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candesartan cilexetil

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Description

Candesartan cilexetil is an angiotensin II receptor blocker (ARB) used to treat high blood pressure and heart failure. It works by blocking the effects of angiotensin II, a hormone that causes blood vessels to constrict. This helps to lower blood pressure and improve heart function. Candesartan cilexetil is synthesized through a multi-step process involving various chemical reactions. It was first synthesized in the late 1980s and has been extensively studied for its cardiovascular effects. The compound is important for treating high blood pressure and heart failure, as it has been shown to reduce the risk of heart attacks, strokes, and other cardiovascular events. It is studied to understand its long-term effects, optimize its dosage, and explore its potential uses in other cardiovascular conditions.'

candesartan cilexetil: a prodrug which is metabolized to an active form candesartan to exert its biological effects [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID2540
CHEMBL ID1014
CHEBI ID3348
SCHEMBL ID40831
MeSH IDM0208739

Synonyms (152)

Synonym
AC-204
AB01274805-01
BRD-A65671304-001-02-6
r85m2x0d68 ,
unii-r85m2x0d68
nsc 758697
amias
h212/91
racanda
parapres
tcv-116
atacand
candesartan hexetil
kenzen
1-{[(cyclohexyloxy)carbonyl]oxy}ethyl 2-(ethyloxy)-1-{[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl}-1h-benzimidazole-7-carboxylate
SPECTRUM_001707
BSPBIO_002691
1-(cyclohexylocarbonyloxy)ethyl-2-ethoxy-1-(2'-(1h-tetrazol-5-yl)biphenyl-4-yl)-1h-benzimidazole-7-carboxylate
1h-benzimidazolium, 7-carboxy-1-(2-((cyclohexylcarbonyl)oxy)ethyl)-2-ethoxy-1-(2'-(1h-tetrazol-5-yl)(1,1'-biphenyl)-4-yl)-, hydroxide, inner salt, (+-)-
candesartan cilexetil [usan]
tcv 116
1h-benzimidazole-7-carboxylic acid, 2-ethoxy-1-((2'-(1h-tetrazol-5-yl)(1,1'-biphenyl)-4-yl)methyl)-, 1-(((cyclohexyloxy)carbonyl)oxy)ethyl ester, (+-)-
(+-)-1-hydroxyethyl 2-ethoxy-1-(p-(o-1h-tetrazol-5-ylphenyl)benzyl)-7-benzimidazolecarboxylate, cyclohexyl carbonate (ester)
SPECTRUM5_001462
candesartan cilexetil
145040-37-5
C07709
DB00796
atacand (tn)
candesartan cilexetil (jp17/usp)
D00626
NCGC00095123-01
NCGC00095123-02
KBIOSS_002187
KBIO2_007323
KBIO2_004755
KBIO2_002187
KBIOGR_001607
KBIO3_001911
SPBIO_000349
SPECTRUM2_000485
SPECTRUM4_001124
SPECTRUM3_000996
SPECTRUM1504261
NCGC00095123-03
HMS2093E20
CHEMBL1014 ,
nsc-758697
candesartan 1-(((cyclohexyloxy)carbonyl)oxy)ethyl ester
chebi:3348 ,
L006257
HMS1922J09
bdbm50318907
2-ethoxy-3-[2''-(2h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid 1-cyclohexyloxycarbonyloxy-ethyl ester
candesartancilexetil
2-ethoxy-3-[2''-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid 1-cyclohexyloxycarbonyloxy-ethyl ester
1-cyclohexyloxycarbonyloxyethyl 2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylate
tox21_302202
NCGC00255218-01
cas-145040-37-5
dtxsid5020239 ,
dtxcid50239
nsc758697
BCP9000480
pharmakon1600-01504261
C2635
MLS004774127
smr003500784
AKOS015920180
candesartan cilexitil
2-ethoxy-3-[2'-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid 1-cyclohe
2-ethoxy-3-[2'-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid 1-cyclohexyloxycarbonyloxy-ethyl ester
CCG-39530
FT-0602914
AB07617
S2037
AKOS015894954
candesartan cilexetil [orange book]
candesartan cilexetil [jan]
candesartan cilexetil [vandf]
1h-benzimidazole-7-carboxylic acid, 2-ethoxy-1-((2'-(1h-tetrazol-5-yl)(1,1'-biphenyl)-4-yl)methyl)-, 1-(((cyclohexyloxy)carbonyl)oxy)ethyl ester, (+/-)-
candesartan cilexetil [ep monograph]
candesartan cilexetil [mart.]
candesartan cilexetil [who-dd]
(+/-)-1-hydroxyethyl 2-ethoxy-1-(p-(o-1h-tetrazol-5-ylphenyl)benzyl)-7-benzimidazolecarboxylate, cyclohexyl carbonate (ester)
candesartan 1-(((cyclohexyloxy)carbonyl)oxy)ethyl ester [mi]
candesartan cilexetil [usp monograph]
candesartan cilexetil [usp-rs]
CCG-222334
HY-17505
1-[[(cyclohexyloxy)carbonyl]oxy]ethyl 2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl]methyl]-1h-benzimidazole-7-carboxylate
1h-benzimidazole-7-carboxylic acid, 2-ethoxy-1-[[2'-(2h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl]methyl]-, 1-[[(cyclohexyloxy)carbonyl]oxy]ethyl ester
AM90293
SCHEMBL40831
KS-1147
1-(cyclohexyloxycarbonyloxy)ethyl 1-((2'-(1h-tetrazol-5-yl)biphenyl-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylate
(+/-)-1-(cyclohexyloxycarbonyloxy)ethyl 2-ethoxy-1-[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methylbenzimidazole-7-carboxylate
(+/-)-1-(cyclohexyloxycarbonyloxy)ethyl 2-ethoxy-1-[2'-(1h-tetrazol-5-yl) biphenyl-4-yl]methylbenzimidazole-7-carboxylate
GHOSNRCGJFBJIB-UHFFFAOYSA-N
1-(cyclohexyloxycarbonyloxy)ethyl-2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl]benzimidazol-7-carboxylate
Q-200786
camptothecine, antibiotic for culture media use only
candesartan cilextil
2-ethoxy-1-[[2'-(2h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl]methyl]-1h-benzimidazole-7-carboxylic acid 1-[[(cyclohexyloxy)carbonyl]oxy]ethyl ester
DS-1302
candesartan cilexetil, pharmaceutical secondary standard; certified reference material
gtpl8352
1-(((cyclohexyloxy)carbonyl)oxy)ethyl 1-((2'-(2h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylate
AB01274805_03
AB01274805_02
tcy 116
mfcd00871371
1-{[(cyclohexyloxy)carbonyl]oxy}ethyl 2-ethoxy-1-{[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl}-1h-benzimidazole-7-carboxylate
STL451065
1261393-19-4
candesartan (cilexetil)
candesartan cilexetil , 97%
SR-05000001976-1
sr-05000001976
candesartan cilexetil, united states pharmacopeia (usp) reference standard
HMS3651I08
candesartan cilexetil, >=98% (hplc)
candesartan cilexetil for peak identification, european pharmacopoeia (ep) reference standard
candesartan cilexetil for system suitability, european pharmacopoeia (ep) reference standard
candesartan cilexetil, european pharmacopoeia (ep) reference standard
SBI-0206767.P001
1-(((cyclohexyloxy)carbonyl)oxy)ethyl 1-((2'-(1h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylate
1-cyclohexyloxycarbonyloxyethyl 2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl] methyl]benzimidazole-4-carboxylate
SW220041-1
NCGC00095123-05
BCP22050
candesartan cilexetil-d11
candesartan cilexetil (atacand)
Q27075664
BRD-A65671304-001-03-4
NCGC00095123-16
NCGC00095123-10
1-cyclohexyloxycarbonyloxyethyl 2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylate.
candesartan 1-[[(cyclohexyloxy)carbonyl]oxy]ethyl ester
candesartan celexetil ester
1-(((cyclohexyloxy)carbonyl)oxy)ethyl1-((2'-(2h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylate
candesartan cilexetil- bio-x
BC164274
EN300-118698
1-{[(cyclohexyloxy)carbonyl]oxy}ethyl 2-ethoxy-1-{[2'-(1h-1,2,3,4-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl]methyl}-1h-1,3-benzodiazole-7-carboxylate
Z1515383338
SY051248
candesartan cilexetil (ep monograph)
candesartan cilexetil (usp monograph)
candesartan cilexetil (mart.)
candesartan cilexetil (usp-rs)
(+/-)1-hydroxyethyl 2-ethoxy-1-(p-(o-1h-tetrazol-5-ylphenyl)benzyl)-7-benzimidazolecarboxylate, cyclohexyl carbonate (ester)

Research Excerpts

Overview

Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. It is a poorly soluble antihypertensive drug.

ExcerptReferenceRelevance
"Candesartan cilexetil is an angiotensin II receptor blocker and it is widely used to treat hypertension and heart failure. "( Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients.
Bae, JW; Cho, CK; Choi, CI; Jang, CG; Jung, EH; Kang, P; Lee, SY; Lee, YJ; Park, HJ, 2021
)
2.06
"Candesartan cilexetil (CC) is a poorly soluble antihypertensive drug with "( New supersaturating drug delivery system as strategy to improve apparent solubility of candesartan cilexetil in biorelevant medium.
Alves, GF; Fernandes, D; França, MT; Leão, AF; Mendes, C; Pinto, JMO; Stulzer, HK, 2020
)
2.22
"Candesartan cilexetil is a highly effective ARB for the treatment of arterial hypertension and heart failure. "( Candesartan cilexetil: an update.
Joost, A; Radke, PW; Schunkert, H, 2011
)
3.25
"Candesartan cilexetil is a potent angiotensin receptor inhibitor with low bioavailability due to poor aqueous solubility. "( Solid lipid nanoparticles loading candesartan cilexetil enhance oral bioavailability: in vitro characteristics and absorption mechanism in rats.
Bu, H; Gao, F; Li, Y; Xiao, J; Zhang, Z, 2012
)
2.1
"Candesartan cilexetil is an angiotensin II type 1 (AT[1]) receptor antagonist (angiotensin receptor blocker [ARB]) that inhibits the actions of angiotensin II on the renin-angiotensin-aldosterone system."( Differential clinical profile of candesartan compared to other angiotensin receptor blockers.
Cernes, R; Mashavi, M; Zimlichman, R, 2011
)
1.09
"Candesartan cilexetil is a new angiotensin II receptor blocker with a high affinity for the angiotensin II-subtype 1 receptor."( Efficacy and safety of oral candesartan cilexetil in patients with congestive heart failure.
Matsumori, A, 2003
)
2.06
"Candesartan cilexetil is an angiotensin II receptor antagonist that is widely used in the treatment of hypertension. "( Erythema multiforme associated with candesartan cilexetil.
Ejaz, AA; Walsh, JS; Wasiluk, A, 2004
)
2.04
"Candesartan cilexetil is an angiotensin receptor blocker with insurmountable binding properties to the angiotensin-1 receptor, long duration of action and improved efficacy."( Candesartan cilexetil in cardiovascular disease.
Papademetriou, V; Ross, A, 2004
)
2.49
"Candesartan cilexetil is a possible treatment for hypertension in renal allograft recipients. "( Evaluation of the effect of candesartan cilexetil on the steady-state pharmacokinetics of tacrolimus in renal transplant patients.
Birkel, M; Kiel, G; Philipp, T; Pietruck, F; Stahlheber-Dilg, B, 2005
)
2.07
"Candesartan cilexetil is a highly potent and long-acting angiotensin II type I (AT1) receptor antagonist. "( Long-acting blood pressure reduction by candesartan cilexetil in patients with hypertension.
Bönner, G; Fuchs, W, 2005
)
2.04
"Candesartan cilexetil is an angiotensin receptor antagonist widely used in the treatment of high blood pressure. "( Hydrolysis and transesterification reactions of candesartan cilexetil observed during the solid phase extraction procedure.
Alonso, RM; Dresen, S; Ferreirós, N; Weinmann, W, 2007
)
2.04
"Candesartan cilexetil is a novel AIIRA that has demonstrated clinical efficacy superior to losartan, has a sustained duration of action over 24 hours (trough:peak ratio close to 100%) and is well tolerated in patients with essential hypertension."( Key features of candesartan cilexetil and a comparison with other angiotensin II receptor antagonists.
Sever, PS, 1999
)
1.37
"Candesartan cilexetil is a potent and long-acting blocker that provides effective 24 hr blood pressure control."( A new class of diacidic nonpeptide angiotensin II receptor antagonists: candesartan cilexetil.
Kubo, K; Naka, T, 1999
)
1.26
"Candesartan cilexetil is a potent and long-acting blocker that, when given once-daily to patients, provides effective 24 hr blood pressure control."( A new class of diacidic nonpeptide angiotensin II receptor antagonists: candesartan cilexetil.
Inada, Y; Kubo, K; Naka, T; Nishikawa, K, 1999
)
1.26
"Candesartan cilexetil is an effective antihypertensive agent that can be used alone or in combination with other antihypertensive drugs."( Candesartan cilexetil: an angiotensin II-receptor blocker.
See, S; Stirling, AL, 2000
)
2.47
"Candesartan cilexetil is a newly synthesized, specific angiotensin II type 1 receptor antagonist. "( Hemodynamic and hormonal effects of the angiotensin II antagonist, candesartan cilexetil, in patients with congestive heart failure.
Yasue, H; Yoshimura, M, 2000
)
1.99
"Candesartan cilexetil is a potent and long-acting blocker that, when given once a day to patients, provides effective 24 hr blood pressure control."( [Angiotensin II receptor antagonists: candesartan cilexetil].
Furukawa, Y; Inada, Y; Kubo, K; Naka, T; Nishikawa, K, 2000
)
1.3
"Candesartan cilexetil is an effective antihypertensive agent with a tolerability profile similar to that of placebo. "( Candesartan cilexetil: an update of its use in essential hypertension.
Easthope, SE; Jarvis, B, 2002
)
3.2

Effects

Cesartan cilexetil has a rapid onset of action (approximately 80% of total blood pressure reduction within the first 2 weeks) It is comparable in efficacy to a number of classes of antihypertensives, and is effective in combination therapy (eg, with hydrochlorothiazide and amlodipine)

ExcerptReferenceRelevance
"Candesartan cilexetil has a rapid onset of action (approximately 80% of total blood pressure reduction within the first 2 weeks) and dose-dependent effects on blood pressure, is comparable in efficacy to a number of classes of antihypertensives, and is effective in combination therapy (eg, with hydrochlorothiazide and amlodipine)."( Key features of candesartan cilexetil and a comparison with other angiotensin II receptor antagonists.
Sever, PS, 1999
)
1.37
"Candesartan cilexetil has been shown to effectively reduce blood pressure and cardiovascular risk. "( Candesartan cilexetil/hydrochlorothiazide combination treatment versus high-dose candesartan cilexetil monotherapy in patients with mild to moderate cardiovascular risk (CHILI Triple T).
Bönner, G; Bramlage, P; Landers, B, 2011
)
3.25
"Candesartan cilexetil has a rapid onset of action (approximately 80% of total blood pressure reduction within the first 2 weeks) and dose-dependent effects on blood pressure, is comparable in efficacy to a number of classes of antihypertensives, and is effective in combination therapy (eg, with hydrochlorothiazide and amlodipine)."( Key features of candesartan cilexetil and a comparison with other angiotensin II receptor antagonists.
Sever, PS, 1999
)
1.37
"Candesartan cilexetil has shown potent and long-lasting antihypertensive effects in clinical trials and in several animal models of hypertension. "( Pharmacologic properties of candesartan cilexetil--possible mechanisms of long-acting antihypertensive action.
Inada, Y; Kanagawa, R; Misumi, Y; Naka, T; Nishikawa, K; Ojima, M, 1999
)
2.04
"Candesartan cilexetil has shown potent and long-lasting antihypertensive effects in clinical trials and in several hypertensive animal models. "( [Pharmacological profiles of candesartan cilexetil (TCV-116)].
Inada, Y, 1999
)
2.04
"Candesartan cilexetil has more than 1000 times more affinity for the angiotensin II, type AT1 receptor ARBs, and the binding affinity and competitive angiotensin II receptor antagonism is stronger than that of losartan."( Candesartan cilexetil: an angiotensin II receptor blocker.
Kaul, AF; McVoy, HJ; Stoukides, CA, 1999
)
2.47
"Candesartan cilexetil has been found to produce a predictable and pronounced dose-dependent decrease in blood pressure, with placebo-like tolerability even at the highest doses studied."( Improving antihypertensive efficacy while maintaining placebo-like tolerability.
Sever, PS, 2000
)
1.03
"Candesartan cilexetil has also been shown to be effective and well tolerated in combination with hydrochlorothiazide in those hypertensive patients who require more than one agent to reach their target blood pressure."( Improving prognosis in hypertension: exploring the benefits of angiotensin II type 1 receptor blockade.
Ruilope, L, 2000
)
1.03

Actions

ExcerptReferenceRelevance
"Candesartan cilexetil did not inhibit antigen-induced bronchoconstriction in sensitized guinea pigs or alter PC(200) in nonsensitized guinea pigs."( Type 1 angiotensin II receptor antagonism reduces antigen-induced airway reactions.
Fujimura, M; Hirose, T; Kurashima, K; Myou, S; Tachibana, H; Watanabe, K, 2000
)
1.03

Treatment

Treatment with candesartan cilexetil lowered systemic blood pressure, normalized PGC at 10 weeks and greatly reduced proteinuria and allograft glomerulosclerosis at 24 weeks.

ExcerptReferenceRelevance
"Candesartan cilexetil-treated banded rat hearts displayed shorter QT intervals and lower vulnerability to atrial and ventricular tachyarrhythmias than vehicle-treated banded hearts."( Candesartan Cilexetil Attenuates Arrhythmogenicity Following Pressure Overload in Rats via the Modulation of Cardiac Electrical and Structural Remodeling and Calcium Handling Dysfunction.
Chang, GJ; Chen, WJ; Ko, YS; Lai, YJ; Lee, YS; Yeh, YH, 2022
)
2.89
"Candesartan cilexetil treatment improved cardiac structural remodeling and cardiac function in SDT rats."( Long-term angiotensin II blockade may improve not only hyperglycemia but also age-associated cardiac fibrosis.
Fukumoto, M; Hayashi, T; Ikeda, T; Jin, D; Kitaura, Y; Miyazaki, M; Oku, H; Sugiyama, T; Takai, S, 2009
)
1.07
"Candesartan cilexetil treatments significantly reduced blood pressure (BP) in rats administered the high dose and moderately in rats receiving the low dose."( Therapeutic effects of postischemic treatment with hypotensive doses of an angiotensin II receptor blocker on transient focal cerebral ischemia.
Fu, H; Hosomi, N; Itano, T; Kohno, M; Liu, G; Masugata, H; Matsumoto, M; Miki, T; Nakano, D; Nishiyama, A; Pelisch, N; Sueda, Y; Ueno, M, 2011
)
1.09
"The candesartan cilexetil-treated patients exhibited improvement of several aspects of QOL, including general symptoms, physical symptoms and well-being, work and satisfaction and sleep scale."( The effects of replacing dihydropyridine calcium-channel blockers with angiotensin II receptor blocker on the quality of life of hypertensive patients.
Fujimoto, H; Kawashima, T; Koide, S; Kunitake, T; Yamamoto, S, 2003
)
0.8
"Candesartan cilexetil is a possible treatment for hypertension in renal allograft recipients. "( Evaluation of the effect of candesartan cilexetil on the steady-state pharmacokinetics of tacrolimus in renal transplant patients.
Birkel, M; Kiel, G; Philipp, T; Pietruck, F; Stahlheber-Dilg, B, 2005
)
2.07
"Candesartan cilexetil treatment reduced neointimal formation both in allografts (Qint 30.2 +/- 8.8% vs."( Candesartan cilexetil reduces graft arteriosclerosis in aortic transplantation model in rat.
Fellström, B; Larsson, E; Zezina, L, 2001
)
2.47
"Treatment with candesartan cilexetil reduced the level of ADMA in hypertensive patients in the chronic stage of cerebral infarction. "( Effects of Candesartan Cilexetil Compared with Amlodipine on Serum Asymmetric Dimethylarginine Levels in the Chronic Stage of Cerebral Infarction: A Preliminary Study.
Katayama, Y; Nishiyama, Y; Nomura, K; Sunami, E, 2016
)
1.18
"Treatment with candesartan cilexetil restored a normal pattern of reactivity in retinal capillaries (l-NMMA: decrease in perfusion by 10%+/-17%, P<0.05) and the central retinal artery (flicker: increase in mean blood flow velocity by 42%+/-31%, P<0.001) in hypertensive patients."( Impaired endothelial function of the retinal vasculature in hypertensive patients.
Delles, C; Harazny, J; Hilgers, KF; Michelson, G; Oehmer, S; Schmieder, RE, 2004
)
0.66
"Treatment with candesartan cilexetil was initiated, and blood pressure control improved markedly."( Erythema multiforme associated with candesartan cilexetil.
Ejaz, AA; Walsh, JS; Wasiluk, A, 2004
)
0.94
"Treatment with candesartan cilexetil lowered systemic blood pressure, normalized PGC at 10 weeks and greatly reduced proteinuria and allograft glomerulosclerosis at 24 weeks."( Candesartan cilexetil reduces chronic renal allograft injury in Fisher-->Lewis rats.
Azuma, H; Brenner, BM; Mackenzie, HS; Nagano, H; Rennke, HG; Tilney, NL; Troy, JL; Ziai, F, 1997
)
2.09
"Treatment with candesartan cilexetil caused significant decreases in blood pressure and amelioration of proteinuria and renal histological scores in the SHRSP/Izm rats."( Effects of AT1 receptor antagonist on proteoglycan gene expression in hypertensive rats.
Nakaya, H; Saruta, T; Sasamura, H; Shimizu-Hirota, R, 2001
)
0.65
"Oral treatment with candesartan cilexetil inhibited all central responses to i.c.v. "( Effects of orally applied candesartan cilexetil on central responses to angiotensin II in conscious rats.
Culman, J; Gohlke, P; Jürgensen, T; Kox, T; Rascher, W; Unger, T; Von Kügelgen, S, 2002
)
0.94

Toxicity

This is the first description of severe hepatotoxicity associated with ductopenia caused by an adverse reaction to candesartan cilexetil. Treatment with 10-mg azilsartan was similar to 8-mg candesARTan cilesetil in its association with rare adverse events.

ExcerptReferenceRelevance
" In double-blind clinical trials in patients with primary hypertension, candesartan cilexetil 2-16 mg once-daily was associated with a low incidence of adverse events and drug-related withdrawals, similar to placebo."( Candesartan cilexetil: safety and tolerability in healthy volunteers and patients with hypertension.
Belcher, G; Elmfeldt, D; George, M; Hübner, R; Lunde, H, 1997
)
1.97
" This pooled safety analysis was performed on adverse event data from five placebo-controlled studies involving a total of 1893 patients, 1287 of whom received candesartan cilexetil and 606 of whom received placebo."( The safety and tolerability of candesartan cilexetil in CHF.
Belcher, G; Erdmann, E; George, M; Held, P; Hiemstra, S; Kolb, D; Pietrek, M; Voet, B, 2000
)
0.79
" To our knowledge, this is the first description of severe hepatotoxicity associated with ductopenia caused by an adverse reaction to candesartan cilexetil."( Candesartan cilexetil-induced severe hepatotoxicity.
Accetta, MG; Basile, G; Ferrara, T; Gangemi, S; Nicita-Mauro, V; Villari, D, 2003
)
1.97
" Eight candesartan patients discontinued treatment because of an adverse event."( Efficacy, safety, and pharmacokinetics of candesartan cilexetil in hypertensive children aged 6 to 17 years.
Hainer, JW; Radcliffe, J; Sorof, JM; Sugg, J; Teng, R; Trachtman, H, 2008
)
0.61
" Candesartan was generally well tolerated; two patients withdrew for adverse events (fatigue and worsening glomerulopathy)."( Efficacy, safety and pharmacokinetics of candesartan cilexetil in hypertensive children from 1 to less than 6 years of age.
Bagdasorova, IV; Drozdz, D; Gimpel, C; Hainer, JW; Montini, G; Schaefer, F; Sorof, J; Sugg, J; Teng, R; van de Walle, J; van Hoeck, K; Zurowska, A, 2010
)
0.63
" Prolonged combined use of CC/PIO did not increase adverse events."( Efficacy and safety of combination therapy with candesartan cilexetil and pioglitazone hydrochloride in patients with hypertension and type 2 diabetes mellitus.
Enya, K; Kaku, K; Sugiura, K; Totsuka, N, 2011
)
0.62
"from a total of 112 treatment-naive patients and 381 previously treated patients eligible for safety analysis, there were only 3 patients with adverse events, and 2 of which were considered possibly related to candesartan (0."( Safety and effectiveness of candesartan and candesartan/HCT fixed dose combination in patients with hypertension.
Pohan, T; Setiawati, A, 2013
)
0.39
" Treatment with 10-mg azilsartan was similar to 8-mg candesartan cilexetil in its association with rare adverse events."( Efficacy and safety of 10-mg azilsartan compared with 8-mg candesartan cilexetil in Japanese patients with hypertension: a randomized crossover non-inferiority trial.
Arai, A; Kaneto, H; Katakami, N; Kusuda, Y; Matsuoka, TA; Shimomura, I; Shindo, M; Shiraiwa, T; Takahara, M, 2014
)
0.9
" N/C combination demonstrated a lower incidence of vasodilatory adverse events than N monotherapy (18."( Nifedipine plus candesartan combination increases blood pressure control regardless of race and improves the side effect profile: DISTINCT randomized trial results.
Cha, G; Gil-Extremera, B; Haller, H; Harvey, P; Heyvaert, F; Kjeldsen, SE; Lewin, AJ; Mancia, G; Sica, D; Villa, G, 2014
)
0.4
"N/C combination was effective in participants with hypertension and showed an improved side effect profile compared with N monotherapy."( Nifedipine plus candesartan combination increases blood pressure control regardless of race and improves the side effect profile: DISTINCT randomized trial results.
Cha, G; Gil-Extremera, B; Haller, H; Harvey, P; Heyvaert, F; Kjeldsen, SE; Lewin, AJ; Mancia, G; Sica, D; Villa, G, 2014
)
0.4
" The primary assessment included the incidence of treatment-emergent adverse events (TEAEs)."( Fixed-dose combination of nifedipine gastrointestinal therapeutic system and candesartan cilexetil in patients with moderate-to-severe essential hypertension: an open-label, long-term safety and efficacy study.
Dzongowski, P; Kjeldsen, SE; Li, N; Radlmaier, A; Wang, L, 2016
)
0.66

Pharmacokinetics

The aim of this series of studies was to determine the potential for pharmacokinetic interaction between candesartan and hydrochlorothiazide (HCTZ), nifedipine, glibenclamide, warfarin, digoxin or the components of an oral contraceptive formulation. The AUC and Cmax showed dose-proportional increases in the dose range of 2-16 mg candeartan cilexetil after both single and repeated once-daily tablet intake.

ExcerptReferenceRelevance
"The pharmacokinetic and pharmacodynamic properties of nonpeptide angiotensin antagonists in humans are reviewed in this paper."( Pharmacokinetic-pharmacodynamic profile of angiotensin II receptor antagonists.
Biollaz, J; Brunner, HR; Buclin, T; Csajka, C, 1997
)
0.3
" The AUC and Cmax of candesartan showed dose-proportional increases in the dose range of 2-16 mg candesartan cilexetil after both single and repeated once-daily tablet intake, indicating linear pharmacokinetics in both younger and elderly healthy subjects."( Pharmacokinetics of candesartan after single and repeated doses of candesartan cilexetil in young and elderly healthy volunteers.
Högemann, AM; Hübner, R; Riddell, JG; Sunzel, M, 1997
)
0.75
"The aim of this series of studies was to determine the potential for pharmacokinetic interaction between candesartan (administered orally as the prodrug candesartan cilexetil) and hydrochlorothiazide (HCTZ), nifedipine, glibenclamide, warfarin, digoxin or the components of an oral contraceptive formulation."( Pharmacokinetic drug interaction studies with candesartan cilexetil.
Högemann, A; Jonkman, JH; Lins, R; Sennewald, R; van Heiningen, PN; van Lier, JJ, 1997
)
0.75
"Five clinical studies were conducted to investigate the pharmacokinetic profile and safety of candesartan cilexetil in patients with either normal or impaired renal or hepatic function."( Pharmacokinetics of candesartan cilexetil in patients with renal or hepatic impairment.
de Zeeuw, D; Kirch, W; Remuzzi, G, 1997
)
0.84
" From these model parameters, a cumulation half-life (t1/2, beta) of 29 h was derived."( Pharmacokinetics and pharmacodynamics of candesartan after administration of its pro-drug candesartan cilexetil in patients with mild to moderate essential hypertension--a population analysis.
Feltkamp, H; Gundert-Remy, U; Högemann, A; Meineke, I, 1997
)
0.52
"Although serum trough levels increased during repeated administration and half-life was higher in patients with impaired renal function, candesartan cilexetil at a dose of 8 mg per day does not lead to drug accumulation in these patients."( Pharmacokinetics and pharmacodynamics of candesartan cilexetil in patients with normal to severely impaired renal function.
Buter, H; de Jong, PE; de Zeeuw, D; Navis, GY; Woittiez, AJ, 1999
)
0.77
"The pharmacokinetic profile of candesartan cilexetil might be altered in patients with end-stage renal disease (ESRD)."( Pharmacokinetics and haemodynamics of candesartan cilexetil in hypertensive patients on regular haemodialysis.
Frey, FJ; Pfister, M; Schaedeli, F; Uehlinger, DE, 1999
)
0.86
"The pharmacodynamic effects of a single oral dose of 16 mg candesartan cilexetil are greater than those of 50 mg losartan and 8 mg candesartan cilexetil."( Pharmacokinetic-pharmacodynamic interactions of candesartan cilexetil and losartan.
Azizi, M; Chatellier, G; Guyene, TT; Ménard, J, 1999
)
0.8
" No relevant pharmacokinetic drug-food or drug-drug interactions are known."( Clinical pharmacokinetics of candesartan.
Gleiter, CH; Mörike, KE, 2002
)
0.31
"This 4-week randomized, double blind, placebo-controlled study (N=240), 1-year open label trial (N=233), and single-dose pharmacokinetic study (N=22) evaluated candesartan cilexetil (3 doses) in hypertensive children aged 6 to 17 years."( Efficacy, safety, and pharmacokinetics of candesartan cilexetil in hypertensive children aged 6 to 17 years.
Hainer, JW; Radcliffe, J; Sorof, JM; Sugg, J; Teng, R; Trachtman, H, 2008
)
0.81
"A single-dose pharmacokinetic profile was obtained in 10 patients."( Efficacy, safety and pharmacokinetics of candesartan cilexetil in hypertensive children from 1 to less than 6 years of age.
Bagdasorova, IV; Drozdz, D; Gimpel, C; Hainer, JW; Montini, G; Schaefer, F; Sorof, J; Sugg, J; Teng, R; van de Walle, J; van Hoeck, K; Zurowska, A, 2010
)
0.63
"There was no pharmacokinetic interaction between candesartan 32 mg and HCT 25 mg during concomitant administration."( Pharmacokinetic interaction study with fixed high dose combinations of candesartan cilexetil and hydrochlorothiazide.
Aberg, JG; Karlson, BW; Olofsson, B, 2011
)
0.6
"There was no pharmacokinetic interaction found between the high doses of candesartan 32 mg and HCT 25 mg."( Pharmacokinetic interaction study with fixed high dose combinations of candesartan cilexetil and hydrochlorothiazide.
Aberg, JG; Karlson, BW; Olofsson, B, 2011
)
0.6
" The method uses 100 µl plasma and covers the calibration range 1-160 ng/ml for CAN and 2-160 ng/ml for HCTZ for routine pharmacokinetic studies in humans."( LC-MS/MS method for simultaneous estimation of candesartan and hydrochlorothiazide in human plasma and its use in clinical pharmacokinetics.
Bharathi, DV; Chatki, PK; Hotha, KK; Satyanarayana, V; Venkateswarlu, V, 2012
)
0.38
" The developed assay was applied to an oral pharmacokinetic study in humans."( LC-MS/MS method for simultaneous estimation of candesartan and hydrochlorothiazide in human plasma and its use in clinical pharmacokinetics.
Bharathi, DV; Chatki, PK; Hotha, KK; Satyanarayana, V; Venkateswarlu, V, 2012
)
0.38
" The pharmacokinetic parameters such as AUC(last), AUC(inf) and C(max) were calculated and the 90% confidence intervals of the ratio (test/reference) pharmacokinetic parameters were obtained by analysis of variance on logarithmically transformed data."( Pharmacokinetic properties and bioequivalence of candesartan cilexetil in Korean healthy volunteers.
Chae, SW; Cho, BS; Choi, YH; Han, SM; Im, YJ; Jang, HY; Jeon, JY; Jo, MJ; Kim, BK; Kim, MG; Kim, Y; Lee, BH; Moon, BK; Shin, DH; Yoo, JS, 2013
)
0.64
" The physicochemical properties, morphology of CC-SLNs were characterized, the pharmacokinetic and pharmacodynamic behaviour of CC-SLNs were evaluated in rats."( Candesartan cilexetil loaded solid lipid nanoparticles for oral delivery: characterization, pharmacokinetic and pharmacodynamic evaluation.
Dudhipala, N; Veerabrahma, K, 2016
)
1.88
"This study was performed to compare the single-dose pharmacokinetic properties and tolerability of DP-R208 (candesartan and rosuvastatin FDC) to those of each component administered alone in healthy Korean male volunteers."( Pharmacokinetic and bioequivalence study comparing a candesartan cilexetil/rosuvastatin calcium fixed-dose combination with the concomitant administration of candesartan cilexetil and rosuvastatin calcium in healthy Korean subjects
.
Jang, K; Jeon, JY; Kim, MG; Lee, BH; Lee, JW; Park, CW; Park, DB, 2017
)
0.7
" We investigated the effect of genetic polymorphism of CYP2C9 enzyme on drug pharmacokinetics using physiologically based pharmacokinetic (PBPK) modeling."( Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients.
Bae, JW; Cho, CK; Choi, CI; Jang, CG; Jung, EH; Kang, P; Lee, SY; Lee, YJ; Park, HJ, 2021
)
0.62
"To evaluate if the combination of the product components in the new FDC capsule formulation affects their respective pharmacokinetic and in vitro dissolution patterns."( Pharmacokinetics of a new fixed-dose combination of candesartan cilexetil, hydrochlorothiazide, and rosuvastatin in healthy adult subjects.
Diaz, L; Feleder, EC; Haddad, T; Halabe, EK; Iglesias, M; Mondelo, N; Roldán, E; Sakson, M; Yerino, GA, 2022
)
0.97

Compound-Compound Interactions

Canesartan cilexetil is an angiotensin II type 1 receptor antagonist. It was well tolerated both alone and in combination with the other agents.

