatin used was 20-40 mg/day, titrated to achieve an LDL-cholesterol target of < or =110 mg/dL."( Insights on treating an over-the-counter-type subgroup: data from the Air Force/Texas Coronary Atherosclerosis Prevention Study Population.
Gotto, AM, 2000
)
0.66
" The two arms were 1) administration of a 20 mg dosage of lovastatin orally and 2) administration of a 20 mg dosage of lovastatin orally 1 h after an intravenous loading dosage and constant infusion of diltiazem."( Intravenous diltiazem and CYP3A-mediated metabolism.
Azie, NE; Brater, DC; Hall, SD; Jones, DR; Masica, AL, 2000
)
0.55
" They should be drugs of first choice in CRD but dosage reduction and close monitoring may be required to avoid side effects in case of renal failure or in combination with calcineurin inhibitors."( [Kidney and statins].
Caillard, S; Moulin, B, 2001
)
0.31
" When used in this dosage and schedule, lovastatin does not appear to be effective for patients with advanced gastric adenocarcinoma."( Phase II study of high-dose lovastatin in patients with advanced gastric adenocarcinoma.
Choi, HJ; Kang, WK; Kim, MM; Kim, WS; Lee, MH; Park, CH; Park, K; Yoon, SS, 2001
)
0.87
"The number of statins available to physicians continues to grow, leading to the question: Are all statins alike? Comparisons of side effects and safety profiles and the dose-response relationship among the different drugs show similar results."( Statins--similarities and differences.
Gaw, A; Pedersen, T, 2001
)
0.31
"0001) when colesevelam and lovastatin were dosed together or dosed apart, respectively."( Low-dose combination therapy with colesevelam hydrochloride and lovastatin effectively decreases low-density lipoprotein cholesterol in patients with primary hypercholesterolemia.
Burke, SK; Davidson, MH; Donovan, JM; Hunninghake, D; Isaacsohn, J; McKenney, J; Toth, P; Weiss, S, 2001
)
0.85
" 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
" 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,
)
0.13
" Participants were dosed with lovastatin IR 40 mg tablets following a standard breakfast, lovastatin ER 40 mg tablets following a standard breakfast, and lovastatin ER 40 mg tablets underfasting conditions."( Comparative pharmacokinetics of lovastatin extended-release tablets and lovastatin immediate-release tablets in humans.
Friedhoff, L; Lukacsko, P; Niecestro, R; Phillips, G; Shen, J; Sun, JX, 2002
)
0.89
"Roxithromycin does not influence the pharmacokinetics of lovastatin in such a way that dosage adjustment of lovastatin seems to be necessary during co-administration."( Effect of roxithromycin on the pharmacokinetics of lovastatin in volunteers.
Bucher, M; Kees, F; Mair, G, 2002
)
0.81
" Once-daily dosing provides ease of administration that should improve compliance and result in a greater proportion of patients meeting their low-density lipoprotein cholesterol goals."( Lovastatin and extended-release niacin combination product: the first drug combination for the management of hyperlipidemia.
Gupta, EK; Ito, MK,
)
1.57
" To evaluate this effect further, dose-response curves with noradrenaline were measured in the presence and absence of 20 micromol/l simvastatin, lovastatin, mevastatin and pravastatin."( Inhibition of smooth muscle cell calcium mobilization and aortic ring contraction by lactone vastatins.
Altieri, PI; Crespo, MJ; Escobales, N; Furilla, RA, 1996
)
0.49
"The purpose of this study was to evaluate pharmacokinetics and dose proportionality of lovastatin extended-release dosage form (ER-lovastatin) in the dosage levels of 10, 20 and 40 mg in 9 healthy male subjects."( Pharmacokinetics of lovastatin extended-release dosage form (Lovastatin XL) in healthy volunteers.
Friedhoff, L; Lamson, M; Lukacsko, P; Niecestro, RM; Phillips, G; Shen, J, 2002
)
0.86
"A micellar electrokinetic chromatographic (MEKC) method was developed for the quantification of lovastatin and simvastatin, cholesterol lowering agents in pharmaceutical dosage forms."( Determination of lovastatin and simvastatin in pharmaceutical dosage forms by MEKC.
Raju, AN; Reddy, GO; Srinivasu, MK, 2002
)
0.87
" Treatment of transformants with various concentrations of rifampicin produced a dose-response curve with maximal induction at 10 microM (5."( A cell-based reporter gene assay for determining induction of CYP3A4 in a high-volume system.
Allen, SW; Raucy, J; Warfe, L; Yueh, MF, 2002
)
0.31
" Southern analysis showed that pML48 had been incorporated by a homologous recombination event, and all high producers possessed two copies of each of the seven genes, mlcA- mlcF and mlcR, suggesting that increased dosage of the biosynthetic gene cluster was responsible for the enhanced production of ML-236B."( Effect of increased dosage of the ML-236B (compactin) biosynthetic gene cluster on ML-236B production in Penicillium citrinum.
Abe, Y; Hosobuchi, M; Iwamoto, K; Mizuno, T; Ono, C; Suzuki, T; Yoshikawa, H, 2002
)
0.31
"The ER formulation of lovastatin provides smooth and sustained delivery of this established and well-tolerated agent over the dosage interval, significantly reducing LDL-cholesterol in patients with primary hypercholesterolaemia."( Lovastatin extended release: a review of its use in the management of hypercholesterolaemia.
Curran, MP; Goa, KL, 2003
)
2.08
"This study evaluated dose-response relationships and safety of a new dual-component drug product containing niacin extended-release (niacin ER) and lovastatin."( A dose-ranging study of a new, once-daily, dual-component drug product containing niacin extended-release and lovastatin.
Brazg, R; Hunninghake, DB; Koren, M; McGovern, ME; Murdock, D; Pearson, T; Weiss, S, 2003
)
0.73
"Niacin ER/lovastatin was more effective than each of its components for improving levels of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG), and exhibited a clear dose-response effect and additivity across the dosage range."( A dose-ranging study of a new, once-daily, dual-component drug product containing niacin extended-release and lovastatin.
Brazg, R; Hunninghake, DB; Koren, M; McGovern, ME; Murdock, D; Pearson, T; Weiss, S, 2003
)
0.93
" Graphs of the dose-response relationships as 3-dimensional surfaces documented the strength and consistency of these responses."( Efficacy of extended-release niacin with lovastatin for hypercholesterolemia: assessing all reasonable doses with innovative surface graph analysis.
Corbelli, J; Crouse, JR; Insull, W; McGovern, ME; Schrott, H; Thompson, P; Zieve, F, 2004
)
0.59
" Dose-response surfaces provide a practical guide for dose selection."( Efficacy of extended-release niacin with lovastatin for hypercholesterolemia: assessing all reasonable doses with innovative surface graph analysis.
Corbelli, J; Crouse, JR; Insull, W; McGovern, ME; Schrott, H; Thompson, P; Zieve, F, 2004
)
0.59
" This open-labeled, multicenter study evaluated the safety of bedtime niacin extended-release/lovastatin when dosed as initial therapy and patient compliance to treatment in various clinical practice settings."( Safety and compliance with once-daily niacin extended-release/lovastatin as initial therapy in the Impact of Medical Subspecialty on Patient Compliance to Treatment (IMPACT) study.
Rubenfire, M, 2004
)
0.78
" Using the same dosages, the second study avoided gestational maternal weight losses and morbidity by starting treatment 14 days before mating with dosing continued to GD 20."( The role of maternal toxicity in lovastatin-induced developmental toxicity.
Cukierski, MA; Lankas, GR; Wise, LD, 2004
)
0.6
" This electrode system was applied to the determination of lovastatin in dosage drug forms and the results were in accordance with the ultraviolet-visible spectroscopy method."( Development of an acetylene black-dihexadecyl hydrogen phosphate composite-modified glassy-carbon electrode, and its application in the determination of lovastatin in dosage drug forms.
Hu, C; Hu, S; Lan, W; Zhang, H, 2004
)
0.77
"01-5 mg kg(-1) day(-1)) and dosage schedules were examined, and collectively the data strongly suggest a powerful anabolic effect but with an unusually flat dose-response curve."( Transdermal application of lovastatin to rats causes profound increases in bone formation and plasma concentrations.
Garrett, IR; Gutierrez, GE; Lalka, D; Mundy, GR; Rossini, G, 2006
)
0.63
" In a second clinical setting, changes in lipid profiles and statin dosage over 30 weeks in patients with type 2 diabetes were retrospectively compared (n = 180 exenatide 10 microg twice daily (BID), n = 168 placebo BID) in a combined analysis of three placebo-controlled, randomized exenatide Phase 3 trials."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.34
" In the exenatide Phase 3 trials, 30-week changes from baseline for low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol, triglycerides and statin dosage were not significantly different between the exenatide and placebo groups treated with statins."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.34
"Despite observed changes in lovastatin bioavailability in the pharmacokinetic drug interaction study, exenatide did not negatively affect long-term lipid profiles or statin dosage in patients with concurrent statin therapy."( Exenatide effects on statin pharmacokinetics and lipid response.
Fineman, M; Han, J; Kothare, PA; Linnebjerg, H; Mace, K; Mitchell, M; Pena, A; Reddy, S; Skrivanek, Z, 2007
)
0.63
" 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 objective of this study was to assess how the dosing method (i."( Comparing pharmacokinetic and pharmacodynamic profiles in female rats orally exposed to lovastatin by gavage versus diet.
Chen, Y; Kapetanovic, IM; Lindeblad, M; Lyubimov, A; Martín-Jiménez, T, 2008
)
0.57
"A liquid chromatographic-mass spectrometricmethod for the determination of lovastatin hydroxy acid in female B6C3F(1) mouse serum was developed for use in supporting toxicokinetic studies of animals dosed with the cholesterol lowering agent lovastatin."( Determination of lovastatin hydroxy acid in female B6C3F1 mouse serum.
Brown, SS; Collins, BJ; Fernando, RA; Fletcher, BL; Lodge, JW; Parham, AJ, 2008
)
0.92
" In conclusion, such kind of combined dosage forms can effectively be formulated to deliver more than one drug so as to have improved patient compliance and better disease management."( Design of floating bilayer tablets of diltiazem hydrochloride and lovastatin.
Bhatia, MS; Kulkarni, AS,
)
0.37
" As it had been 10 months since her last dosage adjustment of diltiazem, it was unlikely that the statin-induced rhabdomyolysis was precipitated by diltiazem."( Rhabdomyolysis caused by a potential sitagliptin-lovastatin interaction.
DiGregorio, RV; Pasikhova, Y, 2009
)
0.61
" In this model, we found that lovastatin inhibits tumor growth at a high dosage (5 or 10 mg/kg/day), suggesting it could be used as an effectively adjuvant chemotherapy for cancer."( In vivo evidence of duality effects for lovastatin in a nude mouse cancer model.
Chang, TC; Shui, HA; Wang, CY, 2010
)
0.92
" In control experiments, the clearance rates were not different between the two strains, either for intraperitoneally dosed LVS, which bypasses SI metabolism, or for orally administered pravastatin, which is known to be poorly metabolized by P450."( Role of intestinal cytochrome P450 (P450) in modulating the bioavailability of oral lovastatin: insights from studies on the intestinal epithelium-specific P450 reductase knockout mouse.
D'Agostino, J; Zhang, QY; Zhu, Y, 2011
)
0.59
"Data were pooled from eight NER studies (administered as NER with a maximum dosage of 1000, 1500, and 2000 mg/day, either as monotherapy or in combination with simvastatin 20 or 40 mg/day [NER/S], or lovastatin 20 or 40 mg/day [NER/L]) to evaluate rates of study discontinuation due to flushing or any treatment-related adverse events."( Niacin extended-release therapy in phase III clinical trials is associated with relatively low rates of drug discontinuation due to flushing and treatment-related adverse events: a pooled analysis.
Brinton, EA; Jiang, P; Kashyap, ML; Padley, RJ; Thakkar, RB; Vo, AN, 2011
)
0.56
" We proposed a systematic classification scheme using FDA-approved drug labeling to assess the DILI potential of drugs, which yielded a benchmark dataset with 287 drugs representing a wide range of therapeutic categories and daily dosage amounts."( FDA-approved drug labeling for the study of drug-induced liver injury.
Chen, M; Fang, H; Liu, Z; Shi, Q; Tong, W; Vijay, V, 2011
)
0.37
" This study shows a simple and fast method validation by reversed-phase high-performance liquid chromatography in the linear range 28 to 52 µg/mL to quantify lovastatin, pravastatin sodium or simvastatin in bulk drug or dosage forms."( Development and validation of a simple and fast HPLC method for determination of lovastatin, pravastatin and simvastatin.
de Oliveira, RB; Oliveira, MA; Silva, TD; Vianna-Soares, CD, 2012
)
0.8
" RMD alone or in combination with lovastatin, does not increase the risk of rhabdomyolysis, even when administered at a high dosage (including HMG-CoA reductase inhibitors >75 mg/day/adult)."( Red mold dioscorea: a potentially safe traditional function food for the treatment of hyperlipidemia.
Chen, CL; Pan, TM, 2012
)
0.66
" An accurate, simple and rapid micellar electrokinetic capillary chromatographic method was developed for the first time for simultaneous determination of lovastatin present in lactone and hydroxy acid forms and citrinin in red rice products provided by different manufacturers and formulated in various dosage forms."( Simultaneous determination of lovastatin and citrinin in red yeast rice supplements by micellar electrokinetic capillary chromatography.
Mornar, A; Nigović, B; Sertić, M, 2013
)
0.88
" Moreover, inappropriate statin dosing restrictions (underdosing of simvastatin and lovastatin) were deliberately utilized in PLATO, potentially contributing to the beneficial effect of ticagrelor."( Exploring the ticagrelor-statin interplay in the PLATO trial.
Dinicolantonio, JJ; Serebruany, VL, 2013
)
0.61
" However, a higher dosage of risperidone was used for treating the disorder in those taking concomitant lovastatin compared to placebo."( Lovastatin for the adjunctive treatment of schizophrenia: a preliminary randomized double-blind placebo-controlled trial.
Akhondzadeh, S; Berk, M; Dehbozorgi, S; Ghanizadeh, A; Rezaee, Z, 2014
)
2.06
"Nutraceuticals (NUT) are forms of compounds with biological activity commonly used to improve health in dosage largely exceeding those obtainable in food."( Effects of a new combination of nutraceuticals with Morus alba on lipid profile, insulin sensitivity and endotelial function in dyslipidemic subjects. A cross-over, randomized, double-blind trial.
Esposito, G; Izzo, R; Manzi, MV; Rozza, F; Santoro, M; Schiattarella, GG; Serino, F; Stabile, E; Trimarco, B; Trimarco, V, 2015
)
0.42
" The subjects were divided into two groups: Group A, treated with an association of 1 g myo-inositol, 5 mg monacolin K and 400 mg lipoic acid for 6 months; Group B, treated with a double dosage of 2 g myo-inositol, 10 mg monacolin K, 800 mg lipoic acid for 6 months."( Polycystic ovary syndrome (PCOS) and hyperandrogenism: the role of a new natural association.
Cappelli, V; De Leo, V; Di Sabatino, A; Massaro, MG; Morgante, G, 2015
)
0.42
"The results have shown good efficacy of both dosages, although women treated with a double dosage of myo-inositol, monacolin K and lipoic acid showed a significantly greater improvement in terms of lipid parameters and those connected with hyperandrogenism."( Polycystic ovary syndrome (PCOS) and hyperandrogenism: the role of a new natural association.
Cappelli, V; De Leo, V; Di Sabatino, A; Massaro, MG; Morgante, G, 2015
)
0.42
" On average, the daily RYR dosage contains less statin than the standard dosage for statins."( ['Red yeast rice' as a cholesterol-lowering substance?Caution is warranted].
Brouwers, JR; Maas, AH; Roeters van Lennep, JE,
)
0.13
" We considered any type and dosage of statin as eligible, as long as the control and experimental arms differed only in the timing of the administration of the same statin."( Chronotherapy versus conventional statins therapy for the treatment of hyperlipidaemia.
Añino Alba, A; Fernandez-Esteban, I; Fernandez-Tabera, JM; Gómez Álvarez, P; Izquierdo-Palomares, JM; Martin-Carrillo, P; Pinar López, Ó; Plana, MN; Saiz, LC, 2016
)
0.43
" Electronic pharmacy records were used to abstract information on the type, length, and dosage of statin exposures starting in the year prior to diagnosis."( Influence of Statins and Cholesterol on Mortality Among Patients With Pancreatic Cancer.
Chang, JI; Huang, BZ; Li, E; Wu, BU; Xiang, AH, 2017
)
0.46
" The desired release profile was achieved by developing an oral dosage form containing lovastatin and coated with 2 different enteric polymers that enabled a pH-dependent "dual pulse" drug release."( Development of a Modified-Release Formulation of Lovastatin Targeted to Intestinal Methanogens Implicated in Irritable Bowel Syndrome With Constipation.
Bristol, A; Chadwick, A; Coughlin, O; Hubert, S; Kokai-Kun, J; Wacher, V, 2018
)
0.96
" NAFLD model was established by high fat food, and rats were administrated with lovastatin, berberine, curcumin, berberine + curcumin at the dosage of 100, 100, 100, 50 + 50 mg/kg bw, respectively."( Natural products berberine and curcumin exhibited better ameliorative effects on rats with non-alcohol fatty liver disease than lovastatin.
Feng, WW; Kuang, SY; Liu, TS; Ma, ZJ; Pang, JY; Tu, C; Wang, JB; Wang, YH; Xiao, XH; Zang, QC; Zhao, YL, 2018
)
0.91
"Twenty male Saanen goats were randomly assigned to four levels of lovastatin supplementation and used to determine the optimal dosage and sustainability of naturally produced lovastatin from fermentation of palm kernel cake (PKC) with Aspergillus terreus on enteric methane (CH4) mitigation."( Effects of naturally-produced lovastatin on feed digestibility, rumen fermentation, microbiota and methane emissions in goats over a 12-week treatment period.
Candyrine, SCL; Chen, WL; Ebrahimi, M; Ganesh, S; Garba, S; Goh, YM; Jahromi, MF; Liang, JB; Mahadzir, MF; Muetzel, S; Ronimus, R; Samsudin, AA; Sazili, AQ, 2018
)
1.01
" Fused-filament fabrication (FFF) offers a platform for the personalization of drug dosage forms, but one of its chief shortcomings compared to other tablet production methods such as dry compression and wet granulation is relatively low throughput."( Mass-customization of oral tablets via the combination of 3D printing and injection molding.
Devine, DM; Doran, P; Fuenmayor, E; Gately, N; Lyons, JG; Major, I; McConville, C; O'Donnell, C, 2019
)
0.51
" Median effective dose was interpolated from the triplicated experiments and the dose-response curves were generated for each drug-virus combination."( A preclinical assessment to repurpose drugs to target type 1 diabetes-associated type B coxsackieviruses.
Honkimaa, A; Hyöty, H; Sioofy-Khojine, AB, 2020
)
0.56
" That is, naringin or vitamin C in the fruit or food may increase the blood concentration of lovastatin; perhaps taking frequency or dosage of lovastatin may be reduced."( Study on the interaction between lovastatin and three digestive enzymes and the effect of naringin and vitamin C on it by spectroscopy and docking methods.
Liu, Y; Liu, Z; Meng, X; Nan, G; Song, N; Wang, Y; Yang, G; Yang, L; Zhang, L, 2020
)
1.06
" However, dosing (methods, time, type of statin, and quantity) varies across studies, limiting the clinical applicability of these findings."( Statin Therapy in Ischemic Stroke Models: A Meta-Analysis.
Christophe, B; Connolly, ES; Karatela, M; Pucci, J; Sanchez, J, 2020
)
0.56
" Twice-weekly dosing with VSW1198 at the previously established maximally tolerated dose in combination with a statin led to hepatotoxicity, while once-weekly VSW1198-based combinations were feasible."( In vivo evaluation of combination therapy targeting the isoprenoid biosynthetic pathway.
Chhonker, Y; Haney, SL; Holstein, SA; Murry, DJ; Smith, LM; Talmon, G; Varney, ML, 2021
)
0.62
"A low dosage of MKA along with lifestyle modifications caused a significant decrease in LDL-C by 15."( Effectiveness and safety of red yeast rice predominated by monacolin K β-hydroxy acid form for hyperlipidemia treatment and management.
Benjian, C; Danping, XU; Huanlin, WU; Huiting, P; Xiaodan, H; Yishi, LI; Yongtao, C, 2022
)
0.72
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
Aspergillus metaboliteAny fungal metabolite produced during a metabolic reaction in the mould, Aspergillus.
prodrugA compound that, on administration, must undergo chemical conversion by metabolic processes before becoming the pharmacologically active drug for which it is a prodrug.
anticholesteremic drugA substance used to lower plasma cholesterol levels.
[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
delta-lactoneA lactone having a six-membered lactone ring.
fatty acid esterA carboxylic ester in which the carboxylic acid component can be any fatty acid.
polyketideNatural and synthetic compounds containing alternating carbonyl and methylene groups ('beta-polyketones'), biogenetically derived from repeated condensation of acetyl coenzyme A (via malonyl coenzyme A), and usually the compounds derived from them by further condensations, etc. Considered by many to be synonymous with the less frequently used terms acetogenins and ketides.
statin (naturally occurring)Any statin that occurs in nature. The class includes compactin (also known as mevastatin), isolated from a fermentation broth of Penicillium citrinum, and lovastatin, isolated from Aspergillus terreus.
hexahydronaphthalenesAny carbobycyclic compound that is an hexahydronaphthalene or a compound obtained from an hexahydronaphthalene by formal substitution of one or more hydrogens.
[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
Lovastatin Action Pathway2143

