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candesartan

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Description

Candesartan 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 narrow. This helps to lower blood pressure and reduce the strain on the heart. Candesartan is a synthetic compound, developed by Takeda Pharmaceuticals, and was first approved for use in the United States in 1998. It is available in both generic and brand-name forms. Candesartan has been shown to be effective in lowering blood pressure and reducing the risk of cardiovascular events, such as heart attacks and strokes. It is often used in combination with other medications, such as diuretics and beta-blockers. The compound is being studied in clinical trials for its potential benefits in treating other conditions, such as diabetic nephropathy and preeclampsia. '

candesartan: a nonpeptide angiotensin II receptor antagonist [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID2541
CHEMBL ID1016
CHEBI ID3347
SCHEMBL ID3938
MeSH IDM0217705

Synonyms (131)

Synonym
BIDD:GT0350
CHEMBL1016 ,
nsc-759858
AB01275447-01
gtpl587
tcv-116 (prodrug)
2-ethoxy-1-{[2'-(1h-tetrazol-5-yl)biphenyl-4ethyl]}-1h-benzimidazole-7-carboxylic acid
CHEBI:3347 ,
2-ethoxy-1-{[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl}-1h-benzimidazole-7-carboxylic acid
cv-11974
2-ethoxy-1-({2'-(1h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl)-1h-benzimidazole-7-carboxylic acid
2-ethoxy-1-(p-(o-1h-tetrazol-5-ylphenyl)benzyl)-7-benzimidazolecarboxylic acid
2-(ethyloxy)-1-{[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl}-1h-benzimidazole-7-carboxylic acid
2-ethoxy-7-carboxy-1-(2'-(1h-tetrazol-5-yl)biphenyl-4-yl)methylbenzimidazole
cv 11974
c24h20n6o3
1h-benzimidazole-7-carboxylic acid, 2-ethoxy-1-((2'-(1h-tetrazol-5-yl)(1,1'-biphenyl)-4-yl)methyl)-
candesartan
139481-59-7
C07468
candesartan (usan/inn)
D00522
NCGC00167474-01
2-ethoxy-1-((2'-(1h-tetrazol-5-yl)(1,1'-biphenyl)-4-yl)methyl)-1h-benzimidazole-7-carboxylic acid
HMS2089M22
2-ethoxy-3-[2''-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid
2-ethoxy-3-[2''-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid(cv-11974)
bdbm50240609
2-ethoxy-3-[2''-(2h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid
L000156
2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid
A807545
2-ethoxy-3-[[4-[2-(2h-1,2,3,4-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid
2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl]methyl]-4-benzimidazolecarboxylic acid
A808309
NCGC00167474-02
unii-s8q36md2xx
ec 604-138-8
hsdb 7520
s8q36md2xx ,
candesartan [usan:inn:ban]
nsc 759858
2-ethoxy-1-((2-(1h-tetrazole-5-yl)biphenyl-4-yl)methyl)-1h-benzamidazole-7-carboxylic acid.
cas-139481-59-7
dtxcid202725
dtxsid0022725 ,
tox21_112478
nsc759858
BCP9000479
pharmakon1600-01502288
smr003500711
1-((2'-(1h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylic acid
MLS004774041
CANDESARTAN - ATACAND
2-ethoxy-3-[[4-[2-(1h-tetrazol-5-yl)phenyl]phenyl]methyl]-3h-benzoimidazole-4-carboxylic acid
2-ethoxy-3-[[4-[2-(1h-tetrazol-5-yl)phenyl]phenyl] methyl]-3h-benzoimidazole-4-carboxylic acid
BCPP000302
smr002203608
MLS003915631
FT-0602912
AB07470
candesartan [vandf]
candesartan [who-dd]
candemore
candesartan [usan]
candesartan [inn]
candesartan [mi]
candesartan cilexetil impurity g [ep impurity]
candesartan [hsdb]
AM84369
S1578
AKOS015888154
gtpl6907
[3h]candesartan
CCG-213059
HY-B0205
SCHEMBL3938
NCGC00167474-04
tox21_112478_1
KS-5003 ,
1-((2'-(1h-tetrazol-5-yl)biphenyl-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylic acid
AKOS025117340
2-ethoxy-3-[2'-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzimidazole-4-carboxylic acid
2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl]-benzimidazole-7-carboxylic acid
2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl]benzimidazole-7-carboxylic acid
HTQMVQVXFRQIKW-UHFFFAOYSA-N
2-ethoxy-1-[[2'-(1 h-tetrazol-5-yl)biphenyl-4-yl]methyl]-benzimidazole-7-carboxylic acid
2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl]methyl]-1h-benzimidazole-7-carboxylic acid
1-((2'-(2h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylic acid
AB01275447_02
AB01275447_03
2-ethoxy-1-({4-[2-(2h-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)-1h-1,3-benzodiazole-7-carboxylic acid
2-ethoxy-3-[2'-(1h-tetrazol-5-yl)-biphenyl-4-ylmethyl]-3h-benzoimidazole-4-carboxylic acid
mfcd00864463
SR-05000001447-5
sr-05000001447
HMS3651C13
SR-05000001447-1
SR-05000001447-2
J-007281
HMS3715F13
NCGC00167474-06
2-ethoxy-1-[[2'-(1h-tetrazol-5-yl)biphenyl-4-yl]methyl]-1h-benzimidazole-7-carboxylic acid (candesartan)
SW199612-2
2-ethoxy-1-[[2'-(2h-tetrazol-5-yl)[1,1'-biphenyl]-4-yl]methyl]-1h-benzimidazole-7-carboxylic acid
DB13919
Q415970
candesartan (atacand)
BCP01137
2-ethoxy-1-{[2'-(2h-1,2,3,4-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl]methyl}-1h-1,3-benzodiazole-7-carboxylic acid
STR09609
CCG-269122
2-ethoxy-3-[[4-[2-(2h-tetrazol-5-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid.
C-266
1-((2'-(2h-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl)methyl)-2-ethoxy-1h-benzo[d]imidazole-7-carboxylicacid
nsc755311
candesartan 100 microg/ml in acetonitrile:methanol
nsc-755311
celexetil
candesartan- bio-x
BC164271
2-ethoxy-1-{[2'-(1h-1,2,3,4-tetrazol-5-yl)-[1,1'-biphenyl]-4-yl]methyl}-1h-1,3-benzodiazole-7-carboxylic acid
EN300-6491073
Z1741968269
1-[(2 inverted exclamation mark -(5-tetrazolyl)-4-biphenylyl)methyl]-2-ethoxybenzimidazole-7-carboxylic acid
SY065768
2-ethoxy-1-((2'-(1h-tetrazol-5-yl)biphenyl-4-yl)methyl)-1h-benzimidazole-7-carboxylic acid
c09ca06
2-ethoxy-1-((2'-(1h-tetrazol-5-yl)biphenyl-4ethyl))-1h-benzimidazole-7-carboxylic acid
candesartanum
2-ethoxy-3-((4-(2-(2h-tetrazol-5-yl)phenyl)phenyl)methyl)-3h-benzoimidazole-4-carboxylic acid

Research Excerpts

Overview

Cedesartan is an angiotensin II receptor antagonist widely used as a blood pressure-lowering drug. The inhibitory potential of candesartan on the NLRP3 inflammasome has not yet been investigated.

ExcerptReferenceRelevance
"Candesartan is an angiotensin II-receptor blocker and has proved neuroprotective properties."( Candesartan protects against d-galactose induced - Neurotoxicity and memory deficit via modulation of autophagy and oxidative stress.
Abo-Saif, MA; Khedr, NF; Werida, RH, 2022
)
2.89
"Candesartan is an angiotensin II (Ang II) receptor antagonist with promising diverse health benefits."( Candesartan Protects Against Cadmium-Induced Hepatorenal Syndrome by Affecting Nrf2, NF-κB, Bax/Bcl-2/Cyt-C, and Ang II/Ang 1-7 Signals.
Ahmed, MA; Ali, FEM; Gad-Elrab, WM; Hassanein, EHM; Kamel, EO; Mohammedsaleh, ZM, 2023
)
3.07
"Candesartan is an angiotensin II receptor antagonist widely used as a blood pressure-lowering drug; however, the inhibitory potential of candesartan on the NLRP3 inflammasome has not yet been investigated."( Repositioning of the Angiotensin II Receptor Antagonist Candesartan as an Anti-Inflammatory Agent With NLRP3 Inflammasome Inhibitory Activity.
Cheng, SM; Chernikov, OV; Chiu, HW; Ho, CL; Hsiao, YY; Hsu, HT; Hua, KF; Li, LH; Lin, WY; Peng, YJ; Wong, WT; Yang, SP, 2022
)
1.69
"Candesartan (Cand) is an angiotensin receptor antagonist widely used for hypertension treatment."( Effect of the structural modification of Candesartan with Zinc on hypertension and left ventricular hypertrophy.
Calleros, L; De Giusti, V; Ferrer, EG; Griera, M; Islas, MS; Jaquenod de Giusti, C; Martinez, VR; Martins Lima, A; Portiansky, EL; Rodriguez Puyol, M; Stergiopulos, N; Velez Rueda, JO; Williams, PAM, 2023
)
1.9
"Candesartan is a nonpeptide angiotensin II receptor blocker that selectively binds to angiotensin II receptor subtype 1. "( Candesartan exhibits low intrinsic permeation capacity and affects buccal tissue viability and integrity: An ex vivo study in porcine buccal mucosa.
Garcia-Tarazona, YM; Gordillo, JFI; Lafaurie, GI; Morantes, SJ; Ramos, FA; Sepúlveda, P, 2023
)
3.8
"Candesartan (Cands) is an angiotensin receptor blocker that has the potential to prevent cognitive deficits."( Effect of safranal or candesartan on 3-nitropropionicacid-induced biochemical, behavioral and histological alterations in a rat model of Huntington's disease.
Abd El-Salam, DM; Hussein, RM; Rizk, SM; Shehata, NI, 2023
)
1.95
"Candesartan is an ARB that has also been known for its anticancer effects but the exact molecular mechanism is remaining elusive."( Antihypertensive drug-candesartan attenuates TRAIL resistance in human lung cancer via AMPK-mediated inhibition of autophagy flux.
Park, SY; Rasheduzzaman, M, 2018
)
1.52
"Candesartan is a poorly water-soluble drug having an anti-hypertensive activity."( Pharmaceutical Cocrystal: A Novel Approach to Tailor the Biopharmaceutical Properties of a Poorly Water Soluble Drug.
Fatima, Z; Kaur, CD; Nashik, SS; Rizvi, DA; Srivastava, D; Tulsankar, SL, 2019
)
1.24
"Candesartan (CDS) is an AT1 receptor antagonist with potential neuroprotective properties."( Antimanic-like activity of candesartan in mice: Possible involvement of antioxidant, anti-inflammatory and neurotrophic mechanisms.
Berk, M; Budni, J; Carvalho, AF; Cavalcante, LM; de Lucena, DF; de Sousa, FC; de Souza Gomes, JA; de Souza, GC; Macêdo, D; Quevedo, J, 2015
)
1.44
"Candesartan is a relatively novel antihypertensive agent of the angiotensin receptor blocker (ARB). "( A systematic review and meta-analysis of candesartan and losartan in the management of essential hypertension.
, 2011
)
2.08
"Candesartan is an angiotensin II type 1 receptor blocker (ARB) that has been to shown to limit ischemic stroke and improve stroke outcome. "( AT1 receptor antagonism is proangiogenic in the brain: BDNF a novel mediator.
Alhusban, A; Ergul, A; Fagan, SC; Kozak, A, 2013
)
1.83
"Candesartan is a novel high-affinity type 1 AT(1)-receptor blocker characterized by prolonged binding to and slow dissociation from the receptor. "( [Candesartan - a novel AT(1)-angiotensin receptor blocker: peculiarities of pharmacology and experience of use in arterial hypertension].
Ivanova, NA; Preobrazhenskiĭ, DV; Sidorenko, BA; Soplevenko, AV; Stetsenko, TM, 2004
)
2.68
"Candesartan is a selective angiotensin II Type I (AT(1)) receptor blocker which binds tightly to, and dissociates slowly from the receptor. "( Candesartan for the treatment of hypertension and heart failure.
Ostergren, J, 2004
)
3.21
"Thus candesartan is considered to be a unique, attractive choice of prophylactic agent for migraine complicated by hypertension."( Efficacy of candesartan in the treatment of migraine in hypertensive patients.
Owada, K, 2004
)
1.16
"Candesartan is a long-acting angiotensin receptor antagonist that is well absorbed from the gastrointestinal tract, with insurmountable receptor binding abilities. "( Candesartan for the management of heart failure: more than an alternative.
McKelvie, RS, 2006
)
3.22
"Candesartan cilexetil is a nonpeptide selective blocker of the angiotensin II receptor sub-type 1. "( Candesartan in heart failure.
Chonlahan, JS; Germany, RE; Ripley, TL, 2006
)
3.22
"Candesartan is an insurmountable blocker with a slow dissociation from the AT1 receptor, and it has been shown to effectively reduce BP in humans and in a variety of genetic and experimental models of hypertension."( Candesartan: a new-generation angiotensin II AT1 receptor blocker: pharmacology, antihypertensive efficacy, renal function, and renoprotection.
Morsing, P, 1999
)
2.47
"Candesartan is an angiotensin II subtype 1 (AT1) receptor antagonist that is administered orally as candesartan cilexetil which is converted in the active compound."( 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
)
1.29
"Candesartan (Atacand) is a novel antagonist of angiotensin II AT1 receptors. "( [Pharma-clinics. The drug of the month. Candesartan (Atacand)].
Kulbertus, H, 1999
)
2.01
"Candesartan cilexetil is an angiotensin II receptor antagonist, and candesartan, its active metabolite, is metabolized by CYP2C9. "( CYP2C9*3 influences the metabolism and the drug-interaction of candesartan in vitro.
Azuma, J; Fukuda, T; Funae, Y; Hanatani, T; Hiroi, T; Ikeda, M; Imaoka, S, 2001
)
1.99

