darapladib profile

darapladib: a selective lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) inhibitor, on biomarkers of cardiovascular (CV) risk [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	9939609
CHEMBL ID	204021
SCHEMBL ID	2742709
MeSH ID	M0521612

Synonym
darapladib
darapladib (jan/usan)
356057-34-6
D03650
bdbm50125265
n-(2-diethylamino-ethyl)-2-[2-(4-fluoro-benzylsulfanyl)-4-oxo-4,5,6,7-tetrahydro-cyclopentapyrimidin-1-yl]-n-(4''-trifluoromethyl-biphenyl-4-ylmethyl)-acetamide
CHEMBL204021 ,
sb-480848
sb 480848;n-[2-(diethylamino)ethyl]-2-[[(4-fluorophenyl)methyl]thio]-4,5,6,7-tetrahydro-4-oxo-n-[[4'-(trifluoromethyl)[1,1'-biphenyl]-4-yl]methyl]-1h-cyclopentapyrimidine-1-acetamide
A822896
BCP9000585
darapladib [usan:inn]
ui1u1myh09 ,
unii-ui1u1myh09
sb 480848
sb480848
1h-cyclopentapyrimidine-1-acetamide, n-(2-(diethylamino)ethyl)-2-(((4-fluorophenyl)methyl)thio)-4,5,6,7-tetrahydro-4-oxo-n-((4'-(trifluoromethyl)(1,1'-biphenyl)-4-yl)methyl)-
n-(2-(diethylamino)ethyl)-2-(2-((4-fluorobenzyl)sulfanyl)-4-oxo-4,5,6,7-tetrahydro-1h-cyclopentapyrimidin-1-yl)-n-((4'-(trifluoromethyl)biphenyl-4-yl)methyl)acetamide
HY-10521
CS-1035
PB30298
S7520
gtpl6696
n-(2-diethylaminoethyl)-2-[2-[(4-fluorophenyl)methylsulfanyl]-4-oxo-6,7-dihydro-5h-cyclopenta[e]pyrimidin-1-yl]-n-[[4-[4-(trifluoromethyl)phenyl]phenyl]methyl]acetamide
darapladib [inn]
n-(2-(diethylamino)ethyl)-2-(2-(4-fluorobenzylsulphanyl)-4-oxo-4,5,6,7-tetrahydrocyclopentapyrimidin-1-yl)-n-(4'-trifluoromethylbiphenyl-4-ylmethyl)acetamide
darapladib [jan]
darapladib [who-dd]
darapladib [mi]
darapladib [usan]
FD5008
MLS006010424
smr004701449
n-[2-(diethylamino)ethyl]-n-[4'-(trifluoromethyl)-1,1'-biphenyl-4-ylmethyl]-2-[2-(4-fluorobenzylthio)-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl]acetamide
SCHEMBL2742709
AKOS025290042
n-(2-(diethylamino)ethyl)-2-(2-((4-fluorobenzyl)thio)-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl)-n-((4'-(trifluoromethyl)-[1,1'-biphenyl]-4-yl)methyl)acetamide
AC-32914
n-[2-(diethylamino)ethyl]-2-[2-[(4-fluorophenyl)methylsulfanyl]-4-oxo-6,7-dihydro-5h-cyclopenta[d]pyrimidin-1-yl]-n-[[4-[4-(trifluoromethyl)phenyl]phenyl]methyl]acetamide
mfcd18251452
DTXSID70189073
5hv ,
n-[2-(diethylamino)ethyl]-2-{2-[(4-fluorobenzyl)sulfanyl]-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl}-n-{[ 4'-(trifluoromethyl)biphenyl-4-yl]methyl}acetamide
HMS3653B13
NCGC00386337-05
SW219569-1
n-[2-(diethylamino)ethyl]-2-{2-[(4-fluorobenzyl)sulfanyl]-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl}-n-{[
n-[2-(diethylamino)ethyl]-2-{2-[(4-fluorobenzyl)sulfanyl]-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl}-n-{[4'-(trifluoromethyl)biphenyl-4-yl]methyl}acetamide
4'-(trifluoromethyl)biphenyl-4-yl]methyl}acetamide
FT-0725571
BCP04908
Q5222103
darapladib (sb-480848)
darapladib; sb-480848
EX-A2245
DB06311
AS-17025
n-[2-(diethylamino)ethyl]-n-[4'-(trifluoromethyl)-1,1'-biphenyl-4-ylmethyl]-2-[2-(4-fluorobenzylthio)-4-oxo-4,5,6,7-tetrahydro-1h-cyclopenta[d]pyrimidin-1-yl]a
n-[2-(diethylamino)ethyl]-2-[[(4-fluorophenyl)methyl]thio]-4,5,6,7-tetrahydro-4-oxo-n-[[4'-(trifluoromethyl)[1,1'-biphenyl]-4-yl]methyl]-1h-cyclopentapyrimidine-1-acetamide
HMS3744E13
CCG-270349
wdpfjwldpvqcaj-uhfffaoysa-n

Excerpt	Reference	Relevance
"Darapladib is a selective oral inhibitor of lipoprotein-associated phospholipase A2."	( Darapladib for preventing ischemic events in stable coronary heart disease. Ardissino, D; Armstrong, PW; Avezum, A; Aylward, PE; Brown, R; Bryce, A; Budaj, A; Cannon, CP; Chen, H; Chen, MF; Corbalan, R; Dalby, AJ; Danchin, N; Davies, RY; De Winter, RJ; Denchev, S; Diaz, R; Elisaf, M; Flather, MD; Goudev, AR; Granger, CB; Grinfeld, L; Harrington, RA; Held, C; Hochman, JS; Husted, S; Kim, HS; Koenig, W; Linhart, A; Lonn, E; López-Sendón, J; Manolis, AJ; Mohler, ER; Nicolau, JC; Pais, P; Parkhomenko, A; Pedersen, TR; Pella, D; Ramos-Corrales, MA; Ruda, M; Sereg, M; Siddique, S; Sinnaeve, P; Smith, P; Sritara, P; Steg, PG; Stewart, R; Swart, HP; Sy, RG; Tarka, E; Teramoto, T; Tse, HF; Viigimaa, M; Vinereanu, D; Wallentin, L; Watson, D; Weaver, WD; Weiss, R; White, HD; Zhu, J, 2014)	2.57
"Darapladib is an oral, selective inhibitor of the Lp-PLA2 enzyme."	( Effect of darapladib on major coronary events after an acute coronary syndrome: the SOLID-TIMI 52 randomized clinical trial. Bode, C; Bonaca, MP; Braunwald, E; Cannon, CP; Crugnale, SE; Davies, RY; Hochman, JS; Im, K; Lukas, MA; Maggioni, AP; Murphy, SA; O'Donoghue, ML; Serruys, PW; Shannon, JB; Steen, DL; Steen, DP; Steg, PG; Tarka, E; Watson, DF; Weaver, WD; White, HD; Wiviott, SD, 2014)	1.53
"Darapladib is a potent and reversible orally active inhibitor of lipoprotein-associated phospholipase A2 (Lp-PLA2 ). "	( The pharmacokinetics and safety of darapladib in subjects with severe renal impairment. Collins, D; Magee, MH; Shaddinger, B; Siddiqi, S; Soffer, J, 2015)	2.14
"Darapladib is a lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor. "	( Single and Multiple Dose Pharmacokinetics, Pharmacodynamics and Safety of the Novel Lipoprotein-Associated Phospholipase A2 Enzyme Inhibitor Darapladib in Healthy Chinese Subjects: An Open Label Phase-1 Clinical Trial. Chen, Q; Gross, AS; Hu, C; Liu, Y; Liu, YM; Magee, M; Tompson, D; Zhao, H; Zhu, W, 2015)	2.06
"Darapladib is an orally available, specific inhibitor of LpPLA2 activity and has been shown to reduce lysophosphatidylcholine content and expression of multiple genes associated with macrophage and T-lymphocyte functioning, with considerable decrease in plaque and necrotic core area."	( Darapladib and atherosclerotic plaque: should lipoprotein-associated phospholipase A2 be a therapeutic target? McCullough, PA, 2009)	2.52
"Darapladib is a selective inhibitor of Lp-PLA(2)."	( Darapladib. Bui, QT; Wilensky, RL, 2010)	2.52
"Darapladib is a selective inhibitor of Lp-PLA(2) and represents a new class of therapeutic agents that target inflammation to treat high-risk atherosclerosis."	( Darapladib. Bui, QT; Wilensky, RL, 2010)	3.25

