dalcetrapib profile

dalcetrapib: inhibits cholesteryl ester transfer protein (CETP) [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	6918540
CHEMBL ID	313006
CHEBI ID	95001
SCHEMBL ID	528622
MeSH ID	M0537680

Synonym
ro4607381
CHEMBL313006 ,
HY-14950
ro-4607381
dalcetrapib
jtt-705
rg-1658
bdbm50092197
s-2-(1-(2-ethylbutyl)cyclohexanecarboxamido)phenyl 2-methylpropanethioate
thioisobutyric acid s-(2-{[1-(2-ethyl-butyl)-cyclohexanecarbonyl]-amino}-phenyl) ester
A25148
jtt-705;s-2-(2-ethylbutyl)-2-formamidocyclohexyl 2-methyl-2-phenylpropanethioate
s-[2-[[1-(2-ethylbutyl)cyclohexanecarbonyl]amino]phenyl] 2-methylpropanethioate
211513-37-0
dalcetrapib (usan/inn)
D09708
3d050liq3h ,
dalcetrapib [usan:inn]
jtt705
jtt 705
unii-3d050liq3h
BCP9000580
dalcetrapib (jtt-705, ro4607381)
AKOS015966940
BCPP000268
PB12356
CS-0916
S2772
2-methylpropanethioic acid s-[2-[1-(2-ethylbutyl)cyclohexylcarboxamido]phenyl] ester
BRD-K18849474-001-01-0
propanethioic acid, 2-methyl-, s-(2-(((1-(2-ethylbutyl)cyclohexyl)carbonyl)amino)phenyl) ester
dalcetrapib [inn]
dalcetrapib [mi]
s-(2-(1-(2-ethylbutyl)cyclohexanecarboxamido)phenyl) 2-methylpropanethioate
dalcetrapib [usan]
dalcetrapib [who-dd]
s-[2-({[1-(2-ethylbutyl)cyclohexyl]carbonyl}amino)phenyl] 2-methylpropanethioate
SCHEMBL528622
s-(2-(1-(2-ethylbutyl)cyclohexane-1-carboxamido)phenyl) 2-methylpropanethioate
AC-27462
J-510086
mfcd06407886
EX-A092
CHEBI:95001
HMS3656F06
NCGC00386198-05
dalcetrapib (jtt-705)
YZQLWPMZQVHJED-UHFFFAOYSA-N
s-[2-[1-(2-ethylbutyl)cyclohexanecarbonylamino]-phenyl] 2-methylthiopropionate
dalcetrapib, >=97% (hplc)
SW219843-1
DB12181
FT-0769704
Q5210285
dalcetrapib pound jtt-705 pound(c)
DTXSID70943475
AMY21305
CCG-264995
AS-55940

Research Excerpts

Overview

Dalcetrapib is a CETP modulator that elevated HDL-C levels but did not reduce the concentration of low-density lipoprotein cholesterol (LDL-C) The effects on cardiovascular outcomes were demonstrated in the dal-OUTCOMES trial to be influenced by correlated polymorphisms in the CETP.

Excerpt	Reference
"Dalcetrapib is a CETP modulator that elevated HDL-C levels but did not reduce the concentration of low-density lipoprotein cholesterol (LDL-C)."	( Future of cholesteryl ester transfer protein (CETP) inhibitors: a pharmacological perspective. Akhlaghi, F; Mohammadpour, AH, 2013)
"Dalcetrapib is a CETP modulator for which effects on cardiovascular outcomes were demonstrated in the dal-OUTCOMES trial to be influenced by correlated polymorphisms in the"	( CETP: Pharmacogenomics-Based Response to the CETP Inhibitor Dalcetrapib. Dubé, MP; Rhainds, D; Rhéaume, E; Tardif, JC, 2017)
"Dalcetrapib is a modulator of cholesteryl ester transfer protein (CETP) activity developed to raise levels of high-density lipoprotein cholesterol (HDL-C) with the goal of further reduction of cardiovascular events additive to standard of care alone. "	( Safety, tolerability and pharmacokinetics of dalcetrapib following single and multiple ascending doses in healthy subjects: a randomized, double-blind, placebo-controlled, phase I study. Anzures-Cabrera, J; Derks, M; Phelan, M; Turnbull, L, 2011)
"Dalcetrapib is a cholesteryl ester transfer protein (CETP) modulator in clinical assessment for cardiovascular outcome benefits. "	( Monitoring Cyp2b10 mRNA expression at cessation of 2-year carcinogenesis bioassay in mouse liver provides evidence for a carcinogenic mechanism devoid of human relevance: the dalcetrapib experience. Braendli-Baiocco, A; Flint, N; Fowler, S; Hoflack, JC; Kuhlmann, O; Mueller, L; Roth, A; Singer, T, 2012)
"Dalcetrapib is a novel molecule acting on CETP with a different chemical structure to torcetrapib."	( Vascular effects and safety of dalcetrapib in patients with or at risk of coronary heart disease: the dal-VESSEL randomized clinical trial. Deanfield, JE; Jukema, JW; Kallend, D; Kaski, JC; Kastelein, JJ; Lüscher, TF; Münzel, T; Taddei, S, 2012)
"Dalcetrapib is an orally administered CETP inhibitor developed for the treatment of primary hypercholesterolaemia and mixed hyperlipidaemia."	( Dalcetrapib , a cholesteryl ester transfer protein modulator. Burnett, JR; Hooper, AJ, 2012)

Effects

Dalcetrapib has a chemical structure that is distinct from other CETP inhibitors, with a smaller molecular weight and a lack of trifluoride moieties. It induces a conformational change in CETP rather than forming a non-productive CETP/HDL-C complex.

Excerpt	Reference
"Dalcetrapib has a chemical structure that is distinct from other CETP inhibitors, with a smaller molecular weight and a lack of trifluoride moieties."	( Future of cholesteryl ester transfer protein (CETP) inhibitors: a pharmacological perspective. Akhlaghi, F; Mohammadpour, AH, 2013)
"Dalcetrapib has a unique chemical structure and induces a conformational change in CETP rather than forming a non-productive CETP/HDL-C complex as do the other CETP inhibitors."	( Dalcetrapib: a review of Phase II data. Robinson, JG, 2010)
"Dalcetrapib has been well tolerated at the 600-mg dose."	( An update on the clinical development of dalcetrapib (RO4607381), a cholesteryl ester transfer protein modulator that increases HDL cholesterol levels. Arsenault, BJ; Brodeur, MR; Rhainds, D; Tardif, JC, 2012)

Actions

Excerpt	Reference
"Dalcetrapib did not increase office blood pressure and the frequency of adverse events was similar between groups."	( Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging (dal-PLAQUE): a randomised clinical trial. Abt, M; Ballantyne, CM; Burgess, T; Farkouh, ME; Fayad, ZA; Fuster, V; Kallend, D; Mani, V; Rudd, JH; Stein, EA; Tardif, JC; Tawakol, A; Woodward, M, 2011)

Treatment

Dalcetrapib treatment increased HDL-C and apolipoprotein A1 by 33.7 and 11.8%, respectively (both P < 0.001) and total cholesterol efflux by 9.5% (P = 0.003) After 4 weeks, principally via an increase in non-ATP-binding cassette transporter (ABC) A1-mediated efflux, without statistically significant changes in pre-β1-HDL levels.