Effects

Candesartan has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%. It has a favorable effect on large artery function in patients with chronic heart failure.

Candesartan has been reported to have a protective effect on cerebral ischemia in vivo and in human ischemic stroke. The drug has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%.

ExcerptReferenceRelevance
"Candesartan has a preventive value against atherosclerotic plaque rupture in hypercholesterolemic rabbits, likely through its reduction of MMP-9 expression, inhibition of macrophage accumulation and increase of collagen content within the plaques."( [Prevention of rupture of atherosclerotic plaque by Candesartan in rabbit model].
Li, SA; Meng, ZM; Qian, HD; Shen, L; Wu, AS; Yin, HC; Yu, T; Zhou, XF; Zhu, WL, 2010
)
2.05
"Candesartan has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%."( Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial.
Granger, CB; Held, P; McMurray, JJ; Michelson, EL; Olofsson, B; Ostergren, J; Pfeffer, MA; Swedberg, K; Yusuf, S, 2003
)
2.15
"Candesartan has a favorable effect on large artery function in patients with chronic heart failure."( Pulsatile hemodynamic effects of candesartan in patients with chronic heart failure: the CHARM Program.
Arnold, JM; Desai, SS; Dunlap, ME; Granger, CB; Marchiori, G; Mitchell, GF; O'Brien, TX; Pfeffer, MA; Warner, E, 2006
)
2.06
"Candesartan has the most positive effects on skin cells."( Side Effects of Frequently Used Antihypertensive Drugs on Wound Healing in vitro.
Bachmann, HS; Besser, M; Severing, AL; Stuermer, EK; Terberger, N, 2019
)
1.24
"Candesartan has been reported to have a protective effect on cerebral ischemia in vivo and in human ischemic stroke. "( Candesartan improves ischemia-induced impairment of the blood-brain barrier in vitro.
Deli, MA; Hayashi, K; Hiu, T; Matsuo, T; Morofuji, Y; Nagata, I; Nakagawa, S; Niwa, M; So, G; Suyama, K; Tanaka, K, 2015
)
3.3
"Candesartan has been reported to reduce cardiovascular events when therapy was started 6 months after PCI with bare-metal stents in patients who survived restenosis. "( Impact of candesartan on cardiovascular events after drug-eluting stent implantation in patients with coronary artery disease: The 4C trial.
Hokimoto, S; Kikuta, K; Kimura, K; Koide, S; Matsui, K; Matsumura, T; Nakao, K; Ogawa, H; Oka, H; Oshima, S; Sakamoto, T; Shimomura, H; Tsujita, K; Yamamoto, N, 2016
)
2.28
"Candesartan has a preventive value against atherosclerotic plaque rupture in hypercholesterolemic rabbits, likely through its reduction of MMP-9 expression, inhibition of macrophage accumulation and increase of collagen content within the plaques."( [Prevention of rupture of atherosclerotic plaque by Candesartan in rabbit model].
Li, SA; Meng, ZM; Qian, HD; Shen, L; Wu, AS; Yin, HC; Yu, T; Zhou, XF; Zhu, WL, 2010
)
2.05
"Candesartan has a moderate impact in preventing admissions for CHF among patients who have heart failure and LVEF higher than 40%."( Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial.
Granger, CB; Held, P; McMurray, JJ; Michelson, EL; Olofsson, B; Ostergren, J; Pfeffer, MA; Swedberg, K; Yusuf, S, 2003
)
2.15
"Candesartan has a favorable effect on large artery function in patients with chronic heart failure."( Pulsatile hemodynamic effects of candesartan in patients with chronic heart failure: the CHARM Program.
Arnold, JM; Desai, SS; Dunlap, ME; Granger, CB; Marchiori, G; Mitchell, GF; O'Brien, TX; Pfeffer, MA; Warner, E, 2006
)
2.06
"Candesartan has no additional effect on the rates of postoperative AF when added to ACEI."( Effect of renin-angiotensin aldosteron system blockers on postoperative atrial fibrillation.
Dede, O; Duver, H; Ibrisim, E; Kapan, S; Ozaydin, M; Peker, O; Turker, Y; Varol, E, 2008
)
1.07
"Candesartan has been reported to produce nitric oxide (NO) and to decrease oxidative stress in animal studies. "( Candesartan decreases carotid intima-media thickness by enhancing nitric oxide and decreasing oxidative stress in patients with hypertension.
Fujiwara, H; Hiei, K; Kawasaki, H; Minatoguchi, S; Mizukusa, T; Ono, H; Takahashi, H; Tsukamoto, T; Uno, T; Watanabe, K; Yamada, Y, 2008
)
3.23
"Candesartan has favorable effects on renal function demonstrated in both humans and animals, and has also been shown to protect the kidney in several models of renal injury."( Candesartan: a new-generation angiotensin II AT1 receptor blocker: pharmacology, antihypertensive efficacy, renal function, and renoprotection.
Morsing, P, 1999
)
2.47

Actions

Cenesartan had a lower Kaplan-Meier rate of NOD than amlodipine. Candesartan promotes angiogenesis and activates MMPs. It may suppress all-cause death and reduce incidence of new-onset diabetes in patients with obesity.

ExcerptReferenceRelevance
"Candesartan had a lower Kaplan-Meier rate of NOD than amlodipine (8.3 vs."( Long-term effects of antihypertensive therapy on cardiovascular events and new-onset diabetes mellitus in high-risk hypertensive patients in Japan.
Ichihara, C; Kitao, H; Konda, M; Kuwabara, Y; Liu, J; Oba, K; Ueshima, K; Yasuno, S, 2018
)
1.2
"Candesartan promotes angiogenesis and activates MMPs."( Sequential Therapy with Minocycline and Candesartan Improves Long-Term Recovery After Experimental Stroke.
Fagan, SC; Fouda, AY; Ishrat, T; Patel, A; Pillai, B; Soliman, S, 2015
)
1.41
"Candesartan treatment may suppress all-cause death and reduce the incidence of new-onset diabetes in patients with obesity."( Role of diabetes and obesity in outcomes of the candesartan antihypertensive survival evaluation in Japan (CASE-J) trial.
Fujimoto, A; Hirata, M; Nakao, K; Oba, K; Ogihara, T; Saruta, T; Ueshima, K; Yasuno, S, 2010
)
1.34
"Candesartan induced an increase in plasma renin activity and plasma angiotensin II associated with a reduction in arterial pressure without affecting heart rate."( Candesartan and arterial baroreflex sensitivity and sympathetic nerve activity in patients with mild heart failure.
Hikosaka, M; Iwasaka, T; Iwasaki, M; Kawamura, A; Mimura, J; Motohiro, M; Sugiura, T; Yuasa, F; Yuyama, R, 2002
)
2.48
"Candesartan promotes a complementary antiproteinuric and a small antihypertensive effect after a treatment period of 8 weeks in patients with chronic glomerulonephritis when given in conjunction with an ACEI. "( Reduction of proteinuria; combined effects of receptor blockade and low dose angiotensin-converting enzyme inhibition.
Bader, BD; Berger, ED; Ebert, C; Erley, CM; Risler, T, 2002
)
1.76

Treatment

Canesartan treatment may suppress all-cause death and reduce the incidence of new-onset diabetes in patients with obesity. The candesartan-treated rats were healthy and had weight gain similar to that of the control rats, although a significant reduction in blood pressure was observed.