Protein Targets (115)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency25.11890.003245.467312,589.2998AID2517
Chain A, TYROSYL-DNA PHOSPHODIESTERASEHomo sapiens (human)Potency22.38720.004023.8416100.0000AID485290
Chain A, Beta-lactamaseEscherichia coli K-12Potency25.28550.044717.8581100.0000AID485341
Chain A, Putative fructose-1,6-bisphosphate aldolaseGiardia intestinalisPotency15.81140.140911.194039.8107AID2451
Chain A, 2-oxoglutarate OxygenaseHomo sapiens (human)Potency39.81070.177814.390939.8107AID2147
Chain A, Ferritin light chainEquus caballus (horse)Potency28.18385.623417.292931.6228AID485281
Chain A, CruzipainTrypanosoma cruziPotency25.11890.002014.677939.8107AID1476
15-lipoxygenase, partialHomo sapiens (human)Potency31.62280.012610.691788.5700AID887
pregnane X receptorRattus norvegicus (Norway rat)Potency44.66840.025127.9203501.1870AID651751
phosphopantetheinyl transferaseBacillus subtilisPotency63.09570.141337.9142100.0000AID1490
hypoxia-inducible factor 1 alpha subunitHomo sapiens (human)Potency59.89183.189029.884159.4836AID1224846; AID1224894
RAR-related orphan receptor gammaMus musculus (house mouse)Potency2.75250.006038.004119,952.5996AID1159521; AID1159523
SMAD family member 2Homo sapiens (human)Potency46.94470.173734.304761.8120AID1346859; AID1346924
USP1 protein, partialHomo sapiens (human)Potency56.23410.031637.5844354.8130AID504865
SMAD family member 3Homo sapiens (human)Potency46.94470.173734.304761.8120AID1346859; AID1346924
TDP1 proteinHomo sapiens (human)Potency18.73700.000811.382244.6684AID686978; AID686979
GLI family zinc finger 3Homo sapiens (human)Potency20.81540.000714.592883.7951AID1259369; AID1259392
Microtubule-associated protein tauHomo sapiens (human)Potency19.95260.180013.557439.8107AID1460
AR proteinHomo sapiens (human)Potency23.88800.000221.22318,912.5098AID1259243; AID1259247; AID1259381; AID743035; AID743036; AID743042; AID743053; AID743054; AID743063
thioredoxin glutathione reductaseSchistosoma mansoniPotency44.66840.100022.9075100.0000AID485364
Smad3Homo sapiens (human)Potency9.18040.00527.809829.0929AID588855
caspase 7, apoptosis-related cysteine proteaseHomo sapiens (human)Potency46.41280.013326.981070.7614AID1346978
hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)Homo sapiens (human)Potency33.14430.00137.762544.6684AID2120; AID914; AID915
PINK1Homo sapiens (human)Potency11.22022.818418.895944.6684AID624263
thyroid stimulating hormone receptorHomo sapiens (human)Potency39.81070.001318.074339.8107AID926; AID938
estrogen receptor 2 (ER beta)Homo sapiens (human)Potency21.84150.000657.913322,387.1992AID1259377; AID1259378
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency78.03950.001022.650876.6163AID1224838; AID1224839
progesterone receptorHomo sapiens (human)Potency36.18530.000417.946075.1148AID1346784; AID1346795
isocitrate dehydrogenase 1, partialHomo sapiens (human)Potency50.11876.309627.099079.4328AID602179
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency13.64230.01237.983543.2770AID1346984; AID1645841
EWS/FLI fusion proteinHomo sapiens (human)Potency15.45760.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency45.21960.000214.376460.0339AID588533; AID720691; AID720692; AID720719
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency64.78440.003041.611522,387.1992AID1159552; AID1159553; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency25.29660.000817.505159.3239AID1159527; AID1159531; AID588546
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency17.13970.001530.607315,848.9004AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
farnesoid X nuclear receptorHomo sapiens (human)Potency46.69430.375827.485161.6524AID743217; AID743220; AID743239
pregnane X nuclear receptorHomo sapiens (human)Potency24.69460.005428.02631,258.9301AID1346982; AID1346985; AID720659
estrogen nuclear receptor alphaHomo sapiens (human)Potency27.05180.000229.305416,493.5996AID1259244; AID1259248; AID1259383; AID743069; AID743075; AID743078; AID743079; AID743080; AID743091
cytochrome P450 2D6Homo sapiens (human)Potency38.90180.00108.379861.1304AID1645840
ParkinHomo sapiens (human)Potency11.22020.819914.830644.6684AID624263
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency11.30670.001024.504861.6448AID588535; AID743212
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency53.78320.001019.414170.9645AID588537; AID743140; AID743191
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency30.02900.023723.228263.5986AID743222; AID743223
caspase-3Homo sapiens (human)Potency46.41280.013326.981070.7614AID1346978
IDH1Homo sapiens (human)Potency12.83210.005210.865235.4813AID686970
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency27.82980.035520.977089.1251AID504332
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency24.63650.001723.839378.1014AID743083
activating transcription factor 6Homo sapiens (human)Potency62.49820.143427.612159.8106AID1159516
thyrotropin-releasing hormone receptorHomo sapiens (human)Potency41.37780.154917.870243.6557AID1346877; AID1346891
nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105), isoform CRA_aHomo sapiens (human)Potency63.720719.739145.978464.9432AID1159509; AID1159518
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency32.61470.057821.109761.2679AID1159526; AID1159528
nuclear receptor subfamily 1, group I, member 2Rattus norvegicus (Norway rat)Potency12.58930.10009.191631.6228AID1346983
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency64.77570.354828.065989.1251AID504847
nuclear factor erythroid 2-related factor 2 isoform 2Homo sapiens (human)Potency23.10930.00419.984825.9290AID504444
potassium voltage-gated channel subfamily H member 2 isoform dHomo sapiens (human)Potency19.95260.01789.637444.6684AID588834
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency47.23530.000323.4451159.6830AID743065; AID743066; AID743067
heat shock protein beta-1Homo sapiens (human)Potency53.29100.042027.378961.6448AID743210; AID743228
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency44.35030.000627.21521,122.0200AID651741; AID743202; AID743219
urokinase-type plasminogen activator precursorMus musculus (house mouse)Potency0.89130.15855.287912.5893AID540303
plasminogen precursorMus musculus (house mouse)Potency0.89130.15855.287912.5893AID540303
urokinase plasminogen activator surface receptor precursorMus musculus (house mouse)Potency0.89130.15855.287912.5893AID540303
nuclear receptor ROR-gamma isoform 1Mus musculus (house mouse)Potency7.07950.00798.23321,122.0200AID2551
gemininHomo sapiens (human)Potency4.63460.004611.374133.4983AID624296; AID624297
survival motor neuron protein isoform dHomo sapiens (human)Potency15.84890.125912.234435.4813AID1458
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency10.00000.031610.279239.8107AID884; AID885
lamin isoform A-delta10Homo sapiens (human)Potency8.42180.891312.067628.1838AID1487
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Voltage-dependent calcium channel gamma-2 subunitMus musculus (house mouse)Potency14.91250.001557.789015,848.9004AID1259244
Cellular tumor antigen p53Homo sapiens (human)Potency66.53450.002319.595674.0614AID651631; AID720552
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Glutamate receptor 2Rattus norvegicus (Norway rat)Potency14.91250.001551.739315,848.9004AID1259244
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Nuclear receptor ROR-gammaHomo sapiens (human)Potency4.73080.026622.448266.8242AID651802
Spike glycoproteinSevere acute respiratory syndrome-related coronavirusPotency1.52180.009610.525035.4813AID1479145; AID1479148
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Rap guanine nucleotide exchange factor 4Homo sapiens (human)Potency35.48133.981146.7448112.2020AID720708
GABA theta subunitRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency10.00001.000012.224831.6228AID885
[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)
Chain A, Antigen Cd11a (p180)Homo sapiens (human)IC50 (µMol)2.40002.40002.40002.4000AID977608
bcl-2-related protein A1Mus musculus (house mouse)IC50 (µMol)100.00000.41907.756335.1000AID432; AID621
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)133.00000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)133.00000.20005.677410.0000AID1473741
Bile salt export pumpHomo sapiens (human)IC50 (µMol)19.30000.11007.190310.0000AID1443990; AID1473738
3-hydroxy-3-methylglutaryl-coenzyme A reductaseHomo sapiens (human)IC50 (µMol)4.01090.00000.79498.9000AID1454766; AID619574; AID625271; AID737914; AID737918; AID81379; AID83165; AID83291; AID83293; AID83294
Integrin beta-2Homo sapiens (human)IC50 (µMol)3.09000.00080.59053.7800AID1647697; AID93340
Intercellular adhesion molecule 1Homo sapiens (human)IC50 (µMol)3.78000.00301.212210.0000AID93340
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)IC50 (µMol)8.75300.00041.877310.0000AID625207
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)Ki8.68000.00322.28879.3160AID625207
ATP-dependent translocase ABCB1Homo sapiens (human)IC50 (µMol)50.02000.00022.318510.0000AID679461; AID679464; AID681126; AID681127; AID681381
Neutrophil elastaseHomo sapiens (human)IC50 (µMol)0.02700.00632.073422.3780AID83484
Insulin receptor Rattus norvegicus (Norway rat)IC50 (µMol)0.02000.00010.78463.3700AID625271
Androgen receptorRattus norvegicus (Norway rat)IC50 (µMol)30.16400.00101.979414.1600AID625228
Androgen receptorRattus norvegicus (Norway rat)Ki20.11000.00031.21858.9270AID625228
Integrin alpha-LHomo sapiens (human)IC50 (µMol)3.09000.00080.60203.7800AID1647697; AID93340
Substance-K receptorHomo sapiens (human)IC50 (µMol)28.22400.00013.12109.5530AID625227
Substance-K receptorHomo sapiens (human)Ki9.40800.00011.92429.7930AID625227
Sodium-dependent noradrenaline transporter Homo sapiens (human)IC50 (µMol)8.75300.00081.541620.0000AID625207
Sodium-dependent noradrenaline transporter Homo sapiens (human)Ki8.68000.00031.465610.0000AID625207
Adenosine receptor A1Homo sapiens (human)IC50 (µMol)26.72000.00020.68187.7010AID625194
Adenosine receptor A1Homo sapiens (human)Ki15.58600.00020.931610.0000AID625194
Prostaglandin G/H synthase 2Homo sapiens (human)IC50 (µMol)0.02000.00010.995010.0000AID625271
3-hydroxy-3-methylglutaryl-coenzyme A reductase Rattus norvegicus (Norway rat)IC50 (µMol)0.05290.00090.20949.0300AID80987; AID81002; AID83463; AID83476; AID83477; AID83478; AID83483; AID83484; AID83485
Sodium-dependent dopamine transporter Homo sapiens (human)IC50 (µMol)10.10400.00071.841946.0000AID625256
Sodium-dependent dopamine transporter Homo sapiens (human)Ki8.02800.00021.11158.0280AID625256
Histone deacetylase 1Homo sapiens (human)IC50 (µMol)11.91100.00010.55439.9000AID737917
Lanosterol 14-alpha demethylaseHomo sapiens (human)IC50 (µMol)200.00000.05001.43904.0000AID322753
Histone deacetylase 2Homo sapiens (human)IC50 (µMol)25.93300.00010.72219.9700AID737916
Canalicular multispecific organic anion transporter 1Homo sapiens (human)IC50 (µMol)133.00002.41006.343310.0000AID1473739
Acyl-CoA:cholesterol acyltransferase Oryctolagus cuniculus (rabbit)IC50 (µMol)16.80000.00600.98467.6000AID298856
Histone deacetylase 6Homo sapiens (human)IC50 (µMol)16.28500.00000.53769.9000AID737915
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)IC50 (µMol)28.00000.05002.37979.7000AID681366
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Integrin alpha-LHomo sapiens (human)Kd12.90000.02000.02000.0200AID722627
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (519)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo 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)
microglial cell activationIntegrin beta-2Homo sapiens (human)
receptor-mediated endocytosisIntegrin beta-2Homo sapiens (human)
phagocytosis, engulfmentIntegrin beta-2Homo sapiens (human)
apoptotic processIntegrin beta-2Homo sapiens (human)
inflammatory responseIntegrin beta-2Homo sapiens (human)
cell adhesionIntegrin beta-2Homo sapiens (human)
leukocyte cell-cell adhesionIntegrin beta-2Homo sapiens (human)
cell-matrix adhesionIntegrin beta-2Homo sapiens (human)
integrin-mediated signaling pathwayIntegrin beta-2Homo sapiens (human)
cell-cell signalingIntegrin beta-2Homo sapiens (human)
regulation of cell shapeIntegrin beta-2Homo sapiens (human)
neutrophil chemotaxisIntegrin beta-2Homo sapiens (human)
receptor internalizationIntegrin beta-2Homo sapiens (human)
positive regulation of superoxide anion generationIntegrin beta-2Homo sapiens (human)
heterotypic cell-cell adhesionIntegrin beta-2Homo sapiens (human)
endodermal cell differentiationIntegrin beta-2Homo sapiens (human)
receptor clusteringIntegrin beta-2Homo sapiens (human)
positive regulation of neutrophil degranulationIntegrin beta-2Homo sapiens (human)
negative regulation of dopamine metabolic processIntegrin beta-2Homo sapiens (human)
regulation of peptidyl-tyrosine phosphorylationIntegrin beta-2Homo sapiens (human)
cellular response to low-density lipoprotein particle stimulusIntegrin beta-2Homo sapiens (human)
positive regulation of protein targeting to membraneIntegrin beta-2Homo sapiens (human)
amyloid-beta clearanceIntegrin beta-2Homo sapiens (human)
cell-cell adhesionIntegrin beta-2Homo sapiens (human)
cell-cell adhesion via plasma-membrane adhesion moleculesIntegrin beta-2Homo sapiens (human)
positive regulation of leukocyte adhesion to vascular endothelial cellIntegrin beta-2Homo sapiens (human)
neutrophil migrationIntegrin beta-2Homo sapiens (human)
positive regulation of prostaglandin-E synthase activityIntegrin beta-2Homo sapiens (human)
cell adhesion mediated by integrinIntegrin beta-2Homo sapiens (human)
regulation of leukocyte mediated cytotoxicityIntercellular adhesion molecule 1Homo sapiens (human)
T cell activation via T cell receptor contact with antigen bound to MHC molecule on antigen presenting cellIntercellular adhesion molecule 1Homo sapiens (human)
T cell antigen processing and presentationIntercellular adhesion molecule 1Homo sapiens (human)
positive regulation of cellular extravasationIntercellular adhesion molecule 1Homo sapiens (human)
cell adhesionIntercellular adhesion molecule 1Homo sapiens (human)
heterophilic cell-cell adhesion via plasma membrane cell adhesion moleculesIntercellular adhesion molecule 1Homo sapiens (human)
leukocyte cell-cell adhesionIntercellular adhesion molecule 1Homo sapiens (human)
membrane to membrane dockingIntercellular adhesion molecule 1Homo sapiens (human)
cell adhesion mediated by integrinIntercellular adhesion molecule 1Homo sapiens (human)
adhesion of symbiont to hostIntercellular adhesion molecule 1Homo sapiens (human)
symbiont entry into host cellIntercellular adhesion molecule 1Homo sapiens (human)
receptor-mediated virion attachment to host cellIntercellular adhesion molecule 1Homo sapiens (human)
leukocyte migrationIntercellular adhesion molecule 1Homo sapiens (human)
establishment of endothelial barrierIntercellular adhesion molecule 1Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeIntercellular adhesion molecule 1Homo sapiens (human)
cellular response to glucose stimulusIntercellular adhesion molecule 1Homo sapiens (human)
T cell extravasationIntercellular adhesion molecule 1Homo sapiens (human)
regulation of ruffle assemblyIntercellular adhesion molecule 1Homo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway via death domain receptorsIntercellular adhesion molecule 1Homo sapiens (human)
cellular response to amyloid-betaIntercellular adhesion molecule 1Homo sapiens (human)
cellular response to leukemia inhibitory factorIntercellular adhesion molecule 1Homo sapiens (human)
negative regulation of endothelial cell apoptotic processIntercellular adhesion molecule 1Homo 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)
proteolysisNeutrophil elastaseHomo sapiens (human)
negative regulation of transcription by RNA polymerase IINeutrophil elastaseHomo sapiens (human)
response to yeastNeutrophil elastaseHomo sapiens (human)
leukocyte migration involved in inflammatory responseNeutrophil elastaseHomo sapiens (human)
biosynthetic process of antibacterial peptides active against Gram-negative bacteriaNeutrophil elastaseHomo sapiens (human)
proteolysisNeutrophil elastaseHomo sapiens (human)
intracellular calcium ion homeostasisNeutrophil elastaseHomo sapiens (human)
response to UVNeutrophil elastaseHomo sapiens (human)
extracellular matrix disassemblyNeutrophil elastaseHomo sapiens (human)
protein catabolic processNeutrophil elastaseHomo sapiens (human)
response to lipopolysaccharideNeutrophil elastaseHomo sapiens (human)
negative regulation of chemokine productionNeutrophil elastaseHomo sapiens (human)
negative regulation of interleukin-8 productionNeutrophil elastaseHomo sapiens (human)
positive regulation of interleukin-8 productionNeutrophil elastaseHomo sapiens (human)
defense response to bacteriumNeutrophil elastaseHomo sapiens (human)
positive regulation of MAP kinase activityNeutrophil elastaseHomo sapiens (human)
positive regulation of smooth muscle cell proliferationNeutrophil elastaseHomo sapiens (human)
negative regulation of inflammatory responseNeutrophil elastaseHomo sapiens (human)
positive regulation of immune responseNeutrophil elastaseHomo sapiens (human)
negative regulation of chemotaxisNeutrophil elastaseHomo sapiens (human)
pyroptosisNeutrophil elastaseHomo sapiens (human)
neutrophil-mediated killing of gram-negative bacteriumNeutrophil elastaseHomo sapiens (human)
neutrophil-mediated killing of fungusNeutrophil elastaseHomo sapiens (human)
positive regulation of leukocyte tethering or rollingNeutrophil elastaseHomo sapiens (human)
phagocytosisNeutrophil elastaseHomo sapiens (human)
acute inflammatory response to antigenic stimulusNeutrophil elastaseHomo sapiens (human)
T cell activation via T cell receptor contact with antigen bound to MHC molecule on antigen presenting cellIntegrin alpha-LHomo sapiens (human)
phagocytosisIntegrin alpha-LHomo sapiens (human)
inflammatory responseIntegrin alpha-LHomo sapiens (human)
cell adhesionIntegrin alpha-LHomo sapiens (human)
heterophilic cell-cell adhesion via plasma membrane cell adhesion moleculesIntegrin alpha-LHomo sapiens (human)
leukocyte cell-cell adhesionIntegrin alpha-LHomo sapiens (human)
cell-matrix adhesionIntegrin alpha-LHomo sapiens (human)
signal transductionIntegrin alpha-LHomo sapiens (human)
integrin-mediated signaling pathwayIntegrin alpha-LHomo sapiens (human)
memory T cell extravasationIntegrin alpha-LHomo sapiens (human)
receptor clusteringIntegrin alpha-LHomo sapiens (human)
cell-cell adhesionIntegrin alpha-LHomo sapiens (human)
cell adhesion mediated by integrinIntegrin alpha-LHomo sapiens (human)
muscle contractionSubstance-K receptorHomo sapiens (human)
tachykinin receptor signaling pathwaySubstance-K receptorHomo sapiens (human)
positive regulation of acetylcholine secretion, neurotransmissionSubstance-K receptorHomo sapiens (human)
intestine smooth muscle contractionSubstance-K receptorHomo sapiens (human)
negative regulation of luteinizing hormone secretionSubstance-K receptorHomo sapiens (human)
operant conditioningSubstance-K receptorHomo sapiens (human)
positive regulation of vascular permeabilitySubstance-K receptorHomo sapiens (human)
positive regulation of monoatomic ion transportSubstance-K receptorHomo sapiens (human)
positive regulation of smooth muscle contractionSubstance-K receptorHomo sapiens (human)
response to electrical stimulusSubstance-K receptorHomo sapiens (human)
prolactin secretionSubstance-K receptorHomo sapiens (human)
positive regulation of uterine smooth muscle contractionSubstance-K receptorHomo sapiens (human)
positive regulation of flagellated sperm motilitySubstance-K receptorHomo sapiens (human)
monoamine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transportSodium-dependent noradrenaline transporter Homo sapiens (human)
chemical synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
response to xenobiotic stimulusSodium-dependent noradrenaline transporter Homo sapiens (human)
response to painSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine uptakeSodium-dependent noradrenaline transporter Homo sapiens (human)
neuron cellular homeostasisSodium-dependent noradrenaline transporter Homo sapiens (human)
amino acid transportSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine uptake involved in synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
sodium ion transmembrane transportSodium-dependent noradrenaline transporter Homo sapiens (human)
temperature homeostasisAdenosine receptor A1Homo sapiens (human)
response to hypoxiaAdenosine receptor A1Homo sapiens (human)
G protein-coupled adenosine receptor signaling pathwayAdenosine receptor A1Homo sapiens (human)
regulation of respiratory gaseous exchange by nervous system processAdenosine receptor A1Homo sapiens (human)
negative regulation of acute inflammatory responseAdenosine receptor A1Homo sapiens (human)
negative regulation of leukocyte migrationAdenosine receptor A1Homo sapiens (human)
positive regulation of peptide secretionAdenosine receptor A1Homo sapiens (human)
positive regulation of systemic arterial blood pressureAdenosine receptor A1Homo sapiens (human)
negative regulation of systemic arterial blood pressureAdenosine receptor A1Homo sapiens (human)
regulation of glomerular filtrationAdenosine receptor A1Homo sapiens (human)
protein targeting to membraneAdenosine receptor A1Homo sapiens (human)
phagocytosisAdenosine receptor A1Homo sapiens (human)
inflammatory responseAdenosine receptor A1Homo sapiens (human)
signal transductionAdenosine receptor A1Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwayAdenosine receptor A1Homo sapiens (human)
cell-cell signalingAdenosine receptor A1Homo sapiens (human)
nervous system developmentAdenosine receptor A1Homo sapiens (human)
negative regulation of cell population proliferationAdenosine receptor A1Homo sapiens (human)
response to inorganic substanceAdenosine receptor A1Homo sapiens (human)
negative regulation of glutamate secretionAdenosine receptor A1Homo sapiens (human)
response to purine-containing compoundAdenosine receptor A1Homo sapiens (human)