Excerpt	Reference
"Dalcetrapib treatment of 600 mg/day produces significant inhibition of CETP activity, and has been utilized in phase II and III studies, including CV endpoint trials."	( Clinical Pharmacokinetics and Pharmacodynamics of Dalcetrapib. Bentley, D; Black, DM; Briggs, E; Chapel, S; Heinonen, T; Lee, J, 2018)
"Dalcetrapib treatment increased HDL-C and apolipoprotein A1 by 33.7 and 11.8%, respectively (both P < 0.001) and total cholesterol efflux by 9.5% (P = 0.003) after 4 weeks, principally via an increase in non-ATP-binding cassette transporter (ABC) A1-mediated efflux, without statistically significant changes in pre-β1-HDL levels."	( The effect of cholesteryl ester transfer protein inhibition on lipids, lipoproteins, and markers of HDL function after an acute coronary syndrome: the dal-ACUTE randomized trial. Anzures-Cabrera, J; Ditmarsch, M; Holme, I; Jones, P; Kallend, D; Lehnert, V; Niesor, EJ; Pauly-Evers, M; Ray, KK; Štásek, J; Suchankova, G; Upmanyu, R; van Hessen, MW, 2014)
"Treatment with dalcetrapib resulted in placebo-adjusted geometric mean percent increases in high-sensitivity C-reactive protein from baseline to end of trial of 18.1% (P=0.0009) and 18.7% (P=0.00001) in participants with the GG and AG genotypes, respectively, but the change was -1.0% (P=0.89) in those with the protective AA genotype."	( Genotype-Dependent Effects of Dalcetrapib on Cholesterol Efflux and Inflammation: Concordance With Clinical Outcomes. Alem, S; Boulé, M; Brodeur, M; Dubé, MP; Feroz Zada, Y; Fouodjio, R; Grégoire, JC; Guertin, MC; Ibrahim, R; L'Allier, PL; Mongrain, I; Olsson, AG; Provost, S; Rhainds, D; Rhéaume, E; Schwartz, GG; Tardif, JC, 2016)
"Treatment with dalcetrapib was safe, but without benefit."	( [Treatment of dyslipidemia - is here still place for CETP-inhibitors?] Kiňová, S; Murín, J; Pernický, M, )
"Treatment with dalcetrapib was generally well tolerated with a similar number of adverse events reported between patient groups and between those receiving dalcetrapib compared with placebo."	( Efficacy and safety of dalcetrapib in type 2 diabetes mellitus and/or metabolic syndrome patients, at high cardiovascular disease risk. Bays, H; Burgess, T; Davidson, MH; Duttlinger-Maddux, R; Goldberg, AC; Kallend, D; Robinson, JG; Stalenhoef, AF, 2012)

Toxicity

Dalcetrapib (RO4607381/JTT-705) is a cholesteryl ester transfer protein inhibitor. It was developed after a report of increased mortality and cardiac events with torcetraib. The drug was generally well tolerated.

Excerpt	Reference
"Efficacy and safety data for dalcetrapib (RO4607381/JTT-705) are presented, following a report of increased mortality and cardiac events with another cholesteryl ester transfer protein inhibitor, torcetrapib, associated with off-target adverse effects (hypertension and the activation of the renin-angiotensin-aldosterone system)."	( Safety and tolerability of dalcetrapib. Buckley, BM; Burgess, T; Capponi, AM; Kallend, D; Kastelein, JJ; Niesor, EJ; Stein, EA; Steiner, G; Stroes, ES, 2009)
" placebo in adverse events, laboratory parameters including aldosterone, electrocardiograms, and vital signs including blood pressure (BP)."	( Safety and tolerability of dalcetrapib (RO4607381/JTT-705): results from a 48-week trial. Burgess, T; Kallend, D; Rhyne, JM; Robinson, JG; Roth, EM; Stein, EA, 2010)
"Tolerability and safety were assessed by monitoring adverse events (AEs), laboratory parameters, vital signs and 12-lead ECG recordings."	( Safety, tolerability and pharmacokinetics of dalcetrapib following single and multiple ascending doses in healthy subjects: a randomized, double-blind, placebo-controlled, phase I study. Anzures-Cabrera, J; Derks, M; Phelan, M; Turnbull, L, 2011)
"Single-dose dalcetrapib up to 4500 mg and multiple doses up to 3900 mg were generally safe and well tolerated."	( Safety, tolerability and pharmacokinetics of dalcetrapib following single and multiple ascending doses in healthy subjects: a randomized, double-blind, placebo-controlled, phase I study. Anzures-Cabrera, J; Derks, M; Phelan, M; Turnbull, L, 2011)
" Treatment with dalcetrapib was generally well tolerated with a similar number of adverse events reported between patient groups and between those receiving dalcetrapib compared with placebo."	( Efficacy and safety of dalcetrapib in type 2 diabetes mellitus and/or metabolic syndrome patients, at high cardiovascular disease risk. Bays, H; Burgess, T; Davidson, MH; Duttlinger-Maddux, R; Goldberg, AC; Kallend, D; Robinson, JG; Stalenhoef, AF, 2012)
" For the coprimary MRI and PET/CT endpoints, CIs were below the no-harm boundary or the adverse change was numerically lower in the dalcetrapib group than in the placebo group."	( Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging (dal-PLAQUE): a randomised clinical trial. Abt, M; Ballantyne, CM; Burgess, T; Farkouh, ME; Fayad, ZA; Fuster, V; Kallend, D; Mani, V; Rudd, JH; Stein, EA; Tardif, JC; Tawakol, A; Woodward, M, 2011)

Pharmacokinetics

Excerpt	Reference
" Primary pharmacokinetic assessments were area under the plasma concentration-time curve (AUC) from time zero to infinity (AUC(∞)) and maximum observed plasma concentration (C(max)) [single doses] and AUC from time zero to 24 hours (AUC(24)) and C(max) (multiple doses)."	( Safety, tolerability and pharmacokinetics of dalcetrapib following single and multiple ascending doses in healthy subjects: a randomized, double-blind, placebo-controlled, phase I study. Anzures-Cabrera, J; Derks, M; Phelan, M; Turnbull, L, 2011)
" Blood samples for pharmacokinetic analyses (AUC(0-36) or AUC(0-∞), C(max)) were collected up to 36, 144, and 96 hours after study drug administration in the fed versus fasting, meal timing/size, and high-fat meal studies, respectively."	( Effects of food intake on the pharmacokinetic properties of dalcetrapib: findings from three phase I, single-dose crossover studies in healthy volunteers. Abt, M; Derks, M; Ishikawa, T; Kawamura, H; Meneses-Lorente, G; Phelan, M, 2011)
"AUC∞ and Cmax of dalcetrapib thiol were increased by 14% and 21%, respectively, by co-administration of probenecid."	( In vivo evaluation of drug-drug interactions linked to UGT inhibition: the effect of probenecid on dalcetrapib pharmacokinetics. Aceves Baldó, P; Anzures-Cabrera, J; Bentley, D, 2013)
" The current clinical development program, representing new advances in precision medicine and focused on a genetically defined population with acute coronary syndrome (ACS), is supported by a large body of pharmacokinetic and pharmacodynamic data as well as substantial clinical experience in over 13,000 patients and volunteers."	( Clinical Pharmacokinetics and Pharmacodynamics of Dalcetrapib. Bentley, D; Black, DM; Briggs, E; Chapel, S; Heinonen, T; Lee, J, 2018)