ExcerptReferenceRelevance
"Candesartan treatment alleviated matrisome protein accumulation and normalized the vascular distensibility and cerebral blood flow."( Candesartan prevents arteriopathy progression in cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy model.
Ando, S; Fujita, N; Fukunaga, M; Hasegawa, M; Hatano, Y; Hirokawa, S; Igarashi, H; Ihara, M; Kakita, A; Kametani, F; Kanazawa, M; Kato, T; Kawashima, Y; Kawata, H; Koyama, A; Manabe, RI; Matsumoto, M; Murayama, S; Nishizawa, M; Nozaki, H; Onodera, O; Saito, R; Saito, S; Sato, T; Sekine, Y; Sugai, A; Sugie, A; Toyoshima, Y; Tsuji, S; Uemura, M, 2021
)
2.79
"Candesartan treatment (10 or 30 mg/kg; orally) was initiated one day post CLI and thereafter once daily for up to 14 days."( Candesartan protects against unilateral peripheral limb ischemia in type-2 diabetic rats: Possible contribution of PI3K-Akt-eNOS-VEGF angiogenic signaling pathway.
Abdelaziz, RR; Elshaer, SL; Khaled, S; Suddek, GM, 2023
)
3.07
"Candesartan treatment reduced the expression of M1 markers, and increased M2 markers."( Candesartan modulates microglia activation and polarization via NF-κB signaling pathway.
Gong, W; Li, W; Liu, Z; Lu, X; Qie, S; Ran, Y; Su, W; Xi, J,
)
2.3
"Candesartan treatment also inhibits the expression of anti-apoptotic protein c-FLIP."( Antihypertensive drug-candesartan attenuates TRAIL resistance in human lung cancer via AMPK-mediated inhibition of autophagy flux.
Park, SY; Rasheduzzaman, M, 2018
)
1.52
"Candesartan treatment improved neurobehavioral and motor function, and decreased infarct size and Hb."( Silencing VEGF-B Diminishes the Neuroprotective Effect of Candesartan Treatment After Experimental Focal Cerebral Ischemia.
Eldahshan, W; Ergul, A; Fagan, SC; Ishrat, T; Pillai, B; Soliman, S, 2018
)
1.45
"Candesartan treatment also increased the amount of fecal short-chain fatty acids (SCFAs) including acetic acid, propionic acid, and butyric acid in SHRs."( Candesartan attenuates hypertension-associated pathophysiological alterations in the gut.
Chen, Y; Cui, J; Ding, L; Du, X; Tang, X; Wang, P; Wang, W; Wu, D; Yin, J; Zhang, T, 2019
)
2.68
"Candesartan and tempol treatments also significantly improved conducted vasodilatation."( Spreading vasodilatation in the murine microcirculation: attenuation by oxidative stress-induced change in electromechanical coupling.
Chaston, DJ; Edwards, FR; Hill, CE; Howitt, L; Matthaei, KI; Sandow, SL, 2013
)
1.11
"All candesartan-treated rabbits showed significantly attenuated atherosclerosis lesions with reduced accumulation of monocytes and had significantly reduced VCAM-1 expression and NF-κβ activity."( Role of NF-κβ and oxidative pathways in atherosclerosis: cross-talk between dyslipidemia and candesartan.
Abdulzahra, MS; Al-Amran, FG; Hadi, NR; Majeed, ML; Mohammad, BI; Yousif, MG; Yousif, NG, 2013
)
1.09
"Candesartan-treated animals showed a significant reduction in the infarct size [t (13) = -5.5, P = 0.0001] accompanied by functional recovery in Bederson [F (1, 13) = 7.9, P = 0.015], beam walk [F (1, 13) = 6.7, P = 0.023], grip strength [F (1, 13) = 15.2, P = 0.0031], and rotarod performance [F (1, 14) = 29.8, P < 0.0001]."( Low-dose candesartan enhances molecular mediators of neuroplasticity and subsequent functional recovery after ischemic stroke in rats.
Ergul, A; Fagan, SC; Fouda, AY; Ishrat, T; Johnson, MH; Kozak, A; Pillai, B; Soliman, S, 2015
)
1.56
"Candesartan treatment restored the functionality of angiotensin-converting enzyme 2-angiotensin-(1-7)-MAS axis by inhibiting the proinflammatory-redox AT1-mediated mechanism."( MAS receptors mediate vasoprotective and atheroprotective effects of candesartan upon the recovery of vascular angiotensin-converting enzyme 2-angiotensin-(1-7)-MAS axis functionality.
da Silva, CHTP; de Oliveira, AM; do Prado, AF; Gerlach, RF; Gomes, MS; Pernomian, L, 2015
)
1.37
"Candesartan treatment was associated with increased iNOS expression (p = .033)."( Support for involvement of the renin-angiotensin system in dysplastic Barrett's esophagus.
Bratlie, SO; Casselbrant, A; Edebo, A; Fändriks, L, 2017
)
1.18
"Candesartan pretreatment reduced the LPS-induced release of TNF-alpha, IL-1beta, and IL-6 into the circulation."( Angiotensin II AT1 blockade reduces the lipopolysaccharide-induced innate immune response in rat spleen.
Baliova, M; Benicky, J; Larrayoz, IM; Nishioku, T; Pavel, J; Saavedra, JM; Sánchez-Lemus, E; Zhou, J, 2009
)
1.07
"Candesartan treatment resulted in increased vascular density in the striatum at 7 days (P=0.037)."( Candesartan augments ischemia-induced proangiogenic state and results in sustained improvement after stroke.
Abdelsaid, M; El-Remessy, AB; Elewa, HF; Ergul, A; Fagan, SC; Johnson, MH; Kozak, A; Machado, LS; Wiley, DC, 2009
)
2.52
"Candesartan treatment significantly elevated (p < 0.01) the total volume of the MD, whereas the total number of MD cells was increased [from 14.2 (0.11) to 19.5 (0.11)]."( The effect of angiotensin II on the number of macula densa cells through the AT1 receptor.
Nyengaard, JR; Razga, Z, 2009
)
1.07
"Candesartan treatment induced a significant improvement in Forns Index, APRI and FibroIndex during treatment in comparison with the control group."( Effect of an angiotensin-II type-1 receptor blocker, candesartan on hepatic fibrosis in chronic hepatitis C: a prospective study.
Koda, M; Mitsuta, A; Murawaki, Y; Shimizu, T; Ueki, M; Yamamoto, T,
)
1.1
"Candesartan treatment significantly reversed the increases in both AQP2 and p-AQP2 expression and targeting."( Changes of renal AQP2, ENaC, and NHE3 in experimentally induced heart failure: response to angiotensin II AT1 receptor blockade.
Frøkiaer, J; Jonassen, T; Kim, SW; Knepper, MA; Kwon, TH; Lütken, SC; Marples, D; Nielsen, S, 2009
)
1.07
"Candesartan-pretreated SHHF (5 mg/kg/day candesartan; weeks 4-8) received during adulthood (20-28 weeks of age) either candesartan at a dose of 1.5 or 5 mg/kg/day or vehicle."( Prehypertensive preconditioning improves adult antihypertensive and cardioprotective treatment.
Baumann, M; Heemann, U; Lutz, J; Roos, M; Sollinger, D, 2010
)
1.08
"Candesartan treatment increased AT1a receptor mRNA expression in the heart but not in the aorta of SHR."( The mechanism of distinct diurnal variations of renin-angiotensin system in aorta and heart of spontaneously hypertensive rats.
Masuyama, T; Matsumoto, M; Naito, Y; Ohyanagi, M; Okuda, S; Sakoda, T; Tsujino, T, 2009
)
1.07
"Candesartan treatment may suppress all-cause death and reduce the incidence of new-onset diabetes in patients with obesity."( Role of diabetes and obesity in outcomes of the candesartan antihypertensive survival evaluation in Japan (CASE-J) trial.
Fujimoto, A; Hirata, M; Nakao, K; Oba, K; Ogihara, T; Saruta, T; Ueshima, K; Yasuno, S, 2010
)
1.34
"Candesartan treatment significantly increased the level of plasma Ile(5)-Ang II (24.0+/-7.6 versus 156.9+/-24.6 fmol/mL; P<0.01); in contrast, there was a markedly lower intrarenal Ile(5)-Ang II content (357.9+/-76.6 versus 21.1+/-2.8 fmol/g; P<0.01)."( Angiotensin II type 1 receptor-mediated augmentation of urinary excretion of endogenous angiotensin II in Val5-angiotensin II-infused rats.
Navar, LG; Seth, DM; Shao, W, 2010
)
1.08
"The candesartan-treated rats were healthy and had weight gain similar to that of the control rats, although a significant reduction in blood pressure was observed. "( Angiotensin type-1 receptor blocker candesartan inhibits calcium oxalate crystal deposition in ethylene glycol-treated rat kidneys.
Akanae, W; Nonomura, N; Okuyama, A; Tsujihata, M; Yoshioka, I, 2011
)
1.2
"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
"Candesartan treatment significantly reduced the morning and office BPs compared with other ARBs in Japanese patients with morning hypertension."( Effect of switching from telmisartan, valsartan, olmesartan, or losartan to candesartan on morning hypertension.
Hasegawa, H; Kameda, Y; Kobayashi, Y; Komuro, I; Kubota, A; Takano, H, 2012
)
1.33
"In candesartan-treated db/db mice (1 mg/kg per day, 4 weeks) increased plasma aldosterone, CYP11B2 expression, and aldosterone secretion were reduced."( Adipocytes produce aldosterone through calcineurin-dependent signaling pathways: implications in diabetes mellitus-associated obesity and vascular dysfunction.
Briones, AM; Burger, D; Burns, KD; Callera, GE; Corrêa, JW; Gagnon, AM; Gomez-Sanchez, CE; Gomez-Sanchez, EP; He, Y; Nguyen Dinh Cat, A; Ooi, TC; Ruzicka, M; Sorisky, A; Touyz, RM; Yogi, A, 2012
)
0.89
"Candesartan treatment acutely recruited microvasculature in both skeletal and cardiac muscle by significantly increasing MBV (P < 0.03 and P = 0.02, respectively) and MBF (P < 0.03 for both) without altering microvascular flow velocity. "( Candesartan acutely recruits skeletal and cardiac muscle microvasculature in healthy humans.
Chai, W; Fowler, DE; Jahn, LA; Liu, J; Liu, Z; Sauder, MA, 2012
)
3.26
"The candesartan treatment was stopped and oral corticosteroid therapy (50 mg/day) initiated."( [Centrilobular nodules with ground-glass opacities in the lungs].
Ella Ondo, T; Iba Ba, J; Mounguengui, D,
)
0.61
"Candesartan treatment reduced the lesion volume after CCI injury by approximately 50%, decreased the number of dying neurons, lessened the number of activated microglial cells, protected cerebral blood flow (CBF), and reduced the expression of the cytokine TGFβ1 while increasing expression of TGFβ3."( Candesartan, an angiotensin II AT₁-receptor blocker and PPAR-γ agonist, reduces lesion volume and improves motor and memory function after traumatic brain injury in mice.
Logan, TT; Saavedra, JM; Sánchez-Lemus, E; Symes, AJ; Villapol, S; Yaszemski, AK, 2012
)
2.54
"Candesartan treatment for 4 weeks significantly reduced these parameters."( Carbonyl stress induces hypertension and cardio-renal vascular injury in Dahl salt-sensitive rats.
Chen, X; Endo, S; Guo, Q; Hu, C; Ito, S; Jiang, Y; Miyata, T; Mori, T; Nakayama, K; Nakayama, M; Ogawa, S; Ohsaki, Y; Yoneki, Y; Zhu, W, 2013
)
1.11
"Candesartan treatment markedly reduced the mean arterial pressure of controls and glucose-intolerant rats."( Renoprotective effects of chronic candesartan treatment in uninephrectomized rat.
Mozaffari, MS; Patel, KB; Schaffer, SW, 2003
)
1.32
"Candesartan-based treatment reduced non-fatal stroke by 27.8% (95% CI, 1.3 to 47.2, P = 0.04), and all stroke by 23.6% (95% CI, -0.7 to 42.1, P = 0.056)."( The Study on Cognition and Prognosis in the Elderly (SCOPE): principal results of a randomized double-blind intervention trial.
Elmfeldt, D; Hansson, L; Hofman, A; Lithell, H; Olofsson, B; Skoog, I; Trenkwalder, P; Zanchetti, A, 2003
)
1.04
"Candesartan treatment reduced (P < 0.05) media area in SHR without affecting vessel or lumen area."( Effect of AT1 receptor blockade on hepatic redox status in SHR: possible relevance for endothelial function?
Cachofeiro, V; Cediel, E; de las Heras, N; González Pacheco, FR; Jiménez, J; Lahera, V; Oubina, MP; Sanz-Rosa, D; Vegazo, O, 2003
)
1.04
"Candesartan treatment decreased cardiac PAI-1 expression only in the dark in WKY rats but throughout the day in SHR."( Circadian gene expression of clock genes and plasminogen activator inhibitor-1 in heart and aorta of spontaneously hypertensive and Wistar-Kyoto rats.