Excerpt	Reference	Relevance
"Darapladib treatment significantly reduced (p<0.05) foam cells number as well as iNOS expression in aorta in rats with T2DM after both treatment times."	( Darapladib inhibits atherosclerosis development in type 2 diabetes mellitus Sprague-Dawley rat model. Adam, AA; Andarini, S; Hanifa, H; Heriansyah, T; Lutfiana, NC; Refialdinata, J; Sholichah, Z; Sulfia, YH; Wihastuti, TA, 2018)	2.64
"Darapladib treatment resulted in a considerable decrease in plaque area and, notably, a markedly reduced necrotic core area and reduced medial destruction, resulting in fewer lesions with an unstable phenotype."	( Inhibition of lipoprotein-associated phospholipase A2 reduces complex coronary atherosclerotic plaque development. Bollinger, JG; Burgert, ME; Fenning, RS; Gelb, MH; Hamamdzic, D; Hoffman, BE; Li, J; Macphee, CH; Mirabile, RC; Mohler, ER; Pelchovitz, DJ; Postle, A; Shi, Y; Walker, MC; Webb, CL; Wilensky, RL; Yang, J; Zalewski, A; Zhang, L; Zhang, P, 2008)	1.07
"Treatment with darapladib led to a ≈65% persistent reduction in median Lp-PLA2 activity."	( Lipoprotein-Associated Phospholipase A2 Activity Is a Marker of Risk But Not a Useful Target for Treatment in Patients With Stable Coronary Heart Disease. Armstrong, PW; Cannon, CP; Davies, RY; Granger, CB; Hagström, E; Harrington, RA; Held, C; Hochman, JS; Koenig, W; Krug-Gourley, S; Mohler, ER; Östlund, O; Siegbahn, A; Steg, PG; Stewart, RA; Tarka, E; Wallentin, L; Weiss, R; White, HD, 2016)	0.77
"Treatment with darapladib was associated with a decrease in necrotic core, but was not associated with a decrease in percentage atheroma volume."	( Relationship between cardiovascular risk factors and biomarkers with necrotic core and atheroma size: a serial intravascular ultrasound radiofrequency data analysis. García-García, HM; Garg, S; Gonzalo, N; Hamm, CW; Klauss, V; Onuma, Y; Serruys, PW; Shannon, J; Wijns, W, 2012)	0.72
"Treatment with darapladib (adjusted OR 0.53; 95% CI: 0.30-0.92) and initial presentation with ACS (adjusted OR 0.42; 95% CI: 0.23-0.77) were associated with less frequent occurrence of a 2-fold increase in hs-cTnI levels."	( Darapladib effect on circulating high sensitive troponin in patients with acute coronary syndromes. Boersma, E; Brugaletta, S; Davies, R; García-García, HM; Oemrawsingh, RM; Serruys, PW; Shannon, J; Vranckx, P, 2012)	2.16

Excerpt	Reference	Relevance
" Darapladib was generally well tolerated, with adverse events (AEs) reported by seven subjects in the hepatic impairment group and three subjects in the healthy matched group (five and one of which were drug-related AEs, respectively)."	( An effect of moderate hepatic impairment on the pharmacokinetics and safety of darapladib. Fang, Z; Glaser, R; Magee, MH; Shaddinger, B; Shearn, S, 2014)	1.54
" Adverse events (AE) were reported in 38% of healthy subjects and 75% of severely renally impaired subjects, most of which were mild or moderate in intensity."	( The pharmacokinetics and safety of darapladib in subjects with severe renal impairment. Collins, D; Magee, MH; Shaddinger, B; Siddiqi, S; Soffer, J, 2015)	0.69
" The most common adverse events (≥ 21% subjects) were abnormal faeces, abnormal urine odour, diarrhoea and nasopharyngitis."	( Single and Multiple Dose Pharmacokinetics, Pharmacodynamics and Safety of the Novel Lipoprotein-Associated Phospholipase A2 Enzyme Inhibitor Darapladib in Healthy Chinese Subjects: An Open Label Phase-1 Clinical Trial. Chen, Q; Gross, AS; Hu, C; Liu, Y; Liu, YM; Magee, M; Tompson, D; Zhao, H; Zhu, W, 2015)	0.62
" The Lp-PLA2 activity and adverse event profile were similar in healthy Chinese and previous reports in Western subjects."	( Single and Multiple Dose Pharmacokinetics, Pharmacodynamics and Safety of the Novel Lipoprotein-Associated Phospholipase A2 Enzyme Inhibitor Darapladib in Healthy Chinese Subjects: An Open Label Phase-1 Clinical Trial. Chen, Q; Gross, AS; Hu, C; Liu, Y; Liu, YM; Magee, M; Tompson, D; Zhao, H; Zhu, W, 2015)	0.62

Excerpt	Reference	Relevance
"Systemic exposure (AUC(0-T), Cmax geometric mean (CVb%)) of darapladib was higher after multiple-dosing (519 ng."	( Single and Multiple Dose Pharmacokinetics, Pharmacodynamics and Safety of the Novel Lipoprotein-Associated Phospholipase A2 Enzyme Inhibitor Darapladib in Healthy Chinese Subjects: An Open Label Phase-1 Clinical Trial. Chen, Q; Gross, AS; Hu, C; Liu, Y; Liu, YM; Magee, M; Tompson, D; Zhao, H; Zhu, W, 2015)	0.86

Excerpt	Reference	Relevance
" After preliminary evaluation of the properties of drug-likeness in vitro and in vivo, compound 37 stands out from this congeneric series of inhibitors for good inhibitory activity and favorable oral bioavailability in male Sprague-Dawley rats, providing a quality candidate for further development."	( Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2. Huang, F; Liu, Q; Shen, J; Wang, K; Xu, Y; Yuan, X; Zou, Y, 2017)	0.46
"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
" Darapladib exhibits favorable pharmacokinetics, minimal predicted drug-drug interactions, sustained blood levels with once-daily oral dosing and limited inhibition of other PLA2 isozymes."	( Darapladib, a reversible lipoprotein-associated phospholipase A2 inhibitor, for the oral treatment of atherosclerosis and coronary artery disease. Corson, MA; Riley, RF, 2009)	2.71
" The area under the plasma concentration-time curve during a dosing interval of duration τ (AUC(0,τ), geometric mean 223 ng ml(-1) h [90% CI 158, 316 ng ml(-1 ) h], in moderate hepatic impaired subjects, vs."	( An effect of moderate hepatic impairment on the pharmacokinetics and safety of darapladib. Fang, Z; Glaser, R; Magee, MH; Shaddinger, B; Shearn, S, 2014)	0.63
" Furthermore, 14c significantly inhibited retinal thickening in STZ-induced diabetic SD rats as a model of diabetic macular edema (DME) after oral dosing for 4 weeks."	( Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema. Chen, M; Chen, X; Du, L; Ma, Q; Mo, M; Shen, J; Wang, K; Wang, Y; Xu, W, 2016)	0.43