ExcerptReferenceRelevance
" Candesartan cilexetil was well tolerated both alone and in combination with the other agents."( Pharmacokinetic drug interaction studies with candesartan cilexetil.
Högemann, A; Jonkman, JH; Lins, R; Sennewald, R; van Heiningen, PN; van Lier, JJ, 1997
)
1.47
"To compare candesartan cilexetil and lisinopril in fixed combination with hydrochlorothiazide with respect to antihypertensive efficacy and tolerability."( Comparison of the AT1-receptor blocker, candesartan cilexetil, and the ACE inhibitor, lisinopril, in fixed combination with low dose hydrochlorothiazide in hypertensive patients.
Istad, H; Keinänen-Kiukaanniemi, S; McInnes, GT; O'Kane, KP; Van Mierlo, HF, 2000
)
0.96
"This multicenter study evaluated the efficacy of candesartan cilexetil, an angiotensin II type 1 receptor antagonist, used alone or in combination with amlodipine or in combination with amlodipine and hydrochlorothiazide in the treatment of patients with moderate-to-severe essential hypertension."( Efficacy of candesartan cilexetil alone or in combination with amlodipine and hydrochlorothiazide in moderate-to-severe hypertension. UK and Israel Candesartan Investigators.
Antonios, TF; He, FJ; MacGregor, GA; Viskoper, JR, 2000
)
0.94

Bioavailability

Candesartan cilexetil is a potent angiotensin receptor inhibitor with low bioavailability due to poor aqueous solubility. To improve bioavailability (BA) of candesartsan, chemical modification was examined to yield candesartans cileXetil. The objective of this study was to compare diff diff candesARTAN and candes ART.

ExcerptReferenceRelevance
"In order to improve the oral bioavailability (BA) of 2-butyl-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]-1H-benzimid azole - 7-carboxylic acid (3: CV-11194) and 2-ethoxy-1-[[2'-(1H-tetrazol-5-yl)biphenyl-4- yl]methyl]-1H-benzimidazole-7-carboxylic acid (4: CV-11974), novel angiotensin II (AII) receptor antagonists, chemical modification to yield prodrugs has been examined."( Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
Furukawa, Y; Inada, Y; Kato, T; Kohara, Y; Kubo, K; Naka, T; Nishikawa, K; Shibouta, Y; Yoshimura, Y, 1993
)
0.29
" Co-administration of candesartan cilexetil with HCTZ produced a statistically significant increase in the bioavailability and Cmax values for candesartan (18% and 25%, respectively)."( Pharmacokinetic drug interaction studies with candesartan cilexetil.
Högemann, A; Jonkman, JH; Lins, R; Sennewald, R; van Heiningen, PN; van Lier, JJ, 1997
)
0.87
" To improve bioavailability (BA) of candesartan, chemical modification was examined to yield candesartan cilexetil, a prodrug of candesartan."( A new class of diacidic nonpeptide angiotensin II receptor antagonists: candesartan cilexetil.
Kubo, K; Naka, T, 1999
)
0.76
" To improve bioavailability of candesartan, chemical modification was examined to yield candesartan cilexetil, a prodrug of candesartan."( A new class of diacidic nonpeptide angiotensin II receptor antagonists: candesartan cilexetil.
Inada, Y; Kubo, K; Naka, T; Nishikawa, K, 1999
)
0.76
" To improve bioavailability of candesartan, chemical modification was examined to yield candesartan cilexetil, a prodrug of candesartan."( [Angiotensin II receptor antagonists: candesartan cilexetil].
Furukawa, Y; Inada, Y; Kubo, K; Naka, T; Nishikawa, K, 2000
)
0.8
" Oral bioavailability is low (about 40%) because of incomplete absorption."( Clinical pharmacokinetics of candesartan.
Gleiter, CH; Mörike, KE, 2002
)
0.31
" In human umbilical endothelial cells, candesartan increased the eNOS protein level AT2-R dependently, inhibited the expression of nicotinamide adenine dinucleotide phosphate oxidase subunits and angiotensin II-induced intracellular reactive oxygen species and nitric oxide, and promoted the extracellular release of nitric oxide, suggesting that it augmented the bioavailability of nitric oxide."( Protective mechanisms of the angiotensin II type 1 receptor blocker candesartan against cerebral ischemia: in-vivo and in-vitro studies.
Kanematsu, Y; Kinouchi, T; Kitazato, KT; Liu, H; Nagahiro, S; Tada, Y; Tamura, T; Uno, M; Yagi, K, 2008
)
0.35
" The objective of the present study was to develop a tablet dosage form of candesartan cilexetil incorporating drug nanoparticles to increase its saturation solubility and dissolution rate for enhancing bioavailability while reducing variability in systemic exposure."( Development and characterization of solid oral dosage form incorporating candesartan nanoparticles.
Harisudhan, T; Nekkanti, V; Pillai, R; Venkateshwarlu, V, 2009
)
0.58
" These findings may explain the known interaction of telmisartan with digoxin and suggest that it may modulate the bioavailability of drugs whose absorption is restricted by P-gp and possibly also by BCRP or MRP2."( Interaction of angiotensin receptor type 1 blockers with ATP-binding cassette transporters.
Benndorf, RA; Böger, RH; Divac, N; Haefeli, WE; Herzog, M; Sauer, A; Schwedhelm, E; Weiss, J, 2010
)
0.36
" However, CC exhibited incomplete intestinal absorption with low oral bioavailability due to its poor aqueous solubility."( Nanoemulsion improves the oral absorption of candesartan cilexetil in rats: Performance and mechanism.
Bu, H; Gao, F; Gao, Z; Huang, Y; Li, Y; Shen, J; Zhang, Z; Zhao, C, 2011
)
0.63
"The poor solubility and wettability of Candesartan cilexetil (CAN) leads to poor dissolution and hence, low bioavailability after oral administration."( Enhancement of solubility and permeability of Candesartan cilexetil by using different pharmaceutical interventions.
Avachat, AM; Shaikh, SM, 2011
)
0.9
" The pharmacokinetic results indicated that the oral bioavailability of candesartan was obviously improved over 12-fold after incorporation into solid lipid nanoparticles."( Solid lipid nanoparticles loading candesartan cilexetil enhance oral bioavailability: in vitro characteristics and absorption mechanism in rats.
Bu, H; Gao, F; Li, Y; Xiao, J; Zhang, Z, 2012
)
0.66
"Candesartan cilexetil is a potent angiotensin receptor inhibitor with low bioavailability due to poor aqueous solubility."( Solid lipid nanoparticles loading candesartan cilexetil enhance oral bioavailability: in vitro characteristics and absorption mechanism in rats.
Bu, H; Gao, F; Li, Y; Xiao, J; Zhang, Z, 2012
)
2.1
" It was thus expected that Fujicalin and Neusilin UFL2-based bi-layer SMET would overcome low oral bioavailability of CDC due to its limited solubility at physiological pH conditions in the gastrointestinal tract."( Development of self-microemulsifying bilayer tablets for pH-independent fast release of candesartan cilexetil.
Kim, SY; Kuh, HJ; Lee, BJ; Lee, GH; Lee, J; Lee, SY; Na, YJ; Seong, I; Sohn, Y, 2012
)
0.6
"The present study was conducted to compare the bioavailability of two candesartan cilexetil 16 mg tablet formulations (test and reference formulations)."( Bioequivalence study of two formulations of candesartan cilexetil tablet in healthy subjects under fasting conditions.
Santoso, ID; Setiawati, E; Simanjuntak, R; Susanto, LW; Tjandrawinata, RR; Yunaidi, DA, 2013
)
0.88
"7-folds increase in apparent bioavailability was noticed with freeze-dried solid dispersions with naringin as compared to free CAN suspension administered alone."( Oral bioavailability and intestinal absorption of candesartan cilexetil: role of naringin as P-glycoprotein inhibitor.
Gurunath, S; Nanjwade, BK; Patil, PA, 2015
)
0.67
"This study demonstrated that increased solubilization (favored by freeze-dried solid dispersion) and efflux pump inhibition (using naringin), the relative bioavailability of CDS can be increased, suggesting an alternative potential for improving oral bioavailability of CAN."( Corroboration of naringin effects on the intestinal absorption and pharmacokinetic behavior of candesartan cilexetil solid dispersions using in-situ rat models.
K Nanjwade, B; Patil, PA; Surampalli, G, 2015
)
0.64
" The in vivo pharmacokinetic study gave many folds increase in oral bioavailability than CC suspension, which was further confirmed by antihypertensive activity in a murine model."( Formulation and Optimization of Candesartan Cilexetil Nano Lipid Carrier: In Vitro and In Vivo Evaluation.
Ahmad, FJ; Ali, A; Fazil, M; Hafeez, A; Imam, SS; Khan, S; Paudel, A, 2017
)
0.74
"Candesartan cilexetil (CC), an antihypertensive drug, has low oral bioavailability due to poor solubility and hepatic first-pass metabolism."( Candesartan cilexetil loaded nanodelivery systems for improved oral bioavailability.
Dudhipala, N; Veerabrahma, K, 2017
)
3.34
"Candesertan cilexetil is a Biopharmaceutics Classification System (BCS) Class II drug possessing high permeability but low aqueous solubility; hence its oral bioavailability is limited in terms of the solubility rate."( DEVELOPMENT OF SOLID LIPID NANOCARRIERS FOR ORAL DELIVERY OF CANDESERTAN CILEXETIL.
Nalbantoglu, A; Sengel-Turk, CT; Ugurlu, T, 2016
)
0.43
" The human absolute bioavailability reported demonstrates that candesartan cilexetil has low permeability and when associated with the low solubility allows to classify it as class 4 of the Biopharmaceutics Classification System."( Polymorphic and Quantum Chemistry Characterization of Candesartan Cilexetil: Importance for the Correct Drug Classification According to Biopharmaceutics Classification System.
da Nova Mussel, W; de Campos, DP; de Souza, J; Lima, RR; Savedra, RML; Silva-Barcellos, NM; Siqueira, MF; Yoshida, MI, 2018
)
0.97
"The drug delivery of candesartan cilexetil encounters an obstacle of low absolute oral bioavailability which is attributed mainly to its low aqueous solubility and efflux by intestinal P-glycoprotein (P-gp) transporters."( A Self-Nanoemulsifying Drug Delivery System for Enhancing the Oral Bioavailability of Candesartan Cilexetil: Ex Vivo and In Vivo Evaluation.
AboulFotouh, K; Allam, AA; El-Badry, M; El-Sayed, AM, 2019
)
1.06
"The objective of this study was to compare different techniques to enhance the solubility and dissolution rate, and hence the bioavailability of candesartan cilexetil."( Applying Different Techniques to Improve the Bioavailability of Candesartan Cilexetil Antihypertensive Drug.
Ali, TFS; Aly, UF; Sarhan, HA; Sharkawy, HAE, 2020
)
1
" Following the preparations, all samples were characterized for their physicochemical properties, and the samples of the best results were subjected to further bioavailability studies."( Applying Different Techniques to Improve the Bioavailability of Candesartan Cilexetil Antihypertensive Drug.
Ali, TFS; Aly, UF; Sarhan, HA; Sharkawy, HAE, 2020
)
0.8
" Results showed a significant increase in the bioavailability of CC from ~15% to ~48%."( Applying Different Techniques to Improve the Bioavailability of Candesartan Cilexetil Antihypertensive Drug.
Ali, TFS; Aly, UF; Sarhan, HA; Sharkawy, HAE, 2020
)
0.8
"The bioavailability of CC was significantly improved from ~15% to ~48% when formulated as SDs with PVP K-90 with 1:4 drug:polymer ratio."( Applying Different Techniques to Improve the Bioavailability of Candesartan Cilexetil Antihypertensive Drug.
Ali, TFS; Aly, UF; Sarhan, HA; Sharkawy, HAE, 2020
)
0.8
"Candesartan cilexetil (CC), a prodrug of candesartan (CDT), is a class II BCS drug that suffers from poor oral bioavailability because of low aqueous solubility, P-gp efflux and first-pass metabolism."( New Peceol™/Span™ 60 Niosomes Coated with Chitosan for Candesartan Cilexetil: Perspective Increase in Absolute Bioavailability in Rats.
AbuElfadl, A; Boughdady, M; Meshali, M, 2021
)
2.31
" The synergistic combination of Peceol™ and Span™ 60 probably surmounted the P-gp efflux with an increase in oral absolute bioavailability of niosomes to five times that of CC suspension."( New Peceol™/Span™ 60 Niosomes Coated with Chitosan for Candesartan Cilexetil: Perspective Increase in Absolute Bioavailability in Rats.
AbuElfadl, A; Boughdady, M; Meshali, M, 2021
)
0.87
"The new niosomal formulations of CC containing Peceol™ with Span™ 60 and cholesterol either uncoated or coated with chitosan were a successful paradigm in achieving high oral absolute bioavailability and increased Caco-2 cells biocompatibility."( New Peceol™/Span™ 60 Niosomes Coated with Chitosan for Candesartan Cilexetil: Perspective Increase in Absolute Bioavailability in Rats.
AbuElfadl, A; Boughdady, M; Meshali, M, 2021
)
0.87

Dosage Studied

The objective of the present study was to develop a tablet dosage form of candesartan cilexetil incorporating drug nanoparticles. The nanoparticles were designed to increase its saturation solubility and dissolution rate for enhancing bioavailability while reducing variability in systemic exposure.

ExcerptRelevanceReference
" The characterisation of their pharmacokinetic-pharmacodynamic relationships deserves further refinement for designing optimal therapeutic regimens and proposing dosage adaptations in specific conditions."( Pharmacokinetic-pharmacodynamic profile of angiotensin II receptor antagonists.
Biollaz, J; Brunner, HR; Buclin, T; Csajka, C, 1997
)
0.3
"A high incidence of maternal toxicity in rabbits characterized by uremia and death was observed when TCV-116, a novel angiotensin II subtype-1 (AT1) receptor antagonist, was orally administered to pregnant rabbits at dosage levels of 3 mg/kg/day or more."( Characterization of the high sensitivity of rabbits to the effects of TCV-116, an angiotensin II receptor antagonist.
Chatani, F; Ito, K; Kito, G; Sato, K, 1997
)
0.3
" Frequent blood samples were collected after the first single dose of candesartan cilexetil, and during the last dosing interval after 1 week repeated once-daily administration."( Pharmacokinetics of candesartan after single and repeated doses of candesartan cilexetil in young and elderly healthy volunteers.
Högemann, AM; Hübner, R; Riddell, JG; Sunzel, M, 1997
)
0.77
" In order to delineate the dose-response curve for candesartan cilexetil (the orally administered prodrug), results from six European placebo-controlled, dose-response studies were pooled."( Candesartan cilexetil, a new generation angiotensin II antagonist, provides dose dependent antihypertensive effect.
Elmfeldt, D; George, M; Hübner, R; Olofsson, B, 1997
)
1.99
" When administered in a flexible dosage regimen of 4-16 mg once-daily, candesartan cilexetil effectively lowered blood pressure (BP) and maintained its antihypertensive effects over the long term (< or =12 months)."( Long-term efficacy and tolerability of candesartan cilexetil in patients with mild to moderate hypertension.
Holzgreve, H; Sever, P, 1997
)
0.8
" The usual maintenance doses of candesartan cilexetil are expected to be 8 mg and 16 mg once-daily and dosage adjustment does not appear to be necessary in elderly patients or those with mild to moderate renal or hepatic impairment."( Candesartan cilexetil: a new, long-acting, effective angiotensin II type 1 receptor blocker.
Sever, P, 1997
)
2.02
", candesartan shifted the dose-response curve to angiotensin II to the right in a nonparallel manner, suggesting a noncompetitive blockade."( Inhibitory effects of candesartan on responses to angiotensin peptides in the hindquarters vascular bed of the cat.
Champion, HC; Kadowitz, PJ; Lambert, DG, 1998
)
0.3
" Before and up to 24 h post dosing angiotensin II was infused in ascending dose steps until blood pressure (systolic and/or diastolic) increased by +25 mmHg."( Angiotensin II antagonism and plasma radioreceptor-kinetics of candesartan in man.
Belz, GG; Breithaupt-Grögler, K; Butzer, R; Fuchs, B; Herrmann, V; Högemann, A; Magin, SG; Malerczyk, C; Mutschler, E; Roll, S; Voith, B, 1998
)
0.3
" DR at 6-9 h post dosing reached a maximum of about 30 and at 24 h still amounted to 4-7, indicating the persistence of a relevant antagonistic effect in vivo."( Angiotensin II antagonism and plasma radioreceptor-kinetics of candesartan in man.
Belz, GG; Breithaupt-Grögler, K; Butzer, R; Fuchs, B; Herrmann, V; Högemann, A; Magin, SG; Malerczyk, C; Mutschler, E; Roll, S; Voith, B, 1998
)
0.3
" In the TCV-116 group, the erythrocyte count, hematocrit value and hemoglobin concentration were decreased by 7-8% as compared with the values in the control group after dosing for 28 days."( Possible mechanism for the anemia induced by candesartan cilexetil (TCV-116), an angiotensin II receptor antagonist, in rats.
Chatani, F; Naeshiro, I; Sato, K; Sato, S, 1998
)
0.56
" In addition, endothelium-dependent and endothelium-independent relaxation was evaluated by dose-response curves to acetylcholine (in the presence or absence of a bradykinin-receptor blocker and of indomethacin) and sodium nitroprusside."( Effects of candesartan cilexetil and enalapril on structural alterations and endothelial function in small resistance arteries of spontaneously hypertensive rats.
Bettoni, G; Castellano, M; Guelfi, D; Muiesan, ML; Pasini, G; Piccoli, A; Porteri, E; Rizzoni, D; Rosei, EA, 1998
)
0.69
"At 2, 3 h and 4 h after dosing with candesartan cilexetil, systolic blood pressure (SBP) and DBP, as well as mean arterial pressure (MAP), were significantly lower than at baseline."( Acute effects of candesartan cilexetil (the new angiotensin II antagonist) on systemic and renal haemodynamics in hypertensive patients.
Andersson, OK; Friberg, P; Fridman, K; Sunzel, M; Wysocki, M, 1998
)
0.91
" No such correlation was detected for each single dose of candesartan cilexetil but a dose-response relationship was present when both doses were combined."( Pharmacokinetic-pharmacodynamic interactions of candesartan cilexetil and losartan.
Azizi, M; Chatellier, G; Guyene, TT; Ménard, J, 1999
)
0.8
" A dose-response curve to norepinephrine was performed at cumulative concentrations in the presence or absence of low- and high-dose insulin."( High-dose, not low-dose insulin increases the vasoconstrictor effect of norepinephrine in spontaneously hypertensive rats: effects of antihypertensive treatment.
Castellano, M; Guelfi, D; Muiesan, ML; Pasini, G; Piccoli, A; Porteri, E; Rizzoni, D; Rosei, EA,
)
0.13
" In these studies, ambulatory blood pressure monitoring is continued throughout the dosing interval and beyond in order to determine when systolic and diastolic blood pressure increase into the hypertensive range."( Comparison of angiotensin II receptor blockers: impact of missed doses of candesartan cilexetil and losartan in systemic hypertension.
Dell'Oro, R; Grassi, G; Mancia, G; Turri, C, 1999
)
0.53
"The purpose of this double-blind, forced titration study was to compare the antihypertensive effect duration of candesartan cilexetil, which has a longlasting binding to the human AT1-receptor, to that of losartan on ambulatory BP (ABP) not only during the 24-h dosing interval but also during the day of a missed dose intake."( A comparison of the efficacy and duration of action of candesartan cilexetil and losartan as assessed by clinic and ambulatory blood pressure after a missed dose, in truly hypertensive patients: a placebo-controlled, forced titration study. Candesartan/Lo
Asmar, R; Lacourcière, Y, 1999
)
0.76
" Dosage adjustments are not necessary in elderly patients or in patients with mild hepatic or renal dysfunction."( Candesartan cilexetil: an angiotensin II receptor blocker.
Kaul, AF; McVoy, HJ; Stoukides, CA, 1999
)
1.75
" Each drug effectively lowers blood pressure during once daily administration to patients with mild to moderate hypertension, with candesartan cilexetil requiring the lowest dosage and providing dose-dependent efficacy."( Newly emerging pharmacologic differences in angiotensin II receptor blockers.
Oparil, S, 2000
)
0.51
" The initial dosage of candesartan was 4 mg/d; the dosage was increased to 16 mg/d if the drug was tolerated."( Randomized trial of candesartan cilexetil in the treatment of patients with congestive heart failure and a history of intolerance to angiotensin-converting enzyme inhibitors.
Bart, BA; Califf, RM; Ertl, G; Granger, CB; Held, P; Kuch, J; Maggioni, AP; McMurray, J; Michelson, EL; Ohlin, G; Pfeffer, MA; Rouleau, JL; Sellers, MA; Sparapani, R; Stevenson, LW; Swedberg, K; Young, J; Yusuf, S, 2000
)
0.63
" Observed trough-to-peak blood pressure ratios support a once-daily dosage regimen."( Candesartan cilexetil: an angiotensin II-receptor blocker.
See, S; Stirling, AL, 2000
)
1.75
"5% 2 h after dosing with 8 mg of candesartan cilexetil."( Hemodynamic and hormonal effects of the angiotensin II antagonist, candesartan cilexetil, in patients with congestive heart failure.
Yasue, H; Yoshimura, M, 2000
)
0.82
" The trough-to-peak ratio is a useful measure of the persistence of antihypertensive efficacy at the end of the dosing interval."( Achieving quality 24-h blood pressure control with candesartan cilexetil.
Meredith, P, 2000
)
0.56
" Oral dosing of L-NAME (100 mg/kg per day) for 7 days significantly raised plasma fibrinogen concentration in rats."( Effect of prolonged nitric oxide synthesis inhibition on plasma fibrinogen concentration in rats.
Fujimura, A; Sugimoto, K; Tsuruoka, S, 2001
)
0.31
" In both treatment groups the dosage could be doubled after > or =2 weeks [according to blood pressure (BP) response] and, if necessary, subsequently decreased if the higher dosage was poorly tolerated."( Antihypertensive treatment in elderly patients aged 75 years or over: a 24-week study of the tolerability of candesartan cilexetil in relation to hydrochlorothiazide.
Forsén, B; Neldam, S, 2001
)
0.52
"Lack of efficacy in the treatment of hypertension with only one drug presents a problem in general practice and often requires switching to another type of drug, because higher dosage of currently used antihypertensives increases the frequency of side effects."( [Change from ACE inhibitor, Ca-antagonist or beta-blocker to candesartan cilexetil: better efficacy and tolerance. SWITCH study (German study segment)].
Baumgart, P; Düsing, R; Pohlmeyer, H; Reismann, J, 2001
)
0.55
"In order to investigate the role of Angiotensin II (AII) for the vasogenic cerebral edema, the AT1 receptor antagonist (TCV-116) was administered to 19-week-old stroke-prone spontaneously hypertensive rats (SHRSP) for 2 weeks at a dosage which did not decrease the blood pressure."( AT1 receptor antagonist prevents brain edema without lowering blood pressure.
Ito, H; Kawai, J; Suzuki, T; Takemori, K, 2000
)
0.31
" The response rate of monotherapy with candesartan in patients with hypertension increases with dosage, but never exceeds 60% at a daily dosage of 16mg of candesartan."( Clinical pharmacokinetics of candesartan.
Gleiter, CH; Mörike, KE, 2002
)
0.31
" Angiotensin II (Ang II) antagonistic effects were determined in vivo from rightward shifts in Ang II dose-response curves for diastolic blood pressure (BP) and dose ratios were calculated."( The pharmacological potency of various AT(1) antagonists assessed by Schild regression technique in man.
Belz, GG; Breithaupt-Grögler, K; Butzer, R; Fuchs, W; Hausdorf, C; Mang, C, 2000
)
0.31
" Significant reductions in systolic BP and diastolic BP are achieved with a once-daily dosage of candesartan cilexetil 2 to 32 mg/day in patients with mild to moderate hypertension."( Candesartan cilexetil: an update of its use in essential hypertension.
Easthope, SE; Jarvis, B, 2002
)
1.97
"A prospective, randomised, double-blind, parallel-group, dose-response trial was conducted to investigate the antiproteinuric effect of candesartan cilexetil, the angiotensin II type 1 receptor blocker, in patients with chronic glomerulonephritis."( Antiproteinuric effect of candesartan cilexetil in patients with chronic glomerulonephritis.
Abe, K; Arakawa, M; Kikkawa, R; Kurokawa, K; Ogawa, N; Onoyama, K; Saruta, T; Tomita, K; Ueda, N, 2002
)
0.82
" Good linearity, precision and selectivity were found, and the two methods were successfully applied to the pharmaceutical dosage form containing the above-mentioned drug combination without any interference by the excipients."( Application of first derivative UV-spectrophotometry and ratio derivative spectrophotometry for the simultaneous determination of candesartan cilexetil and hydrochlorothiazide.
Erk, N, 2003
)
0.52
" The experiment protocol included sham-operated rats (Sham), MI-control rats (MI-control), MI rats treated with ramipril 3 mg/kg (MI-ramipril) or TCV116 2 mg/kg (MI-TCV116) per day, half dosage (MI-1/2R&T) or full dosage (MI-R&T) combination of the two."( Combined effects of ramipril and angiotensin II receptor blocker TCV116 on rat congestive heart failure after myocardial infarction.
Huang, YW; Tao, ZW; Xia, Q; Xu, QW, 2005
)
0.33
"The results suggest that treatment with appropriate dosage combination of a chronic ACEI and a chronic ARB may further improve cardiac remodeling and cardiac function after MI."( Combined effects of ramipril and angiotensin II receptor blocker TCV116 on rat congestive heart failure after myocardial infarction.
Huang, YW; Tao, ZW; Xia, Q; Xu, QW, 2005
)
0.33
"Both candesartan and valsartan similarly alter taste sensitivity after the repeated dosing of the drug."( Angiotensin II receptor blocker-induces blunted taste sensitivity: comparison of candesartan and valsartan.
Ando, H; Fujimura, A; Ioka, T; Sugimoto, K; Tsuruoka, S; Wakaumi, M; Yamamoto, H, 2005
)
0.33
"Twenty-four-hour ambulatory blood pressure monitoring (ABPM) provides the most accurate efficacy assessment of an antihypertensive agent throughout a 24-hour dosing interval."( A multicentre, 12-week study of imidapril and candesartan cilexetil in patients with mild to moderate hypertension using ambulatory blood pressure monitoring.
Alegría, E; Gonzalez-Juanatey, JR; Marquez, E; Olivan, J; Palma-Gamiz, JL; Pêgo, M; Pujol, M; Sagastagoitia-Gorostiza, JD, 2007
)
0.6
"Imidapril in once-daily doses of up to 20mg was shown to be at least as effective as candesartan cilexetil given in once-daily doses of up to 16 mg in reducing BP throughout the entire 24-hour dosing interval."( A multicentre, 12-week study of imidapril and candesartan cilexetil in patients with mild to moderate hypertension using ambulatory blood pressure monitoring.
Alegría, E; Gonzalez-Juanatey, JR; Marquez, E; Olivan, J; Palma-Gamiz, JL; Pêgo, M; Pujol, M; Sagastagoitia-Gorostiza, JD, 2007
)
0.82
" All of these were similar in design: i) a 4-week placebo run-in period, ii) a 4- to 6-week period (V1) with CC 8 mg once daily (od), after which the dosage was doubled if BP was not normalized (BP > 140/90 or BP >130/80 mmHg in diabetes), and iii) a 4- to 6-week period (V2) with CC 8 or 16 mg od."( Effect of candesartan cilexetil on diabetic and non-diabetic hypertensive patients: meta-analysis of five randomized double-blind clinical trials.
Asmar, R; Féghali, RE; Nisse-Durgeat, S, 2007
)
0.74
" Depending on the BP response, dosage of CC 8 mg was doubled at the follow-up visit if BP >or=140/90 mmHg."( [Efficacy of candesartan cilexetil in hypertensive patients with or without diabetes].
Asmar, R; El Féghali, R; Nisse-Durgeat, S, 2007
)
0.71
" Patients underwent a 7-day washout period prior to initiation of weight-based dosing of candesartan cilexetil (2-8 mg daily)."( Candesartan cilexetil effectively reduces blood pressure in hypertensive children.
Franks, AM; Gardner, SF; O'Brien, CE; Stowe, CD; Wells, TG, 2008
)
2.01
" RI was compared to the ARB, candesartan (3 mg/kg/day PO), and to the ACEI, enalapril (60 mg/kg/day PO) in a 4-week dosing paradigm."( A nonpeptide, piperidine renin inhibitor provides renal and cardiac protection in double-transgenic mice expressing human renin and angiotensinogen genes.
Carlson, T; Kowala, MC; Leadley, R; Major, TC; Okerberg, C; Olszewski, B; Ostroski, R; Rosebury, W; Schroeder, R, 2008
)
0.35
" The objective of the present study was to develop a tablet dosage form of candesartan cilexetil incorporating drug nanoparticles to increase its saturation solubility and dissolution rate for enhancing bioavailability while reducing variability in systemic exposure."( Development and characterization of solid oral dosage form incorporating candesartan nanoparticles.
Harisudhan, T; Nekkanti, V; Pillai, R; Venkateshwarlu, V, 2009
)
0.58
" Candesartan was uptitrated to 32 mg/day (target dose if tolerated) during 6 weeks followed by constant dosing over 16 weeks."( Effects of candesartan cilexetil "add-on" treatment in congestive heart failure outpatients in daily practice.
Appel, KF; Dereli, S; Hamm, CW; Mitrovic, V; Proskynitopoulos, N, 2009
)
0.74
" After a 4-week wash-out period, 209 patients were randomized to either CC 8 mg or AML 5 mg once daily for a minimum of 1 month, after which, if BP was not normalized, the dosage was doubled, followed by the addition of hydrochlorothiazide 12."( Effects of candesartan cilexetil on carotid remodeling in hypertensive diabetic patients: the MITEC study.
Asmar, R; Baguet, JP; Mallion, JM; Nisse-Durgeat, S; Valensi, P, 2009
)
0.74
"3%, thus a flow-through dissolution apparatus was recommended for testing prolonged release dosage forms."( The effect of polysorbate 20 on solubility and stability of candesartan cilexetil in dissolution media.
Hoppe, K; Sznitowska, M, 2014
)
0.64
"DISTINCT (reDefining Intervention with Studies Testing Innovative Nifedipine GITS - Candesartan Therapy) aimed to determine the dose-response and tolerability of nifedipine GITS and/or candesartan cilexetil therapy in participants with hypertension."( Nifedipine plus candesartan combination increases blood pressure control regardless of race and improves the side effect profile: DISTINCT randomized trial results.
Cha, G; Gil-Extremera, B; Haller, H; Harvey, P; Heyvaert, F; Kjeldsen, SE; Lewin, AJ; Mancia, G; Sica, D; Villa, G, 2014
)
0.59
" A positive dose-response was observed, with all combinations providing statistically better blood pressure (BP) reductions from baseline versus respective monotherapies (P < 0."( Nifedipine plus candesartan combination increases blood pressure control regardless of race and improves the side effect profile: DISTINCT randomized trial results.
Cha, G; Gil-Extremera, B; Haller, H; Harvey, P; Heyvaert, F; Kjeldsen, SE; Lewin, AJ; Mancia, G; Sica, D; Villa, G, 2014
)
0.4
"To ensure safe oral administration, pediatric patients require an appropriate dosage form to be swallowed without relevant difficulties."( Choice of excipients for gelly-like pulp prepared ex tempore "on a spoon"- "placebo" and with sartans.
Boniecka, M; Kluk, A; Sznitowska, M; Wolska, E; Zarazińska, M, 2016
)
0.43
" A trend to dose-response relationship was observed in each subgroup."( Nifedipine GITS/Candesartan Combination Therapy Lowers Blood Pressure Across Different Baseline Systolic and Diastolic Blood Pressure Categories: DISTINCT Study Subanalyses.
Cha, G; Kjeldsen, SE; Mancia, G; Villa, G, 2016
)
0.43
" The purpose of this study was to explore the optimal dosage of a fixed-dose combination of candesartan cilexetil (CAN) and amlodipine besylate (AML), by examining the tolerability and efficacy of CAN/AML combination therapy compared with those of monotherapy with either drug in patients with essential hypertension."( Efficacy and Tolerability of Combination Therapy Versus Monotherapy with Candesartan and/or Amlodipine for Dose Finding in Essential Hypertension: A Phase II Multicenter, Randomized, Double-blind Clinical Trial.
Ahn, T; Chae, SC; Cho, EJ; Cho, JH; Choi, JY; Chung, WB; Hong, TJ; Ihm, SH; Jeon, HK; Jeong, MH; Kim, CJ; Kim, WS; Kim, YK; Lee, HY; Lee, JH; Nam, CW; Park, JI; Park, SM; Shin, ES; Sohn, IS; Yang, TH; Yoon, JH; Youn, HJ, 2017
)
0.68
" In addition, by introducing the age and ethnicity into the model, we developed a model that can propose an appropriate dosage regimen taking into account the individual characteristics of each patient."( Physiologically based pharmacokinetic modeling of candesartan related to CYP2C9 genetic polymorphism in adult and pediatric patients.
Bae, JW; Cho, CK; Choi, CI; Jang, CG; Jung, EH; Kang, P; Lee, SY; Lee, YJ; Park, HJ, 2021
)
0.62
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Drug Classes (1)