lipid catabolic processAdenosine receptor A1Homo sapiens (human)
negative regulation of synaptic transmission, GABAergicAdenosine receptor A1Homo sapiens (human)
positive regulation of nucleoside transportAdenosine receptor A1Homo sapiens (human)
negative regulation of neurotrophin productionAdenosine receptor A1Homo sapiens (human)
positive regulation of protein dephosphorylationAdenosine receptor A1Homo sapiens (human)
vasodilationAdenosine receptor A1Homo sapiens (human)
negative regulation of circadian sleep/wake cycle, non-REM sleepAdenosine receptor A1Homo sapiens (human)
negative regulation of apoptotic processAdenosine receptor A1Homo sapiens (human)
positive regulation of potassium ion transportAdenosine receptor A1Homo sapiens (human)
positive regulation of MAPK cascadeAdenosine receptor A1Homo sapiens (human)
negative regulation of hormone secretionAdenosine receptor A1Homo sapiens (human)
cognitionAdenosine receptor A1Homo sapiens (human)
leukocyte migrationAdenosine receptor A1Homo sapiens (human)
detection of temperature stimulus involved in sensory perception of painAdenosine receptor A1Homo sapiens (human)
negative regulation of lipid catabolic processAdenosine receptor A1Homo sapiens (human)
positive regulation of lipid catabolic processAdenosine receptor A1Homo sapiens (human)
regulation of sensory perception of painAdenosine receptor A1Homo sapiens (human)
negative regulation of synaptic transmission, glutamatergicAdenosine receptor A1Homo sapiens (human)
fatty acid homeostasisAdenosine receptor A1Homo sapiens (human)
excitatory postsynaptic potentialAdenosine receptor A1Homo sapiens (human)
long-term synaptic depressionAdenosine receptor A1Homo sapiens (human)
mucus secretionAdenosine receptor A1Homo sapiens (human)
negative regulation of mucus secretionAdenosine receptor A1Homo sapiens (human)
triglyceride homeostasisAdenosine receptor A1Homo sapiens (human)
regulation of cardiac muscle cell contractionAdenosine receptor A1Homo sapiens (human)
apoptotic signaling pathwayAdenosine receptor A1Homo sapiens (human)
regulation of presynaptic cytosolic calcium ion concentrationAdenosine receptor A1Homo sapiens (human)
negative regulation of long-term synaptic potentiationAdenosine receptor A1Homo sapiens (human)
negative regulation of long-term synaptic depressionAdenosine receptor A1Homo sapiens (human)
G protein-coupled receptor signaling pathwayAdenosine receptor A1Homo 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 transcription by RNA polymerase IINuclear receptor ROR-gammaHomo sapiens (human)
xenobiotic metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
regulation of glucose metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
regulation of steroid metabolic processNuclear receptor ROR-gammaHomo sapiens (human)
intracellular receptor signaling pathwayNuclear receptor ROR-gammaHomo sapiens (human)
circadian regulation of gene expressionNuclear receptor ROR-gammaHomo sapiens (human)
cellular response to sterolNuclear receptor ROR-gammaHomo sapiens (human)
positive regulation of circadian rhythmNuclear receptor ROR-gammaHomo sapiens (human)
regulation of fat cell differentiationNuclear receptor ROR-gammaHomo sapiens (human)
positive regulation of DNA-templated transcriptionNuclear receptor ROR-gammaHomo sapiens (human)
adipose tissue developmentNuclear receptor ROR-gammaHomo sapiens (human)
T-helper 17 cell differentiationNuclear receptor ROR-gammaHomo sapiens (human)
regulation of transcription by RNA polymerase IINuclear receptor ROR-gammaHomo sapiens (human)
monoamine transportSodium-dependent dopamine transporter Homo sapiens (human)
neurotransmitter transportSodium-dependent dopamine transporter Homo sapiens (human)
lactationSodium-dependent dopamine transporter Homo sapiens (human)
sensory perception of smellSodium-dependent dopamine transporter Homo sapiens (human)
locomotory behaviorSodium-dependent dopamine transporter Homo sapiens (human)
response to xenobiotic stimulusSodium-dependent dopamine transporter Homo sapiens (human)
response to iron ionSodium-dependent dopamine transporter Homo sapiens (human)
dopamine transportSodium-dependent dopamine transporter Homo sapiens (human)
adenohypophysis developmentSodium-dependent dopamine transporter Homo sapiens (human)
response to nicotineSodium-dependent dopamine transporter Homo sapiens (human)
positive regulation of multicellular organism growthSodium-dependent dopamine transporter Homo sapiens (human)
regulation of dopamine metabolic processSodium-dependent dopamine transporter Homo sapiens (human)
response to cocaineSodium-dependent dopamine transporter Homo sapiens (human)
dopamine biosynthetic processSodium-dependent dopamine transporter Homo sapiens (human)
dopamine catabolic processSodium-dependent dopamine transporter Homo sapiens (human)
response to ethanolSodium-dependent dopamine transporter Homo sapiens (human)
cognitionSodium-dependent dopamine transporter Homo sapiens (human)
dopamine uptake involved in synaptic transmissionSodium-dependent dopamine transporter Homo sapiens (human)
response to cAMPSodium-dependent dopamine transporter Homo sapiens (human)
norepinephrine uptakeSodium-dependent dopamine transporter Homo sapiens (human)
prepulse inhibitionSodium-dependent dopamine transporter Homo sapiens (human)
dopamine uptakeSodium-dependent dopamine transporter Homo sapiens (human)
hyaloid vascular plexus regressionSodium-dependent dopamine transporter Homo sapiens (human)
amino acid transportSodium-dependent dopamine transporter Homo sapiens (human)
norepinephrine transportSodium-dependent dopamine transporter Homo sapiens (human)
sodium ion transmembrane transportSodium-dependent dopamine transporter Homo 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)
steroid biosynthetic processLanosterol 14-alpha demethylaseHomo sapiens (human)
cholesterol biosynthetic processLanosterol 14-alpha demethylaseHomo sapiens (human)
sterol metabolic processLanosterol 14-alpha demethylaseHomo sapiens (human)
negative regulation of protein catabolic processLanosterol 14-alpha demethylaseHomo sapiens (human)
negative regulation of protein secretionLanosterol 14-alpha demethylaseHomo sapiens (human)
negative regulation of amyloid-beta clearanceLanosterol 14-alpha demethylaseHomo sapiens (human)
adaptive immune responseRap guanine nucleotide exchange factor 4Homo sapiens (human)
G protein-coupled receptor signaling pathwayRap guanine nucleotide exchange factor 4Homo sapiens (human)
adenylate cyclase-activating G protein-coupled receptor signaling pathwayRap guanine nucleotide exchange factor 4Homo sapiens (human)
calcium-ion regulated exocytosisRap guanine nucleotide exchange factor 4Homo sapiens (human)
regulation of exocytosisRap guanine nucleotide exchange factor 4Homo sapiens (human)
insulin secretionRap guanine nucleotide exchange factor 4Homo sapiens (human)
positive regulation of insulin secretionRap guanine nucleotide exchange factor 4Homo sapiens (human)
regulation of synaptic vesicle cycleRap guanine nucleotide exchange factor 4Homo sapiens (human)
Ras protein signal transductionRap guanine nucleotide exchange factor 4Homo sapiens (human)
regulation of insulin secretionRap guanine nucleotide exchange factor 4Homo 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 processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
negative regulation of gene expressionCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bile acid and bile salt transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
heme catabolic processCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic export from cellCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transepithelial transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
leukotriene transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
monoatomic anion transmembrane transportCanalicular multispecific organic anion transporter 1Homo sapiens (human)
transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transport across blood-brain barrierCanalicular multispecific organic anion transporter 1Homo 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)
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 (148)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo 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)
cargo receptor activityIntegrin beta-2Homo sapiens (human)
amyloid-beta bindingIntegrin beta-2Homo sapiens (human)
complement component C3b bindingIntegrin beta-2Homo sapiens (human)
integrin bindingIntegrin beta-2Homo sapiens (human)
protein bindingIntegrin beta-2Homo sapiens (human)
protein kinase bindingIntegrin beta-2Homo sapiens (human)
ICAM-3 receptor activityIntegrin beta-2Homo sapiens (human)
heat shock protein bindingIntegrin beta-2Homo sapiens (human)
metal ion bindingIntegrin beta-2Homo sapiens (human)
cell adhesion molecule bindingIntegrin beta-2Homo sapiens (human)
virus receptor activityIntercellular adhesion molecule 1Homo sapiens (human)
transmembrane signaling receptor activityIntercellular adhesion molecule 1Homo sapiens (human)
integrin bindingIntercellular adhesion molecule 1Homo sapiens (human)
protein bindingIntercellular adhesion molecule 1Homo sapiens (human)
signaling receptor activityIntercellular adhesion molecule 1Homo 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)
protease bindingNeutrophil elastaseHomo sapiens (human)
transcription corepressor activityNeutrophil elastaseHomo sapiens (human)
endopeptidase activityNeutrophil elastaseHomo sapiens (human)
serine-type endopeptidase activityNeutrophil elastaseHomo sapiens (human)
protein bindingNeutrophil elastaseHomo sapiens (human)
heparin bindingNeutrophil elastaseHomo sapiens (human)
peptidase activityNeutrophil elastaseHomo sapiens (human)
cytokine bindingNeutrophil elastaseHomo sapiens (human)
protein bindingIntegrin alpha-LHomo sapiens (human)
ICAM-3 receptor activityIntegrin alpha-LHomo sapiens (human)
metal ion bindingIntegrin alpha-LHomo sapiens (human)
cell adhesion molecule bindingIntegrin alpha-LHomo sapiens (human)
integrin bindingIntegrin alpha-LHomo sapiens (human)
tachykinin receptor activitySubstance-K receptorHomo sapiens (human)
protein bindingSubstance-K receptorHomo sapiens (human)
substance K receptor activitySubstance-K receptorHomo sapiens (human)
actin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
protein bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
alpha-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
metal ion bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
beta-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
G protein-coupled receptor bindingAdenosine receptor A1Homo sapiens (human)
purine nucleoside bindingAdenosine receptor A1Homo sapiens (human)
protein bindingAdenosine receptor A1Homo sapiens (human)
heat shock protein bindingAdenosine receptor A1Homo sapiens (human)
G-protein beta/gamma-subunit complex bindingAdenosine receptor A1Homo sapiens (human)
heterotrimeric G-protein bindingAdenosine receptor A1Homo sapiens (human)
protein heterodimerization activityAdenosine receptor A1Homo sapiens (human)
G protein-coupled adenosine receptor activityAdenosine receptor A1Homo 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)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificNuclear receptor ROR-gammaHomo sapiens (human)
DNA-binding transcription factor activityNuclear receptor ROR-gammaHomo sapiens (human)
protein bindingNuclear receptor ROR-gammaHomo sapiens (human)
oxysterol bindingNuclear receptor ROR-gammaHomo sapiens (human)
zinc ion bindingNuclear receptor ROR-gammaHomo sapiens (human)
ligand-activated transcription factor activityNuclear receptor ROR-gammaHomo sapiens (human)
sequence-specific double-stranded DNA bindingNuclear receptor ROR-gammaHomo sapiens (human)
nuclear receptor activityNuclear receptor ROR-gammaHomo sapiens (human)
protease bindingSodium-dependent dopamine transporter Homo sapiens (human)
signaling receptor bindingSodium-dependent dopamine transporter Homo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent dopamine transporter Homo sapiens (human)
dopamine:sodium symporter activitySodium-dependent dopamine transporter Homo sapiens (human)
protein bindingSodium-dependent dopamine transporter Homo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent dopamine transporter Homo sapiens (human)
dopamine bindingSodium-dependent dopamine transporter Homo sapiens (human)
amine bindingSodium-dependent dopamine transporter Homo sapiens (human)
protein-containing complex bindingSodium-dependent dopamine transporter Homo sapiens (human)
metal ion bindingSodium-dependent dopamine transporter Homo sapiens (human)
protein phosphatase 2A bindingSodium-dependent dopamine transporter Homo sapiens (human)
heterocyclic compound bindingSodium-dependent dopamine transporter Homo sapiens (human)
norepinephrine:sodium symporter activitySodium-dependent dopamine transporter Homo 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)
iron ion bindingLanosterol 14-alpha demethylaseHomo sapiens (human)
sterol 14-demethylase activityLanosterol 14-alpha demethylaseHomo sapiens (human)
heme bindingLanosterol 14-alpha demethylaseHomo sapiens (human)
oxidoreductase activityLanosterol 14-alpha demethylaseHomo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygenLanosterol 14-alpha demethylaseHomo sapiens (human)
guanyl-nucleotide exchange factor activityRap guanine nucleotide exchange factor 4Homo sapiens (human)
protein bindingRap guanine nucleotide exchange factor 4Homo sapiens (human)
cAMP bindingRap guanine nucleotide exchange factor 4Homo sapiens (human)
protein-macromolecule adaptor activityRap guanine nucleotide exchange factor 4Homo sapiens (human)
small GTPase bindingRap guanine nucleotide exchange factor 4Homo 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)
protein bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP bindingCanalicular multispecific organic anion transporter 1Homo sapiens (human)
organic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type xenobiotic transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
bilirubin transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATP hydrolysis activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
xenobiotic transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityCanalicular multispecific organic anion transporter 1Homo sapiens (human)
ABC-type transporter activityCanalicular multispecific organic anion transporter 1Homo 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)
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 (100)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo 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)
plasma membraneIntegrin beta-2Homo sapiens (human)
external side of plasma membraneIntegrin beta-2Homo sapiens (human)
cell surfaceIntegrin beta-2Homo sapiens (human)
membraneIntegrin beta-2Homo sapiens (human)
integrin alphaL-beta2 complexIntegrin beta-2Homo sapiens (human)
integrin alphaM-beta2 complexIntegrin beta-2Homo sapiens (human)
integrin alphaX-beta2 complexIntegrin beta-2Homo sapiens (human)
specific granule membraneIntegrin beta-2Homo sapiens (human)
plasma membrane raftIntegrin beta-2Homo sapiens (human)
extracellular exosomeIntegrin beta-2Homo sapiens (human)
tertiary granule membraneIntegrin beta-2Homo sapiens (human)
ficolin-1-rich granule membraneIntegrin beta-2Homo sapiens (human)
extracellular vesicleIntegrin beta-2Homo sapiens (human)
integrin complexIntegrin beta-2Homo sapiens (human)
receptor complexIntegrin beta-2Homo sapiens (human)
focal adhesionIntegrin beta-2Homo sapiens (human)
cell surfaceIntegrin beta-2Homo sapiens (human)
immunological synapseIntercellular adhesion molecule 1Homo sapiens (human)
extracellular spaceIntercellular adhesion molecule 1Homo sapiens (human)
plasma membraneIntercellular adhesion molecule 1Homo sapiens (human)
focal adhesionIntercellular adhesion molecule 1Homo sapiens (human)
external side of plasma membraneIntercellular adhesion molecule 1Homo sapiens (human)
cell surfaceIntercellular adhesion molecule 1Homo sapiens (human)
membraneIntercellular adhesion molecule 1Homo sapiens (human)
membrane raftIntercellular adhesion molecule 1Homo sapiens (human)
collagen-containing extracellular matrixIntercellular adhesion molecule 1Homo sapiens (human)
extracellular exosomeIntercellular adhesion molecule 1Homo sapiens (human)
plasma membraneIntercellular adhesion molecule 1Homo 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)
extracellular regionNeutrophil elastaseHomo sapiens (human)
extracellular spaceNeutrophil elastaseHomo sapiens (human)
cytoplasmNeutrophil elastaseHomo sapiens (human)
cytosolNeutrophil elastaseHomo sapiens (human)
cell surfaceNeutrophil elastaseHomo sapiens (human)
secretory granuleNeutrophil elastaseHomo sapiens (human)
azurophil granule lumenNeutrophil elastaseHomo sapiens (human)
specific granule lumenNeutrophil elastaseHomo sapiens (human)
phagocytic vesicleNeutrophil elastaseHomo sapiens (human)
collagen-containing extracellular matrixNeutrophil elastaseHomo sapiens (human)
extracellular exosomeNeutrophil elastaseHomo sapiens (human)
transcription repressor complexNeutrophil elastaseHomo sapiens (human)
extracellular spaceNeutrophil elastaseHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
plasma membraneGlutamate receptor 2Rattus norvegicus (Norway rat)
plasma membraneIntegrin alpha-LHomo sapiens (human)
cell surfaceIntegrin alpha-LHomo sapiens (human)
membraneIntegrin alpha-LHomo sapiens (human)
integrin alphaL-beta2 complexIntegrin alpha-LHomo sapiens (human)
specific granule membraneIntegrin alpha-LHomo sapiens (human)
extracellular exosomeIntegrin alpha-LHomo sapiens (human)
integrin complexIntegrin alpha-LHomo sapiens (human)
external side of plasma membraneIntegrin alpha-LHomo sapiens (human)
plasma membraneSubstance-K receptorHomo sapiens (human)
sperm flagellumSubstance-K receptorHomo sapiens (human)
sperm headSubstance-K receptorHomo sapiens (human)
sperm midpieceSubstance-K receptorHomo sapiens (human)
sperm midpieceSubstance-K receptorHomo sapiens (human)
plasma membraneSubstance-K receptorHomo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
cell surfaceSodium-dependent noradrenaline transporter Homo sapiens (human)
membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
neuronal cell body membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
presynaptic membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
axonSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneAdenosine receptor A1Homo sapiens (human)
plasma membraneAdenosine receptor A1Homo sapiens (human)
basolateral plasma membraneAdenosine receptor A1Homo sapiens (human)
axolemmaAdenosine receptor A1Homo sapiens (human)
asymmetric synapseAdenosine receptor A1Homo sapiens (human)
presynaptic membraneAdenosine receptor A1Homo sapiens (human)
neuronal cell bodyAdenosine receptor A1Homo sapiens (human)
terminal boutonAdenosine receptor A1Homo sapiens (human)
dendritic spineAdenosine receptor A1Homo sapiens (human)
calyx of HeldAdenosine receptor A1Homo sapiens (human)
postsynaptic membraneAdenosine receptor A1Homo sapiens (human)
presynaptic active zoneAdenosine receptor A1Homo sapiens (human)
synapseAdenosine receptor A1Homo sapiens (human)
dendriteAdenosine receptor A1Homo sapiens (human)
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)
nucleusNuclear receptor ROR-gammaHomo sapiens (human)
nucleoplasmNuclear receptor ROR-gammaHomo sapiens (human)
nuclear bodyNuclear receptor ROR-gammaHomo sapiens (human)
chromatinNuclear receptor ROR-gammaHomo sapiens (human)
nucleusNuclear receptor ROR-gammaHomo sapiens (human)
virion membraneSpike glycoproteinSevere acute respiratory syndrome-related coronavirus
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
cytoplasmSodium-dependent dopamine transporter Homo sapiens (human)
plasma membraneSodium-dependent dopamine transporter Homo sapiens (human)
cell surfaceSodium-dependent dopamine transporter Homo sapiens (human)
membraneSodium-dependent dopamine transporter Homo sapiens (human)
axonSodium-dependent dopamine transporter Homo sapiens (human)
neuron projectionSodium-dependent dopamine transporter Homo sapiens (human)
neuronal cell bodySodium-dependent dopamine transporter Homo sapiens (human)
axon terminusSodium-dependent dopamine transporter Homo sapiens (human)
membrane raftSodium-dependent dopamine transporter Homo sapiens (human)
postsynaptic membraneSodium-dependent dopamine transporter Homo sapiens (human)
dopaminergic synapseSodium-dependent dopamine transporter Homo sapiens (human)
flotillin complexSodium-dependent dopamine transporter Homo sapiens (human)
axonSodium-dependent dopamine transporter Homo sapiens (human)
presynaptic membraneSodium-dependent dopamine transporter Homo sapiens (human)
plasma membraneSodium-dependent dopamine transporter Homo sapiens (human)
neuronal cell body membraneSodium-dependent dopamine transporter Homo 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)
endoplasmic reticulum membraneLanosterol 14-alpha demethylaseHomo sapiens (human)
membraneLanosterol 14-alpha demethylaseHomo sapiens (human)
cytosolRap guanine nucleotide exchange factor 4Homo sapiens (human)
plasma membraneRap guanine nucleotide exchange factor 4Homo sapiens (human)
membraneRap guanine nucleotide exchange factor 4Homo sapiens (human)
hippocampal mossy fiber to CA3 synapseRap guanine nucleotide exchange factor 4Homo sapiens (human)
plasma membraneRap guanine nucleotide exchange factor 4Homo 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 membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
cell surfaceCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo sapiens (human)
intercellular canaliculusCanalicular multispecific organic anion transporter 1Homo sapiens (human)
apical plasma membraneCanalicular multispecific organic anion transporter 1Homo 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)
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 (464)