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	23.9185	0.0123	8.9648	39.8107	AID1645842
cytochrome P450 2D6	Homo sapiens (human)	Potency	9.5221	0.0010	8.3798	61.1304	AID1645840
Interferon beta	Homo sapiens (human)	Potency	23.9185	0.0033	9.1582	39.8107	AID1645842
HLA class I histocompatibility antigen, B alpha chain	Homo sapiens (human)	Potency	23.9185	0.0123	8.9648	39.8107	AID1645842
Inositol hexakisphosphate kinase 1	Homo sapiens (human)	Potency	23.9185	0.0123	8.9648	39.8107	AID1645842
cytochrome P450 2C9, partial	Homo sapiens (human)	Potency	23.9185	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)
Cytochrome P450 3A4	Homo sapiens (human)	IC50 (µMol)	27.0000	0.0001	1.7536	10.0000	AID54918
Cytochrome P450 2D6	Homo sapiens (human)	IC50 (µMol)	26.0000	0.0000	2.0151	10.0000	AID54596
Platelet-activating factor acetylhydrolase	Homo sapiens (human)	IC50 (µMol)	0.0003	0.0000	0.3837	3.9000	AID103814; AID1256582; AID1256589; AID1293618; AID1308811; AID1322513; AID1322514; AID1331350; AID1373370; AID1373371; AID1472155; AID746823
Platelet-activating factor acetylhydrolase	Homo sapiens (human)	Ki	0.0001	0.0000	0.0001	0.0001	AID103824
Platelet-activating factor acetylhydrolase	Mus musculus (house mouse)	IC50 (µMol)	0.0003	0.0003	0.3001	0.6000	AID1256582
[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)
Platelet-activating factor acetylhydrolase	Homo sapiens (human)	Kd	0.0497	0.0497	0.0497	0.0497	AID1312391
[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)
lipid hydroxylation	Cytochrome P450 3A4	Homo sapiens (human)
lipid metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
steroid catabolic process	Cytochrome P450 3A4	Homo sapiens (human)
xenobiotic metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
steroid metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
cholesterol metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
androgen metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
estrogen metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
alkaloid catabolic process	Cytochrome P450 3A4	Homo sapiens (human)
monoterpenoid metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
calcitriol biosynthetic process from calciol	Cytochrome P450 3A4	Homo sapiens (human)
xenobiotic catabolic process	Cytochrome P450 3A4	Homo sapiens (human)
vitamin D metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
vitamin D catabolic process	Cytochrome P450 3A4	Homo sapiens (human)
retinol metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
retinoic acid metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
long-chain fatty acid biosynthetic process	Cytochrome P450 3A4	Homo sapiens (human)
aflatoxin metabolic process	Cytochrome P450 3A4	Homo sapiens (human)
oxidative demethylation	Cytochrome P450 3A4	Homo sapiens (human)
xenobiotic metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
steroid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
cholesterol metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
estrogen metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
coumarin metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
alkaloid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
alkaloid catabolic process	Cytochrome P450 2D6	Homo sapiens (human)
monoterpenoid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
isoquinoline alkaloid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
xenobiotic catabolic process	Cytochrome P450 2D6	Homo sapiens (human)
retinol metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
long-chain fatty acid biosynthetic process	Cytochrome P450 2D6	Homo sapiens (human)
negative regulation of binding	Cytochrome P450 2D6	Homo sapiens (human)
oxidative demethylation	Cytochrome P450 2D6	Homo sapiens (human)
negative regulation of cellular organofluorine metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
arachidonic acid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
peptide hormone processing	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
low-density lipoprotein particle remodeling	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
lipid oxidation	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
plasma lipoprotein particle oxidation	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
phosphatidylcholine catabolic process	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
platelet activating factor metabolic process	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
positive regulation of inflammatory response	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
platelet activating factor catabolic process	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
positive regulation of monocyte chemotaxis	Platelet-activating factor acetylhydrolase	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)
monooxygenase activity	Cytochrome P450 3A4	Homo sapiens (human)
steroid binding	Cytochrome P450 3A4	Homo sapiens (human)
iron ion binding	Cytochrome P450 3A4	Homo sapiens (human)
protein binding	Cytochrome P450 3A4	Homo sapiens (human)
steroid hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
retinoic acid 4-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
oxidoreductase activity	Cytochrome P450 3A4	Homo sapiens (human)
oxygen binding	Cytochrome P450 3A4	Homo sapiens (human)
enzyme binding	Cytochrome P450 3A4	Homo sapiens (human)
heme binding	Cytochrome P450 3A4	Homo sapiens (human)
vitamin D3 25-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
caffeine oxidase activity	Cytochrome P450 3A4	Homo sapiens (human)
quinine 3-monooxygenase activity	Cytochrome P450 3A4	Homo sapiens (human)
testosterone 6-beta-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
1-alpha,25-dihydroxyvitamin D3 23-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
anandamide 8,9 epoxidase activity	Cytochrome P450 3A4	Homo sapiens (human)
anandamide 11,12 epoxidase activity	Cytochrome P450 3A4	Homo sapiens (human)
anandamide 14,15 epoxidase activity	Cytochrome P450 3A4	Homo sapiens (human)
aromatase activity	Cytochrome P450 3A4	Homo sapiens (human)
vitamin D 24-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
estrogen 16-alpha-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
estrogen 2-hydroxylase activity	Cytochrome P450 3A4	Homo sapiens (human)
1,8-cineole 2-exo-monooxygenase activity	Cytochrome P450 3A4	Homo sapiens (human)
monooxygenase activity	Cytochrome P450 2D6	Homo sapiens (human)
iron ion binding	Cytochrome P450 2D6	Homo sapiens (human)
oxidoreductase activity	Cytochrome P450 2D6	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen	Cytochrome P450 2D6	Homo sapiens (human)
heme binding	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 8,9 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 11,12 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 14,15 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
1-alkyl-2-acetylglycerophosphocholine esterase activity	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
phospholipid binding	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
hydrolase activity, acting on ester bonds	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
calcium-independent phospholipase A2 activity	Platelet-activating factor acetylhydrolase	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)
cytoplasm	Cytochrome P450 3A4	Homo sapiens (human)
endoplasmic reticulum membrane	Cytochrome P450 3A4	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 3A4	Homo sapiens (human)
mitochondrion	Cytochrome P450 2D6	Homo sapiens (human)
endoplasmic reticulum	Cytochrome P450 2D6	Homo sapiens (human)
endoplasmic reticulum membrane	Cytochrome P450 2D6	Homo sapiens (human)
cytoplasm	Cytochrome P450 2D6	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 2D6	Homo sapiens (human)
extracellular region	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
low-density lipoprotein particle	Platelet-activating factor acetylhydrolase	Homo sapiens (human)
high-density lipoprotein particle	Platelet-activating factor acetylhydrolase	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]

Bioassays (96)