ClassDescription
biphenylsBenzenoid aromatic compounds containing two phenyl or substituted-phenyl groups which are joined together by a single bond.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (95)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, HADH2 proteinHomo sapiens (human)Potency39.81070.025120.237639.8107AID893
Chain B, HADH2 proteinHomo sapiens (human)Potency39.81070.025120.237639.8107AID893
Chain A, 2-oxoglutarate OxygenaseHomo sapiens (human)Potency31.62280.177814.390939.8107AID2147
Chain A, ATP-DEPENDENT DNA HELICASE Q1Homo sapiens (human)Potency28.18380.125919.1169125.8920AID2549
Chain A, CruzipainTrypanosoma cruziPotency10.21750.002014.677939.8107AID1476; AID1478
LuciferasePhotinus pyralis (common eastern firefly)Potency56.37190.007215.758889.3584AID1224835
acetylcholinesteraseHomo sapiens (human)Potency70.96800.002541.796015,848.9004AID1347397
15-lipoxygenase, partialHomo sapiens (human)Potency31.62280.012610.691788.5700AID887
hypoxia-inducible factor 1 alpha subunitHomo sapiens (human)Potency42.39813.189029.884159.4836AID1224846; AID1224894
RAR-related orphan receptor gammaMus musculus (house mouse)Potency22.53630.006038.004119,952.5996AID1159521; AID1159523
SMAD family member 2Homo sapiens (human)Potency17.36470.173734.304761.8120AID1346859; AID1346924
USP1 protein, partialHomo sapiens (human)Potency22.38720.031637.5844354.8130AID504865
SMAD family member 3Homo sapiens (human)Potency17.36470.173734.304761.8120AID1346859; AID1346924
TDP1 proteinHomo sapiens (human)Potency26.10110.000811.382244.6684AID686978; AID686979
GLI family zinc finger 3Homo sapiens (human)Potency25.01120.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency30.66260.000221.22318,912.5098AID1259243; AID1259247; AID743035; AID743042; AID743054; AID743063
caspase 7, apoptosis-related cysteine proteaseHomo sapiens (human)Potency54.43720.013326.981070.7614AID1346978
estrogen receptor 2 (ER beta)Homo sapiens (human)Potency10.86170.000657.913322,387.1992AID1259378
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency52.46390.001022.650876.6163AID1224838; AID1224893
progesterone receptorHomo sapiens (human)Potency29.33190.000417.946075.1148AID1346784; AID1346795
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency2.39190.01237.983543.2770AID1645841
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency44.17590.000214.376460.0339AID720691; AID720692; AID720719
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency47.16020.003041.611522,387.1992AID1159552; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency30.27300.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency43.54170.001530.607315,848.9004AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
farnesoid X nuclear receptorHomo sapiens (human)Potency43.61810.375827.485161.6524AID743217
pregnane X nuclear receptorHomo sapiens (human)Potency24.31620.005428.02631,258.9301AID1346982
estrogen nuclear receptor alphaHomo sapiens (human)Potency45.99440.000229.305416,493.5996AID1259244; AID1259248; AID743069; AID743075; AID743077; AID743078; AID743079
GVesicular stomatitis virusPotency4.77240.01238.964839.8107AID1645842
cytochrome P450 2D6Homo sapiens (human)Potency13.45040.00108.379861.1304AID1645840
glucocerebrosidaseHomo sapiens (human)Potency0.11220.01268.156944.6684AID2101
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency23.35300.001019.414170.9645AID743140; AID743191
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency8.71540.023723.228263.5986AID743222; AID743223; AID743241
caspase-3Homo sapiens (human)Potency54.43720.013326.981070.7614AID1346978
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency48.51720.001723.839378.1014AID743083
activating transcription factor 6Homo sapiens (human)Potency48.94030.143427.612159.8106AID1159516; AID1159519
thyrotropin-releasing hormone receptorHomo sapiens (human)Potency19.01370.154917.870243.6557AID1346877
nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105), isoform CRA_aHomo sapiens (human)Potency42.099619.739145.978464.9432AID1159509; AID1159518
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency29.93950.057821.109761.2679AID1159526; AID1159528
Histone H2A.xCricetulus griseus (Chinese hamster)Potency44.98050.039147.5451146.8240AID1224845; AID1224896
Caspase-7Cricetulus griseus (Chinese hamster)Potency43.24100.006723.496068.5896AID1346980
hemoglobin subunit betaHomo sapiens (human)Potency19.95260.31629.086131.6228AID910
cellular tumor antigen p53 isoform aHomo sapiens (human)Potency25.11890.316212.443531.6228AID902; AID924
15-hydroxyprostaglandin dehydrogenase [NAD(+)] isoform 1Homo sapiens (human)Potency31.62280.001815.663839.8107AID894
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency44.66840.354828.065989.1251AID504847
caspase-3Cricetulus griseus (Chinese hamster)Potency43.24100.006723.496068.5896AID1346980
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency23.83280.000323.4451159.6830AID743065; AID743067
heat shock protein beta-1Homo sapiens (human)Potency38.87470.042027.378961.6448AID743210; AID743228
mitogen-activated protein kinase 1Homo sapiens (human)Potency35.48130.039816.784239.8107AID1454
ubiquitin carboxyl-terminal hydrolase 2 isoform aHomo sapiens (human)Potency0.79430.65619.452025.1189AID927
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency31.27810.000627.21521,122.0200AID743202; AID743219
nuclear receptor ROR-gamma isoform 1Mus musculus (house mouse)Potency24.70280.00798.23321,122.0200AID2546; AID2551
DNA polymerase kappa isoform 1Homo sapiens (human)Potency28.18380.031622.3146100.0000AID588579
cytochrome P450 3A4 isoform 1Homo sapiens (human)Potency12.58930.031610.279239.8107AID884; AID885
histone acetyltransferase KAT2A isoform 1Homo sapiens (human)Potency19.95260.251215.843239.8107AID504327
Gamma-aminobutyric acid receptor subunit piRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Polyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)Potency25.11890.316212.765731.6228AID881
Voltage-dependent calcium channel gamma-2 subunitMus musculus (house mouse)Potency61.07960.001557.789015,848.9004AID1259244
Interferon betaHomo sapiens (human)Potency4.77240.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency4.77240.01238.964839.8107AID1645842
Cellular tumor antigen p53Homo sapiens (human)Potency24.63740.002319.595674.0614AID651631; AID720552
Integrin beta-3Homo sapiens (human)Potency25.11890.316211.415731.6228AID924
Integrin alpha-IIbHomo sapiens (human)Potency25.11890.316211.415731.6228AID924
Gamma-aminobutyric acid receptor subunit beta-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit deltaRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Glutamate receptor 2Rattus norvegicus (Norway rat)Potency61.07960.001551.739315,848.9004AID1259244
Gamma-aminobutyric acid receptor subunit alpha-5Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-4Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit gamma-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit alpha-6Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Histamine H2 receptorCavia porcellus (domestic guinea pig)Potency25.11890.00638.235039.8107AID881
Spike glycoproteinSevere acute respiratory syndrome-related coronavirusPotency39.81070.009610.525035.4813AID1479145
Gamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-3Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Gamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Disintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)Potency0.79431.584913.004325.1189AID927
GABA theta subunitRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency4.77240.01238.964839.8107AID1645842
Gamma-aminobutyric acid receptor subunit epsilonRattus norvegicus (Norway rat)Potency12.58931.000012.224831.6228AID885
cytochrome P450 2C9, partialHomo sapiens (human)Potency4.77240.01238.964839.8107AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
CruzipainTrypanosoma cruziIC50 (µMol)105.00000.00022.04508.0000AID484274; AID484275
Type-1 angiotensin II receptorOryctolagus cuniculus (rabbit)IC50 (µMol)0.20000.00010.09130.5000AID568911
NEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)IC50 (µMol)16.43000.00030.04710.1800AID1728035
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)IC50 (µMol)2.45470.10472.71957.0795AID977603
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)Ki1.90000.08002.46889.8000AID977604
DNA polymerase kappaHomo sapiens (human)IC50 (µMol)7.40003.40005.95009.2000AID1315755; AID1315756
DNA polymerase iotaHomo sapiens (human)IC50 (µMol)6.20000.06202.11236.2000AID1315759
Broad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)IC50 (µMol)5.00000.00401.966610.0000AID1873191
DNA polymerase etaHomo sapiens (human)IC50 (µMol)11.20000.06200.06850.0750AID1315758
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)IC50 (µMol)0.72440.05002.37979.7000AID977600
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)Ki0.40000.04401.36305.0000AID977601
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Peroxisome proliferator-activated receptor gammaHomo sapiens (human)EC50 (µMol)4.20000.00000.992210.0000AID1737435
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (386)

Processvia Protein(s)Taxonomy
lipid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
phospholipid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
apoptotic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell population proliferationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of macrophage derived foam cell differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonic acid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell migrationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
prostate gland developmentPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
regulation of epithelial cell differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of chemokine productionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of peroxisome proliferator activated receptor signaling pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
positive regulation of keratinocyte differentiationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of cell cyclePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
negative regulation of growthPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
hepoxilin biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
endocannabinoid signaling pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cannabinoid biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipoxin A4 biosynthetic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleic acid metabolic processPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipid oxidationPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipoxygenase pathwayPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA 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-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
negative regulation of low-density lipoprotein receptor activityIntegrin beta-3Homo sapiens (human)
positive regulation of protein phosphorylationIntegrin beta-3Homo sapiens (human)
positive regulation of endothelial cell proliferationIntegrin beta-3Homo sapiens (human)
positive regulation of cell-matrix adhesionIntegrin beta-3Homo sapiens (human)
cell-substrate junction assemblyIntegrin beta-3Homo sapiens (human)
cell adhesionIntegrin beta-3Homo sapiens (human)
cell-matrix adhesionIntegrin beta-3Homo sapiens (human)
integrin-mediated signaling pathwayIntegrin beta-3Homo sapiens (human)
embryo implantationIntegrin beta-3Homo sapiens (human)
blood coagulationIntegrin beta-3Homo sapiens (human)
positive regulation of endothelial cell migrationIntegrin beta-3Homo sapiens (human)
positive regulation of gene expressionIntegrin beta-3Homo sapiens (human)
negative regulation of macrophage derived foam cell differentiationIntegrin beta-3Homo sapiens (human)
positive regulation of fibroblast migrationIntegrin beta-3Homo sapiens (human)
negative regulation of lipid storageIntegrin beta-3Homo sapiens (human)
response to activityIntegrin beta-3Homo sapiens (human)
smooth muscle cell migrationIntegrin beta-3Homo sapiens (human)
positive regulation of smooth muscle cell migrationIntegrin beta-3Homo sapiens (human)
platelet activationIntegrin beta-3Homo sapiens (human)
positive regulation of vascular endothelial growth factor receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
cell-substrate adhesionIntegrin beta-3Homo sapiens (human)
activation of protein kinase activityIntegrin beta-3Homo sapiens (human)
negative regulation of lipid transportIntegrin beta-3Homo sapiens (human)
regulation of protein localizationIntegrin beta-3Homo sapiens (human)
regulation of actin cytoskeleton organizationIntegrin beta-3Homo sapiens (human)
cell adhesion mediated by integrinIntegrin beta-3Homo sapiens (human)
positive regulation of cell adhesion mediated by integrinIntegrin beta-3Homo sapiens (human)
positive regulation of osteoblast proliferationIntegrin beta-3Homo sapiens (human)
heterotypic cell-cell adhesionIntegrin beta-3Homo sapiens (human)
substrate adhesion-dependent cell spreadingIntegrin beta-3Homo sapiens (human)
tube developmentIntegrin beta-3Homo sapiens (human)
wound healing, spreading of epidermal cellsIntegrin beta-3Homo sapiens (human)
cellular response to platelet-derived growth factor stimulusIntegrin beta-3Homo sapiens (human)
apolipoprotein A-I-mediated signaling pathwayIntegrin beta-3Homo sapiens (human)
wound healingIntegrin beta-3Homo sapiens (human)
apoptotic cell clearanceIntegrin beta-3Homo sapiens (human)
regulation of bone resorptionIntegrin beta-3Homo sapiens (human)
positive regulation of angiogenesisIntegrin beta-3Homo sapiens (human)
positive regulation of bone resorptionIntegrin beta-3Homo sapiens (human)
symbiont entry into host cellIntegrin beta-3Homo sapiens (human)
platelet-derived growth factor receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
positive regulation of fibroblast proliferationIntegrin beta-3Homo sapiens (human)
mesodermal cell differentiationIntegrin beta-3Homo sapiens (human)
positive regulation of smooth muscle cell proliferationIntegrin beta-3Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationIntegrin beta-3Homo sapiens (human)
negative regulation of lipoprotein metabolic processIntegrin beta-3Homo sapiens (human)
negative chemotaxisIntegrin beta-3Homo sapiens (human)
regulation of release of sequestered calcium ion into cytosolIntegrin beta-3Homo sapiens (human)
regulation of serotonin uptakeIntegrin beta-3Homo sapiens (human)
angiogenesis involved in wound healingIntegrin beta-3Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeIntegrin beta-3Homo sapiens (human)
platelet aggregationIntegrin beta-3Homo sapiens (human)
cellular response to mechanical stimulusIntegrin beta-3Homo sapiens (human)
cellular response to xenobiotic stimulusIntegrin beta-3Homo sapiens (human)
positive regulation of glomerular mesangial cell proliferationIntegrin beta-3Homo sapiens (human)
blood coagulation, fibrin clot formationIntegrin beta-3Homo sapiens (human)
maintenance of postsynaptic specialization structureIntegrin beta-3Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor internalizationIntegrin beta-3Homo sapiens (human)
regulation of postsynaptic neurotransmitter receptor diffusion trappingIntegrin beta-3Homo sapiens (human)
positive regulation of substrate adhesion-dependent cell spreadingIntegrin beta-3Homo sapiens (human)
positive regulation of adenylate cyclase-inhibiting opioid receptor signaling pathwayIntegrin beta-3Homo sapiens (human)
regulation of trophoblast cell migrationIntegrin beta-3Homo sapiens (human)
regulation of extracellular matrix organizationIntegrin beta-3Homo sapiens (human)
cellular response to insulin-like growth factor stimulusIntegrin beta-3Homo sapiens (human)
negative regulation of endothelial cell apoptotic processIntegrin beta-3Homo sapiens (human)
positive regulation of T cell migrationIntegrin beta-3Homo sapiens (human)
cell migrationIntegrin beta-3Homo sapiens (human)
positive regulation of leukocyte migrationIntegrin alpha-IIbHomo sapiens (human)
cell-matrix adhesionIntegrin alpha-IIbHomo sapiens (human)
integrin-mediated signaling pathwayIntegrin alpha-IIbHomo sapiens (human)
angiogenesisIntegrin alpha-IIbHomo sapiens (human)
cell-cell adhesionIntegrin alpha-IIbHomo sapiens (human)
cell adhesion mediated by integrinIntegrin alpha-IIbHomo sapiens (human)
negative regulation of gene expressionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of cholesterol effluxPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
long-chain fatty acid transportPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of osteoblast differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of smooth muscle cell proliferationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of receptor signaling pathway via STATPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of low-density lipoprotein receptor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of signaling receptor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of gene expressionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of BMP signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of MAP kinase activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of adiponectin secretionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of miRNA transcriptionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of cardiac muscle hypertrophy in response to stressPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of connective tissue replacement involved in inflammatory response wound healingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of transcription by RNA polymerase IIPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
placenta developmentPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
regulation of transcription by RNA polymerase IIPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
lipid metabolic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
signal transductionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
G protein-coupled receptor signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
response to nutrientPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
regulation of blood pressurePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of gene expressionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of gene expressionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
macrophage derived foam cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of macrophage derived foam cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of cholesterol storagePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of lipid storagePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of sequestering of triglyceridePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of angiogenesisPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
monocyte differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
BMP signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
epithelial cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cellular response to insulin stimulusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
response to lipidPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
peroxisome proliferator activated receptor signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
glucose homeostasisPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
regulation of circadian rhythmPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
mRNA transcription by RNA polymerase IIPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
lipoprotein transportPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of blood vessel endothelial cell migrationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
innate immune responsePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cell fate commitmentPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of fat cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of DNA-templated transcriptionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of DNA-templated transcriptionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
retinoic acid receptor signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cell maturationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
rhythmic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
white fat cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of DNA-binding transcription factor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
lipid homeostasisPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of type II interferon-mediated signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of SMAD protein signal transductionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
regulation of cholesterol transporter activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cellular response to low-density lipoprotein particle stimulusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cellular response to hypoxiaPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of mitochondrial fissionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
regulation of cellular response to insulin stimulusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of extracellular matrix assemblyPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of miRNA transcriptionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of miRNA transcriptionPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of cellular response to transforming growth factor beta stimulusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of adipose tissue developmentPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of vascular associated smooth muscle cell proliferationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of vascular associated smooth muscle cell apoptotic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of vascular endothelial cell proliferationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of fatty acid metabolic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
fatty acid metabolic processPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
negative regulation of inflammatory responsePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cell differentiationPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
hormone-mediated signaling pathwayPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to hypoxiaDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
neutrophil mediated immunityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
germinal center formationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of leukocyte chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane protein ectodomain proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch receptor processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell population proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to xenobiotic stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of T cell chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
signal releaseDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
B cell differentiationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell growthDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to lipopolysaccharideDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of chemokine productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
regulation of mast cell apoptotic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
T cell differentiation in thymusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesion mediated by integrinDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
wound healing, spreading of epidermal cellsDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of blood vessel endothelial cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor-activated receptor activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
spleen developmentDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell motilityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
defense response to Gram-positive bacteriumDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cellular response to high density lipoprotein particle stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
commissural neuron axon guidanceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of cold-induced thermogenesisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor-mediated signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of vascular endothelial cell proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
signal transductionNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
mitotic DNA replication checkpoint signalingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
regulation of apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
regulation of neuron apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein neddylationNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
neuron apoptotic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin-dependent protein catabolic processNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein ubiquitinationNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
DNA damage responseNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
proteolysisNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
endomitotic cell cycleNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein modification processNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
post-translational protein modificationNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein neddylationNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
regulation of cell cycleNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
DNA replicationDNA polymerase kappaHomo sapiens (human)
DNA repairDNA polymerase kappaHomo sapiens (human)
nucleotide-excision repair, DNA gap fillingDNA polymerase kappaHomo sapiens (human)
DNA damage responseDNA polymerase kappaHomo sapiens (human)
cellular response to UVDNA polymerase kappaHomo sapiens (human)
error-prone translesion synthesisDNA polymerase kappaHomo sapiens (human)
DNA replicationDNA polymerase iotaHomo sapiens (human)
DNA repairDNA polymerase iotaHomo sapiens (human)
error-prone translesion synthesisDNA polymerase iotaHomo sapiens (human)
translesion synthesisDNA polymerase iotaHomo sapiens (human)
lipid transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid biosynthetic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate metabolic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transmembrane transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transepithelial transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
renal urate salt excretionBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
export across plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
cellular detoxificationBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
DNA synthesis involved in DNA repairDNA polymerase etaHomo sapiens (human)
DNA replicationDNA polymerase etaHomo sapiens (human)
DNA repairDNA polymerase etaHomo sapiens (human)
regulation of DNA repairDNA polymerase etaHomo sapiens (human)
pyrimidine dimer repairDNA polymerase etaHomo sapiens (human)
response to UV-CDNA polymerase etaHomo sapiens (human)
error-free translesion synthesisDNA polymerase etaHomo sapiens (human)
cellular response to UV-CDNA polymerase etaHomo sapiens (human)
response to radiationDNA polymerase etaHomo sapiens (human)
error-prone translesion synthesisDNA polymerase etaHomo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (122)

Processvia Protein(s)Taxonomy
iron ion bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
calcium ion bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
protein bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
lipid bindingPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleate 13S-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonate 8(S)-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
arachidonate 15-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
linoleate 9S-lipoxygenase activityPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
fibroblast growth factor bindingIntegrin beta-3Homo sapiens (human)
C-X3-C chemokine bindingIntegrin beta-3Homo sapiens (human)
insulin-like growth factor I bindingIntegrin beta-3Homo sapiens (human)
neuregulin bindingIntegrin beta-3Homo sapiens (human)
virus receptor activityIntegrin beta-3Homo sapiens (human)
fibronectin bindingIntegrin beta-3Homo sapiens (human)
protease bindingIntegrin beta-3Homo sapiens (human)
protein disulfide isomerase activityIntegrin beta-3Homo sapiens (human)
protein kinase C bindingIntegrin beta-3Homo sapiens (human)
platelet-derived growth factor receptor bindingIntegrin beta-3Homo sapiens (human)
integrin bindingIntegrin beta-3Homo sapiens (human)
protein bindingIntegrin beta-3Homo sapiens (human)
coreceptor activityIntegrin beta-3Homo sapiens (human)
enzyme bindingIntegrin beta-3Homo sapiens (human)
identical protein bindingIntegrin beta-3Homo sapiens (human)
vascular endothelial growth factor receptor 2 bindingIntegrin beta-3Homo sapiens (human)
metal ion bindingIntegrin beta-3Homo sapiens (human)
cell adhesion molecule bindingIntegrin beta-3Homo sapiens (human)
extracellular matrix bindingIntegrin beta-3Homo sapiens (human)
fibrinogen bindingIntegrin beta-3Homo sapiens (human)
protein bindingIntegrin alpha-IIbHomo sapiens (human)
identical protein bindingIntegrin alpha-IIbHomo sapiens (human)
metal ion bindingIntegrin alpha-IIbHomo sapiens (human)
extracellular matrix bindingIntegrin alpha-IIbHomo sapiens (human)
molecular adaptor activityIntegrin alpha-IIbHomo sapiens (human)
fibrinogen bindingIntegrin alpha-IIbHomo sapiens (human)
integrin bindingIntegrin alpha-IIbHomo sapiens (human)
transcription cis-regulatory region bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
transcription coregulator bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
nucleic acid bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
chromatin bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
double-stranded DNA bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA-binding transcription factor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
nuclear receptor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
prostaglandin receptor activityPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
protein bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
zinc ion bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
enzyme bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
peptide bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
identical protein bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
sequence-specific DNA bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
nuclear retinoid X receptor bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
arachidonic acid bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA binding domain bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
LBD domain bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
alpha-actinin bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
R-SMAD bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
E-box bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
STAT family protein bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA-binding transcription factor bindingPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
endopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
interleukin-6 receptor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
integrin bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
peptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metallopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
SH3 domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytokine bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
PDZ domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
tumor necrosis factor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metal ion bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activity involved in amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein bindingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin protein ligase bindingNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein heterodimerization activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
ubiquitin activating enzyme activityNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
ATP bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
NEDD8 activating enzyme activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
NEDD8 transferase activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
identical protein bindingNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein heterodimerization activityNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
serine-type endopeptidase inhibitor activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
damaged DNA bindingDNA polymerase kappaHomo sapiens (human)
metal ion bindingDNA polymerase kappaHomo sapiens (human)
DNA-directed DNA polymerase activityDNA polymerase kappaHomo sapiens (human)
damaged DNA bindingDNA polymerase iotaHomo sapiens (human)
DNA-directed DNA polymerase activityDNA polymerase iotaHomo sapiens (human)
protein bindingDNA polymerase iotaHomo sapiens (human)
metal ion bindingDNA polymerase iotaHomo sapiens (human)
protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ABC-type xenobiotic transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
efflux transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP hydrolysis activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATPase-coupled transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
identical protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
protein homodimerization activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
damaged DNA bindingDNA polymerase etaHomo sapiens (human)
DNA-directed DNA polymerase activityDNA polymerase etaHomo sapiens (human)
protein bindingDNA polymerase etaHomo sapiens (human)
metal ion bindingDNA polymerase etaHomo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (75)

Processvia Protein(s)Taxonomy
nucleusPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cytosolPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
cytoskeletonPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
plasma membranePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
adherens junctionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
focal adhesionPolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
membranePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
extracellular exosomePolyunsaturated fatty acid lipoxygenase ALOX15BHomo sapiens (human)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
glutamatergic synapseIntegrin beta-3Homo sapiens (human)
nucleusIntegrin beta-3Homo sapiens (human)
nucleoplasmIntegrin beta-3Homo sapiens (human)
plasma membraneIntegrin beta-3Homo sapiens (human)
cell-cell junctionIntegrin beta-3Homo sapiens (human)
focal adhesionIntegrin beta-3Homo sapiens (human)
external side of plasma membraneIntegrin beta-3Homo sapiens (human)
cell surfaceIntegrin beta-3Homo sapiens (human)
apical plasma membraneIntegrin beta-3Homo sapiens (human)
platelet alpha granule membraneIntegrin beta-3Homo sapiens (human)
lamellipodium membraneIntegrin beta-3Homo sapiens (human)
filopodium membraneIntegrin beta-3Homo sapiens (human)
microvillus membraneIntegrin beta-3Homo sapiens (human)
ruffle membraneIntegrin beta-3Homo sapiens (human)
integrin alphav-beta3 complexIntegrin beta-3Homo sapiens (human)
melanosomeIntegrin beta-3Homo sapiens (human)
synapseIntegrin beta-3Homo sapiens (human)
postsynaptic membraneIntegrin beta-3Homo sapiens (human)
extracellular exosomeIntegrin beta-3Homo sapiens (human)
integrin alphaIIb-beta3 complexIntegrin beta-3Homo sapiens (human)
glycinergic synapseIntegrin beta-3Homo sapiens (human)
integrin complexIntegrin beta-3Homo sapiens (human)
protein-containing complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-PKCalpha complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-IGF-1-IGF1R complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-HMGB1 complexIntegrin beta-3Homo sapiens (human)
receptor complexIntegrin beta-3Homo sapiens (human)
alphav-beta3 integrin-vitronectin complexIntegrin beta-3Homo sapiens (human)
alpha9-beta1 integrin-ADAM8 complexIntegrin beta-3Homo sapiens (human)
focal adhesionIntegrin beta-3Homo sapiens (human)
cell surfaceIntegrin beta-3Homo sapiens (human)
synapseIntegrin beta-3Homo sapiens (human)
plasma membraneIntegrin alpha-IIbHomo sapiens (human)
focal adhesionIntegrin alpha-IIbHomo sapiens (human)
cell surfaceIntegrin alpha-IIbHomo sapiens (human)
platelet alpha granule membraneIntegrin alpha-IIbHomo sapiens (human)
extracellular exosomeIntegrin alpha-IIbHomo sapiens (human)
integrin alphaIIb-beta3 complexIntegrin alpha-IIbHomo sapiens (human)
blood microparticleIntegrin alpha-IIbHomo sapiens (human)
integrin complexIntegrin alpha-IIbHomo sapiens (human)
external side of plasma membraneIntegrin alpha-IIbHomo sapiens (human)
plasma membraneGamma-aminobutyric acid receptor subunit gamma-2Rattus norvegicus (Norway rat)
plasma membraneGlutamate receptor 2Rattus norvegicus (Norway rat)
nucleusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
nucleusPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
nucleoplasmPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
cytosolPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
intracellular membrane-bounded organellePeroxisome proliferator-activated receptor gammaHomo sapiens (human)
RNA polymerase II transcription regulator complexPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
chromatinPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
receptor complexPeroxisome proliferator-activated receptor gammaHomo sapiens (human)
virion membraneSpike glycoproteinSevere acute respiratory syndrome-related coronavirus
plasma membraneGamma-aminobutyric acid receptor subunit alpha-1Rattus norvegicus (Norway rat)
plasma membraneGamma-aminobutyric acid receptor subunit beta-2Rattus norvegicus (Norway rat)
cell-cell junctionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
focal adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
ruffle membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Golgi membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytoplasmDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
endoplasmic reticulum lumenDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytosolDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell surfaceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
actin cytoskeletonDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
apical plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane raftDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytosolNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
plasma membraneNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
protein-containing complexNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
cytoplasmNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
nucleusNEDD8-activating enzyme E1 regulatory subunitHomo sapiens (human)
nucleusNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
cytosolNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
protein-containing complexNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
cytoplasmNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
nucleusNEDD8-activating enzyme E1 catalytic subunitHomo sapiens (human)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
site of DNA damageDNA polymerase kappaHomo sapiens (human)
nucleusDNA polymerase kappaHomo sapiens (human)
nucleoplasmDNA polymerase kappaHomo sapiens (human)
nuclear bodyDNA polymerase kappaHomo sapiens (human)
nucleusDNA polymerase kappaHomo sapiens (human)
nucleoplasmDNA polymerase iotaHomo sapiens (human)
nuclear speckDNA polymerase iotaHomo sapiens (human)
cytoplasmic ribonucleoprotein granuleDNA polymerase iotaHomo sapiens (human)
nucleoplasmBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
brush border membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
mitochondrial membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
membrane raftBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
external side of apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
nucleoplasmDNA polymerase etaHomo sapiens (human)
cytosolDNA polymerase etaHomo sapiens (human)
nucleusDNA polymerase etaHomo sapiens (human)
replication forkDNA polymerase etaHomo sapiens (human)
site of double-strand breakDNA polymerase etaHomo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (138)