Compound-Compound Interactions

The potential for orlistat to affect the bioavailability of concomitantly administered dalcetrapib was studied in an open-label 2-cohort study in 24 healthy volunteers. The exposure of ethinylestradiol and levonorgestrel was similar when Microgynon® 30 was administered with or without dalCETrapib. For ethinylESTradiol the geometric mean ratio %, (90% confidence interval (CI)) for AUC0-24 and Cmax were 92 (86 - 98) and 105 (95 - 115)

Excerpt	Reference
" This study examined the use of the CETP inhibitor JTT-705 combined with pravastatin."	( Effectiveness of inhibition of cholesteryl ester transfer protein by JTT-705 in combination with pravastatin in type II dyslipidemia. de Grooth, GJ; Kastelein, JJ; Kawamura, H; Klerkx, AH; Kuivenhoven, JA; Trip, MD; Wilhelm, F, 2005)
" It is in clinical development for the prevention of cardiovascular events and will likely be used in combination with standard of care, including statins."	( Coadministration of dalcetrapib with pravastatin, rosuvastatin, or simvastatin: no clinically relevant drug-drug interactions. Abt, M; Bech, N; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Turnbull, L; White, AM, 2010)
" The exposure of ethinylestradiol and levonorgestrel was similar when Microgynon® 30 was administered with or without dalcetrapib; for ethinylestradiol the geometric mean ratio %, (90% confidence interval (CI)) for AUC0-24 and Cmax were 92 (86 - 98) and 105 (95 - 115) and for levonorgestrel 92 (88 - 96) and 93 (87 - 99), respectively."	( No clinically relevant drug-drug interactions when dalcetrapib is co-administered with a monophasic oral contraceptive (Microgynon® 30). Anzures-Cabrera, J; Derks, M; Young, A, 2012)
" Thus, the potential for orlistat to affect the bioavailability of concomitantly administered dalcetrapib was studied in an open-label 2-cohort study in 24 healthy volunteers as follows: single 600-mg doses of dalcetrapib were administered with increasing doses of orlistat (cohort A: 10, 40, 120 mg; cohort B: 20, 60, 120 mg)."	( Evidence of a drug-drug interaction linked to inhibition of ester hydrolysis by orlistat. Bentley, D; Carlile, D; Gross, G; Rowell, L; Tardio, J; Young, AM, 2012)
"This case study illustrates the difficulty in predicting clinically relevant drug-drug interactions for UGT substrates based only on the fraction metabolized by glucuronidation."	( In vivo evaluation of drug-drug interactions linked to UGT inhibition: the effect of probenecid on dalcetrapib pharmacokinetics. Aceves Baldó, P; Anzures-Cabrera, J; Bentley, D, 2013)

Bioavailability

Dalcetrapib, a modulator of cholesteryl ester transfer protein (CETP) inhibitor activity, was ∼60% higher when administered in the fed state compared with the fasting state. This article reports on 3 studies conducted to assess the effects of food intake, timing of administration with respect to meals, and meal size and content.

Excerpt	Reference
"Preclinical studies have reported that the relative bioavailability of dalcetrapib, a modulator of cholesteryl ester transfer protein (CETP) inhibitor activity, was ∼60% higher when administered in the fed state compared with the fasting state."	( Effects of food intake on the pharmacokinetic properties of dalcetrapib: findings from three phase I, single-dose crossover studies in healthy volunteers. Abt, M; Derks, M; Ishikawa, T; Kawamura, H; Meneses-Lorente, G; Phelan, M, 2011)
"This article reports on 3 studies conducted to assess the effects of food intake, timing of administration with respect to meals, and meal size and content on the relative bioavailability of dalcetrapib in healthy male subjects."	( Effects of food intake on the pharmacokinetic properties of dalcetrapib: findings from three phase I, single-dose crossover studies in healthy volunteers. Abt, M; Derks, M; Ishikawa, T; Kawamura, H; Meneses-Lorente, G; Phelan, M, 2011)
" Thus, the potential for orlistat to affect the bioavailability of concomitantly administered dalcetrapib was studied in an open-label 2-cohort study in 24 healthy volunteers as follows: single 600-mg doses of dalcetrapib were administered with increasing doses of orlistat (cohort A: 10, 40, 120 mg; cohort B: 20, 60, 120 mg)."	( Evidence of a drug-drug interaction linked to inhibition of ester hydrolysis by orlistat. Bentley, D; Carlile, D; Gross, G; Rowell, L; Tardio, J; Young, AM, 2012)
"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)

Dosage Studied

Dalcetrapib increased (3)H-cholesterol in plasma HDL vs non-HDL, after oral dosing of labeled cholesterol. In the interval study (n = 52), serial and concurrent co-administration of atorvastatin resulted in similar reductions in dalcatrapib exposure that were comparable to those observed in the concurrent dosing study.

Excerpt	Reference
"Two crossover studies were performed in healthy subjects: a two-period study of dalcetrapib 900 mg concurrently with atorvastatin (concurrent dosing study) and a three-period study of dalcetrapib 600 mg (dose chosen for Phase III) with atorvastatin concurrently or serially 4 h after dalcetrapib (interval dosing study)."	( No clinically relevant drug-drug interactions when dalcetrapib is co-administered with atorvastatin. Abt, M; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Young, AM, 2010)
" In the interval study (n = 52), serial and concurrent co-administration of atorvastatin resulted in similar reductions in dalcetrapib exposure that were comparable to those observed in the concurrent dosing study."	( No clinically relevant drug-drug interactions when dalcetrapib is co-administered with atorvastatin. Abt, M; Derks, M; Meneses-Lorente, G; Parr, G; Phelan, M; Young, AM, 2010)
" 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)
" Pharmacodynamic assessments included CETP activity and lipids (multiple dosing only)."	( Safety, tolerability and pharmacokinetics of dalcetrapib following single and multiple ascending doses in healthy subjects: a randomized, double-blind, placebo-controlled, phase I study. Anzures-Cabrera, J; Derks, M; Phelan, M; Turnbull, L, 2011)
" Exposure was independent of dosing time."	( Effects of food intake on the pharmacokinetic properties of dalcetrapib: findings from three phase I, single-dose crossover studies in healthy volunteers. Abt, M; Derks, M; Ishikawa, T; Kawamura, H; Meneses-Lorente, G; Phelan, M, 2011)
" Dalcetrapib did not change plasma (3)H-cholesterol level but increased (3)H-cholesterol in plasma HDL vs non-HDL, after oral dosing of labeled cholesterol."	( Effect of dalcetrapib, a CETP modulator, on non-cholesterol sterol markers of cholesterol homeostasis in healthy subjects. Blum, D; Chaput, E; Derks, M; Kallend, D; Niesor, EJ; Staempfli, A, 2011)