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.
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.
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.
AID1293638	Oral bioavailability in Sprague-Dawley rat at 50 mg/kg after 0.5 to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID746824	Inhibition of Lp-PLA2 in human plasma using [3H]PAF as substrate at 10 nM incubated for 5 mins prior to substrate addition measured after 10 mins by liquid scintillation counting analysis relative to control	2013	Bioorganic & medicinal chemistry letters, May-15, Volume: 23, Issue:10	Triazole derivatives: a series of Darapladib analogues as orally active Lp-PLA2 inhibitors.
AID1472149	Inhibition of recombinant human full length GST-tagged group-7B PLA2 expressed in Escherichia coli Rosetta(DE3) pLysS using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent ba	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID1652350	Inhibition of recombinant human Lp-PLA2 (47 to 429 residues) in presence of 8-BODIPY by fluorescence polarization-based assay	2020	Journal of medicinal chemistry, 07-09, Volume: 63, Issue:13	Identification of Highly Selective Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors by a Covalent Fragment-Based Approach.
AID1322514	Inhibition of recombinant human Lp-PLA2 pre-incubated for 30 mins before PED6 fluorogenic substrate	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID746825	Inhibition of Lp-PLA2 in rabbit plasma using [3H]PAF as substrate at 10 nM incubated for 5 mins prior to substrate addition measured after 10 mins by liquid scintillation counting analysis relative to control	2013	Bioorganic & medicinal chemistry letters, May-15, Volume: 23, Issue:10	Triazole derivatives: a series of Darapladib analogues as orally active Lp-PLA2 inhibitors.
AID127500	Inhibitory concentration against monocyte chemotaxis	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1308811	Inhibition of human recombinant Lp-PLA2 using 2-thio-PAF as substrate after 20 mins by CPM-based fluorescence assay	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1373368	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 1 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID1293628	AUC (0 to 24 hrs) in Sprague-Dawley rat at 10 mg/kg, iv after 5 mins to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1652354	Inhibition of recombinant human Lp-PLA2 (47 to 429 residues) expressed in Escherichia coli RosettaTM2 (DE3) pLysS	2020	Journal of medicinal chemistry, 07-09, Volume: 63, Issue:13	Identification of Highly Selective Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors by a Covalent Fragment-Based Approach.
AID1322516	Ratio of IC50 for Lp-PLA2 in whole human plasma by Thio-PAF assay to IC50 for recombinant human Lp-PLA2 by Thio-PAF assay	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1373370	Inhibition of Lp-PLA2 in human plasma LDL fractions using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID102345	Inhibitory concentration against lyso-PtdCho production in human LDL	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1256582	Inhibition of Lp-PLA2 (unknown origin)	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1322512	Inhibition of Lp-PLA2 in whole human plasma pre-incubated for 15 mins before 2-thio-PAF substrate addition	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1373367	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 10 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID1331356	Lipophilicity, logD of the compound at pH 7.4 by chromatography	2017	ACS medicinal chemistry letters, Jan-12, Volume: 8, Issue:1	Investigation of a Bicyclo[1.1.1]pentane as a Phenyl Replacement within an LpPLA
AID729789	Inhibition of plasma Lp-PLA2 in Apo-E mouse model at 50 mg/kg, ip measured after 12 hrs by in vivo inhibition assay	2013	Bioorganic & medicinal chemistry letters, Mar-01, Volume: 23, Issue:5	Design and synthesis of imidazole and triazole derivatives as Lp-PLA₂ inhibitors and the unexpected discovery of highly potent quaternary ammonium salts.
AID103822	Non specific binding effect against Lp-PLA2 was determined in human plasma at 10 nM	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1256583	Invivo inhibition of Lp-PLA2 in mouse plasma at 100 nM after 24 hrs	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID103966	Non specific binding effect against Lp-PLA2 was determined in rabbit plasma at 100 nM	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1293632	Clearance in Sprague-Dawley rat at 10 mg/kg, iv after 5 mins to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID54596	Inhibitory activity against Cytochrome P450 2D6	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1308817	Lipophilicity, log D of the compound at pH 7.4 by reversed phase HPLC method	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1293636	Cmax in Sprague-Dawley rat at 50 mg/kg, po after 0.5 to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1293637	Tmax in Sprague-Dawley rat at 50 mg/kg, po after 0.5 to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID103814	Inhibitory activity against recombinant human Lp-PLA2	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1331350	Inhibition of human recombinant LpPLA2	2017	ACS medicinal chemistry letters, Jan-12, Volume: 8, Issue:1	Investigation of a Bicyclo[1.1.1]pentane as a Phenyl Replacement within an LpPLA
AID1293635	AUC (0 to 24 hrs) in Sprague-Dawley rat at 50 mg/kg, po after 0.5 to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1256585	Inhibition of Lp-PLA2 in Sprague-Dawley rat plasma at 10 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1322517	Solubility in pH 7.4 PBS by CLND assay	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1293626	Inhibition of Lp-PLA2 in rat plasma at 10 nM using 2-thio-PAF as substrate measured for 10 mins by plate reader analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1293625	Inhibition of Lp-PLA2 in rat plasma at 100 nM using 2-thio-PAF as substrate measured for 10 mins by plate reader analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1293618	Inhibition of recombinant human Lp-PLA2 using 2-thio-PAF as substrate measured for 10 mins by plate reader analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1472156	Inhibition of Lp-PLA2 in human plasma at 50 nM using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent based assay relative to control	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID1308815	Selectivity ratio of IC50 for human recombinant PLA2-7B to IC50 for human recombinant Lp-PLA2	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1373369	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 0.1 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID1256589	Inhibition of recombinant human Lp-PLA2 using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1293624	Inhibition of Lp-PLA2 in human plasma at 1 nM using 2-thio-PAF as substrate measured for 10 mins by plate reader analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1256592	Cmax in Sprague-Dawley rat at 50 mg/kg, po after 48 hrs by LC-MS method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1373371	Inhibition of human Lp-PLA2	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID1472172	In vivo inhibition of Lp-PLA2 in Sprague-Dawley rat plasma at 3 mg/kg, po after 24 hrs by DNTB reagent based assay	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID13421	Oral bioavailability in fasted rat	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1331352	Thermodynamic solubility of the compound in fasted state simulated intestinal fluid	2017	ACS medicinal chemistry letters, Jan-12, Volume: 8, Issue:1	Investigation of a Bicyclo[1.1.1]pentane as a Phenyl Replacement within an LpPLA
AID1312391	Binding affinity to human Lp-PLA2 by ITC assay	2016	Journal of medicinal chemistry, 05-26, Volume: 59, Issue:10	Structural and Thermodynamic Characterization of Protein-Ligand Interactions Formed between Lipoprotein-Associated Phospholipase A2 and Inhibitors.
AID1472150	Inhibition of Lp-PLA2 in rat plasma at 250 nM using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent based assay by DNTB reagent based assay relative to control	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID1373366	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 100 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID729791	Inhibition of human plasma Lp-PLA2 at 1 nM by liquid scintillation counting	2013	Bioorganic & medicinal chemistry letters, Mar-01, Volume: 23, Issue:5	Design and synthesis of imidazole and triazole derivatives as Lp-PLA₂ inhibitors and the unexpected discovery of highly potent quaternary ammonium salts.
AID1308816	Ratio of IC50 for Lp-PLA2 in human whole plasma to IC50 for human recombinant Lp-PLA2	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1322524	Permeability at pH 7.05 by PAMPA method	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1256590	Inhibition of recombinant human Lp-PLA2 at 100 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1256597	AUC (0 to infinity) in Sprague-Dawley rat at 50 mg/kg, po after 48 hrs by LC-MS method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID13422	Oral bioavailability in fed rat	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1322519	Lipophilicity, log D of the compound by chromatography	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1322515	Inhibition of recombinant human PLA2-VIIB by Thio-PAF assay	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1331353	Permeability of the compound at pH 7.05 by PAMPA	2017	ACS medicinal chemistry letters, Jan-12, Volume: 8, Issue:1	Investigation of a Bicyclo[1.1.1]pentane as a Phenyl Replacement within an LpPLA
AID103828	Inhibition of Lp-PLA2 within the atherosclerotic plaque 2 hr after an oral dose of 30 mg/kg to the WHHL rabbit	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID54918	Inhibitory activity against CYP450 3A4 isozyme	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1308813	Inhibition of Lp-PLA2 in human whole plasma using 2-thio-PAF as substrate preincubated for 15 mins followed by substrate addition measured after 3 mins by CPM-based fluorescence assay	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID729794	Inhibition of rabbit plasma Lp-PLA2 at 100 nM by liquid scintillation counting	2013	Bioorganic & medicinal chemistry letters, Mar-01, Volume: 23, Issue:5	Design and synthesis of imidazole and triazole derivatives as Lp-PLA₂ inhibitors and the unexpected discovery of highly potent quaternary ammonium salts.
AID1331351	Kinetic solubility of the compound by chemiluminescent nitrogen detection assay	2017	ACS medicinal chemistry letters, Jan-12, Volume: 8, Issue:1	Investigation of a Bicyclo[1.1.1]pentane as a Phenyl Replacement within an LpPLA
AID1472158	Inhibition of Lp-PLA2 in rat plasma at 50 nM using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent based assay relative to control	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID1256584	Inhibition of Lp-PLA2 in mouse plasma at 1 uM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1256599	Terminal half life in Sprague-Dawley rat at 50 mg/kg, po after 48 hrs by LC-MS method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1472155	Inhibition of human recombinant GST-tagged Lp-PLA2 (47 to 429 residues) expressed in Escherichia coli Rosetta(DE3) pLysS using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID9332	Oral bioavailability in dog	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1373364	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 1000 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID103813	Inhibitory activity against Lp-PLA2 in whole human plasma	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID746823	Inhibition of recombinant human Lp-PLA2 using [3H]PAF as substrate at 10 nM incubated for 5 mins prior to substrate addition measured after 10 mins by liquid scintillation counting analysis	2013	Bioorganic & medicinal chemistry letters, May-15, Volume: 23, Issue:10	Triazole derivatives: a series of Darapladib analogues as orally active Lp-PLA2 inhibitors.
AID1256586	Inhibition of Lp-PLA2 in Sprague-Dawley rat plasma at 100 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID21274	Permeability in plasma	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1308819	Apparent permeability of the compound after 3 hrs by HPLC-UV method	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1472152	Inhibition of Lp-PLA2 in human plasma at 250 nM using 2-thio-PAF as substrate preincubated for 30 min followed by substrate addition measured every minute for 10 mins by DNTB reagent based assay relative to control	2017	Journal of medicinal chemistry, 12-28, Volume: 60, Issue:24	Structure-Guided Discovery of Novel, Potent, and Orally Bioavailable Inhibitors of Lipoprotein-Associated Phospholipase A2.
AID1373365	Inhibition of Lp-PLA2 in human plasma LDL fractions assessed as residual enzyme activity at 500 nM using 2-thio platelet-activating factor as substrate by TMB dye based spectrophotometry	2018	Bioorganic & medicinal chemistry letters, 02-15, Volume: 28, Issue:4	Regioselectivity of thiouracil alkylation: Application to optimization of Darapladib synthesis.
AID1308820	Binding affinity to human serum albumin/alpha-1 acidglycoprotein after 6 mins by HPLC method	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1256588	Inhibition of Lp-PLA2 in human plasma at 100 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1256587	Inhibition of Lp-PLA2 in human plasma at 10 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID1256594	Inhibition of recombinant human Lp-PLA2 at 10 nM using 2-thio-PAF substrate after 10 mins	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Discovery of a Novel Series of Imidazo[1,2-a]pyrimidine Derivatives as Potent and Orally Bioavailable Lipoprotein-Associated Phospholipase A2 Inhibitors.
AID746826	Inhibition of Lp-PLA2 in rabbit plasma using [3H]PAF as substrate at 100 nM incubated for 5 mins prior to substrate addition measured after 10 mins by liquid scintillation counting analysis relative to control	2013	Bioorganic & medicinal chemistry letters, May-15, Volume: 23, Issue:10	Triazole derivatives: a series of Darapladib analogues as orally active Lp-PLA2 inhibitors.
AID103824	Inhibitory activity against recombinant human Lp-PLA2 by mechanistic studies	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
