anacetrapib profile

ID Source	ID
PubMed CID	11556427
CHEMBL ID	1800807
SCHEMBL ID	531448
MeSH ID	M0524107

Synonym
anacetrapib ,
HY-12090
D08855
875446-37-0
anacetrapib (jan/usan)
mk-0859;(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-[[4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl]methyl]-4-methyl-1,3-oxazolidin-2-one
A24886
unii-p7t269pr6s
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-2'-methoxy-5'-(propan-2- yl)-4-(trifluoromethyl)(1,1'-biphenyl)-2-yl)methyl)-4-methyl-1,3-oxazolidin-2-one
anacetrapib [usan:inn]
2-oxazolidinone, 5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-2'-methoxy-5'-(1- methylethyl)-4-(trifluoromethyl)(1,1'-biphenyl)-2-yl)methyl)-4-methyl-, (4s,5r)-
p7t269pr6s ,
CHEMBL1800807 ,
mk-0859
mk0859
BCP9000299
anacetrapib (mk-0859)
bdbm50348228
BCPP000402
NCGC00346671-01
CS-0636
anacetrapib [who-dd]
anacetrapib [usan]
anacetrapib [mi]
anacetrapib [mart.]
anacetrapib [jan]
anacetrapib [inn]
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-2'-methoxy-5'-(propan-2-yl)-4-(trifluoromethyl)(1,1'-biphenyl)-2-yl)methyl)-4-methyl-1,3-oxazolidin-2-one
S2748
MLS006010190
smr004701293
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-[[4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl]methyl]-4-methyl-1,3-oxazolidin-2-one
SCHEMBL531448
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-{[4'-fluoro-5'isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl]methyl}-4-methyl-1,3-oxazolidin-2-one
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-{[4'-fluoro-5'isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl]methyl}4-methyl-1,3-oxazolidin-2-one
J-501484
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl)methyl)-4-methyl-1 ,3-oxazolidin-2-one
mfcd16294903
AKOS025290725
gtpl8400
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-[[2-(4-fluoro-2-methoxy-5-propan-2-ylphenyl)-5-(trifluoromethyl)phenyl]methyl]-4-methyl-1,3-oxazolidin-2-one
AC-25517
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)biphenyl-2-yl)methyl)-4-methyloxazolidin-2-one
DTXSID90236452
EX-A420
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-({2-[4-fluoro-2-methoxy-5-(propan-2-yl)phenyl]-5-(trifluoromethyl)phenyl}methyl)-4-methyl-1,3-oxazolidin-2-one
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)-[1,1'-biphenyl]-2-yl)methyl)-4-methyloxazolidin-2-one
Q4750639
(4s,5r)-5-(3,5-bis(trifluoromethyl)phenyl)-3-((4'-fluoro-5'-isopropyl-2'-methoxy-4-(trifluoromethyl)-[1,1'-biphenyl]-2-yl)methyl)-4-methyloxazolidin-2-one.
DB06630
AS-19552
BCP02374
AMY19494
CCG-270307
15?-hydroxy testosterone
(4s,5r)-5-[3,5-bis(trifluoromethyl)phenyl]-3-[[4'-fluoro-2'-methoxy-5'-(1-methylethyl)-4-(trifluoromethyl)[1,1'-biphenyl]-2-yl]methyl]-4-methyl-2-oxazolidinone

Excerpt	Reference	Relevance
"Anacetrapib is an inhibitor of cholesteryl ester transfer protein (CETP) previously under development as a lipid-modifying agent that reduces LDL-cholesterol and increases HDL-cholesterol in hypercholesterolemic patients. "	( Impact of drug distribution into adipose on tissue function: The cholesteryl ester transfer protein (CETP) inhibitor anacetrapib as a test case. Bateman, T; Blaustein, RO; Chen, Y; Hubert, J; Johns, DG; Rosa, R; Wang, SP; Xu, S, 2019)	2.17
"Anacetrapib is a novel cholesteryl-ester transfer protein (CETP) inhibitor in late-stage clinical development, shown in preceding clinical trials to have residual pharmacological activity after prolonged washout after chronic dosing. "	( Chronic Administration of Anacetrapib Is Associated With Accumulation in Adipose and Slow Elimination. Blaustein, RO; Chawla, A; Cote, J; Gheyas, F; Gutstein, DE; Hagen, DR; Krishna, R; Liu, Y; Walker, B, 2017)	2.2
"Anacetrapib is a cholesteryl ester transfer protein (CETP) inhibitor being developed for the treatment of mixed dyslipidemia. "	( Pharmacokinetics and Pharmacodynamics of Anacetrapib Following Single Doses in Healthy, Young Japanese and White Male Subjects. Cote, J; Denker, AE; Gheyas, F; Krishna, R; Laterza, O; Liu, Y; Ruckle, JL; Wagner, JA, 2018)	2.19
"Anacetrapib is a cholesteryl ester transfer protein inhibitor intended for the treatment of dyslipidemia. "	( Pharmacokinetics and Pharmacodynamics of Anacetrapib in Black and White Healthy Subjects. Corr, C; Cote, J; Gheyas, F; Gutstein, DE; Krishna, R; Liu, Y; Wagner, J, 2018)	2.19
"Anacetrapib is an inhibitor of cholesteryl ester transfer protein (CETP), associated with reduction in LDL cholesterol and increase in HDL cholesterol in hypercholesterolemic patients. "	( Characterization of Anacetrapib Distribution into the Lipid Droplet of Adipose Tissue in Mice and Human Cultured Adipocytes. Bateman, T; Blaustein, RO; Chen, Y; Hartmann, G; Johns, DG; Krsmanovic, M; LeVoci, L; Lu, M; Wang, SP; Xu, S, 2019)	2.28
"Anacetrapib is a novel cholesteryl ester transfer protein (CETP) inhibitor in development for treatment of dyslipidemia. "	( Effects of Rifampin, a potent inducer of drug-metabolizing enzymes and an inhibitor of OATP1B1/3 transport, on the single dose pharmacokinetics of anacetrapib. Anderson, MS; Auger, P; Cote, J; Gutstein, DE; Hohnstein, A; Johnson-Levonas, AO; Liu, Y; Rasmussen, S; Stypinski, D, 2013)	2.03
"Anacetrapib is a cholesteryl ester transfer protein inhibitor in Phase III development. "	( Single therapeutic and supratherapeutic doses of anacetrapib, a cholesteryl ester transfer protein inhibitor, do not prolong the QTcF interval in healthy volunteers. Farmer, HF; Johnson-Levonas, AO; Lai, E; Larson, P; Lauring, B; Li, XS; Liu, Y; Moreau, A; Wagner, JA, 2014)	2.1
"Anacetrapib is a cholesteryl ester transfer protein (CETP) inhibitor currently in Phase III of development as a treatment for those with dyslipidemia and the risk of cardiovascular disease. "	( Anacetrapib: a potential new therapy for dyslipidemia. Frishman, WH; Robinson, LB, )	3.02
"Anacetrapib is a cholesteryl ester transfer protein (CETP) inhibitor that has previously been shown to reduce low-density lipoprotein cholesterol (LDL-C) and raise high-density lipoprotein cholesterol (HDL-C) in patients with or at high risk of coronary heart disease in the 76-week, placebo-controlled, Determining the Efficacy and Tolerability of CETP Inhibition with Anacetrapib (DEFINE) trial. "	( Lipids, safety parameters, and drug concentrations after an additional 2 years of treatment with anacetrapib in the DEFINE study. Barter, P; Brinton, EA; Cannon, CP; Chatterjee, MS; Dansky, HM; Gotto, AM; Kher, U; Li, XS; Liu, Y; Mitchel, Y; Moon, JE; Shah, S; Vaidya, S, 2014)	2.06
"Anacetrapib is an orally active, potent inhibitor of cholesteryl ester transfer protein (CETP), which is in development for the treatment of dyslipidaemia. "	( Assessment of a pharmacokinetic and pharmacodynamic interaction between simvastatin and anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy subjects. Bieberdorf, FA; Chodakewitz, J; Garg, A; Jin, B; Keshavarz, SS; Krishna, R; Wagner, JA, 2009)	2.02
"Anacetrapib is a cholesteryl ester transfer protein (CETP) inhibitor that raises HDL-C and reduces LDL-C when administered alone or with a statin."	( Design of the DEFINE trial: determining the EFficacy and tolerability of CETP INhibition with AnacEtrapib. Barter, P; Binkowitz, B; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gibbons, P; Gotto, AM; Gould, AL; Hermanowski-Vosatka, A; Liu, SX; Mitchel, Y; Rubino, J; Shah, S; Stepanavage, M, 2009)	1.29
"Anacetrapib is an orally active and potent inhibitor of CETP in development for the treatment of dyslipidaemia. "	( Single-dose pharmacokinetics and pharmacodynamics of anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy subjects. Al-Huniti, N; Archer, L; Bergman, AJ; Chavez-Eng, C; Chen, J; Cote, J; Dykstra, K; Garg, A; Gottesdiener, K; Hilliard, D; Jin, B; Krishna, R; Laethem, T; Lasseter, KC; Lutz, R; Panebianco, D; Snyder, K; Van Bortel, L; Van Dyck, K; Van Hoydonck, P; Wagner, JA, 2009)	2.05
"Anacetrapib is a novel cholesteryl ester transfer protein inhibitor being developed for the treatment of primary hypercholesterolemia and mixed dyslipidemia. "	( Metabolism and excretion of anacetrapib, a novel inhibitor of the cholesteryl ester transfer protein, in humans. Bergman, AJ; Biddle, Z; Braun, MP; Dean, DC; Dru, J; Gendrano, IN; Graves, MW; Hartmann, G; Ho, JZ; Jones, AN; Karanam, B; Krishna, R; Kumar, S; Staskiewicz, SJ; Tan, EY; Wagner, JA, 2010)	2.1
"Anacetrapib is a cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and reduces low-density lipoprotein (LDL) cholesterol."	( Safety of anacetrapib in patients with or at high risk for coronary heart disease. Ashraf, TB; Barter, P; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gibbons, P; Gotto, AM; Liu, SX; Mitchel, Y; Shah, S; Stepanavage, M; Zafarino, J, 2010)	2.21
"Anacetrapib is a cholesteryl-ester-transfer-protein (CETP) inhibitor, a new class of experimental drugs in the treatment of primary hypercholesterolemia and dyslipidaemia associated with the metabolic syndrome. "	( Anacetrapib: a new weapon against dyslipidemia. Alivanis, P; Aperis, G; Paliouras, C; Papakonstantinou, N; Tsampikaki, E, 2011)	3.25
"Anacetrapib is a potent, reversible CETP inhibitor that is not only able to increase HDL-cholesterol, but also further decrease LDL-cholesterol when taken in combination with a statin. "	( Anacetrapib, a cholesteryl ester transfer protein inhibitor. Burnett, JR; Hooper, AJ, 2012)	3.26
"Anacetrapib is a novel CETP inhibitor in development."	( Lack of a meaningful effect of anacetrapib on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Ali, M; Connolly, SM; Cote, J; Degroot, B; Garg, A; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2012)	1.39
"Anacetrapib (MK-0859) is a CETP inhibitor currently under development."	( Effect of the cholesteryl ester transfer protein inhibitor, anacetrapib, on lipoproteins in patients with dyslipidaemia and on 24-h ambulatory blood pressure in healthy individuals: two double-blind, randomised placebo-controlled phase I studies. Anderson, MS; Bergman, AJ; Bieberdorf, F; Bloomfield, DM; Chavez-Eng, C; Chodakewitz, J; Cote, J; Doherty, J; Fallon, M; Gottesdiener, KM; Gutierrez, M; Jin, B; Krishna, R; Lutz, R; Rosko, K; Wagner, JA, 2007)	1.3