Assay IDTitleYearJournalArticle
AID749449Inhibition of Hepatitis C virus CON1 NS5B RNA dependent RNA polymerase after 2 hrs by scintillation counting analysis2013Bioorganic & medicinal chemistry, Jun-01, Volume: 21, Issue:11
Inhibitors for the hepatitis C virus RNA polymerase explored by SAR with advanced machine learning methods.
AID1519950Cell cycle arrest in human A549 cells assessed as accumulation at G1 phase at 75 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 63.84 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID183922Inhibitory activity on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 5 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1519984Induction of apoptosis in human A549 cells assessed as increase in PARP cleavage at 50 to 100 uM by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1315759Inhibition of human DNA polymerase iota preincubated for 15 mins followed by replicating non-damaged DNA substrate addition measured after 30 mins in presence of dCTP and dGTP by radioactive gel-based primer extension assay2016Journal of medicinal chemistry, Oct-27, Volume: 59, Issue:20
Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.
AID1519924Antiproliferative activity against human HepG2 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519966Binding affinity to biotin-labeled GST-tagged NAE (unknown origin) incubated for 1 hr by SPR assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1737435Agonist activity at human PPARgammaDEF receptor expressed in african green monkey COS7 cells transfected with pGal5-TK-pGL3/pRenilla-CMV assessed as intrinsic activity measured after 39 hrs by dual luciferase reporter assay2020European journal of medicinal chemistry, Jun-01, Volume: 195Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells.
AID183920Inhibitory activity on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 24 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1519996Antitumor activity against human A549 cells xenografted in nude mouse assessed as decrease in tumor weight at 30 mg/kg, ip qd measured after 22 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID183923Inhibitory activity on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 7 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1728034Antiproliferative activity against human A549 cells assessed as inhibition of cell proliferation at 100 uM incubated for 48 hrs by CCK-8 assay relative to control2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID26234Bioavailability determined from the ratio of AUC(plasma) for 0 to infinity after oral dosing of the test compound (10 mg/kg) to intravenous administration of CD-11194 (1 mg/kg) in rats1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1519991Competitive inhibition of Nedd8-Ubc12 (unknown origin) adduct formation assessed as decrease in Ubc12-Nedd8 adduct formation at 50 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID484275Inhibition of Trypanosoma cruzi cruzaine preincubated for 5 mins before substrate addition by fluorescence assay in presence of 0.01% Triton X-1002010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1519956Induction of apoptosis in human A549 cells assessed as early apoptotic cells at 50 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 2.19 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519952Cell cycle arrest in human A549 cells assessed as accumulation at G2 phase at 75 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 12.69 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519987Antitumor activity against human A549 cells xenografted in nude mouse assessed as decrease in tumor size at 60 mg/kg, ip qd measured after 22 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID568922Antihypertensive activity in po dosed conscious rat2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID1519967Antiproliferative activity against human A549 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519993Inhibition of cullin-RING ligase in human A549 cells assessed as accumulation of p27 level at 50 to 125 uM and measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID183921Inhibitory activity on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 3 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1519953Cell cycle arrest in human A549 cells assessed as accumulation at sub-G1 phase at 75 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 0.89 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1737443Cytotoxicity against human HS5 cells assessed as cell death at 10 uM measured after 72 hrs by Propidium iodide stain based FACS analysis2020European journal of medicinal chemistry, Jun-01, Volume: 195Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells.
AID1519947Cell cycle arrest in human A549 cells assessed as accumulation at S phase at 50 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 21.54 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1728036Antiproliferative activity against human A549 cells incubated for 48 hrs by CCK-8 assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1519946Cell cycle arrest in human A549 cells assessed as accumulation at G1 phase at 50 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 63.84 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519970Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin3-Nedd8 adduct level at 50 uM measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1315755Inhibition of human DNA polymerase kappa (19 to 526 residues) preincubated for 15 mins followed by replicating non-damaged DNA substrate addition measured after 30 mins in presence of dCTP and dGTP by radioactive gel-based primer extension assay2016Journal of medicinal chemistry, Oct-27, Volume: 59, Issue:20
Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.
AID484277Colloidal aggregation in fed state simulated intestinal fluid by dynamic light scattering assay in presence of 0.25% DMSO2010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1728033Inhibition of NAE (unknown origin)-mediated neddylation assessed as suppression of cullin1-Nedd8 adduct formation at 25 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis relative to control2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID484297Colloidal aggregation in fed state simulated intestinal fluid assessed as colloid radius at 550 uM by dynamic light scattering assay in presence of 1% DMSO2010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1519955Induction of apoptosis in human A549 cells assessed as late apoptotic cells at 25 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 1.71 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519942Cell cycle arrest in human A549 cells assessed as accumulation at G1 phase at 25 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 63.84 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519973Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin1-Nedd8 adduct level measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519945Cell cycle arrest in human A549 cells assessed as accumulation at sub-G1 phase at 25 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 0.89 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID27680Tested for Half- life in rat liver homogenate (2%)1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1315756Inhibition of human DNA polymerase kappa (19 to 526 residues)-mediated TLS past acrolein derived ring-opened reduced form of gamma-HOPdG lesions preincubated for 15 mins followed by DNA substrate addition measured after 30 mins in presence of dCTP and dGT2016Journal of medicinal chemistry, Oct-27, Volume: 59, Issue:20
Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.
AID1519951Cell cycle arrest in human A549 cells assessed as accumulation at S phase at 75 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 21.54 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID183919Inhibitory activity on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 2 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID39653Relative binding affinity of compound to Angiotensin II receptor, type 1 was determined2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID1519929Antiproliferative activity against human MGC803 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1728035Inhibition of NAE (unknown origin)-mediated neddylation assessed as suppression of cullin1-Nedd8 adduct formation preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1737437Cytotoxicity against African green monkey COS7 cells assessed as effect on metabolic activity at 20 uM measured after 72 hrs by MTT assay2020European journal of medicinal chemistry, Jun-01, Volume: 195Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells.
AID484274Inhibition of Trypanosoma cruzi cruzaine preincubated for 5 mins before substrate addition by fluorescence assay in absence of Triton X-1002010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1737436Cytotoxicity against African green monkey COS7 cells assessed as effect on metabolic activity at 10 uM measured after 72 hrs by MTT assay2020European journal of medicinal chemistry, Jun-01, Volume: 195Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells.
AID1728038Cytotoxicity against human 16H6E cells incubated for 48 hrs by CCK-8 assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1519948Cell cycle arrest in human A549 cells assessed as accumulation at G2 phase at 50 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 12.69 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519962Inhibition of Nedd8-cullin1 (unknown origin) assessed as decrease in cullin1-Nedd8 adduct formation at 25 to 50 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519923Antiproliferative activity against human H1299 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519965Competitive inhibition of Nedd8-cullin1 (unknown origin) adduct formation at 12.5 to 50 uM assessed as increase in substrate Km by Lineweaver-Burk plot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519969Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin2-Nedd8 adduct level at 50 uM measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID484380Colloidal aggregation in fed state simulated intestinal fluid assessed as colloid radius at 50 uM by dynamic light scattering assay in presence of 1% DMSO2010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID27681Tested for Half- life in rat plasma homogenate (10%) at 37 degree Centigrade1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1737434Agonist activity at human PPARgammaDEF receptor expressed in african green monkey COS7 cells transfected with pGal5-TK-pGL3/pRenilla-CMV assessed as maximal activation at 10 uM measured after 39 hrs by dual luciferase reporter assay relative to pioglitazo2020European journal of medicinal chemistry, Jun-01, Volume: 195Identification and development of non-cytotoxic cell death modulators: Impact of sartans and derivatives on PPARγ activation and on growth of imatinib-resistant chronic myelogenous leukemia cells.
AID977603pIC50 values for sodium fluorescein (10 uM) uptake in OATP1B3-transfected CHO cells2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1519930Antiproliferative activity against human PLC cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID18418Oral bioavailability was evaluated in rat; Range is 28-33 %1996Journal of medicinal chemistry, Feb-02, Volume: 39, Issue:3
Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy.
AID1519931Cytotoxicity against human BEAS2B cells after 48 hrs by CCK-8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519976Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin4a-Nedd8 adduct level measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519963Inhibition of Nedd8-Ubc12 (unknown origin) assessed as decrease in Ubc12-Nedd8 adduct formation at 50 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1873191Inhibition of human ABCG2 expressed in dog MDCK-II-BCRP cells mediated pheophorbide A efflux and measured after 60 mins using pheophorbide A as fluorescent substrate by flow cytometry2022European journal of medicinal chemistry, Jul-05, Volume: 237Targeting breast cancer resistance protein (BCRP/ABCG2): Functional inhibitors and expression modulators.
AID1519922Antiproliferative activity against human EKVX cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519957Induction of apoptosis in human A549 cells assessed as late apoptotic cells at 50 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 1.71 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519994Effect on Ub-modified protein level in human A549 cells by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID484296Colloidal aggregation in fed state simulated intestinal fluid by dynamic light scattering assay in presence of 2.75% DMSO2010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1519932Cytotoxicity against human 16HBE cells after 48 hrs by CCK-8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519990Competitive inhibition of Nedd8-cullin1 (unknown origin) adduct formation assessed as decrease in cullin1-Nedd8 adduct formation at 50 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519968Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin1-Nedd8 adduct level at 50 uM measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519954Induction of apoptosis in human A549 cells assessed as early apoptotic cells at 25 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 2.19 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519975Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin3-Nedd8 adduct level measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1519979Inhibition of UbcH10 in human A549 cells assessed as reduction in protein ubiquitination by measuring Ubc10-ub adduct formation at 50 to 100 uM by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519927Antiproliferative activity against human MCF7 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519986Antitumor activity against human A549 cells xenografted in nude mouse assessed as decrease in tumor weight at 60 mg/kg, ip qd measured after 22 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519972Inhibition of UBE2F in human A549 cells assessed as decrease in Cullin5-Nedd8 adduct level at 50 uM measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID679592TP_TRANSPORTER: inhibition of Digoxin transepithelial transport (basal to apical)(Digoxin: 0.1 uM, Candesartan cilexetil: 50 uM) in MDR1-expressing LLC-PK1 cells2002Life sciences, Feb-15, Volume: 70, Issue:13
Interaction of digoxin with antihypertensive drugs via MDR1.
AID568869Oral bioavailability in rat2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID484392Colloidal aggregation in fed state simulated intestinal fluid at 550 uM by dynamic light scattering-based beads autocorrelation assay in presence of 2.75% DMSO2010Journal of medicinal chemistry, May-27, Volume: 53, Issue:10
Colloid formation by drugs in simulated intestinal fluid.
AID1519978Inhibition of Ubc9 in human A549 cells assessed as reduction in protein sumoylation by measuring Ubc9-Sumo adduct formation at 50 to 100 uM by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID977604Ki values for sodium fluorescein (10 uM) uptake in OATP1B3-transfected CHO cells2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID184050Inhibitory activity on AII (100 ng/kg iv)-induced pressor response at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 1 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID26947Total oral bioavailability was determined2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID1519980Effect on SUMO1 level in human A549 cells by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519988Toxicity in nude mouse xenografted with human A549 cells assessed as effect on body weight at 30 to 60 mg/kg, ip qd measured every 2 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1728053Toxicity in nude mouse assessed as effect on body weight at 30 mg/kg, qd after 24 days2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1519926Antiproliferative activity against human T47D cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519958Induction of apoptosis in human A549 cells assessed as early apoptotic cells at 75 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 2.19 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID27685Tested for half- life in rat small intestine homogenate (1%)1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1519997Antitumor activity against human A549 cells xenografted in nude mouse assessed as decrease in tumor size at 30 mg/kg, ip qd measured after 22 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519925Antiproliferative activity against human HuH7 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519971Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin4a-Nedd8 adduct level at 50 uM measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID568911Antagonist activity at angiotensin AT1 receptor in rabbit aortic strip assessed as inhibition of angiotensin 2-induced contractile response2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1519974Inhibition of UBC12 in human A549 cells assessed as decrease in Cullin2-Nedd8 adduct level measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1519928Antiproliferative activity against human MKN45 cells measured after 48 hrs by CCK8 assay2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519943Cell cycle arrest in human A549 cells assessed as accumulation at S phase at 25 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 21.54 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID176435Oral effective dose required for inhibition of Ang II pressor response in rats1996Journal of medicinal chemistry, Feb-02, Volume: 39, Issue:3
Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy.
AID1519985Inhibition of colony formation in human A549 cells measured after 10 days2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519960Inhibition of Nedd8-cullin1 (unknown origin) adduct formation assessed as decrease in cullin1 neddylation at 50 uM preincubated for 10 mins followed by ATP addition and measured after 30 mins by immunoblot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519959Induction of apoptosis in human A549 cells assessed as late apoptotic cells at 75 uM measured after 48 hrs by AnnexinV-FITC/propidium iodide staining based FACS analysis (Rvb = 1.71 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID977601Ki values for sodium fluorescein (10 uM) uptake in OATP1B1-transfected CHO cells2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1519992Inhibition of cullin-RING ligase in human A549 cells assessed as accumulation of Wee1 level at 50 to 125 uM and measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519977Inhibition of UBE2F in human A549 cells assessed as decrease in Cullin5-Nedd8 adduct level measured after 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1728039Cytotoxicity against human BEAS-2B cells incubated for 48 hrs by CCK-8 assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1519949Cell cycle arrest in human A549 cells assessed as accumulation at sub-G1 phase at 50 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 0.89 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1728037Antiproliferative activity against human H1299 cells incubated for 48 hrs by CCK-8 assay2021European journal of medicinal chemistry, Jan-15, Volume: 210Development of novel benzimidazole-derived neddylation inhibitors for suppressing tumor growth invitro and invivo.
AID1315758Inhibition of human DNA polymerase eta (1 to 437 residues) preincubated for 15 mins followed by replicating non-damaged DNA substrate addition measured after 30 mins in presence of dCTP and dGTP by radioactive gel-based primer extension assay2016Journal of medicinal chemistry, Oct-27, Volume: 59, Issue:20
Targeting the Translesion Synthesis Pathway for the Development of Anti-Cancer Chemotherapeutics.
AID1519961Inhibition of Nedd8-cullin1 adduct formation in human A549 cells assessed as decrease in cullin1 neddylation at 100 uM incubated for 6 to 12 hrs by Western blot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID1519964Competitive inhibition of Nedd8-cullin1 (unknown origin) adduct formation at 12.5 to 50 uM assessed as substrate Vmax by Lineweaver-Burk plot analysis2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID977600pIC50 values for sodium fluorescein (10 uM) uptake in OATP1B1-transfected CHO cells2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1519944Cell cycle arrest in human A549 cells assessed as accumulation at G2 phase at 25 uM measured after 24 hrs by propidium iodide/RNase A staining based flow cytometry analysis (Rvb = 12.69 %)2020European journal of medicinal chemistry, Jan-01, Volume: 185Discovery of candesartan cilexetic as a novel neddylation inhibitor for suppressing tumor growth.
AID184209Inhibitory effect on AII (100 ng/kg iv)-induced pressor response after administration at 0.1 mg/kg po in conscious male Sprague-Dawley rats at 0.5 h.1993Journal of medicinal chemistry, Aug-06, Volume: 36, Issue:16
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of potential prodrugs of benzimidazole-7-carboxylic acids.
AID1347161Confirmatory screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347169Tertiary RLuc qRT-PCR qHTS assay for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347149Furin counterscreen qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347153Confirmatory screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347152Confirmatory screen NINDS AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347168HepG2 cells viability qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347158ZIKV-mCherry secondary qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347164384 well plate NINDS Rhodamine confirmatory qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347170Vero cells viability counterscreen for qRT-PCR qHTS assay of selected Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347172Secondary qRT-PCR qHTS assay for selected Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347163384 well plate NINDS AMC confirmatory qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347156DAPI mCherry counterscreen qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347171Orthogonal mCherry assay for qRT-PCR qHTS of selected Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347167Vero cells viability qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (605)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's208 (34.38)18.2507
2000's248 (40.99)29.6817
2010's127 (20.99)24.3611
2020's22 (3.64)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 90.74