Fujioka, Y; Iwasaki, T; Kawasaki, D; Masai, M; Morimoto, S; Naito, Y; Ohyanagi, M; Okumura, T; Sakoda, T; Tsujino, T, 2003
)
1.04
"Candesartan treatment prevented the hypertension (87 +/- 3 mmHg) and led to increased plasma Ang II concentrations (441 +/- 27 fmol/ml), but prevented increases in kidney (120 +/- 15 fmol/g) and renal interstitial fluid (2.15 +/- 0.12 pmol/ml) Ang II concentrations."( Angiotensin II type 1 receptor-mediated augmentation of renal interstitial fluid angiotensin II in angiotensin II-induced hypertension.
Navar, LG; Nishiyama, A; Seth, DM, 2003
)
1.04
"Candesartan cilexetil treatment significantly reduced the fibrosis development. "( Anti-fibrogenic effects of captopril and candesartan cilexetil on the hepatic fibrosis development in rat. The effect of AT1-R blocker on the hepatic fibrosis.
Bayram, I; Ozbek, H; Tuncer, I; Ugras, S, 2003
)
2.03
"Candesartan treatment reduced primary end point risk (5.9% vs 12.3% for control subjects; relative risk, 0.47; 95% CI, 0.24 to 0.93)."( Effects of low-dose angiotensin II receptor blocker candesartan on cardiovascular events in patients with coronary artery disease.
Kondo, J; Kono, T; Kosaka, T; Matsui, H; Morishima, I; Mukawa, H; Murohara, T; Numaguchi, Y; Okumura, K; Sone, T; Tsuboi, H; Uesugi, M; Yoshida, T, 2003
)
1.29
"Candesartan treatment, however, attenuated the chronic tubulointerstitial injury in obstructed kidneys and was associated with significant preservation of kidney tissue mass."( AT1A-mediated activation of kidney JNK1 and SMAD2 in obstructive uropathy: preservation of kidney tissue mass using candesartan.
Padda, R; Sheikh-Hamad, D; Truong, LD; Tsao, CC; Wamsley-Davis, A; Zhang, P, 2004
)
1.25
"Candesartan treatment resulted in a significant decrease of systolic and diastolic blood pressures, LV mass index (LVMI), homeostasis model assessment (HOMA) index, and plasma brain natriuretic peptide (BNP)."( Candesartan, an angiotensin II receptor blocker, improves left ventricular hypertrophy and insulin resistance.
Anan, F; Hara, M; Ooie, T; Saikawa, T; Takahashi, N; Yoshimatsu, H, 2004
)
2.49
"Candesartan treatment in macroalbuminuric patients significantly changed 15 of the 113 polypeptides in the diabetic renal damage pattern toward levels in normoalbuminuric patients."( Impact of diabetic nephropathy and angiotensin II receptor blockade on urinary polypeptide patterns.
Christensen, PK; Hillmann, M; Kaiser, T; Mischak, H; Parving, HH; Rossing, K; Walden, M, 2005
)
1.05
"Candesartan treatment was continued for 28 days."( Effects of angiotensin II receptor blocker (candesartan) in daunorubicin-induced cardiomyopathic rats.
Aizawa, Y; Kamal, FA; Kodama, M; Kunisaki, M; Ma, M; Mito, S; Palaniyandi, S; Prakash, P; Soga, M; Tachikawa, H; Veeraveedu, P; Watanabe, K, 2006
)
1.32
"Candesartan treatment completely suppressed the increases of p21, p27, p53 and Rb."( Angiotensin II receptor antagonist attenuates expression of aging markers in diabetic mouse heart.
Izumi, T; Kosugi, R; Machida, Y; Shioi, T; Takahashi, K; Watanabe-Maeda, K; Yoshida, Y, 2006
)
1.06
"Candesartan treatment increased Aogen, ACE and AT2 receptor in SHR, and increased ACE and decreased Aogen in WKY rats, without affecting the (pro)renin and AT1 receptors."( AT1 receptor blockade regulates the local angiotensin II system in cerebral microvessels from spontaneously hypertensive rats.
Delgiacco, E; Dou, J; Ge, L; Imboden, H; Macova, M; Nishioku, T; Pavel, J; Saavedra, JM; Yu, ZX; Zhou, J, 2006
)
1.06
"With candesartan-based treatment, compared with control, the relative risk of non-fatal stroke was 0.72 (P = 0.04) and of major cardiovascular events 0.89 (P = 0.19)."( The Study on COgnition and Prognosis in the Elderly (SCOPE)--recent analyses.
Trenkwalder, P, 2006
)
0.79
"Candesartan treatment from the onset of obstruction attenuated the reduction in GFR (3.1 +/- 0.4 vs."( Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction.
Frische, S; Frøkiaer, J; Jensen, AM; Knepper, MA; Li, C; Nielsen, S; Nørregaard, R; Praetorius, HA, 2006
)
1.06
"Candesartan-treated mice demonstrated significantly lower liver weights and reduced lipid droplets in hepatic cells compared with control mice."( Angiotensin-II receptor antagonist alleviates non-alcoholic fatty liver in KKAy obese mice with type 2 diabetes.
Itoh, T; Kanda, T; Kawaura, K; Kusaka, K; Morimoto, S; Moriya, J; Sumino, H; Takahashi, T; Yamakawa, J; Yu, F,
)
0.85
"With candesartan pretreatment, LV fractional shortening and ejection fraction increased (P<0.05) by 37% and 28%, and LV chamber dilation was attenuated (P<0.05)."( Pretreatment with angiotensin receptor blockade prevents left ventricular dysfunction and blunts left ventricular remodeling associated with acute myocardial infarction.
Castellano, L; Do, R; Gaballa, MA; Goldman, S; Juneman, E; Phan, H; Thai, H, 2006
)
0.79
"In candesartan-treated piglets, the l-NAME-induced GFR reduction seen in normal and nonobstructed kidneys was absent in the partial obstructed kidneys."( Glomerular and tubular function during AT1 receptor blockade in pigs with neonatal induced partial ureteropelvic obstruction.
Djurhuus, JC; Eskild-Jensen, A; Ferreira, LS; Frøkiaer, J; Nielsen, S; Nyengaard, JR; Paulsen, LF; Rawashdeh, YF; Rungø, C; Thomsen, K, 2007
)
0.85
"Candesartan treatment also notably decreased staining intensity of oxidative stress markers, as well as attenuating intra-islet fibrosis and improving blood supply in the islet."( Angiotensin II receptor blocker provides pancreatic beta-cell protection independent of blood pressure lowering in diabetic db/db mice.
Du, H; Iwashita, N; Kawamori, R; Shao, JQ; Wang, J; Wang, YT; Wang, YY; Watada, H; Zhao, M, 2007
)
1.06
"Candesartan treatment of DS rats with established diastolic heart failure reversed cardiac remodeling, improved cardiac relaxation abnormality, and prolonged survival, being accompanied by the attenuation of the increase in cardiac superoxide, reduced nicotinamide-adenine dinucleotide phosphate oxidase, and xanthine oxidoreductase activities."( Role of xanthine oxidoreductase in the reversal of diastolic heart failure by candesartan in the salt-sensitive hypertensive rat.
Dong, YF; Kataoka, K; Kim-Mitsuyama, S; Matsuba, S; Ogawa, H; Tokutomi, Y; Yamamoto, E; Yamashita, T, 2007
)
1.29
"Candesartan treatment improved myocardial injury in obese mice with acute viral myocarditis and induced expression of cardiac adiponectin with the induction of C/EBPalpha as well as the reduction of cardiac NF-kappaB and TNF-alpha."( Candesartan improves myocardial damage in obese mice with viral myocarditis and induces cardiac adiponectin.
Chen, R; Iwai, K; Kanda, T; Matsumoto, M; Morimoto, S; Nakahashi, T; Sumino, H; Takahashi, T; Yu, F, 2008
)
3.23
"Candesartan treatment significantly improved RBF (+40% +/- 6% vs."( Low-dose candesartan improves renal blood flow and kidney oxygen tension in rats with endotoxin-induced acute kidney dysfunction.
Grimberg, E; Guron, G; Nitescu, N, 2008
)
1.48
"In candesartan-treated DM rats, UT-A3 increased in IM tip (160 +/- 14%) and base (210 +/- 19%)."( Candesartan augments compensatory changes in medullary transport proteins in the diabetic rat kidney.
Blount, MA; Kent, KJ; Klein, JD; Price, SR; Sands, JM; Smith, TD, 2008
)
2.3
"Candesartan treatment attenuated the sodium-retaining action of hyperinsulinaemia."( Effect of an angiotensin II receptor antagonist, candesartan, on insulin resistance and pressor mechanisms in essential hypertension.
Higashiura, K; Miyazaki, Y; Shimamoto, K; Ura, N, 1999
)
1.28
"Candesartan treatment normalized blood pressure and the shift toward higher blood pressures at both the upper and lower limits of cerebrovascular autoregulation in SHR. "( Angiotensin II AT(1) blockade normalizes cerebrovascular autoregulation and reduces cerebral ischemia in spontaneously hypertensive rats.
Ito, T; Nishimura, Y; Saavedra, JM, 2000
)
1.75
"Candesartan treatment for 1 week reduced aortic and cardiac PAI-1 expression in spontaneously hypertensive rats by 94% and 72%, respectively (P<0.05), but did not affect vascular PAI-1 levels in Wistar-Kyoto rats."( Role of the angiotensin AT(1) receptor in rat aortic and cardiac PAI-1 gene expression.
Bouchie, JL; Chen, HC; Clermont, AC; Feener, EP; Hampe, J; Izumo, S; Perez, AS, 2000
)
1.03
"Candesartan-treated animals maintained mesenteric and jejunal mucosal perfusion during 40% hypovolemia compared to CTRL animals, while no differences were observed in the hepatic and renal circulation."( Angiotensin II blockade in existing hypovolemia: effects of candesartan in the porcine splanchnic and renal circulation.
Aneman, A; Ewert, S; Fändriks, L; Laesser, M; Pettersson, A, 2000
)
1.27
"Candesartan treatment (n=8) also prevented increases in kidney (215+/-19 fmol/g), endosomal (96+/-29 fmol/mg protein), and intermicrovillar cleft Ang II levels (11+/-2 fmol/mg protein)."( Ang II accumulation in rat renal endosomes during Ang II-induced hypertension: role of AT(1) receptor.
Benes, E; Hammond, TG; Imig, JD; Navar, LG; Orengo, S; Zhuo, JL, 2002
)
1.04
"Candesartan treatment normalised the lower part of the autoregulatory curve in SHR, and markedly decreased cerebral ischaemia as a consequence of middle cerebral artery occlusion with reperfusion."( Pre-treatment with candesartan protects from cerebral ischaemia.
Ito, T; Nishimura, Y; Saavedra, J, 2001
)
1.36
"Candesartan treatment ameliorated the glomerular morphological findings at six weeks after disease induction."( Fractalkine expression and the recruitment of CX3CR1+ cells in the prolonged mesangial proliferative glomerulonephritis.
Gejyo, F; Ikezumi, Y; Ito, Y; Kawachi, H; Koike, H; Morioka, Y; Nakamura, T; Nakatsue, T; Natori, Y; Oyanagi, A; Shimizu, F, 2002
)
1.04
"Treatment with candesartan and C21 was started on day 1, before VCR treatment, and continued until day 7."( Neuroprotective effect of angiotensin II type 2 receptor stimulation in vincristine-induced mechanical allodynia.
Bessaguet, F; Bouchenaki, H; Danigo, A; Demiot, C; Desmoulière, A; Duchesne, M; Magy, L; Richard, L; Sturtz, F, 2018
)
0.82
"Treatment with candesartan had no influence on serum YKL-40 levels."( Angiotensin II blockade, YKL-40 and maintenance of sinus rhythm after electrical cardioversion for atrial fibrillation.
Arnesen, H; Seljeflot, I; Smith, P; Svendsen, JH; Tveit, A, 2013
)
0.73
"Treatment with candesartan completely abrogated the emergence of the enlarged cells but did not reverse the Ito, and IKur in normal-sized cells in DCM hearts."( Effects of candesartan on electrical remodeling in the hearts of inherited dilated cardiomyopathy model mice.
Daida, H; Inoue, H; Konishi, M; Kurebayashi, N; Morimoto, S; Murayama, T; Nakazato, Y; Odagiri, F; Sakurai, T; Shioya, T; Sugihara, M; Suzuki, T, 2014
)
1.13
"Treatment with candesartan in the early phases of acute necrotizing pancreatitis effective on microcirculation of pancreatic tissue (Tab. "( Candesartan mediates microcirculation in acute necrotizing pancreatitis.
Bostanci, H; Dikmen, AU; Dikmen, K; Gulbahar, O; Poyraz, A; Sahin, TT; Tekin, E; Yuksel, O, 2015
)
2.21