[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Class	Description
anilide	Any aromatic amide obtained by acylation of aniline.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
cytochrome P450 family 3 subfamily A polypeptide 4	Homo sapiens (human)	Potency	9.5221	0.0123	7.9835	43.2770	AID1645841
G	Vesicular stomatitis virus	Potency	1.8999	0.0123	8.9648	39.8107	AID1645842
Interferon beta	Homo sapiens (human)	Potency	1.8999	0.0033	9.1582	39.8107	AID1645842
HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)	Potency	1.8999	0.0123	8.9648	39.8107	AID1645842
Inositol hexakisphosphate kinase 1	Homo sapiens (human)	Potency	1.8999	0.0123	8.9648	39.8107	AID1645842
cytochrome P450 2C9, partial	Homo sapiens (human)	Potency	1.8999	0.0123	8.9648	39.8107	AID1645842
[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)	4.1000	0.0030	0.2169	4.1000	AID1476688
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell activation involved in immune response	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to virus	Interferon beta	Homo sapiens (human)
positive regulation of autophagy	Interferon beta	Homo sapiens (human)
cytokine-mediated signaling pathway	Interferon beta	Homo sapiens (human)
natural killer cell activation	Interferon beta	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT protein	Interferon beta	Homo sapiens (human)
cellular response to interferon-beta	Interferon beta	Homo sapiens (human)
B cell proliferation	Interferon beta	Homo sapiens (human)
negative regulation of viral genome replication	Interferon beta	Homo sapiens (human)
innate immune response	Interferon beta	Homo sapiens (human)
positive regulation of innate immune response	Interferon beta	Homo sapiens (human)
regulation of MHC class I biosynthetic process	Interferon beta	Homo sapiens (human)
negative regulation of T cell differentiation	Interferon beta	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Interferon beta	Homo sapiens (human)
defense response to virus	Interferon beta	Homo sapiens (human)
type I interferon-mediated signaling pathway	Interferon beta	Homo sapiens (human)
neuron cellular homeostasis	Interferon beta	Homo sapiens (human)
cellular response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
cellular response to virus	Interferon beta	Homo sapiens (human)
negative regulation of Lewy body formation	Interferon beta	Homo sapiens (human)
negative regulation of T-helper 2 cell cytokine production	Interferon beta	Homo sapiens (human)
positive regulation of apoptotic signaling pathway	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell differentiation	Interferon beta	Homo sapiens (human)
natural killer cell activation involved in immune response	Interferon beta	Homo sapiens (human)
adaptive immune response	Interferon beta	Homo sapiens (human)
T cell activation involved in immune response	Interferon beta	Homo sapiens (human)
humoral immune response	Interferon beta	Homo sapiens (human)
positive regulation of T cell mediated cytotoxicity	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
adaptive immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independent	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of T cell anergy	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
defense response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
detection of bacterium	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of interleukin-12 production	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of interleukin-6 production	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protection from natural killer cell mediated cytotoxicity	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
innate immune response	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
regulation of dendritic cell differentiation	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class Ib	HLA class I histocompatibility antigen, B alpha chain	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)
inositol phosphate metabolic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
negative regulation of cold-induced thermogenesis	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol phosphate biosynthetic process	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
cytokine activity	Interferon beta	Homo sapiens (human)
cytokine receptor binding	Interferon beta	Homo sapiens (human)
type I interferon receptor binding	Interferon beta	Homo sapiens (human)
protein binding	Interferon beta	Homo sapiens (human)
chloramphenicol O-acetyltransferase activity	Interferon beta	Homo sapiens (human)
TAP binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
signaling receptor binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protein binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
peptide antigen binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
TAP binding	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
protein-folding chaperone binding	HLA class I histocompatibility antigen, B alpha chain	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)
inositol-1,3,4,5,6-pentakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol heptakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 5-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
protein binding	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
ATP binding	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 1-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol hexakisphosphate 3-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activity	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
extracellular space	Interferon beta	Homo sapiens (human)
extracellular region	Interferon beta	Homo sapiens (human)
Golgi membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
endoplasmic reticulum	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
Golgi apparatus	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
plasma membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
cell surface	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
ER to Golgi transport vesicle membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
secretory granule membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
phagocytic vesicle membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
early endosome membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
recycling endosome membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
extracellular exosome	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
lumenal side of endoplasmic reticulum membrane	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
MHC class I protein complex	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
extracellular space	HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)
external side of plasma membrane	HLA class I histocompatibility antigen, B alpha chain	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)
fibrillar center	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
nucleoplasm	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
cytosol	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
nucleus	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
cytoplasm	Inositol hexakisphosphate kinase 1	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
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.
AID1347160	Primary screen NINDS Rhodamine 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.
AID1347159	Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay	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.
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.
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.
AID166506	In vivo percent elevation evaluated from the plasma HDL levels in JW rabbits by oral administration of 100 mg/kg once a day for 3 days	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
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.
AID311047	Decrease in aortic arch lesions in cholesterol fed rabbit	2007	Bioorganic & medicinal chemistry, Jul-15, Volume: 15, Issue:14	The biology and chemistry of hyperlipidemia.
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.
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.
AID51943	Percent inhibition of cholesteryl ester transfer protein in human plasma at 9 uM	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
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.
AID166645	In vivo percent inhibition of cholesteryl ester transfer protein was measured 3h after oral administration of 10 mg/kg JW rabbits plasma	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
AID166646	In vivo percent inhibition of cholesteryl ester transfer protein was measured 3h after oral administration of 30 mg/kg JW rabbits plasma	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
AID166507	In vivo percent elevation evaluated from the plasma HDL levels in JW rabbits by oral administration of 30 mg/kg once a day for 3 days	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
AID51787	In vitro concentration required to inhibit 50% of cholesteryl ester transfer protein mediated cholesteryl ester transfer from HDL to VLDL and LDL in human plasma	2000	Journal of medicinal chemistry, Sep-21, Volume: 43, Issue:19	bis(2-(Acylamino)phenyl) disulfides, 2-(acylamino)benzenethiols, and S-(2-(acylamino)phenyl) alkanethioates as novel inhibitors of cholesteryl ester transfer protein.
AID51791	In vitro inhibition of CETP activity was assessed by measuring the rate of [3H]- cholesteryl ester transfer from HDL to apoprotein B-containing lipoproteins in human plasma	2004	Bioorganic & medicinal chemistry letters, May-17, Volume: 14, Issue:10	S-(2-(acylamino)phenyl) 2,2-dimethylpropanethioates as CETP inhibitors.
[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	43 (26.38)	29.6817
2010's	101 (61.96)	24.3611
2020's	19 (11.66)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	38 (22.89%)	5.53%
Reviews	45 (27.11%)	6.00%
Case Studies	0 (0.00%)	4.05%
Observational	0 (0.00%)	0.25%
Other	83 (50.00%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (18)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Double-blind, Placebo-controlled, Phase 2a Proof-of-concept Trial of Dalcetrapib in Patients With Confirmed Mild to Moderate COVID-19[NCT04676867]	Phase 2	227 participants (Actual)	Interventional	2021-01-11	Completed
A Phase III, Double-blind, Randomized Placebo-controlled Study to Evaluate the Effects of Dalcetrapib on Cardiovascular (CV) Risk in a Genetically Defined Population With a Recent Acute Coronary Syndrome (ACS): The Dal-GenE Trial[NCT02525939]	Phase 3	6,147 participants (Actual)	Interventional	2016-04-30	Completed