Assay IDTitleYearJournalArticle
AID1347154Primary screen GU AMC 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.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID249811Weight of cholesterol in liver wet tissue after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID83856Effect on total serum cholesterol in male hamsters at a dose of 10 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID358047Reversal of reduction in survivin mRNA expression in human SW480 cells at 20 uM after 48 hrs by RT-PCR technique in presence of 100 uM mevalonate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID613072Inhibition of Listeria monocytogenes recombinant HMGR class II expressed in Escherichia coli using HMG-CoA as substrate2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
AID1315657Inhibition of human HMGR catalytic domain at 200 uM using HMG-CoA as substrate measured every 20 secs for 10 mins relative to control2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID476519Induction of bone formation in SAMP6 mouse right femora assessed as trabecular resorption surface percentage at 10 mg/kg/day, po measured after 3 months by bone histomorphometry2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID180697In vitro inhibitory potency for cholesterol synthesis was measured in rat testes1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
AID249808Weight of serum cholesterol after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
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.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID406850Antiplasmodial activity against chloroquine-sensitive Plasmodium falciparum IMT0312007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID680013TP_TRANSPORTER: inhibition of Fexofenadine uptake (Fexofenadine: 2 uM, Lovastatin: 100 uM) in Xenopus laevis oocytes1999Drug metabolism and disposition: the biological fate of chemicals, Aug, Volume: 27, Issue:8
OATP and P-glycoprotein transporters mediate the cellular uptake and excretion of fexofenadine.
AID540209Volume of distribution at steady state in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID28681Partition coefficient (logD6.5)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID83864Effect on total serum cholesterol in male hamsters at a dose of 5 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID1202383Upregulation of BMP-2 expression in mouse MC3T3-E1 cells at 0.4 uM after 24 hrs by luciferase reporter gene assay relative to control2015European journal of medicinal chemistry, , Volume: 96Synthesis of a novel class of substituted benzothiophene or benzofuran derivatives as BMP-2 up-regulators and evaluation of the BMP-2-up-regulating effects in vitro and the effects on glucocorticoid-induced osteoporosis in rats.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1072584Induction of apoptosis in human MDA-MB-231 cells assessed as viable cells at 1 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 93.2 +/-0.9%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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]
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.
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.
AID51950Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 0.3 mg/kg four weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID619573Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 100 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID59808Tested in vivo for hypocholesterolemic activity by measuring its ability to decrease serum LDL-cholesterol, after oral administration of 10 mg/kg per day for 119 days in male Beagle dogs.1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
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.
AID362087Inhibition of sICAM1/LFA1 interaction-mediated human THP1 cell adhesion at 6.25 ug/mL after 1 hr by ELISA2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition.
AID527846Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in HDL to total cholesterol ratio at 25 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID1324339Induction of CHK1 phosphorylation in human MDA-MB-231 cells at 10 uM after 6 to 24 hrs by Western blot method2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID476520Induction of bone formation in SAMP6 mouse right femora assessed as average osteoid width at 10 mg/kg/day, po measured after 3 months by bone histomorphometry2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID1072578Induction of apoptosis in human MDA-MB-231 cells assessed as viable cells at 10 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 93.2 +/-0.9%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID619482Hypolipidemic activity in high fat diet fed Syrian golden hamster assessed as reduction of triglyceride level at 25 mg/kg, po for 7 days2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID425652Total body clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID512645Antiviral activity against Hepatitis C virus (isolate Con1) genotype 1b in human Huh-7/3-1 cells assessed as inhibition of HCV replication after 72 hrs by luciferase assay2005Nature chemical biology, Nov, Volume: 1, Issue:6
Host sphingolipid biosynthesis as a target for hepatitis C virus therapy.
AID681366TP_TRANSPORTER: inhibition of estradiol-17beta-glucuronide uptake(estradiol-17beta-glucuronide:0.02uM) in OATP1B1-expressing HEK293 cells2005Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4
Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID85817Percentage lowering of the total serum cholesterol in male hamsters at a dose of 5 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID180695In vitro inhibitory potency for cholesterol synthesis was measured in rat spleen1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
AID1240157Lipid lowering activity in human HepG2 cells assessed as decrease in oleic acid elicited lipid accumulation after 6 hrs by oil-red O staining method2015Bioorganic & medicinal chemistry letters, Sep-01, Volume: 25, Issue:17
Lipid-lowering polyketides from a soft coral-derived fungus Cladosporium sp. TZP29.
AID1443995Hepatotoxicity in human assessed as drug-induced liver injury2014Hepatology (Baltimore, Md.), Sep, Volume: 60, Issue:3
Human drug-induced liver injury severity is highly associated with dual inhibition of liver mitochondrial function and bile salt export pump.
AID165824Tested in vivo for hypocholesterolemic activity by measuring its ability to decrease serum total cholesterol, after oral administration of 20 mg/kg body wt. per day in normolipidemic NZW rabbits1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID85814Percentage lowering of the total serum cholesterol in male hamsters at a dose of 200 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID1072592Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at G2/M phase at 1 uM after 30 hrs by flow cytometer (Rvb = 17.1 +/-2.1%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID476517Induction of bone formation in SAMP6 mouse right femora assessed as trabecular bone volume percentage at 10 mg/kg/day, po measured after 3 months by bone histomorphometry2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
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).
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.
AID406848Antiplasmodial activity against chloroquine-sensitive Plasmodium falciparum D62007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID1210013Inhibition of recombinant CYP2J2 (unknown origin)-mediated terfenadine hydroxylation assessed as remaining activity at 30 uM after 5 mins by LC-MS analysis relative to control2012Drug metabolism and disposition: the biological fate of chemicals, May, Volume: 40, Issue:5
Identifying a selective substrate and inhibitor pair for the evaluation of CYP2J2 activity.
AID342987Decrease in hepatic triglyceride level in hypercholesterolemic Wistar rat at 20 mg/kg, po for 1 week with diet2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Synthesis, DNA binding, and cytotoxic evaluation of new analogs of diallyldisulfide, an active principle of garlic.
AID444056Fraction escaping gut-wall elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1204211Induction of apoptosis in human RPMI8226 cells assessed as increase in caspase-3 cleavage at 20 uM incubated for 48 hrs by immunoblot method2015Bioorganic & medicinal chemistry letters, Jun-01, Volume: 25, Issue:11
N-Oxide derivatives of 3-(3-pyridyl)-2-phosphonopropanoic acids as potential inhibitors of Rab geranylgeranylation.
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.
AID1324330Induction of reactive oxygen species in human MDA-MB-231 cells at 30 uM after 24 hrs by DCFH-DA probe-based flow cytometric method2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID165823Tested in vivo for hypocholesterolemic activity by measuring its ability to decrease serum total cholesterol, after oral administration of 10 mg/kg body wt. per day in normolipidemic NZW rabbits1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID1473809Drug concentration at steady state in human at 10 to 80 mg, po QD after 24 hrs2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID84867The compound was evaluated for its ability to reduce liver cholesterol esters(LCE) in cholesterol-fed hamsters; NE=no effect at 10 mg/kg1998Journal of medicinal chemistry, Mar-12, Volume: 41, Issue:6
Discovery of 1-(4-fluorophenyl)-(3R)-[3-(4-fluorophenyl)-(3S)-hydroxypropyl]-(4S)-(4 -hydroxyphenyl)-2-azetidinone (SCH 58235): a designed, potent, orally active inhibitor of cholesterol absorption.
AID1519520Inhibition of GGtase-1 in human RPMI8226 cells assessed as disruption of Rap1a geranylgeranylation at 0.5 uM after 48 hrs by immunoblot analysis2019Bioorganic & medicinal chemistry letters, 12-15, Volume: 29, Issue:24
Novel benzimidazole phosphonates as potential inhibitors of protein prenylation.
AID358062Reversal of inhibition of FBS-stimulated increase in Ras protein expression in human SW480 cells assessed as GTP-bound protein at 20 uM by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID680566TP_TRANSPORTER: inhibition of estradiol-17beta-D-glucuronide uptake (Lovastatin:10 uM) in OATP1B1-expressing HeLa cells2005Drug metabolism and disposition: the biological fate of chemicals, May, Volume: 33, Issue:5
Hepatic uptake of the novel antifungal agent caspofungin.
AID83478Inhibition of rat liver microsomal HMG-CoA reductase1993Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23
Inhibitors of cholesterol biosynthesis. 2. 3,5-Dihydroxy-7-(N-pyrrolyl)-6-heptenoates, a novel series of HMG-CoA reductase inhibitors.
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]
AID51948Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 0.1 mg/kg four weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID613070Inhibition of Streptococcus pneumoniae recombinant HMGR class II expressed in Escherichia coli using HMG-CoA as substrate2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
AID80987Inhibitory activity against partially purified rat liver HMG-CoA reductase in vitro; 0.23-0.711993Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23
HMG-CoA reductase inhibitors: design, synthesis, and biological activity of tetrahydroindazole-substituted 3,5-dihydroxy-6-heptenoic acid sodium salts.
AID678719Metabolic stability in human liver microsomes assessed as medium signal/noise ratio (S/N of 10 to 100) by measuring GSH adduct formation at 100 uM after 90 mins by HPLC-MS analysis2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1220876Apparent permeability of the compound in BCRP knockdown human Caco2 cells at 10 uM up to 120 mins by reverse-phase liquid chromatography with triple-quadrupole tandem mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Use of transporter knockdown Caco-2 cells to investigate the in vitro efflux of statin drugs.
AID737914Inhibition of HMG-CoA reductase in human A549 cells after 5 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.
AID619574Inhibition of HMG-CoA reductase using HMG-CoA as substrate by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID291329Cell cycle arrest in human STS-26T cells assessed as accumulation in G1 phase at 1 uM after 24 hrs2007Journal of medicinal chemistry, Jul-12, Volume: 50, Issue:14
Synthesis, biochemical, and cellular evaluation of farnesyl monophosphate prodrugs as farnesyltransferase inhibitors.
AID1519519Inhibition of FTase in human RPMI8226 cells assessed as disruption of H-ras farnesylation at 0.5 uM after 48 hrs by immunoblot analysis2019Bioorganic & medicinal chemistry letters, 12-15, Volume: 29, Issue:24
Novel benzimidazole phosphonates as potential inhibitors of protein prenylation.
AID311524Oral bioavailability in human2007Bioorganic & medicinal chemistry, Dec-15, Volume: 15, Issue:24
Hologram QSAR model for the prediction of human oral bioavailability.
AID629781Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 25 uM2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID181824Compound was evaluated for the percentage of acute inhibition of cholesterol synthesis (AICS) in male rats through peroral rout.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
Inhibitors of cholesterol biosynthesis. 4. trans-6-[2-(substituted-quinolinyl)ethenyl/ethyl]tetrahydro-4-hydroxy-2 H-pyran-2-ones, a novel series of HMG-CoA reductase inhibitors.
AID81725Concentration required to inhibit HMG-CoA reductase by 50% was determined in HES 9 cell line1992Journal of medicinal chemistry, Sep-04, Volume: 35, Issue:18
Synthesis and biological evaluation of dihydroeptastatin, a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase.
AID619565Hypolipidemic activity in high fat diet fed Syrian golden hamster assessed as increase in HDL-cholesterol-total cholesterol ratio at 25 mg/kg, po for 7 days2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1695293Antileishmanial activity against amastigote form of Leishmania infantum MCAN_UY_2015_mCO8 isolate assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
AID1072581Induction of apoptosis in human MDA-MB-231 cells assessed as viable cells at 5 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 93.2 +/-0.9%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1324341Induction of ATM phosphorylation in human MDA-MB-231 cells at 10 uM after 6 to 24 hrs by Western blot method2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID342986Decrease in serum cholesterol level in hypercholesterolemic Wistar rat at 20 mg/kg, po for 1 week with diet2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Synthesis, DNA binding, and cytotoxic evaluation of new analogs of diallyldisulfide, an active principle of garlic.
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.
AID231147Ratio of the mean IC50 for sterol-synthesis inhibition of adrenal relative to hepatocytes in rat1989Journal of medicinal chemistry, Sep, Volume: 32, Issue:9
A potent, tissue-selective, synthetic inhibitor of HMG-CoA reductase.
AID1072607Growth inhibition of ER-negative, HER2-positive human AU565 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1324333Cytotoxicity against human PC3 cells assessed as growth inhibition after 48 hrs by SRB assay2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID83861Effect on total serum cholesterol in male hamsters at a dose of 200 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID681381TP_TRANSPORTER: inhibition of calcein-AM efflux in MDR1-expressing MDCK cells2005Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4
Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID1204210Induction of apoptosis in human RPMI8226 cells assessed as increase in PARP cleavage at 20 uM incubated for 48 hrs by immunoblot method2015Bioorganic & medicinal chemistry letters, Jun-01, Volume: 25, Issue:11
N-Oxide derivatives of 3-(3-pyridyl)-2-phosphonopropanoic acids as potential inhibitors of Rab geranylgeranylation.
AID51949Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 0.1 mg/kg two weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID613075Inhibition of Pseudomonas mevalonii recombinant HMGR class II expressed in Escherichia coli using HMG-CoA as substrate2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
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).
AID23913Calculated partition coefficient (clogP) (active dihydroxy acid form)1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID357813Induction of apoptosis in human SW480 cells at 20 uM after 48 hrs by annexin-V propidium iodide staining method2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1454766Inhibition of HMG-CoA reductase (unknown origin) using [14C]-HMG-CoA as substrate after 5 mins in presence of NADPH2018Journal of medicinal chemistry, 03-22, Volume: 61, Issue:6
Natural-Products-Inspired Use of the gem-Dimethyl Group in Medicinal Chemistry.
AID1409607IC50 for antiviral activity against SARS-CoV-2 in the Vero E6 cell line at 48 h by immunofluorescence-based assay (detecting the viral NP protein in the nucleus of the Vero E6 cells).2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID629783Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 100 uM2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID1315653Antimalarial activity against multi-drug-resistant Plasmodium falciparum K1 by microculture radioisotope technique2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID1315655Cytotoxicity against human MCF7 cells by resazurin microplate assay2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
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).
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
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).
AID358057Reversal of decrease in isoprenylated Ras level in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of farnesyl pyrophosphate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID357812Induction of apoptosis in human SW480 cells assessed as increase in hypodiploid DNA content at 20 uM after 48 hrs by flow cytometry relative to control2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
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.
AID567091Drug absorption in human assessed as human intestinal absorption rate2011European journal of medicinal chemistry, Jan, Volume: 46, Issue:1
Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID681126TP_TRANSPORTER: inhibition of Rhodamine 123 efflux in NIH-3T3-G185 cells2001Biochemical and biophysical research communications, Nov-30, Volume: 289, Issue:2
Active transport of fluorescent P-glycoprotein substrates: evaluation as markers and interaction with inhibitors.
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1315656Cytotoxicity against African green monkey Vero cells2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID1220877Apparent permeability of the compound in MRP2 knockdown human Caco2 cells at 10 uM up to 120 mins by reverse-phase liquid chromatography with triple-quadrupole tandem mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Use of transporter knockdown Caco-2 cells to investigate the in vitro efflux of statin drugs.
AID51953Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 1.0 mg/kg two weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
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.
AID29363Dissociation constant (pKa)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
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.
AID172947In vivo inhibition of hepatic cholesterol de novo synthesis in rat after oral administration of 5 mg/kg dose1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1072577Induction of apoptosis in human MDA-MB-231 cells assessed as apoptotic cells at 10 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 2.4 +/-0.5%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID85691Percentage lowering of the total serum cholesterol in male hamsters at a dose of 100 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID476504Induction of bone mineral density in SAMP6 mouse assessed as whole body BMD at 10 mg/kg/day, po measured after 3 months2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID631127Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as increase in serum ratio of HDL/total cholesterol level at 25 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.
AID1315660Binding affinity to human HMGR catalytic domain at 50 uM in presence of 800 to 3200 uM HMG-CoA as substrate measured every 20 secs for 10 mins2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID619560Hypolipidemic activity in high fat diet fed Syrian golden hamster assessed as reduction of glycerol level at 25 mg/kg, po for 7 days2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID358049Inhibition of survivin expression in survivin gene transfected human LS180 cells at 20 uM immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID680574TP_TRANSPORTER: inhibition of Pravastatin uptake (Pravastatin: 0.5 uM, Lovastatin: 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.
AID1742238Hypolipidemic activity in mouse 3T3-L1 preadipocytes assessed as reduction in lipid content at 10 uM by Oil Red O staining based assay relative to control2020European journal of medicinal chemistry, Nov-01, Volume: 205Synthesis of natural 3'-Prenylchalconaringenin and biological evaluation of ameliorating non-alcoholic fatty liver disease and metabolic syndrome.
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.
AID83293Inhibition of cellular HMG-CoA reductase in cultures of hepatic cells (HEP G2, a human hepatoma cell line)1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID1072612Total growth inhibition of PR, ER, HER2-negative human MDA-MB-231 cells at >10 uM after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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).
AID179204Compound was tested for its Cholesterol Synthesis Inhibition ability in rats.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
Inhibitors of cholesterol biosynthesis. 4. trans-6-[2-(substituted-quinolinyl)ethenyl/ethyl]tetrahydro-4-hydroxy-2 H-pyran-2-ones, a novel series of HMG-CoA reductase inhibitors.
AID83483In vitro inhibition of rat liver HMG-CoA reductase1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 1. Lactones of pyridine- and pyrimidine-substituted 3,5-dihydroxy-6-heptenoic (-heptanoic) acids.
AID1072576Induction of apoptosis in human MDA-MB-231 cells assessed as necrotic cells at 10 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 4.4 +/-0.4%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1072599Cytotoxicity against PR, ER, HER2-negative human MDA-MB-468 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID183243Inhibition of hepatic cholesterol de novo synthesis in male rats after po administration,1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID83305Relative potency for the inhibitory activity of HMG-CoA reductase to that (arbitrarily assigned a value of 1.00)1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 1. Lactones of pyridine- and pyrimidine-substituted 3,5-dihydroxy-6-heptenoic (-heptanoic) acids.
AID102357Compound was tested in vitro for up-regulation of low density lipoprotein (LDL) receptor in human hepatocytes (HepG2 cells) at a concentration 3 uM1996Journal of medicinal chemistry, Aug-16, Volume: 39, Issue:17
New low-density lipoprotein receptor upregulators acting via a novel mechanism.
AID527843Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in triglyceride level at 25 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID476518Induction of bone formation in SAMP6 mouse right femora assessed as trabecular formation surface percentage at 10 mg/kg/day, po measured after 3 months by bone histomorphometry2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
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.
AID1072588Induction of p21 expression in human PR, ER, HER2-negative human MDA-MB-231 cells at 1 to 10 uM after 24 hrs by western blot analysis2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID83484In vitro inhibitory activity was measured against rat liver HMG-CoA reductase1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
AID1695288Antileishmanial activity against amastigote form of Leishmania infantum MHOM/BR/2002/LPC-RPV assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
AID1443992Total Cmax in human administered as single dose2014Hepatology (Baltimore, Md.), Sep, Volume: 60, Issue:3
Human drug-induced liver injury severity is highly associated with dual inhibition of liver mitochondrial function and bile salt export pump.
AID358050Blockade of growth inhibition of survivin gene transfected human LS180 cells after 72 hrs by MTS method2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
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.
AID613074Inhibition of Archaeoglobus fulgidus HMGCR 1 recombinant HMGR class II expressed in Escherichia coli using HMG-CoA as substrate2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
AID619572Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 50 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID613071Ratio Ki for lovastatin to compound for recombinant Streptococcus pneumoniae HMGR class II2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID251127Percent decrease in weight of serum cholesterol after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID291330Cell cycle arrest in human STS-26T cells assessed as accumulation in G2/M phase at 1 uM after 24 hrs2007Journal of medicinal chemistry, Jul-12, Volume: 50, Issue:14
Synthesis, biochemical, and cellular evaluation of farnesyl monophosphate prodrugs as farnesyltransferase inhibitors.
AID613073Inhibition of Staphylococcus aureus recombinant HMGR class II expressed in Escherichia coli using HMG-CoA as substrate2011Bioorganic & medicinal chemistry, Jun-01, Volume: 19, Issue:11
Specific inhibitions of annonaceous acetogenins on class II 3-hydroxy-3-methylglutaryl coenzyme A reductase from Streptococcus pneumoniae.
AID357805Growth inhibition of human SW480 cells after 96 hrs by MTS assay2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1072602Growth inhibition of ER-positive, HER2-positive human MDA-MB-361 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1072591Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 10 uM after 30 hrs by flow cytometer (Rvb = 49.8 +/-1.5%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID631126Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum LDL level at 25 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.
AID243389Percent decrease in HMG-CoA reductase activity in rat2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID1695289Antileishmanial activity against amastigote form of Leishmania infantum MCAN_UY_2015_gPL8 isolate assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
AID165482Percent decrease in total plasma cholesterol in rabbit was determined after oral administration of a dose of 10 mg/kg for 6 days1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
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.
AID83463Compound was evaluated for the inhibition of HMG-CoA reductase (COR) in rats.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
Inhibitors of cholesterol biosynthesis. 4. trans-6-[2-(substituted-quinolinyl)ethenyl/ethyl]tetrahydro-4-hydroxy-2 H-pyran-2-ones, a novel series of HMG-CoA reductase inhibitors.
AID476508Induction of bone mineral density in SAMP6 mouse assessed as whole body BMD at 30 mg/kg/day, po measured after 2 months2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
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.
AID231149Ratio of the mean IC50 for sterol-synthesis inhibition of spleen relative to hepatocytes in rat1989Journal of medicinal chemistry, Sep, Volume: 32, Issue:9
A potent, tissue-selective, synthetic inhibitor of HMG-CoA reductase.
AID126805In vivo percent change of HDL cholesterol in monkeys at 20 mg/kg/day for 5 days dose1997Journal of medicinal chemistry, Jul-04, Volume: 40, Issue:14
(1 alpha, 2 beta, 3 beta, 4 alpha)-1,2-bis[N-propyl-N-(4-phenoxybenzyl) amino]carbonyl]cyclobutane-3,4-dicarboxylic acid (A-87049): a novel potent squalene synthase inhibitor.
AID51951Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 0.3 mg/kg two weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID1502953Reduction in triglyceride level in patient with moderate hypercholesterolemia at 20 to 80 mg/day2017European journal of medicinal chemistry, Nov-10, Volume: 140Lipid lowering agents of natural origin: An account of some promising chemotypes.
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]
AID722627Binding affinity to I-domain of human integrin alphaL (amino acid residues 128 to 307) plus initial methionine expressed in Escherichia coli by NMR spectroscopy2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Design, synthesis, and functional evaluation of leukocyte function associated antigen-1 antagonists in early and late stages of cancer development.
AID629782Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 50 uM2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID231148Ratio of the mean IC50 for sterol-synthesis inhibition of hepatocytes relative to hepatocytes in rat1989Journal of medicinal chemistry, Sep, Volume: 32, Issue:9
A potent, tissue-selective, synthetic inhibitor of HMG-CoA reductase.
AID83865Effect on total serum cholesterol in male hamsters at a dose of 50 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID631125Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as increase in serum HDL level at 25 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.
AID1324342Induction of CHK1/2 phosphorylation in human MDA-MB-231 cells assessed as increase in p53 phosphorylation at 10 uM after 6 to 24 hrs by Western blot method2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID476507Induction of bone mineral density in SAMP6 mouse assessed as spine BMD at 10 mg/kg/day, po measured last 2 months2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID57493Percent decrease in plasma LDL-cholesterol in dog was determined after oral administration of a dose of 10 mg/kg for 19 days1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID1315652Antimycobacterial activity against Mycobacterium tuberculosis H37Rv measured daily for 8 days by GFP-based fluorescence assay2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID85689Percentage lowering of the total serum cholesterol in male hamsters at a dose of 10 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
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).
AID444057Fraction escaping hepatic elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1695290Antileishmanial activity against amastigote form of Leishmania infantum MCAN_UY_2015_bPL7 isolate assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
AID357815Reversal of reduction in survivin expression in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of 100 uM mevalonate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1072575Growth inhibition of PR, ER, HER2-negative human MDA-MB-231 cells at 1 uM after 48 hrs by WST-1 assay in presence of mevalonate2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID342985Decrease in hepatic cholesterol level in hypercholesterolemic Wistar rat at 20 mg/kg, po for 1 week with diet2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Synthesis, DNA binding, and cytotoxic evaluation of new analogs of diallyldisulfide, an active principle of garlic.
AID234423The compound was tested for the relative potency with respect to standard compound BMY-219501990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
AID357809Induction of cell cycle arrest in human SW480 cells by accumulation at G0/G1 phase at 20 uM after 48 hrs by flow cytometry2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID251131Percent decrease in weight of cholesterol in liver wet tissue after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
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.
AID540210Clearance in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1140415Inhibition of HMG-coA reductase in human RPMI-8226 cells assessed as disruption of Rap1a geranylgeranylation at 10 uM after 48 hrs by western blot analysis in presence of 1 mM mevalonate2014Bioorganic & medicinal chemistry, May-01, Volume: 22, Issue:9
Geranyl and neryl triazole bisphosphonates as inhibitors of geranylgeranyl diphosphate synthase.
AID85818Percentage lowering of the total serum cholesterol in male hamsters at a dose of 50 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID187296Inhibition of hepatic cholesterol de novo synthesis in male rats after po administration, relative to mevinolin1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID444052Hepatic clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID81002Tested for inhibition of rat liver microsomal HMG-CoA reductase1994Journal of medicinal chemistry, Sep-30, Volume: 37, Issue:20
Synthesis and biological activity of bile acid-derived HMG-CoA reductase inhibitors. The role of 21-methyl in recognition of HMG-CoA reductase and the ileal bile acid transport system.
AID249812Weight of triglyceride in liver wet tissue after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID83304Inhibition of cellular HMG-CoA reductase in cultures of hepatic cells (HEP G2, a human hepatoma cell line) relative to mevinolin1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID83862Effect on total serum cholesterol in male hamsters at a dose of 25 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID1309366Inhibition of GGDPS in human RPMI8266 cells assessed as lambda light chain levels at 5 uM after 48 hrs by ELISA in presence of GGDP2016Bioorganic & medicinal chemistry, 08-15, Volume: 24, Issue:16
A new motif for inhibitors of geranylgeranyl diphosphate synthase.
AID81173Potency relative to mevinolin was determined with respect to IC50. Mevinolin was assigned a value of 1001991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID358046Decrease in survivin mRNA expression in human SW480 cells at 20 uM after 48 hrs by RT-PCR technique2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
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).
AID1473810Ratio of drug concentration at steady state in human at 10 to 80 mg, po QD after 24 hrs to IC50 for human BSEP overexpressed in Sf9 insect cells2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID358056Reversal of decrease in isoprenylated Ras level in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of mevalonate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1742233Hypolipidemic activity in oleic, palmitic, linoleic and arachidonic acid 29:47:18:6 (v/v)-induced hyperlipidemia in human HepG2 cells assessed as reduction in lipid content at 10 uM by Oil Red O staining based assay relative to control2020European journal of medicinal chemistry, Nov-01, Volume: 205Synthesis of natural 3'-Prenylchalconaringenin and biological evaluation of ameliorating non-alcoholic fatty liver disease and metabolic syndrome.
AID444054Oral bioavailability in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID358053Reversal of growth inhibition of human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of geranylgeranyl pyrophosphate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1324334Cytotoxicity against human MCF7 cells assessed as growth inhibition after 24 to 48 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID1220875Apparent permeability of the compound in P-gp knockdown human Caco2 cells at 10 uM up to 120 mins by reverse-phase liquid chromatography with triple-quadrupole tandem mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Use of transporter knockdown Caco-2 cells to investigate the in vitro efflux of statin drugs.
AID180692In vitro inhibitory potency for cholesterol synthesis was measured in rat adrenals1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
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).
AID1140416Inhibition of HMG-coA reductase in human RPMI-8226 cells assessed as disruption of Rap1a geranylgeranylation at 10 uM after 48 hrs by western blot analysis in presence of 10 uM GGPP2014Bioorganic & medicinal chemistry, May-01, Volume: 22, Issue:9
Geranyl and neryl triazole bisphosphonates as inhibitors of geranylgeranyl diphosphate synthase.
AID228653The compound was tested in vivo for the inhibition of cholesterol biosynthesis in chow-fed rats at 1.0 mg/kg.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID322753Inhibition of human CYP51 expressed in Topp 3 cells by lanosterol demethylase assay2007Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 35, Issue:3
Three-dimensional quantitative structure-activity relationship analysis of human CYP51 inhibitors.
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.
AID1072594Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 1 uM after 30 hrs by flow cytometer (Rvb = 49.8 +/-1.5%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1072609Total growth inhibition of ER-positive, HER2-negative human MCF7 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID86397Tested for inhibition of cholesterol biosynthesis in HEP G2 cells1994Journal of medicinal chemistry, Sep-30, Volume: 37, Issue:20