"Treatment with candesartan in the acute phase of stroke was not associated with clear long-term clinical benefits. "( Effects of candesartan in acute stroke on vascular events during long-term follow-up: results from the Scandinavian Candesartan Acute Stroke Trial (SCAST).
Bath, PM; Berge, E; Boysen, G; Hornslien, AG; Igland, J; Murray, GD; Sandset, EC; Terént, A, 2015
)
1.16
"Treatment with candesartan did not influence the levels of hs-TnI."( High-Sensitivity Troponin I and Rhythm Outcome after Electrical Cardioversion for Persistent Atrial Fibrillation.
Arnesen, H; Horjen, AW; Norseth, J; Seljeflot, I; Smith, P; Tveit, A; Ulimoen, SR, 2016
)
0.77
"Treatment with candesartan in type 2 diabetic patients with mild to moderate retinopathy might induce improvement of retinopathy."( Effect of candesartan on progression and regression of retinopathy in type 2 diabetes (DIRECT-Protect 2): a randomised placebo-controlled trial.
Bilous, R; Chaturvedi, N; Fuller, J; Klein, R; Orchard, T; Parving, HH; Porta, M; Sjølie, AK, 2008
)
1.1
"Treatment with candesartan, but not hydralazine, reduced these values to levels in db/m mice."( Urinary oxidative stress markers closely reflect the efficacy of candesartan treatment for diabetic nephropathy.
Hashimoto, T; Hirawa, N; Imai, N; Ishigami, T; Kihara, M; Kitamura, H; Kiuchi, Y; Nomura, K; Tamura, K; Toya, Y; Umemura, S; Yasuzaki, H; Yoshida, S, 2009
)
0.93
"Pretreatment with candesartan profoundly modifies the response to stress."( Peripherally administered angiotensin II AT1 receptor antagonists are anti-stress compounds in vivo.
Benicky, J; Murakami, Y; Pavel, J; Saavedra, JM; Sanchez-Lemus, E, 2008
)
0.67
"Treatment with candesartan was associated with a shorter FPD in patients remaining in sinus rhythm for 6 months."( Effects of angiotensin receptor blockade on serial P-wave signal-averaged electrocardiograms after electrical cardioversion of persistent atrial fibrillation.
Arnesen, H; Grundvold, I; Hegbom, F; Smith, P; Tveit, A, 2009
)
0.71
"Treatment with candesartan did not reduce or prevent the development of excessive excretion of urinary albumin."( Albuminuria in chronic heart failure: prevalence and prognostic importance.
Gerstein, HC; Granger, CB; Jackson, CE; McMurray, JJ; Michelson, EL; Olofsson, B; Pfeffer, MA; Solomon, SD; Swedberg, K; Yusuf, S; Zetterstrand, S, 2009
)
0.69
"When treated with candesartan, but not CCBs, CAVI significantly decreased from 8.7 to 7.7 by 11%."( Blood pressure-independent effect of candesartan on cardio-ankle vascular index in hypertensive patients with metabolic syndrome.
Bokuda, K; Ichihara, A; Itoh, H; Kinouchi, K; Mito, A; Sakoda, M, 2010
)
0.96
"The treatment with candesartan significantly reduced CTGF expression and effectively suppressed the development of fibrotic deposition in diabetic animals."( Angiotensin II type 1 receptor blocker attenuates diabetes-induced atrial structural remodeling.
Aizawa, T; Fu, LT; Kaneko, S; Kato, T; Sagara, K; Sekiguchi, A; Takamura, M; Tsuneda, T; Yamashita, T, 2011
)
0.69
"Treatment with candesartan improved lipid peroxidation and primary hemostasis."( [Dynamics of primary hemostasis activity in patients with arterial hypertension and metabolic syndrome treated with candesartan].
Medvedev, IN; Simonenko, VB; Tolmachev, VV, 2011
)
0.92
"Pretreatment with candesartan, spironolactone, or candesartan and spironolactone significantly inhibited retinal ischemic injury."( Activation of the aldosterone/mineralocorticoid receptor system and protective effects of mineralocorticoid receptor antagonism in retinal ischemia-reperfusion injury.
Fujita, T; Hirooka, K; Itano, T; Lei, B; Liu, Y; Nakamura, T; Nishiyama, A; Shiraga, F; Zhang, J, 2012
)
0.7
"Treatment with Candesartan (2mg/kg per day) could effectively downregulate Smad3 and fibronectin accompanied by upregulating of Smad7."( Candesartan antagonizes pressure overload-evoked cardiac remodeling through Smad7 gene-dependent MMP-9 suppression.
Li, H; Liu, X; Wang, S; Yu, H; Zhao, G, 2012
)
2.16
"Pretreatment with candesartan significantly inhibited Ang II- induced JAK/STAT3 phosphorylation."( Effect of angiotensin II on proliferation and differentiation of mouse induced pluripotent stem cells into mesodermal progenitor cells.
Goshima, H; Ishizuka, T; Ozawa, A; Watanabe, Y, 2012
)
0.7
"Treatment with candesartan alone increased cortical BZ(1) binding, and decreased γ(2) subunit mRNA expression in the cingulate cortex."( Angiotensin II AT1 receptor blocker candesartan prevents the fast up-regulation of cerebrocortical benzodiazepine-1 receptors induced by acute inflammatory and restraint stress.
Honda, M; Saavedra, JM; Sánchez-Lemus, E, 2012
)
0.99
"Pretreatment with candesartan for 10 days reduced significantly the ulcer index induced by indomethacin injection."( Immunomodulatory effect of candesartan on indomethacin-induced gastric ulcer in rats.
Awad, AS; El Morsy, EM; Kamel, R, 2012
)
1
"Oral treatment with candesartan increased the nonlinearity and reduced the linearity in SHR."( Potentiated sympathetic nervous and renin-angiotensin systems reduce nonlinear correlation between sympathetic activity and blood pressure in conscious spontaneously hypertensive rats.
Imai, M; Kumagai, H; Matsuura, T; Onami, T; Osaka, M; Sakata, K; Saruta, T, 2002
)
0.63
"Treatment with candesartan, but not FK506, prevented the upregulation of ACE and TGF-beta1 gene expression."( AT1 receptor blockade reduces cardiac calcineurin activity in hypertensive rats.
Ichihara, S; Iwase, M; Izawa, H; Nagasaka, T; Nagata, K; Nakashima, N; Obata, K; Odashima, M; Somura, F; Yamada, Y; Yokota, M, 2002
)
0.65
"Pretreatment with candesartan for 3 days or nicardipine for 28 days was ineffective."( Protection against ischemia and improvement of cerebral blood flow in genetically hypertensive rats by chronic pretreatment with an angiotensin II AT1 antagonist.
Bregonzio, C; Falcón-Neri, A; Ito, T; Saavedra, JM; Terrón, JA; Yamakawa, H, 2002
)
0.64
"Treatment with candesartan, an angiotensin-II-receptor blocker (ARB), controlled both hypertension and proteinuria satisfactorily without worsening of his renal function."( A case of nephrotic syndrome associated with renovascular hypertension successfully treated with candesartan.
Chinda, J; Hasebe, N; Hirayama, T; Imamoto, C; Kikuchi, K; Okada, M; Takahashi, F; Takeuchi, T, 2003
)
0.88
"Treatment with candesartan enhanced (P < 0.05) ACh relaxations in SHR and reduced (P < 0.05) ACh + l-NAME contractions in both strains."( Effect of AT1 receptor blockade on hepatic redox status in SHR: possible relevance for endothelial function?
Cachofeiro, V; Cediel, E; de las Heras, N; González Pacheco, FR; Jiménez, J; Lahera, V; Oubina, MP; Sanz-Rosa, D; Vegazo, O, 2003
)
0.66
"pretreatment with candesartan, 0.1 and 0.3 mg/kg, dose-dependently decreased MAP before, during and after ischaemic injury but did not improve recovery from brain ischaemia."( Chronic pretreatment with candesartan improves recovery from focal cerebral ischaemia in rats.
Blume, A; Culman, J; Gohlke, P; Groth, W; Unger, T, 2003
)
0.94
"Pre-treatment with candesartan resulted in higher survival rate (83%, 10 out of 12 animals) compared with 50% (6 of 12) in control animals and 27% (3 of 11) in animals treated during endotoxinemia. "( The angiotensin II receptor blocker candesartan improves survival and mesenteric perfusion in an acute porcine endotoxin model.
Aneman, A; Ewert, S; Fändriks, L; Laesser, M; Oi, Y, 2004
)
0.93
"Treatment with candesartan, but not the combination of hydralazine and hydrochlorothiazide, significantly increased the expression of Cx37 and Cx40, although blood pressure decreased similarly."( Angiotensin II receptor blockade corrects altered expression of gap junctions in vascular endothelial cells from hypertensive rats.
Abe, I; Fujii, K; Goto, K; Iida, M; Kansui, Y; Nakamura, K; Oniki, H; Shibata, Y, 2004
)
0.66
"Treatment with candesartan attenuated all of these changes and prevented significant albuminuria."( Candesartan reduced advanced glycation end-products accumulation and diminished nitro-oxidative stress in type 2 diabetic KK/Ta mice.
Fan, Q; Gohda, T; Gu, L; Horikoshi, S; Kobayashi, M; Liao, J; Suzuki, Y; Tomino, Y; Wang, LN; Yamashita, M, 2004
)
2.11
"Treatment with candesartan increased EB extravasation in the kidney in normovolaemic controls."( Effects of candesartan and enalaprilat on the organ-specific microvascular permeability during haemorrhagic shock in rats.
Binkowski, K; Dendorfer, A; Eichler, W; Klotz, KF; Puchakayala, MR; Schumacher, J, 2006
)
1.06
"Pretreatment with candesartan before an acute MI improves global LV function, prevents LV dilation, and blunts the increase in constitutive microtubulin, with minimal effects on LV hemodynamics, regional function, or tissue endothelial nitric oxide synthase. "( Pretreatment with angiotensin receptor blockade prevents left ventricular dysfunction and blunts left ventricular remodeling associated with acute myocardial infarction.
Castellano, L; Do, R; Gaballa, MA; Goldman, S; Juneman, E; Phan, H; Thai, H, 2006
)
0.67
"Treatment with candesartan markedly increased mRNA expression of angiotensin II type-2 receptor and methyl methanesulfonate sensitive-2 in the brain in KK-A(y) mice, determined by quantitative RT-PCR."( Amelioration of cognitive impairment in the type-2 diabetic mouse by the angiotensin II type-1 receptor blocker candesartan.
Fujita, T; Horiuchi, M; Iwai, M; Iwanami, J; Li, JM; Min, LJ; Mogi, M; Sakata, A; Tsukuda, K, 2007
)
0.89
"Treatment with candesartan did not affect the levels of NT-proBNP."( Candesartan, NT-proBNP and recurrence of atrial fibrillation after electrical cardioversion.
Abdelnoor, M; Arnesen, H; Grundvold, I; Seljeflot, I; Smith, P; Tveit, A, 2009
)
2.14
"Pretreatment with candesartan and ramipril (low dose) did not reduce blood pressure during MCAO, whereas ramipril high dose did. "( Candesartan but not ramipril pretreatment improves outcome after stroke and stimulates neurotrophin BNDF/TrkB system in rats.
Krikov, M; Müller, S; Thone-Reineke, C; Unger, T; Villringer, A, 2008
)
2.12
"Cotreatment with candesartan reversed the inhibitory effects of Ang II on the expression levels of these mRNAs."( Aldosterone breakthrough caused by chronic blockage of angiotensin II type 1 receptors in human adrenocortical cells: possible involvement of bone morphogenetic protein-6 actions.
Goto, J; Inagaki, K; Kano, Y; Makino, H; Miyoshi, T; Ogura, T; Otani, H; Otsuka, F; Suzuki, J, 2008
)
0.67
"Treatment with candesartan, pioglitazone, and their combination resulted in significantly reduced mRNA expression of the inflammatory markers CXCL1 and TNFalpha in vivo (P<0.01)."( Comparison between single and combined treatment with candesartan and pioglitazone following transient focal ischemia in rat brain.
Kintscher, U; Krikov, M; Müller, S; Schefe, JH; Schmerbach, K; Thoene-Reineke, C; Unger, T; Villringer, A, 2008
)
0.93
"Treatment with candesartan, 16 mg o.d., with or without hydrochlorothiazide, for 24 weeks, significantly reduced left ventricular mass and arterial hypertrophy in patients with hypertension. "( Effects of candesartan on cardiac and arterial structure and function in hypertensive subjects.
Shiels, A; Spratt, JC; Webb, DJ; Williams, B, 2001
)
1.05