A 4-Weeks Treatment, Randomised, Double-Blind, Parallel-Group Study Evaluating The Efficacy and Safety of JTT-705 300 to 900mg in Comparison With Placebo in Patients With Type II Hyperlipidaemia[NCT00686010]	Phase 2	198 participants (Actual)	Interventional	2000-05-31	Completed
A 4-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study Evaluating the Safety and Efficacy of JTT-705 600 mg Versus Placebo Administered Once Daily in Combination With Simvastatin 40 mg in Patients With Low HDL Levels[NCT00688558]	Phase 2	92 participants (Actual)	Interventional	2004-02-29	Completed
A 4-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study Evaluating the Efficacy and Safety of JTT-705 (300 mg or 600 mg) Versus Placebo in Combination With Pravastatin 40 mg in Patients With Type II Hyperlipidemia[NCT00688896]	Phase 2	155 participants (Actual)	Interventional	2002-06-30	Completed
A 4-Week, Randomized, Double-Blind, Placebo-Controlled, Parallel Group Study Evaluating the Safety and Efficacy of JTT-705 600 mg Versus Placebo Administered Once Daily in Combination With Atorvastatin 20 mg in Patients With Low HDL Levels[NCT00689442]	Phase 2	105 participants (Actual)	Interventional	2004-01-31	Completed
Phase III, Double-blind, Randomized Placebo-controlled Study to Evaluate the Effects of Dalcetrapib on Cardiovascular (CV) Risk in a Genetically Defined Population With a Recent Acute Coronary Syndrome (ACS)[NCT05918861]	Phase 3	2,000 participants (Anticipated)	Interventional	2023-10-03	Recruiting
A Phase II, Placebo-Controlled, Double-Blind Extension Study of Study NC19453 Assessing Long-term Safety and Efficacy of RO4607381[NCT00400439]	Phase 2	77 participants (Actual)	Interventional	2007-01-31	Completed
A Randomized, Placebo-controlled Study of the Effect of RO4607381 on Progression or Regression of Atherosclerotic Plaque in Patients With Coronary Heart Disease (CHD) Including Patients With Other CHD Risk Factors[NCT00655473]	Phase 2	130 participants (Actual)	Interventional	2008-03-31	Completed
A Phase II, Double-Blind, Randomized, Placebo-controlled, Parallel Group Study, Evaluating the Efficacy and Safety of RO4607381 Over a 24-week Period in Patients With CHD or a CHD Risk Equivalent[NCT00353522]	Phase 2	135 participants (Actual)	Interventional	2006-07-31	Completed
A Phase 3b, Multi-Center, Double-Blind, Placebo-Controlled, Parallel Group, Study to Evaluate the Effect of Dalcetrapib 600 mg on Cardiovascular (CV) Events in Adult Patients With Stable Coronary Heart Disease (CHD), CHD Risk Equivalents or at Elevated Ri[NCT01516541]	Phase 3	2,220 participants (Actual)	Interventional	2012-01-31	Completed
A Single-center, Randomized, Open-label, Four Treatments, Four Periods, Four Sequence, Four-way Crossover Study to Explore the Pharmacokinetic Performance of Dalcetrapib and Atorvastatin Fixed Dose Combination Prototype Formulations in Healthy Volunteers[NCT01363999]	Phase 1	24 participants (Actual)	Interventional	2011-06-30	Completed
A Phase III, Double-blind, Randomized, Placebo-controlled, Multi-center Study Evaluating the Efficacy and Safety of Dalcetrapib on Lipids, Lipoproteins, Apolipoproteins and Markers of Cardiovascular (CV) Risk in Patients Hospitalized for an Acute Coronary[NCT01323153]	Phase 3	300 participants (Actual)	Interventional	2011-03-31	Completed
An Open Label, Single Centre Study to Investigate the Metabolic Profile of Dalcetrapib After a Single Oral Dose in Healthy Male Subjects[NCT01476267]	Phase 1	6 participants (Actual)	Interventional	2011-10-31	Completed
A Randomized, Double-blind, Placebo-controlled Study Assessing the Effect of RO4607381 on Cardiovascular Mortality and Morbidity in Clinically Stable Patients With a Recent Acute Coronary Syndrome[NCT00658515]	Phase 3	15,871 participants (Actual)	Interventional	2008-04-30	Completed
A Randomized, Double-blind Study of the Effect of RO4607381 in Combination With Pravastatin on HDL-cholesterol (HDL-C) Levels in Patients With Low or Average HDL-C Levels[NCT00697203]	Phase 2	292 participants (Actual)	Interventional	2005-07-31	Completed
A Multi-Center, Double-blind, Randomized, Placebo Controlled, Parallel Group Study of the Effect of Dalcetrapib on Atherosclerotic Disease Progression As Measured by Coronary Intravascular Ultrasound, Carotid B-Mode Ultrasound and Coronary Angiography[NCT01059682]	Phase 3	936 participants (Actual)	Interventional	2010-01-31	Terminated(stopped due to Termination of the clinical development program by the Sponsor)
A Randomized, Placebo-controlled Study of the Safety, Tolerability and Effect on Endothelial Function, as Measured by Flow Mediated Dilatation, of RO4607381 in Patients With Coronary Heart Disease (CHD) or CHD Risk Equivalents.[NCT00655538]	Phase 2	476 participants (Actual)	Interventional	2008-02-29	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00353522 (6) [back to overview]	Change From Baseline in Cholesterol Ester Transfer Protein (CETP) Activity
NCT00353522 (6) [back to overview]	Percent Change From Baseline in Cholesterol Ester Transfer Protein (CETP) Mass
NCT00353522 (6) [back to overview]	Percent Change From Baseline in HDL-C
NCT00353522 (6) [back to overview]	Change From Baseline in Total Cholesterol (TC), Triglycerides (TG), HDL-C, LDL-C, Apolipoproteins A1 (ApoA1), Apolipoproteins B (ApoB)
NCT00353522 (6) [back to overview]	Change in Mesenteric Lymph Nodes
NCT00353522 (6) [back to overview]	Absolute Change From Baseline in HDL-C
NCT00400439 (2) [back to overview]	Percent Change From Baseline in HDL-C
NCT00400439 (2) [back to overview]	Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C), Total Cholesterol (TC), Low Density Lipoprotein Cholesterol (LDL-C), Triglycerides (TG), Apolipoprotein B (ApoB) and Apolipoprotein A1 (ApoA1)
NCT00655473 (2) [back to overview]	Change From Baseline in Target (Plaque) to Background (Blood) Ratio From an Index Vessel.
NCT00655473 (2) [back to overview]	Percent Change From Baseline in Mean Wall Thickness
NCT00655538 (8) [back to overview]	Change From Baseline in % Flow Mediated Dilatation (FMD)
NCT00655538 (8) [back to overview]	Percent Change in HDL-C, LDL-C, Total Cholesterol, Triglycerides, ApoA1, ApoB
NCT00655538 (8) [back to overview]	Percent Change From Baseline of sP-Selectin, sE-Selectin, Soluble Intracellular Adhesion Molecule, Soluble Vascular Cell Molecule, Lipoprotein-associated phospholipaseA2s, Matrix Metalloproteinase-3, Matrix metalloproteinase9
NCT00655538 (8) [back to overview]	Percent Change CETP Mass
NCT00655538 (8) [back to overview]	Change From Baseline in Mean BP, Measured by BP Monitoring
NCT00655538 (8) [back to overview]	Change From Baseline in Mean BP, Measured by BP Monitoring
NCT00655538 (8) [back to overview]	Change From Baseline in % FMD
NCT00655538 (8) [back to overview]	CETP Activity
NCT00658515 (3) [back to overview]	Composite Endpoint:All Cause Mortality
NCT00658515 (3) [back to overview]	Change From Baseline for HDL Cholesterol
NCT00658515 (3) [back to overview]	Incidence of Cardiovascular Mortality and Morbidity
NCT00697203 (5) [back to overview]	Absolute Change From Baseline in HDL-C Level\
NCT00697203 (5) [back to overview]	Percent Change From Baseline in HDL-C Level\
NCT00697203 (5) [back to overview]	Percent Change of Fasting Glucose Level
NCT00697203 (5) [back to overview]	Change From Baseline in: Total Cholesterol, Triglycerides, HDL-C, LDL-C, HDL-2, HDL-3, ApoA1, ApoA2, ApoB, LpAI
NCT00697203 (5) [back to overview]	Ratios of Total HDL-C/LDL-C, HDL-2/HDL-3, ApoA1/ApoB
NCT01059682 (4) [back to overview]	Nominal Change From Baseline to Study End in Coronary Percent Atheroma Volume (PAV) of the Target Coronary Artery Assessed by IVUS.
NCT01059682 (4) [back to overview]	Nominal Changes From Baseline in Minimal Lumen Diameter as Assessed by Quantitative Coronary Angiography
NCT01059682 (4) [back to overview]	Nominal Changes in Percent Diameter Stenosis as Assessed by Quantitative Coronary Angiography
NCT01059682 (4) [back to overview]	Rate of Change From Baseline to Study End in Carotid Intima-media Thickness (CIMT) Using B-mode Ultrasound
NCT01323153 (1) [back to overview]	Percent Change From Baseline in High-density Lipoprotein C (HDL-C) Levels After 4 Weeks of Treatment
NCT01363999 (4) [back to overview]	Plasma Concentration of Dalcetrapib Active Form
NCT01363999 (4) [back to overview]	Plasma Concentration of Atorvastatin Metabolites
NCT01363999 (4) [back to overview]	Safety: Incidence of Serious Adverse Events
NCT01363999 (4) [back to overview]	Plasma Concentration of Atorvastatin
NCT01476267 (1) [back to overview]	Metabolic Profile: Percentage of Free Thiophenol M1 in the Blood Plasma
NCT02525939 (3) [back to overview]	Composite of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, and Non-Fatal Stroke
NCT02525939 (3) [back to overview]	Composite Endpoint of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, Non-Fatal Stroke, Hospitalization for ACS (With Electrocardiogram Abnormalities) or Unanticipated Coronary Revascularization
NCT02525939 (3) [back to overview]	Composite Endpoint of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, Non-Fatal Stroke or Hospitalization for New or Worsening Heart Failure
NCT04676867 (10) [back to overview]	Time to Complete Clinical Resolution
NCT04676867 (10) [back to overview]	Time to Complete Clinical Resolution (Excluding Cough, Sense of Smell and Taste) Defined in the Same Way as the Primary Endpoint, But Considering That All Symptoms Must Resolve to a Score of 0 for 72 Hours
NCT04676867 (10) [back to overview]	Time to Sustained Clinical Resolution of Symptoms of COVID-19 (Excluding Cough, Sense of Smell and Taste) in Subjects With Confirmed, Mild to Moderate, Symptomatic COVID-19 Treatment With Dalcetrapib
NCT04676867 (10) [back to overview]	Time to Sustained Complete Clinical Resolution of Symptoms in Subjects With Confirmed, Mild to Moderate, Symptomatic COVID-19 Treatment With Dalcetrapib
NCT04676867 (10) [back to overview]	Change From Baseline in Coronavirus Disease of 2019 (COVID-19) Total Symptom Severity Score Collected at All Time Points
NCT04676867 (10) [back to overview]	Change From Baseline in log10 Viral Load (Nasal Swab)
NCT04676867 (10) [back to overview]	Duration of Hospitalization
NCT04676867 (10) [back to overview]	Viral Clearance Using Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) Polymerase Chain Reaction (PCR)
NCT04676867 (10) [back to overview]	Scoring of World Health Organization (WHO) Clinical Outcome Scale (9-point Scale) at Screening, Days 1, 3, 5, End of Treatment (Day 10), Follow-Up Visit (Day 14), and Day 28
NCT04676867 (10) [back to overview]	Change From Baseline in log10 Viral Load (Saliva)