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

MetricThis Compound (vs All)
Research Demand Index90.74 (24.57)
Research Supply Index6.66 (2.92)
Research Growth Index4.40 (4.65)
Search Engine Demand Index164.75 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (90.74)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials151 (24.04%)5.53%
Reviews94 (14.97%)6.00%
Case Studies10 (1.59%)4.05%
Observational6 (0.96%)0.25%
Other367 (58.44%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (158)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Phase 2, Double-Blind, Randomized, Placebo-Controlled Dose-Ranging Study of the Efficacy, Safety and Tolerability of TAK-536 in Subjects With Mild to Moderate Uncomplicated Essential Hypertension [NCT01289132]Phase 2926 participants (Actual)Interventional2007-07-31Completed
Phase IV Study for Effect of Intensive Blood-Pressure Control Using Anti-hypertensive Agents in Essential Hypertension With History of Stroke [NCT01198496]Phase 45,000 participants (Anticipated)Interventional2010-10-31Recruiting
Clinical Study Evaluating the Efficacy of Renin Angiotensin System Inhibitors on the Extent of Liver Fibrosis in Patients With Chronic Hepatitis C [NCT03770936]Phase 345 participants (Anticipated)Interventional2018-10-01Recruiting
Influence of Blockade of the Renin-angiotensin System for Preservation of Cognitive Function, Hormonal Counter-regulatory Response, Symptomatology and Cardiac Repolarisation During Hypoglycaemia in Patients With Type 1 Diabetes [NCT01116180]9 participants (Actual)Interventional2010-04-30Completed
A Randomized, Double-blind, Candesartan-controlled, Parallel Group Comparison Clinical Study to Evaluate the Antihypertensive Efficacy and Safety of Fimasartan in Patients With Mild to Moderate Essential Hypertension (Phase IIIb) [NCT01135212]Phase 3290 participants (Actual)Interventional2010-04-30Completed
A Randomized, Double-blind, Multi-center, Phase III Clinical Trial to Evaluate the Antihypertensive Efficacy and Safety of Amlodipine Besylate and Candesartan Cilexetil Combination in Patients With Essential Hypertension Who Are Not Adequately Controlled [NCT02368665]Phase 3180 participants (Actual)Interventional2014-12-31Completed
A Randomized, Double-blind, Multi-center, Phase III Clinical Trial to Evaluate the Antihypertensive Efficacy and Safety of Amlodipine Besylate and Candesartan Cilexetil Combination in Patients With Essential Hypertension Who Are Not Adequately Controlled [NCT02368652]Phase 3181 participants (Actual)Interventional2014-12-31Completed
Comparison of Vascular Remodeling Between Different Antianginal Medication Evaluated by Noninvasive ECG-gated Fundus Photographic Evaluation [NCT01162902]Phase 4150 participants (Anticipated)Interventional2013-09-30Not yet recruiting
Single Dose Study to Compare the Pharmacokinetics as Well as Safety and Tolerability of a Novel Fixed Dose Combination of Nifedipine GITS and Candesartan, the Loose Combination of Both and the Single Components Alone and to Investigate the Bioequivalence [NCT01227603]Phase 149 participants (Actual)Interventional2010-11-30Completed
Candesartan's Effects on Alzheimer's Disease And Related Biomarkers [NCT02646982]Phase 277 participants (Actual)Interventional2016-06-30Completed
Single Dose Study to Compare the Pharmacokinetics as Well as Safety and Tolerability of a Novel Fixed Dose Combination of Nifedipine GITS and Candesartan and the Loose Combination of Both Components and to Investigate the Bioequivalence Between the Fixed [NCT01350609]Phase 149 participants (Actual)Interventional2011-04-30Completed
A Randomized, Open-label, Multiple Doses, Crossover Study to Evaluate a Pharmacokinetic Drug Interaction and Safety of Amlodipine Between Free Combination of Amlodipine and Candesartan and Amlodipine Monotherapy in Healthy Male Volunteers [NCT02064556]Phase 124 participants (Actual)Interventional2014-05-31Completed
A Randomized, Double-blind, Multi-center, PhaseⅡ Clinical Trial to Evaluate the Antihypertensive Efficacy and Safety of Candesartan Cilexetil and Amlodipine Besylate for the Dose Selection in Patients With Essential Hypertension [NCT02059616]Phase 2384 participants (Anticipated)Interventional2014-02-28Recruiting
An Open-label, Multiple-dosing, Two-arm, One-sequence, Crossover Study to Evaluate the Safety and Pharmacokinetics After Oral Concurrent Administration of Candesartan 32 mg and Rosuvastatin 20 mg in Healthy Male Volunteers [NCT02079506]Phase 140 participants (Actual)Interventional2014-02-28Completed
Single Dose Escalation Study to Investigate the Pharmacokinetics as Well as Safety and Tolerability of a Concomitant Administration of Nifedipne GITS and Candesartan Tablets Under Fasting Conditions in Healthy Male Subjects in an Open Label, Non-randomize [NCT03136666]Phase 112 participants (Actual)Interventional2010-04-19Completed
DIRECT: DIabetic Retinopathy Candesartan Trials. Effects of Candesartan Cilexetil (Candesartan) on Diabetic Retinopathy in Type 1 Diabetic Patients With Retinopathy. [NCT00252720]Phase 31,850 participants (Actual)Interventional2001-08-31Completed
Efficacy and Safety Evaluation of the New Association on Fixed Dose of Candesartan + Chlorthalidone, Produced by EMS S.A,in Arterial Hypertension Control [NCT02521233]Phase 30 participants (Actual)Interventional2016-11-30Withdrawn(stopped due to Sponsor decision)
An Open-Label, Randomised, Single Dose, Two-Way Crossover Pilot Study to Determine the Relative Bioavailability of a Fixed Dose Combination Tablet Formulation of GSK587323 (16mg Candesartan Cilexetil/12.5mg Hydrochlorothiazide) Relative to Respective Refe [NCT02094924]Phase 116 participants (Actual)Interventional2014-04-17Completed
The Effect of Continuing or Discontinuing ACE-I/ARBs Therapy on the Incidence of Contrast-induced Nephropathy in Patients With Chronic Kidney Disease Undergoing Coronary Angiography; a Randomized Controlled Trial [NCT05271448]600 participants (Anticipated)Interventional2021-06-01Recruiting
A Randomized, Open-label, Single-dosing, 2x2 Crossover Study to Compare the Safety and Pharmacokinetics of CKD-330 (Fixed-dose Combination of Candesartan 8 mg and Amlodipine 5 mg) With Coadministration of the Two Separate Drugs in Healthy Male Volunteers [NCT02186496]Phase 132 participants (Actual)Interventional2014-07-31Completed
A Randomized, Open-label, Multiple Doses, Crossover Study to Evaluate a Pharmacokinetic Drug Interaction and Safety of Candesartan Between Free Combination of Candesartan and Amlodipine and Candesartan Monotherapy in Healthy Male Volunteers [NCT02064621]Phase 124 participants (Actual)Interventional2014-06-30Completed
Open-label, Randomized, Single-dose, Crossover Study to Evaluate the Pharmacokinetics and Safety Following Administration of CJ-30059 and Co-administration of Candesartan Cilexetil and Amlodipine Besylate in Healthy Volunteers. [NCT02173912]Phase 132 participants (Anticipated)Interventional2014-06-30Recruiting
Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) [NCT00081731]Phase 3947 participants (Actual)Interventional2004-04-30Completed
Candesartan in Heart Fail. Assess. of Reduction in Mortality & Morbidity. Candesartan in Patients With Heart Failure Who Are ACE Inhibitor Intolerant and Have Depressed Left Ventricular Systolic Function [NCT00634400]Phase 36,268 participants (Anticipated)Interventional1999-03-31Completed
Efficacy and Safety Evaluation of the New Association on Fixed Dose of Candesartan Cilexetil + Chlorthalidone (16mg + 12.5mg and 16mg + 25mg) Compared With HYZAAR® in Hypertension Control [NCT02521246]Phase 30 participants (Actual)Interventional2016-11-30Withdrawn(stopped due to Sponsor decision)
Phase 2/3 Study of Effect of AT1RB Versus ACE Inhibitor in Addition to XO Inhibitor on Progression of LV Remodeling and Dysfunction in Diabetic Patients With Acute MI. [NCT01052272]Phase 2/Phase 372 participants (Actual)Interventional2005-07-31Completed
A Single Dose Study to Evaluate the Safety and Tolerability, Pharmacokinetics and Pharmacodynamics of MK5478 in Subjects and in Patients With Hypertension [NCT01025843]Phase 120 participants (Actual)Interventional2009-12-01Completed
A Randomized, Open-label, Single-dosing, 2x2 Crossover Study to Compare the Safety and Pharmacokinetics of CKD-330 (Fixed-dose Combination of Candesartan 16 mg and Amlodipine 5 mg) With Coadministration of the Two Separate Drugs in Healthy Male Volunteers [NCT02801526]Phase 132 participants (Actual)Interventional2015-04-30Completed
A Randomized, Double-blind, Multi-center Clinical Trial to Evaluate Efficacy and Safety of Ezetimibe/Rosuvastatin Combination Tablets and Candesartan Cilexetil/Amlodipine Besylate Combination Tablets [NCT03847506]Phase 4127 participants (Actual)Interventional2018-07-05Completed
A Randomized, Double-blind, Multi-center, Phase 2 Trial to Evaluate the Efficacy and Safety of Candesartan/Amlodipine Combined or Alone and Select Better Dose of CKD-330 in Patients With Essential Hypertension [NCT02206165]Phase 2456 participants (Anticipated)Interventional2014-03-31Recruiting
A Multicenter, Multifactorial, Randomized, Double-Blind, Placebo-Controlled Dose-Finding Study of Nifedipine GITS and Candesartan in Combination Compared to Monotherapy in Adult Patients With Essential Hypertension [NCT01303783]Phase 21,381 participants (Actual)Interventional2011-04-30Completed
An Open-label, Randomized, Single Dose, Three-way Crossover, Six Sequence Pilot Study to Determine the Relative Bioavailability of Candesartan Cilexetil 16mg From Two Candidate Tablet Formulations of GW615775 Relative to One 16mg Tablet of Reference Cande [NCT02254447]Phase 118 participants (Actual)Interventional2014-12-02Completed
A Multicenter, Double-blind, Controlled, Randomized Trial to Evaluate the Association Candesartan Cilexetil + Chlorthalidone + Amlodipine Versus Exforge HCT®️ for Systemic Arterial Hypertension [NCT05920005]Phase 3698 participants (Anticipated)Interventional2023-08-22Recruiting
Clinical Study to Evaluate the Efficacy and Safety of the Combination Therapy Candesartan Cilexetil 32 mg Plus Hydrochlorothiazide 25 mg in Patients With Severe Hypertension [NCT01012479]Phase 4107 participants (Actual)Interventional2009-10-31Completed
Directed Use of REmote Patient Management System AMia to Achieve Prescribed Dry Weight [NCT04002440]28 participants (Actual)Interventional2018-11-08Active, not recruiting
Association Between Angiotensin Converting Enzyme Inhibitor or Angiotensin Receptor Blocker Use and COVID-19 Severity and Mortality Among US Veterans [NCT04467931]22,213 participants (Actual)Observational2020-01-19Completed
The Precision Hypertension Care Study [NCT02774460]Phase 4280 participants (Actual)Interventional2017-02-20Completed
Candesartan Cilexetil in Heart Failure Assessment of Reduction in Mortality and Morbidity. Clinical Study of Candesartan in Patients With Heart Failure and Preserved Left Ventricular Systolic Function [NCT00634712]Phase 3734 participants (Anticipated)Interventional1999-06-30Completed
A Randomized, Single-dose, Open, Crossover Clinical Trial to Compare the Pharmacokinetics of DP-R208 (Candesartan Cilexetil and Rosuvastatin Calcium Fixed Dose Combinations) in Comparison to Each Component Administered Alone in Healthy Male Volunteers [NCT02707224]Phase 140 participants (Actual)Interventional2015-01-31Completed
Randomized, Controlled, Parallel Arm, PROBE Study to Evaluate Different Effects of Imidapril and Candesartan on Fibrinolysis and Insulin-Sensitivity in Patients With Mild to Moderate Hypertension [NCT00644475]Phase 360 participants (Anticipated)Interventional2008-03-31Recruiting
CandeSpartan Study Candesartan Spanish Response-prediction and Tolerability Study Observational Study on Response Predictors and Tolerability of Candesartan in Usual Clinical Practice [NCT04138316]85 participants (Actual)Observational [Patient Registry]2020-01-02Completed
"A REtrospective Study on the Effects of cAndesartan vs. Losartan on Blood Pressure, Health Care Consumption and cardiovascuLar Events In a Real-liFe GP sEtting in Sweden" [NCT00620178]14,000 participants (Anticipated)Observational2008-03-31Completed
A Randomized, Open-label, Single-dosing, 2x2 Crossover Study to Compare the Safety and Pharmacokinetics of CKD-330(Fixed-dose Combination of Candesartan 16 mg and Amlodipine 5 mg) With Coadministration of the Two Separate Drugs in Healthy Male Volunteers [NCT02811731]Phase 132 participants (Actual)Interventional2015-04-30Completed
A Randomized, Double-blind, Multi-center, Phase 3 Trial to Evaluate the Efficacy and Safety of a Combination Therapy of Candesartan and Amlodipine Versus Candesartan Monotherapy in Hypertensive Patients Inadequately Controlled by Candesartan Monotherapy [NCT02651870]Phase 3135 participants (Actual)Interventional2015-04-22Completed
A Double-blind, Randomised, 4-arm Parallel Group, Multicentre, 8-week, Phase III Study to Assess the Antihypertensive Efficacy and Safety of the Combination of Candesartan Cilexetil (CC) 32 mg and Hydrochlorothiazide (HCT) 25 mg Compared With CC 32 mg, HC [NCT00434967]Phase 32,207 participants (Actual)Interventional2007-01-31Completed
Candesartan vs Propranolol for Migraine Prevention: A Double Blind, Placebo Controlled, Double Dummy, Triple Cross-over Study [NCT00884663]Phase 2/Phase 372 participants (Actual)Interventional2009-04-30Completed
A Double Blind Randomized Controlled Trial to Assess the Efficacy and Safety of a Quadruple Ultra-low-dose Treatment for Hypertension (QUARTET USA) [NCT03640312]Phase 262 participants (Actual)Interventional2019-08-30Active, not recruiting
Evaluation of the Pharmacokinetic Interaction Between Candesartan and Felodipine in a Combination Package Compared to the Separate Intake of the Reference Brands Atacand and Splendil After a Fasting Period. [NCT00905333]Phase 136 participants (Actual)Interventional2008-10-31Completed
Angiotensin Receptor Blockade an Anti-Fibrotic Intervention in Patients With Chronic Hepatitis C [NCT00930995]Phase 20 participants (Actual)InterventionalWithdrawn(stopped due to Not Awarded)
Single Dose Crossover Comparative Bioavailability Study of Candesartan Cilexetil 32 mg Tablets in Healthy Adult Subjects Under Fasting Conditions [NCT04012307]Phase 140 participants (Actual)Interventional2019-07-11Completed
Does Telmisartan Compared to Candesartan Due to a Distinctly Larger Volume of Distribution Exert Stronger Effects in Relevant Peripheral Tissues, e.g. Renal and Adrenal Tissues [NCT02261116]Phase 424 participants (Actual)Interventional2002-04-30Completed
A 24-Week Multicentre, Randomized, Double-Blind, Controlled, Parallel Group Non-Inferiority Study to Assess the Efficacy and Safety of Olmesartan Medoxomil Versus Candesartan Cilexetil in Patients With Symptomatic Heart Failure (NYHA II-IV) [NCT00679484]Phase 3400 participants (Anticipated)Interventional2008-06-30Terminated(stopped due to Lack of subject recruitment)
Observational Usage and Efficacy Study of Candesartan in Heart Failure Treatment in France [NCT00679640]450 participants (Actual)Observational2008-01-31Completed
[NCT02614352]Phase 160 participants (Anticipated)InterventionalNot yet recruiting
The Potential of Candesartan to Retard the Progression of Aortic Stenosis Influences of Medical Therapy to the Atheroinflammatory Process in Stenotic Aortic Valves [NCT00699452]Phase 3120 participants (Anticipated)Interventional2009-05-31Recruiting
[NCT02609711]Phase 190 participants (Anticipated)Interventional2015-11-30Active, not recruiting
"Candesartan Added Therapy for Treatment Optimization of Symptomatic Heart Failure With Diastolic Dysfunction in Diabetic and Hypertensive Patients A Randomized, Placebo-controlled, Double-blind, Parallel-group and Multicenter Clinical Phase III Study Inv [NCT00775840]Phase 322 participants (Actual)Interventional2008-01-31Completed
Prognostic Value of the Circadian Pattern of Ambulatory Blood Pressure for Multiple Risk Assessment [NCT00741585]Phase 421,983 participants (Actual)Interventional2008-09-01Completed
A Single Dose, 2-Period, Cross-over, Bioequivalence Study in Healthy Subjects to Evaluate the Proposed Commercial Oral Suspension of Candesartan Cilexetil [NCT00844324]Phase 136 participants (Actual)Interventional2009-03-31Completed
Effects Of Candesartan Cilexetil vs Standard Therapy on Serum Levels of Brain Natriuretic Peptide in Patients Suffering From Chronic Heart Failure With Depressed and Preserved Systolic Function [NCT00843154]Phase 3571 participants (Actual)Interventional2005-12-31Terminated(stopped due to Insufficient enrollment)
Effects of Telmisartan Compared With Candesartan on Ischemic Cardiovascular Events in High-risk Hypertensive Patients: a Multi-center, Prospective, Randomized, Open-labeled, Blinded Endpoints Trial [NCT00863980]1,500 participants (Actual)Interventional2009-04-30Terminated(stopped due to Principle investigator resigned in 2013)
A 28-week, Randomised, Open-label, Parallel-Group, Multi-Center Study To Find the Effective Dose of Candesartan Cilexetil (Atacand) for Renoprotection in Korean Hypertensive Patients With Non-diabetic Nephropathy [NCT00573430]Phase 4128 participants (Actual)Interventional2007-12-31Completed
Open Label, Comparative, Multiple-dose, Fixed-sequence Steady State Trial in Healthy Volunteers to Assess the Pharmacokinetic Interaction of Candesartan, Atorvastatin and Amlodipine After a Multiple Oral Dose Administration [NCT04245046]Phase 118 participants (Actual)Interventional2019-01-18Completed
An Open-label Extension Study of Candesartan Cilexetil in Hypertensive Pediatric Subjects Ages 1 to <11 Years: a Long Term Study [NCT00690612]Phase 335 participants (Actual)Interventional2007-09-30Completed
Open-label, Randomised, 2-Arm Parallel Group, Multicentre, 8-week, Phase IV Study to Assess the Antihypertensive Efficacy and Safety of the Candesartan Cilexetil 16 mg and Hydrochlorothiazide 12.5 mg Combination Therapy in Comparison With Candesartan 16 m [NCT00621153]Phase 4214 participants (Actual)Interventional2008-02-29Completed
Effects of Antihypertensive Treatment on Cardiac Remodelling and Metabolic Profile in HIV Infected Patients: Randomized Longitudinal Study With Candesartan Versus Lercanidipine [NCT00564057]Phase 430 participants (Anticipated)Interventional2007-09-30Recruiting
Double-blind, Randomized Trial to Investigate the Antihypertensive and Metabolic Effects of Candesartan in Insulin-resistant Obese Patients With a Hypertension Not Adequately Controlled by Previous ß-blocker or Calcium Channel Blocker [NCT00775814]Phase 4188 participants (Actual)Interventional2006-10-31Completed
A Multicenter, Randomized, Double-Blind, Monotherapy-Controlled Study of Nifedipine Gastrointestinal Therapeutic System and Candesartan Cilexetil in Combination Taken Orally for 8 Weeks in Adult Subjects With Essential Hypertension Who Are Inadequately Co [NCT02047019]Phase 30 participants (Actual)Interventional2017-12-01Withdrawn(stopped due to GPDC decided to terminate the study)
Bariatric Surgery and Pharmacokinetics Candesartan: BAR-MEDS Candesartan [NCT03460327]12 participants (Anticipated)Observational2016-11-02Recruiting
Effects of Candesartan Cilexetil (Candesartan) on Diabetic Retinopathy in Type 1 Diabetic Patients Without Retinopathy. [NCT00252733]Phase 35,238 participants (Actual)Interventional2001-06-30Completed
Characterization of Vascular Effects of Candesartan and Pioglitazone. [NCT00154037]40 participants Interventional2005-10-31Completed
Which is the Best Treatment for Non-diabetic Hypertension With Obesity: Telmisartan, Amlodipine or Candesartan, Alone or Plus MEtformin? (HOT-ACME 1) [NCT00538486]Phase 4360 participants (Actual)Interventional2008-02-29Completed
Effects of Candesartan Cilexetil (Candesartan) on Diabetic Retinopathy in Type 2 Diabetic Patients With Retinopathy. [NCT00252694]Phase 34,717 participants (Actual)Interventional2001-08-31Completed
A Multicenter, Non-comparative, Phase IV Study to Evaluate the Effect of Candesartan Based Therapy in the Percent Change of proBNP Level After 24 Week Treatment in the Patients With Hypertension With Left Ventricular Hypertrophy [NCT00348686]Phase 4315 participants (Actual)Interventional2006-06-30Completed
A Double-Blind, Randomised, Dose Ranging, Multi-Centre, Phase IIIb Study to Evaluate the Efficacy and Safety of High Doses of Candesartan Cilexetil (Atacand®) on the Reduction of Proteinuria in the Treatment of Subjects With Hypertension and Moderate to S [NCT00242346]Phase 3270 participants Interventional2003-04-30Completed
An Open-label, Randomised, Single Dose, Two-way Crossover Pilot Study to Determine the Relative Bioavailability of One 8mg Tablet Formulation of Candesartan Cilexetil (GW615775) Relative to One 8mg Reference Tablet of Candesartan Cilexetil (Atacand) in He [NCT02006589]Phase 116 participants (Actual)Interventional2013-12-11Completed
An Open-label, Randomised, Single Dose, Two-way Crossover Pilot Study to Determine the Relative Bioavailability of One 16mg Tablet Formulation of Candesartan Cilexetil (GW615775) Relative to One 16mg Reference Tablet of Candesartan Cilexetil (Atacand) in [NCT02006602]Phase 116 participants (Actual)Interventional2013-12-13Completed
Host Response Mediators in Coronavirus (COVID-19) Infection - Is There a Protective Effect of Losartan and Other ARBs on Outcomes of Coronavirus Infection? [NCT04606563]Phase 3341 participants (Actual)Interventional2020-10-09Terminated(stopped due to DSMC recommendation due to futility)
Open Label, Randomized, Active Drug Comparative, Parallel Group, Multi-center, Phase IV Study to Compare and Evaluate the Efficacy and Safety of Candemore Tab and Atacand Tab. [NCT01682564]Phase 4169 participants (Actual)Interventional2012-01-31Completed
Beneficial Effect of Angiotensin-blocking Agent Candesartan on Alcoholic Liver Fibrosis: A Randomized Controlled Trial [NCT00990639]Phase 1/Phase 285 participants (Actual)Interventional2005-09-30Completed
A Randomized, Open-label, Single-dosing, Crossover Study to Compare the Safety and Pharmacokinetics of CKD-330(Fixed-dose Combination of Candesartan Cilexetil 8 mg and Amlodipine 5 mg) With Coadministration of the Two Separate Drugs in Healthy Male Volunt [NCT02548286]Phase 153 participants (Actual)Interventional2015-08-31Completed
A Multi-center, Randomized, Double-blind, Parellel Phase III Clinical Trial to Evaluate the Efficacy and Safety of DP-R208 and Each Monotherapy in Patients With Hypertension and Primary Hypercholesterolemia. [NCT02770261]Phase 3219 participants (Actual)Interventional2015-12-31Completed
DP-R208 Pharmacokinetic Study Phase I [NCT02709187]Phase 137 participants (Actual)Interventional2016-03-31Completed
The Renin-angiotensin System (RAS) in Barrett's Esophagus as Future Biomarkers for Dysplasia and Cancer? A Randomized Controlled Trial [NCT02879721]Early Phase 133 participants (Actual)Interventional2009-10-31Completed
Candesartan Cilexetil in Heart Failure Assessment of Reduction in Mortality and Morbidity. Clinical Study of Candesartan in Patients With Heart Failure and Depressed Left Ventricular Systolic Function [NCT00634309]Phase 3597 participants (Anticipated)Interventional1999-06-30Completed
Comparison Between ARB and ARB Plus CCB on Incidence of Renal and Cardiovascular Events in Hypertensive ADPKD Patients [NCT00541853]Phase 4150 participants (Anticipated)Interventional2007-12-31Not yet recruiting
An Open-label, Multicenter Study to Evaluate the Efficacy and Safety of a 4 Week Therapy With Aliskiren 300 mg Plus Hydrochlorothiazide 25 mg in Hypertensive Patients Not Adequately Responding to a 4 Week Therapy With Candesartan 32 mg Plus Hydrochlorothi [NCT00867490]Phase 3186 participants (Actual)Interventional2009-03-31Completed
Angiotensin-II Blockade in Mitral Regurgitation [NCT00587470]Phase 460 participants (Actual)Interventional1998-08-31Completed
A Phase-3 Randomized, Double-Blind, Parallel-Group Efficacy and Safety Study Evaluating the Fixed-Dose Combination of Candesartan Plus Amlodipine (8/5 mg) in Chinese Subjects With Mild/Moderate Essential Hypertension, Who Do Not Achieve Target Blood Press [NCT02969265]Phase 30 participants (Actual)Interventional2017-05-09Withdrawn(stopped due to Business reasons unrelated to product safety)
ACE/ACE2 Ratio in Diabetic Patients Treated With Antihypertensive Drugs [NCT00192803]Phase 420 participants InterventionalNot yet recruiting
Prospective, Randomized, Pharmacological Intervention Study; Evaluating Effect of the Angiotensin II-receptor (AT1) Blocker Candesartan vs Placebo in Prevention of Trastuzumab-associated Cardiotoxicity in Patients Treated With Trastuzumab [NCT00459771]Phase 3210 participants (Actual)Interventional2007-06-30Completed
Heart Outcomes Prevention Evaluation-3 [NCT00468923]Phase 412,705 participants (Actual)Interventional2007-05-31Completed
Genetic Epidemiology of Responses to Antihypertensives [NCT00005520]1,200 participants (Actual)Observational1997-02-28Completed
Neurohumoral and Oxidative Influences of Candesartan, Atenolol, Hydrochlorothiazide and Drug Combinations in Essential Hypertensive Patients. [NCT00232882]Phase 486 participants (Actual)Interventional2003-12-31Completed
A 36 Week Three-Center Double-Blind Randomized Cross-Over Trial Comparing Metabolic Effects of Candesartan, Hydrochlorothiazide and Placebo [NCT00282178]Phase 226 participants (Actual)Interventional2005-04-30Completed
Scandinavian Candesartan Acute Stroke Trial [NCT00120003]Phase 32,500 participants (Anticipated)Interventional2005-06-30Completed
Left Ventricular Reverse Remodelling After Aortic Valve Replacement in Severe Valvular Aortic Stenosis - Effect of Blockade of the Angiotensin-II Receptor [NCT00294775]Phase 3140 participants (Anticipated)Interventional2006-02-28Active, not recruiting
Candesartan Antihypertensive Survival Evaluation in Japan (CASE-J) Trial of Cardiovascular Events in High-Risk Hypertensive Patients [NCT00125463]Phase 33,200 participants Interventional2001-09-30Active, not recruiting
Effects of Candesartan Cilexetil on Cardiovascular Events in Japanese Patients With Hypertension After Sirolimus- or Paclitaxel-Eluting Stents Implantation [NCT00139386]Phase 41,119 participants (Actual)Interventional2005-10-31Completed
[NCT00154050]22 participants Interventional2004-05-31Completed
Prophylactic Treatment of Episodic Cluster Headache With an Angiotensin II Receptor Blocker (Candesartan Cilexetil); a Randomized, Placebo Controlled Parallel Study [NCT00184587]Phase 240 participants (Actual)Interventional2005-03-31Completed
Non-interventional Study on Uncontrolled Hypertensive Patients for Evaluating Efficacy of Candesartan Cilexetil as Monotherapy or add-on Therapy. [NCT00573742]1,940 participants (Actual)Observational2007-09-30Completed
Candesartan Use in Hypertrophic and Non-Obstructive Cardiomyopathy Estate (The CHANCE): a Double-Blind, Placebo-Controlled, Randomized, Multicenter Study [NCT00430833]Phase 20 participants InterventionalActive, not recruiting
A Multi-center, Randomized, Double-blind, Phase II Clinical Trial to Evaluate the Efficacy and Safety of Combination Therapy vs. Monotherapy of Candesartan and Amlodipine for Dose-Finding in Patients With Essential Hypertension [NCT02944734]Phase 2392 participants (Actual)Interventional2014-09-30Completed
[NCT00530595]0 participants InterventionalCompleted
Effect of ACE Inhibitor Plus High Dose Candesartan on BNP and Inflammation in Patients With LV Dysfunction: Impact of Renin-angiotensin-aldosterone System Genetic Polymorphisms [NCT00400582]Phase 4300 participants (Anticipated)Interventional2006-11-30Completed
A Double Blind, Randomised, 3-Arm Parallel Group, Multicentre, 8-Week, Phase III Study to Assess Antihypertensive Efficacy and Safety of the Combination of Candesartan Cilexetil (CC) /HCT 32/12.5mg and 32/25mg vs. CC 32mg Alone in Patients With Inadequate [NCT00383929]Phase 31,979 participants (Actual)Interventional2006-09-30Completed
Acute Candesartan Cilexetil Outcomes Stroke Trial (ACCOST) [NCT00108706]Phase 450 participants Interventional2004-12-31Active, not recruiting
Action to Control Cardiovascular Risk in Diabetes (ACCORD) [NCT00000620]Phase 310,251 participants (Actual)Interventional1999-09-30Completed
The Renin-Angiotensin System in Essential Hypertension [NCT00141583]11 participants (Anticipated)Interventional2004-04-30Terminated(stopped due to Insufficient accrual rate)
An Open-label, Multiple-dose, Two-arm, One-sequence, Crossover Study to Evaluate the Safety and Pharmacokinetics After Oral Concurrent Administration of amlodipine10mg and candesartan32mg in Healthy Male Volunteers [NCT01806311]Phase 134 participants (Anticipated)Interventional2012-12-31Completed
[NCT00130975]Phase 3200 participants Interventional2001-04-30Completed
Danish Hypertension Prevention Project [NCT00150631]Phase 3100 participants (Actual)Interventional2000-11-30Active, not recruiting
A Dose-ranging Safety and Pharmacokinetics Study of Candesartan Cilexetil in Hypertensive Pediatric Subjects 1 to Less That 6 Years of Age: A 4-week, Multicenter, Randomized, Double-blind Study With a 1-year, Open-label, Follow-up Period. [NCT00244621]Phase 395 participants (Actual)Interventional2004-11-30Completed
Define in Humans With Compensated CHF and Renal Dysfunction, the Modulating Action of Chronic AT1 Receptor Blockade in Addition to ACE Inhibition on Cardiorenal and Humoral Function [NCT01678794]Phase 1/Phase 233 participants (Actual)Interventional2012-02-29Completed
Pulse Wave Velocity, Pulse Wave Morphology and Blocking of the Reninangiotensin System in Patients With Chronic Kidney Disease: An Interventional and Methodological Study [NCT00235287]Phase 460 participants (Anticipated)Interventional2005-09-30Recruiting
A Randomized, Double-blind, Placebo-controlled, Multicenter, Long-term Trial of Preventing Hypertension Using Candesartan Cilexetil 16 mg in Patients With High Normal Blood Pressure (TROPHY) [NCT00227318]Phase 31,000 participants Interventional1998-07-31Completed
A Randomized, Comparative Study of the Effects of Candesartan and Telmisartan on the Home Blood Pressure, Glucose and Lipid Metabolism in the Hypertensive Patients With the Accumulation of Visceral Fat by the Central Registration System [NCT00288717]300 participants Interventional2006-02-28Recruiting
Angiotensin II Antagonism of TGF-Beta 1: A Candesartan Dose - TGF-Beta 1 Response Relationship Study [NCT00320970]36 participants Interventional2002-08-31Completed
Multi-Arm Multi-Stage Adaptive Platform Trial (APT) for the Acute Treatment of Traumatic Brain Injury [NCT05826912]Phase 2672 participants (Anticipated)Interventional2024-03-29Not yet recruiting
Studies of Early Diabetic Glomerulopathy-the Relation Between Histopathology, Kidney Function and Metabolic Control. Natural History and Effect of ARB [NCT00328302]Phase 413 participants Interventional2000-09-30Active, not recruiting
Effects of Sodium Intake on Pharmacokinetic/Pharmacodynamic Relationship of a Single Dose of a Renin Angiotensin System-Blocker, or a Beta-Blocker in Normotensive Sodium-Depleted or Replated Volunteers in a Cross-Over Study [NCT00310778]Phase 164 participants (Actual)Interventional2006-03-31Completed
[NCT01629225]Phase 4500 participants (Anticipated)Interventional2013-07-31Recruiting
Effect of Lower Body Negative Pressure and Angiotensin II Receptor Blockade on Renal Hemodynamic, Neuro-hormonal and Tubular Response in Pre-hypertensive States: a Randomized Controlled Trial. [NCT01734096]Phase 478 participants (Actual)Interventional2009-05-31Completed
Renin-Angiotensin-System Quantification in Patients Treated With Aliskiren or Candesartan (RASQAL) [NCT01827202]Phase 424 participants (Actual)Interventional2012-12-31Completed
Open-label, Randomized, Single-dose, Crossover Study to Evaluate the Pharmacokinetic Interactions of Candesartan Cilexetil and Amlodipine Besylate in Healthy Male Volunteers. [NCT01845272]Phase 140 participants (Anticipated)Interventional2013-04-30Active, not recruiting
A Multicenter, Randomized, Active Controlled, Open Label, Platform Trial on the Efficacy and Safety of Experimental Therapeutics for Patients With COVID-19 (Caused by Infection With Severe Acute Respiratory Syndrome Coronavirus-2) [NCT04351724]Phase 2/Phase 3500 participants (Anticipated)Interventional2020-04-16Recruiting
Effects of Cerebral Hypoperfusion and Its Reversal on Late-Life Depression [NCT01794455]Phase 41 participants (Actual)Interventional2013-05-31Terminated(stopped due to Enrollment difficulties)
The Effect of Multidisciplinary Intervention on Patients With Persistent Post-traumatic Headache [NCT05328635]100 participants (Anticipated)Observational2021-09-01Recruiting
A Randomized, Multi-center, Double-blind, Placebo-controlled, Parallel-group Comparison, Phase 2 Study to Evaluate the Dose-response Relationship of the Efficacy and Safety of Oral Administration of TAK-272 in Patients With Type 2 Diabetes Mellitus and Mi [NCT02332824]Phase 2415 participants (Actual)Interventional2014-10-16Completed
An Open-label, Randomized, Cross-over Study to Evaluate Pharmacokinetics and the Safety of HL068 16/10mg Compared to Candesartan 16mg and Amlodipine 10mg Co-administered in Healthy Male Volunteers. [NCT02988362]Phase 140 participants (Anticipated)Interventional2016-12-31Not yet recruiting
Adiposity and Endothelin Receptor Function [NCT03583866]Early Phase 125 participants (Actual)Interventional2018-05-21Active, not recruiting
Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy: A Randomized, Placebo-controlled, 2x2 Factorial, Double Blind Trial of Candesartan and Metoprolol [NCT01434134]Phase 2130 participants (Actual)Interventional2011-09-30Completed
Molecular - Genetic Alterations in Adipose Tissue After Change in Therapy From ACE Inhibitors to AT1 Receptor Blockers in Patients With Essential Hypertension [NCT01444833]35 participants (Anticipated)Interventional2008-10-31Recruiting
An Investigator Initiated, International Multi-Centre, Multi-Arm, Multi-Stage Randomised Double Blind Placebo Controlled Trial of Angiotensin Receptor Blocker (ARB) & Chemokine Receptor Type 2 (CCR2) Antagonist for the Treatment of COVID-19 [NCT05122182]Phase 249 participants (Actual)Interventional2022-01-07Terminated(stopped due to Withdrawal of funding support from the trial funder.)
Candesartan for Migraine Prevention: A Multicentre, Binational, Triple Blind, Placebo Controlled, Parallel Group Study of Two Doses of Candesartan (8 and 16 mg) [NCT04574713]Phase 2450 participants (Anticipated)Interventional2020-04-26Recruiting
"Unisia Combination Tablets LD, HD Special Drug Use Surveillance Hypertension: Long-Term Use" [NCT02068495]3,409 participants (Actual)Observational2010-06-15Completed
An Open-label, Multicenter Study to Evaluate the Efficacy and Tolerability of a 4 Week Therapy With the Fixed Dose Combination of Valsartan 160 mg Plus HCTZ 25 mg in Hypertensive Patients Not Adequately Responding to a 4 Week Therapy With the Free Combina [NCT00360178]Phase 3198 participants (Actual)Interventional2006-07-31Completed
An ACE Inhibitor or an Angiotensin Receptor Blocker as a Treatment for Methamphetamine Dependence [NCT01062451]Phase 180 participants (Actual)Interventional2009-05-31Completed
Strain-based vs. Left Ventricular Ejection Fraction-based Cardiotoxicity Prevention Strategy in Patients With Breast Cancer Who Treated With Adjuvant Trastuzumab [NCT04429633]136 participants (Anticipated)Interventional2019-07-19Recruiting
Efficacy and Safety of a Sequential Therapy Change From Candesartan 32 mg to the Fixed Combination of Olmesartan 40 mg/Amlodipine 10 mg in Patients With Poorly Controlled Moderate Hypertension - an Open Phase IV Trial [NCT01611077]Phase 488 participants (Actual)Interventional2012-01-31Completed
Sevicontrol-1: Efficacy and Safety of a Fixed Combination of Olmesartan 40 mg / Amlodipine 10 mg in Patients With Insufficiently Controlled Hypertension Under Monotherapy With Candesartan 32 mg - an Open Phase IIIb Trial [NCT01613209]Phase 383 participants (Actual)Interventional2011-12-31Completed
"A Randomized, Double Blind, Cross-Over, Placebo-Controlled Clinical Trial to Assess the Effects of Candesartan on the Carbohydrate Metabolism, of Non Diabetic, Non Hypertensive Subjects With Dysglycemia and Abdominal Obesity.ARAMIA" [NCT00319202]Phase 456 participants (Actual)Interventional2006-06-30Terminated(stopped due to Difficulties in completing the required sample size)
"Early Treatment With Candesartan vs Placebo in Asymptomatic Genetic Carriers of Dilated Cardiomyopathy (EARLY-GENE Trial)" [NCT05321875]Phase 3320 participants (Anticipated)Interventional2022-06-02Recruiting
CAndesartan vs LIsinopril Effects on the BRain and Endothelial Function in eXecutive MCI (CALIBREX) [NCT01984164]Phase 2176 participants (Actual)Interventional2014-08-20Completed
ECARD Combination Tablets LD&HD Special Drug Use Surveillance: Long-term Use (12 Months) [NCT02016183]3,222 participants (Actual)Observational2009-04-01Completed
Cardiovascular and Metabolic Effects of Combination Therapy With Ramipril and Candesartan In Hypertensive Patients [NCT00356395]Phase 440 participants Interventional2003-08-31Completed
[NCT00360763]Phase 4600 participants InterventionalRecruiting
A Pilot, Proof of Concept, Placebo-controlled Trial of Candesartan as an Adjunctive Treatment for Bipolar Depression [NCT04430959]Early Phase 10 participants (Actual)Interventional2020-10-01Withdrawn(stopped due to The reason the study was withdrawn was due to lack of funds. In addition, the PI is moving to a different institution and it would not be feasible to proceed with the study under these circumstances.)
An Open-label, Multiple-dosing, Two-arm, One-sequence, Crossover Study to Evaluate the Safety and Pharmacokinetics After Oral Concurrent Administration of Amlodipine 10mg and Candesartan 32mg in Healthy Male Volunteers [NCT01926652]Phase 134 participants (Actual)Interventional2013-07-31Completed
The RAS, Fibrinolysis and Cardiopulmonary Bypass [NCT00607672]Phase 4111 participants (Actual)Interventional2006-08-31Completed
Pilot Study, Single-blind, Candesartan Versus Usual Care of Peripheral Neuropathy Development Induced by Vincristine (PNIV) in Patients Treated for Lymphoma B [NCT03688633]Phase 29 participants (Actual)Interventional2019-05-01Terminated(stopped due to Patient Recruitment Failure)
The Antihypertensives and Vascular, Endothelial and Cognitive Function Trial (AVEC Trial) [NCT00605072]Phase 253 participants (Actual)Interventional2008-01-31Completed
Pilot Study of Candesartan: An Angiotensin Receptor Blocker as a Treatment for Cocaine Dependence [NCT01938664]Phase 230 participants (Actual)Interventional2013-01-31Terminated(stopped due to Results of interim efficacy analysis showed results were not promising.)
A Randomised, Open-Label, Drug-Drug Interaction Study to Evaluate the Effect of Colestilan on the Pharmacokinetics of Single Oral Doses of Candesartan Cilexetil in Healthy Subjects [NCT01976572]Phase 118 participants (Actual)Interventional2013-10-31Completed
"Candesartan Cilexetil Tablets Specified Drug-use Survey Hypertension: Survey on Patients With Metabolic Syndrome" [NCT02166697]14,151 participants (Actual)Observational2006-06-30Completed
Multicenter, Open-Label, Long-Term Safety and Efficacy Study of the Fixed Dose Combination of Nifedipine Gastrointestinal Therapeutic System and Candesartan Cilexetil in Adult Subjects With Moderate to Severe Essential Hypertension [NCT01788358]Phase 3508 participants (Actual)Interventional2013-02-14Completed
Blopress Tablets Special Drug Use Surveillance 「Challenge - Quality Control」 [NCT02211638]18,113 participants (Actual)Observational2011-06-13Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00000620 (6) [back to overview]First Occurrence of a Major Cardiovascular Event (MCE); Specifically Nonfatal Heart Attack, Nonfatal Stroke, or Cardiovascular Death (Measured Throughout the Study) in the Glycemia Trial.
NCT00000620 (6) [back to overview]Death From Any Cause in the Glycemia Trial.
NCT00000620 (6) [back to overview]First Occurrence of Major Cardiovascular Event (MCE) in the Blood Pressure Trial.
NCT00000620 (6) [back to overview]First Occurrence of Major Cardiovascular Event (MCE) in the Lipid Trial.
NCT00000620 (6) [back to overview]First Occurrence of MCE or Revascularization or Hospitalization for Congestive Heart Failure (CHF) in Lipid Trial.
NCT00000620 (6) [back to overview]Stroke in the Blood Pressure Trial.
NCT00081731 (7) [back to overview]Stroke
NCT00081731 (7) [back to overview]Hospitalization for Congestive Heart Failure
NCT00081731 (7) [back to overview]Need for Renal Replacement Therapy
NCT00081731 (7) [back to overview]Myocardial Infarction
NCT00081731 (7) [back to overview]30% Reduction of eGFR From Baseline, Persisting for Greater Than or Equal to 60 Days
NCT00081731 (7) [back to overview]Cardiovascular or Renal Death
NCT00081731 (7) [back to overview]Composite Endpoint: Death From Cardiovascular or Renal Causes, Stroke, Myocardial Infarction, Hospitalization for CHF, Progressive Renal Insufficiency, or Permanent Renal Replacement Therapy
NCT00244621 (4) [back to overview]Mean Change From Baseline to Week 4 in Systolic Blood Pressure (SBP)
NCT00244621 (4) [back to overview]Change in Albumin/Creatinine (A/C) Ratio for Each Assigned Dose Level From Baseline to Day 28
NCT00244621 (4) [back to overview]Change in Protein/Creatinine (P/C) Ratio for Each Assigned Dose Level From Baseline to Day 28
NCT00244621 (4) [back to overview]Mean Change From Baseline to Week 4 in Diastolic Blood Pressure (DBP)
NCT00252694 (4) [back to overview]Number of Participants With at Least a 3 Step Improvement or a Persistent 2-step Improvement in the ETDRS Severity Scale.
NCT00252694 (4) [back to overview]Number of Participants With a 3-step or Greater Increase in Early Treatment of Diabetic Retinopathy Study (EDTRS) Severity Scale
NCT00252694 (4) [back to overview]Number of Participants With Incident Clinically Significant Macular Edema (CSME) and/or Proliferative Diabetic Retinopathy (PDR).
NCT00252694 (4) [back to overview]Rate of Change in Urinary Albumin Excretion Rate (UAER).
NCT00252720 (4) [back to overview]Number of Participants With a Regression of Diabetic Retinopathy.
NCT00252720 (4) [back to overview]Rate of Change in Urinary Albumin Excretion Rate (UAER).
NCT00252720 (4) [back to overview]Number of Participants With a 3-step or Greater Increase in Early Treatment of Diabetic Retinopathy Study (EDTRS) Severity Scale
NCT00252720 (4) [back to overview]Number of Participants With Incident Clinically Significant Macular Edema (CSME) and/or Proliferative Diabetic Retinopathy (PDR).
NCT00252733 (2) [back to overview]Number of Participants With a 2-step or Greater Increase in Early Treatment Diabetic Retinopathy Study (ETDRS) Severity Scale.
NCT00252733 (2) [back to overview]Rate of Change in Urinary Albumin Excretion Rate (UAER).
NCT00348686 (6) [back to overview]Percent Change of proBNP(B Type Natriuretic Peptides) in Patients Treated With Candesartan Only
NCT00348686 (6) [back to overview]Percent Change of proBNP(B Type Natriuretic Peptides) in Patients With Candesartan Plus Felodipine
NCT00348686 (6) [back to overview]Percent Change of B Type Natriuretic Peptides (BNP) Level
NCT00348686 (6) [back to overview]LVH(Left Ventricular Hypertrophy) Regression by Echocardiac Parameter, Left Ventricular Mass Index
NCT00348686 (6) [back to overview]Change of Systolic Blood Pressure (SBP)
NCT00348686 (6) [back to overview]Change of Diastolic Blood Pressure (DBP)
NCT00434967 (3) [back to overview]The Number of Patients With Controlled Sitting DBP and Sitting SBP in Each Treatment Group at the End of the Study
NCT00434967 (3) [back to overview]Change in Sitting Systolic Blood Pressure (SBP) From Baseline to the End of the Study (Baseline to 8 Weeks)
NCT00434967 (3) [back to overview]Change in Sitting Diastolic Blood Pressure (DBP) From Baseline to the End of the Study (From Baseline to 8 Weeks).
NCT00573430 (5) [back to overview]Estimated GFR Predicted From the Modification of Diet in Renal Disease (MDRD) Equation
NCT00573430 (5) [back to overview]Inflammatory Marker (Hs-C-peptide Reactive Protein)
NCT00573430 (5) [back to overview]The Change in Urinary Protein/Creatinine Ratio From Baseline to 28 Weeks
NCT00573430 (5) [back to overview]Treatment-emergent Adverse Events
NCT00573430 (5) [back to overview]Change of Systolic and Diastolic Blood Pressure From Baseline
NCT00605072 (5) [back to overview]Cognitive Assessment: Trail Making Test Part B
NCT00605072 (5) [back to overview]Cognitive Assessment: Hopkins Verbal Learning- Immediate Recall
NCT00605072 (5) [back to overview]Cognitive Assessment: Forward Digit Span Test
NCT00605072 (5) [back to overview]Blood Pressure Outcome: Systolic BP
NCT00605072 (5) [back to overview]Blood Flow Velocity, Sitting
NCT00607672 (13) [back to overview]Re-exploration for Bleeding
NCT00607672 (13) [back to overview]New Onset Atrial Fibrillation
NCT00607672 (13) [back to overview]Length of Hospital Stay
NCT00607672 (13) [back to overview]Blood Loss
NCT00607672 (13) [back to overview]Acute Kidney Injury
NCT00607672 (13) [back to overview]Vasopressor Drug Use
NCT00607672 (13) [back to overview]Tissue-type Plasminogen Activator (t-PA) Antigen Response
NCT00607672 (13) [back to overview]Plasminogen Activator Inhibitor-1 (PAI-1) Response
NCT00607672 (13) [back to overview]Interleukin-8 (IL-8) Response
NCT00607672 (13) [back to overview]Interleukin-6 (IL-6) Response
NCT00607672 (13) [back to overview]Interleukin-10 (IL-10) Response
NCT00607672 (13) [back to overview]Stroke
NCT00607672 (13) [back to overview]Blood Product Transfusion Requirement
NCT00621153 (1) [back to overview]Changes in Mean Sitting DBP From Baseline After 4 Weeks of Therapy
NCT00690612 (2) [back to overview]Mean Change From Baseline to Final Visit in Diastolic Blood Pressure (DBP).
NCT00690612 (2) [back to overview]Mean Change From Baseline to Final Visit in Systolic Blood Pressure (SBP).
NCT00867490 (12) [back to overview]Change in Mean Sitting Systolic Blood Pressure (msSBP) During the Core Phase of the Study
NCT00867490 (12) [back to overview]Change in Mean Sitting Systolic Blood Pressure (msSBP) During the Extension Phase of the Study
NCT00867490 (12) [back to overview]Change in Sitting Pulse Pressure During the Core Phase of the Study
NCT00867490 (12) [back to overview]Change in Sitting Pulse Pressure During the Extension Phase of the Study
NCT00867490 (12) [back to overview]Change in Sitting Pulse Rate During the Core Phase of the Study
NCT00867490 (12) [back to overview]Change in Sitting Pulse Rate During the Extension Phase of the Study
NCT00867490 (12) [back to overview]Percentage of Patients Who Achieved a Protocol-defined Blood Pressure Response During the Core Phase of the Study
NCT00867490 (12) [back to overview]Percentage of Patients Who Achieved a Protocol-defined Blood Pressure Response During the Core Phase of the Study
NCT00867490 (12) [back to overview]Percentage of Patients Who Achieved Normalized Blood Pressure During the Core Phase of the Study
NCT00867490 (12) [back to overview]Percentage of Patients Who Achieved Normalized Blood Pressure During the Core Phase of the Study
NCT00867490 (12) [back to overview]Change in Mean Sitting Diastolic Blood Pressure (msDBP) During the Core Phase of the Study
NCT00867490 (12) [back to overview]Change in Mean Sitting Diastolic Blood Pressure (msDBP) During the Extension Phase of the Study
NCT01025843 (4) [back to overview]Area Under the Plasma Concentration Versus Time Curve (AUC 0-infinity) of MK-5478 and Candesartan
NCT01025843 (4) [back to overview]Maximum Plasma Concentration (Cmax) of MK-5478 and Candesartan
NCT01025843 (4) [back to overview]Number of Participants Who Discontinued Treatment Due to an AE
NCT01025843 (4) [back to overview]Number of Participants With One or More Adverse Events (AEs)
NCT01052272 (7) [back to overview]Left Ventricular End Diastolic Volume Indexed to Body Surface Area (LVEDV/BSA)
NCT01052272 (7) [back to overview]Left Ventricular End Systolic Volume Indexed to Body Surface Area (LVESV/BSA)
NCT01052272 (7) [back to overview]Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume (LVED Mass/LVEDV)
NCT01052272 (7) [back to overview]Left Ventricular End-Diastolic Radius to Wall Thickness (LVED Radius/Wall Thickness)
NCT01052272 (7) [back to overview]LV End Systolic Maximum Shortening (LVES Max Shortening)
NCT01052272 (7) [back to overview]Peak Early Filling Rate Normalized to EDV
NCT01052272 (7) [back to overview]Left Ventricular Ejection Fraction (LVEF)
NCT01678794 (2) [back to overview]Change in Urinary Sodium Excretion
NCT01678794 (2) [back to overview]Change in Glomerular Filtration Rate
NCT01788358 (9) [back to overview]Number of Subjects With Clinically Relevant Changes in Laboratory Parameters
NCT01788358 (9) [back to overview]Number of Subjects With All Treatment-emergent Adverse Events (TEAEs) and Drug-related TEAEs up to Week 52/End of Study (EOS)
NCT01788358 (9) [back to overview]Number of Subjects With All Treatment-emergent Adverse Events (TEAEs) and Drug-related TEAEs up to Week 28
NCT01788358 (9) [back to overview]Change From Baseline In Mean Seated Systolic Blood Pressure (MSSBP) At Weeks 28 And 52
NCT01788358 (9) [back to overview]Change From Baseline in Mean Seated Diastolic Blood Pressure (MSDBP) at Weeks 28 and 52
NCT01788358 (9) [back to overview]Blood Pressure Response Rate at Weeks 28 and 52
NCT01788358 (9) [back to overview]Number of Subjects With Treatment-emergent Adverse Events (TEAEs) of Special Interest up to Week 28
NCT01788358 (9) [back to overview]Blood Pressure Control Rate at Weeks 28 and 52
NCT01788358 (9) [back to overview]Number of Subjects With Treatment-emergent Adverse Events (TEAEs) of Special Interest up to Week 52/End of Study (EOS)
NCT01794455 (2) [back to overview]Quick Inventory of Depressive Symptoms, Self-Rated (QIDS-SR16)
NCT01794455 (2) [back to overview]Montgomery-Asberg Depression Rating Scale
NCT01938664 (3) [back to overview]# of Participants Retained in Study
NCT01938664 (3) [back to overview]# of Participants With Presence of Cocaine Metabolites Via Urinalysis
NCT01938664 (3) [back to overview]# of Participants With Adverse Events
NCT01976572 (4) [back to overview]T1/2
NCT01976572 (4) [back to overview]Cmax of Candesartan
NCT01976572 (4) [back to overview]AUC0-t of Candesartan
NCT01976572 (4) [back to overview]Tmax
NCT01984164 (8) [back to overview]Memory
NCT01984164 (8) [back to overview]Attention Measured Using Digit Span Backward
NCT01984164 (8) [back to overview]Attention Measured Using Digit Span Forward
NCT01984164 (8) [back to overview]Cerebral Perfusion
NCT01984164 (8) [back to overview]Language
NCT01984164 (8) [back to overview]Executive Function
NCT01984164 (8) [back to overview]"NINDS-initiated EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research or EXAMINER Tool Box."
NCT01984164 (8) [back to overview]White Matter Lesion Volume
NCT02016183 (4) [back to overview]Changes From Baseline in Systolic Blood Pressure (SBP) at Each Time Point
NCT02016183 (4) [back to overview]Number of Participants Who Experience at Least One Adverse Drug Reactions (ADRs)
NCT02016183 (4) [back to overview]Changes From Baseline in Diastolic Blood Pressure (DBP) at Each Time Point
NCT02016183 (4) [back to overview]Changes From Baseline in Pulse Rate at Each Time Point
NCT02068495 (6) [back to overview]Changes From Baseline in Diastolic Blood Pressure (DBP) at Final Assessment
NCT02068495 (6) [back to overview]Changes From Baseline in Pulse Rate at Final Assessment
NCT02068495 (6) [back to overview]Changes From Baseline in Systolic Blood Pressure (SBP) at Final Assessment
NCT02068495 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Drug Reactions (ADRs)
NCT02068495 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Events
NCT02068495 (6) [back to overview]Percentage of Participants Who Meet Targeted Blood Pressure Level at Baseline and Final Assessment
NCT02166697 (6) [back to overview]Number of Participants Reporting One or More Adverse Drug Reactions (ADR)
NCT02166697 (6) [back to overview]Number of Participants Reporting One or More Serious Adverse Drug Reactions (SADR)
NCT02166697 (6) [back to overview]Incidence of Cerebrovascular/Cardiovascular Events
NCT02166697 (6) [back to overview]Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity + Blood Glucose Abnormalities + Lipid Abnormalities
NCT02166697 (6) [back to overview]Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity + Blood Glucose Abnormalities, Obesity + Lipid Abnormalities, or Blood Glucose Abnormalities + Lipid Abnormalities
NCT02166697 (6) [back to overview]Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity, Blood Glucose Abnormalities, or Lipid Abnormalities
NCT02211638 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Drug Reactions
NCT02211638 (6) [back to overview]Changes in Clinic Blood Pressure in the Sitting Position
NCT02211638 (6) [back to overview]Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Continued Candesartan Therapy at Week 14
NCT02211638 (6) [back to overview]Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to ARB Combination Drug Therapy at Week 14
NCT02211638 (6) [back to overview]Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to Calcium Channel Blocker (CCB)-Containing ARB Combination Drug Therapy at Week 14
NCT02211638 (6) [back to overview]Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to Diuretic-containing ARB Combination Drug Therapy at Week 14
NCT02332824 (5) [back to overview]Urine Albumin/Creatinine Ratio (UACR) at Each Assessment Point
NCT02332824 (5) [back to overview]Remission Rate From Early-Stage Nephropathy (Stage 2) to Pre-Nephropathy Stage (Stage 1) at the End of Treatment (Week 12)
NCT02332824 (5) [back to overview]Change From End of Pre-treatment Period (Week 0) in Log-transformed Urine Albumin/Creatinine Ratio (UACR) at the End of Treatment Period (Week 12)
NCT02332824 (5) [back to overview]Number of Participants Who Experience at Least One Treatment Emergent Adverse Event (TEAE)
NCT02332824 (5) [back to overview]Progression Rate From Early-Stage Nephropathy (Stage 2) to Overt Nephropathy (Stage 3) During the Treatment Period (Week 12)
NCT02646982 (22) [back to overview]Number of Participants Discontinuing Study Medication
NCT02646982 (22) [back to overview]Number of Participants With Hyperkalemia
NCT02646982 (22) [back to overview]Number of Participants With Elevated Serum Creatinine
NCT02646982 (22) [back to overview]Number of Participants With a Hypotensive Episode
NCT02646982 (22) [back to overview]EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research (EXAMINER) Toolbox Composite Score
NCT02646982 (22) [back to overview]Trail Making Test (TMT) Part B - A
NCT02646982 (22) [back to overview]Trail Making Test (TMT) Part B
NCT02646982 (22) [back to overview]Pulse Wave Velocity (PWV)
NCT02646982 (22) [back to overview]Hopkins Verbal Learning Test (HVLT) Delayed Recall Score
NCT02646982 (22) [back to overview]Hippocampal Volume
NCT02646982 (22) [back to overview]Global Standardized Uptake Value Ratio (SUVR) of [18F]T807
NCT02646982 (22) [back to overview]Global Standardized Uptake Value Ratio (SUVR) of (11)C-Pittsburgh Compound B ((11)C-PiB)
NCT02646982 (22) [back to overview]Clinical Dementia Rating (CDR) Score
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Total Tau Levels
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) of Tau Phosphorylated at Threonine 181 (p-tau181) Levels
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ42/Aβ40 Levels
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ42 Levels
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ40 Levels
NCT02646982 (22) [back to overview]Augmentation Index (AI)
NCT02646982 (22) [back to overview]Vasoreactivity
NCT02646982 (22) [back to overview]Number of Participants With Symptoms of Hypotension
NCT02646982 (22) [back to overview]Number of Participants With Hypotensive Episodes and Symptoms
NCT03640312 (17) [back to overview]Proportion of Patients With Adverse Event Free Hypertension Control
NCT03640312 (17) [back to overview]Rate of Adverse Events of Special Interest
NCT03640312 (17) [back to overview]Health-related Quality of Life
NCT03640312 (17) [back to overview]Proportion of Patients With Hypertension Control
NCT03640312 (17) [back to overview]Mean Diastolic Blood Pressure
NCT03640312 (17) [back to overview]Mean Systolic Blood Pressure
NCT03640312 (17) [back to overview]Medication Adherence
NCT03640312 (17) [back to overview]Number of Patients Requiring Step up Treatment
NCT03640312 (17) [back to overview]Percentage of Participants With Potentially Related Adverse Events
NCT03640312 (17) [back to overview]Percentage of Participants With Serious Adverse Events (SAEs)
NCT03640312 (17) [back to overview]Mean Change in Serum Sodium
NCT03640312 (17) [back to overview]Mean Change in Serum Potassium
NCT03640312 (17) [back to overview]Mean Change in Serum Creatinine
NCT03640312 (17) [back to overview]Mean Change in Blood Urea Nitrogen
NCT03640312 (17) [back to overview]Change in Mean Systolic Blood Pressure
NCT03640312 (17) [back to overview]Change in Mean Systolic Blood Pressure
NCT03640312 (17) [back to overview]Change in Mean Diastolic Blood Pressure