Toxicity

Candesartan was well tolerated with no serious drug-related adverse events reported. A low dose of HCTZ in combination with candesartans reduces blood pressure effectively without adverse effects on the glucose and lipid profiles.

ExcerptReferenceRelevance
" No serious or severe adverse events were reported."( Pharmacokinetics and safety of candesartan cilexetil in subjects with normal and impaired liver function.
Högemann, A; Hoogkamer, JF; Kirch, W; Kleinbloesem, CH; Nokhodian, A; Ouwerkerk, M; Weidekamm, E, 1998
)
0.59
" We hypothesized that higher doses will be safe and well tolerated."( Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Ashton, M; Weinberg, AJ; Weinberg, MS; Zappe, DH,
)
0.13
"Candesartan was well tolerated with no serious drug-related adverse events reported."( Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Ashton, M; Weinberg, AJ; Weinberg, MS; Zappe, DH,
)
1.57
"The results of this pilot study suggest that supramaximal doses of ARBs are safe and well tolerated in patients with chronic kidney disease, while reducing both blood pressure and proteinuria."( Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Ashton, M; Weinberg, AJ; Weinberg, MS; Zappe, DH,
)
0.13
" The incidence of adverse events during both phases was comparably low and the results of laboratory tests were unremarkable."( Efficacy and safety of combination therapy using high- or low-dose hydrochlorothiazide with valsartan or other Angiotensin-receptor blockers.
Ansari, A; Fuenfstueck, R; Hempel, RD; Klebs, S; Weidinger, G,
)
0.13
"To evaluate the evidence for temporal reporting patterns, such as the Weber effect, in spontaneous post-marketing adverse event (AE) reports submitted to the Food and Drug Administration (FDA), for four members of the angiotensin II receptor blockers drug class (ARBs)."( Identifying patterns of adverse event reporting for four members of the angiotensin II receptor blockers class of drugs: revisiting the Weber effect.
Dal Pan, GJ; Governale, LA; Hammad, TA; McAdams, MA; Swartz, L, 2008
)
0.35
" Adverse events leading to drug discontinuation were more frequent in the candesartan group: placebo/candesartan risk (%), lowest compared with highest age category: hyperkalemia (0."( Benefits and safety of candesartan treatment in heart failure are independent of age: insights from the Candesartan in Heart failure--Assessment of Reduction in Mortality and morbidity programme.
Cohen-Solal, A; Granger, CB; McMurray, JJ; Michelson, EL; Pfeffer, MA; Puu, M; Solomon, SD; Swedberg, K; Yusuf, S, 2008
)
0.89
"Older patients were at a greater absolute risk of adverse CV mortality and morbidity outcomes but derived a similar relative risk reduction and, therefore, a greater absolute benefit from treatment with candesartan, despite receiving a somewhat lower mean daily dose of candesartan."( Benefits and safety of candesartan treatment in heart failure are independent of age: insights from the Candesartan in Heart failure--Assessment of Reduction in Mortality and morbidity programme.
Cohen-Solal, A; Granger, CB; McMurray, JJ; Michelson, EL; Pfeffer, MA; Puu, M; Solomon, SD; Swedberg, K; Yusuf, S, 2008
)
0.84
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."( Developing structure-activity relationships for the prediction of hepatotoxicity.
Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010
)
0.36
"5 mg candesartan would be safe in the rabbit eyes."( Intraocular toxicity and pharmacokinetics of candesartan in a rabbit model.
Lee, JE; Lee, SM; Lim, DW; Oum, BS; Park, HJ; Shin, JH, 2011
)
1.14
"The regular dose of an angiotensin II type-1 receptor blocker (ARB) in renal transplant patients for hypertension is shown to be safe and effective; however, information on the appropriate dosing of ARBs in renal transplant patients is limited."( Safety and efficacy of administering the maximal dose of candesartan in renal transplant recipients.
Abe, T; Ichimaru, N; Imamura, R; Isaka, Y; Kawada, N; Kitamura, H; Kojima, Y; Kokado, Y; Moriyama, T; Nonomura, N; Okumi, M; Rakugi, H; Takahara, S, 2011
)
0.61
"The gradual increase of an ARB to its maximal dose in renal transplant patients is safe when carefully monitored."( Safety and efficacy of administering the maximal dose of candesartan in renal transplant recipients.
Abe, T; Ichimaru, N; Imamura, R; Isaka, Y; Kawada, N; Kitamura, H; Kojima, Y; Kokado, Y; Moriyama, T; Nonomura, N; Okumi, M; Rakugi, H; Takahara, S, 2011
)
0.61
" A low dose of HCTZ in combination with candesartan reduces blood pressure effectively without adverse effects on the glucose and lipid profiles."( Low dose of hydrochlorothiazide, in combination with angiotensin receptor blocker, reduces blood pressure effectively without adverse effect on glucose and lipid profiles.
Fujiwara, W; Ishii, J; Izawa, H; Kinoshita, K; Morimoto, S; Mukaide, D; Nomura, M; Ozaki, Y; Ukai, G; Yokoi, H, 2013
)
0.66
" In the present analysis we aim to investigate the effect of change in blood pressure during the first 2 days of stroke on the risk of early adverse events and poor outcome."( Relation between change in blood pressure in acute stroke and risk of early adverse events and poor outcome.
Bath, PM; Berge, E; Kjeldsen, SE; Murray, GD; Sandset, EC, 2012
)
0.38
" The primary effect parameter was early adverse events (recurrent stroke, stroke progression, and symptomatic hypotension) during the first 7 days, analyzed using logistic regression, with the group with a small decrease in SBP as the reference group."( Relation between change in blood pressure in acute stroke and risk of early adverse events and poor outcome.
Bath, PM; Berge, E; Kjeldsen, SE; Murray, GD; Sandset, EC, 2012
)
0.38
" 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
)
0.75
"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
)
0.75
" We evaluated the impact of 3 generic angiotensin II receptor blockers commercialization on adverse events: hospitalizations or emergency room consultations."( Impact of the Commercialization of Three Generic Angiotensin II Receptor Blockers on Adverse Events in Quebec, Canada: A Population-Based Time Series Analysis.
Blais, C; Guénette, L; Hamel, D; Leclerc, J; Poirier, P; Rochette, L, 2017
)
0.46
" Rates of adverse events for losartan, valsartan, and candesartan users (N=136 177) aged ≥66 years were calculated monthly, 24 months before and 12 months after generics commercialization."( Impact of the Commercialization of Three Generic Angiotensin II Receptor Blockers on Adverse Events in Quebec, Canada: A Population-Based Time Series Analysis.
Blais, C; Guénette, L; Hamel, D; Leclerc, J; Poirier, P; Rochette, L, 2017
)
0.7
"Among generic users, immediate or delayed differences in adverse events rates were observed right after generic commercialization for 3 antihypertensive drugs."( Impact of the Commercialization of Three Generic Angiotensin II Receptor Blockers on Adverse Events in Quebec, Canada: A Population-Based Time Series Analysis.
Blais, C; Guénette, L; Hamel, D; Leclerc, J; Poirier, P; Rochette, L, 2017
)
0.46
" Rates of adverse events were similar for patients using and not using preventive medications."( Efficacy and safety of lasmiditan in patients using concomitant migraine preventive medications: findings from SAMURAI and SPARTAN, two randomized phase 3 trials.
Ailani, J; Baygani, S; Hundemer, HP; Krege, JH; Loo, LS; Port, M; Schim, J, 2019
)
0.51

Pharmacokinetics

The pharmacokinetic parameters on days 1 and 7 revealed no statistically significant influence of liver impairment on the pharmacokinetics of candesartan. The half-life of candeartan was short in the vitreous, and modification of the delivery method would be required to extend the action duration.