Change From Baseline in Cholesterol Ester Transfer Protein (CETP) Activity

(NCT00353522)
Timeframe: Baseline and 48 Weeks

Intervention	percent change in pMOL/mcL/hr (Least Squares Mean)
Dalcetrapib	-56.5
Placebo	-5.69

Intervention	Percent change in mg/dL (Least Squares Mean)
	Total Cholesterol	Triglycerides	HDL-C	LDL-C	ApoA1	ApoB
Dalcetrapib	10.17	0.94	33.76	4.75	16.43	4.98
Placebo	2.67	4.11	3.69	2.97	8.15	2.48

Intervention	Number of Nodes (Number)
	Number Increased in Volume	Number Decreased in Volume
Dalcetrapib	4	6
Placebo	11	18

Intervention	Percent change in ng/mL (Mean)
	sP-Selectin	sE-Selectin	Soluble intracellular adhesion molecule	Soluble vascular cell molecule	Lipoprotein-associated phospholipaseA2s	Matrix metalloproteinase-3	Matrix metalloproteinase9
Dalcetrapib	-1.83	6.01	1.05	3.60	23.24	3.46	28.12
Placebo	0.24	6.08	2.01	1.86	5.80	3.44	20.36

Intervention	mg/dL (Least Squares Mean)
Dalcetrapib 300mg	17.18
Dalcetrapib 600mg	31.42
Dalcetrapib 900mg	36.45
Placebo	2.31

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

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

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

Intervention	ng/mL (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet	285
B, RO5317116/F03 Bilayer Tablet	272
C, RO5317116/F04 Active-coated Tablet	294
D, RO4607381/F49 Tablet	231

Intervention	ng/ml (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet	2.50
B, RO5317116/F03 Bilayer Tablet	2.51
C, RO5317116/F04 Active-coated Tablet	2.95
D, RO4607381/F49 Tablet	2.77

Intervention	ng/mL (Geometric Mean)
A, RO5317116/F01 Bilayer Tablet	3.56
B, RO5317116/F03 Bilayer Tablet	3.55
C, RO5317116/F04 Active-coated Tablet	4.26
D, RO4607381/F49 Tablet	3.86

Intervention	days (Median)
Placebo Tablets	29.0
900 mg Dose	28.0
1800 mg Dose	29.0
3600 mg Dose	28.5

Intervention	score on a scale (Mean)
	Baseline	Day 2	Change from baseline to Day 2	Day 3	Change from baseline to Day 3	Day 4	Change from baseline to Day 4	Day 5	Change from baseline to Day 5	Day 6	Change from baseline to Day 6	Day 7	Change from baseline to Day 7	Day 8	Change from baseline to Day 8	Day 9	Change from baseline to Day 9	Day 10	Change from baseline to Day 10	Follow-up visit 1 (Day 14)	Change from baseline to follow-up visit 1	Follow-up visit 2 (Day 28/End of Study)	Change from baseline to follow-up visit 2
1800 mg Dose	10.88	11.55	0.68	10.57	-0.38	10.75	-0.13	9.29	-1.58	8.09	-2.44	8.39	-2.24	7.02	-3.64	6.86	-4.00	5.85	-4.59	4.23	-6.59	2.89	-7.78
3600 mg Dose	9.02	11.39	2.35	10.12	1.08	9.34	0.23	8.36	-0.56	8.24	-0.71	6.91	-2.02	5.50	-3.48	4.90	-3.95	4.00	-4.77	3.40	5.21	1.75	-7.17
900 mg Dose	11.11	10.76	-0.39	9.42	-1.69	9.60	-1.55	8.89	-2.26	7.94	-3.23	5.75	-5.29	5.82	-5.38	5.22	-6.20	4.37	-6.96	3.39	-7.90	2.23	-9.02
Placebo Tablets	10.70	10.30	-0.40	8.85	-1.85	8.24	-2.54	7.90	-2.79	6.98	-3.67	6.0	-4.65	5.06	-5.48	4.44	-6.10	3.90	-6.67	3.22	-7.42	1.84	-8.96