Excerpt	Reference	Relevance
"Anacetrapib has a good safety profile."	( Cardiovascular outcomes trial with anacetrapib in subjects with high cardiovascular risk - are major benefits REVEALed? Doggrell, SA, 2018)	1.48
"Anacetrapib has been shown to raise HDL-C by up to 138% and decrease low-density lipoprotein cholesterol by up to 39% compared with placebo."	( Anacetrapib: a potential new therapy for dyslipidemia. Frishman, WH; Robinson, LB, )	2.3

Excerpt	Reference	Relevance
"Anacetrapib treatment was associated with a small increase in blood pressure, but was devoid of major side effects and was also associated with a small reduction in diabetes mellitus."	( Trials and Tribulations of CETP Inhibitors. Rader, DJ; Tall, AR, 2018)	1.2
"Anacetrapib may be a new treatment option that has a cardiovascular benefit for the management of dyslipidemia."	( The effect and safety of anacetrapib in the treatment of dyslipidemia: a systematic review and meta-analysis. Chen, D; Gao, P; Wang, Y; Zhang, Q; Zhou, J, 2018)	1.51
"Anacetrapib treatment was associated with considerable increases in the LDL triglyceride/cholesterol ratio and LDL size by NMR."	( Anacetrapib lowers LDL by increasing ApoB clearance in mildly hypercholesterolemic subjects. Baer, AL; deGoma, EM; Donovan, DS; Dunbar, RL; Ginsberg, HN; Gutstein, DE; Holleran, S; Johnson-Levonas, AO; Jumes, P; Karmally, W; Lassman, ME; Liu, Y; Millar, JS; Obunike, J; Pollan, L; Rader, DJ; Rafeek, H; Ramakrishnan, R; Reyes-Soffer, G; Tohyama, J; Wagner, JA, 2015)	2.58
"Anacetrapib treatment increased plasma HDL cholesterol levels by 65% and between 48 and 82% in hamsters and humans, respectively."	( Inhibition of cholesteryl ester transfer protein by anacetrapib does not impair the anti-inflammatory properties of high density lipoprotein. Chen, Y; Ehrhardt, AG; Fischer, P; Fisher, T; Gagen, K; Han, S; Johns, DG; Levoci, L; Peier, AM; Wang, SP; Xie, D, 2013)	1.36
"Treatment with anacetrapib reduced LDL-C (BQ) by 37% (95% confidence interval -42.5, -31.0) and increased HDL-C by 118% (95% confidence interval 110.6, 125.7) relative to placebo (p <0.001 for both)."	( A Multiregional, Randomized Evaluation of the Lipid-Modifying Efficacy and Tolerability of Anacetrapib Added to Ongoing Statin Therapy in Patients With Hypercholesterolemia or Low High-Density Lipoprotein Cholesterol. Ashraf, TB; Ballantyne, CM; Briones, IR; Dong, Y; Ferreira Rossi, PR; Johnson-Levonas, AO; Kang, DH; Mitchel, YB; Moiseeva, Y; Sahin, T; Sapre, A; Shah, S; Sheu, WH; Tobias, SC; Ye, P, 2017)	1.02
"Treatment with anacetrapib during the 2-year extension was well tolerated with a safety profile similar to patients on placebo."	( Lipids, safety parameters, and drug concentrations after an additional 2 years of treatment with anacetrapib in the DEFINE study. Barter, P; Brinton, EA; Cannon, CP; Chatterjee, MS; Dansky, HM; Gotto, AM; Kher, U; Li, XS; Liu, Y; Mitchel, Y; Moon, JE; Shah, S; Vaidya, S, 2014)	0.96
"Treatment with anacetrapib in this model was also found to lead to statistically significant reductions in plasma PCSK9 and to reduce cholesterol excursion in the combined chylomicron and remnant lipoprotein fraction isolated from plasma by fast protein liquid chromatography."	( Effects of anacetrapib on plasma lipids, apolipoproteins and PCSK9 in healthy, lean rhesus macaques. Ai, X; Akinsanya, KO; Albanese, K; Chen, Y; Cleary, MA; Dansky, HM; Donnelly, M; Dunn, K; Forrest, G; Gai, C; Gewain, A; Jensen, KK; Johns, DG; Kulick, A; Lederman, H; McLaren, DG; Previs, SF; Roddy, TP; Szeto, D; Vachal, P; Xie, D, 2014)	1.13
"Treatment with anacetrapib had robust effects on LDL and HDL cholesterol, had an acceptable side-effect profile, and, within the limits of the power of this study, did not result in the adverse cardiovascular effects observed with torcetrapib. "	( Safety of anacetrapib in patients with or at high risk for coronary heart disease. Ashraf, TB; Barter, P; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gibbons, P; Gotto, AM; Liu, SX; Mitchel, Y; Shah, S; Stepanavage, M; Zafarino, J, 2010)	1.12