AID1293623	Inhibition of Lp-PLA2 in human plasma at 10 nM using 2-thio-PAF as substrate measured for 10 mins by plate reader analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID729792	Inhibition of human plasma Lp-PLA2 at 10 nM by liquid scintillation counting	2013	Bioorganic & medicinal chemistry letters, Mar-01, Volume: 23, Issue:5	Design and synthesis of imidazole and triazole derivatives as Lp-PLA₂ inhibitors and the unexpected discovery of highly potent quaternary ammonium salts.
AID1308818	Solubility of the compound in pH 7.4 phosphate buffered saline after 1 hr by chemiluminescent nitrogen detection assay	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1322513	Inhibition of recombinant human Lp-PLA2 incubated for 20 mins by Thio-PAF assay	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID729793	Inhibition of rabbit plasma Lp-PLA2 at 10 nM by liquid scintillation counting	2013	Bioorganic & medicinal chemistry letters, Mar-01, Volume: 23, Issue:5	Design and synthesis of imidazole and triazole derivatives as Lp-PLA₂ inhibitors and the unexpected discovery of highly potent quaternary ammonium salts.
AID1293630	Half life in Sprague-Dawley rat at 10 mg/kg, iv after 5 mins to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1308812	Inhibition of human recombinant PLA2-7B using 2-thio-PAF as substrate after 20 mins by CPM-based fluorescence assay	2016	Journal of medicinal chemistry, 06-09, Volume: 59, Issue:11	Exploitation of a Novel Binding Pocket in Human Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Discovered through X-ray Fragment Screening.
AID1293634	Volume of distribution at steady state in Sprague-Dawley rat at 10 mg/kg, iv after 5 mins to 24 hrs by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Mar-24, Volume: 59, Issue:6	Discovery of Potent and Orally Active Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Inhibitors as a Potential Therapy for Diabetic Macular Edema.
AID1345232	Human PLA2-G7 (Hydrolases)	2016	Journal of medicinal chemistry, 12-08, Volume: 59, Issue:23	Fragment-Based Approach to the Development of an Orally Bioavailable Lactam Inhibitor of Lipoprotein-Associated Phospholipase A2 (Lp-PLA
AID1345232	Human PLA2-G7 (Hydrolases)	2003	Bioorganic & medicinal chemistry letters, Mar-24, Volume: 13, Issue:6	The identification of clinical candidate SB-480848: a potent inhibitor of lipoprotein-associated phospholipase A2.
[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	13 (12.62)	29.6817
2010's	78 (75.73)	24.3611
2020's	12 (11.65)	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	28 (26.92%)	5.53%
Reviews	25 (24.04%)	6.00%
Case Studies	0 (0.00%)	4.05%
Observational	1 (0.96%)	0.25%
Other	50 (48.08%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (22)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
An Open-Label, Non-Randomized, Pharmacokinetic and Safety Study of Multiple Oral Doses of SB-480848 in Healthy Subjects and Subjects With Moderate Hepatic Impairment [NCT01154114]	Phase 1	24 participants (Actual)	Interventional	2010-07-01	Completed
Lp-PLA2, Progenitor Cells and Coronary Atherosclerosis in Humans AIM III [NCT01067339]	Phase 3	70 participants (Actual)	Interventional	2010-02-04	Completed
A Phase II Clinical Study of SB-480848 in Dyslipidemic Patients- A Multicenter, Randomized, Double-blind, Placebo-controlled Study of SB-480848 to Evaluate the Efficacy and Safety - [NCT00734032]	Phase 2	107 participants (Actual)	Interventional	2008-08-26	Completed
A Clinical Outcomes Study of Darapladib Versus Placebo in Subjects Following Acute Coronary Syndrome to Compare the Incidence of Major Adverse Cardiovascular Events (MACE). [NCT01000727]	Phase 3	13,026 participants (Actual)	Interventional	2009-12-01	Completed
An Open Label Study on the Effects of a Short Course of SB480848 (Darapladib) on Contents of Cantharidin-Induced Inflammatory Blisters in Subjects With Type 2 Diabetes Mellitus [NCT02058641]	Phase 1	9 participants (Actual)	Interventional	2014-02-26	Completed
SB-480848 in Major Adverse Cardiovascular Events - Integrated Phase III Summary of Efficacy and Safety [NCT01636271]		28,855 participants (Actual)	Observational	2011-10-31	Completed
An International, Multicenter, Randomized, Placebo-controlled, Parallel-group, 1 Year Treatment, Integrated Biomarkers and Imaging Study in Subjects With Angiographically Documented Coronary Heart Disease (CHD) to Examine the Effects of the Novel Lipoprot [NCT00268996]	Phase 2	336 participants (Actual)	Interventional	2005-11-10	Completed
A Study to Evaluate the Pharmacokinetics of the Enteric-Coated Micronized Free Base Formulation of Darapladib [SB-480848] and Its Metabolites in Healthy Volunteers. [NCT00743860]	Phase 1	20 participants (Actual)	Interventional	2008-09-30	Completed
An Open Label, Single Session Study to Collect Tolerability Information Following Repeat Dosing of Darapladib in Healthy Adult Subjects [NCT00704431]	Phase 1	2 participants (Actual)	Interventional	2008-05-31	Completed
LPL100601, A Clinical Outcomes Study of Darapladib Versus Placebo in Subjects With Chronic Coronary Heart Disease to Compare the Incidence of Major Adverse Cardiovascular Events (MACE) [NCT00799903]	Phase 3	15,828 participants (Actual)	Interventional	2008-12-01	Completed
An Open-label, Single-sequence Study to Evaluate the Potential CYP 3A4 Pharmacokinetic Interaction of Darapladib (SB-480848) in Healthy Subjects [NCT01873339]	Phase 1	26 participants (Actual)	Interventional	2013-06-19	Completed
A Multi-centre, Randomised, Double-blind, Placebo-controlled, Parallel-group Study to Investigate the Effect of the Lp-PLA2 Inhibitor SB-480848 (40, 80mg od) on Carotid Plaque Composition in Patients With Carotid Artery Disease and Planned Carotid Endarte [NCT01916720]	Phase 2	103 participants (Actual)	Interventional	2003-01-31	Completed
A Study to Evaluate the Pharmacokinetics, Pharmacodynamics and Safety of 160 mg Enteric-coated Micronised Free Base Darapladib in Healthy Chinese Subjects. [NCT02000804]	Phase 1	24 participants (Actual)	Interventional	2013-10-23	Completed
Phase I Study of SB-480848 (Darapladib) -A Double Blind, Randomised, Placebo-controlled, Parallel-group, Repeat Dose Study to Investigate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of SB-480848 in Healthy Japanese Male Subjects- [NCT00622830]	Phase 1	18 participants (Anticipated)	Interventional	2008-01-31	Completed
A Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of Single Oral Doses of Darapladib (SB480848) in Healthy Japanese Male Subjects [NCT00551317]	Phase 1	18 participants (Actual)	Interventional	2007-07-31	Completed
An Open-Label, Three Period, Single Sequence Study To Determine The Effect Of Repeat Oral Dosing Of Diltiazem On The Pharmacokinetics Of Repeat Oral Dosing Of Darapladib (SB-480848). [NCT01852565]	Phase 1	36 participants (Actual)	Interventional	2013-05-14	Completed
A Study to Evaluate the Effect of Repeat Oral Doses of Darapladib on Cardiac Conduction as Compared to Placebo and a Single Oral Dose of Moxifloxacin [NCT00411073]	Phase 1	72 participants (Anticipated)	Interventional	2006-12-31	Completed
A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Dose-ranging Study of SB-480848, an Oral Lipoprotein-associated Phospholipase A2 (Lp-PLA2) Inhibitor, in Subjects With Stable Coronary Heart Disease (CHD) or CHD-risk Equivalent [NCT00269048]	Phase 2	969 participants (Actual)	Interventional	2005-11-30	Completed
A Phase 2, Multi-national, Multi-centre, Double Masked, Randomised, Placebo Controlled, Parallel-group Study to Investigate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics and Efficacy of Darapladib Administered for 3 Months to Adult Subjects [NCT01506895]	Phase 2	54 participants (Actual)	Interventional	2012-02-29	Completed
An Open-Label, Non-Randomized, Pharmacokinetic and Safety Study of Multiple Oral Doses of SB-480848 in Healthy Subjects and in Subjects With Severe Renal Impairment [NCT01711723]	Phase 1	16 participants (Actual)	Interventional	2012-10-29	Completed
A Two-Part, Open-label, Sequential, Double Cohort, Study to Evaluate the Safety, Tolerability and Pharmacokinetics of Rosuvastatin When Co Administered With Darapladib in Healthy Adult Subjects [NCT01751074]	Phase 1	18 participants (Actual)	Interventional	2012-12-17	Completed
A Randomised, Double-blind, Placebo-controlled, Parallel Group, Repeat Dose Study to Assess the Effect of SB-480848 on Overall Asthma Control in Adult Subjects With Persistent Asthma Controlled on Stable, Low-dose, Inhaled Corticosteroids [NCT00368576]	Phase 1	67 participants (Actual)	Interventional	2006-08-31	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00268996 (18) [back to overview]	Mean sCD40L Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52
NCT00268996 (18) [back to overview]	Mean Myeloperoxidase (MPO) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52
NCT00268996 (18) [back to overview]	Change From Baseline in Mean Plaque Area, Mean Vessel Area, and Mean Lumen Area as IVUS-Grey Scale Assessments at Week 52.
NCT00268996 (18) [back to overview]	Mean Matrix Metaloproteinases-9 (MMP-9) Levels as Circulating Biomarkers Associated With Plaque Instability at Week 26 and Week 52.
NCT00268996 (18) [back to overview]	Mean Lipoprotein Phospholipase A2 (Lp-PLA2) Activity at the End of Week 26 and Week 52
NCT00268996 (18) [back to overview]	Mean Levels of Oxidised Phospholipids/ Apolipoprotein B100 (oxPL/apoB) Ratio as Target Circulating Biomarkers at the End of Week 26 and Week 52.
NCT00268996 (18) [back to overview]	Mean Interlukin 6 (IL-6) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52
NCT00268996 (18) [back to overview]	Mean Intercellular Adhesion Molecule-1 (ICAM-1) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52
NCT00268996 (18) [back to overview]	Change From Baseline in Vessel Volume and Lumen Volume as IVUS-Grey Scale Assessments at Week 52.
NCT00268996 (18) [back to overview]	Change From Baseline in Fibrous Tissue Volume and Fibro-fatty Volume as IVUS-VH Assessments at Week 52
NCT00268996 (18) [back to overview]	Change From Baseline in Fibrous Tissue and Fibro-fatty as a Percent of IVUS-VH Plaque as IVUS-VH Assessments at Week 52
NCT00268996 (18) [back to overview]	Mean Circulating High Sensitivity C- Reactive Protein (Hs-CRP) Levels at Week 52.
NCT00268996 (18) [back to overview]	Circulating Hs-CRP at the End of Week 26.
NCT00268996 (18) [back to overview]	Change From Baseline in the Density of Rotterdam Classification (ROC) Grade III/IV Strain Spots/10 Millimeter (mm) Within the Region of Interest (ROI) on IVUS Grey Scale Based Palpography at the End of Week 52.
NCT00268996 (18) [back to overview]	Change From Baseline in Necrotic Core as a Percent of IVUS-VH Plaque at the End of Week 52.
NCT00268996 (18) [back to overview]	Change From Baseline in Necrotic Core Volume as Intravenous Ultrasound-Virtual Histology (IVUS-VH) Assessments at Week 52
NCT00268996 (18) [back to overview]	Change From Baseline in Percent Obstruction Volume as IVUS-Grey Scale Assessments at Week 52
NCT00268996 (18) [back to overview]	Change From Baseline in Plaque Volume as IVUS-Grey Scale Assessments at Week 52
NCT00734032 (3) [back to overview]	Change From Baseline to Week 4 in Plasma Lipoprotein-associated Phospholipase A2 (Lp-PLA2) Activity
NCT00734032 (3) [back to overview]	Change From Baseline in Lp-PLA2 Activity at Week 1, 2 and Follow-up
NCT00734032 (3) [back to overview]	Percent Inhibition of Lp-PLA2 Activity in Plasma Over Time
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of Any Component of the Composite of All-cause Mortality, Non-fatal MI, or Non-fatal Stroke During the Time Period for Follow-up of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With All-cause Mortality During the Time Period for Vital Status
NCT00799903 (8) [back to overview]	Number of Participants With CV Death During the Time Period for Follow-up of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of Any Component of the Composite of Major Adverse Cardiovascular Events (Cardiovascular [CV] Death, Non-fatal Myocardial Infarction [MI] or Non-fatal Stroke) During the Time Period for Follow-up of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of Any Event in the Composite of Major Coronary Events (Coronary Heart Disease [CHD] Death, Non-fatal MI, or Urgent Coronary Revascularization [CR] for MI) During the Time Period for Follow-up (FU) of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of Any Event in the Composite of Total Coronary Events (CHD Death, Non-fatal MI, Hospitalization for Unstable Angina, or Any Coronary Revascularization Procedure) During Time Period for FU of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of MI (Fatal/Non-fatal) During the Time Period for Follow-up of CV Events
NCT00799903 (8) [back to overview]	Number of Participants With First Occurrence of Stroke (Fatal/Non-fatal) During the Time Period for Follow-up of CV Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Component of the Composite of Major Adverse Cardiovascular Events (Cardiovascular [CV] Death, Non-fatal MI or Non-fatal Stroke) During the Time Period for Follow-up of CV Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Component of the Composite of All-cause Mortality, Non-fatal MI, or Nonfatal Stroke During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With CHD Death During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With Cardiovascular Death During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With All-cause Mortality During the Time Period for Vital Status
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Stroke (Fatal/Non-fatal) During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of MI (Fatal/Nonfatal) During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Coronary Revascularization Procedures (Excluding Coronary Revascularization Planned Prior to Randomization, But Performed After Randomization) During the Time Period for Follow-up of Cardiovascular Event
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Event in the Composite of Total Coronary Events (CHD Death, Non-fatal MI, Hospitalization for Unstable Angina, or Any Coronary Revascularization Procedure) During the Time Period for FU of CV Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Event in the Composite of Major Coronary Events During the Time Period for Follow-up (FU) of Cardiovascular (CV) Event
NCT01000727 (12) [back to overview]	Number of Participants With Urgent Coronary Revascularization for Myocardial Ischemia During the Time Period for Follow-up of Cardiovascular Events
NCT01000727 (12) [back to overview]	Number of Participants With First Occurrence of Any Event in the Composite of CHD Death and Non-fatal MI During the Time Period for Follow-up of Cardiovascular Events
NCT01067339 (2) [back to overview]	Percentage Change in Coronary Blood Flow (CBF)
NCT01067339 (2) [back to overview]	Percentage Change in Coronary Artery Diameter