Intervention	Participants (Count of Participants)
	Viral Clearance (saliva)72361239		Viral Clearance (saliva)72361240	Viral Clearance (saliva)72361241	Viral Clearance (saliva)72361242	Viral Clearance (nasal swab)72361240	Viral Clearance (nasal swab)72361239	Viral Clearance (nasal swab)72361241	Viral Clearance (nasal swab)72361242
	Yes	No
Placebo Tablets	12
900 mg Dose	10
1800 mg Dose	9
3600 mg Dose	14
Placebo Tablets	41
900 mg Dose	44
1800 mg Dose	39
3600 mg Dose	36
Placebo Tablets	25
900 mg Dose	22
1800 mg Dose	12
Placebo Tablets	28
900 mg Dose	32
1800 mg Dose	36

Intervention	Participants (Count of Participants)
	Screening72361239									Screening72361240	Screening72361241	Screening72361242	Day 172361241	Day 172361242	Day 172361239	Day 172361240	Day 372361241	Day 372361240	Day 372361242	Day 372361239	Day 572361240	Day 572361239	Day 572361241	Day 572361242	End of Treatment (Day 10)72361240	End of Treatment (Day 10)72361241	End of Treatment (Day 10)72361242	End of Treatment (Day 10)72361239	Follow-up visit 1 (Day 14)72361239	Follow-up visit 1 (Day 14)72361242	Follow-up visit 1 (Day 14)72361240	Follow-up visit 1 (Day 14)72361241	Follow-up visit 2 (Day 28/End Of Study)72361239	Follow-up visit 2 (Day 28/End Of Study)72361240	Follow-up visit 2 (Day 28/End Of Study)72361241	Follow-up visit 2 (Day 28/End Of Study)72361242
	WHO Clinical Outcome Scale Score 7	WHO Clinical Outcome Scale Score 8	WHO Clinical Outcome Scale Score 0	WHO Clinical Outcome Scale Score 1	WHO Clinical Outcome Scale Score 2	WHO Clinical Outcome Scale Score 3	WHO Clinical Outcome Scale Score 4	WHO Clinical Outcome Scale Score 5	WHO Clinical Outcome Scale Score 6
1800 mg Dose	0
Placebo Tablets	18
900 mg Dose	15
1800 mg Dose	19
3600 mg Dose	23
Placebo Tablets	35
900 mg Dose	40
1800 mg Dose	29
3600 mg Dose	29
Placebo Tablets	15
900 mg Dose	13
1800 mg Dose	17
Placebo Tablets	38
900 mg Dose	42
1800 mg Dose	31
3600 mg Dose	34
Placebo Tablets	0
900 mg Dose	0
900 mg Dose	16
1800 mg Dose	15
900 mg Dose	38
1800 mg Dose	32
3600 mg Dose	25
Placebo Tablets	17
Placebo Tablets	34
900 mg Dose	31
3600 mg Dose	27
Placebo Tablets	3
900 mg Dose	5
3600 mg Dose	1
Placebo Tablets	29
900 mg Dose	27
3600 mg Dose	18
Placebo Tablets	19
900 mg Dose	20
1800 mg Dose	22
3600 mg Dose	31
Placebo Tablets	1
3600 mg Dose	0
900 mg Dose	2
Placebo Tablets	10
900 mg Dose	14
1800 mg Dose	12
3600 mg Dose	13
Placebo Tablets	31
1800 mg Dose	23
Placebo Tablets	11
900 mg Dose	18
1800 mg Dose	8
3600 mg Dose	11
900 mg Dose	1
Placebo Tablets	28
3600 mg Dose	19
Placebo Tablets	20
900 mg Dose	21
1800 mg Dose	21
3600 mg Dose	24
Placebo Tablets	5
900 mg Dose	12
1800 mg Dose	5
3600 mg Dose	8
1800 mg Dose	1

Condition	Indicated	Relationship Strength	Studies	Trials
Arteriosclerosis Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.	0	5.1	7	0
Disease Exacerbation [description not available]	0	4.75	2	1
Atherogenesis [description not available]	0	14.2	28	10
Hyperlipemia [description not available]	0	7.54	9	2
Hyperlipidemias Conditions with excess LIPIDS in the blood.	1	9.54	9	2
Atherosclerosis A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.	0	14.2	28	10
Hypertriglyceridemia A condition of elevated levels of TRIGLYCERIDES in the blood.	0	3.39	2	0
Congenital Zika Syndrome [description not available]	0	2.25	1	0
Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.	0	2.83	3	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	12.89	21	10
Cardiovascular Diseases Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.	1	14.63	30	4
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	14.89	21	10
2019 Novel Coronavirus Disease [description not available]	0	5.1	11	0
Apoplexy [description not available]	0	7.11	4	1
Asystole [description not available]	0	5.41	2	1
Cardiovascular Stroke [description not available]	0	8.06	5	2
Heart Arrest Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.	0	5.41	2	1
Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).	0	8.06	5	2
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	7.11	4	1
Acute Coronary Syndrome An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.	1	14.8	37	12
Angina at Rest [description not available]	0	5.93	3	1
Angina, Unstable Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.	0	5.93	3	1
Diabetes Mellitus, Adult-Onset [description not available]	0	4.84	2	1
Prediabetes [description not available]	0	4.55	1	1
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	4.84	2	1
Prediabetic State The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).	0	4.55	1	1
Chronic Kidney Diseases [description not available]	0	2.31	1	0
Renal Insufficiency, Chronic Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)	0	2.31	1	0
Dyslipidemia [description not available]	0	16.67	17	6
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.	1	13.67	17	6
Recrudescence [description not available]	0	5.73	2	1
Heart Disease, Ischemic [description not available]	0	4.48	1	1
Myocardial Ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).	0	4.48	1	1
Vascular Diseases Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.	0	2.58	2	0
Arteriosclerosis, Coronary [description not available]	0	8.38	9	2
Coronary Artery Disease Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.	0	8.38	9	2
Atheroma [description not available]	0	9.1	7	5
Arterial Diseases, Carotid [description not available]	0	7.51	4	4
Aortic Diseases Pathological processes involving any part of the AORTA.	0	7.67	5	4
Carotid Artery Diseases Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.	0	7.51	4	4
Innate Inflammatory Response [description not available]	0	8.78	6	4
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	8.78	6	4
alpha-Lipoprotein Deficiency Disease, Familial [description not available]	0	3.48	1	1
Cardiac Diseases [description not available]	0	3.39	2	0
Hyperlipoproteinemia [description not available]	0	4.11	3	0
Heart Diseases Pathological conditions involving the HEART including its structural and functional abnormalities.	0	3.39	2	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	4.11	3	0
Kidney Diseases Pathological processes of the KIDNEY or its component tissues.	0	4.8	2	1
Lipid Metabolism, Inborn Error [description not available]	0	3.67	3	0
Vascular Calcification Deposition of calcium into the blood vessel structures. Excessive calcification of the vessels are associated with ATHEROSCLEROTIC PLAQUES formation particularly after MYOCARDIAL INFARCTION (see MONCKEBERG MEDIAL CALCIFIC SCLEROSIS) and chronic kidney diseases which in turn increase VASCULAR STIFFNESS.	0	3.51	1	1
Angiitis [description not available]	0	3.51	1	1
Vasculitis Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.	0	3.51	1	1
Elevated Cholesterol [description not available]	0	10.63	13	5
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.	0	10.63	13	5
Cardiac Failure [description not available]	0	3.06	1	0
Heart Failure A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.	0	3.06	1	0
Apolipoprotein B-100, Familial Defective [description not available]	0	4.75	2	1
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).	0	4.75	2	1
Lymphatic Diseases Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.	0	3.44	1	1
Adrenal Cancer [description not available]	0	2.05	1	0
Blood Pressure, High [description not available]	0	3.85	2	1
Hypertension Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.	0	3.85	2	1
Arrhythmia [description not available]	0	3.44	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	3.44	1	1
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	3.39	2	0
Diabetic Angiopathies VASCULAR DISEASES that are associated with DIABETES MELLITUS.	0	2.07	1	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	8.39	2	0
Coronary Artery Stenosis [description not available]	0	4.77	2	1
Adverse Drug Event [description not available]	0	4.37	1	1
Coronary Stenosis Narrowing or constriction of a coronary artery.	0	4.77	2	1
Drug-Related Side Effects and Adverse Reactions Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.	0	4.37	1	1
Diabetes Mellitus A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.	0	2.06	1	0
A-alphalipoprotein Neuropathy [description not available]	0	3.83	2	1
Liver Dysfunction [description not available]	0	3.47	1	1
Liver Diseases Pathological processes of the LIVER.	0	3.47	1	1
Body Weight The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.	0	2.01	1	0
Cancer of Liver [description not available]	0	2.01	1	0
Liver Neoplasms Tumors or cancer of the LIVER.	0	2.01	1	0
Angiogenesis, Pathologic [description not available]	0	2.02	1	0
Hypolipoproteinemia [description not available]	0	2.92	1	0