First Occurrence of a Major Cardiovascular Event (MCE); Specifically Nonfatal Heart Attack, Nonfatal Stroke, or Cardiovascular Death (Measured Throughout the Study) in the Glycemia Trial.

"Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. This was the primary outcome measure in all three trials: Glycemia (all participants), Blood Pressure (subgroup of participants not in Lipid Trial), and Lipid (subgroup of participants not in Blood Pressure Trial).~In the Glycemia Trial, a finding of higher mortality in the intensive arm group led to an early discontinuation of therapy after a mean of 3.5 years of follow-up. Intensive arm participants were transitioned to standard arm strategy over a period of 0.2 year and followed for an additional 1.2 years to the planned end of the Glycemia Trial while participating in one of the other sub-trials (BP or Lipid) to their planned completion." (NCT00000620)
Timeframe: 4.9 years

Interventionparticipants (Number)
Glycemia Trial: Intensive Control503
Glycemia Trial: Standard Control543

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Death From Any Cause in the Glycemia Trial.

"Time to death from any cause. Secondary measure for Glycemia Trial.~A finding of higher mortality in the intensive-therapy group led to an early discontinuation of therapy after a mean of 3.5 years of follow-up. Intensive arm participants were transitioned to standard arm strategy over a period of 0.2 year and followed for an additional 1.2 years to the planned end of the Glycemia Trial while participating in one of the other sub-trials (BP or Lipid)." (NCT00000620)
Timeframe: 4.9 years

Interventionparticipants (Number)
Glycemia Trial: Intensive Control391
Glycemia Trial: Standard Control327

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First Occurrence of Major Cardiovascular Event (MCE) in the Blood Pressure Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. Primary outcome for Blood Pressure Trial. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
BP Trial: Intensive Control208
BP Trial: Standard Control237

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First Occurrence of Major Cardiovascular Event (MCE) in the Lipid Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death in Lipid Trial participants. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
Lipid Trial: Fenofibrate291
Lipid Trial: Placebo310

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First Occurrence of MCE or Revascularization or Hospitalization for Congestive Heart Failure (CHF) in Lipid Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, cardiovascular death, revascularization procedure or hospitalization for CHF in Lipid Trial participants. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
Lipid Trial: Fenofibrate641
Lipid Trial: Placebo667

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Stroke in the Blood Pressure Trial.

Time to first occurrence of nonfatal or fatal stroke among participants in the BP Trial. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
BP Trial: Intensive Control36
BP Trial: Standard Control62

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Stroke

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy16
Stenting12

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Hospitalization for Congestive Heart Failure

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy26
Stenting27

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Need for Renal Replacement Therapy

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy3
Stenting4

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Myocardial Infarction

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy27
Stenting30

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30% Reduction of eGFR From Baseline, Persisting for Greater Than or Equal to 60 Days

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy77
Stenting68

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Cardiovascular or Renal Death

(NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy20
Stenting20

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Composite Endpoint: Death From Cardiovascular or Renal Causes, Stroke, Myocardial Infarction, Hospitalization for CHF, Progressive Renal Insufficiency, or Permanent Renal Replacement Therapy

Only the first event per participant is included in the composite (NCT00081731)
Timeframe: Measured at every 3 months for the first year and annually thereafter

Interventionparticipants (Number)
Optimal Medical Therapy169
Stenting161

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Mean Change From Baseline to Week 4 in Systolic Blood Pressure (SBP)

(NCT00244621)
Timeframe: From randomisation to end of double-blind treatment (4 weeks)

Interventionmm Hg (Mean)
Atacand .05 mg-6.0
Atacand .20 mg-8.9
Atacand .40 mg-12.0

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Change in Albumin/Creatinine (A/C) Ratio for Each Assigned Dose Level From Baseline to Day 28

(NCT00244621)
Timeframe: From randomisation to day 28

InterventionPercent change (Median)
Atacand .05 mg-11.1
Atacand .20 mg-40.6
Atacand .40 mg-50.0

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Change in Protein/Creatinine (P/C) Ratio for Each Assigned Dose Level From Baseline to Day 28

(NCT00244621)
Timeframe: From randomisation to day 28

InterventionPercent change (Median)
Atacand .05 mg0.0
Atacand .20 mg-29.2
Atacand .40 mg0.0

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Mean Change From Baseline to Week 4 in Diastolic Blood Pressure (DBP)

(NCT00244621)
Timeframe: From randomisation to end of double-blind treatment (4 weeks)

Interventionmm Hg (Mean)
Atacand .05 mg-5.2
Atacand .20 mg-7.9
Atacand .40 mg-11.1

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Number of Participants With at Least a 3 Step Improvement or a Persistent 2-step Improvement in the ETDRS Severity Scale.

3 steps were defined as either a 1-step change in one eye and a 2-step change in the other eye or as a 3-step change in one eye only. EDRTS is a scale with 11 steps (1-11). (NCT00252694)
Timeframe: From baseline to end of study, i.e. 5 years.

InterventionParticipants (Number)
Candesartan180
Placebo136

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Number of Participants With a 3-step or Greater Increase in Early Treatment of Diabetic Retinopathy Study (EDTRS) Severity Scale

3 steps were defined as either a 1-step change in one eye and a 2-step change in the other eye or as a 3-step change in one eye only. EDRTS is a scale with 11 steps (1-11). A generlized log-rank test was used to test difference between treatments. (NCT00252694)
Timeframe: From baseline to end of study, i.e. 5 years, with visits after a half year, one year and thereafter one visit per year.

InterventionParticipants (Number)
Candesartan161
Placebo182

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Number of Participants With Incident Clinically Significant Macular Edema (CSME) and/or Proliferative Diabetic Retinopathy (PDR).

Clinically Significant Macular Edema (CSME) and Proliferative Diabetic Retinopathy (PDR) are diagnosed via retinal photographs. (NCT00252694)
Timeframe: From baseline to end of study, i.e. 5 years.

InterventionParticipants (Number)
Candesartan192
Placebo193

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Rate of Change in Urinary Albumin Excretion Rate (UAER).

An estimate of the slope from fitting a linear regression of log(UAER) over time (post-randomisation, yearly assessments) for each patient. (NCT00252694)
Timeframe: From Baseline to end of study, i.e. 5 years.

Interventionlog (µg/min)/1000 year (Least Squares Mean)
Candesartan656
Placebo718

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Number of Participants With a Regression of Diabetic Retinopathy.

Regression of diabetic retinopathy was defined as at least a 3 step improvement or a persistent 2-step improvement (confirmed in 2 consecutive photography sets) in the Early Treatment of Diabetic Retinopathy Study (ETDRS) severity scale. 3 steps were defined as either a 1-step change in one eye and a 2-step change in the other eye or as a 3-step change in one eye only. EDRTS is a scale with 11 steps (1-11). (NCT00252720)
Timeframe: From baseline to the end of the study, i.e., 5 years

InterventionParticipants (Number)
Candesartan140
Placebo139

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Rate of Change in Urinary Albumin Excretion Rate (UAER).

An estimate of the slope from fitting a linear regression of log (UAER) over time (post-randimisation, yearly assessments) for each patient (NCT00252720)
Timeframe: From baseline to end of study, i.e. 5 years.

Interventionlog (µg/min)/year (Least Squares Mean)
Candesartan0.569
Placebo0.642

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Number of Participants With a 3-step or Greater Increase in Early Treatment of Diabetic Retinopathy Study (EDTRS) Severity Scale

Retinopathy progression was defined as the first occurrence of at least a 3-step increase in the ETDRS severity scale. 3 steps were defined as either a 1-step change in one eye and a 2-step change in the other eye or as a 3-step change in one eye only. EDRTS is a scale with 11 steps (1-11). A generlized log-rank test was used to test difference between treatments. (NCT00252720)
Timeframe: From baseline to end of study, i.e. 5 years, with visits after a half year, one year and thereafter one visit per year.

InterventionParticipants (Number)
Candesartan127
Placebo124

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Number of Participants With Incident Clinically Significant Macular Edema (CSME) and/or Proliferative Diabetic Retinopathy (PDR).

Clinically Significant Macular Edema (CSME) and Proliferative Diabetic Retinopathy (PDR) are diagnosed via retinal photographs. (NCT00252720)
Timeframe: From baseline to end of study, i.e. 5 years.

InterventionParticipants (Number)
Candesartan110
Placebo107

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Number of Participants With a 2-step or Greater Increase in Early Treatment Diabetic Retinopathy Study (ETDRS) Severity Scale.

Two steps were defined as either a 1-step change in each eye or as a 2-step change in one eye only. ETDRS is a scale with 11 steps (1-11, where a score of 1 represents no retinopathy and a score of 11 represents proliferative retinopathy). A generalized log-rank test was used to test difference between treatments. (NCT00252733)
Timeframe: From baseline to end of study, i.e. 5 years, with visits after a half year, one year and thereafter one visit per year.

InterventionParticipants (Number)
Candesartan178
Placebo217

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Rate of Change in Urinary Albumin Excretion Rate (UAER).

An estimate of the slope from fitting a linear regression of log(UAER) over time for each patient. (NCT00252733)
Timeframe: From baseline to end of study, i.e. 5 years.

Interventionlog (µg/min)/year (Least Squares Mean)
Candesartan0.510
Placebo0.543

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Percent Change of proBNP(B Type Natriuretic Peptides) in Patients Treated With Candesartan Only

Percent change of proBNP(B type Natriuretic Peptides) was calculated and collected through the way of Last Observational carried forward. (NCT00348686)
Timeframe: At Baseline and 24 weeks

Interventionpercent change (Median)
Candesartan-18.9

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Percent Change of proBNP(B Type Natriuretic Peptides) in Patients With Candesartan Plus Felodipine

Percent change of proBNP(B type Natriuretic Peptides) was calculated and collected through the way of Last Observational carried forward. (NCT00348686)
Timeframe: At Baseline and 24 weeks

Interventionpercent change (Median)
Candesartan-36.1

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Percent Change of B Type Natriuretic Peptides (BNP) Level

Change of B Type Natriuretic Peptides Level of the Subjects With Hypertension and Left Ventricular Hypertrophy (LVH) Treated With Candesartan Based Therapy for 24 Weeks was calculated just as the later time point minus the earlier time point. No specific calculation was used. (NCT00348686)
Timeframe: At Baseline and 24 weeks

InterventionPercent Change (Median)
Candesartan-29.2

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LVH(Left Ventricular Hypertrophy) Regression by Echocardiac Parameter, Left Ventricular Mass Index

Change of Left Ventricular Hypertrophy(LVH) by Echocardiac Parameter, Left Ventricular mass Index (LVMI) was calculated and collected through the way of Last Observational carried forward. LVH/Index was calculated like this: Divide LV mass with Body Surface Area. (NCT00348686)
Timeframe: At Baseline and 24 weeks

Interventiong/m^2 (Median)
Candesartan-10.90

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Change of Systolic Blood Pressure (SBP)

Change of Systolic Blood Pressure was calculated and collected through the way of Last Observational carried forward. (NCT00348686)
Timeframe: At Baseline and 24 weeks

InterventionmmHg (Median)
Candesartan-32.0

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Change of Diastolic Blood Pressure (DBP)

"Change of Diastolic Blood Pressure was calculated and collected through the way of Last Observational carried forward.~Only who has diastolic blood pressure data both baseline and follow up was analyzed. Most of patient who enrolled, 302 have a data." (NCT00348686)
Timeframe: At Baseline and 24 weeks

InterventionmmHg (Median)
Candesartan-20.0

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The Number of Patients With Controlled Sitting DBP and Sitting SBP in Each Treatment Group at the End of the Study

Controlled sitting SBP and sitting DBP are defined as having sitting SBP < 140 mmHg and sitting DBP < 90 mmHg at the end of the study (NCT00434967)
Timeframe: 8 weeks

Interventionparticipants (Number)
Placebo8
Candesartan 32 mg198
HCT 25 mg168
Candesartan/HCT 32/25 mg304

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Change in Sitting Systolic Blood Pressure (SBP) From Baseline to the End of the Study (Baseline to 8 Weeks)

Change (reduction) in sitting SBP at the end of the study, when compared to sitting SBP at baseline. (NCT00434967)
Timeframe: 8 weeks

Interventionmm Hg (Least Squares Mean)
Placebo-3.7
Candesartan 32 mg-13.1
HCT 25 mg-11.6
Candesartan/HCT 32/25 mg-21.4

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Change in Sitting Diastolic Blood Pressure (DBP) From Baseline to the End of the Study (From Baseline to 8 Weeks).