Synthesis and biological activity of bile acid-derived HMG-CoA reductase inhibitors. The role of 21-methyl in recognition of HMG-CoA reductase and the ileal bile acid transport system.
AID1519525Inhibition of GGTase-2 in human RPMI8226 cells assessed as ratio of calnexin to Rab6 level at 10 uM after 48 hrs by immunoblot analysis relative to control2019Bioorganic & medicinal chemistry letters, 12-15, Volume: 29, Issue:24
Novel benzimidazole phosphonates as potential inhibitors of protein prenylation.
AID83858Effect on total serum cholesterol in male hamsters at a dose of 100 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID629779Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 5 uM2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID1220874Apparent permeability of the compound in vector transfected human Caco2 cells at 10 uM up to 120 mins by reverse-phase liquid chromatography with triple-quadrupole tandem mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 39, Issue:7
Use of transporter knockdown Caco-2 cells to investigate the in vitro efflux of statin drugs.
AID357810Induction of cell cycle arrest in human SW480 cells by accumulation at S phase at 20 uM after 48 hrs by flow cytometry2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID358063Inhibition of FBS-stimulated increase in Akt phosphorylation in human SW480 cells at 20 uM by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID629780Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 10 uM2011Bioorganic & medicinal chemistry letters, Nov-15, Volume: 21, Issue:22
Discovery and synthesis of novel substituted benzocoumarins as orally active lipid modulating agents.
AID444058Volume of distribution at steady state in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID85815Percentage lowering of the total serum cholesterol in male hamsters at a dose of 25 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID358054Reversal of growth inhibition of human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of squalene2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID231150Ratio of the mean IC50 for sterol-synthesis inhibition of testes relative to hepatocytes in rat1989Journal of medicinal chemistry, Sep, Volume: 32, Issue:9
A potent, tissue-selective, synthetic inhibitor of HMG-CoA reductase.
AID430556Enhancement of BMP-2 expression in mouse MC3T3-E1 cells assessed as upregulation rate at 0.4 uM2009Bioorganic & medicinal chemistry letters, Aug-01, Volume: 19, Issue:15
Synthesis and evaluation of 1-(benzo[b]thiophen-2-yl)ethanone analogues as novel anti-osteoporosis agents acting on BMP-2 promotor.
AID679601TP_TRANSPORTER: inhibition of Digoxin transepithelial transport (basal to apical) (Digoxin: 5 uM, Lovastatin: 100 uM) in Caco-2 cells1999Pharmaceutical research, Mar, Volume: 16, Issue:3
Interrelationship between substrates and inhibitors of human CYP3A and P-glycoprotein.
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.
AID180693In vitro inhibitory potency for cholesterol synthesis was measured in rat ileum1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
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).
AID1072582Induction of apoptosis in human MDA-MB-231 cells assessed as necrotic cells at 1 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 4.4 +/-0.4%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID678835TP_TRANSPORTER: transepithelial transport (basal to apical) in MDR1-expressing LLC-PK1 cells1999Pharmaceutical research, Mar, Volume: 16, Issue:3
Interrelationship between substrates and inhibitors of human CYP3A and P-glycoprotein.
AID1409613Selectivity ratio: ratio of AUC (viral infection %) of SARS-CoV-2 in the Vero E6 cell line compared to AUC (cytotoxicity %) of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID1502951Reduction in total cholesterol level in patient with moderate hypercholesterolemia at 20 to 80 mg/day2017European journal of medicinal chemistry, Nov-10, Volume: 140Lipid lowering agents of natural origin: An account of some promising chemotypes.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
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.
AID1443991Induction of mitochondrial dysfunction in Sprague-Dawley rat liver mitochondria assessed as inhibition of mitochondrial respiration per mg mitochondrial protein measured for 20 mins by A65N-1 oxygen probe based fluorescence assay2014Hepatology (Baltimore, Md.), Sep, Volume: 60, Issue:3
Human drug-induced liver injury severity is highly associated with dual inhibition of liver mitochondrial function and bile salt export pump.
AID358058Reversal of decrease in isoprenylated Ras level in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of geranylgeranyl pyrophosphate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
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.
AID1072589Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at G2/M phase at 10 uM after 30 hrs by flow cytometer (Rvb = 17.1 +/-2.1%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1473808AUC in human at 10 to 80 mg, po QD after 24 hrs2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID412236Lipophilicity, log P of the compound2009Bioorganic & medicinal chemistry, Jan-01, Volume: 17, Issue:1
Comparison of benzil and trifluoromethyl ketone (TFK)-mediated carboxylesterase inhibition using classical and 3D-quantitative structure-activity relationship analysis.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID83485In vitro inhibitory activity was measured against rat liver HMG-CoA reductase using [2-14C]-acetate incorporation1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
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).
AID680260TP_TRANSPORTER: inhibition of Taurocholate uptake (Taurocholate: 0.5 uM, Lovastatin: 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.
AID189706Compound was tested for its relative Cholesterol Synthesis Inhibition as compared to compactin in rats.1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
Inhibitors of cholesterol biosynthesis. 4. trans-6-[2-(substituted-quinolinyl)ethenyl/ethyl]tetrahydro-4-hydroxy-2 H-pyran-2-ones, a novel series of HMG-CoA reductase inhibitors.
AID357806Growth inhibition of human LS180 cells after 96 hrs by MTS assay2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
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.
AID406852Antiplasmodial activity against chloroquine-resistant Plasmodium falciparum Bre12007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID358051Blockade of growth inhibition of human LS180 cells after 72 hrs by MTS method2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID357807Growth inhibition of human HT29 cells after 96 hrs by MTS assay2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID83294Inhibition of cellular HMG-CoA reductase in cultures of human HEP G2 cells, determined by decreased incorporation of sodium [14C]acetate into cholesterol.1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 1. Lactones of pyridine- and pyrimidine-substituted 3,5-dihydroxy-6-heptenoic (-heptanoic) acids.
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.
AID1502950Increase in HDL-C level in patient with moderate hypercholesterolemia at 20 to 80 mg/day2017European journal of medicinal chemistry, Nov-10, Volume: 140Lipid lowering agents of natural origin: An account of some promising chemotypes.
AID362085Inhibition of sICAM1/LFA1 interaction-mediated human THP1 cell adhesion at 25 ug/mL after 1 hr by ELISA2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition.
AID515874Inhibition of FDPS in human K562 cells assessed as reduction Ras protein farnesylation after 48 hrs by Western blotting in presence of mevalonate and FPP2010Bioorganic & medicinal chemistry, Oct-15, Volume: 18, Issue:20
Synthesis and biological evaluation of a series of aromatic bisphosphonates.
AID406853Antiplasmodial activity against chloroquine-resistant Plasmodium falciparum FCR32007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID1309365Inhibition of GGDPS in human RPMI8266 cells assessed as disruption of Rap1a geranylgeranylation at 5 uM after 48 hrs by immunoblot analysis in presence of GGDP2016Bioorganic & medicinal chemistry, 08-15, Volume: 24, Issue:16
A new motif for inhibitors of geranylgeranyl diphosphate synthase.
AID527844Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in total cholesterol level at 25 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID1502949Reduction in LDL-C level in patient with moderate hypercholesterolemia at 20 to 80 mg/day2017European journal of medicinal chemistry, Nov-10, Volume: 140Lipid lowering agents of natural origin: An account of some promising chemotypes.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID406849Antiplasmodial activity against chloroquine-sensitive Plasmodium falciparum 3D72007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID57499Percent increase in plasma HDL-cholesterol in dog was determined after oral administration of a dose of 10 mg/kg for 19 days1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID81379Inhibition of the incorporation of sodium [14C]acetate into cholesterol in HEP G2 cells.1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID228837Inhibition of v-ras posttranslational processing in NIH3T3 cells at 15 uM1994Journal of medicinal chemistry, Mar-18, Volume: 37, Issue:6
Pseudopeptide inhibitors of Ras farnesyl-protein transferase.
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.
AID476513Induction of bone mineral density in SAMP6 mouse assessed as left hind leg BMD at 10 mg/kg/day, po measured after 3 months2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID81380Inhibition of HMG-CoA reductase compared to mevinolin.1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
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]
AID1072574Growth inhibition of PR, ER, HER2-negative human MDA-MB-231 cells after 48 hrs by WST-1 assay in presence of geranylgeranyl pyrophosphate2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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]
AID167720Tested for inhibition of Na+ -dependent [3H]taurocholate uptake into rabbit ileal brush border membrane vesicles1994Journal of medicinal chemistry, Sep-30, Volume: 37, Issue:20
Synthesis and biological activity of bile acid-derived HMG-CoA reductase inhibitors. The role of 21-methyl in recognition of HMG-CoA reductase and the ileal bile acid transport system.
AID126807In vivo percent change of total cholesterol in monkeys at 20 mg/kg/day for 5 days dose1997Journal of medicinal chemistry, Jul-04, Volume: 40, Issue:14
(1 alpha, 2 beta, 3 beta, 4 alpha)-1,2-bis[N-propyl-N-(4-phenoxybenzyl) amino]carbonyl]cyclobutane-3,4-dicarboxylic acid (A-87049): a novel potent squalene synthase inhibitor.
AID1324336Cytotoxicity against human MDA-MB-231 cells assessed as growth inhibition after 24 to 48 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID357814Decrease in survivin expression in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID83860Effect on total serum cholesterol in male hamsters at a dose of 150 mg/kg orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID242962Ratio of HMG-CoA reductase to mevalinate2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID1742243Hypolipidemic activity in mouse 3T3-L1 mature adipocytes assessed as reduction in lipid content at 10 uM by Oil Red O staining based assay relative to control2020European journal of medicinal chemistry, Nov-01, Volume: 205Synthesis of natural 3'-Prenylchalconaringenin and biological evaluation of ameliorating non-alcoholic fatty liver disease and metabolic syndrome.
AID1695291Antileishmanial activity against amastigote form of Leishmania infantum MCAN_UY_2015_gCH2 isolate assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
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).
AID1409611AUC (cytotoxicity %) of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID681370TP_TRANSPORTER: inhibition of calcein-AM efflux in MRP2-expressing MDCK cells2005Drug metabolism and disposition: the biological fate of chemicals, Apr, Volume: 33, Issue:4
Differential interaction of 3-hydroxy-3-methylglutaryl-coa reductase inhibitors with ABCB1, ABCC2, and OATP1B1.
AID540213Half life in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID362084Inhibition of sICAM1/LFA1 interaction-mediated human THP1 cell adhesion after 1 hr by ELISA2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition.
AID1072590Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at S phase at 10 uM after 30 hrs by flow cytometer (Rvb = 33.1 +/-0.3%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID362088Inhibition of sICAM1/LFA1 interaction-mediated human THP1 cell adhesion at 3.13 ug/mL after 1 hr by ELISA2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition.
AID425653Renal clearance in human2009Journal of medicinal chemistry, Aug-13, Volume: 52, Issue:15
Physicochemical determinants of human renal clearance.
AID358055Decrease in isoprenylated Ras level in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1739429Cytotoxicity against mouse MC3T3-E1 cells at 100 uM2020European journal of medicinal chemistry, Aug-15, Volume: 200Substituted benzothiophene and benzofuran derivatives as a novel class of bone morphogenetic Protein-2 upregulators: Synthesis, anti-osteoporosis efficacies in ovariectomized rats and a zebrafish model, and ADME properties.
AID342988Decrease in serum triglyceride level in hypercholesterolemic Wistar rat at 20 mg/kg, po for 1 week with diet2008Bioorganic & medicinal chemistry, Aug-01, Volume: 16, Issue:15
Synthesis, DNA binding, and cytotoxic evaluation of new analogs of diallyldisulfide, an active principle of garlic.
AID444053Renal clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
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.
AID527845Antihyperlipidemic activity against high fat diet fed gloden syrian hamster assessed as change in HDL level at 25 mg/kg, po for 7 days2010Bioorganic & medicinal chemistry letters, Nov-15, Volume: 20, Issue:22
Synthesis and antihyperlipidemic activity of novel coumarin bisindole derivatives.
AID81401Tested for ability to inhibit incorporation of [14C]acetate into cholesterol in cultured human hepatoma (HEP-G2) cells; 0.061-0.101993Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23
HMG-CoA reductase inhibitors: design, synthesis, and biological activity of tetrahydroindazole-substituted 3,5-dihydroxy-6-heptenoic acid sodium salts.
AID1072580Induction of apoptosis in human MDA-MB-231 cells assessed as apoptotic cells at 5 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 2.4 +/-0.5%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1072611Cytotoxicity against PR, ER, HER2-negative human MDA-MB-231 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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.
AID358059Reversal of decrease in isoprenylated Ras level in human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of squalene2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID51952Hypocholesterolemic activity in Cholestyramine-primed Beagle dogs at dose of 1.0 mg/kg four weeks after.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID1072579Induction of apoptosis in human MDA-MB-231 cells assessed as necrotic cells at 5 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 4.4 +/-0.4%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID619568Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 1 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1309367Inhibition of GGDPS in human RPMI8266 cells assessed as disruption of Rap1a geranylgeranylation at 5 uM after 48 hrs by immunoblot analysis in presence of mevalonate2016Bioorganic & medicinal chemistry, 08-15, Volume: 24, Issue:16
A new motif for inhibitors of geranylgeranyl diphosphate synthase.
AID180694In vitro inhibitory potency for cholesterol synthesis was measured in rat lens epithelium1990Journal of medicinal chemistry, Nov, Volume: 33, Issue:11
Synthesis, biological profile, and quantitative structure-activity relationship of a series of novel 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID83477In vitro inhibition of HMG-CoA reductase of rat liver1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID406851Antiplasmodial activity against chloroquine-resistant Plasmodium falciparum W22007Antimicrobial agents and chemotherapy, Jul, Volume: 51, Issue:7
Atorvastatin is 10-fold more active in vitro than other statins against Plasmodium falciparum.
AID680264TP_TRANSPORTER: inhibition of Pravastatin uptake (Pravastatin: 0.5 uM, Lovastatin: 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.
AID444055Fraction absorbed in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID358045Effect on Bax expression in human SW480 cells2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID515870Inhibition of GGTase1 in human K562 cells assessed as reduction of Rap1a protein geranylgeranylation after 48 hrs by Western blotting2010Bioorganic & medicinal chemistry, Oct-15, Volume: 18, Issue:20
Synthesis and biological evaluation of a series of aromatic bisphosphonates.
AID167721Tested for inhibition of Na+ -dependent [3H]taurocholate uptake into rabbit ileal brush border membrane vesicles1994Journal of medicinal chemistry, Sep-30, Volume: 37, Issue:20
Synthesis and biological activity of bile acid-derived HMG-CoA reductase inhibitors. The role of 21-methyl in recognition of HMG-CoA reductase and the ileal bile acid transport system.
AID93340In vitro inhibition of recombinant ICAM-1 binding to purified immobilized LFA-1 using cell-free assay2004Bioorganic & medicinal chemistry letters, May-17, Volume: 14, Issue:10
Statin-derived 1,3-oxazinan-2-ones as submicromolar inhibitors of LFA-1/ICAM-1 interaction: stabilization of the metabolically labile vanillyl side chain.
AID1631436Antiviral activity against Dengue virus 2 NGC infected in human A549 cells assessed as reduction in virus replication after 48 hrs by renilla luciferase reporter gene assay2016Journal of medicinal chemistry, 06-23, Volume: 59, Issue:12
The Medicinal Chemistry of Dengue Virus.
AID1129361Unbound fraction in HEK293 cell homogenate at 0.1 uM by equilibrium dialysis based UPLC-MS/MS analysis2014Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7
A high-throughput cell-based method to predict the unbound drug fraction in the brain.
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).
AID357808Reversal of growth inhibition of human SW480 cells at 20 uM after 48 hrs by MTS assay in presence of >50 uM mevalonate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID298856Inhibition of ACAT in Albino rabbit intestinal mucosa2007Bioorganic & medicinal chemistry letters, Apr-01, Volume: 17, Issue:7
Synthesis and biological evaluation of unprecedented classes of spiro-beta-lactams and azido-beta-lactams as acyl-CoA:cholesterol acyltransferase inhibitors.
AID619569Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 5 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1168422Lipid-lowering effect in human HepG2 cells assessed as reduction in oleic acid-induced triglyceride accumulation at 10 uM after 24 hrs by oil-red O staining based spectrophotometry2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Lipid-lowering effects of farnesylquinone and related analogues from the marine-derived Streptomyces nitrosporeus.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID1739396Upregulation of Runx2 transcriptional activity in mouse MC3T3-E1 cells transfected with p6OSE2-luc at 10 uM incubated for 48 hrs by firefly luciferase reporter gene assay relative to control2020European journal of medicinal chemistry, Aug-15, Volume: 200Substituted benzothiophene and benzofuran derivatives as a novel class of bone morphogenetic Protein-2 upregulators: Synthesis, anti-osteoporosis efficacies in ovariectomized rats and a zebrafish model, and ADME properties.
AID540212Mean residence time in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID619487Hypolipidemic activity in high fat diet fed Syrian golden hamster assessed as reduction of total cholesterol level at 25 mg/kg, po for 7 days2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1647697Inhibition of human integrin alphaL beta2 assessed as reduction in integrin alphaL beta2/ICAM1 protein-protein interaction by ELISA2020Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11
Insights into Protein-Ligand Interactions in Integrin Complexes: Advances in Structure Determinations.
AID444050Fraction unbound in human plasma2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1324335Cytotoxicity against human T47D cells assessed as growth inhibition after 24 to 48 hrs by MTT assay2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID1072593Cell cycle arrest in PR, ER, HER2-negative human MDA-MB-231 cells assessed as accumulation at S phase at 1 uM after 30 hrs by flow cytometer (Rvb = 33.1 +/-0.3%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
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.
AID251132Percent decrease in weight of triglyceride in liver wet tissue after treatment with compound at 20 mg/kg dose for seven days2004Bioorganic & medicinal chemistry letters, Nov-01, Volume: 14, Issue:21
Bis[3-(4'-substituted phenyl)prop-2-ene]disulfides as a new class of antihyperlipidemic compounds.
AID625277FDA Liver Toxicity Knowledge Base Benchmark Dataset (LTKB-BD) drugs of less concern for DILI2011Drug discovery today, Aug, Volume: 16, Issue:15-16
FDA-approved drug labeling for the study of drug-induced liver injury.
AID1283271Inhibition of HMGCoA reductase in Dhcr7-deficient mouse Neuro2a cells assessed as decrease in 7-DHC levels at 1 uM by LC-MS/GC-MS analysis2016Journal of medicinal chemistry, Feb-11, Volume: 59, Issue:3
The Effect of Small Molecules on Sterol Homeostasis: Measuring 7-Dehydrocholesterol in Dhcr7-Deficient Neuro2a Cells and Human Fibroblasts.
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).
AID476511Induction of BMP2 expression in mouse calcarial MC3T3-E1 cells stably transfected with mouse BMP2 promotor-luciferase assessed as upregulation rate at 0.4 uM2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
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).
AID167719Tested for inhibition of Na+ -dependent [3H]taurocholate uptake into rabbit ileal brush border membrane vesicles1994Journal of medicinal chemistry, Sep-30, Volume: 37, Issue:20
Synthesis and biological activity of bile acid-derived HMG-CoA reductase inhibitors. The role of 21-methyl in recognition of HMG-CoA reductase and the ileal bile acid transport system.
AID680569TP_TRANSPORTER: inhibition of Taurocholate uptake (Taurocholate: 0.5 uM, Lovastatin: 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.
AID126806In vivo percent change of LDL cholesterol in monkeys at 20 mg/kg/day for 5 days dose1997Journal of medicinal chemistry, Jul-04, Volume: 40, Issue:14
(1 alpha, 2 beta, 3 beta, 4 alpha)-1,2-bis[N-propyl-N-(4-phenoxybenzyl) amino]carbonyl]cyclobutane-3,4-dicarboxylic acid (A-87049): a novel potent squalene synthase inhibitor.
AID476503Induction of bone mineral density in SAMP6 mouse assessed as spine BMD at 10 mg/kg/day, po measured after 3 months2010Journal of medicinal chemistry, Feb-25, Volume: 53, Issue:4
Substituted benzothiophene or benzofuran derivatives as a novel class of bone morphogenetic protein-2 up-regulators: synthesis, structure-activity relationships, and preventive bone loss efficacies in senescence accelerated mice (SAMP6) and ovariectomized
AID1168421Lipid-lowering effect in human HepG2 cells assessed as reduction in oleic acid-induced total cholesterol accumulation at 10 uM after 24 hrs by oil-red O staining based spectrophotometry2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Lipid-lowering effects of farnesylquinone and related analogues from the marine-derived Streptomyces nitrosporeus.
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
AID722629Binding affinity to integrin alpha2 I-domain (unknown origin)2013Journal of medicinal chemistry, Feb-14, Volume: 56, Issue:3
Design, synthesis, and functional evaluation of leukocyte function associated antigen-1 antagonists in early and late stages of cancer development.
AID619570Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 10 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
AID1072583Induction of apoptosis in human MDA-MB-231 cells assessed as apoptotic cells at 1 uM after 48 hrs by annexin V/propidium iodide based flow cytometry (Rvb = 2.4 +/-0.5%)2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID631055Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum total cholesterol level at 25 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.
AID619571Inhibition of HMG-CoA reductase using HMG-CoA as substrate at 20 uM by spectrophotometry in presence of NADPH2011European journal of medicinal chemistry, Oct, Volume: 46, Issue:10
Discovery of a new class of HMG-CoA reductase inhibitor from Polyalthia longifolia as potential lipid lowering agent.
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.
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.
AID1140414Inhibition of HMG-coA reductase in human RPMI-8226 cells assessed as disruption of Rap1a geranylgeranylation at 10 uM after 48 hrs by western blot analysis2014Bioorganic & medicinal chemistry, May-01, Volume: 22, Issue:9
Geranyl and neryl triazole bisphosphonates as inhibitors of geranylgeranyl diphosphate synthase.
AID681127TP_TRANSPORTER: inhibition of LDS-751 efflux in NIH-3T3-G185 cells2001Biochemical and biophysical research communications, Nov-30, Volume: 289, Issue:2
Active transport of fluorescent P-glycoprotein substrates: evaluation as markers and interaction with inhibitors.
AID291332Apoptosis in human STS-26T cells at 1 uM after 24 hrs2007Journal of medicinal chemistry, Jul-12, Volume: 50, Issue:14
Synthesis, biochemical, and cellular evaluation of farnesyl monophosphate prodrugs as farnesyltransferase inhibitors.
AID29811Oral bioavailability in human2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID357811Induction of cell cycle arrest in human SW480 cells by accumulation at G2/M phase at 20 uM after 48 hrs by flow cytometry2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID358048Inhibition of survivin expression in parent human LS180 cells at 20 uM by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1409608AUC (viral infection %) for SARS-CoV-2 in the Vero E6 cell line at 48 h by immunofluorescence-based assay (detecting the viral NP protein in the nucleus of the Vero E6 cells).2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
AID85813Percentage lowering of the total serum cholesterol in male hamsters at a dose of 150 mg/dL orally administered for 14 days1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Selective inhibition of mammalian lanosterol 14 alpha-demethylase: a possible strategy for cholesterol lowering.
AID1443990Inhibition of recombinant human BSEP expressed in baculovirus infected sf9 cell plasma membrane vesicles assessed as reduction in ATP-dependent [3H]-taurocholate uptake in to vesicles after 15 to 20 mins2014Hepatology (Baltimore, Md.), Sep, Volume: 60, Issue:3
Human drug-induced liver injury severity is highly associated with dual inhibition of liver mitochondrial function and bile salt export pump.
AID1409609Cytotoxicity of compound against Vero E6 cells by MTT assay.2020Nature, 07, Volume: 583, Issue:7816
A SARS-CoV-2 protein interaction map reveals targets for drug repurposing.
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.
AID540211Fraction unbound in human after iv administration2008Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7
Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1309368Inhibition of GGDPS in human RPMI8266 cells assessed as lambda light chain levels at 5 uM after 48 hrs by ELISA in presence of mevalonate2016Bioorganic & medicinal chemistry, 08-15, Volume: 24, Issue:16
A new motif for inhibitors of geranylgeranyl diphosphate synthase.
AID1168417Lipid-lowering effect in human HepG2 cells assessed as reduction in oleic acid-induced lipid accumulation at 1 uM after 6 hrs by oil-red O staining based spectrophotometry2014Bioorganic & medicinal chemistry letters, Nov-15, Volume: 24, Issue:22
Lipid-lowering effects of farnesylquinone and related analogues from the marine-derived Streptomyces nitrosporeus.
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.
AID83291Concentration required to inhibit HMG-CoA reductase by 50% was determined in Hep G2 cell line1992Journal of medicinal chemistry, Sep-04, Volume: 35, Issue:18
Synthesis and biological evaluation of dihydroeptastatin, a novel inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase.
AID1210014Inhibition of recombinant CYP2J2 (unknown origin)-mediated astemizole O-demethylation assessed as remaining activity at 30 uM after 5 mins by LC-MS/MS analysis relative to control2012Drug metabolism and disposition: the biological fate of chemicals, May, Volume: 40, Issue:5
Identifying a selective substrate and inhibitor pair for the evaluation of CYP2J2 activity.
AID27167Delta logD (logD6.5 - logD7.4)2000Journal of medicinal chemistry, Jun-29, Volume: 43, Issue:13
QSAR model for drug human oral bioavailability.
AID1351280Hypocholesterolemic effect in hypercholesterolemia patient assessed as decrease in LDL cholesterol level2018European journal of medicinal chemistry, Jan-20, Volume: 144Polymeric bile acid sequestrants: Review of design, in vitro binding activities, and hypocholesterolemic effects.
AID81171In vitro inhibition of solubilized, partially purified rat liver HMG-CoA reductase relative to mevinolin1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID362086Inhibition of sICAM1/LFA1 interaction-mediated human THP1 cell adhesion at 12.50 ug/mL after 1 hr by ELISA2008Bioorganic & medicinal chemistry letters, Aug-15, Volume: 18, Issue:16
Alkamides from the fruits of Piper longum and Piper nigrum displaying potent cell adhesion inhibition.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1072597Cytotoxicity against human HMEC assessed as growth inhibition after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID1315654Cytotoxicity against human KB cells by resazurin microplate assay2016Journal of natural products, 06-24, Volume: 79, Issue:6
Lovastatin Analogues from the Soil-Derived Fungus Aspergillus sclerotiorum PSU-RSPG178.
AID291331Cell cycle arrest in human STS-26T cells assessed as accumulation in S phase at 1 uM after 24 hrs2007Journal of medicinal chemistry, Jul-12, Volume: 50, Issue:14
Synthesis, biochemical, and cellular evaluation of farnesyl monophosphate prodrugs as farnesyltransferase inhibitors.
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.
AID358061Inhibition of FBS-stimulated increase in Ras protein expression in human SW480 cells assessed as GTP-bound protein at 20 uM by immunoblot analysis2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1072600Total growth inhibition of PR, ER, HER2-negative human MDA-MB-468 cells after 48 hrs by WST-1 assay2014Bioorganic & medicinal chemistry, Mar-15, Volume: 22, Issue:6
Characterization of lovastatin-docosahexaenoate anticancer properties against breast cancer cells.
AID83476In vitro inhibition of HMG-CoA reductase in solubilized rat liver.1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID444051Total clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID83165Tested in vitro for the inhibition of HMG-CoA reductase from partially purified microsomal preparations.1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID187304Potency relative to mevinolin was determined with respect to IC50. Mevinolin was assigned a value of 1001991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID358052Reversal of growth inhibition of human SW480 cells at 20 uM after 48 hrs by immunoblot analysis in presence of farnesyl pyrophosphate2007The Journal of biological chemistry, Jul-06, Volume: 282, Issue:27
Survivin down-regulation plays a crucial role in 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor-induced apoptosis in cancer.
AID1695292Antileishmanial activity against amastigote form of Leishmania infantum MCAN_UY_2015_bCH11 isolate assessed as decrease in parasite viability measured after 72 hrs by resazurin assay2020RSC medicinal chemistry, Aug-01, Volume: 11, Issue:8
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.
AID631054Antidyslipidemic activity in high fat diet-fed dyslipidemic syrian golden hamster model assessed as decrease in serum triglyceride level at 25 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.
AID1324340Induction of CHK2 phosphorylation in human MDA-MB-231 cells at 10 uM after 6 to 24 hrs by Western blot method2016Bioorganic & medicinal chemistry letters, 11-15, Volume: 26, Issue:22
Synthesis and biological evaluation of lovastatin-derived aliphatic hydroxamates that induce reactive oxygen species.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS 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.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
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.
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.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588459High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504810Antagonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588461High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, Validation compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588460High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, Validation Compound Set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID504812Inverse Agonists of the Thyroid Stimulating Hormone Receptor: HTS campaign2010Endocrinology, Jul, Volume: 151, Issue:7
A small molecule inverse agonist for the human thyroid-stimulating hormone receptor.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
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.
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.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
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.
AID1346822Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1990Journal of medicinal chemistry, Jan, Volume: 33, Issue:1
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 2. Derivatives of 7-(1H-pyrrol-3-yl)-substituted-3,5-dihydroxyhept-6(E)-enoic (-heptanoic) acids.
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1991Journal of medicinal chemistry, Jan, Volume: 34, Issue:1
Inhibitors of cholesterol biosynthesis. 4. trans-6-[2-(substituted-quinolinyl)ethenyl/ethyl]tetrahydro-4-hydroxy-2 H-pyran-2-ones, a novel series of HMG-CoA reductase inhibitors.
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1991Journal of medicinal chemistry, Oct, Volume: 34, Issue:10
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.
AID1346822Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1980Proceedings of the National Academy of Sciences of the United States of America, Jul, Volume: 77, Issue:7
Mevinolin: a highly potent competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase and a cholesterol-lowering agent.
AID1346838Rat hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1993Journal of medicinal chemistry, Nov-12, Volume: 36, Issue:23
Inhibitors of cholesterol biosynthesis. 2. 3,5-Dihydroxy-7-(N-pyrrolyl)-6-heptenoates, a novel series of HMG-CoA reductase inhibitors.
AID1346822Human hydroxymethylglutaryl-CoA reductase (Lanosterol biosynthesis pathway)1992Journal of medicinal chemistry, May-29, Volume: 35, Issue:11
Inhibitors of cholesterol biosynthesis. 6. trans-6-[2-(2-N-heteroaryl-3,5-disubstituted- pyrazol-4-yl)ethyl/ethenyl]tetrahydro-4-hydroxy-2H-pyran-2-ones.
AID1346741Human Pregnane X receptor (1I. Vitamin D receptor-like receptors)1998The Journal of clinical investigation, Sep-01, Volume: 102, Issue:5
The human orphan nuclear receptor PXR is activated by compounds that regulate CYP3A4 gene expression and cause drug interactions.
AID1811Experimentally measured binding affinity data derived from PDB1999Journal of molecular biology, Sep-10, Volume: 292, Issue:1
Structural basis for LFA-1 inhibition upon lovastatin binding to the CD11a I-domain.
AID977608Experimentally measured binding affinity data (IC50) for protein-ligand complexes derived from PDB1999Journal of molecular biology, Sep-10, Volume: 292, Issue:1
Structural basis for LFA-1 inhibition upon lovastatin binding to the CD11a I-domain.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1224864HCS microscopy assay (F508del-CFTR)2016PloS one, , Volume: 11, Issue:10
Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (4,596)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990450 (9.79)18.7374
1990's1937 (42.15)18.2507
2000's1234 (26.85)29.6817
2010's796 (17.32)24.3611
2020's179 (3.89)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 80.74