dalcetrapib

Description

Cross-References

Synonyms (59)

Research Excerpts

Overview

Effects

Actions

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Drug Classes (1)

Protein Targets (7)

Potency Measurements

Inhibition Measurements

Biological Processes (64)

Molecular Functions (24)

Ceullar Components (24)

Bioassays (18)

Research

Studies (163)

Study Types

Clinical Trials (18)

Trial Overview

Trial Outcomes

Change From Baseline in Cholesterol Ester Transfer Protein (CETP) Activity

Percent Change From Baseline in Cholesterol Ester Transfer Protein (CETP) Mass

Percent Change From Baseline in HDL-C

Change From Baseline in Total Cholesterol (TC), Triglycerides (TG), HDL-C, LDL-C, Apolipoproteins A1 (ApoA1), Apolipoproteins B (ApoB)

Change in Mesenteric Lymph Nodes

Absolute Change From Baseline in HDL-C

Percent Change From Baseline in HDL-C

Change From Baseline in High Density Lipoprotein Cholesterol (HDL-C), Total Cholesterol (TC), Low Density Lipoprotein Cholesterol (LDL-C), Triglycerides (TG), Apolipoprotein B (ApoB) and Apolipoprotein A1 (ApoA1)

Change From Baseline in Target (Plaque) to Background (Blood) Ratio From an Index Vessel.

Percent Change From Baseline in Mean Wall Thickness

Change From Baseline in % Flow Mediated Dilatation (FMD)

Percent Change in HDL-C, LDL-C, Total Cholesterol, Triglycerides, ApoA1, ApoB

Percent Change From Baseline of sP-Selectin, sE-Selectin, Soluble Intracellular Adhesion Molecule, Soluble Vascular Cell Molecule, Lipoprotein-associated phospholipaseA2s, Matrix Metalloproteinase-3, Matrix metalloproteinase9

Percent Change CETP Mass

Change From Baseline in Mean BP, Measured by BP Monitoring

Change From Baseline in Mean BP, Measured by BP Monitoring

Change From Baseline in % FMD

CETP Activity

Composite Endpoint:All Cause Mortality

Change From Baseline for HDL Cholesterol

Incidence of Cardiovascular Mortality and Morbidity

Absolute Change From Baseline in HDL-C Level\

Percent Change From Baseline in HDL-C Level\

Percent Change of Fasting Glucose Level

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

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

Nominal Change From Baseline to Study End in Coronary Percent Atheroma Volume (PAV) of the Target Coronary Artery Assessed by IVUS.

Nominal Changes From Baseline in Minimal Lumen Diameter as Assessed by Quantitative Coronary Angiography

Nominal Changes in Percent Diameter Stenosis as Assessed by Quantitative Coronary Angiography

Rate of Change From Baseline to Study End in Carotid Intima-media Thickness (CIMT) Using B-mode Ultrasound

Percent Change From Baseline in High-density Lipoprotein C (HDL-C) Levels After 4 Weeks of Treatment

Plasma Concentration of Dalcetrapib Active Form

Plasma Concentration of Atorvastatin Metabolites

Safety: Incidence of Serious Adverse Events

Plasma Concentration of Atorvastatin

Metabolic Profile: Percentage of Free Thiophenol M1 in the Blood Plasma

Composite of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, and Non-Fatal Stroke

Composite Endpoint of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, Non-Fatal Stroke, Hospitalization for ACS (With Electrocardiogram Abnormalities) or Unanticipated Coronary Revascularization

Composite Endpoint of Cardiovascular Death, Resuscitated Cardiac Arrest, Non-Fatal Myocardial Infarction, Non-Fatal Stroke or Hospitalization for New or Worsening Heart Failure

Time to Complete Clinical Resolution

Time to Complete Clinical Resolution (Excluding Cough, Sense of Smell and Taste) Defined in the Same Way as the Primary Endpoint, But Considering That All Symptoms Must Resolve to a Score of 0 for 72 Hours

Time to Sustained Clinical Resolution of Symptoms of COVID-19 (Excluding Cough, Sense of Smell and Taste) in Subjects With Confirmed, Mild to Moderate, Symptomatic COVID-19 Treatment With Dalcetrapib

Time to Sustained Complete Clinical Resolution of Symptoms in Subjects With Confirmed, Mild to Moderate, Symptomatic COVID-19 Treatment With Dalcetrapib

Change From Baseline in Coronavirus Disease of 2019 (COVID-19) Total Symptom Severity Score Collected at All Time Points

Change From Baseline in log10 Viral Load (Nasal Swab)

Duration of Hospitalization

Viral Clearance Using Severe Acute Respiratory Syndrome CoronaVirus 2 (SARS-CoV-2) Polymerase Chain Reaction (PCR)

Scoring of World Health Organization (WHO) Clinical Outcome Scale (9-point Scale) at Screening, Days 1, 3, 5, End of Treatment (Day 10), Follow-Up Visit (Day 14), and Day 28

Change From Baseline in log10 Viral Load (Saliva)

Related Drugs (66)

Related Conditions (81)