Mean sCD40L Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52

Blood was collected at baseline, Week 4, 13, 26 and 52 for evaluation of biomarkers. Mean sCD40L levels as circulating biomarker associated with inflammatory burden at Week 26 and Week 52 were assessed and reported. sCD40L had a skewed distribution and values were log transformed before analysis. The statistics was calculated on the log transformed data and back transformed. The adjusted geometric means of sCD40L levels at Week 26 and 52 were reported. The levels were analyzed using ANCOVA, with ACS status, pooled country and treatment included as covariates. (NCT00268996)
Timeframe: Week 26 and Week 52

Intervention	pg/ml (Least Squares Mean)
	Week 26	Week 52
Darapladib 160 mg EC Tablet	206.351	254.200
Placebo	178.738	183.449

Intervention	picomole per litre (pmol/L) (Geometric Mean)
	Week 26 (LOCF)	Week 52 (LOCF)
Darapladib 160 mg EC Tablet	378.811	405.339
Placebo	324.534	370.999

Intervention	mm2 (Least Squares Mean)
	Mean plaque area	Mean vessel area	Mean lumen area
Darapladib 160 mg EC Tablet	-0.124	-0.194	-0.069
Placebo	-0.112	-0.242	-0.130

Intervention	microgram per litre (mcg/L) (Geometric Mean)
	Week 26 LOCF	Week 52 LOCF
Darapladib 160 mg EC Tablet	471.477	498.709
Placebo	481.581	488.998

Intervention	mm^3 (Least Squares Mean)
	Vessel volume	Lumen volume
Darapladib 160 mg EC Tablet	-9.453	-4.066
Placebo	-11.211	-6.693

Intervention	mm^3 (Least Squares Mean)
	Fibrous tissue volume	Fibro-fatty volume
Darapladib 160 mg EC Tablet	-7.569	-1.415
Placebo	-6.985	-3.342

Intervention	Percentage of VH (Least Squares Mean)
	Fibrous tissue as percentage of VH plaque	Fibro-fatty as percentage of VH plaque
Darapladib 160 mg EC Tablet	-2.007	-0.043
Placebo	-4.007	-0.782

Intervention	Log(millimole per milliliter per minute) (Geometric Mean)
Placebo	0.961
SB-480848 40 mg	0.494
SB-480848 80 mg	0.404
SB-480848 160 mg	0.313

Intervention	Log(millimole per milliliter per minute) (Geometric Mean)
	Week 1	Week 2	Week 7 (Follow-up)
Placebo	0.957	0.977	0.964
SB-480848 160 mg	0.332	0.313	0.860
SB-480848 40 mg	0.495	0.499	0.917
SB-480848 80 mg	0.430	0.403	0.902

Intervention	Percent inhibiton of Lp-PLA2 activity (Mean)
	Week 1	Week 2	Week 4	Week 7 (Follow-up)
Placebo	-4.06	-1.96	-3.59	-3.16
SB-480848 160 mg	-66.03	-67.52	-67.73	-13.36
SB-480848 40 mg	-48.25	-49.05	-49.05	-7.65
SB-480848 80 mg	-55.83	-58.95	-58.67	-9.40