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 Index80.74 (24.57)
Research Supply Index8.62 (2.92)
Research Growth Index4.91 (4.65)
Search Engine Demand Index148.83 (26.88)
Search Engine Supply Index2.01 (0.95)

This Compound (80.74)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials698 (14.46%)5.53%
Reviews347 (7.19%)6.00%
Case Studies233 (4.83%)4.05%
Observational2 (0.04%)0.25%
Other3,548 (73.49%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (60)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Linking Inhibition From Molecular to Systems and Cognitive Levels: a Preclinical and Clinical Approach in Autism Spectrum Disorders and Neurofibromatosis. [NCT03826940]16 participants (Actual)Interventional2019-02-19Completed
A Phase 2 Trial of Lovastatin for Modification of Abnormal Breast Duct Cytology and Risk-Associated Biomarkers in Women at High Inherited Risk of Breast Cancer [NCT00285857]Phase 230 participants (Actual)Interventional2005-11-30Terminated(stopped due to Slow accrual)
Open-label, Pilot Study to Assess Cholesterol-Lovastatin Solution in the Treatment of Syndromic Ichthyoses [NCT01110642]Phase 20 participants (Actual)Interventional2011-07-31Withdrawn(stopped due to Study was withdrawn due to lack of eligible population for study)
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
Human Cytochrome P450 4F Enzymes and Drug Interactions [NCT01250535]Phase 119 participants (Actual)Interventional2010-12-31Completed
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)
The Effect of Lovastatin Gel in the Treatment of Chronic Periodontitis Randomized Controlled Trial Split-mouth [NCT03178526]Phase 2/Phase 315 participants (Actual)Interventional2015-12-24Completed
[NCT02389868]Phase 215 participants (Anticipated)Interventional2015-02-28Completed
Neurophysiological and Acute Pharmacological Studies in FXS Patients [NCT02998151]Early Phase 129 participants (Actual)Interventional2016-01-31Completed
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
Topical Treatment for Superficial Disseminated Actinic Porokeratosis: A Single-Blinded Comparison Between Lovastatin/Cholesterol and Lovastatin [NCT04359823]Phase 131 participants (Actual)Interventional2020-08-24Completed
Lovastatin for Treatment of Brain Arteriovenous Malformations:a Double-blind, Placebo-controlled Randomized Trial [NCT04297033]Phase 21,244 participants (Anticipated)Interventional2021-01-01Not yet recruiting
Antiretroviral Effect of Lovastatin on HIV-1-infected Individuals Without Highly Active Antiretroviral Therapy (HAART): A Phase-II Randomized Clinical Trial (RCT) [NCT00721305]Phase 2112 participants (Actual)Interventional2008-08-31Completed
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
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
An Open-randomized, Balanced, Crossover Relative Bioavailability Study of Lovastatin and Its ß-hydroxy Acid From Four 600 mg LipoCol Forte® Capsules Compared to That of One 20 mg Mevacor® Tablet in Healthy Subjects [NCT01346670]Phase 414 participants (Actual)Interventional2006-10-31Completed
A Phase II Study of the Synergistic Interaction of Lovastatin and Paclitaxel For Patients With Refractory or Relapsed Ovarian Cancer [NCT00585052]Phase 211 participants (Actual)Interventional2003-08-31Terminated(stopped due to Slow accrual, PI left the institution)
A Dose Escalation Phase I/II Study of Lovastatin With High-Dose Cytarabine for Patients With Refractory or Relapsed Acute Myeloid Leukemia [NCT00583102]Phase 1/Phase 223 participants (Actual)Interventional2001-06-30Terminated(stopped due to Slow accrual, PI left institution)
Higher Potency Statins and the Risk of New Diabetes: Multicentre, Observational Study of Administrative Databases [NCT02518503]136,966 participants (Actual)Observational2012-07-31Completed
Lovastatin as a Neuroprotective Treatment for Early Stage Parkinson's Disease: a Single-center, Double-blind, Placebo-controlled Randomized Trial [NCT03242499]Phase 280 participants (Anticipated)Interventional2017-05-15Recruiting
A Single Dose Crossover Comparative Bioavailability Study of Lovastatin 40mg Tablets in Healthy Male Volunteers/Fasting State [NCT00685685]Phase 154 participants (Actual)Interventional2004-09-30Completed
A Single Site, Randomized Open Label Cross-Over Study to Compare Pharmacokinetic Profiles (PK) of XueZhiKang (XZK) Capsules Versus Lovastatin Tablets in Healthy Male Volunteers [NCT02603770]Phase 120 participants (Actual)Interventional2015-11-30Completed
A Pilot Study Exploring the Safety and Synergistic Effect of a Minocycline/Lovastatin Combined Treatment on the Behavior of Individuals With Fragile X Syndrome; Validation of New Biochemical and Neurophysiological Markers (LovaMiX) [NCT02680379]Phase 222 participants (Actual)Interventional2016-03-31Completed
A Randomized Placebo-Controlled Study of Lovastatin in Children With Neurofibromatosis Type 1 [NCT00853580]Phase 2146 participants (Actual)Interventional2009-07-31Completed
Neurobiology and Treatment of Reading Disability in NF1 [NCT02964884]Phase 2120 participants (Anticipated)Interventional2016-11-30Recruiting
A Study of the Proper Dosage of Lovastatin and Docetaxel for Patients With Cancer [NCT00584012]Phase 19 participants (Actual)Interventional2004-04-30Terminated(stopped due to Funding issues)
Pharmacological Treatment of Rett Syndrome With 3-Hydroxy-3 Methylglutaryl-coenzyme A Reductase Inhibitor-Lovastatin (Mevacor) [NCT02563860]Phase 220 participants (Actual)Interventional2015-07-31Completed
A Phase II Study to Prevent Radiation-Induced Rectal Injury With Lovastatin [NCT00580970]Phase 273 participants (Actual)Interventional2007-04-30Completed
Effect of a Nutritional Supplement (AB-LIFE Plus Monacolin K) to Reduce Total and LDL Cholesterol Levels [NCT04677335]40 participants (Actual)Interventional2014-10-01Completed
Phase 2 Study of Interferon Alfa-2b and Lovastatin Combination Therapy for Patients With High-risk Resected or Unresectable Malignant Melanoma [NCT00963664]Phase 2250 participants (Anticipated)Interventional2009-12-31Withdrawn(stopped due to Modifications will be necessary before full IRB approval will be secured.)
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
Evaluation of Lovastatin in Severe Persistent Asthma [NCT00689806]Phase 1/Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to Study never opened)
Imaging Biomarkers of Pulmonary Inflammation [NCT00741013]Early Phase 122 participants (Actual)Interventional2007-03-31Completed
the Histomorphometric Study of Nanocrystalline Hydroxyapatite (Nano Bone) With Lovastatin in the Preservation of the Tooth Socket [NCT03981601]Phase 220 participants (Anticipated)Interventional2018-02-22Recruiting
[NCT00000463]Phase 30 participants Interventional1987-04-30Completed
A Double Blind, Placebo Controlled, Phase II, Randomized Study of Lovastatin Therapy in the Treatment of Mildly Active Rheumatoid Arthritis [NCT00302952]Phase 264 participants (Actual)Interventional2007-11-06Terminated(stopped due to Slow enrollment &Study Drug Expiration (Target: 40 randomized participants /arm))
A Phase 2 Safety Study in Which Ischemic Stroke Patients Will be Randomized Within 24 Hours of Symptom Onset to Placebo or Oral Lovastatin 640 mg Per Day for 3 Days. [NCT01976936]Phase 2164 participants (Actual)Interventional2009-02-28Completed
A Phase II Study Using Lovastatin to Improve Cosmetic Outcome After Radiation Therapy for Breast Cancer [NCT00902668]Phase 23 participants (Actual)Interventional2009-04-30Terminated(stopped due to Slow accrual)
Naturopathic Treatment for the Prevention of Cardiovascular Disease: a Pragmatic Randomized Controlled Trial [NCT00718796]Phase 3300 participants (Anticipated)Interventional2008-04-30Completed
Trial to Evaluate the Safety of Lovastatin in Individuals With Neurofibromatosis Type I (NF1) [NCT00352599]Phase 144 participants (Actual)Interventional2009-09-30Completed
Lovastatin as a Potential Modulator of Apoptosis in COPD [NCT00700921]Phase 230 participants (Actual)Interventional2008-04-30Completed
Pharmacodynamic Trial of Pre-Prostatectomy Lovastatin on MYC (V-myc Myelocytomatosis Viral Oncogene Homolog) Down-Regulation in Localized Prostate Cancer [NCT01478828]2 participants (Actual)Interventional2012-07-13Terminated(stopped due to The study was stopped due to an unanticipated serious adverse event.)
SPOTRIAS: Neuroprotection With Statin Therapy for Acute Recovery Trial [NCT00243880]Phase 133 participants (Actual)Interventional2005-09-30Completed
A Consumer Use Study of OTC Lovastatin (CUSTOM): A 6-Month Consumer Behavior Study of the Lovastatin OTC Self-Management System [NCT00092846]Phase 31,000 participants (Anticipated)Interventional2002-12-04Completed
A Double-Blind, Placebo-Controlled Angiographic Study to Evaluate the Effect of Lovastatin on the Progression Rate of Atherosclerosis in the Coronary Arteries of Patients With Coronary Heart Disease [NCT00116870]Phase 2/Phase 3270 participants Interventional1985-06-30Completed
The Pharmacokinetic Study of Red Yeast Rice Capsule Compared to Lovastatin Tablet in Healthy Subjects. [NCT01527669]Phase 412 participants (Actual)Interventional2012-02-29Completed
Familial Atherosclerosis Treatment Study [NCT00000512]Phase 3146 participants (Actual)Interventional1984-01-31Completed
The Dose Response of Niacin ER/Lovastatin on Peak Walking Time (PWT) in Patients With Intermittent Claudication - a Matrix Design [NCT00071266]Phase 3870 participants Interventional2003-10-31Completed
Effect of Niacin ER/Lovastatin on Peak Walking Time and Claudication Onset Time in Patients With Intermittent Claudication [NCT00062556]Phase 3366 participants Interventional2003-01-31Completed
[NCT00000477]Phase 20 participants Interventional1990-07-31Completed
The Effects of Multiple Dose Fluoxetine and Metabolites on CYP1A2, CYP2C19, CYP2D6 and CYP3A4 Activity [NCT01361217]10 participants (Actual)Interventional2011-09-30Completed
Extended-Release Niacin/Lovastatin Versus Usual Care for Treatment of Dyslipidemia in a Primary Care Setting (EXTEND Study) [NCT00345657]Phase 4100 participants Interventional2003-07-31Completed
[NCT00000469]Phase 20 participants Interventional1988-05-31Completed
Effects of Diet and Medication in Patients With Cerebrotendinous Xanthomatosis (CTX) [NCT00004346]Phase 25 participants Interventional1996-01-31Recruiting
Evaluation of the Efficacy and Safety of Single, Daily Oral Doses of SYN-010 Compared to Placebo in Adult Patients With Irritable Bowel Syndrome With Constipation (EASE-DO) [NCT03763175]Phase 259 participants (Actual)Interventional2018-12-24Terminated(stopped due to Interim Futility Analysis)
A Single Dose Crossover Comparative Bioavailability Study of Lovastatin 40mg Tablets in Healthy Male Volunteers/Fed State [NCT00684723]Phase 154 participants (Actual)Interventional2004-07-31Completed
A Randomized, Double-Blind, Placebo-Controlled Phase II Clinical Trial of Lovastatin for Various Endpoints of Melanoma Pathobiology [NCT00462280]Phase 280 participants (Actual)Interventional2007-05-31Completed
A Phase 2 Efficacy and Safety Dose-Ranging Study of LY3015014 in Patients With Primary Hypercholesterolemia [NCT01890967]Phase 2527 participants (Actual)Interventional2013-06-30Completed
Combining Lovastatin and a Parent-Implemented Language Intervention in a Multimodal Treatment for Fragile X Syndrome [NCT02642653]Phase 430 participants (Actual)Interventional2016-01-31Completed
Improvement of Synaptic Plasticity and Cognitive Function in RAS Pathway Disorders [NCT03504501]Phase 216 participants (Actual)Interventional2019-03-22Terminated(stopped due to The study has been terminated prematurely due to recruitment difficulties. Current status: recruitment stopped and cleaning of the database is ongoing.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00285857 (4) [back to overview]Change in Low Density Lipoprotein (LDL) After Treatment With Lovastatin 80 mg/Day
NCT00285857 (4) [back to overview]Change in Mammographic Density Before and After Treatment With Lovastatin 80 mg/Day
NCT00285857 (4) [back to overview]Change in Total Cholesterol After Treatment With Lovastatin 80 mg/Day
NCT00285857 (4) [back to overview]Change in the Incidence of Abnormal Breast Duct Cytology After Treatment With Lovastatin 80 mg/Day
NCT00302952 (15) [back to overview]Adjusted Mean Change From Baseline in Serum Anti-cyclic Citrullinated Peptide (Anti-CCP) by ELISA (ELISA: Enzyme-linked Immunosorbent Assay)
NCT00302952 (15) [back to overview]Adjusted Mean Change From Baseline in Serum IgM Rheumatoid Factor by ELISA (ELISA: Enzyme-linked Immunosorbent Assay)
NCT00302952 (15) [back to overview]Adjusted Mean Change From Baseline in the Disease Activity Score Using C-reactive Protein (DAS28-CRP) on Day 84
NCT00302952 (15) [back to overview]Change From Baseline in CPK at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Hematocrit (Hct) at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Alkaline Phosphatase, Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST) at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Mean Corpuscular Hemoglobin (MCH) at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Mean Corpuscular Volume (MCV) at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Red Cell Distribution Width (RDW) at Day 84
NCT00302952 (15) [back to overview]Percentage of Participants Meeting ACR20 Response Criteria at Day 84 (ACR: American College of Rheumatology)
NCT00302952 (15) [back to overview]Change From Baseline in Albumin, Total Protein, Hemoglobin, and Mean Corpuscular Hemoglobin Concentration (MCHC) at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Counts: White Blood Cells (WBC), Neutrophils, Bands, Lymphocytes, Monocytes, Eosinophils, Basophils, Platelets, and Reticulocytes at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Potassium, Sodium, Chloride, and Total CO2 at Day 84
NCT00302952 (15) [back to overview]Change From Baseline in Total Bilirubin, Creatinine, BUN, Phosphorus, Calcium, and Glucose at Day 84
NCT00302952 (15) [back to overview]Adjusted Mean Change From Baseline in Log Transformed C - Reactive Protein (CRP) at Day 84
NCT00462280 (27) [back to overview]At Least 1 Study-related Adverse Event Reported During the Study
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - VEGF: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - RelA: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - RelA: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - p21 (WAF1/CIP1): Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - p21 (WAF1/CIP1): Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - Ki-67: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - Ki-67: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - HIF1alpha: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - HIF1alpha: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - (n)-Cadherin: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - (n)-Cadherin: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - (e)-Cadherin: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - (e)-Cadherin: Pathologist 3's Evaluation
NCT00462280 (27) [back to overview]Histopathologic Regression of Target Atypical Nevi With Treatment - Pathologist 2's Evaluation
NCT00462280 (27) [back to overview]Histopathologic Regression of Target Atypical Nevi With Treatment - Pathologist 1's Evaluation
NCT00462280 (27) [back to overview]Clinical Regression of Atypical Moles - Average of Three Reviewers' Evaluations
NCT00462280 (27) [back to overview]Change in Triglycerides (mg/dL) From Baseline After Treatment
NCT00462280 (27) [back to overview]Change in SGOT/AST (U/L) From Baseline After Treatment
NCT00462280 (27) [back to overview]Change in SGOT/ALT (U/L) From Baseline After Treatment
NCT00462280 (27) [back to overview]Serum and Molecular Biomarkers - VEGF: Pathologist 4's Evaluation
NCT00462280 (27) [back to overview]Change in HDL (mg/dL) From Baseline After Treatment
NCT00462280 (27) [back to overview]Change in CPK (U/L) From Baseline After Treatment
NCT00462280 (27) [back to overview]Change in Cholesterol (mg/dL) From Baseline After Treatment
NCT00462280 (27) [back to overview]Change in C-reactive Protein (mg/dL) From Baseline After Treatment
NCT00462280 (27) [back to overview]Total Nevus Number on Patient's Back - Combined Three Reviewers' Evaluations
NCT00462280 (27) [back to overview]Change in LDL (mg/dL) From Baseline After Treatment
NCT00580970 (1) [back to overview]Percentage of Participants With Physician Reported Rectal Toxicity ≥ Grade 2 During the First 2 Years of Radiation Treatment
NCT00585052 (1) [back to overview]Time to Progression Using the Combination of Lovastatin and Paclitaxel.
NCT00684723 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 Extrapolated to Infinity [AUC(0-∞)]
NCT00684723 (3) [back to overview]Maximum Plasma Concentration (Cmax)
NCT00684723 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]
NCT00685685 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 Extrapolated to Infinity [AUC(0-∞)]
NCT00685685 (3) [back to overview]Area Under the Concentration Versus Time Curve From Time 0 to Time t [AUC(0-t)]
NCT00685685 (3) [back to overview]Maximum Plasma Concentration (Cmax)
NCT00741013 (2) [back to overview]Change in Ki (Measure of [18F]Fluorodeoxyglucose ([18F]FDG) Uptake Determined by Patlak Graphical Analysis) in the Right Lung 24 Hours After LPS Instillation
NCT00741013 (2) [back to overview]Number of Total Nucleated Cells From Bronchoalveolar Lavage (BAL) Fluid 24 Hours After Endotoxin Instillation
NCT00853580 (20) [back to overview]Object Assembly (WISC-III)
NCT00853580 (20) [back to overview]Judgement of Line Orientation Test
NCT00853580 (20) [back to overview]Internalizing Behaviors, Behavior Assessment System for Children Second Edition
NCT00853580 (20) [back to overview]Creature Counting (Test of Everyday Attention for Children)
NCT00853580 (20) [back to overview]Controlled Oral Word Association Test
NCT00853580 (20) [back to overview]Commission Errors (Conners Continuous Performance Test, Second Edition; CPT-II)
NCT00853580 (20) [back to overview]Behavior Rating Inventory of Executive Function Global Executive Composite
NCT00853580 (20) [back to overview]Score! (Test of Everyday Attention for Children)
NCT00853580 (20) [back to overview]Stop Signal Task (Cambridge Neuropsychological Test Automated Battery)
NCT00853580 (20) [back to overview]Stockings of Cambridge (Cambridge Neuropsychological Test Automated Battery) Automated Battery).
NCT00853580 (20) [back to overview]Internalizing Behaviors, Behavior Assessment System for Children Second Edition
NCT00853580 (20) [back to overview]Spatial Working Memory (Cambridge Neuropsychological Test Automated Battery)
NCT00853580 (20) [back to overview]Sky Search DT (Test of Everyday Attention for Children)
NCT00853580 (20) [back to overview]Sky Search (Test of Everyday Attention for Children)
NCT00853580 (20) [back to overview]Quality of Life Pediatric Quality of Life Inventory (PedsQL)
NCT00853580 (20) [back to overview]Psychosocial Quality of Life PedsQL
NCT00853580 (20) [back to overview]Paired Associate Learning (Cambridge Neuropsychological Test Automated Battery).
NCT00853580 (20) [back to overview]Omission Errors (Conners Continuous Performance Test, Second Edition; CPT-II)
NCT00853580 (20) [back to overview]ADHD Hyperactive/Impulsive Scale, Conners ADHD Scales
NCT00853580 (20) [back to overview]ADHD Inattentive Scale, Conners ADHD Scales
NCT01361217 (2) [back to overview]Lovastatin AUC in the Presence of Fluoxetine
NCT01361217 (2) [back to overview]AUC of Dextromethorphan, Midazolam and Omeprazole in the Presence of Fluoxetine
NCT01478828 (1) [back to overview]Number of Participants That Can Achieve 60% MYC Modulation Response
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Apolipoprotein A1 (Apo A1), Apolipoprotein B (Apo B)
NCT01890967 (10) [back to overview]Percentage Change From Baseline in LDL-C, Total Cholesterol (TC), High-Density Lipoprotein Cholesterol (HDL-C), Triglycerides (TG), Non-HDL-C
NCT01890967 (10) [back to overview]Number of Participants 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]Number of Participants With an Injection Site Reaction
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Free Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Lipoprotein(a) [Lp(a)]
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C)
NCT01890967 (10) [back to overview]Percentage Change From Baseline in Total Proprotein Convertase Subtilisin/Kexin Type 9 Antibody (PCSK9) Levels
NCT01890967 (10) [back to overview]Pharmacokinetics (PK): Area Under the Concentration-Time Curve at Steady-State (AUC,ss) for LY3015014
NCT02563860 (2) [back to overview]Visual Memory Novelty Score as Assessed by TobiiTX 300 Eyetracking System
NCT02563860 (2) [back to overview]Gait Velocity as Measured by GAITRite System
NCT02642653 (14) [back to overview]FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Spoken Language Impairment
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Spoken Language Impairment
NCT02642653 (14) [back to overview]Clinical Global Impression-Improvement (CGI-I) Scale
NCT02642653 (14) [back to overview]Expressive Language Sample Composite Score in the Home
NCT02642653 (14) [back to overview]Expressive Language Sample Composite Score in the Home
NCT02642653 (14) [back to overview]Clinical Global Impression-Improvement (CGI-I) Scale
NCT02642653 (14) [back to overview]Clinical Global Impression- Severity (CGI-S)
NCT02642653 (14) [back to overview]FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Spoken Language Impairment
NCT02642653 (14) [back to overview]FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Social Impairment
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Social Impairment
NCT02642653 (14) [back to overview]Visual Analog Scale (VAS) - Social Impairment
NCT02998151 (5) [back to overview]Change in EEG Relative Gamma Power
NCT02998151 (5) [back to overview]Change From Pre-dose in the Repeatable Battery for the Assessment of Neuropsychological Status at 4 Hours Post Dose
NCT02998151 (5) [back to overview]Woodcock Johnson Test of Cognitive Abilities - Auditory Attention Task
NCT02998151 (5) [back to overview]Test of Attentional Performance for Children (KiTAP) Test of Alertness
NCT02998151 (5) [back to overview]Clinical Global Impressions-Improvement
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]Percentage of Participants Reporting >=15 Percent (%) Reduction in LDL-C Level at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in 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 Apolipoprotein (Apo) B at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
NCT03510715 (13) [back to overview]Number of Participants With Tanner Staging at Baseline, Weeks 12, 24 and 48
NCT03510715 (13) [back to overview]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 Low-Density Lipoprotein Cholesterol at Week 12: On-treatment Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) at Week 12: Intent-to-Treat (ITT) Analysis
NCT03510715 (13) [back to overview]Percent Change From Baseline in Fasting Triglycerides (TG) 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 Apolipoprotein A1 (Apo A1) at Weeks 12, 24 and 48: ITT Analysis/On-treatment Analysis
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 Week 12: ITT 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]Number of Participants With Tanner Staging at Baseline and Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 130 mg/dL (3.37 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol < 110 mg/dL (2.84 mmol/L) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved at Least 50% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants 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 Achieved at Least 30% Reduction in Low Density Lipoprotein Cholesterol Level From Baseline at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Weeks 8, 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Low Density Lipoprotein Cholesterol at Weeks 12, and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Lipoprotein (a) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein A1 at Weeks 12 and 24: On-treatment Estimand
NCT03510884 (44) [back to overview]DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]DB Period: Number of Participants With Treatment-Emergent (TE) Positive Anti-Alirocumab Antibodies (ADA) Response
NCT03510884 (44) [back to overview]DB Period: Absolute Change From Baseline in Apo B/Apo A-1 Ratio at Weeks 12 and 24: ITT Estimand
NCT03510884 (44) [back to overview]Change From Baseline in Cogstate Battery Test - Overall Composite Score at Weeks 24, 68 and 104
NCT03510884 (44) [back to overview]OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: On-treatment Estimand
NCT03510884 (44) [back to overview]OL Period: Percent Change in Low Density Lipoprotein Cholesterol From Baseline to Week 104: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level Lower Than (<) 130 mg/dL (3.37 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Achieving Low Density Lipoprotein Cholesterol <110 mg/dL (2.84 mmol/L) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Total Cholesterol (Total-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Non-High Density Lipoprotein Cholesterol 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: 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: 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 Apolipoprotein A1 at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B (Apo B) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Apolipoprotein B at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 12: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in Fasting Triglycerides (TG) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percent Change From Baseline in High-Density Lipoprotein Cholesterol (HDL-C) at Week 24: ITT Estimand
NCT03510884 (44) [back to overview]DB Period: Percentage of Participants Who Achieved Low Density Lipoprotein Cholesterol Level <130 mg/dL (3.37 mmol/L) at Week 12: ITT Estimand
NCT03763175 (9) [back to overview]Proportion of Overall Responders During the 12-week Treatment Period
NCT03763175 (9) [back to overview]Proportion of Patients With Adequate Relief
NCT03763175 (9) [back to overview]Proportion of Patients Using Rescue Medication
NCT03763175 (9) [back to overview]Proportion of Overall Stool Frequency Responders During the 12-week Treatment Period
NCT03763175 (9) [back to overview]Proportion of Overall Bloating Responders During the 12-week Treatment Period
NCT03763175 (9) [back to overview]Proportion of Overall Abdominal Pain Intensity Responders During the 12-week Treatment Period
NCT03763175 (9) [back to overview]Mean Change From Baseline in the Area-under-the-curve (AUC) of Breath Methane Production, Based on the 120-minute Lactulose Breath Test.
NCT03763175 (9) [back to overview]Change From Baseline in the Weekly Average Number of Completely Spontaneous Bowel Movements (CSBM) Compared to the 12-week Treatment Period
NCT03763175 (9) [back to overview]Change From Baseline in Breath Methane Production Based on a Single-point Breath Methane Test
NCT04359823 (7) [back to overview]Application Frequency Influence on Disseminated Actinic Porokeratosis General Assessment Severity Index
NCT04359823 (7) [back to overview]Improvement in Color of DSAP Lesions
NCT04359823 (7) [back to overview]Improvement in Dermatology Quality of Life Index Questionnaire
NCT04359823 (7) [back to overview]Improvement in Overall Appearance of DSAP Lesions
NCT04359823 (7) [back to overview]Improvement in Size of DSAP Lesions
NCT04359823 (7) [back to overview]Measurement of Treatment Efficacy Determined by DSAP-GASI Score (Disseminated Actinic Porokeratosis General Assessment Severity Index)
NCT04359823 (7) [back to overview]Pain and Itch Associated With Treatment