Excerpt	Reference	Relevance
" Anacetrapib was well tolerated, and the incidence of adverse events was similar for placebo and all active treatment groups."	( Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib as monotherapy and coadministered with atorvastatin in dyslipidemic patients. Bloomfield, D; Carlson, GL; Littlejohn, TW; McKenney, JM; Mitchel, Y; Pasternak, RC; Sapre, A; Sisk, CM; Tribble, D, 2009)	1.5
" The primary end points were the percent change from baseline in LDL cholesterol at 24 weeks (HDL cholesterol level was a secondary end point) and the safety and side-effect profile of anacetrapib through 76 weeks."	( Safety of anacetrapib in patients with or at high risk for coronary heart disease. Ashraf, TB; Barter, P; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gibbons, P; Gotto, AM; Liu, SX; Mitchel, Y; Shah, S; Stepanavage, M; Zafarino, J, 2010)	0.95
"Treatment with anacetrapib had robust effects on LDL and HDL cholesterol, had an acceptable side-effect profile, and, within the limits of the power of this study, did not result in the adverse cardiovascular effects observed with torcetrapib."	( Safety of anacetrapib in patients with or at high risk for coronary heart disease. Ashraf, TB; Barter, P; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gibbons, P; Gotto, AM; Liu, SX; Mitchel, Y; Shah, S; Stepanavage, M; Zafarino, J, 2010)	1.12
" ANA was well tolerated, and dose-dependent relationships for adverse events were not observed across treatment groups."	( Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib in Japanese patients with dyslipidemia. Kikuchi, M; McCrary Sisk, C; Nakagomi, M; Numaguchi, H; Shirakawa, M; Surks, HK; Tamura, S; Teramoto, T, 2013)	0.62
"1%, with an acceptable side-effect profile, in patients with or at high risk for coronary heart disease in the Determining the Efficacy and Tolerability of CETP Inhibition With Anacetrapib (DEFINE) trial."	( Evaluation of lipids, drug concentration, and safety parameters following cessation of treatment with the cholesteryl ester transfer protein inhibitor anacetrapib in patients with or at high risk for coronary heart disease. Barter, P; Brinton, EA; Cannon, CP; Dansky, HM; Davidson, M; Gotto, AM; Kher, U; Li, XS; Mitchel, Y; Moon, JE; Shah, S; Vaidya, S, 2014)	0.79
" No clinically important abnormalities in liver enzymes, blood pressure, electrolytes, or adverse experiences were observed during the extension."	( Lipids, safety parameters, and drug concentrations after an additional 2 years of treatment with anacetrapib in the DEFINE study. Barter, P; Brinton, EA; Cannon, CP; Chatterjee, MS; Dansky, HM; Gotto, AM; Kher, U; Li, XS; Liu, Y; Mitchel, Y; Moon, JE; Shah, S; Vaidya, S, 2014)	0.62
" There were no differences between the groups in the proportion of patients who discontinued drug due to an adverse event or abnormalities in liver enzymes, creatinine kinase, blood pressure, electrolytes or adjudicated cardiovascular events."	( Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib in Japanese patients with heterozygous familial hypercholesterolemia. Arai, H; Blaustein, RO; Daida, H; Ikewaki, K; Johnson-Levonas, AO; Kakikawa, T; Maeda, Y; Nakagomi, M; Numaguchi, H; Shirakawa, M; Teramoto, T; Vaidya, S, 2016)	0.67
" There were no significant effects on non-vascular mortality, site-specific cancer, or other serious adverse events."	( Long-term safety and efficacy of anacetrapib in patients with atherosclerotic vascular disease. Angermann, C; Armitage, J; Baigent, C; Barter, P; Baxter, A; Blaustein, R; Bowman, L; Braunwald, E; Brenner, S; Cannon, C; Chen, F; Chen, Y; Chen, Z; Collins, R; Dayanandan, R; DeLucca, P; Ertl, G; Fabbri, G; Fajardo-Moser, M; Goodenough, R; Goto, S; Gray, A; Hao, D; Haynes, R; Herrington, W; Hill, M; Hopewell, JC; Knott, C; Landray, M; Lay, M; Liu, J; Lucci, D; Macdonnell, S; Maggioni, A; Mihaylova, B; Mitchel, Y; Mosegaard, S; Murphy, K; Sammons, E; Stevens, W; Tobert, J; Valdes-Marquez, E; Wallendszus, K; Wanner, C; Wincott, E; Wiviott, S; Wuhan, B; Zhang, H, 2022)	1
"The beneficial effects of anacetrapib on major coronary events increased with longer follow-up, and no adverse effects emerged on non-vascular mortality or morbidity."	( Long-term safety and efficacy of anacetrapib in patients with atherosclerotic vascular disease. Angermann, C; Armitage, J; Baigent, C; Barter, P; Baxter, A; Blaustein, R; Bowman, L; Braunwald, E; Brenner, S; Cannon, C; Chen, F; Chen, Y; Chen, Z; Collins, R; Dayanandan, R; DeLucca, P; Ertl, G; Fabbri, G; Fajardo-Moser, M; Goodenough, R; Goto, S; Gray, A; Hao, D; Haynes, R; Herrington, W; Hill, M; Hopewell, JC; Knott, C; Landray, M; Lay, M; Liu, J; Lucci, D; Macdonnell, S; Maggioni, A; Mihaylova, B; Mitchel, Y; Mosegaard, S; Murphy, K; Sammons, E; Stevens, W; Tobert, J; Valdes-Marquez, E; Wallendszus, K; Wanner, C; Wincott, E; Wiviott, S; Wuhan, B; Zhang, H, 2022)	1.3

Excerpt	Reference	Relevance
" Because of the likely use of anacetrapib with hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, we aimed to evaluate the potential for a pharmacokinetic interaction with simvastatin."	( Assessment of a pharmacokinetic and pharmacodynamic interaction between simvastatin and anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy subjects. Bieberdorf, FA; Chodakewitz, J; Garg, A; Jin, B; Keshavarz, SS; Krishna, R; Wagner, JA, 2009)	0.86
"There appears to be no clinically meaningful effect of anacetrapib on the pharmacokinetic parameters of simvastatin."	( Assessment of a pharmacokinetic and pharmacodynamic interaction between simvastatin and anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy subjects. Bieberdorf, FA; Chodakewitz, J; Garg, A; Jin, B; Keshavarz, SS; Krishna, R; Wagner, JA, 2009)	0.82
"Anacetrapib was rapidly absorbed, with peak concentrations occurring at approximately 4 h post-dose and an apparent terminal half-life ranging from approximately 9 to 62 h in the fasted state and from approximately 42 to approximately 83 h in the fed state."	( Single-dose pharmacokinetics and pharmacodynamics of anacetrapib, a potent cholesteryl ester transfer protein (CETP) inhibitor, in healthy subjects. Al-Huniti, N; Archer, L; Bergman, AJ; Chavez-Eng, C; Chen, J; Cote, J; Dykstra, K; Garg, A; Gottesdiener, K; Hilliard, D; Jin, B; Krishna, R; Laethem, T; Lasseter, KC; Lutz, R; Panebianco, D; Snyder, K; Van Bortel, L; Van Dyck, K; Van Hoydonck, P; Wagner, JA, 2009)	2.05
" WHAT THIS STUDY: ADDS • This is the first study to show that there is no clinically meaningful pharmacokinetic interaction between anacetrapib and warfarin."	( Lack of a meaningful effect of anacetrapib on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Ali, M; Connolly, SM; Cote, J; Degroot, B; Garg, A; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2012)	0.87
" After warfarin concentrations and prothrombin time were measured, standard pharmacokinetic, pharmacodynamic and statistical (linear mixed effects model) analyses were applied."	( Lack of a meaningful effect of anacetrapib on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Ali, M; Connolly, SM; Cote, J; Degroot, B; Garg, A; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2012)	0.66
" Log-transformed anacetrapib AUC0-∞ and Cmax were analyzed by a linear mixed effects model."	( Effects of Rifampin, a potent inducer of drug-metabolizing enzymes and an inhibitor of OATP1B1/3 transport, on the single dose pharmacokinetics of anacetrapib. Anderson, MS; Auger, P; Cote, J; Gutstein, DE; Hohnstein, A; Johnson-Levonas, AO; Liu, Y; Rasmussen, S; Stypinski, D, 2013)	0.93
"Anacetrapib, a cholesterol ester transfer protein (CETP) inhibitor, has been reported to have longer elimination half-life after longer treatment."	( Assessment of the persistence of anacetrapib and evacetrapib concentrations using two pharmacokinetic modeling approaches. Friedrich, S; Hall, SD; Ke, AB; Mantlo, N; Rotelli, M; Small, DS, 2015)	2.14
" We review its pharmacokinetic properties."	( Pharmacokinetic drug evaluation of anacetrapib for the treatment of dyslipidemia. Borghi, C; Cicero, AF, 2017)	0.73
" Although there was no apparent race-related pharmacokinetic effect, attenuation of the lipid response was observed in black subjects."	( Pharmacokinetics and Pharmacodynamics of Anacetrapib in Black and White Healthy Subjects. Corr, C; Cote, J; Gheyas, F; Gutstein, DE; Krishna, R; Liu, Y; Wagner, J, 2018)	0.75

Excerpt	Reference	Relevance
"Ion mobility was performed on stored plasma samples collected from patients before and after treatment with anacetrapib alone (150 and 300 mg/d) or in combination with atorvastatin (20 mg/d) in a previously conducted 8-week phase IIb study."	( Changes in LDL particle concentrations after treatment with the cholesteryl ester transfer protein inhibitor anacetrapib alone or in combination with atorvastatin. Dansky, HM; Johnson-Levonas, AO; Krauss, RM; Liu, Y; Pinto, CA, )	0.56