ExcerptReferenceRelevance
"The pharmacokinetic parameters on days 1 and 7 revealed no statistically significant influence of liver impairment on the pharmacokinetics of candesartan."( Pharmacokinetics and safety of candesartan cilexetil in subjects with normal and impaired liver function.
Högemann, A; Hoogkamer, JF; Kirch, W; Kleinbloesem, CH; Nokhodian, A; Ouwerkerk, M; Weidekamm, E, 1998
)
0.79
"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
" No relevant pharmacokinetic drug-food or drug-drug interactions are known."( Clinical pharmacokinetics of candesartan.
Gleiter, CH; Mörike, KE, 2002
)
0.61
" These pharmacodynamic differences warrant further investigation and clarification."( Pharmacodynamic studies on the angiotensin II type 1 antagonists irbesartan and candesartan based on angiotensin II dose response in humans.
Belz, GG; Butzer, R; Kober, S; Mutschler, E, 2002
)
0.54
" Finally, some relevant pharmacokinetics and metabolic properties of the database of 53 compounds are calculated using the VolSurf and MetaSite software to allow the simultaneous characterization of pharmacodynamic and pharmacokinetics properties of the chemical space of angiotensin II receptor antagonists."( Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
Berellini, G; Cruciani, G; Mannhold, R, 2005
)
0.33
" The mean dose-adjusted area under the concentration curve from 0 to 12 h (AUC(0-12)) and AUC(0-6) of MPA co-administered with telmisartan were significantly lower than that without ARB (98 vs."( Effect of telmisartan, valsartan and candesartan on mycophenolate mofetil pharmacokinetics in Japanese renal transplant recipients.
Habuchi, T; Inoue, T; Kagaya, H; Miura, M; Ohkubo, T; Saito, M; Satoh, S; Suzuki, T, 2009
)
0.63
" The half-life of candesartan was short in the vitreous, and modification of the delivery method would be required to extend the action duration for clinical applications."( Intraocular toxicity and pharmacokinetics of candesartan in a rabbit model.
Lee, JE; Lee, SM; Lim, DW; Oum, BS; Park, HJ; Shin, JH, 2011
)
0.96
" 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
)
0.64
" 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
)
0.64
" CYP2C9 variants were associated only with losartan pharmacokinetics: the half-life of losartan was higher in CYP2C9*3 allele carriers (3."( Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
Abad-Santos, F; Cabaleiro, T; López-Rodríguez, R; Novalbos, J; Ochoa, D; Prieto-Pérez, R; Román, M; Talegón, M; Wojnicz, A, 2013
)
0.39
"Compared with control group and nephrotic group received enalapril alone respectively, Tmax of enalaprilat in nephrotic group received both enalapril and candesartan cilexetil prolonged about 21."( The effect of candesartan on the pharmacokinetics of enalaprilat in nephrotic rats.
Bi, BT; Lin, HB; Lin, T; Ma, AD; Xu, JP; Yang, XM; Yang, YB, 2012
)
0.94
"Dietary sodium, the main determinant of the pharmacodynamic response to renin-angiotensin system blockade, influences the pharmacokinetics of various cardiovascular drugs."( Effect of contrasted sodium diets on the pharmacokinetics and pharmacodynamic effects of renin-angiotensin system blockers.
Azizi, M; Blanchard, A; Charbit, B; Ezan, E; Funck-Brentano, C; Ménard, J; Peyrard, S; Wuerzner, G, 2013
)
0.39
" Pharmacokinetic assessments were performed over 48 hours for candesartan in part 1 and 72 hours for amlodipine in part 2 after drug administration on Day 10."( No pharmacokinetic interactions between candesartan and amlodipine following multiple oral administrations in healthy subjects.
Huh, W; Kim, JR; Kim, S; Ko, JW, 2018
)
0.99
" The method was successfully applied to investigate pharmacokinetic interaction between PIT and CAN in wistar rats."( Quantitative bio-analysis of pitavastatin and candesartan in rat plasma by HPLC-UV: Assessment of pharmacokinetic drug-drug interaction.
Kothari, C; Patel, M, 2020
)
0.82
" Repeat dose pharmacokinetic and pharmacodynamic study of the nano-fixed dose combination (FDC) was done in dexamethasone-induced animal model."( Pharmacokinetic and pharmacodynamic evaluation of nano-fixed dose combination for hypertension.
Bhandari, RK; Bhatia, A; Kaur, N; Malhotra, S; Pandey, AK; Rather, IIG; Shafiq, N; Sharma, S, 2020
)
0.56
" In pharmacokinetic analysis a sustained-release for 7 days was observed in nano-FDC group."( Pharmacokinetic and pharmacodynamic evaluation of nano-fixed dose combination for hypertension.
Bhandari, RK; Bhatia, A; Kaur, N; Malhotra, S; Pandey, AK; Rather, IIG; Shafiq, N; Sharma, S, 2020
)
0.56
" The present studies describe quality-by-design-based development and characterization of Candesartan loaded SNEDDS for improving its pharmacodynamic potential."( Design and optimization of candesartan loaded self-nanoemulsifying drug delivery system for improving its dissolution rate and pharmacodynamic potential.
Kaushik, D; Verma, R, 2020
)
1.08

Compound-Compound Interactions

A randomized clinical trial was used to compare the effects of an angiotensin II type 1 receptor inhibitor, candesartan, singly or in combination with a reducing sodium diet, the DASH diet, on the quality of life (QOL) No clinically relevant pharmacokinetic drug-drug interaction between nifedipine and candeartan was observed.

ExcerptReferenceRelevance
"A randomized clinical trial was used to compare the effects of an angiotensin II type 1 receptor inhibitor, candesartan, singly or in combination with a reducing sodium diet, the DASH diet, on the quality of life (QOL) in outpatients with hypertension."( Assessment of quality of life in a randomized clinical trial of candesartan only or in combination with DASH diet for hypertensive patients.
Geleris, P; Kirpizidis, H; Stavrati, A, 2005
)
0.78
"Angiotensin II type 1 receptor blockade with a therapeutic dosage of candesartan maintains significant control of blood pressure and may improve QOL-scores, especially when combined with a reducing sodium diet."( Assessment of quality of life in a randomized clinical trial of candesartan only or in combination with DASH diet for hypertensive patients.
Geleris, P; Kirpizidis, H; Stavrati, A, 2005
)
0.8
"Fenofibrate combined with candesartan improves endothelial function and reduces inflammatory markers to a greater extent than monotherapy in hypertriglyceridemic hypertensive patients."( Additive beneficial effects of fenofibrate combined with candesartan in the treatment of hypertriglyceridemic hypertensive patients.
Ahn, JY; Chung, WJ; Han, SH; Kim, JA; Koh, KK; Lee, Y; Quon, MJ; Shin, EK, 2006
)
0.88
" An ARB (candesartan, 4 mg/ day) in combination with an ACEI (enalapril, 5 mg/day) was started."( Treatment with candesartan combined with angiotensin-converting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem cell transplantation.
Hosoi, G; Ikemiya, M; Ishii, T; Noma, H; Osugi, Y; Sako, M; Yamada, H, 2006
)
1.1
" Pioglitazone monotherapy significantly attenuated cardiovascular p22(phox) and Rac1 in SHRSP, whereas pioglitazone combined with candesartan more attenuated p22(phox) and significantly reduced Nox1."( Beneficial effects of pioglitazone on hypertensive cardiovascular injury are enhanced by combination with candesartan.
Dong, YF; Kataoka, K; Kim-Mitsuyama, S; Matsuba, S; Nakamura, T; Ogawa, H; Tokutomi, Y; Yamamoto, E; Yamashita, T, 2008
)
0.76
"Previous studies have shown highly effective lowering of blood pressure with thiazide diuretics in combination with angiotensin receptor blockers."( Low dose of hydrochlorothiazide, in combination with angiotensin receptor blocker, reduces blood pressure effectively without adverse effect on glucose and lipid profiles.
Fujiwara, W; Ishii, J; Izawa, H; Kinoshita, K; Morimoto, S; Mukaide, D; Nomura, M; Ozaki, Y; Ukai, G; Yokoi, H, 2013
)
0.39
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012
)
0.38
"To determine the bioequivalence of a nifedipine and candesartan fixed-dose combination (FDC) with the corresponding loose combination, and to investigate the pharmacokinetic drug-drug interaction potential between both drugs."( Investigation of bioequivalence of a new fixed-dose combination of nifedipine and candesartan with the corresponding loose combination as well as the drug-drug interaction potential between both drugs under fasting conditions.
Brendel, E; Dietrich, H; Froede, C; Thomas, D; Weimann, B, 2013
)
0.87
" each drug alone, the 90% CIs remained within the range of 80 - 125% indicating the absence of a clinically relevant pharmacokinetic drug-drug interaction."( Investigation of bioequivalence of a new fixed-dose combination of nifedipine and candesartan with the corresponding loose combination as well as the drug-drug interaction potential between both drugs under fasting conditions.
Brendel, E; Dietrich, H; Froede, C; Thomas, D; Weimann, B, 2013
)
0.62
" No clinically relevant pharmacokinetic drug-drug interaction between nifedipine and candesartan was observed."( Investigation of bioequivalence of a new fixed-dose combination of nifedipine and candesartan with the corresponding loose combination as well as the drug-drug interaction potential between both drugs under fasting conditions.
Brendel, E; Dietrich, H; Froede, C; Thomas, D; Weimann, B, 2013
)
0.84
"To investigate the effect of low-dose carvedilol combined with candesartan in the prevention of acute and chronic cardiotoxicity of anthracycline drugs in adjuvant chemotherapy of breast cancer."( [Preventive effect of low-dose carvedilol combined with candesartan on the cardiotoxicity of anthracycline drugs in the adjuvant chemotherapy of breast cancer].
Han, YL; Liang, XF; Liu, L; Liu, YY; Liu, ZZ; Xie, XD; Zheng, ZD, 2013
)
0.88
"Forty patients were randomly divided into two groups: the experimental group with chemotherapy plus low-dose carvedilol combined with candesartan (20 cases) and control group with chemotherapy alone (20 cases)."( [Preventive effect of low-dose carvedilol combined with candesartan on the cardiotoxicity of anthracycline drugs in the adjuvant chemotherapy of breast cancer].
Han, YL; Liang, XF; Liu, L; Liu, YY; Liu, ZZ; Xie, XD; Zheng, ZD, 2013
)
0.84
"The use of low-dose carvedilol combined with candesartan can reduce the acute and chronic cardiotoxicity of anthracycline drugs, and with tolerable toxicities."( [Preventive effect of low-dose carvedilol combined with candesartan on the cardiotoxicity of anthracycline drugs in the adjuvant chemotherapy of breast cancer].
Han, YL; Liang, XF; Liu, L; Liu, YY; Liu, ZZ; Xie, XD; Zheng, ZD, 2013
)
0.9
" Hence, there is no evidence for a potential drug-drug interaction between PIT and CAN."( Quantitative bio-analysis of pitavastatin and candesartan in rat plasma by HPLC-UV: Assessment of pharmacokinetic drug-drug interaction.
Kothari, C; Patel, M, 2020
)
0.82
" Candesartan in combination with RDN prolonged trough BP and attenuated renal hemodynamic responses to blood loss."( Renal Denervation in Combination With Angiotensin Receptor Blockade Prolongs Blood Pressure Trough During Hemorrhage.
Booth, LC; Denton, KM; Head, GA; May, CN; McArdle, Z; Moritz, KM; Schlaich, MP; Singh, RR, 2022
)
1.63

Bioavailability

Canesartan or ACE inhibitor captopril markedly attenuated eNOS-derived O(2)*(-) and hydrogen peroxide production while augmenting NO* bioavailability in diabetic aortas.