Substance	Relationship Strength	Studies	Trials	Classes	Roles
carbamates [no description available]	2.49	2	0	amino-acid anion
probucol Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).. probucol : A dithioketal that is propane-2,2-dithiol in which the hydrogens attached to both sulfur atoms are replaced by 3,5-di-tert-butyl-4-hydroxyphenyl groups. An anticholesteremic drug with antioxidant and anti-inflammatory properties, it is used to treat high levels of cholesterol in blood.	3.56	2	0	dithioketal; polyphenol	anti-inflammatory drug; anticholesteremic drug; antilipemic drug; antioxidant; cardiovascular drug
pirinixic acid pirinixic acid: structure	2.05	1	0	aryl sulfide; organochlorine compound; pyrimidines
5,5-dimethylhydantoin 5,5-dimethylhydantoin: RN given refers to parent cpd	2.13	1	0	imidazolidine-2,4-dione
benzenesulfonamide [no description available]	2.13	1	0	sulfonamide
pyrroles 1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.	4.75	2	1	pyrrole; secondary amine
thiophenes Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.	2.05	1	0	mancude organic heteromonocyclic parent; monocyclic heteroarene; thiophenes; volatile organic compound	non-polar solvent
quinazolines Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.	3.16	1	0	azaarene; mancude organic heterobicyclic parent; ortho-fused heteroarene; quinazolines
isoxazoles Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.. isoxazole : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing three carbon atoms and an oxygen and nitrogen atom adjacent to each other. It is the parent of the class of isoxazoles.. isoxazoles : Oxazoles in which the N and O atoms are adjacent.	2.05	1	0	isoxazoles; mancude organic heteromonocyclic parent; monocyclic heteroarene
phenyl acetate phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.	6.51	9	0	benzenes; phenyl acetates
simvastatin Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.	3.06	1	0	delta-lactone; fatty acid ester; hexahydronaphthalenes; statin (semi-synthetic)	EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor; EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor; ferroptosis inducer; geroprotector; prodrug
atorvastatin [no description available]	5.53	3	1	aromatic amide; dihydroxy monocarboxylic acid; monofluorobenzenes; pyrroles; statin (synthetic)	environmental contaminant; xenobiotic
valsartan Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.	2.1	1	0	biphenylyltetrazole; monocarboxylic acid amide; monocarboxylic acid	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
oxazolidin-2-one Oxazolidinones: Derivatives of oxazolidin-2-one. They represent an important class of synthetic antibiotic agents.. oxazolidin-2-one : An oxazolidinone that is 1,3-oxazolidine with an oxo substituent at position 2.. oxazolidinone : An oxazolidine containing one or more oxo groups.	3.56	2	0	carbamate ester; oxazolidinone	metabolite
tanshinone tanshinone: from root of Salvia miltiorrhiza Bunge; RN given refers to tanshinone I; cardioprotective agent and neuroprotective agent	2.31	1	0	abietane diterpenoid	anticoronaviral agent
bay x 1005 2-(4-(quinolin-2-yl-methoxy)phenyl)-2-cyclopentylacetic acid: inhibits synthesis of leukotriene B4 and 5-hydroxyeicosatetraenoic acid; inhibits five-lipoxygenase activating protein(FLAP)and leukotriene A4 hydrolase(LTA4H); structure given in first source;	2.05	1	0
ivabradine Ivabradine: A benzazepine derivative and selective HYPERPOLARIZATION-ACTIVATED CYCLIC NUCLEOTIDE-GATED CHANNELS inhibitor that lowers the heart rate. It is used in the treatment of CHRONIC STABLE ANGINA in patients unable to take BETA-ADRENERGIC BLOCKERS, and in the treatment of HEART FAILURE.. ivabradine : A member of the class of benzazepines that is 7,8-dimethoxy-1,3,4,5-tetrahydro-3-benzazepin-2-one in which the amide hydrogen is replaced by a [{[(7S)-3,4-dimethoxybicyclo[4.2.0]octa-1,3,5-trien-7-yl]methyl}(methyl)amino]propyl} group. Used (as its hydrochloride salt) to treat patients with angina who have intolerance to beta blockers and/or heart failure.	2.1	1	0	aromatic ether; benzazepine; carbobicyclic compound; tertiary amino compound	cardiotonic drug
varespladib [no description available]	6.02	7	0	aromatic ether; benzenes; dicarboxylic acid monoamide; indoles; monocarboxylic acid; primary carboxamide	anti-inflammatory drug; antidote; EC 3.1.1.4 (phospholipase A2) inhibitor
angiotensin ii Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).	2.31	1	0	amino acid zwitterion; angiotensin II	human metabolite
tbc-11251 sitaxsentan: endothelin A receptor antagonist; structure in first source	2.05	1	0	benzodioxoles
succinobucol succinobucol: monosuccinic acid ester of probucol; a metabolically stable modification of probucol, an equipotent antioxidant to probucol but is pharmacologically distinct	3.56	2	0	benzoate ester; phenols
n-phenylacrylamide N-phenylacrylamide: structure in first source	2.25	1	0
thiouracil Thiouracil: Occurs in seeds of Brassica and Crucifera species. Thiouracil has been used as antithyroid, coronary vasodilator, and in congestive heart failure although its use has been largely supplanted by other drugs. It is known to cause blood dyscrasias and suspected of terato- and carcinogenesis.. thiouracil : A nucleobase analogue that is uracil in which the oxo group at C-2 is replaced by a thioxo group.	7.17	1	0	nucleobase analogue; thiocarbonyl compound	antithyroid drug; metabolite
lysophosphatidylcholines lysophosphatidylcholine : An acylglycerophosphocholine resulting from partial hydrolysis of a phosphatidylcholine, which removes one of the fatty acyl groups. The structure is depicted in the image where R1 = acyl, R2 = H or where R1 = H, R2 = acyl.	5.9	2	1	1-O-acyl-sn-glycero-3-phosphocholine
enalapril Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).	2.1	1	0	dicarboxylic acid monoester; dipeptide	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; geroprotector; prodrug
dalcetrapib dalcetrapib: inhibits cholesteryl ester transfer protein (CETP)	3.16	1	0	anilide
mocetinostat mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).	3.46	1	1	aminopyrimidine; benzamides; pyridines; secondary amino compound; secondary carboxamide; substituted aniline	antineoplastic agent; apoptosis inducer; autophagy inducer; cardioprotective agent; EC 3.5.1.98 (histone deacetylase) inhibitor; hepatotoxic agent
varespladib methyl varespladib methyl : A methyl ester resulting from the formal condensation of the carboxy group of varespladib with methanol. It is a potential therapy for the treatment of snakebite envenomings in which toxicity depends on the action of PLA2s.	4.08	2	0	aromatic ether; benzenes; indoles; methyl ester; primary carboxamide	anti-inflammatory drug; antidote; EC 3.1.1.4 (phospholipase A2) inhibitor; prodrug
sb-435495 SB-435495: structure in first source	2.01	1	0
anacetrapib [no description available]	3.56	2	0
phosphatidylcholines Phosphatidylcholines: Derivatives of PHOSPHATIDIC ACIDS in which the phosphoric acid is bound in ester linkage to a CHOLINE moiety.	2.04	1	0	1,2-diacyl-sn-glycero-3-phosphocholine
cardiovascular agents Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.	8.41	6	3
natriuretic peptide, brain Natriuretic Peptide, Brain: A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.	4.45	1	1	polypeptide
d-4f peptide D-4F peptide: an apo A-I mimetic peptide synthesized from D-amino acids; may play a role in reducing inflammatory responses to influenza virus in mice; may also have anti-atherosclerotic properties	3.16	1	0
rvx 208 apabetalone: a bromodomain and extra-terminal domain protein (BET) inhibitor; prevents interactions between BET proteins and acetyl-lysine residues on histone tails to modify epigenetic regulation	3.16	1	0
pyrimidinones Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.	3.52	2	0