Excerpt	Reference	Relevance
" Anacetrapib exhibited a low clearance in both species and a moderate oral bioavailability of approximately 38% in rats and approximately 13% in monkeys."	( Pharmacokinetics, metabolism, and excretion of anacetrapib, a novel inhibitor of the cholesteryl ester transfer protein, in rats and rhesus monkeys. Bradley, S; Braun, MP; Chen, Q; Dean, DC; Doss, G; Hartmann, G; Ho, JZ; Kumar, S; Pereira, A; Tan, EY; Tang, W; Zhang, AS, 2010)	1.53
" The population pharmacokinetic model described differences between the liquid-filled capsule used in phase I and phase IIb and the hot-melt extruded (HME) tablet formulation introduced in phase III, allowing for bridging of the two formulations, and quantified the complex relationship of apparent anacetrapib bioavailability with subject meal intake."	( Model-based development of anacetrapib, a novel cholesteryl ester transfer protein inhibitor. Bergman, AJ; Dockendorf, MF; Dykstra, K; Green, M; Krishna, R; Wagner, JA, 2011)	0.84
" In order to further support the development of anacetrapib, we prepared [M + 6]MK-0859, which was required in support of an absolute bioavailability study of the active pharmaceutical ingredient (API)."	( Synthesis of stable isotope labeled anacetrapib, its major metabolites and [(14) C]anacetrapib. Kuethe, JT; Quinn, CA; Royster, P; Soli, ED, 2013)	0.92
" However, there are limited published data on the impact of nanoparticle size on bioavailability in vivo and, to our knowledge, there have been no published examples looking at the impact of differential size of in situ-generated nanoparticles from an ASD."	( Effect of Amorphous Nanoparticle Size on Bioavailability of Anacetrapib in Dogs. Galipeau, K; Harmon, P; Kesisoglou, F; Okoh, G; Wang, M; Xu, W, 2019)	0.76
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51

Excerpt	Relevance	Reference
" Overall, it appears that anacetrapib exhibits a low-to-moderate degree of absorption after oral dosing and majority of the absorbed dose is eliminated via oxidation to a series of hydroxylated metabolites that undergo conjugation with glucuronic acid before excretion into bile."	( Pharmacokinetics, metabolism, and excretion of anacetrapib, a novel inhibitor of the cholesteryl ester transfer protein, in rats and rhesus monkeys. Bradley, S; Braun, MP; Chen, Q; Dean, DC; Doss, G; Hartmann, G; Ho, JZ; Kumar, S; Pereira, A; Tan, EY; Tang, W; Zhang, AS, 2010)	0.92
" Their mechanism of action, potential for significant raising of HDL-C, once-daily dosing regimen, and favorable lipid-altering effects when added to hydroxymethylglutaryl-CoA reductase inhibitors are key elements."	( Anacetrapib and dalcetrapib: two novel cholesteryl ester transfer protein inhibitors. Miyares, MA, 2011)	1.81
" Thus, no dosage adjustment for digoxin is necessary when co-administered with anacetrapib."	( Lack of an effect of anacetrapib on the pharmacokinetics of digoxin in healthy subjects. Ali, M; Connolly, SM; DeGroot, B; Garg, A; Gendrano, IN; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2011)	0.92
" A drug interaction study for warfarin with a novel CETP inhibitor is expected to be helpful in defining dosing regimens."	( Lack of a meaningful effect of anacetrapib on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Ali, M; Connolly, SM; Cote, J; Degroot, B; Garg, A; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2012)	0.66
" Thus, no dosage adjustment for warfarin is necessary when co-administered with anacetrapib."	( Lack of a meaningful effect of anacetrapib on the pharmacokinetics and pharmacodynamics of warfarin in healthy subjects. Ali, M; Connolly, SM; Cote, J; Degroot, B; Garg, A; Krishna, R; Li, S; Liu, Y; Maes, A; Stoch, SA; Stypinski, D; Wagner, JA, 2012)	0.89
" This open-label, fixed-sequence, 3-period study was intended to evaluate the potential of anacetrapib to be a victim of OATP1B1/3 inhibition and strong CYP3A induction using acute and chronic dosing of rifampin, respectively, as a probe."	( Effects of Rifampin, a potent inducer of drug-metabolizing enzymes and an inhibitor of OATP1B1/3 transport, on the single dose pharmacokinetics of anacetrapib. Anderson, MS; Auger, P; Cote, J; Gutstein, DE; Hohnstein, A; Johnson-Levonas, AO; Liu, Y; Rasmussen, S; Stypinski, D, 2013)	0.81
" Mice were dosed orally with 10 mg/kg anacetrapib daily for 42 days."	( Disposition into Adipose Tissue Determines Accumulation and Elimination Kinetics of the Cholesteryl Ester Transfer Protein Inhibitor Anacetrapib in Mice. Burton, A; Chavez-Eng, C; Gheyas, F; Gutstein, D; Hartmann, G; Jackson, T; Johns, D; Kumar, S; Lederman, H; Lutz, R; Mitra, K; Shen, X, 2016)	0.91
" Consumption of a traditional Japanese breakfast prior to dosing increased the plasma pharmacokinetics of anacetrapib in Japanese subjects compared with fasted conditions, to a similar extent as in white subjects."	( Pharmacokinetics and Pharmacodynamics of Anacetrapib Following Single Doses in Healthy, Young Japanese and White Male Subjects. Cote, J; Denker, AE; Gheyas, F; Krishna, R; Laterza, O; Liu, Y; Ruckle, JL; Wagner, JA, 2018)	0.96
"Drug half-life has important implications for dosing regimen and peak-to-trough ratio at the steady state."	( Relevance of Half-Life in Drug Design. Beaumont, K; Di, L; Maurer, TS; Smith, DA, 2018)	0.48

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
EWS/FLI fusion protein	Homo sapiens (human)	Potency	20.0556	0.0013	10.1577	42.8575	AID1259253; AID1259256
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Cholesteryl ester transfer protein	Homo sapiens (human)	IC50 (µMol)	0.0343	0.0030	0.2169	4.1000	AID1282099; AID1330817; AID1435500; AID1476688; AID1500868; AID1646834; AID1692975; AID1783824; AID1783852; AID607213; AID638019
Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)	IC50 (µMol)	30.0000	0.0009	1.9014	10.0000	AID1783859
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)	EC50 (µMol)	3.9000	0.0020	3.5196	10.0000	AID1783834
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
negative regulation of DNA-templated transcription	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
regulation of DNA-templated transcription	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
xenobiotic metabolic process	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
signal transduction	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
steroid metabolic process	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
positive regulation of gene expression	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
intracellular receptor signaling pathway	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
xenobiotic catabolic process	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
xenobiotic transport	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
positive regulation of DNA-templated transcription	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
cell differentiation	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
triglyceride metabolic process	Cholesteryl ester transfer protein	Homo sapiens (human)
lipid transport	Cholesteryl ester transfer protein	Homo sapiens (human)
cholesterol metabolic process	Cholesteryl ester transfer protein	Homo sapiens (human)
negative regulation of macrophage derived foam cell differentiation	Cholesteryl ester transfer protein	Homo sapiens (human)
regulation of cholesterol efflux	Cholesteryl ester transfer protein	Homo sapiens (human)
phospholipid transport	Cholesteryl ester transfer protein	Homo sapiens (human)
cholesterol transport	Cholesteryl ester transfer protein	Homo sapiens (human)
positive regulation of cholesterol transport	Cholesteryl ester transfer protein	Homo sapiens (human)
triglyceride transport	Cholesteryl ester transfer protein	Homo sapiens (human)
very-low-density lipoprotein particle remodeling	Cholesteryl ester transfer protein	Homo sapiens (human)
low-density lipoprotein particle remodeling	Cholesteryl ester transfer protein	Homo sapiens (human)
high-density lipoprotein particle remodeling	Cholesteryl ester transfer protein	Homo sapiens (human)
cholesterol homeostasis	Cholesteryl ester transfer protein	Homo sapiens (human)
reverse cholesterol transport	Cholesteryl ester transfer protein	Homo sapiens (human)
phosphatidylcholine metabolic process	Cholesteryl ester transfer protein	Homo sapiens (human)
lipid homeostasis	Cholesteryl ester transfer protein	Homo sapiens (human)
phospholipid homeostasis	Cholesteryl ester transfer protein	Homo sapiens (human)
triglyceride homeostasis	Cholesteryl ester transfer protein	Homo sapiens (human)
positive regulation of phospholipid transport	Cholesteryl ester transfer protein	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of heart rate by hormone	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of membrane potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
positive regulation of DNA-templated transcription	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion homeostasis	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cardiac muscle contraction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of ventricular cardiac muscle cell membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cellular response to xenobiotic stimulus	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane depolarization during action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of heart rate by cardiac conduction	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
membrane repolarization during ventricular cardiac muscle cell action potential	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
negative regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
positive regulation of potassium ion transmembrane transport	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
negative regulation of potassium ion export across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
potassium ion import across plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
RNA polymerase II transcription regulatory region sequence-specific DNA binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
nuclear receptor activity	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
protein binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
zinc ion binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
nuclear receptor binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
sequence-specific double-stranded DNA binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
phospholipid transporter activity	Cholesteryl ester transfer protein	Homo sapiens (human)
lipid binding	Cholesteryl ester transfer protein	Homo sapiens (human)
cholesterol binding	Cholesteryl ester transfer protein	Homo sapiens (human)
triglyceride binding	Cholesteryl ester transfer protein	Homo sapiens (human)
phosphatidylcholine binding	Cholesteryl ester transfer protein	Homo sapiens (human)
cholesterol transfer activity	Cholesteryl ester transfer protein	Homo sapiens (human)
transcription cis-regulatory region binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
inward rectifier potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
delayed rectifier potassium channel activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
ubiquitin protein ligase binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
identical protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
protein homodimerization activity	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
C3HC4-type RING finger domain binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity involved in cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
scaffold protein binding	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
nucleoplasm	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
transcription regulator complex	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
nuclear body	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
intermediate filament cytoskeleton	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
chromatin	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
nucleus	Nuclear receptor subfamily 1 group I member 2	Homo sapiens (human)
extracellular region	Cholesteryl ester transfer protein	Homo sapiens (human)
extracellular space	Cholesteryl ester transfer protein	Homo sapiens (human)
vesicle	Cholesteryl ester transfer protein	Homo sapiens (human)
extracellular exosome	Cholesteryl ester transfer protein	Homo sapiens (human)
high-density lipoprotein particle	Cholesteryl ester transfer protein	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
cell surface	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
perinuclear region of cytoplasm	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
voltage-gated potassium channel complex	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
inward rectifier potassium channel complex	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
plasma membrane	Potassium voltage-gated channel subfamily H member 2	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (128)