Change (reduction) in sitting DBP at the end of the study, when compared to sitting DBP at baseline. (NCT00434967)
Timeframe: 8 weeks

Interventionmm Hg (Least Squares Mean)
Placebo-3.3
Candesartan 32 mg-9.3
HCT 25 mg-7.7
Candesartan/HCT 32/25 mg-13.9

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Estimated GFR Predicted From the Modification of Diet in Renal Disease (MDRD) Equation

GFR (mL/min/1.73 m2) = 186 x (Scr)-1.154 x (Age)-0.203 x (0.742 if female) x (1.210 if African-American) (conventional units) (NCT00573430)
Timeframe: 28 weeks

InterventionmL/min/1.73 m2 (Mean)
Candesartan 8 mg1.28
Candesartan 16mg1.20
Candesartan 32mg0.56

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Inflammatory Marker (Hs-C-peptide Reactive Protein)

To evaluate how to reduce and relate with cardiovascular risk (NCT00573430)
Timeframe: baseline to 28 weeks

Interventionmg/dL (Mean)
Candesartan 8 mg0.01
Candesartan 16mg-0.17
Candesartan 32mg-0.01

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The Change in Urinary Protein/Creatinine Ratio From Baseline to 28 Weeks

Decrease of urinary protein/creatinine ratio means improvement of renal disease. (NCT00573430)
Timeframe: baseline to 28 weeks

Interventionmg/g (Mean)
Candesartan 8 mg794.0
Candesartan 16mg639.9
Candesartan 32mg819.0

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Treatment-emergent Adverse Events

Prevalence of adverse events after treatment regardless causality. An adverse event is the development of an undesirable medical condition or the deterioration of a pre-existing medical condition from the signing of the informed consent, whether or not considered causally related to the product. (NCT00573430)
Timeframe: Baseline to 28 weeks

InterventionParticipants (Number)
Candesartan 8 mg28
Candesartan 16mg27
Candesartan 32mg25

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Change of Systolic and Diastolic Blood Pressure From Baseline

(NCT00573430)
Timeframe: baseline to 28 weeks

,,
InterventionmmHg (Mean)
SystolicDiastolic
Candesartan 16mg-13.30-8.00
Candesartan 32mg-16.10-13.00
Candesartan 8 mg-11.70-8.90

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Cognitive Assessment: Trail Making Test Part B

This test requires the connection of sequentially numbered circles (A), and the connection of circles marked by numbers and letters in alternating sequence (B). This test is considered a benchmark of executive function. The test score is the time required to complete the task in seconds. (NCT00605072)
Timeframe: Baseline-12 months

Interventionseconds (Least Squares Mean)
ACEI (Lisinopril)-14
ARB (Candesartan)17
HCTZ4

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Cognitive Assessment: Hopkins Verbal Learning- Immediate Recall

This is a 12-item list learning test in which individuals are presented three learning and recall trials followed by a delayed recall and 24 item recognition test. The HVLT-R has been identified as an ideal memory measure for elderly patients, and appropriate reliability and validity have been shown in older individuals. The test score is the number of correct answers in the delayed recall ( score range 0-12) (NCT00605072)
Timeframe: Baseline-12 months

Interventionnumber words remembered (Least Squares Mean)
ACEI (Lisinopril)-1
ARB (Candesartan)-2
HCTZ-3

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Cognitive Assessment: Forward Digit Span Test

This test consists of series of digits of increasing length, some of which are recited as presented, and some of which are to be recited in reversed order. The forward digit span score ranges from 0 (ie cannot repeat two digits) to 8 ( participant can repeat up to 8 digits) (NCT00605072)
Timeframe: Baseline-12 months

Interventionnumber of digits repeated (Least Squares Mean)
ACEI (Lisinopril)-0.3
ARB (Candesartan)0.02
HCTZ-0.04

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Blood Pressure Outcome: Systolic BP

Blood pressure was measured as follows: the participant was in the sitting position, rested for 5 minutes, no caffeine or smoking 2 hours prior to measurement, using appropriate cuff size (covering 60% of upper arm length and 80% of arm circumference), correct cuff placement (1-2 inches above brachial pulse on bare arm), and the bell of the stethoscope. The systolic blood pressure was defined as the pressure corresponding to the first korotkoff sounds (K1) and the diastolic as the pressure corresponding to the last korotkoff sound (K5). Blood pressure was measured in both arms and recorded (NCT00605072)
Timeframe: Baseline-12 months

Interventionmm Hg (Least Squares Mean)
ACEI (Lisinopril)28
ARB (Candesartan)27
HCTZ21

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Blood Flow Velocity, Sitting

This reports the change in the least square mean from baseline to 12 months, adjusted for age (NCT00605072)
Timeframe: Baseline-12 months

Interventioncm/sec (Least Squares Mean)
ACEI (Lisinopril)-0.3
ARB (Candesartan)-2.85
HCTZ0.35

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Re-exploration for Bleeding

The percentage of patients that were taken back to the operating room for re-exploration because of bleeding (NCT00607672)
Timeframe: From arrival in intensive care unit until discharge from hospital

Interventionpercentage of patients (Number)
Placebo3.6
Ramipril (ACEI)8.3
Candesartan (ARB)4.5

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New Onset Atrial Fibrillation

New onset atrial fibrillation based on electrocardiogram (ECG) rhythm strips with a duration longer than 10 seconds (NCT00607672)
Timeframe: From arrival in intensive care unit until discharge from hospital

Interventionpercentage of patients (Number)
Placebo17.9
Ramipril (ACEI)16.7
Candesartan (ARB)27.3

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Length of Hospital Stay

(NCT00607672)
Timeframe: From the start of surgery until discharge from hospital

Interventiondays (Mean)
Placebo7.7
Ramipril (ACEI)6.3
Candesartan (ARB)8.1

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Blood Loss

Blood loss over 24 hours as measured by chest tube output (NCT00607672)
Timeframe: First 24 hours after arrival in the intensive care unit

InterventionmL (Mean)
Placebo437
Ramipril (ACEI)470
Candesartan (ARB)511

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Acute Kidney Injury

Acute kidney injury (AKI) was defined according to Acute Kidney Injury Network (AKIN) criteria,specifically any increase in subject serum creatinine concentration of 50% or 0.3 mg/dL (26.5 umol/L) within 72 hours of surgery. (NCT00607672)
Timeframe: From the start of surgery until postoperative day 3

Interventionpercentage of patients (Number)
Placebo28.6
Ramipril (ACEI)23.8
Candesartan (ARB)36.4

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Vasopressor Drug Use

(NCT00607672)
Timeframe: From the end of cardiopulmonary bypass until arrival in intensive care unit

,,
Interventionpercentage of patients (Number)
DobutamineMlrinoneNorepinephrineEpinephrine
Candesartan (ARB)27.322.795.513.6
Placebo35.725.085.77.1
Ramipril (ACEI)29.225.079.24.3

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Tissue-type Plasminogen Activator (t-PA) Antigen Response

To compare the effects of angiotensin II type I (AT1) receptor antagonism or angiotensin-converting enzyme (ACE) inhibition versus placebo on the fibrinolytic responses to cardiopulmonary bypass (CPB) as measured by t-PA antigen response (NCT00607672)
Timeframe: From the start of surgery until postoperative day 2

,,
Interventionng/mL (Mean)
Pre CPB60min of CPBPost surgeryPostoperative day 1Postoperative day 2
Candesartan (ARB)11.9724.8931.4715.7512.89
Placebo14.3627.6534.5620.2516.56
Ramipril (ACEI)14.0536.6741.1117.1012.49

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Plasminogen Activator Inhibitor-1 (PAI-1) Response

To compare the effects of AT1 receptor antagonism or ACE inhibition versus placebo on the fibrinolytic responses to CPB as measured by PAI-1 response (NCT00607672)
Timeframe: From the start of surgery until postoperative day 2

,,
Interventionng/mL (Mean)
Pre CPB60min of CPBPost surgeryPostoperative day 1Postoperative day 2
Candesartan (ARB)18.2824.1949.1021.7013.4
Placebo15.1420.4339.6931.8321.59
Ramipril (ACEI)16.2519.4141.6226.2717.33

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Interleukin-8 (IL-8) Response

To compare the effects of AT1 receptor antagonism or ACE inhibition versus placebo on the inflammatory response to CPB as measured by IL-8 (NCT00607672)
Timeframe: From the start of surgery until postoperative day 2

,,
Interventionpg/mL (Mean)
Pre CPBPost surgeryPostoperative day 1Postoperative day 2
Candesartan (ARB)13.3876.7637.1137.77
Placebo16.1866.4446.1834.39
Ramipril (ACEI)11.8680.0737.3928.06

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Interleukin-6 (IL-6) Response

To compare the effects of AT1 receptor antagonism or ACE inhibition versus placebo on the inflammatory response to CPB as measured by IL-6 (NCT00607672)
Timeframe: From the start of surgery until postoperative day 2

,,
Interventionpg/mL (Mean)
Pre CPBPost surgeryPostoperative day 1Postoperative day 2
Candesartan (ARB)6.44144.76218.16243.72
Placebo6.29116.04224.96166.96
Ramipril (ACEI)9.33167.51172.65144.67

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Interleukin-10 (IL-10) Response

To compare the effects of AT1 receptor antagonism or ACE inhibition versus placebo on the inflammatory response to CPB as measured by the IL-10 response (NCT00607672)
Timeframe: From the start of surgery until postoperative day 2

,,
Interventionpg/mL (Mean)
Pre CPBPost surgeryPostoperative day 1Postoperative day 2
Candesartan (ARB)4.21749.5622.5514.26
Placebo4.45461.9030.7016.74
Ramipril (ACEI)5.36815.7426.8914.59

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Stroke

New onset neurological deficit with a duration of longer than 24 hours (NCT00607672)
Timeframe: From arrival in intensive care unit until discharge from hospital

Interventionpercentage of patients (Number)
Placebo7.1
Ramipril (ACEI)4.2
Candesartan (ARB)4.5

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Blood Product Transfusion Requirement

Percentage of patients that received blood product transfusion (NCT00607672)
Timeframe: From the start of surgery until discharge from hospital

,,
Interventionpercentage of patients (Number)
Packed red blood cellsPlasmaPlateletsCryoprecipitate
Candesartan (ARB)2.731.822.74.5
Placebo67.960.746.47.1
Ramipril (ACEI)62.529.229.24.2

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Changes in Mean Sitting DBP From Baseline After 4 Weeks of Therapy

Mean of the changed DBP from baseline after 4 weeks (NCT00621153)
Timeframe: 4 weeks

InterventionmmHg (Least Squares Mean)
Candesartan Cilexetil/Hydroclorozide Combination Therapy-17.0
Candesartan Cilexetil Monotherapy-14.1

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Mean Change From Baseline to Final Visit in Diastolic Blood Pressure (DBP).

Blood pressure response was defined as Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) less than the 95th percentile based on population height-adjusted charts for age and gender. Response rates were based on the proportion of patients meeting the criteria at each evaluation time point or the last available measure. (NCT00690612)
Timeframe: every 3 months - baseline to final visit

Interventionmm Hg (Mean)
Atacand Candesartan Cilexetil-0.43

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Mean Change From Baseline to Final Visit in Systolic Blood Pressure (SBP).

Blood pressure response was defined as Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) less than the 95th percentile based on population height-adjusted charts for age and gender. Response rates were based on the proportion of patients meeting the criteria at each evaluation time point or the last available measure. (NCT00690612)
Timeframe: Every 3 months- baseline to final visit

InterventionMillimeters of Mercury (mm Hg) (Mean)
Atacand Candesartan Cilexetil-2.86

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Change in Mean Sitting Systolic Blood Pressure (msSBP) During the Core Phase of the Study

The arm in which the highest sitting diastolic pressures were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, systolic/diastolic blood pressure were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionmmHg (Mean)
Phase 2 - Aliskiren+HCTZ-2.81

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Change in Mean Sitting Systolic Blood Pressure (msSBP) During the Extension Phase of the Study

The arm in which the highest sitting diastolic pressures were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, systolic/diastolic blood pressure were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionmmHg (Mean)
Phase III - Aliskiren+HCTZ+Amlodipine-9.20

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Change in Sitting Pulse Pressure During the Core Phase of the Study

Pulse pressure is systolic pressure (SP) minus diastolic pressure (DP). The arm in which the highest sitting DPs were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, SP and DP were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionmmHg (Mean)
Phase 2 - Aliskiren+HCTZ0.31

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Change in Sitting Pulse Pressure During the Extension Phase of the Study

Pulse pressure is systolic pressure (SP) minus diastolic pressure (DP). The arm in which the highest sitting DPs were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, SP and DP were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionmmHg (Mean)
Phase III - Aliskiren+HCTZ+Amlodipine-3.33

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Change in Sitting Pulse Rate During the Core Phase of the Study

Pulse rate was measured once for 30 seconds just prior to blood pressure measurements in the sitting position. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionBPM (beats per minute) (Mean)
Phase 2 - Aliskiren+HCTZ0.27

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Change in Sitting Pulse Rate During the Extension Phase of the Study

Pulse rate was measured once for 30 seconds just prior to blood pressure measurements in the sitting position. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionBPM (beats per minute) (Mean)
Phase III - Aliskiren+HCTZ+Amlodipine0.03

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Percentage of Patients Who Achieved a Protocol-defined Blood Pressure Response During the Core Phase of the Study

Blood pressure response was defined as msSBP < 140 mmHg or a 20 mmHg decrease in msSBP at the end of Phase 2 compared to Baseline in Phase 2 or a msDBP < 90 mmHg or a 10 mmHg decrease in msDBP at the end of Phase 2 compared to Baseline in Phase 2. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionPercentage of patients (Number)
msSBP responsemsDBP response
Phase 2 - Aliskiren+HCTZ37.434.1

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Percentage of Patients Who Achieved a Protocol-defined Blood Pressure Response During the Core Phase of the Study

Blood pressure response was defined as msSBP < 140 mmHg or a 20 mmHg decrease in msSBP at the end of Phase 2 compared to Baseline in Phase 2 or a msDBP < 90 mmHg or a 10 mmHg decrease in msDBP at the end of Phase 2 compared to Baseline in Phase 2. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionPercentage of patients (Number)
msSBP responsemsDBP response
Phase III - Aliskiren+HCTZ+Amlodipine54.147.5

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Percentage of Patients Who Achieved Normalized Blood Pressure During the Core Phase of the Study

Normalized blood pressure was defined as a msSBP < 140 mmHg and/or a msDBP < 90 mmHg. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionPercentage of patients (Number)
msSBP < 140 mmHgmsDBP < 90 mmHg
Phase 2 - Aliskiren+HCTZ37.433.3

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Percentage of Patients Who Achieved Normalized Blood Pressure During the Core Phase of the Study

Normalized was defined as a msSBP < 140 mm Hg and/or a msDBP < 90 mm Hg. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionPercentage of patients (Number)
msSBP < 140 mmHgmsDBP < 90 mmHg
Phase III - Aliskiren+HCTZ+Amlodipine54.144.3

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Change in Mean Sitting Diastolic Blood Pressure (msDBP) During the Core Phase of the Study

The arm in which the highest sitting diastolic pressures were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, systolic/diastolic blood pressure were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 2 to end of Phase 2

InterventionmmHg (Mean)
Phase 2 - Aliskiren+HCTZ-3.12

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Change in Mean Sitting Diastolic Blood Pressure (msDBP) During the Extension Phase of the Study

The arm in which the highest sitting diastolic pressures were found at study entry was the arm used for all subsequent readings. A calibrated sphygmomanometer and appropriate size cuff were used to measure arterial sitting blood pressure (BP) at trough with the arm supported at the level of the heart. At each study visit, after having the patient in a sitting position for at least 5 minutes, systolic/diastolic blood pressure were measured 3 times at 1-2 minute intervals. A mean was calculated from the 3 measurements. A negative change indicates improvement. (NCT00867490)
Timeframe: Baseline Phase 3 to end of Phase 3

InterventionmmHg (Mean)
Phase III - Aliskiren+HCTZ+Amlodipine-5.87

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Area Under the Plasma Concentration Versus Time Curve (AUC 0-infinity) of MK-5478 and Candesartan

Blood was collected at the following time points: pre-dose, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 36, and 48 hours post-dose in order to measure AUC 0-infinity of MK-5478 and Candesartan (NCT01025843)
Timeframe: Pre-dose and up to 48 hours postdose

Interventionumol.hr/L (Mean)
MK-5478 1 mg0.236
MK-5478 2 mg0.494
MK-5478 5 mg1.87
MK-5478 8 mg1.80
MK-5478 12 mg1.36
MK-5478 18 mg2.23
MK-5478 24 mg3.15
MK-5478 38 mg4.50
MK-5478 2 mg - Fed0.504
Candesartan 32 mg5.89
Candesartan 32 mg - Fed4.46

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Maximum Plasma Concentration (Cmax) of MK-5478 and Candesartan

Blood was collected at the following time points: pre-dose, 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 16, 24, 36, and 48 hours post-dose in order to measure the Cmax of MK-5478 and Candesartan (NCT01025843)
Timeframe: Pre-dose and up to 48 hours postdose

Interventionµmol/L (Mean)
MK-5478 1 mg0.0291
MK-5478 2 mg0.0573
MK-5478 5 mg0.254
MK-5478 8 mg0.227
MK-5478 12 mg0.120
MK-5478 18 mg0.245
MK-5478 24 mg0.321
MK-5478 38 mg0.532
MK-5478 2 mg - Fed0.0553
Candesartan 32 mg0.476
Candesartan 32 mg - Fed0.451

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Number of Participants Who Discontinued Treatment Due to an AE

An AE is any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the SPONSOR's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the SPONSOR's product, is also an AE. (NCT01025843)
Timeframe: Up to 24 hours after administration of study drug

InterventionParticipants (Number)
MK-5478 1 mg0
MK-5478 2 mg0
MK-5478 5 mg0
MK-5478 8 mg0
MK-5478 12 mg0
MK-5478 18 mg0
MK-5478 24 mg0
MK-5478 38 mg0
MK-5478 2 mg - Fed0
Candesartan 32 mg0
Candesartan 32 mg - Fed0
Candesartan Placebo0
MK-5478 Placebo0

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Number of Participants With One or More Adverse Events (AEs)

An AE is any unfavorable and unintended change in the structure, function, or chemistry of the body temporally associated with the use of the SPONSOR's product, whether or not considered related to the use of the product. Any worsening (i.e., any clinically significant adverse change in frequency and/or intensity) of a preexisting condition which is temporally associated with the use of the SPONSOR's product, is also an AE. (NCT01025843)
Timeframe: Up to 14 days after administration of last dose of study drug (up to Day 52)

InterventionParticipants (Number)
MK-5478 1 mg5
MK-5478 2 mg3
MK-5478 5 mg3
MK-5478 8 mg4
MK-5478 12 mg4
MK-5478 18 mg3
MK-5478 24 mg2
MK-5478 38 mg2
MK-5478 2 mg - Fed1
Candesartan 32 mg9
Candesartan 32 mg - Fed0
Candesartan Placebo1
MK-5478 Placebo6

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Left Ventricular End Diastolic Volume Indexed to Body Surface Area (LVEDV/BSA)

LVEDV/BSA: As an indicator of heart size, the blood volume of the heart is related to the body size. The relation of heart blood volume to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventionml/m^2 (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil78.0678.6093.5785.4490.2082.74NA84.2876.65
Candesartan Cilexetil and Allopurinol79.0378.01NA79.7563.184.9575.2779.7275.05
Ramipril73.0374.1073.2375.3481.1975.2871.9970.4648.68
Ramipril and Allopurinol78.5286.13NA83.95108.2567.96NA71.63NA

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Left Ventricular End Systolic Volume Indexed to Body Surface Area (LVESV/BSA)

LVESV/BSA: The end systolic volume is the blood volume of the heart at the end of contraction and is an index of the pump function of the heart. This relation to body size is more accurate in determining pathology because larger people require a larger heart blood volume. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventionml/m^2 (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month 12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil35.2635.2653.8742.2754.0437.76NA41.7235.13
Candesartan Cilexetil and Allopurinol39.4934.15NA36.0728.7437.1832.9935.9934.22
Ramipril36.2034.7725.6436.8239.4235.3035.2331.1723.98
Ramipril and Allopurinol37.9142.88NA42.3470.4830.39NA31.56NA

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Left Ventricular End-diastolic Mass Indexed to Left Ventricular End-diastolic Volume (LVED Mass/LVEDV)

LVED Mass/LVEDV: As an indicator of heart muscle mass and heart blood volume, the mass indexed to end diastolic volume determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a three-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventiong/ml (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month 12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil0.950.830.670.780.700.79NA0.800.64
Candesartan Cilexetil and Allopurinol0.870.82NA0.860.680.800.690.820.69
Ramipril0.920.870.750.840.810.790.950.840.93
Ramipril and Allopurinol0.860.71NA0.720.570.83NA0.80NA

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Left Ventricular End-Diastolic Radius to Wall Thickness (LVED Radius/Wall Thickness)

LVED Radius/Wall thickness As an indicator of heart muscle mass and heart volume chamber diameter, the end-diastolic radius indexed to end diastolic wall thickness determines whether there is an adequate amount of heart muscle to pump the heart blood volume obtained from a two-dimensional analysis. The values that are too high or too low indicate a diseased myocardium. This is a measure of LV Geometry. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventionunitless (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month 12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil3.143.394.143.684.103.71NA3.584.04
Candesartan Cilexetil and Allopurinol3.453.63NA3.423.903.564.243.564.29
Ramipril3.233.323.423.433.443.602.923.463.12
Ramipril and Allopurinol3.574.04NA4.014.573.60NA3.61NA

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LV End Systolic Maximum Shortening (LVES Max Shortening)

By identifying three points in three different planes in the heart muscle, the maximum shortening is the average of the difference between the distance between these three points at the end of filling of the heart and the end of contraction divided by the length at the end of filling times 100. The maximum shortening is a three dimensional analysis. The higher values indicate a healthy heart. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventionpercent of length at end of filling (Mean)
Month 0 (n=17,17,17,18)Month 6(n=14,11,10,12)Month 9(n=1,2,0,0)Month 12(n=11,11,10,10)Month 15(n=3,2,1,1)Month 18(n=10,12,7,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil16.6817.5019.0817.1316.2817.55NA16.6220.38
Candesartan Cilexetil and Allopurinol16.0018.50NA18.5116.3617.5217.8917.8516.59
Ramipril15.8116.8818.4314.5717.0617.2616.6815.6713.70
Ramipril and Allopurinol15.8418.72NA17.9614.2217.46NA17.52NA

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Peak Early Filling Rate Normalized to EDV

The Peak Early Filling Rate Normalized to EDV is calculated from the slope of the volume during the early filling of the heart with respect to time. The higher values indicate a very healthy heart muscle and lower values are indicative of a very stiff muscle. This is a measure of LV Diastolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes. (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Intervention1/sec (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month 12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil2.012.021.131.901.481.93NA1.651.10
Candesartan Cilexetil and Allopurinol2.01.98NA1.772.282.052.501.822.15
Ramipril1.931.742.501.802.021.911.692.051.34
Ramipril and Allopurinol2.112.03NA1.931.561.89NA1.88NA

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Left Ventricular Ejection Fraction (LVEF)

LVEF is a calculation of heart pump function determined from the volume after complete filling minus the volume after complete contraction divided by the volume after complete filling. A value of 55% or greater is normal. This is a measure of LV Systolic Function. Since some visits did not occur at the scheduled 6 month intervals, the results have been divided into 3-month visit intervals for reporting purposes (NCT01052272)
Timeframe: 5 visits per Participant over 2 years (about every 6 months)

,,,
Interventionpercent (Mean)
Month 0 (n=17,17,18,18)Month 6(n=14,11,11,12)Month 9(n=1,2,0,0)Month 12(n=12,11,11,11)Month 15(n=3,2,1,1)Month 18(n=10,12,8,8)Month 21(n=3,0,0,1)Month 24 (n=11,9,8,10)Month 27 (n=1,1,0,1)
Candesartan Cilexetil56.3656.8242.6252.3739.8856.33NA51.7054.17
Candesartan Cilexetil and Allopurinol52.6857.28NA56.1154.4657.8256.1755.7954.40
Ramipril52.1954.2064.9852.7652.1355.0251.2757.1850.73
Ramipril and Allopurinol53.3752.80NA51.7434.8954.05NA55.59NA

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Change in Urinary Sodium Excretion

Urinary sodium excretion correlates with elevated blood pressure in subjects at low cardiovascular risk. The body continually monitors blood volume and sodium concentration. When either becomes too high, sensors in the heart, blood vessels, and kidneys detect the increases and stimulate the kidneys to increase sodium excretion, thus returning blood volume to normal. Measured as mEq/min (NCT01678794)
Timeframe: baseline to 3 months

InterventionmEq/min (Median)
Candesartan-8.50
Placebo10.00

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Change in Glomerular Filtration Rate

Glomerular Filtration Rate estimates how much blood passes through the glomeruli each minute. Glomeruli are the tiny filters in the kidneys that filter waste from the blood. Measured as ml/min/1.73 m2 (NCT01678794)
Timeframe: baseline to 3 months

Interventionml/min/1.73 m2 (Median)
Candesartan-5
Placebo1.00

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Number of Subjects With Clinically Relevant Changes in Laboratory Parameters

Laboratory evaluations of blood and urine samples were performed, including hematology (hematocrit, hemoglobin, red blood cells count, white blood cells count, neutrophils, lymphocytes, monocytes, eosinophils, basophils, platelets), blood chemistry (sodium, potassium, chloride, bicarbonate, uric acid, total protein, albumin, calcium, blood urea nitrogen, creatinine, aspartate transaminase, alanine transaminase, lactate dehydrogenase, gamma glutamyl transferase, alkaline phosphatase, creatine kinase, total bilirubin, direct bilirubin, total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, triglycerides, fasting glucose), urinalysis (pH, blood, specific gravity, glucose, protein, cells/sediment). A laboratory test abnormality considered clinically relevant, for example, causing withdrawal by subject, requiring treatment or causing apparent clinical manifestations, or judged relevant by the investigator, were reported as AEs. (NCT01788358)
Timeframe: Baseline (Week 0) up to Week 52/EOS

InterventionSubjects (Number)
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)0

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Change From Baseline In Mean Seated Systolic Blood Pressure (MSSBP) At Weeks 28 And 52

(NCT01788358)
Timeframe: Baseline (Week 0), Weeks 28 and 52

Interventionmillimeter of mercury (mmHg) (Mean)
BaselineChange at Week 28Change at Week 52
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)170.7-30.4-30.1

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Change From Baseline in Mean Seated Diastolic Blood Pressure (MSDBP) at Weeks 28 and 52

(NCT01788358)
Timeframe: Baseline (Week 0), Weeks 28 and 52

Interventionmillimeter of mercury (mmHg) (Mean)
BaselineChange at Week 28Change at Week 52
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)95.6-12.7-12.8

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Blood Pressure Response Rate at Weeks 28 and 52

Response rate was defined as the percentage of subjects who achieved a systolic blood pressure response (MSSBP of <140 mmHg or a reduction of MSSBP of more than (>) 20 mmHg from baseline value), or a diastolic blood pressure response (MSDBP of <90 mmHg or a reduction of MSDBP of >10 mmHg from baseline value). (NCT01788358)
Timeframe: Weeks 28 and 52

Interventionpercentage of subjects (Number)
Week 28Week 52
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)86.686.2

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Number of Subjects With Treatment-emergent Adverse Events (TEAEs) of Special Interest up to Week 28

An AE is any untoward medical occurrence (that is, any unfavorable and unintended sign [including abnormal laboratory findings], symptom or disease) in a subject or clinical investigation subject after providing written informed consent for participation in the study. AEs were considered to be treatment-emergent if they had started or worsened after first application of study medication. TEAEs of special interest included the incidence of symptomatic hypotension and the incidence and severity of vasodilatory adverse events (such as oedema, headache, and flushing). Only subjects who had TEAEs of special interest as mild, moderate or severe were reported. (NCT01788358)
Timeframe: From the time of first study drug administration up to Week 28

InterventionSubjects (Number)
Oedema (mild)Oedema (moderate)Oedema (severe)Headache (mild)Headache (moderate)Flushing (mild)Symptomatic hypotension (mild)
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)124547311534

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Blood Pressure Control Rate at Weeks 28 and 52

Control rate was defined as the percentage of subjects that reached a predetermined blood pressure (BP) target of BP less than (<) 140/90 mmHg. (NCT01788358)
Timeframe: Weeks 28 and 52

Interventionpercentage of subjects (Number)
Week 28Week 52
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)51.451.6

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Number of Subjects With Treatment-emergent Adverse Events (TEAEs) of Special Interest up to Week 52/End of Study (EOS)

An AE is any untoward medical occurrence (that is, any unfavorable and unintended sign [including abnormal laboratory findings], symptom or disease) in a subject or clinical investigation subject after providing written informed consent for participation in the study. AEs were considered to be treatment-emergent if they had started or worsened after first application of study medication. TEAEs of special interest included the incidence of symptomatic hypotension and the incidence and severity of vasodilatory adverse events (such as oedema, headache, and flushing). Only subjects who had TEAEs of special interest as mild, moderate or severe were reported. (NCT01788358)
Timeframe: From the time of study treatment up to Week 52/EOS

InterventionSubjects (Number)
Oedema (mild)Oedema (moderate)Oedema(severe)Headache (mild)Headache (moderate)Flushing (mild)Symptomatic hypotension (mild)
Nifedipine GITS/Candesartan Cilexetil FDC (BAY98-7106)131567311734

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Quick Inventory of Depressive Symptoms, Self-Rated (QIDS-SR16)

Self-report measure of depression severity (range 0 - 27, higher scores indicate more severe depressive symptoms). This applies to the candesartan Phase 2 arm. (NCT01794455)
Timeframe: Week 20

Interventionunits on a scale (Number)
Phase 2: Candesartan11

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Montgomery-Asberg Depression Rating Scale

MADRS is a measure of depression severity (range 0 - 60, higher scores indicate more severe depressive symptoms). This outcome applies to the candesartan Phase 2 arm. (NCT01794455)
Timeframe: Week 20

Interventionunits on a scale (Number)
Phase 2: Candesartan22

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# of Participants Retained in Study

(NCT01938664)
Timeframe: 8 weeks

Interventionparticipants (Number)
Candesartan w Cognitive Behavior Therapy5
Placebo w Cognitive Behavior Therapy0

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# of Participants With Presence of Cocaine Metabolites Via Urinalysis

(NCT01938664)
Timeframe: thrice weekly, baseline thru week 8

Interventionparticipants (Number)
Candesartan w Cognitive Behavior Therapy20
Placebo w Cognitive Behavior Therapy10

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# of Participants With Adverse Events

Candesartan will be well tolerated without significant side effects. (NCT01938664)
Timeframe: 8 weeks

Interventionparticipants (Number)
Candesartan w Cognitive Behavior Therapy0
Placebo w Cognitive Behavior Therapy0

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T1/2

Apparent plasma terminal elimination half-life (NCT01976572)
Timeframe: 0, 1, 2, 3, 4, 5, 6, 8, 12, 24, 36, and 48 hours post-dose

Interventionhr (Mean)
Candesartan Alone13.50
T-1hr9.61
T0hr10.44
T+3hr10.01

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Cmax of Candesartan

Maximum observed plasma concentration (NCT01976572)
Timeframe: 0, 1, 2, 3, 4, 5, 6, 8, 12, 24, 36, and 48 hours post-dose

Interventionng/mL (Mean)
Candesartan Alone106.7
T-1hr94.7
T0hr42.8
T+3hr99.5

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AUC0-t of Candesartan

Area under the plasma concentration-time curve from time zero up to the last quantifiable time-point (NCT01976572)
Timeframe: 0, 1, 2, 3, 4, 5, 6, 8, 12, 24, 36, and 48 hours post-dose

Interventionng*hr/mL (Mean)
Candesartan Alone1118
T-1hr826
T0hr494
T+3hr759

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Tmax

Time of maximum observed plasma concentration (NCT01976572)
Timeframe: 0, 1, 2, 3, 4, 5, 6, 8, 12, 24, 36, and 48 hours post-dose

Interventionhr (Median)
Candesartan Alone3.00
T-1hr3.00
T0hr5.05
T+3hr2.05

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Memory

To assess episodic memory, the Hopkins Verbal Learning Test-Revised (HVLT-R) will be used. The retention (%) score is calculated by dividing the delayed recall trial by the higher of 3 learning trials. Each trial scores 0 (min) to 12 (max). The HVLT-R retention score is a percentage, and a higher percentage represents a better outcome. (NCT01984164)
Timeframe: 12 months

Interventionpercentage of retention (Least Squares Mean)
Candesartan82.71
Lisinopril79.47

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Attention Measured Using Digit Span Backward

The Digit Span test is a subtest of both the Wechsler Adult Intelligence Scale (WAIS) and the Wechsler Memory Scales (WMS). For the digit span backwards, subjects are read a sequence of numbers and asked to repeat the same sequence back to the examiner in reverse order (backward span). Backward span is an executive task particularly dependent on working memory. The Digit Span backward is scored for backwards performance. Scale: 0 (minimum) to 16 (maximum). A higher score represents a better outcome. (NCT01984164)
Timeframe: 12 months

InterventionNumber of correct responses (Least Squares Mean)
Candesartan5.14
Lisinopril5.16

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Attention Measured Using Digit Span Forward

This will be measured using Digit Span Forward. The Digit Span test is a subtest of both the Wechsler Adult Intelligence Scale (WAIS) and the Wechsler Memory Scales (WMS). For the digit span forward, subjects are read a sequence of numbers and asked to repeat the same sequence back to the examiner in the correct order (forward span). Forward span captures attention efficiency and capacity. The Digit Span forward is scored for forwards performance. Scale: 0 (minimum) to 16 (maximum). A higher score represents a better outcome. (NCT01984164)
Timeframe: 12 months

InterventionNumber of correct responses (Least Squares Mean)
Candesartan9.67
Lisinopril8.93

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Cerebral Perfusion

ASL-MRI: Arterial Spin Labeling (ASL) MRI is non-invasive measure of perfusion that does not require contrast, and allows multiple brain regions mapping of perfusion and reserve. ASL-MRI provides measures of cerebral blood flow (CBF). Higher values indicates higher CBF. (NCT01984164)
Timeframe: 12 months

Interventionml/100g/min (Least Squares Mean)
Candesartan45.48
Lisinopril47.65

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Language

This will be measured using the Boston Naming Test. BNT is a neuropsychological test used to assess visual confrontation naming and language performance in participants with cognitive decline. Its short 15-item version consists of drawings of objects ranging from common objects to less familiar objects. Scale: 0 (min score) to 15 (max score). For this test, a higher score/response represents a better outcome. (NCT01984164)
Timeframe: 12 months

Interventionnumber of correct responses (Least Squares Mean)
Candesartan13.42
Lisinopril13.84

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Executive Function

Executive function will be assessed using Trail Making Test (part B-A). Part A was collected to correct for motor speed and visual-perceptual demands on TMT by subtracting completion time for TMT Part A from completion time for Part B (TMT B - A). TMT Part B-A provides a relatively purer measure of executive functioning. It has a timed scale from 0 sec (min) to 300 secs (max). Along this scale, a lower score is better. (NCT01984164)
Timeframe: 12 months

Interventionseconds (Least Squares Mean)
Candesartan87.23
Lisinopril111.37

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"NINDS-initiated EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research or EXAMINER Tool Box."

"EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research or EXAMINER tool box. This test batteryThe battery includes 11 tasks that generate 15 primary variables. Within this set, the EXAMINER includes: working memory, inhibition, set shifting, and fluency. The parts of EXAMINER that were used for this study include: Flanker task (inhibition) which involves responding to a central stimulus while ignoring flanking stimuli that are either compatible or incompatible with the central stimulus; Set-shifting, a measure of mental flexibility; Spatial 1-Back test assesses spatial working memory; Dot Counting test assesses verbal working memory; Verbal Fluency tested using a List Generation test which require the participant to generate words beginning with a specific letter, and category fluency in which the participant generates words from a specified category (e.g., animals, fruits). Higher are reflective of better executive function (-1 to +1)" (NCT01984164)
Timeframe: 12 months

Interventionunits on a scale (Least Squares Mean)
Candesartan0.07
Lisinopril0.25

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White Matter Lesion Volume

White Matter Lesion volume: high-resolution anatomical images are acquired for the measurement of microvascular disease. WMH volumes will be obtained from Fluid attenuated inversion recovery (FLAIR) imaging sequence and reported as total volume (in mm3). Higher values means greater WMH (NCT01984164)
Timeframe: 12 months

Interventionmm^3 (Least Squares Mean)
Candesartan2.68
Lisinopril5.73

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Changes From Baseline in Systolic Blood Pressure (SBP) at Each Time Point

Reported data are changes in SBP from baseline at Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and final assessment. (NCT02016183)
Timeframe: Baseline, and Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and Final assessment (up to 12 months)

InterventionmmHg (Mean)
Change in SBP at Month 1Change in SBP at Month 2Change in SBP at Month 3Change in SBP at Month 4Change in SBP at Month 5Change in SBP at Month 6Change in SBP at Month 7Change in SBP at Month 8Change in SBP at Month 9Change in SBP at Month 10Change in SBP at Month 11Change in SBP at Month 12Change in SBP at Final
Candesartan Cilexetil/Hydrochlorothiazide-13.3-14.8-15.4-15.7-15.6-16.1-15.8-15.8-16.4-16.6-17.0-18.1-17.5

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Number of Participants Who Experience at Least One Adverse Drug Reactions (ADRs)

ADRs are defined as adverse events (AEs) which are in the investigator's opinion of causal relationship to the study treatment. AEs are defined as any unfavorable and unintended signs, symptoms or diseases temporally associated with the use of a medicinal product reported from the first dose of study drug to the last dose of study drug. (NCT02016183)
Timeframe: Up to 12 months

InterventionParticipants (Count of Participants)
Candesartan Cilexetil/Hydrochlorothiazide283

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Changes From Baseline in Diastolic Blood Pressure (DBP) at Each Time Point

Reported data are changes in DBP from baseline at Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and final assessment. (NCT02016183)
Timeframe: Baseline, and Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and Final assessment (up to 12 months)

InterventionmmHg (Mean)
Change in DBP at Month 1Change in DBP at Month 2Change in DBP at Month 3Change in DBP at Month 4Change in DBP at Month 5Change in DBP at Month 6Change in DBP at Month 7Change in DBP at Month 8Change in DBP at Month 9Change in DBP at Month 10Change in DBP at Month 11Change in DBP at Month 12Change in DBP at Final
Candesartan Cilexetil/Hydrochlorothiazide-6.5-7.3-7.6-7.8-7.8-8.0-8.1-8.2-8.5-8.7-8.5-9.1-8.5

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Changes From Baseline in Pulse Rate at Each Time Point

Reported data are changes in Pulse Rate from baseline at Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and final assessment. (NCT02016183)
Timeframe: Baseline, and Month 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, and Final assessment (up to 12 months)

InterventionBeats per minutes (Mean)
Change in Pulse Rate at Month 1Change in Pulse Rate at Month 2Change in Pulse Rate at Month 3Change in Pulse Rate at Month 4Change in Pulse Rate at Month 5Change in Pulse Rate at Month 6Change in Pulse Rate at Month 7Change in Pulse Rate at Month 8Change in Pulse Rate at Month 9Change in Pulse Rate at Month 10Change in Pulse Rate at Month 11Change in Pulse Rate at Month 12Change in Pulse Rate at Final assessment
Candesartan Cilexetil/Hydrochlorothiazide-1.3-1.1-1.3-1.5-1.3-1.5-1.1-1.5-1.6-1.7-1.5-1.8-1.6

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Changes From Baseline in Diastolic Blood Pressure (DBP) at Final Assessment

Reported data are changes in DBP from baseline at final assessment (up to 12 months). (NCT02068495)
Timeframe: Baseline and final assessment (up to 12 Months)

InterventionmmHg (Mean)
Candesartan Cilexetil/Amlodipine-7.2

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Changes From Baseline in Pulse Rate at Final Assessment

Reported data are changes in Pulse Rate from baseline at final assessment (up to 12 months). (NCT02068495)
Timeframe: Baseline and final assessment (up to 12 Months)

InterventionBeats per minute (Mean)
Candesartan Cilexetil/Amlodipine-1.2

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Changes From Baseline in Systolic Blood Pressure (SBP) at Final Assessment

Reported data are changes in SBP from baseline at final assessment (up to 12 months). (NCT02068495)
Timeframe: Baseline and final assessment (up to 12 Months)

InterventionmmHg (Mean)
Candesartan Cilexetil/Amlodipine-14.6

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Number of Participants Who Experience at Least One Adverse Drug Reactions (ADRs)

ADRs are defined as adverse events (AEs) which are in the investigator's opinion of causal relationship to the study treatment. AEs are defined as any unfavorable and unintended signs, symptoms or diseases temporally associated with the use of a medicinal product reported from the first dose of study drug to the last dose of study drug. (NCT02068495)
Timeframe: Up to 12 Months

InterventionParticipants (Count of Participants)
Candesartan Cilexetil/Amlodipine85

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Number of Participants Who Experience at Least One Adverse Events

(NCT02068495)
Timeframe: Up to 12 Months

InterventionParticipants (Count of Participants)
Candesartan Cilexetil/Amlodipine286

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Percentage of Participants Who Meet Targeted Blood Pressure Level at Baseline and Final Assessment

Reported data are percentage of participants who meet targeted blood pressure level at baseline and final assessment in analysis population. Targeted blood pressure level of SBP/DBP was less than 140/90 mmHg. (NCT02068495)
Timeframe: Baseline and final assessment (up to 12 Months)

InterventionPercentage of Participants (Number)
BaselineFinal Assessment
Candesartan Cilexetil/Amlodipine28.566.9

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Number of Participants Reporting One or More Adverse Drug Reactions (ADR)

ADR are defined as adverse events (AEs) which are in the investigator's opinion of causal relationship to the study treatment. AEs are defined as any unfavorable and unintended signs, symptoms or diseases temporally associated with the use of a medicinal product reported from the first dose of study drug to the last dose of study drug. (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionParticipants (Number)
Candesartan Cilexetil230

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Number of Participants Reporting One or More Serious Adverse Drug Reactions (SADR)

SADR are defined as serious adverse events (SAEs) which are in the investigator's opinion of causal relationship to the study treatment. SADR was an ADR resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionParticipants (Number)
Candesartan Cilexetil320

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Incidence of Cerebrovascular/Cardiovascular Events

Cerebrovascular/cardiovascular events reported to be associated with Blopress were reported. The composite events classified under primary major adverse cardiac Events (MACE) 1 and primary MACE2 were defined as: MACE1: sudden death, cerebral hemorrhage, cerebral infarction, subarachnoid hemorrhage, and acute myocardial infarction; MACE2: MACE1 + hospitalization for cardiac failure and intervention/hospitalization for angina pectoris. Renal events include (transition to dialysis + renal transplant). (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionNumber of events per 1,000 person-years (Number)
Sudden DeathCerebral HemorrhageCerebral InfarctionSubarachnoid HemorrhageAcute Myocardial InfarctionHospitalization for Heart FailureIntervention/Hospitalization for Angina PectorisAtrial FibrillationTransition to DialysisRenal TransplantDissecting Aortic AneurysmDiabetic RetinopathyNew-Onset DiabetesPrimary MACEPrimary MACE 2Renal Events
Candesartan Cilexetil0.240.572.340.150.990.271.741.350.300.000.060.154.354.296.290.30

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Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity + Blood Glucose Abnormalities + Lipid Abnormalities

Participants reporting cerebrovascular/cardiovascular events who had obesity, blood glucose and lipid abnormalities associated with Blopress at the time of enrollment were reported. The composite events classified under primary MACE1 and primary MACE2 were defined as: MACE1: sudden death, cerebral hemorrhage, cerebral infarction, subarachnoid hemorrhage, and acute myocardial infarction; MACE2: MACE1 + hospitalization for cardiac failure and intervention/hospitalization for angina pectoris. Renal events include (transition to dialysis + renal transplant). (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionNumber of events/1,000 person-years (Number)
Sudden DeathCerebral HemorrhageCerebral InfarctionSubarachnoid HemorrhageAcute Myocardial InfarctionHospitalization for Heart FailureIntervention/Hospitalization for Angina PectorisAtrial FibrillationTransition to DialysisRenal TransplantDissecting Aortic AneurysmDiabetic RetinopathyNew-Onset DiabetesPrimary MACEPrimary MACE 2Renal Events
Candesartan Cilexetil0.350.813.480.231.280.352.781.970.700.000.120.355.226.149.270.70

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Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity + Blood Glucose Abnormalities, Obesity + Lipid Abnormalities, or Blood Glucose Abnormalities + Lipid Abnormalities

Participants reporting cerebrovascular/cardiovascular events who had multiple underlying risk factors which included either obesity + blood glucose abnormalities, obesity + lipid abnormalities OR blood glucose + lipid abnormalities associated with Blopress at the time of enrollment were reported. The composite events classified under primary MACE1 and primary MACE2 were defined as: MACE1: sudden death, cerebral hemorrhage, cerebral infarction, subarachnoid hemorrhage, and acute myocardial infarction; MACE2: MACE1 + hospitalization for cardiac failure and intervention/hospitalization for angina pectoris. Renal events include (transition to dialysis + renal transplant). (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionNumber of events/1,000 person-years (Number)
Sudden DeathCerebral HemorrhageCerebral InfarctionSubarachnoid HemorrhageAcute Myocardial InfarctionHospitalization for heart FailureIntervention/Hospitalization for Angina PectorisAtrial FibrillationTransition to DialysisRenal TransplantDissecting Aortic AneurysmDiabetic RetinopathyNew-Onset DiabetesPrimary MACEPrimary MACE 2Renal Events
Candesartan Cilexetil0.200.532.190.131.060.331.331.460.070.000.070.074.514.115.770.07

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Incidence of Cerebrovascular/Cardiovascular Events Affected by Underlying Risk Factors of Obesity, Blood Glucose Abnormalities, or Lipid Abnormalities

Participants reporting cerebrovascular/cardiovascular events who had either obesity, blood glucose abnormalities, or lipid abnormalities as any one of the underlying risk factors associated with Blopress at the time of enrollment were reported.The composite events classified under primary MACE1 and primary MACE2 were defined as: MACE1: sudden death, cerebral hemorrhage, cerebral infarction, subarachnoid hemorrhage, and acute myocardial infarction; MACE2: MACE1 + hospitalization for cardiac failure and intervention/hospitalization for angina pectoris. Renal events include (transition to dialysis + renal transplant). (NCT02166697)
Timeframe: Baseline up to 3 years

InterventionNumber of events/1,000 person-years (Number)
Sudden DeathCerebral HemorrhageCerebral InfarctionSubarachnoid HemorrhageAcute Myocardial InfarctionHospitalization for Heart FailureIntervention/Hospitalization for Angina PectorisAtrial FibrillationTransition to DialysisRenal TransplantDissecting Aortic AneurysmDiabetic RetinopathyNew-Onset DiabetesPrimary MACEPrimary MACE 2Renal Events
Candesartan Cilexetil0.210.411.550.100.620.101.450.620.310.000.000.103.322.904.450.31

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Number of Participants Who Experience at Least One Adverse Drug Reactions

Adverse drug reactions are defined as adverse events (AEs) which are in the investigator's opinion of causal relationship to the study treatment. AEs are defined as any unfavorable and unintended signs, symptoms or diseases temporally associated with the use of a medicinal product reported from the first dose of study drug to the last dose of study drug. Among these, events which are considered possibly associated with a medicinal product are defined as adverse drug reactions. (NCT02211638)
Timeframe: Up to Month 3

InterventionParticipants (Count of Participants)
Candesartan Cilexetil 4 mg to 8 mg132

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Changes in Clinic Blood Pressure in the Sitting Position

Changes in clinic blood pressure (systolic blood pressure -SBP and diastolic blood pressure -DBP) in the sitting position measured at Month 3, last dose of candesartan (up to Month 6) relative to baseline were reported. (NCT02211638)
Timeframe: Baseline, Month 3 and Last dose of Candesartan (up to Month 6)

InterventionmmHg (Mean)
Month 3, SBPLast Dose of Candesartan, SBPMonth 3, DBPLast Dose of Candesartan, DBP
Candesartan Cilexetil 4 mg to 8 mg-20.1-18.1-10.4-9.3

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Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Continued Candesartan Therapy at Week 14

Changes in clinic blood pressure (systolic blood pressure -SBP and diastolic blood pressure -DBP) in the sitting position measured at Month 3, last dose of candesartan (up to Month 6) relative to baseline in only participants who continued candesartan therapy at Week 14 were reported. (NCT02211638)
Timeframe: Baseline, Month 3 and Last dose of Candesartan (up to Month 6)

InterventionmmHg (Mean)
Month 3, SBPLast Dose of Candesartan, SBPMonth 3, DBPLast Dose of Candesartan, DBP
Candesartan Cilexetil 4 mg to 8 mg-19.8-19.5-10.1-10.0

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Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to ARB Combination Drug Therapy at Week 14

Changes in clinic blood pressure (systolic blood pressure -SBP and diastolic blood pressure -DBP) in the sitting position measured at Month 3, last dose of candesartan and last dose of ARB Combination Drug (up to Month 6) relative to baseline were reported. The data was for only participants who switched to ARB combination drug therapy from candesartan therapy at Week 14 as part of routine medical care. (NCT02211638)
Timeframe: Baseline, Month 3, Last dose of Candesartan, and Last dose of ARB Combination Drug (up to Month 6)

InterventionmmHg (Mean)
Month 3, SBPLast Dose of Candesartan, SBPLast dose of ARB Combination Drug, SBPMonth 3, DBPLast Dose of Candesartan, DBPLast dose of ARB Combination Drug, DBP
Candesartan Cilexetil 4 mg to 8 mg-21.7-12.3-26.4-11.8-6.4-14.4

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Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to Calcium Channel Blocker (CCB)-Containing ARB Combination Drug Therapy at Week 14

Changes in clinic blood pressure (systolic blood pressure -SBP and diastolic blood pressure -DBP) in the sitting position measured at last dose of ARB combination drug (up to Month 6) relative to baseline were reported. The data was for only participants who switched to calcium channel blocker (CCB)-containing ARB combination drug therapy from candesartan therapy at Week 14 as part of routine medical care. (NCT02211638)
Timeframe: Baseline and Last dose of ARB Combination Drug (up to Month 6)

InterventionmmHg (Mean)
SBPDBP
Candesartan Cilexetil 4 mg to 8 mg-26.9-14.7

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Changes in Clinic Blood Pressure in the Sitting Position for Participants Who Switched to Diuretic-containing ARB Combination Drug Therapy at Week 14

Changes in clinic blood pressure (systolic blood pressure -SBP and diastolic blood pressure -DBP) in the sitting position measured at last dose of diuretic-containing ARB combination drug (up to Month 6) relative to baseline were reported. The data was for only participants who switched to diuretic-containing ARB combination drug therapy from candesartan therapy at Week 14 as part of routine medical care. (NCT02211638)
Timeframe: Baseline and Last dose of ARB Combination Drug (up to Month 6)

InterventionmmHg (Mean)
SBPDBP
Candesartan Cilexetil 4 mg to 8 mg-24.5-13.2

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Urine Albumin/Creatinine Ratio (UACR) at Each Assessment Point

The first morning void urine (the first urine immediately after rising prior to activities in standing position in the morning) samples on the day of each visit, and 1 day and 2 days before the day of each visit (3 consecutive days) were collected to calculate UACR. Reported data is geometric mean ratio of UACR at each assessment point relative to Baseline. (NCT02332824)
Timeframe: Weeks 2, 4, 8, 12, follow-up (Week 14) and End of Treatment

,,,,,
Interventionmg/gCr (Geometric Mean)
Week 2Week 4Week 8Week 12Follow-up (Week 14)End of treatment
Candesartan Cilexetil 8 mg0.760.720.710.700.850.69
Placebo1.041.031.071.131.111.15
TAK-272 20 mg0.800.800.750.710.950.72
TAK-272 40 mg0.730.660.630.610.800.62
TAK-272 5 mg0.840.820.850.850.920.85
TAK-272 80 mg0.720.710.620.590.860.61

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Remission Rate From Early-Stage Nephropathy (Stage 2) to Pre-Nephropathy Stage (Stage 1) at the End of Treatment (Week 12)

Remission rate is defined as percentage of participants who have UACR <30 mg/gCr and whose UACR decreased by ≥30% from the value at the end of the pre-treatment period (Week 0). (NCT02332824)
Timeframe: Week 12

Interventionpercentage of participants (Number)
Placebo0.0
TAK-272 5 mg9.0
TAK-272 20 mg9.5
TAK-272 40 mg17.9
TAK-272 80 mg24.6
Candesartan Cilexetil 8 mg14.3

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Change From End of Pre-treatment Period (Week 0) in Log-transformed Urine Albumin/Creatinine Ratio (UACR) at the End of Treatment Period (Week 12)

The first morning void urine (the first urine immediately after rising prior to activities in standing position in the morning) samples on the day of each visit, and 1 day and 2 days before the day of each visit (3 consecutive days) were collected to calculate UACR. (NCT02332824)
Timeframe: Week 0 and Week 12

Interventionlog (mg/gCr) (Least Squares Mean)
Placebo0.152
TAK-272 5 mg-0.173
TAK-272 20 mg-0.317
TAK-272 40 mg-0.478
TAK-272 80 mg-0.497
Candesartan Cilexetil 8 mg-0.377

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Number of Participants Who Experience at Least One Treatment Emergent Adverse Event (TEAE)

An Adverse Event (AE) is defined as any untoward medical occurrence in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. A treatment-emergent adverse event (TEAE) is defined as an adverse event with an onset that occurs after receiving study drug. (NCT02332824)
Timeframe: Up to Week 14

InterventionParticipants (Count of Participants)
Placebo28
TAK-272 5 mg22
TAK-272 20 mg26
TAK-272 40 mg28
TAK-272 80 mg36
Candesartan Cilexetil 8 mg30

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Progression Rate From Early-Stage Nephropathy (Stage 2) to Overt Nephropathy (Stage 3) During the Treatment Period (Week 12)

Progression rate is defined as percentage of participants who have UACR ≥300 mg/gCr and whose UACR increased by ≥30% from the value at the end of the pre-treatment period [Week 0]. Meanwhile, the definition of transition to overt nephropathy also includes the case that UACR decreased to <300 mg/gCr after the transition to overt nephropathy. (NCT02332824)
Timeframe: Week 12

Interventionpercentage of participants (Number)
Placebo18.2
TAK-272 5 mg3.0
TAK-272 20 mg0.0
TAK-272 40 mg0.0
TAK-272 80 mg0.0
Candesartan Cilexetil 8 mg1.4

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Number of Participants Discontinuing Study Medication

The number of participants who discontinued the study medication is presented here. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan0
Placebo1

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Number of Participants With Hyperkalemia

The levels of potassium were obtained from blood samples. Hyperkalemia is defined as potassium levels >5.9 milliequivalent per deciliter (meq/dL). Hyperkalemia is an indication of kidney dysfunction. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan0
Placebo1

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Number of Participants With Elevated Serum Creatinine

The levels of creatinine were obtained from blood samples. Elevated serum creatinine is defined as levels >2.5 milligram per deciliter (mg/dL). Elevated serum creatinine is indicative of decreased renal function. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan0
Placebo0

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Number of Participants With a Hypotensive Episode

Hypotension is defined as blood pressure <100/40 mm Hg. Blood pressure was measured according to the American Heart Association guidelines with the subject in the sitting position and rested for 5 minutes. An appropriate cuff size (covering 60% of upper arm length and 80% of arm circumference) was used and correct cuff placement (1-2 inches above the brachial pulse on bare arm) was ensured. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan16
Placebo4

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EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research (EXAMINER) Toolbox Composite Score

The EXAMINER toolbox battery includes 11 tasks that generate 15 primary variables. Within this set, the EXAMINER includes working memory, inhibition, set shifting, and fluency. The parts of EXAMINER that were used for this study include: Flanker task (inhibition) which involves responding to a central stimulus while ignoring flanking stimuli that are either compatible or incompatible with the central stimulus; Set-shifting, a measure of mental flexibility; Spatial 1-Back test assesses spatial working memory; Dot Counting test assesses verbal working memory; Verbal Fluency tested using a List Generation test which require the participant to generate words beginning with a specific letter, and category fluency in which the participant generates words from a specified category (e.g., animals, fruits). A composite score is calculated where scores range from -1 to +1 and higher are reflective of better executive function. (NCT02646982)
Timeframe: Baseline, Month 6, Month 12

,
Interventionscore on a scale (Least Squares Mean)
BaselineMonth 6Month 12
Candesartan0.030.180.07
Placebo-0.050.04-0.06

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Trail Making Test (TMT) Part B - A

In Parts A and B of the TMT, participants connect circles labeled with numbers, in ascending order. The score is the amount of time (in seconds) it takes for the participant to complete the task. The TMT Part A score reflects visuoperceptual abilities, and subtracting the score for Part A from the score from Part B (Part B-A, in seconds) provides a more accurate assessment of executive function. A lower score indicates greater executive function. (NCT02646982)
Timeframe: Baseline, Month 6, Month 12

,
Interventionseconds (Least Squares Mean)
BaselineMonth 6Month 12
Candesartan108.0881.59103.64
Placebo91.56102.38103.50

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Trail Making Test (TMT) Part B

The Trail Making Test assesses executive function. In Part B of the TMT participants connect circles labeled with letters and numbers, in ascending order. The score is the amount of time it takes for the participant to complete the task. The average time is 75 seconds and times greater than 273 seconds indicate a deficit with executive function. (NCT02646982)
Timeframe: Baseline, Month 6, Month 12

,
Interventionseconds (Least Squares Mean)
BaselineMonth 6Month 12
Candesartan149.44122.04148.06
Placebo142.93152.91152.96

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Pulse Wave Velocity (PWV)

Arterial stiffness was assessed by Pulse Wave Velocity (PWV). PWV is calculated as PWV=distance (d)/time (t) and the unit of measure is reported as meters per second (m/s). Lower values indicate a preferable measurement of arterial stiffness. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionm/s (Least Squares Mean)
BaselineMonth 12
Candesartan7.817.71
Placebo8.738.14

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Hopkins Verbal Learning Test (HVLT) Delayed Recall Score

The Hopkins Verbal Learning Test (HVLT) is used to assess memory domains. Participants are read a list of 12 words and are asked to recall as many as they can remember. This is repeated for 3 trials followed by a 20 minute delay, and then participants are asked to recall as many words as they can. The delayed recall score ranges from 0 to 12 and higher scores indicate better memory. (NCT02646982)
Timeframe: Baseline, Month 6, Month 12

,
Interventionnumber of words recalled (Least Squares Mean)
BaselineMonth 6Month 12
Candesartan4.835.405.10
Placebo5.295.085.39

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Hippocampal Volume

Structural MRI images were acquired in order to assess hippocampal volume. Decreased hippocampal volume suggests neurodegenerative changes (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionmm^3 (Mean)
BaselineMonth 12
Candesartan6949.826761.12
Placebo6662.216521.30

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Global Standardized Uptake Value Ratio (SUVR) of [18F]T807

In-vivo tau-PET imaging was conducted using the radiotracer [18F]T807. SUVR is a ratio of PET uptake measured in the brain region of interest and a disease free reference region. A higher SUVR is an indication of increased PET radiotracer uptake and worsening disease. (NCT02646982)
Timeframe: Baseline, 12 Months

,
InterventionRatio of target and reference regions (Mean)
BaselineMonth 12
Candesartan1.331.34
Placebo1.361.34

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Global Standardized Uptake Value Ratio (SUVR) of (11)C-Pittsburgh Compound B ((11)C-PiB)

In-vivo amyloid imaging with positron emission tomography (PET) was conducted after intravenous administration of 15±1.5 millicurie (mCi) of the radiotracer (11)C-PiB. SUVR is a ratio of PET uptake measured in the brain region of interest and a disease free reference region. A higher SUVR is an indication of increased PET radiotracer uptake and worsening disease. (NCT02646982)
Timeframe: Baseline, 12 Months

,
InterventionRatio of target and reference regions (Mean)
BaselineMonth 12
Candesartan1.321.34
Placebo1.421.46

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Clinical Dementia Rating (CDR) Score

The CDR rates each of the six general domains involving memory, orientation, judgment and problem-solving, community affairs, home and hobbies, and personal care. An overall score, ranging from 0 to 3, can be calculated. A score of 0 = normal, 0.5 = very mild dementia, 1 = mild dementia, 2 = moderate dementia, and 3 = severe dementia. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionscore on a scale (Least Squares Mean)
BaselineMonth 12
Candesartan1.862.18
Placebo1.852.21

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Cerebrospinal Fluid (CSF) Total Tau Levels

CSF total tau (t-tau) levels were analyzed from CSF samples obtained via lumbar puncture. Normal values for t-tau are < 450 pg/ml. Elevated levels of t-tau indicate worsening disease. (NCT02646982)
Timeframe: Baseline, Month 12

,
InterventionPicograms per milliliter (pg/ml) (Least Squares Mean)
Baseline Total TauMonth 12 Total Tau
Candesartan638.31571.96
Placebo529.04441.25

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Cerebrospinal Fluid (CSF) of Tau Phosphorylated at Threonine 181 (p-tau181) Levels

CSF levels of p-tau181 were analyzed from CSF samples obtained via lumbar puncture. P-tau181 is a biomarker that is elevated in persons with Alzheimer's disease. Higher values indicate worsening disease. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionpg/ml (Least Squares Mean)
Baseline p-tauMonth 12 p-tau
Candesartan100.2988.52
Placebo81.5868.49

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Cerebrospinal Fluid (CSF) Amyloid Aβ42/Aβ40 Levels

CSF Aβ42/Aβ40 levels were analyzed from CSF samples obtained via lumbar puncture. A lower ratio indicates worsening disease. (NCT02646982)
Timeframe: Baseline, Month 12

,
InterventionRatio (Least Squares Mean)
Baseline Aβ42/Aβ40 ratioMonth 12 Aβ42/Aβ40 ratio
Candesartan0.0490.050
Placebo0.0520.051

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Cerebrospinal Fluid (CSF) Amyloid Aβ42 Levels

CSF Aβ42 levels were analyzed from CSF samples obtained via lumbar puncture. Aβ42 is a biomarker for Alzheimer's disease and lower values indicate worsening disease and an increased accumulation of amyloid in the brain. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionpg/ml (Least Squares Mean)
Baseline Aβ42Month 12 Aβ42
Candesartan554.80557.60
Placebo523.03476.32

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Cerebrospinal Fluid (CSF) Amyloid Aβ40 Levels

CSF Aβ40 levels were analyzed from CSF samples obtained via lumbar puncture. Lower values indicate worsening disease and an increased brain accumulation of amyloid. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionpg/ml (Least Squares Mean)
Baseline Aβ40Month 12 Aβ40
Candesartan11624.0011769.00
Placebo10802.009735.00

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Augmentation Index (AI)

Arterial stiffness was assessed by Augmentation Index (AI). The AI is a ratio measure of augmentation of central arterial pressure reflected in a pulse wave; the value is multiplied by 100 to provide a percentage. AI increases with age and is higher in persons with cardiovascular disease states. A lower value indicates a preferable state of arterial stiffness. (NCT02646982)
Timeframe: Baseline, Month 12

,
Interventionpercentage of arterial stiffness (Least Squares Mean)
BaselineMonth 12
Candesartan29.9528.36
Placebo31.2226.66

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Vasoreactivity

Cerebrovascular reactivity (CVR) is assessed with blood oxygenation level-dependent (BOLD) MRI. Vasoreactivity (VR) is the degree of change in BOLD signal relative to change in end tidal CO2. CVR is an indicator of microvascular function (higher indicates better function) (NCT02646982)
Timeframe: Month 12

Intervention(ml/100g/min)/mmHg (Least Squares Mean)
Candesartan0.27
Placebo-0.17

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Number of Participants With Symptoms of Hypotension

Participants were asked to report any symptoms of hypotension (dizziness, weakness, fatigue and lightheadedness). All participants were given a telephone number to reach physician 24-hours per day to report symptoms they experience. The number of participants reporting symptoms of hypotension is reported here. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan7
Placebo10

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Number of Participants With Hypotensive Episodes and Symptoms

The number of participants with reported episodes hypotension as well as symptoms of hypotension. (NCT02646982)
Timeframe: Up to Month 12

InterventionParticipants (Count of Participants)
Candesartan4
Placebo1

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Proportion of Patients With Adverse Event Free Hypertension Control

Proportion of patients with adverse event free hypertension control (percent with SBP < 130 mmHg and DBP <80 mmHg). (NCT03640312)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
QUARTET LDQT6
Candesartan9

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Rate of Adverse Events of Special Interest

Rate of pre-specified adverse events that are known side effects of active ingredients at the participant level. (NCT03640312)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
QUARTET LDQT16
Candesartan10

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Proportion of Patients With Hypertension Control

Proportion of patients with hypertension control (percent with SBP < 130 mmHg and DBP <80 mmHg). (NCT03640312)
Timeframe: 6 and 12 weeks

,
Interventionproportion of participants (Number)
6 weeks12 weeks
Candesartan0.39290.5769
QUARTET LDQT0.68750.6667

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Mean Diastolic Blood Pressure

Mean automated office diastolic blood pressure adjusted for baseline values. (NCT03640312)
Timeframe: 6 weeks

Interventionmm Hg (Least Squares Mean)
QUARTET LDQT73.01
Candesartan77.88

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Mean Systolic Blood Pressure

Mean automated office systolic blood pressure adjusted for baseline values. (NCT03640312)
Timeframe: 6 weeks

Interventionmm Hg (Least Squares Mean)
QUARTET LDQT122.37
Candesartan127.15

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Medication Adherence

Medication adherence defined by objective pill counts (NCT03640312)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
QUARTET LDQT21
Candesartan21

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Number of Patients Requiring Step up Treatment

Number of patients requiring step-up treatment. (NCT03640312)
Timeframe: 6 weeks

InterventionParticipants (Count of Participants)
QUARTET LDQT6
Candesartan16

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Percentage of Participants With Serious Adverse Events (SAEs)

Percentage of participants with any Serious Adverse Events (SAE) according to Good Clinical Practice definition: adverse events that result in death, are life threatening, require hospitalization or prolong existing hospitalization, result in persistent disability, result in congenital anomaly or birth defect, or unimportant medical event that requires intervention to prevent any of the above. (NCT03640312)
Timeframe: 12 weeks

InterventionParticipants (Count of Participants)
QUARTET LDQT2
Candesartan0

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Mean Change in Serum Sodium

Mean change (from baseline) in continuous serum sodium. (NCT03640312)
Timeframe: 12 weeks

InterventionmEq/L (Mean)
QUARTET LDQT-0.81
Candesartan-0.15

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Mean Change in Serum Potassium

Mean change (from baseline) in continuous serum potassium. (NCT03640312)
Timeframe: 12 weeks

InterventionmEq/L (Mean)
QUARTET LDQT0.01
Candesartan0.02

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Mean Change in Serum Creatinine

Mean change in continuous serum creatinine. (NCT03640312)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
QUARTET LDQT-0.04
Candesartan-0.04

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Mean Change in Blood Urea Nitrogen

Mean change (from baseline) in continuous blood urea nitrogen. (NCT03640312)
Timeframe: 12 weeks

Interventionmg/dL (Mean)
QUARTET LDQT0.38
Candesartan-0.40

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Change in Mean Systolic Blood Pressure

Mean change (from baseline) in automated office systolic blood pressure adjusted for baseline values. (NCT03640312)
Timeframe: 6 weeks

Interventionmm Hg (Least Squares Mean)
QUARTET LDQT-15.65
Candesartan-10.87

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Change in Mean Systolic Blood Pressure

Mean change (from baseline) in automated office systolic blood pressure adjusted for baseline values. (NCT03640312)
Timeframe: 12 weeks

Interventionmm Hg (Least Squares Mean)
QUARTET LDQT-15.65
Candesartan-10.87

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Change in Mean Diastolic Blood Pressure

Mean change (from baseline) in automated office diastolic blood pressure adjusted for baseline values. (NCT03640312)
Timeframe: 6 weeks

Interventionmm Hg (Least Squares Mean)
QUARTET LDQT-11.60
Candesartan-6.74

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