Change in Low Density Lipoprotein (LDL) After Treatment With Lovastatin 80 mg/Day

(NCT00285857)
Timeframe: 6 months

Interventionmg/dL (Mean)
Lovastatin 80 mg/Day-6

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Change in Mammographic Density Before and After Treatment With Lovastatin 80 mg/Day

"Bilateral mammography was performed at study entry (before lovastatin therapy) and at study conclusion (after lovastatin therapy) . Mammograms were assessed for a decline in mean breast density, using the American College of Radiology Breast Imaging Reporting and Data System (BI-RAD) composition system for mammographic density assessment.~Category 0 Need additional imaging evaluation~Negative~Benign~Probably benign~Suspicious abnormality~Highly suggestive of malignancy~Known biopsy-proven malignancy" (NCT00285857)
Timeframe: 6 months

InterventionBI-RADS (Mean)
Lovastatin 80 mg/Day-0.10

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Change in Total Cholesterol After Treatment With Lovastatin 80 mg/Day

(NCT00285857)
Timeframe: 6 months

Interventionmg/dL (Mean)
Lovastatin 80 mg/Day-8

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Change in the Incidence of Abnormal Breast Duct Cytology After Treatment With Lovastatin 80 mg/Day

"Assessed on that basis of pre- and post-treatment evaluation with RPFNA (random periareolar fine needle aspiration). All subjects received a prescription for lovastatin 80 mg/day, to be taken as 40 mg twice-a-day.~Cytology was qualitatively and quantitatively, using the Masood semiquantitative scale to assign a number to each specimen, with higher numbers indicating increasing degrees of abnormality, as follows:~06-10 Non-proliferative breast disease (NPBD)~11-14 Proliferative breast disease without atypia (PBD-A)~15-18 Proliferative breast disease with atypia (PBD+A)~19-24 Carcinoma in situ and invasive cancer (CIS/IC)~If no cells could be obtained after multiple RPFNA attempts, the classification was acellular.~Change from NPBD to PBD-A was considered Unfavorable.~Change from NPBD to Acellular was considered Equivocal.~Change from PBD-A to NPBD was considered Favorable." (NCT00285857)
Timeframe: 6 months

,,
Interventionparticipants (Number)
Post-treatment NPBDPost-treatment PBD-APost-treatment PBD+APost-treatment CIS/ICPost-treatment biopsy acellular
Baseline Biopsy Acellular10000
Baseline Non-proliferative Breast Disease (NPBD)82003
Baseline Proliferative Breast Disease Without Atypia (PBD-A)57000

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Adjusted Mean Change From Baseline in Serum Anti-cyclic Citrullinated Peptide (Anti-CCP) by ELISA (ELISA: Enzyme-linked Immunosorbent Assay)

Anti-CCP antibodies are autoantibodies frequently detected in the serum of individuals with rheumatoid arthritis. In this study, a positive value for anti-CCP was 8 IU/mL or greater; a negative value for anti-CCP was <8 IU/mL. Change= subtraction of Day 0 from Day 84 anti-CCP value. In general, high levels of the antibody indicate an aggressive rheumatoid arthritis and a higher risk of joint damage. Participants with measurements for designated time points included in analysis. (NCT00302952)
Timeframe: Baseline ( Day 0), Day 84 (Wk 12)

InterventionIU/mL (Mean)
Lovastatin 80 mg16.3
Placebo-1.0

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Adjusted Mean Change From Baseline in Serum IgM Rheumatoid Factor by ELISA (ELISA: Enzyme-linked Immunosorbent Assay)

Rheumatoid factor (RF) is an antibody often present in the blood of a person with rheumatoid arthritis. In this study, a positive value for RF was 0.5 IU/mL or greater; a negative value for RF was <0.5 IU/mL. Change= Day 84 value minus Baseline value. In general, presence of the antibody indicates aggressive rheumatoid arthritis and higher risk of joint damage. Participants with measurements for designated time points included in analysis. (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

InterventionIU/mL (Mean)
Lovastatin 80 mg-5.4
Placebo2.8

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Adjusted Mean Change From Baseline in the Disease Activity Score Using C-reactive Protein (DAS28-CRP) on Day 84

The DAS28-CRP score is on a scale of 0 to 10 and indicates current activity of rheumatoid arthritis (>5.1=high disease activity; 3.2-<=5.1=moderate disease activity; <=3.2=low disease activity; <2.6=remission). The score uses a combination of four variables: 1) the number of tender joints (of the 28 that are measured); 2) the number of swollen joints (of the 28 that are measured); 3) serum C-reactive protein (CRP) lab value in mg/L , and 4) Patient Global Assessment of Disease Activity. Using a formula, the physician determines the score. Participants with measurements for designated time points included in analysis. (NCT00302952)
Timeframe: Baseline (Day 0) to Day 84 (Wk 12)

InterventionScores on a scale (Mean)
Lovastatin 80 mg-0.5
Placebo-0.5

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Change From Baseline in CPK at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

InterventionU/L (Mean)
Lovastatin 80 mg-2.4
Placebo8.0

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Change From Baseline in Hematocrit (Hct) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

Intervention% of packed red blood cells by volume (Mean)
Lovastatin 80 mg-0.5
Placebo-0.5

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Change From Baseline in Alkaline Phosphatase, Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

,
InterventionU/L (Mean)
Alkaline PhosphataseALTAST
Lovastatin 80 mg-3.0-1.8-1.2
Placebo0.40.70.8

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Change From Baseline in Mean Corpuscular Hemoglobin (MCH) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

Interventionpg (Mean)
Lovastatin 80 mg-0.4
Placebo0.0

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Change From Baseline in Mean Corpuscular Volume (MCV) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

InterventionfL (Mean)
Lovastatin 80 mg-0.4
Placebo0.7

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Change From Baseline in Red Cell Distribution Width (RDW) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

Intervention% of mean corpuscle volume (Mean)
Lovastatin 80 mg-0.4
Placebo0.2

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Percentage of Participants Meeting ACR20 Response Criteria at Day 84 (ACR: American College of Rheumatology)

Patients were ACR20 Responders if they had: at least 20% improvement in both tender joint count (28 examined) and swollen joint count (28 examined), and 20% improvement in at least three of the following 5 remaining ACR core measures: • Patient's pain assessment (Visual Analogue Scale (VAS) 100 mm) • Patient's global assessment of disease activity (VAS 100 mm) • Physician's global assessment of disease activity (VAS 100 mm) • Patient self-assessed disability (Health Assessment Questionnaire (HAQ)) score • Acute phase reactant C-reactive protein. Participants with measurements for designated time points were included in analysis. (NCT00302952)
Timeframe: Day 84 (Wk 12)

InterventionPercentage of participants (Number)
Lovastatin 80 mg29.0
Placebo40.0

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Change From Baseline in Albumin, Total Protein, Hemoglobin, and Mean Corpuscular Hemoglobin Concentration (MCHC) at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

,
Interventiong/dL (Mean)
AlbuminTotal ProteinHemoglobinMCHC
Lovastatin 80 mg0.00.0-0.3-0.3
Placebo0.10.1-0.3-0.4

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Change From Baseline in Counts: White Blood Cells (WBC), Neutrophils, Bands, Lymphocytes, Monocytes, Eosinophils, Basophils, Platelets, and Reticulocytes at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

,
Intervention10^3/uL (Mean)
WBCNeutrophilsBandsLymphocytesMonocytesEosinophilsBasophilsPlatelet CountReticulocytes
Lovastatin 80 mg0.10.20.0-0.10.10.00.0-8.2-4.7
Placebo-0.4-0.60.00.10.00.00.0-5.60.0

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Change From Baseline in Potassium, Sodium, Chloride, and Total CO2 at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

,
Interventionmmol/L (Mean)
PotassiumSodiumChlorideTotal CO2
Lovastatin 80 mg0.0-0.2-0.10.7
Placebo0.0-0.20.5-0.5

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Change From Baseline in Total Bilirubin, Creatinine, BUN, Phosphorus, Calcium, and Glucose at Day 84

Blood samples were taken from participants at Baseline and Day 84. Participants with measurements for designated time points included in analysis. Change=Day 84 value minus Baseline value. A positive difference reflects an increased laboratory parameter value over time; a negative difference reflects a decreased laboratory parameter value over time. Normal laboratory values depend on a subject age, gender, and the specific laboratory methods that were used to determine the lab values. Reference: http://www.merckmanuals.com/professional/appendixes/normal_laboratory_values/blood_tests_normal_values.html (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

,
Interventionmg/dL (Mean)
Total BilirubinCreatinineBUNPhosphorusCalciumGlucose
Lovastatin 80 mg0.00.0-0.40.00.0-4.3
Placebo0.10.0-0.50.00.0-1.2

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Adjusted Mean Change From Baseline in Log Transformed C - Reactive Protein (CRP) at Day 84

Blood draw for CRP, an acute phase reactant used to identify the presence of nonspecific inflammation. Change=Day 84 value minus Baseline value. Normal serum CRP reference range in this study is 0-4 mg/L (log transformed: -4.2 to 1.4). Participants with measurements for designated time points were included in analysis. An increased CRP level indicates the presence of inflammation. Reduced CRP levels could mean a decrease in inflammation. (NCT00302952)
Timeframe: Baseline (Day 0), Day 84 (Wk 12)

Interventionmg/L (Mean)
Lovastatin 80 mg-0.4
Placebo-0.3

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Serum and Molecular Biomarkers - VEGF: Pathologist 3's Evaluation

VEGF expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin4.81
Placebo-0.63

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Serum and Molecular Biomarkers - RelA: Pathologist 4's Evaluation

RelA expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin3.73
Placebo-3.44

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Serum and Molecular Biomarkers - RelA: Pathologist 3's Evaluation

RelA expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin0.83
Placebo-1.25

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Serum and Molecular Biomarkers - p21 (WAF1/CIP1): Pathologist 4's Evaluation

p21 expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin2.05
Placebo-0.13

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Serum and Molecular Biomarkers - p21 (WAF1/CIP1): Pathologist 3's Evaluation

p21 expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin1.00
Placebo1.18

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Serum and Molecular Biomarkers - Ki-67: Pathologist 4's Evaluation

Ki-67 expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin0.57
Placebo0.28

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Serum and Molecular Biomarkers - Ki-67: Pathologist 3's Evaluation

Ki-67 expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin0.73
Placebo0.50

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Serum and Molecular Biomarkers - HIF1alpha: Pathologist 4's Evaluation

HIF1alpha expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin-0.04
Placebo-0.04

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Serum and Molecular Biomarkers - HIF1alpha: Pathologist 3's Evaluation

HIF1alpha expression was assessed via nuclear staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin0.05
Placebo-0.32

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Serum and Molecular Biomarkers - (n)-Cadherin: Pathologist 4's Evaluation

(n)-cadherin expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin4.24
Placebo-3.52

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Serum and Molecular Biomarkers - (n)-Cadherin: Pathologist 3's Evaluation

(n)-cadherin expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin5.91
Placebo-9.17

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Serum and Molecular Biomarkers - (e)-Cadherin: Pathologist 4's Evaluation

(e)-cadherin expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin4.23
Placebo-7.40

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Serum and Molecular Biomarkers - (e)-Cadherin: Pathologist 3's Evaluation

(e)-cadherin expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin0.67
Placebo-7.37

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Histopathologic Regression of Target Atypical Nevi With Treatment - Pathologist 2's Evaluation

The level of atypia will be graded in a standard fashion which leads to seven levels of atypia, with zero being no atypia and six being a melanoma. For each patient, the change from baseline in the level of atypia was calculated. Only the Two Matched Nevi Group - Lovastatin and Two Matched Nevi Group - Placebo data were used and analyzed for the primary outcome. One-Large Nevi Group - Lovastatin and One-Large Nevi Group - Placebo sample data were not used or analyzed due to insufficient numbers. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionscore (Mean)
Two Matched Nevi Group - Lovastatin0.17
Two Matched Nevi Group - Placebo0.04

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Histopathologic Regression of Target Atypical Nevi With Treatment - Pathologist 1's Evaluation

The level of atypia will be graded in a standard fashion which leads to seven levels of atypia, with zero being no atypia and six being a melanoma. For each patient, the change from baseline in the level of atypia was calculated. Only the Two Matched Nevi Group - Lovastatin and Two Matched Nevi Group - Placebo data were used and analyzed for the primary outcome. One-Large Nevi Group - Lovastatin and One-Large Nevi Group - Placebo sample data were not used or analyzed due to insufficient numbers. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionscore (Mean)
Two Matched Nevi Group - Lovastatin0.50
Two Matched Nevi Group - Placebo-0.12

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Clinical Regression of Atypical Moles - Average of Three Reviewers' Evaluations

From close-up photos of target atypical nevi, lesions will be graded clinically. After unblinding of pre- or post-treatment status for photos, the grading score was as follows: 1= Post-treatment (Post-TX) photo shows a complete resolution of atypia relative to pre-treatment (Pre-TX) photo, 2 = Post-TX photo shows a strong lessening of atypia relative to Pre-TX photo, 3 = Post-TX photo shows a mild lessening of atypia relative to Pre-TX photo, 4 = Post-TX and Pre-TX photos show same degree of atypia, 5 = Pre-TX photo shows a mild lessening of atypia relative to Post-TX photo, 6 = Pre-TX photo shows a strong lessening of atypia relative to Post-TX photo, 7 = Pre-TX photo shows a complete resolution of atypia relative to Post-TX photo. The Wilcoxon rank sum test will be applied to compare the scores for patients treated with placebo vs. those treated with lovastatin. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionscore (Mean)
Lovastatin4.03
Placebo3.98

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Change in Triglycerides (mg/dL) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

Interventionmg/dL (Mean)
Lovastatin1.21
Placebo1.65

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Change in SGOT/AST (U/L) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

InterventionU/L (Mean)
Lovastatin3.42
Placebo-0.75

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Change in SGOT/ALT (U/L) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

InterventionU/L (Mean)
Lovastatin5.61
Placebo2.93

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Serum and Molecular Biomarkers - VEGF: Pathologist 4's Evaluation

VEGF expression was assessed via cytoplasmic staining, and the change in the percentage of positive stained cells from baseline to 24 weeks is calculated. (NCT00462280)
Timeframe: From baseline up to 24 weeks

Interventionpercentage of cells that are positive (Mean)
Lovastatin-1.83
Placebo-2.24

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Change in HDL (mg/dL) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

Interventionmg/dL (Mean)
Lovastatin-1.42
Placebo-2.63

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Change in CPK (U/L) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

InterventionU/L (Mean)
Lovastatin20.94
Placebo9.1

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Change in Cholesterol (mg/dL) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

Interventionmg/dL (Mean)
Lovastatin-27.25
Placebo-3.77

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Change in C-reactive Protein (mg/dL) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

Interventionmg/dL (Mean)
Lovastatin-0.3
Placebo-0.11

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Total Nevus Number on Patient's Back - Combined Three Reviewers' Evaluations

Assessed by photos of subjects' back pre and post treatment. These photos will be used to count, by blinded evaluators, the number of nevi on the back pre and post therapy. (NCT00462280)
Timeframe: From baseline up to 24 weeks

,
Interventionpairs of photos (Number)
Fewer nevi after the treatmentSame number of nevi after treatmentMore nevi after the treatment
Lovastatin4641
Placebo3677

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Change in LDL (mg/dL) From Baseline After Treatment

(NCT00462280)
Timeframe: Baseline up to 24 weeks

Interventionmg/dL (Mean)
Lovastatin-25.28
Placebo-0.4

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Percentage of Participants With Physician Reported Rectal Toxicity ≥ Grade 2 During the First 2 Years of Radiation Treatment

The primary endpoint of this study was percentage of participants with physician reported rectal toxicity ≥Grade 2 during the first 2 years after treatment. A one sided test will be conducted in order to evaluate reduction of risk from adding Lovastatin. The analysis is using a one-stage design, 5% level of significance, and 83% power. (NCT00580970)
Timeframe: 24 months

Interventionpercentage of participants (Number)
Supportive Care (Lovastatin) (Evaluable)38

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Time to Progression Using the Combination of Lovastatin and Paclitaxel.

To determine the time to progression using the combination of lovastatin and paclitaxel. (NCT00585052)
Timeframe: Up to one year

Interventionyears (Mean)
Paclitaxel and Lovastatin0.41

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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. (NCT00684723)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng-hr/mL (Mean)
Lovastatin 40 mg Tablets48.72
Mevacor® 40 mg Tablets52.98

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Maximum Plasma Concentration (Cmax)

The maximum or peak concentration that the drug reaches in the plasma. (NCT00684723)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng/mL (Mean)
Lovastatin 40 mg Tablets9.26
Mevacor® 40 mg Tablets10.01

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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. (NCT00684723)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng-hr/mL (Mean)
Lovastatin 40 mg Tablets47.86
Mevacor® 40 mg Tablets51.64

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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. (NCT00685685)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng-hr/mL (Mean)
Lovastatin 40 mg Tablets34.52
Mevacor® 40 mg Tablets33.80

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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. (NCT00685685)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng-hr/mL (Mean)
Lovastatin 40 mg Tablets30.64
Mevacor® 40 mg Tablets30.36

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Maximum Plasma Concentration (Cmax)

The maximum or peak concentration that the drug reaches in the plasma. (NCT00685685)
Timeframe: serial pharmacokinetic plasma concentrations were drawn prior to dose administration (0 hour) and at 0.33, 0.67, 1, 1.33, 1.67, 2, 2.33, 2.67, 3, 3.33, 3.67, 4, 4.5, 5, 5.5, 6, 7, 8, 10, 14, 18, 24, 36, and 48 hours after drug administration.

Interventionng/mL (Mean)
Lovastatin 40 mg Tablets1.86
Mevacor® 40 mg Tablets1.96

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Change in Ki (Measure of [18F]Fluorodeoxyglucose ([18F]FDG) Uptake Determined by Patlak Graphical Analysis) in the Right Lung 24 Hours After LPS Instillation

Calculated Ki was used to measure the amount of lung inflammation before and after instillation of endotoxin to assess the effect of placebo, lovastatin, and rhAPC treatment (NCT00741013)
Timeframe: 24 hours after endotoxin instillation

InterventionChange in Ki (Mean)
Placebo Pill and Intravenous (i.v.) Placebo18.8
Lovastatin Pill and i.v. Placebo8.4
Placebo Pill and Recombinant Human Activated Protein C i.v.14.2

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Number of Total Nucleated Cells From Bronchoalveolar Lavage (BAL) Fluid 24 Hours After Endotoxin Instillation

Number of total nucleated cells isolated from the first aliquoe of BAL obtained to correlate with PET data. (NCT00741013)
Timeframe: 24 hours after endotoxin instillation

Interventioncells per cubic mm (Mean)
Placebo Pill and Intravenous (i.v.) Placebo545
Lovastatin Pill and i.v. Placebo311
Placebo Pill and Recombinant Human Activated Protein C i.v.520

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Object Assembly (WISC-III)

A measure of visuoperceptual organization. Participants were required to rebuild an item puzzle based on disassembled pieces. Age scaled scores are reported, which have a population mean of 10 and standard deviation of 3 (range 1-19). Higher scores indicate better performances. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionScores on a scale (Mean)
BaselinePost-treatment
Lovastatin6.67.8
Placebo6.97.5

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Judgement of Line Orientation Test

A test of visuospatial judgement. The test measured the participant's ability to match the angle and orientation of lines in space. There were 30 trial in total. Correct response in a trial was awarded one point (range 0-30). Higher scores represent better performances. Raw data are reported. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionTotal correct responses (Mean)
BaselinePost-treatment
Lovastatin15.017.2
Placebo14.616.7

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Internalizing Behaviors, Behavior Assessment System for Children Second Edition

A parent-reported questionnaire assessing internalizing behaviors of anxiety, depression and somatization. T-scores are reported. Higher scores indicate increased internalizing behaviors. A score below 60 is considered healthy, 61-65 a possible significant problem, and 66+ is considered a significant problem. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin55.252.6
Placebo53.852.5

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Creature Counting (Test of Everyday Attention for Children)

"Creature Counting is a measure of attentional control. Participants were required to count creatures from top of the page to the bottom, using arrows as cues to switch from counting up to counting down (and vice versa). There were seven testing trials. The outcome variable was the total number of correct trials (range 0-7). Higher scores represent better performances." (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionScores on a scale (Mean)
BaselinePost-treatment
Lovastatin4.04.5
Placebo3.84.6

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Controlled Oral Word Association Test

A measure of verbal fluency. Participants were required to spontaneously produce as many words as they could, beginning with a designated letter in 60 seconds. Three letters were used. Higher scores represent better performances. Raw data are reported summing total words generated for all three letters. Scale does not have a maximum range. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionTotal words (Mean)
BaselinePost-treatment
Lovastatin22.222.2
Placebo21.222.6

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Commission Errors (Conners Continuous Performance Test, Second Edition; CPT-II)

A computerised measure of impulse control. Letters were presented serially on a screen in a random order. All letters were considered target stimuli, except for the letter 'X' which is a non-target stimulus. Participants responded to target stimuli by pressing the space bar of a computer keyboard (90% of the stimuli) while withholding responses to non-target stimuli (10% of the test). Commission errors represented the number of times a participant incorrectly responded to the non-target (letter 'X'). T-scores are reported, as generated by the test software. Higher scores indicate poorer performances. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin57.558.8
Placebo62.164.1

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Behavior Rating Inventory of Executive Function Global Executive Composite

A parent-rated questionnaire of executive behaviour assessing behavioral regulation (inhibit, shift, emotional control) and metacognition (initiate, working memory, plan/organize, organization of materials, self-monitoring). T-scores for the Global Executive Composite (overall summary score) are reported. Higher scores indicate poorer executive behaviors. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin63.559.2
Placebo61.458.8

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Score! (Test of Everyday Attention for Children)

Score! is a measure of sustained attention. Participants were required to silently count a series of aurally presented tones and say the total number of tones counted at the end of each trial. The number of tones ranged from 9 to 15, with a total of 10 trials (range 0-10). Higher values represent better performance. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionUnits on a scale (Mean)
BaselinePost-treatment
Lovastatin6.07.3
Placebo5.76.8

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Stop Signal Task (Cambridge Neuropsychological Test Automated Battery)

"A computerized measure of inhibitory control. The participant quickly responded to an arrow stimulus by pressing one of two buttons (left or right), depending on the direction in which the arrow pointed on the screen. If an audio tone is present, the subject was supposed to withhold the response.~The difficulty of the task was manipulated by altering the delay before a stop signal (auditory tone) was presented, known as the stop signal delay. The outcome from this measure was stop signal reaction time (last half of test), which was computed by subtracting the mean stop signal delay at which the participant was able to stop on 50% of trials from the mean reaction time on go trials. Poorer response inhibition was reflected by a larger stop signal reaction time. Scale does not have a maximum range." (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionMilliseconds (Mean)
BaselinePost-treatment
Lovastatin264.7227.2
Placebo237.2227.0

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Stockings of Cambridge (Cambridge Neuropsychological Test Automated Battery) Automated Battery).

"A computerized measure of spatial planning based on the Tower of London test. It required participants to move balls in a lower display to match a pattern shown in the upper display in a certain number of moves.~More specifically, the participant was shown two displays containing three coloured balls. The displays were presented in such a way that they could be perceived as stacks of coloured balls held in socks suspended from a beam. The test administrator first demonstrated to the participant how to move the balls in the lower display to copy the pattern in the upper display and completed one demonstration problem, where the solution required one move. The participant then completed problems that increased in difficulty, from one through to five move problems.~The unit of measure was the mean number of moves taken to complete a problem that could not be completed in less than five moves. The higher the score, the poorer the performance (range 5-12)." (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionMoves (Mean)
BaselinePost-treatment
Lovastatin7.97.3
Placebo8.07.9

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Internalizing Behaviors, Behavior Assessment System for Children Second Edition

A self-reported questionnaire assessing internalizing behaviors such as anxiety and depression. T-scores are reported. Higher scores indicate increased internalizing behaviors. A score below 60 is considered healthy, 61-65 a possible significant problem, and 66+ is considered a significant problem. (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin50.947.9
Placebo51.249.2

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Spatial Working Memory (Cambridge Neuropsychological Test Automated Battery)

"A computerized measure of spatial working memory. This task assessed the participant's ability to retain spatial information and to manipulate remembered items in working memory.~In this test, participants were shown an array of boxes on a computer screen and they were required to search through the boxes for hidden tokens. One box at a time was touched until a blue token was found inside. Participants then commenced a new search for the next token. The key instruction was that, once a token had been located, that box would not be used again to hide another token.~Unit of measure was between search errors, determined by the number of boxes a participant reopens in which a token had previously been found. Higher score indicated poorer performance. Scale does not have a maximum range." (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionErrors (Mean)
BaselinePost-treatment
Lovastatin47.040.4
Placebo47.941.6

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Quality of Life Pediatric Quality of Life Inventory (PedsQL)

Parent-rated questionnaire of psychosocial Quality of Life (including emotional, social and school functioning). Summary scores are reported. Higher scores indicate increased increased quality of life (range 0-100). (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionScores on a scale (Mean)
BaselinePost-treatment
Lovastatin62.869.2
Placebo64.668.1

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Psychosocial Quality of Life PedsQL

Self-rated questionnaire of psychosocial Quality of Life (including emotional, social and school functioning). Summary scores are reported. Higher scores indicate higher quality of life (range 0-100). (NCT00853580)
Timeframe: Baseline and Post-treatment (week 16)

,
InterventionScores on a scale (Mean)
BaselinePost-treatment
Lovastatin67.262.6
Placebo70.067.3

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Paired Associate Learning (Cambridge Neuropsychological Test Automated Battery).