Assay ID	Title	Year	Journal	Article
AID607212	Inhibition of human recombinant CETP-mediated cholesteryl ester transfer activity at 100 uM after 1 hr by fluorescent cholesteryl esters transfer assay relative to control	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID607213	Inhibition of human recombinant CETP-mediated cholesteryl ester transfer activity after 1 hr by fluorescent cholesteryl esters transfer assay	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID607217	Dose-normalized AUC in C57BL/6 mouse at 0.6 mg/kg, iv	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1500870	Antihyperlipidemic activity in transgenic ap2-CETPTg mouse model assessed as increase in plasma HDL cholesterol levels at 30 mg/kg, po qd for 14 days measured 2 hrs post dose on day 14 by automated lipid analyzer relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1692973	In vivo inhibition of CETP in human assessed as increase in HDL-C level	2021	Bioorganic & medicinal chemistry letters, 01-15, Volume: 32	Cholesteryl ester transfer protein (CETP) inhibitors based on cyclic urea, bicyclic urea and bicyclic sulfamide cores.
AID1654610	Lipophilicity, logD of the compound	2020	Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12	Metabolic and Pharmaceutical Aspects of Fluorinated Compounds.
AID1476712	Drug uptake in LDL fraction of human serum from human donors with normal triglyceride levels (<150 mg/dL) by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1476721	Inhibition of CETP in Syrian hamster blood at 3 and 10 mg/kg, po dosed once daily for 2 weeks and measured 24 hrs post last dose	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783843	Half life in C57BL/6 mouse at 0.6 mg/kg, iv	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476714	Drug uptake in triglyceride rich lipoprotein fraction of human serum from human donors with normal triglyceride levels (<150 mg/dL) by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1166852	Drug concentration in testes of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1500879	Antihyperlipidemic activity in high-fat fed guinea pig model assessed as increase in plasma HDL cholesterol level at 30 mg/kg administered via oral gavage as qd for 14 days measured 2 hrs post dose on day 14 relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1282099	Inhibition of full-length human recombinant CETP expressed in CHO cells by BODIPY-CE dye based fluorescence assay	2016	Bioorganic & medicinal chemistry, Apr-15, Volume: 24, Issue:8	Discovery of novel N,N-3-phenyl-3-benzylaminopropionanilides as potent inhibitors of cholesteryl ester transfer protein in vivo.
AID1476702	Increase in HDL cholesterol level in Syrian hamster plasma at 0.3 and 10 mg/kg, po dosed once daily for 2 weeks and measured 24 hrs post last dose by HPLC size exclusion chromatography method relative to control	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1166849	Drug concentration in muscle of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1500873	Inhibition of recombinant human CETP at 10 uM using fluorescent cholesteryl containing HDL after 3 hrs by fluorescence assay	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1500886	Octanol-water partition coefficient, log P of the compound at pH 7.4 by HPLC based shake flask method	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1783825	Inhibition of recombinant CETP (unknown origin) assessed as maximal inhibition of transfer of [3H]cholesteryl oleate or [3H]triolein between exogenous [3H]LDL in 95% human serum at 10 uM by liquid scintillation analysis	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1166869	Drug concentration in adipose fat of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 21 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1692982	In vivo inhibition of CETP in human assessed as reduction in LDL-C level	2021	Bioorganic & medicinal chemistry letters, 01-15, Volume: 32	Cholesteryl ester transfer protein (CETP) inhibitors based on cyclic urea, bicyclic urea and bicyclic sulfamide cores.
AID1654613	Drug recovery in bile duct-cannulated Sprague-Dawley rat feces at 10 mg/kg, po administered as single dose using 14C labelled compound measured after 48 hrs	2020	Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12	Metabolic and Pharmaceutical Aspects of Fluorinated Compounds.
AID1367800	Half life in human	2018	Journal of medicinal chemistry, 05-24, Volume: 61, Issue:10	Relevance of Half-Life in Drug Design.
AID1783846	Increase in HDL-C in C57BL/6-transgenic mouse expressing human CETP at 10 mg/kg, po bid	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476710	Ex vivo inhibition of CETP activity in hamster hypertriglyceridemia model treated with 100 mg/kg, iv Triton WR-1339 dosed 5 hrs post compound dose measured every 15 mins for 120 mins by fluorescence method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1646833	Inhibition of human CETP at 10 uM relative to control	2020	Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2	Synthesis, biological evaluation and SAR studies of ursolic acid 3β-ester derivatives as novel CETP inhibitors.
AID1476713	Drug uptake in lipoprotein deficient serum fraction of human serum from human donors with normal triglyceride levels (<150 mg/dL) by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783824	Inhibition of recombinant CETP (unknown origin) assessed as inhibition of transfer of [3H]cholesteryl oleate or [3H]triolein between exogenous [3H]LDL in 95% human serum by liquid scintillation analysis	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476706	Drug uptake in Syrian hamster plasma at 10 mg/kg, po dosed once daily for 14 days measured 24 hrs post last dose by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1476715	Toxicty in human NCI-H295R cells assessed as increase in aldosterone levels at 0.1 to 10000 nM after 24 hrs by scintillation proximity assay	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID638018	Cardioprotective activity in transgenic B6 mouse expressing cynomolgus monkey CETP assessed as increase in HDL-cholesterol level at 10 mg/kg, po BID measured after 24 hrs of first dose	2012	Bioorganic & medicinal chemistry letters, Jan-01, Volume: 22, Issue:1	SAR studies on the central phenyl ring of substituted biphenyl oxazolidinone-potent CETP inhibitors.
AID1783859	Inhibition of [S35]-MK-0499 binding to human ERG expressed in HEK293 cells	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1654611	Volume of distribution at steady state in Sprague-Dawley rat at 0.5 mg/kg, iv administered as single dose measured after 0.083 to 48 hrs	2020	Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12	Metabolic and Pharmaceutical Aspects of Fluorinated Compounds.
AID1166848	Drug concentration in plasma of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1692975	Inhibition of CETP in 95% human serum assessed as inhibition of transfer of [3H] cholesteryl oleate or [3H] triolein between LDL and HDL	2021	Bioorganic & medicinal chemistry letters, 01-15, Volume: 32	Cholesteryl ester transfer protein (CETP) inhibitors based on cyclic urea, bicyclic urea and bicyclic sulfamide cores.
AID1783853	Inhibition of recombinant CETP (unknown origin) assessed as maximal inhibition of transfer of [3H]cholesteryl oleate or [3H]triolein using exogenous LDL and HDL in 2% human serum at 10 uM measured after 2 hrs by liquid scintillation analysis relative to c	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1166868	Drug concentration in testes of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 21 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1476725	Drug uptake in triglyceride rich lipoprotein fraction of human serum from human donors with triglyceride levels ( 300-500 and >750 mg/dL) by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783840	Dose normalized AUC in C57BL/6 mouse at 2 mg/kg, po	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476690	1-Octanol-phosphate buffered saline partition coefficient, log D of compound at pH 7.6 by tandem mass spectrometry method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1166825	Terminal elimination half life in healthy human administered as single oral dose	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1783855	Induction of aldosterone elevation in po dosed NFR-transgenic- mouse assessed as no-effect level in plasma measured after 60 mins by mass-spectrometry (MS)-based assay	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1166836	Increase in HDL-cholesterol in hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1476688	Inhibition of CETP in human plasma measured every 30 mins for 120 mins by fluorescence method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID607209	Increase in HDL-cholesterol level in C57BL/6 mouse expressing cynomolgus monkey CETP gene assessed as change in HDL-C level at 1 mg/kg, po BID measured 24 hrs after first dose	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID607208	Increase in HDL-cholesterol level in C57BL/6 mouse expressing cynomolgus monkey CETP gene assessed as change in HDL-C level at 0.3 mg/kg, po BID measured 24 hrs after first dose	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1500880	Hypolipidemic activity in high-fat fed guinea pig model assessed as reduction in plasma LDL cholesterol levels at 30 mg/kg administered via oral gavage as qd for 14 days measured 2 hrs post dose on day 14 relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID607211	Increase in HDL-cholesterol level in C57BL/6 mouse expressing cynomolgus monkey CETP gene assessed as change in HDL-C level at 10 mg/kg, po BID measured 24 hrs after first dose	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1783928	Terminal half life in DIO NFR-transgenic mouse adipose tissue at 100 mg/kg, po once daily for 14 days	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1646834	Inhibition of human CETP	2020	Bioorganic & medicinal chemistry letters, 01-15, Volume: 30, Issue:2	Synthesis, biological evaluation and SAR studies of ursolic acid 3β-ester derivatives as novel CETP inhibitors.