Condition	Indicated	Relationship Strength	Studies	Trials
Alloxan Diabetes [description not available]	0	3.26	5	0
Central Retinal Edema, Cystoid [description not available]	0	3.91	2	1
Diabetic Retinopathy Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.	1	6.21	3	1
Macular Edema Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)	0	8.91	2	1
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	4.4	4	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
Infections, Plasmodium [description not available]	0	2.41	1	0
Plasmodium falciparum Malaria [description not available]	0	2.41	1	0
Malaria A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.	0	2.41	1	0
Malaria, Falciparum Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.	0	2.41	1	0
Benign Neoplasms [description not available]	0	7.79	5	4
Neoplasms New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.	0	7.79	5	4
Diabetes Mellitus, Adult-Onset [description not available]	0	2.59	2	0
Diabetic Glomerulosclerosis [description not available]	0	2.21	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	2.59	2	0
Diabetic Nephropathies KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.	0	2.21	1	0
Electron Transport Chain Deficiencies, Mitochondrial [description not available]	0	2.25	1	0
Glial Cell Tumors [description not available]	0	2.25	1	0
Glioma Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)	0	7.25	1	0
Mitochondrial Diseases Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.	0	2.25	1	0
Allergic Encephalomyelitis [description not available]	0	2.31	1	0
Innate Inflammatory Response [description not available]	0	8.57	12	1
MS (Multiple Sclerosis) [description not available]	0	2.31	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	8.57	12	1
Multiple Sclerosis An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)	0	2.31	1	0
Chronic Illness [description not available]	0	2.31	1	0
Daytime Sleepiness [description not available]	0	2.31	1	0
Cardiovascular Diseases Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.	0	9.92	12	3
Chronic Disease Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).	0	2.31	1	0
Disorders of Excessive Somnolence Disorders characterized by hypersomnolence during normal waking hours that may impair cognitive functioning. Subtypes include primary hypersomnia disorders (e.g., IDIOPATHIC HYPERSOMNOLENCE; NARCOLEPSY; and KLEINE-LEVIN SYNDROME) and secondary hypersomnia disorders where excessive somnolence can be attributed to a known cause (e.g., drug affect, MENTAL DISORDERS, and SLEEP APNEA SYNDROME). (From J Neurol Sci 1998 Jan 8;153(2):192-202; Thorpy, Principles and Practice of Sleep Medicine, 2nd ed, p320)	0	2.31	1	0
Cirrhosis [description not available]	0	2.31	1	0
Cardiac Hypertrophy Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.	0	2.31	1	0
Fibrosis Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.	0	2.31	1	0
Cardiomegaly Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.	0	2.31	1	0
Cancer of Pancreas [description not available]	0	2.31	1	0
Cachexia General ill health, malnutrition, and weight loss, usually associated with chronic disease.	0	7.31	1	0
Pancreatic Neoplasms Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).	0	2.31	1	0
Chronic Kidney Diseases [description not available]	0	3.7	1	1
Arteriosclerosis, Coronary [description not available]	0	11.55	16	7
Symptom Cluster [description not available]	0	3.7	1	1
Coronary Artery Disease Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.	0	16.55	16	7
Syndrome A characteristic symptom complex.	0	3.7	1	1
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	3.7	1	1
Coronary Heart Disease [description not available]	0	13.17	24	15
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.	0	13.17	24	15
Atheroma [description not available]	0	11.77	17	8
Disease Exacerbation [description not available]	0	5.87	4	2
Apoplexy [description not available]	0	9.59	9	5
Cardiac Failure [description not available]	0	6.96	5	3
Cardiovascular Stroke [description not available]	0	11.08	12	7
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	6.96	5	3
Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).	0	11.08	12	7
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	9.59	9	5
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	12.09	10	6
Necrosis The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.	0	8.2	6	6
Recrudescence [description not available]	0	5.35	2	2
Atherogenesis [description not available]	0	9.07	24	1
Atherosclerosis A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.	1	11.07	24	1
Insulin Sensitivity [description not available]	0	2.17	1	0
Pregnancy in Diabetes [description not available]	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
Pregnancy The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.	0	2.17	1	0
Dyslipidemia [description not available]	0	3.91	2	1
Angiogenesis, Pathologic [description not available]	0	2.17	1	0
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	3.91	2	1
Angina at Rest [description not available]	0	4.88	2	1
Anterior Circulation Transient Ischemic Attack [description not available]	0	3.59	1	1
Angina, Unstable Precordial pain at rest, which may precede a MYOCARDIAL INFARCTION.	0	4.88	2	1
Ischemic Attack, Transient Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)	0	3.59	1	1
Cognitive Decline [description not available]	0	4.51	1	1
Cognitive Dysfunction Diminished or impaired mental and/or intellectual function.	0	4.51	1	1
Carotid Artery Narrowing [description not available]	0	4.4	1	1
Carotid Stenosis Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)	0	4.4	1	1
Liver Dysfunction [description not available]	0	3.48	1	1
Liver Diseases Pathological processes of the LIVER.	0	3.48	1	1
Heart Disease, Ischemic [description not available]	0	5.71	2	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	5.71	2	1
Elevated Cholesterol [description not available]	0	2.8	3	0
Diabetes Mellitus A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.	0	2.5	2	0
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	7.8	3	0
Kidney Failure A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.	0	4.84	2	1
Renal Insufficiency Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.	0	4.84	2	1
Genetic Predisposition [description not available]	0	2.13	1	0
Arterial Obstructive Diseases [description not available]	0	2.13	1	0
Arterial Occlusive Diseases Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.	0	2.13	1	0
Astrocytosis [description not available]	0	2.15	1	0
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	2.97	1	0
Hyperlipemia [description not available]	0	2.99	1	0
Hyperlipidemias Conditions with excess LIPIDS in the blood.	0	2.99	1	0
Peripheral Arterial Diseases [description not available]	0	3.45	1	1
Peripheral Arterial Disease Lack of perfusion in the EXTREMITIES resulting from atherosclerosis. It is characterized by INTERMITTENT CLAUDICATION, and an ANKLE BRACHIAL INDEX of 0.9 or less.	0	3.45	1	1
Cancer of Cervix [description not available]	0	2.08	1	0
Uterine Cervical Neoplasms Tumors or cancer of the UTERINE CERVIX.	0	2.08	1	0
Body Weight The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.	0	2.08	1	0

darapladib

Description

Cross-References

Synonyms (62)

Research Excerpts

Overview

Treatment

Toxicity

Pharmacokinetics

Bioavailability

Dosage Studied

Protein Targets (11)

Potency Measurements

Inhibition Measurements

Activation Measurements

Biological Processes (79)

Molecular Functions (45)

Ceullar Components (27)

Bioassays (96)

Research

Studies (103)

Market Indicators

Research Demand Index: 34.22

Study Types

Clinical Trials (22)

Trial Overview

Trial Outcomes

Mean sCD40L Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52

Mean Myeloperoxidase (MPO) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52

Change From Baseline in Mean Plaque Area, Mean Vessel Area, and Mean Lumen Area as IVUS-Grey Scale Assessments at Week 52.

Mean Matrix Metaloproteinases-9 (MMP-9) Levels as Circulating Biomarkers Associated With Plaque Instability at Week 26 and Week 52.

Mean Lipoprotein Phospholipase A2 (Lp-PLA2) Activity at the End of Week 26 and Week 52

Mean Levels of Oxidised Phospholipids/ Apolipoprotein B100 (oxPL/apoB) Ratio as Target Circulating Biomarkers at the End of Week 26 and Week 52.

Mean Interlukin 6 (IL-6) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52

Mean Intercellular Adhesion Molecule-1 (ICAM-1) Levels as Circulating Biomarkers Associated With Inflammatory Burden at Week 26 and Week 52

Change From Baseline in Vessel Volume and Lumen Volume as IVUS-Grey Scale Assessments at Week 52.

Change From Baseline in Fibrous Tissue Volume and Fibro-fatty Volume as IVUS-VH Assessments at Week 52

Change From Baseline in Fibrous Tissue and Fibro-fatty as a Percent of IVUS-VH Plaque as IVUS-VH Assessments at Week 52

Mean Circulating High Sensitivity C- Reactive Protein (Hs-CRP) Levels at Week 52.

Circulating Hs-CRP at the End of Week 26.

Change From Baseline in the Density of Rotterdam Classification (ROC) Grade III/IV Strain Spots/10 Millimeter (mm) Within the Region of Interest (ROI) on IVUS Grey Scale Based Palpography at the End of Week 52.

Change From Baseline in Necrotic Core as a Percent of IVUS-VH Plaque at the End of Week 52.

Change From Baseline in Necrotic Core Volume as Intravenous Ultrasound-Virtual Histology (IVUS-VH) Assessments at Week 52

Change From Baseline in Percent Obstruction Volume as IVUS-Grey Scale Assessments at Week 52

Change From Baseline in Plaque Volume as IVUS-Grey Scale Assessments at Week 52

Change From Baseline to Week 4 in Plasma Lipoprotein-associated Phospholipase A2 (Lp-PLA2) Activity

Change From Baseline in Lp-PLA2 Activity at Week 1, 2 and Follow-up

Percent Inhibition of Lp-PLA2 Activity in Plasma Over Time

Number of Participants With First Occurrence of Any Component of the Composite of All-cause Mortality, Non-fatal MI, or Non-fatal Stroke During the Time Period for Follow-up of CV Events

Number of Participants With All-cause Mortality During the Time Period for Vital Status

Number of Participants With CV Death During the Time Period for Follow-up of CV Events

Number of Participants With First Occurrence of Any Component of the Composite of Major Adverse Cardiovascular Events (Cardiovascular [CV] Death, Non-fatal Myocardial Infarction [MI] or Non-fatal Stroke) During the Time Period for Follow-up of CV Events

Number of Participants With First Occurrence of Any Event in the Composite of Major Coronary Events (Coronary Heart Disease [CHD] Death, Non-fatal MI, or Urgent Coronary Revascularization [CR] for MI) During the Time Period for Follow-up (FU) of CV Events

Number of Participants With First Occurrence of Any Event in the Composite of Total Coronary Events (CHD Death, Non-fatal MI, Hospitalization for Unstable Angina, or Any Coronary Revascularization Procedure) During Time Period for FU of CV Events

Number of Participants With First Occurrence of MI (Fatal/Non-fatal) During the Time Period for Follow-up of CV Events

Number of Participants With First Occurrence of Stroke (Fatal/Non-fatal) During the Time Period for Follow-up of CV Events

Number of Participants With First Occurrence of Any Component of the Composite of Major Adverse Cardiovascular Events (Cardiovascular [CV] Death, Non-fatal MI or Non-fatal Stroke) During the Time Period for Follow-up of CV Events

Number of Participants With First Occurrence of Any Component of the Composite of All-cause Mortality, Non-fatal MI, or Nonfatal Stroke During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With CHD Death During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With Cardiovascular Death During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With All-cause Mortality During the Time Period for Vital Status

Number of Participants With First Occurrence of Stroke (Fatal/Non-fatal) During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With First Occurrence of MI (Fatal/Nonfatal) During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With First Occurrence of Any Coronary Revascularization Procedures (Excluding Coronary Revascularization Planned Prior to Randomization, But Performed After Randomization) During the Time Period for Follow-up of Cardiovascular Event

Number of Participants With First Occurrence of Any Event in the Composite of Total Coronary Events (CHD Death, Non-fatal MI, Hospitalization for Unstable Angina, or Any Coronary Revascularization Procedure) During the Time Period for FU of CV Events

Number of Participants With First Occurrence of Any Event in the Composite of Major Coronary Events During the Time Period for Follow-up (FU) of Cardiovascular (CV) Event

Number of Participants With Urgent Coronary Revascularization for Myocardial Ischemia During the Time Period for Follow-up of Cardiovascular Events

Number of Participants With First Occurrence of Any Event in the Composite of CHD Death and Non-fatal MI During the Time Period for Follow-up of Cardiovascular Events

Percentage Change in Coronary Blood Flow (CBF)

Percentage Change in Coronary Artery Diameter

Related Drugs (36)

Related Conditions (95)