A computerized test of visuospatial learning. Participants had to remember patterns associated with different locations on the screen, and during the test phase, as each pattern is presented, point to the appropriate location. The test starts at a very simple level and gradually increases in difficulty. Higher number of errors indicates poorer performance. Scale does not have a maximum range. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionPAL Total Errors (Mean)
BaselinePost-treatment
Lovastatin15.810.3
Placebo17.011.7

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Omission Errors (Conners Continuous Performance Test, Second Edition; CPT-II)

A computerised measure of vigilance and concentration. Letters were presented serially on a screen in a random order. All letters were considered target stimuli, except for the letter 'X' which is a non-target stimulus. Participants responded to target stimuli by pressing the space bar of a computer keyboard (90% of the stimuli) while withholding responses to non-target stimuli (10% of the test). Omission errors represented the number of times a participant fails to respond to target letters (all other than 'X'). T-scores are reported, as generated by the test software. Higher scores indicate poorer performances. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin54.754.2
Placebo56.955.5

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ADHD Hyperactive/Impulsive Scale, Conners ADHD Scales

Parent rated hyperactive/impulsive ADHD symptoms, based on Diagnostic and Statistical Manual of Mental Disorders criteria, 4th edition.T-scores are reported. Higher scores indicate increased ADHD-related symptoms. A score below 60 is considered healthy, 61-65 a possible significant problem, and 66+ is considered a significant problem. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin65.562.3
Placebo62.962.3

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ADHD Inattentive Scale, Conners ADHD Scales

Parent rated inattentive ADHD symptoms, based on Diagnostic and Statistical Manual of Mental Disorders criteria, 4th edition. T-scores are reported. Higher scores indicate increased ADHD-related symptoms. A score below 60 is considered healthy, 61-65 a possible significant problem, and 66+ is considered a significant problem. (NCT00853580)
Timeframe: Baseline and Post-treatment (16 weeks)

,
InterventionT score (Mean)
BaselinePost-treatment
Lovastatin66.259.5
Placebo64.061.1

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Lovastatin AUC in the Presence of Fluoxetine

Our primary outcome measure will be the interaction of fluoxetine with CYP3A4. A 50% increase in the AUC for lovastatin plus hydroxy-lovastatin acid (the active form of lovastatin) between treatment day 14 (study day 20) and control days (study day 2) is considered clinically significant. (NCT01361217)
Timeframe: The primary outcome will be assessed within 2 months after the last subject is enrolled or at 2 years from the start of study enrollment, which ever is sooner.

Interventionnmol*hr/L (Mean)
Lovastatin AUC After Fluoxetine Dosing170
Lovastatin Before Fluoxetine180

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AUC of Dextromethorphan, Midazolam and Omeprazole in the Presence of Fluoxetine

Our secondary outcome measure will be the interaction between fluoxetine and each CYP evaluated in the cocktail. A 50% increase in the AUC of caffeine (CYP1A2), dextromethorphan (CYP2D6), omeprazole (CYP2C19) or midazolam (CYP3A4) between treatment and control days is considered clinically significant. The interaction of fluoxetine with caffeine (CYP1A2) will be considered as a negative control for the study. These AUCs will be measured on study day 1 (control day) and study day 18 (NCT01361217)
Timeframe: The secondary outcome will be assessed within 2 months after the last subject is enrolled or at 2 years from the start of study enrollment, which ever is sooner.

Interventionnmol*hr/L (Mean)
caffeine control AUCCaffeine treatment AUCdextromethophan control AUCDextromethorphan treatment AUCOmeprazole control AUComeprazole treatment AUCmidazolam control AUCmidazolam treatment AUC
Midazolam, Caffeine, Omeprazole, Caffeine AUC After Fluoxetine4300043000681850120085003024

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Number of Participants That Can Achieve 60% MYC Modulation Response

Number of participants who achieve V-myc Myelocytomatosis Viral Oncogene Homolog (MYC) down-regulation in prostatectomy specimens in intermediate-/high-risk localized prostate cancer patients. (NCT01478828)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Lovastatin0

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

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

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

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

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

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

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

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

InterventionPercentage change (Least Squares Mean)
Placebo Q4W9.9
20 mg LY3015014 Q4W-16.3
120 mg LY3015014 Q4W-36.6
300 mg LY3015014 Q4W-68.0
100 mg LY3015014 Q8W-4.4
300 mg LY3015014 Q8W-35.2

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

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

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

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

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

InterventionPercentage change (Least Squares Mean)
Placebo Q4W7.6
20 mg LY3015014 Q4W-14.9
120 mg LY3015014 Q4W-40.5
300 mg LY3015014 Q4W-50.5
100 mg LY3015014 Q8W-14.9
300 mg LY3015014 Q8W-37.1

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

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

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

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

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

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

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Visual Memory Novelty Score as Assessed by TobiiTX 300 Eyetracking System

"Novelty score is considered a composite measure of visual memory.Test is a standardized neuropsychological test( Rose test) adapted for eye tracking system.~The present study made use of a well-established battery of visual paired comparison problems .There were nine problems: five using achromatic photos of faces and four using multicolored abstract patterns paired stimuli , separated by 23°. For each problem, two identical stimuli are briefly presented side by side for familiarization, then the familiar and a new one are paired on test~Recognition(memory) is indexed by a novelty score (percentage of looking to the novel target on test).~Higher novelty scores were related to better recognition (index of better memory) Scores range from 0.0-1.0 (0-100%) and indicate 1) more overall looking at novel target and (2) more fixations to novel targets.~Score of .5 (50%) indicates looking by change only with no recognition." (NCT02563860)
Timeframe: final week of treatment, Week 32

Interventionpercent (Median)
Pre-treatmentPost treatment
Open Label44.8558.93

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Gait Velocity as Measured by GAITRite System

To perform quantitative gait assessment using a computerized walkway with embedded pressure sendors (GAIT rite) (NCT02563860)
Timeframe: During final week of treatment, week 32

Interventioncm/sec (Median)
Open Label58.6

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FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale

The ABC-C is a 58-item caregiver-rated behavior scale used to examine treatment effects on challenging behaviors for individuals with FXS in the following domains: (1) irritability; (2) lethargy/social withdrawal; (3) stereotypic behavior; (4) hyperactivity; and (5) inappropriate speech. Caregiver rates the subject's behavior as follows: 0 = not a problem, l = the behavior is a problem but slight in degree, 2 = the problem is moderately serious, 3 = the problem is severe in degree. Sansone et al. (2012) further subdivided social withdrawal to rate social avoidance in FXS. The subscale includes 4 items which were originally part of the Lethargy/Withdrawal subscale. This subscale captures core aspects of the FXS phenotype related to gaze avoidance, social ''escape'' behaviors, and social anxiety. Subscale score ranges from 0 to 12, higher scores reflect a more problematic behavior. (NCT02642653)
Timeframe: Baseline

Interventionscore on a scale (Mean)
Lovastatin and PILI2.5
Placebo and PILI4.31

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Visual Analog Scale (VAS) - Spoken Language Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Spoken Language Impairment scale, at 10-weeks. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: 10 weeks

Interventioncentimeters (Mean)
Lovastatin and PILI5.28
Placebo and PILI3.09

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Visual Analog Scale (VAS) - Spoken Language Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Spoken Language Impairment scale, at 20-weeks. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: 20 weeks

Interventioncentimeters (Mean)
Lovastatin and PILI5.66
Placebo and PILI4.18

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Clinical Global Impression-Improvement (CGI-I) Scale

A clinician rated scale utilizing history from the parents or caregiver and incorporating it into a clinical rating to assess for overall therapeutic response. The 7-point scale ranges from: 1 = Very much improved; 2 = Much improved; 3 = Minimally improved; 4 = No change; 5 = Minimally worse; 6 = Much worse; and 7 = Very much worse. Therefore, the lower the score, the greater the overall improvement as rated by the clinician. The CGI-I was used at the 10 week and 20 week visits. Shown here are the CGI-I mean scores from the 20-weeks end-of-study visit. (NCT02642653)
Timeframe: 20 weeks

Interventionunits on a scale (Mean)
Lovastatin and PILI2.42
Placebo and PILI2.38

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Expressive Language Sample Composite Score in the Home

The primary outcome reflects the diversity of vocabulary used. Higher scores reflect more skill. The lowest possible value is zero. No theoretical maximum can be defined because the wordless picture books can lead to a large and indeterminate set of options for the amount of talk and the vocabulary used. In a previous study of a nonpharmacological intervention, the range at baseline was 9-177, and at post-treatment, the range for the combined treated and nontreated groups was 23-214, although these values were not corrected for the number of C-units produced (McDuffie at el. 2018 Developmental Neurorehabilitation). (NCT02642653)
Timeframe: Baseline

Interventionscore on a scale (Mean)
Lovastatin and PILI39.63
Placebo and PILI42.47

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Expressive Language Sample Composite Score in the Home

The primary outcome reflects the diversity of vocabulary used. Higher scores reflect more skill. The lowest possible value is zero. No theoretical maximum can be defined because the wordless picture books can lead to a large and indeterminate set of options for the amount of talk and the vocabulary used. In a previous study of a nonpharmacological intervention, the range at baseline was 9-177, and at post-treatment, the range for the combined treated and nontreated groups was 23-214, although these values were not corrected for the number of C-units produced (McDuffie at el. 2018 Developmental Neurorehabilitation). (NCT02642653)
Timeframe: 20 weeks

Interventionscore on a scale (Mean)
Lovastatin and PILI59.32
Placebo and PILI54.81

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Clinical Global Impression-Improvement (CGI-I) Scale

A clinician rated scale utilizing history from the parents or caregiver and incorporating it into a clinical rating to assess for overall therapeutic response. The 7-point scale ranges from: 1 = Very much improved; 2 = Much improved; 3 = Minimally improved; 4 = No change; 5 = Minimally worse; 6 = Much worse; and 7 = Very much worse. Therefore, the lower the score, the greater the overall improvement as rated by the clinician. The CGI-I was used at the 10 week and 20 week visits. Shown here are the CGI-I mean scores from the 10-weeks end-of-study visit. (NCT02642653)
Timeframe: 10 weeks

Interventionunits on a scale (Mean)
Lovastatin and PILI2.92
Placebo and PILI3.00

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Clinical Global Impression- Severity (CGI-S)

A clinician rated scale utilizing history from the parents or caregiver and incorporating it into a clinical rating for severity. The CGI-S was used at the pre-treatment assessment to judge symptom severity. The 7-point scale ranges from: 1 = Normal; 2 = Borderline Ill; 3 = Mildly Ill; 4 = Moderately Ill; 5 = Markedly Ill; 6 = Severely Ill; and 7 = Extremely Ill. Therefore, the higher the score, the greater the severity of the patient's illness. Shown here are the CGI-S mean scores from the baseline visit. (NCT02642653)
Timeframe: Baseline

Interventionunits on a scale (Mean)
Lovastatin and PILI4.58
Placebo and PILI4.50

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FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale

The ABC-C is a 58-item caregiver-rated behavior scale used to examine treatment effects on challenging behaviors for individuals with FXS in the following domains: (1) irritability; (2) lethargy/social withdrawal; (3) stereotypic behavior; (4) hyperactivity; and (5) inappropriate speech. Caregiver rates the subject's behavior as follows: 0 = not a problem, l = the behavior is a problem but slight in degree, 2 = the problem is moderately serious, 3 = the problem is severe in degree. Sansone et al. (2012) further subdivided social withdrawal to rate social avoidance in FXS. The subscale includes 4 items which were originally part of the Lethargy/Withdrawal subscale. This subscale captures core aspects of the FXS phenotype related to gaze avoidance, social ''escape'' behaviors, and social anxiety. Subscale score ranges from 0 to 12, higher scores reflect a more problematic behavior. Shown are the ABC social avoidance subscale mean scores from the 20-weeks end-of-study visit. (NCT02642653)
Timeframe: 20 weeks

Interventionscore on a scale (Mean)
Lovastatin and PILI2.42
Placebo and PILI3.38

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Visual Analog Scale (VAS) - Spoken Language Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Spoken Language Impairment scale, at baseline. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: Baseline

Interventioncentimeters (Mean)
Lovastatin and PILI4.06
Placebo and PILI1.94

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FXS- Normed Aberrant Behavior Checklist (ABC) Social Avoidance Subscale

The ABC-C is a 58-item caregiver-rated behavior scale used to examine treatment effects on challenging behaviors for individuals with FXS in the following domains: (1) irritability; (2) lethargy/social withdrawal; (3) stereotypic behavior; (4) hyperactivity; and (5) inappropriate speech. Caregiver rates the subject's behavior as follows: 0 = not a problem, l = the behavior is a problem but slight in degree, 2 = the problem is moderately serious, 3 = the problem is severe in degree. Sansone et al. (2012) further subdivided social withdrawal to rate social avoidance in FXS. The subscale includes 4 items which were originally part of the Lethargy/Withdrawal subscale. This subscale captures core aspects of the FXS phenotype related to gaze avoidance, social ''escape'' behaviors, and social anxiety. Subscale score ranges from 0 to 12, higher scores reflect a more problematic behavior. Shown here are the ABC social avoidance subscale mean scores from the 10-weeks follow-up visit. (NCT02642653)
Timeframe: 10 weeks

Interventionscore on a scale (Mean)
Lovastatin and PILI2.5
Placebo and PILI3.53

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Visual Analog Scale (VAS) - Social Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Social Impairment scale, at 10-weeks. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: 10-weeks

Interventioncentimeters (Mean)
Lovastatin and PILI4.57
Placebo and PILI3.41

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Visual Analog Scale (VAS) - Social Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Social Impairment scale, at 20-weeks. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: 20-weeks

Interventioncentimeters (Mean)
Lovastatin and PILI5.18
Placebo and PILI3.99

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Visual Analog Scale (VAS) - Social Impairment

"The measure was used to assess parental impressions of progress in two key symptoms: spoken language impairment and social impairment. The distance of the mark from one end is used as the outcome variable for analysis. Caregivers mark on a visual line measuring 10 cm with worst behavior at 0 cm and best behavior at 10 cm. For each behavior the caregiver is instructed to mark their impression of the behavior at baseline visit and again at the 10-weeks and 20-weeks visits. The calculated distance in cm between the marks drawn at the baseline and follow-up visits thereby demonstrates whether each behavior improved, worsened, or stayed the same during the study, and by how much. Shown here is the mean distance in cm from the worst behavior side for the Social Impairment scale, at baseline. The smaller the value, the worse the behavior. The range is minimum 0 cm to maximum 10 cm." (NCT02642653)
Timeframe: Baseline

Interventioncentimeters (Mean)
Lovastatin and PILI3.73
Placebo and PILI2.55

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Change in EEG Relative Gamma Power

EEG relative gamma power at rest was calculated as the percent of power in the gamma frequencies relative to the sum of power in all frequency bands, averaged across electrodes, and calculated separately at pre-dose and post-dose timepoints. To assess the impact of drug, the pre-dose relative gamma power was subtracted from post-dose relative gamma power. Higher numbers indicate more relative gamma power post-dose; lower numbers indicate more relative gamma power pre-dose. (NCT02998151)
Timeframe: Pre-dose, 4-hour post-dose

Interventionpercent of power in gamma frequencies (Mean)
Placebo0.0024
Acamprosate-0.0077
Lovastatin-0.0039
Minocycline0.0019
Baclofen-0.0160

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Change From Pre-dose in the Repeatable Battery for the Assessment of Neuropsychological Status at 4 Hours Post Dose

Four 10-item lists of unrelated words were presented orally to the examinee who was then required to immediately recall words presented, at both pre-dose and post-dose timepoints. The impact of drug was assessed by subtracting the number of words remembered post-dose from the number of words remembered pre-dose. Lower numbers indicate more words remembered post-dose; higher numbers indicate more words remembered pre-dose. (NCT02998151)
Timeframe: Pre-dose, 4-hour post dose

Interventionnumber of words remembered (Mean)
Placebo-.20
Acamprosate-1.47
Lovastatin-1.25
Minocycline-.69
Baclofen-.88

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Woodcock Johnson Test of Cognitive Abilities - Auditory Attention Task

Woodcock Johnson Test of Cognitive Abilities III Auditory Attention subscale. Participants must identify orally presented words amid increasingly intense background noise. The scores for this subtask range from 0-50, with higher scores indicating a better outcome. Raw scores for this subscale are reported (rather than standard scores, or age- or grade-equivalents). (NCT02998151)
Timeframe: 4-hour post-dose

Interventionscore on a scale (Mean)
Placebo32.84
Acamprosate33.07
Lovastatin32.93
Minocycline33.24
Baclofen33

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Test of Attentional Performance for Children (KiTAP) Test of Alertness

Computerized task where an examinee is required to push a key when a target stimulus is presented on the screen. Scores are presented as change in median reaction time (RT), in milliseconds. (NCT02998151)
Timeframe: Predose, 4-hour post-dose

Interventionchange in median RT in milliseconds (Mean)
Placebo13.76
Acamprosate-28.64
Lovastatin18.59
Minocycline26.85
Baclofen-31.44

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Clinical Global Impressions-Improvement

The Clinical Global Impressions - Improvement (CGI-I) requires the clinician to assess how much the patient's illness has changed relative to pre-dose, from 1 (very much improved) to 7 (very much worse). (NCT02998151)
Timeframe: 4-hour post-dose

Interventionscore on a scale (Mean)
Placebo3.70
Acamprosate3.88
Lovastatin3.97
Minocycline3.81
Baclofen3.94

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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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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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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 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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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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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 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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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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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 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 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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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 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 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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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 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: 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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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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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 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 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 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: 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: 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 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 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 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 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 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 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 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 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: 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: 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: 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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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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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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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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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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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 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: 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: 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 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 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: 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: 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 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 (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 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: 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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Proportion of Overall Responders During the 12-week Treatment Period

An overall 12-week responder is defined as a patient with a weekly response in at least 50% of the weeks of treatment (6 of 12 weeks). A weekly response is defined as a decrease in the patient's weekly average score for worst abdominal pain in the past 24 hours of at least 30% compared to baseline and a stool frequency increase of 1 or more CSBMs per week compared with baseline. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg1
SYN-010 42 mg2
Placebo6

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Proportion of Patients With Adequate Relief

Outcome will be assessed by evaluating proportion of patients reporting adequate relief pre- and post-treatment on validated questionnaire. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg1
SYN-010 42 mg2
Placebo6

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Proportion of Patients Using Rescue Medication

Subjects will record their use of rescue medication throughout the study period. Proportion of patients using rescue medication after completing the 12-week course of treatment will be compared to those reporting usage at baseline screening period. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg9
SYN-010 42 mg11
Placebo8

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Proportion of Overall Stool Frequency Responders During the 12-week Treatment Period

An overall stool frequency responder is defined as a patient with a weekly stool frequency response in at least 50% of the weeks of treatment (6 of 12 weeks). A weekly stool frequency response is defined as a stool frequency increase of 1 or more CSBMs per week compared with baseline, with abdominal pain unchanged or improved compared with baseline. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg4
SYN-010 42 mg6
Placebo9

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Proportion of Overall Bloating Responders During the 12-week Treatment Period

An overall bloating responder is defined as a patient with a weekly bloating response in at least 50% of the weeks of treatment (6 of 12 weeks). A weekly bloating response is defined as a weekly average bloating score of at least 30% improvement compared to baseline, with stool frequency unchanged or improved compared with baseline. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg3
SYN-010 42 mg3
Placebo1

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Proportion of Overall Abdominal Pain Intensity Responders During the 12-week Treatment Period

An overall abdominal pain intensity responder is defined as a patient with a weekly abdominal pain intensity response in at least 50% of the weeks of treatment (6 of 12 weeks). A weekly response abdominal pain intensity response is defined as a decrease in the patient's weekly average score for worst abdominal pain in the past 24 hours of at least 30% compared to baseline, with stool frequency unchanged or improved compared with baseline. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionParticipants (Count of Participants)
SYN-010 21 mg4
SYN-010 42 mg4
Placebo7

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Mean Change From Baseline in the Area-under-the-curve (AUC) of Breath Methane Production, Based on the 120-minute Lactulose Breath Test.

Change in exhaled methane level as a potential predictor of constipation improvement will be evaluated by comparing lactulose breath tests pre- and post-treatment. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

Interventionparticles per million * min (Mean)
SYN-010 21 mg-18.678
SYN-010 42 mg-20.137
Placebo-39.199

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Change From Baseline in the Weekly Average Number of Completely Spontaneous Bowel Movements (CSBM) Compared to the 12-week Treatment Period

Subjects will record their daily bowel movements throughout the duration of the study. Change in weekly average number of CSBMs will be evaluated by comparing reported values pre- and post-treatment. (NCT03763175)
Timeframe: After completing 12-week course of SYN-010

InterventionWeekly average CSBMs (Least Squares Mean)
SYN-010 21 mg1.53
SYN-010 42 mg0.32
Placebo0.51

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Change From Baseline in Breath Methane Production Based on a Single-point Breath Methane Test

Change in exhaled methane level as a potential predictor of constipation improvement will be evaluated by comparing single-point breath tests pre- and post-treatment. (NCT03763175)
Timeframe: After completing course of SYN-010

Interventionparticles per million (Mean)
SYN-010 21 mg-22.623
SYN-010 42 mg-4.785
Placebo-10.081

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Application Frequency Influence on Disseminated Actinic Porokeratosis General Assessment Severity Index

Measure if applying once or twice a day had an affect on treatment efficacy using the DSAP-GASI described in the primary outcome. Factors included plaque/rim elevation, scaling, and color. (0= clear, 1=almost clear, 2=mild, 3=moderate, and 4=severe). Lower score indicates better outcome. (NCT04359823)
Timeframe: 12 weeks

Interventionscore on a scale (Mean)
DSAP-GASI Score With Once a Day Application1.42
DSAP-GASI Score With Twice a Day Application1.54

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Improvement in Color of DSAP Lesions

Patients were asked if their color was lighter, unchanged, darker. The responses were collected at weeks 4, 8, and 12. Only the final visit (week 12) was used in analysis. Lighter coloring is reported in the data table. (NCT04359823)
Timeframe: 12 weeks

Interventionparticipants denoting a score of lighter (Number)
Statin/Cholesterol Combination Group13
Statin Alone Group12

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Improvement in Dermatology Quality of Life Index Questionnaire

"The patient quality of life scale asks 10 questions gaging how the patient skin condition is currently impacting their life. This questionnaire is a common validated tool, available free online. DLQI interpretation: no effect (0-1), mild effect (2-5), moderate effect (6-10), very large effect (11-20), extreme large effect (21-30). Lower scores represent improved quality of life.~This was given after every visit at weeks 0, 4, 8, and 12 to access if the cream has contributed to quality of life improvement. The mean difference between the first (week 0) and last score (week 12) was used as the final improvement score." (NCT04359823)
Timeframe: 12 weeks

InterventionPercent improvement in quality of life (Number)
Statin/Cholesterol Combination Group48
Statin Alone Group38

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Improvement in Overall Appearance of DSAP Lesions

Patients were asked if their overall appearance was better, unchanged, worse. The responses were collected at weeks 4, 8, and 12. Only the final visit (week 12) was used in analysis. Better overall improvement is reported in the data table. (NCT04359823)
Timeframe: 12 weeks

Interventionparticipants denoting a score of better (Number)
Statin/Cholesterol Combination Group14
Statin Alone Group12

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Improvement in Size of DSAP Lesions

Patients were asked if their lesion size was smaller, unchanged, or larger. The responses were collected at weeks 4, 8, and 12. Only the final visit (week 12) was used in analysis. The number of participants reporting smaller lesions is reported in the data table. (NCT04359823)
Timeframe: 12 weeks

Interventionparticipants denoting smaller size (Number)
Statin/Cholesterol Combination Group12
Statin Alone Group11

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Measurement of Treatment Efficacy Determined by DSAP-GASI Score (Disseminated Actinic Porokeratosis General Assessment Severity Index)

The primary endpoint was the percentage of lesion clearance after 12 weeks of therapy using an exploratory clinical measure modified from a validated psoriasis index. The Disseminated Actinic Porokeratosis General Assessment Severity Index (DSAP-GASI) included plaque/rim elevation, scaling, and color (0= clear, 1=almost clear, 2=mild, 3=moderate, and 4=severe). Lesions of each patient were graded by 2 blinded physicians before and after treatment. (NCT04359823)
Timeframe: 12 weeks

InterventionPercent decrease in mean DSAP-GASI score (Number)
Statin/Cholesterol Combination Group50.0
Statin Alone Group51.4

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Pain and Itch Associated With Treatment

Pain and Itch were measured as increased or decreased at weeks 0, 4, 8, and 12. Week 12 findings reported. (NCT04359823)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
Statin/Cholesterol Combination Group Itch Decrease5
Statin/Cholesterol Combination Group Itch Increase1
Statin Alone Group Itch Decrease1
Statin Alone Group Itch Increase1
Statin/Cholesterol Combination Group Pain Decrease2
Statin/Cholesterol Combination Group Pain Increase0
Statin Alone Group Pain Decrease0
Statin Alone Group Pain Increase0

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