AID638019	Inhibition of CETP-mediated neutral lipid transfer by fluorometric analysis	2012	Bioorganic & medicinal chemistry letters, Jan-01, Volume: 22, Issue:1	SAR studies on the central phenyl ring of substituted biphenyl oxazolidinone-potent CETP inhibitors.
AID1330817	Inhibition of recombinant CETP (unknown origin) assessed as inhibition of BODIPY-labeled cholesteryl transfer to fluorescent substrate by fluorimetric assay	2016	European journal of medicinal chemistry, Nov-10, Volume: 123	Design, synthesis and biological evaluation of novel cholesteryl ester transfer protein inhibitors bearing a cycloalkene scaffold.
AID1166867	Drug concentration in kidney of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 21 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1654612	Volume of distribution at steady state in rhesus monkey at 0.1 mg/kg, iv administered as single dose measured after 0.083 to 48 hrs	2020	Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12	Metabolic and Pharmaceutical Aspects of Fluorinated Compounds.
AID1500892	Induction of plasma triglyceride levels in transgenic ap2-CETPTg mouse model at 30 mg/kg, po qd for 14 days measured 2 hrs post dose on day 14 by automated lipid analyzer relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1330823	In vivo inhibition of CETP in high-fat fed syrian hamster model assessed as increase in plasma HDL-cholesterol level at 30 mg/kg, po administered once daily for 5 days measured 2 hrs post last dose relative to control	2016	European journal of medicinal chemistry, Nov-10, Volume: 123	Design, synthesis and biological evaluation of novel cholesteryl ester transfer protein inhibitors bearing a cycloalkene scaffold.
AID1783834	Transactivation of PXR (unknown origin)	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476705	Reduction in LDL cholesterol level in Syrian hamster plasma at 0.3 and 10 mg/kg, po dosed once daily for 2 weeks and measured 24 hrs post last dose by HPLC size exclusion chromatography method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1435500	Inhibition of recombinant full length human CETP expressed in CHO cells assessed as reduction in BODIPY-CE transfer measured after 1 to 3 hrs by fluorescence assay	2017	European journal of medicinal chemistry, Jan-27, Volume: 126	Fragment-based discovery of novel pentacyclic triterpenoid derivatives as cholesteryl ester transfer protein inhibitors.
AID607220	Tmax in C57BL/6 mouse at 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1166853	Drug concentration in adipose fat of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1166839	Plasma concentration in hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 5 and day 7 post dose	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1500868	Inhibition of recombinant human CETP after 3 hrs using fluorescent cholesteryl containing HDL after 3 hrs by fluorescence assay	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1476707	Drug uptake in Syrian hamster adipose tissue at 10 mg/kg, po dosed once daily for 14 days measured 24 hrs post last dose by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783854	Lipophilicity, logD of the compound at pH 7.3 by HPLC analysis	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1783926	Terminal half life in DIO NFR-transgenic mouse plasma at 100 mg/kg, po once daily for 14 days	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1783852	Inhibition of recombinant CETP (unknown origin) assessed as inhibition of transfer of [3H]cholesteryl oleate or [3H]triolein using exogenous LDL and HDL in 2% human serum by liquid scintillation analysis	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1783845	Oral bioavailability in C57BL/6 mouse at 2 mg/kg	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID607221	Oral bioavailability in C57BL/6 mouse at 2 mg/kg	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1476704	Reduction in LDL cholesterol level in Syrian hamster plasma at 0.3 and 10 mg/kg, po dosed once daily for 2 weeks and measured 24 hrs post last dose by HPLC size exclusion chromatography method relative to control	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1166851	Drug concentration in kidney of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1166850	Drug concentration in liver of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 3 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1166866	Drug concentration in muscle of hemizygous human CETP transgenic mouse at 10 mg/kg, po dosed for 5 consecutive days measured on day 21 after cessation of drug treatment	2014	Journal of medicinal chemistry, Nov-13, Volume: 57, Issue:21	Potent cholesteryl ester transfer protein inhibitors of reduced lipophilicity: 1,1'-spiro-substituted hexahydrofuroquinoline derivatives.
AID1783835	Transactivation of PXR (unknown origin) at 10 uM relative to control	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1783837	Solubility of the compound in pH 7 phosphate buffer	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476709	Inhibition of CETP activity in human serum at upto 1200 mg/dl serum triglyceride concentration by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1476708	Drug uptake in Syrian hamster adrenal tissue at 10 mg/kg, po dosed once daily for 14 days measured 24 hrs post last dose by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID607218	Dose-normalized AUC in C57BL/6 mouse at 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID607207	Increase in HDL-cholesterol level in C57BL/6 mouse expressing cynomolgus monkey CETP gene assessed as change in HDL-C level administered orally twice daily and measured 24 hrs after first dose	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1783856	Induction of aldosterone elevation in C57BL/6 mouse assessed as no-effect level in plasma at 30 mg/kg, po measured after 60 mins by mass-spectrometry (MS)-based assay	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1500893	Induction of plasma total cholesterol levels in transgenic ap2-CETPTg mouse model at 30 mg/kg, po qd for 14 days measured 2 hrs post dose on day 14 by automated lipid analyzer relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID607215	Volume of distribution in C57BL/6 mouse at 0.6 mg/kg, iv and 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1783927	Terminal half life in DIO NFR-transgenic mouse liver at 100 mg/kg, po once daily for 14 days	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1235235	Inhibition of CETP in rabbit serum at 100 uM incubated for 1 hr using NBD-labeled cholesterol in HDL and LDL by fluorescence based assay	2015	Bioorganic & medicinal chemistry, Aug-01, Volume: 23, Issue:15	Synthesis and biological evaluation of isoflavone amide derivatives with antihyperlipidemic and preadipocyte antiproliferative activities.
AID1500874	Hypolipidemic activity in transgenic ap2-CETPTg mouse model assessed as reduction in plasma LDL cholesterol levels at 30 mg/kg, po qd for 14 days measured 2 hrs post dose on day 14 by automated lipid analyzer relative to control	2017	European journal of medicinal chemistry, Oct-20, Volume: 139	Discovery of pentacyclic triterpene 3β-ester derivatives as a new class of cholesterol ester transfer protein inhibitors.
AID1783993	Increase in HDL-cholesterol in transgenic mouse at 100 mg/kg, po treated for 2 weeks relative to control	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1476703	Increase in HDL cholesterol levels in hamster plasma by HPLC size exclusion chromatography method relative to control	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783838	Cmax in C57BL/6 mouse at 0.6 mg/kg, iv and 2 mg/kg, po	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1692974	Inhibition of recombinant CETP (unknown origin) assessed as inhibition of transfer of [3H] cholesteryl oleate or [3H] triolein between exogenous LDL and HDL in 2% human serum	2021	Bioorganic & medicinal chemistry letters, 01-15, Volume: 32	Cholesteryl ester transfer protein (CETP) inhibitors based on cyclic urea, bicyclic urea and bicyclic sulfamide cores.
AID1783841	Total clearance in C57BL/6 mouse in whole blood at 0.6 mg/kg, iv	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID607214	Blood clearance in C57BL/6 mouse at 0.6 mg/kg, iv and 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID607216	Terminal half life in C57BL/6 mouse at 0.6 mg/kg, iv and 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID657499	Inhibition of CETP in human plasma assessed as reduction in fluorescent intensity by fluorescence analysis	2012	Bioorganic & medicinal chemistry letters, May-01, Volume: 22, Issue:9	Design, synthesis and structure-activity-relationship of 1,5-tetrahydronaphthyridines as CETP inhibitors.
AID607210	Increase in HDL-cholesterol level in C57BL/6 mouse expressing cynomolgus monkey CETP gene assessed as change in HDL-C level at 3 mg/kg, po BID measured 24 hrs after first dose	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1783847	Terminal half life in C57BL/6-transgenic mouse expressing human CETP at 200 mg/kg, po qd treated for 7 days measured for 240 hrs	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID1654614	Drug recovery in bile duct-cannulated rhesus monkey feces at 10 mg/kg, po administered as single dose using 14C labelled compound measured after 96 hrs	2020	Journal of medicinal chemistry, 06-25, Volume: 63, Issue:12	Metabolic and Pharmaceutical Aspects of Fluorinated Compounds.
AID1476711	Drug uptake in HDL fraction of human serum from human donors with normal triglyceride levels (<150 mg/dL) by LC-MS/MS method	2017	Journal of medicinal chemistry, 10-26, Volume: 60, Issue:20	Discovery of a Novel Piperidine-Based Inhibitor of Cholesteryl Ester Transfer Protein (CETP) That Retains Activity in Hypertriglyceridemic Plasma.
AID1783991	In vivo inhibition of CETP in transgenic mouse assessed as CETP activity measured at 100 mg/kg, po treated for 2 weeks relative to control	2021	Journal of medicinal chemistry, 09-23, Volume: 64, Issue:18	Invention of MK-8262, a Cholesteryl Ester Transfer Protein (CETP) Inhibitor Backup to Anacetrapib with Best-in-Class Properties.
AID607219	Cmax in C57BL/6 mouse at 2 mg/kg, po	2011	Journal of medicinal chemistry, Jul-14, Volume: 54, Issue:13	Biphenyl-substituted oxazolidinones as cholesteryl ester transfer protein inhibitors: modifications of the oxazolidinone ring leading to the discovery of anacetrapib.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	15 (8.77)	29.6817
2010's	140 (81.87)	24.3611
2020's	16 (9.36)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	33 (18.44%)	5.53%
Reviews	46 (25.70%)	6.00%
Case Studies	0 (0.00%)	4.05%
Observational	0 (0.00%)	0.25%
Other	100 (55.87%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (16)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Single Dose Study to Investigate the Pharmacokinetics of MK0859 in Patients With Hepatic Insufficiency [NCT01114490]	Phase 1	24 participants (Actual)	Interventional	2010-05-31	Completed
A Single-Dose Study to Investigate the Pharmacokinetics of MK0859 in Subjects With Impaired Renal Function [NCT01122667]	Phase 1	24 participants (Actual)	Interventional	2010-06-30	Completed
A Phase IIb, Multicenter, Randomized, Placebo-Controlled, Double-Blind, Dose-Ranging Study to Assess the Efficacy and Safety of MK0859 in Japanese Patients With Dyslipidemia [NCT00977288]	Phase 2	408 participants (Actual)	Interventional	2009-09-30	Completed
A 76-Week, Worldwide, Multicenter, Double-Blind, Randomized, Placebo-Controlled Study to Assess the Tolerability and Efficacy of Anacetrapib When Added to Ongoing Therapy With a Statin in Patients With Coronary Heart Disease (CHD) or CHD Risk-Equivalent D [NCT00685776]	Phase 3	1,623 participants (Actual)	Interventional	2008-03-24	Completed
A Multiple Dose Study to Investigate the Effect of MK0859 on Lipoprotein Metabolism When Added to Ongoing Statin Therapy in Dyslipidemic Patients [NCT00990808]	Phase 1	46 participants (Actual)	Interventional	2009-11-30	Completed
A 24-Week, Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo- Controlled Study to Assess the Efficacy and Tolerability of Anacetrapib When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Medication(s) in Patients Wi [NCT01860729]	Phase 3	589 participants (Actual)	Interventional	2013-05-13	Completed
REVEAL: Randomized EValuation of the Effects of Anacetrapib Through Lipid-modification. A Large-scale, Randomized Placebo-controlled Trial of the Clinical Effects of Anacetrapib Among People With Established Vascular Disease [NCT01252953]	Phase 3	30,449 participants (Actual)	Interventional	2011-06-30	Active, not recruiting
[NCT00565292]	Phase 1	50 participants (Actual)	Interventional	2006-07-31	Completed
A Cross-sectional REVEAL Sub-study Evaluating the Effect of Anacetrapib on Vascular Function and Arterial Stiffness [An Investigator Led Sub-study of HPS3/TIMI 55: REVEAL] [NCT02931188]		103 participants (Actual)	Observational	2017-01-31	Completed
[NCT00565006]	Phase 1	22 participants (Actual)	Interventional	2006-07-31	Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Dose-Ranging Study to Assess the Efficacy, Safety, and Tolerability of MK-0859 in Patients With Primary Hypercholesterolemia or Mixed Hyperlipidemia [NCT00325455]	Phase 2	500 participants (Actual)	Interventional	2006-06-30	Terminated
A 24-Week, Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Assess the Efficacy and Tolerability of Anacetrapib When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Medication(s) in Patients Wit [NCT01717300]	Phase 3	459 participants (Actual)	Interventional	2012-11-06	Completed
A Multicenter, 24-Week, Double-Blind, Randomized, Placebo-Controlled, Phase III Study With 28-Week Open Labeled Extension Period to Assess the Efficacy and Safety of MK-0859 When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Medica [NCT01760460]	Phase 3	307 participants (Actual)	Interventional	2013-03-14	Completed
A 12-Week, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Assess the Efficacy and Safety of MK-0859 When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Therapies in Japanese Patients With Heterozygous F [NCT01824238]	Phase 3	68 participants (Actual)	Interventional	2013-05-31	Completed
A Worldwide, Multicenter, Double-Blind, Randomized, Placebo-Controlled, 12-Week Study to Assess the Efficacy and Tolerability of Anacetrapib When Added to Ongoing Lipid-Lowering Therapy in Adult Patients With Homozygous Familial Hypercholesterolemia (HoFH [NCT01841684]	Phase 3	2 participants (Actual)	Interventional	2013-06-30	Terminated
A 1-Year, Worldwide, Multicenter, Double-Blind, Randomized, Parallel, Placebo-Controlled Study to Assess the Efficacy and Tolerability of Anacetrapib When Added to Ongoing Statin Therapy With or Without Other Lipid Modifying Medication(s) in Patients With [NCT01524289]	Phase 3	306 participants (Actual)	Interventional	2012-02-03	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT01252953 (4) [back to overview]	Number of Participants With Major Atherosclerotic Event
NCT01252953 (4) [back to overview]	Number of Participants With Major Coronary Event
NCT01252953 (4) [back to overview]	Number of Participants With Major Vascular Event
NCT01252953 (4) [back to overview]	Number of Participants With Presumed Ischaemic Stroke
NCT01524289 (22) [back to overview]	Percent Change From Baseline in Apolipoprotein (Apo) A-1 Levels
NCT01524289 (22) [back to overview]	Percent Change From Baseline in Apolipoprotein (Apo) B Levels
NCT01524289 (22) [back to overview]	Percent Change From Baseline in High-Density Lipoprotein Cholesterol Levels
NCT01524289 (22) [back to overview]	Percent Change From Baseline in Lipoprotein(a) (Lp[a]) Levels
NCT01524289 (22) [back to overview]	Percent Change From Baseline in Low-Density Lipoprotein Cholesterol (LDL-C) - Treatment Phase
NCT01524289 (22) [back to overview]	Percent Change From Baseline in Non-High-Density Lipoprotein Cholesterol Levels
NCT01524289 (22) [back to overview]	Percentage of Participants Adjudicated Cardiovascular (CV) SAE
NCT01524289 (22) [back to overview]	Percentage of Participants Discontinuing Study Treatment Due to an Adverse Event - Treatment Phase
NCT01524289 (22) [back to overview]	Percentage of Participants Who Died From Any Cause - Treatment Phase
NCT01524289 (22) [back to overview]	Percentage of Participants With Any Adverse Event - Treatment Phase
NCT01524289 (22) [back to overview]	Percentage of Participants With Any Serious Adverse Event - Treatment Phase
NCT01524289 (22) [back to overview]	Percentage of Participants With Any Treatment-Related Adverse Event - Treatment Phase
NCT01524289 (22) [back to overview]	Percentage of Participants With Bicarbonate Levels > ULN
NCT01524289 (22) [back to overview]	Percentage of Participants With Changes in Diastolic Blood Pressure (DBP) >= 10 mm Hg
NCT01524289 (22) [back to overview]	Percentage of Participants With Changes in SBP >= 15 mm Hg
NCT01524289 (22) [back to overview]	Percentage of Participants With Changes in Systolic Blood Pressure (SBP) >= 10 mm Hg
NCT01524289 (22) [back to overview]	Percentage of Participants With Chloride Levels > ULN
NCT01524289 (22) [back to overview]	Percentage of Participants With CK Level >=10 x ULN With Muscle Spasms
NCT01524289 (22) [back to overview]	Percentage of Participants With Consecutive Changes in Alanine Aminotransferase (ALT) and/or Aspartate Aminotransferase (AST) of >=3 x ULN
NCT01524289 (22) [back to overview]	Percentage of Participants With Creatine Kinase (CK) Level >=10 x ULN
NCT01524289 (22) [back to overview]	Percentage of Participants With Potassium Levels < Lower Limit of Normal (LLN)
NCT01524289 (22) [back to overview]	Percentage of Participants With Sodium Levels > Upper Limit of Normal (ULN)

Number of Participants With Major Atherosclerotic Event

"Major atherosclerotic events (defined as coronary death, myocardial infarction or presumed ischaemic stroke; the key secondary outcome).~Secondary assessments involve intention-to-treat comparisons among all randomized participants of the effects of allocation to anacetrapib versus placebo during the scheduled treatment period." (NCT01252953)
Timeframe: Randomized treatment phase during median follow-up period of 4.1years

Intervention	Participants (Count of Participants)
Anacetrapib	1383
Placebo Anacetrapib	1483

Condition	Indicated	Relationship Strength	Studies	Trials
Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.	0	3.53	7	0
Hyperlipemia [description not available]	0	7.72	7	2
Hyperlipidemias Conditions with excess LIPIDS in the blood.	1	9.72	7	2
Hypertriglyceridemia A condition of elevated levels of TRIGLYCERIDES in the blood.	0	2.15	1	0
Dyslipidemia [description not available]	0	13.41	33	9
Dyslipidemias Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.	0	13.41	33	9
Congenital Zika Syndrome [description not available]	0	2.25	1	0
Zika Virus Infection A viral disease transmitted by the bite of AEDES mosquitoes infected with ZIKA VIRUS. Its mild DENGUE-like symptoms include fever, rash, headaches and ARTHRALGIA. The viral infection during pregnancy, in rare cases, is associated with congenital brain and ocular abnormalities, called Congenital Zika Syndrome, including MICROCEPHALY and may also lead to GUILLAIN-BARRE SYNDROME.	0	2.25	1	0
Coronary Heart Disease [description not available]	0	11.19	15	5
Coronary Disease An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.	1	13.19	15	5
Cardiovascular Diseases Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.	1	12.76	30	1
Atherogenesis [description not available]	0	10.95	20	2
Cardiovascular Stroke [description not available]	0	6.03	3	1
Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).	0	6.03	3	1
Atherosclerosis A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.	0	10.95	20	2
Neointima The new and thickened layer of scar tissue that forms on a PROSTHESIS, or as a result of vessel injury especially following ANGIOPLASTY or stent placement.	0	7.55	2	0
Hyperplasia An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.	0	7.55	2	0
Weight Reduction [description not available]	0	2.21	1	0
Obesity A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).	0	4.18	3	1
Weight Loss Decrease in existing BODY WEIGHT.	0	2.21	1	0
Elevated Cholesterol [description not available]	0	11.84	17	6
Hypercholesterolemia A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.	1	13.84	17	6
Liver Steatosis [description not available]	0	2.17	1	0
Insulin Sensitivity [description not available]	0	2.17	1	0
Fatty Liver Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.	0	2.17	1	0
Insulin Resistance Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.	0	2.17	1	0
Diabetes Mellitus, Adult-Onset [description not available]	0	3.09	1	0
Diabetes Mellitus, Type 2 A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.	0	3.09	1	0
Arteriosclerosis, Coronary [description not available]	0	3.39	2	0
Coronary Artery Disease Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.	0	3.39	2	0
Apolipoprotein B-100, Familial Defective [description not available]	0	7.74	4	2
Hyperlipoproteinemia Type II A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).	1	12.06	8	4
Arrhythmia [description not available]	0	3.48	1	1
Arrhythmias, Cardiac Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.	0	3.48	1	1
Liver Dysfunction [description not available]	0	8.63	5	4
Kidney Diseases Pathological processes of the KIDNEY or its component tissues.	0	8.62	5	4
Liver Diseases Pathological processes of the LIVER.	0	8.63	5	4
Apoplexy [description not available]	0	3.01	1	0
Stroke A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)	0	3.01	1	0
Disease Exacerbation [description not available]	0	2.11	1	0
Cardiac Diseases [description not available]	0	3.67	3	0
Hyperlipoproteinemia [description not available]	0	3.01	1	0
Heart Diseases Pathological conditions involving the HEART including its structural and functional abnormalities.	0	3.67	3	0
Hyperlipoproteinemias Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.	0	3.01	1	0
Lipid Metabolism, Inborn Error [description not available]	0	3.71	3	0
Vascular Injuries [description not available]	0	2.11	1	0
Diseases, Peripheral Vascular [description not available]	0	2.11	1	0
Ischemia A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.	0	2.11	1	0
Peripheral Vascular Diseases Pathological processes involving any one of the BLOOD VESSELS in the vasculature outside the HEART.	0	2.11	1	0
Sensitivity and Specificity Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)	0	3.86	2	1
Genetic Predisposition [description not available]	0	2.15	1	0
Aldosteronism [description not available]	0	2.04	1	0
Hyperaldosteronism A condition caused by the overproduction of ALDOSTERONE. It is characterized by sodium retention and potassium excretion with resultant HYPERTENSION and HYPOKALEMIA.	0	2.04	1	0
Innate Inflammatory Response [description not available]	0	2.05	1	0
Inflammation A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.	0	2.05	1	0
Cardiometabolic Syndrome A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components not only include metabolic dysfunctions of METABOLIC SYNDROME but also HYPERTENSION, and ABDOMINAL OBESITY.	0	3.86	2	0
Metabolic Syndrome A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome include ABDOMINAL OBESITY; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state.	0	3.86	2	0
Acute Coronary Syndrome An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.	0	3.39	2	0
Recrudescence [description not available]	0	2.99	1	0
Atheroma [description not available]	0	2.99	1	0
A-alphalipoprotein Neuropathy [description not available]	0	2.07	1	0

anacetrapib

Cross-References

Synonyms (56)

Research Excerpts

Overview

Effects

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Protein Targets (4)

Potency Measurements

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Biological Processes (53)

Molecular Functions (26)

Ceullar Components (16)

Bioassays (128)

Research

Studies (171)

Market Indicators

Research Demand Index: 38.08

Study Types

Clinical Trials (16)

Trial Overview

Trial Outcomes

Number of Participants With Major Atherosclerotic Event

Number of Participants With Major Coronary Event

Number of Participants With Major Vascular Event

Number of Participants With Presumed Ischaemic Stroke

Percent Change From Baseline in Apolipoprotein (Apo) A-1 Levels

Percent Change From Baseline in Apolipoprotein (Apo) B Levels

Percent Change From Baseline in High-Density Lipoprotein Cholesterol Levels

Percent Change From Baseline in Lipoprotein(a) (Lp[a]) Levels

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

Percent Change From Baseline in Non-High-Density Lipoprotein Cholesterol Levels

Percentage of Participants Adjudicated Cardiovascular (CV) SAE

Percentage of Participants Discontinuing Study Treatment Due to an Adverse Event - Treatment Phase

Percentage of Participants Who Died From Any Cause - Treatment Phase

Percentage of Participants With Any Adverse Event - Treatment Phase

Percentage of Participants With Any Serious Adverse Event - Treatment Phase

Percentage of Participants With Any Treatment-Related Adverse Event - Treatment Phase

Percentage of Participants With Bicarbonate Levels > ULN

Percentage of Participants With Changes in Diastolic Blood Pressure (DBP) >= 10 mm Hg

Percentage of Participants With Changes in SBP >= 15 mm Hg

Percentage of Participants With Changes in Systolic Blood Pressure (SBP) >= 10 mm Hg

Percentage of Participants With Chloride Levels > ULN

Percentage of Participants With CK Level >=10 x ULN With Muscle Spasms

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

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

Percentage of Participants With Potassium Levels < Lower Limit of Normal (LLN)

Percentage of Participants With Sodium Levels > Upper Limit of Normal (ULN)

Related Drugs (90)

Related Conditions (61)