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
" This might be ascribed to their improved bioavailability by increased lipophilicity."( Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
Imamiya, E; Inada, Y; Kohara, Y; Kubo, K; Naka, T; Wada, T, 1996
)
0.29
" Oral bioavailability is low (about 40%) because of incomplete absorption."( Clinical pharmacokinetics of candesartan.
Gleiter, CH; Mörike, KE, 2002
)
0.61
" Estrogen has been shown to downregulate angiotensin type 1 (AT1) receptor expression and to increase the bioavailability of endothelium-derived NO, which decreases AT1 receptor expression."( Postovariectomy hypertension is linked to increased renal AT1 receptor and salt sensitivity.
Harrison-Bernard, LM; Raij, L; Schulman, IH, 2003
)
0.32
"Candesartan is a long-acting angiotensin receptor antagonist that is well absorbed from the gastrointestinal tract, with insurmountable receptor binding abilities."( Candesartan for the management of heart failure: more than an alternative.
McKelvie, RS, 2006
)
3.22
" Ang II receptor type 1 blocker candesartan or ACE inhibitor captopril markedly attenuated eNOS-derived O(2)*(-) and hydrogen peroxide production while augmenting NO* bioavailability in diabetic aortas, implicating recoupling of eNOS."( Attenuation of angiotensin II signaling recouples eNOS and inhibits nonendothelial NOX activity in diabetic mice.
Cai, H; Oak, JH, 2007
)
0.62
" Human oral bioavailability is an important pharmacokinetic property, which is directly related to the amount of drug available in the systemic circulation to exert pharmacological and therapeutic effects."( Hologram QSAR model for the prediction of human oral bioavailability.
Andricopulo, AD; Moda, TL; Montanari, CA, 2007
)
0.34
"Salt-sensitive (SS) hypertension is a vascular diathesis characterized by reduced cardiovascular and renal nitric oxide bioavailability and local upregulation of ANG II."( Upregulation of cortical COX-2 in salt-sensitive hypertension: role of angiotensin II and reactive oxygen species.
Jaimes, EA; Pearse, DD; Puzis, L; Raij, L; Zhou, MS, 2008
)
0.35
"In addition to a class effect of ARBs, telmisartan may have additional effects on nitric oxide bioavailability and atherosclerotic change through its PPAR gamma-mediated effects in genetically hyperlipidemic rabbits."( Effects of telmisartan, a unique angiotensin receptor blocker with selective peroxisome proliferator-activated receptor-gamma-modulating activity, on nitric oxide bioavailability and atherosclerotic change.
Akasaka, T; Goto, M; Ikejima, H; Imanishi, T; Kobayashi, K; Kuroi, A; Mochizuki, S; Muragaki, Y; Shiomi, M; Tsujioka, H; Yoshida, K, 2008
)
0.35
" An increase in production of superoxide anion and hydrogen peroxide, reduction of nitric oxide synthesis, and a decrease in bioavailability of antioxidants have been demonstrated in human hypertension."( [Oxidative stress and mild hypertension].
Kurabayashi, M; Nakamura, T; Saito, Y, 2008
)
0.35
" 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 solubility, absorption and distribution of a drug are involved in the basic aspects of oral bioavailability Solubility is an essential characteristic and influences the efficiency of the drug."( Preparation of candesartan and atorvastatin nanoparticles by solvent evaporation.
Dohnal, J; Grunwaldova, V; Jampilek, J; Kral, V; Vaculikova, E, 2012
)
0.73
" There was a marked decrease in nitric oxide (NO) bioavailability and antioxidant enzyme capacity."( Combination therapy with spironolactone and candesartan protects against streptozotocin-induced diabetic nephropathy in rats.
El-Moselhy, MA; Hofni, A; Khalifa, MM; Taye, A, 2014
)
0.66
" Generic drug equivalence is evaluated through comparative bioavailability studies."( Impact of the Commercialization of Three Generic Angiotensin II Receptor Blockers on Adverse Events in Quebec, Canada: A Population-Based Time Series Analysis.
Blais, C; Guénette, L; Hamel, D; Leclerc, J; Poirier, P; Rochette, L, 2017
)
0.46
"9 fold in terms of bioavailability as compared to the pure drug."( Pharmaceutical Cocrystal: A Novel Approach to Tailor the Biopharmaceutical Properties of a Poorly Water Soluble Drug.
Fatima, Z; Kaur, CD; Nashik, SS; Rizvi, DA; Srivastava, D; Tulsankar, SL, 2019
)
0.51
"The prepared cocrystal was found to be relatively more soluble than the pure drug and also showed an enhanced oral bioavailability as compared to the pure drug."( Pharmaceutical Cocrystal: A Novel Approach to Tailor the Biopharmaceutical Properties of a Poorly Water Soluble Drug.
Fatima, Z; Kaur, CD; Nashik, SS; Rizvi, DA; Srivastava, D; Tulsankar, SL, 2019
)
0.51
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51
" The buccal mucosa has been extensively studied as an alternative route for drug delivery as it improves the bioavailability of drugs administered via the peroral route."( Candesartan exhibits low intrinsic permeation capacity and affects buccal tissue viability and integrity: An ex vivo study in porcine buccal mucosa.
Garcia-Tarazona, YM; Gordillo, JFI; Lafaurie, GI; Morantes, SJ; Ramos, FA; Sepúlveda, P, 2023
)
2.35

Dosage Studied

The response rate of monotherapy with candesartan in patients with hypertension increases with dosage, but never exceeds 60% at a daily dosage of 16mg. At the lowest dose studied (20 microgram/kg iv), the inhibitory effects of candesArtan were competitive, whereas at the highest dose the dose-response curve for angiotensin II was shifted to the right.

ExcerptRelevanceReference
", the dose-response curve for angiotensin II was shifted to the right in a parallel manner, whereas the administration of higher doses resulted in nonparallel rightward shifts of the angiotensin II dose-response curves."( Analysis of the effects of candesartan in the mesenteric vascular bed of the cat.
Champion, HC; Kadowitz, PJ, 1997
)
0.59
" 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
)
0.54
" 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
)
0.54
" A moderate drug accumulation of 20%, which does not require a dose adjustment, was observed following once-daily dosing in both groups."( Pharmacokinetics and safety of candesartan cilexetil in subjects with normal and impaired liver function.
Högemann, A; Hoogkamer, JF; Kirch, W; Kleinbloesem, CH; Nokhodian, A; Ouwerkerk, M; Weidekamm, E, 1998
)
0.59
" At this concentration, candesartan only produces a slight rightward shift of the angiotensin II dose-response curve."( The effects of candesartan on human AT1 receptor-expressing Chinese hamster ovary cells.
De Backer, JP; Fierens, FL; Vanderheyden, PM; Vauquelin, G, 1999
)
0.96
", candesartan shifted the dose-response curve to AngII to the right in an insurmountable manner, indicating an insurmountable blockade of AT1 receptors."( Analysis of the effects of candesartan on responses to angiotensin II in the hindquarters vascular bed of the cat.
Bivalacqua, TJ; Champion, HC; Kadowitz, PJ; Lambert, DG; McNamara, DB, 1999
)
1.32
" At the lowest dose studied (20 microgram/kg iv), the inhibitory effects of candesartan were competitive, whereas at the highest dose (100 microgram/kg iv) the dose-response curve for angiotensin II was shifted to the right in a nonparallel manner with inhibitory effects that could not be surmounted."( Role of AT(1) receptors and autonomic nervous system in mediating acute pressor responses to ANG II in anesthetized mice.
Bivalacqua, TJ; Champion, HC; Dalal, A; Kadowitz, PJ, 1999
)
0.53
" Data are reviewed to demonstrate that ACE escape reflects inadequate ACE dosage rather than a decrease in ACE inhibition occurring with time."( Therapeutic implications of escape from angiotensin-converting enzyme inhibition in patients with chronic heart failure.
Berlowitz, M; Ennezat, PV; Le Jemtel, TH; Sonnenblick, EH, 2000
)
0.31
" h(-1)) was found at the 4- to 8-hour interval after dosing in a subset of subjects (n=5) who received the 16-mg dose 4 hours earlier than the other subjects."( Renal hemodynamic and hormonal responses to the angiotensin II antagonist candesartan.
Fisher, ND; Hollenberg, NK; Lansang, MC; Osei, SY; Price, DA, 2000
)
0.54
" Dose-response curves for drinking response to intracerebroventricular injections of ANG II were compared between SD and TG rats."( Glial angiotensinogen regulates brain angiotensin II receptors in transgenic rats TGR(ASrAOGEN).
Bader, M; Böhm, M; Bricca, G; Ganten, D; Monti, J; Schinke, M, 2001
)
0.31
" To investigate blockade of postsynaptic AT1 receptors, we studied the effect of the AT1 antagonists on dose-response curves elicited by exogenous Ang II."( Inhibition of facilitation of sympathetic neurotransmission and angiotensin II-induced pressor effects in the pithed rat: comparison between valsartan, candesartan, eprosartan and embusartan.
Balt, JC; Mathy, MJ; Pfaffendorf, M; van Zwieten, PA, 2001
)
0.51
" Interestingly, the greatest doses of the AT1 antagonists caused less than maximal reduction in the stimulation-induced increase in DBP, resulting in a U-shaped dose-response relationship."( Inhibition of facilitation of sympathetic neurotransmission and angiotensin II-induced pressor effects in the pithed rat: comparison between valsartan, candesartan, eprosartan and embusartan.
Balt, JC; Mathy, MJ; Pfaffendorf, M; van Zwieten, PA, 2001
)
0.51
" In this study we investigated the importance of drug dosing in mediating these differences by comparing the AT(1)-receptor blockade induced by 3 doses of valsartan with that obtained with 3 other antagonists at given doses."( Comparative angiotensin II receptor blockade in healthy volunteers: the importance of dosing.
Brunner, HR; Burnier, M; Centeno, C; Maillard, MP; Nussberger, J; Würzner, G, 2002
)
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
)
0.88
" In this study, we examined the relative contribution of non-ACE pathways, by comparing the response to candesartan and to captopril at the top of the dose-response in normal humans when in balance on a low-salt, as well as a high-salt, diet."( Salt intake and non-ACE pathways for intrarenal angiotensin II generation in man.
Fisher, ND; Hollenberg, NK; Lansang, MC; Osei, SY; Price, DA, 2001
)
0.53
" Chronic candesartan therapy, 16 mg once-daily effectively suppresses pressor responses to Ang II over the duration of the dosing interval."( The effects of candesartan on vascular responses to angiotensin II and norepinephrine in normal volunteers.
Howes, L; Phoon, S; Tran, D, 2001
)
1.08
" The authors established with an initial dose-response curve using escalating concentrations of CN that 10 nmol/L abrogated vasoconstriction induced by angiotensin II (0."( Increased AT2R protein expression but not increased apoptosis during cardioprotection induced by AT1R blockade.
Jugdutt, BI; Kumar, D; Moudgil, R; Musat-Marcu, S; Xu, Y, 2002
)
0.31
" The authors established with an initial dose-response curve using escalating concentrations of CN that 10 nmol/L abrogated vasoconstriction induced by angiotensin II (0."( Increased AT(2)R protein expression but not increased apoptosis during cardioprotection induced by AT(1)R blockade.
Jugdutt, BI; Kumar, D; Moudgil, R; Musat-Marcu, S; Xu, Y, 2002
)
0.31
" The selected studies were included in a meta-analysis of the dose-response relationship for each drug."( The relationships between dose and antihypertensive effect of four AT1-receptor blockers. Differences in potency and efficacy.
Elmfeldt, D; Meredith, P; Olofsson, B, 2002
)
0.31
"There was a wide range of changes in RPF and GFR in response to the two agents, each administered at the top of its dose-response range."( Glomerular hemodynamics and the renin-angiotensin system in patients with type 1 diabetes mellitus.
Fisher, ND; Gordon, MS; Hollenberg, NK; Laffel, LM; Lansang, MC; Perkins, B; Price, DA; Williams, GH, 2003
)
0.32
" Further research is necessary to determine which AT1RBs and which dosing regimens are optimal."( Emerging role of angiotensin II type 1 receptor blockers for the treatment of endothelial dysfunction and vascular inflammation.
Mancini, GB, 2002
)
0.31
" While the biphenyltetrazole compound candesartan dissociated slowly and behaved as an insurmountable antagonist for WT-AT(1), it dissociated swiftly and only produced a rightward shift of the angiotensin Ang II- and -IV dose-response curves for inositol phosphate (IP) accumulation in cells expressing N111G."( Peptide and nonpeptide antagonist interaction with constitutively active human AT1 receptors.
Hunyady, L; Kersemans, V; Le, MT; Szaszák, M; Vanderheyden, PM; Vauquelin, G, 2003
)
0.59
" score of test increased) after repeated dosing of the drug, although the subjects did not notice such changes."( Subclinical alteration of taste sensitivity induced by candesartan in healthy subjects.
Araki, N; Fujimura, A; Harada, K; Nishiki, K; Sugimoto, K; Tsuruoka, S; Wakaumi, M, 2004
)
0.57
"These data suggest that candesartan subclinically reduces taste sensitivity after repeated dosing in healthy subjects."( Subclinical alteration of taste sensitivity induced by candesartan in healthy subjects.
Araki, N; Fujimura, A; Harada, K; Nishiki, K; Sugimoto, K; Tsuruoka, S; Wakaumi, M, 2004
)
0.88
" Patients received candesartan titrated to a targeted dosage of 160 mg/day (5 times above the currently approved maximum dose) and remained at that dosage for the subsequent 4 weeks."( Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Ashton, M; Weinberg, AJ; Weinberg, MS; Zappe, DH,
)
0.46
" This study demonstrates the need to further investigate the optimal dosing strategy for ARBs in reducing the progression of renal disease."( Safety and tolerability of high-dose angiotensin receptor blocker therapy in patients with chronic kidney disease: a pilot study.
Ashton, M; Weinberg, AJ; Weinberg, MS; Zappe, DH,
)
0.13
" Dose-response curves were established for the noradrenaline-induced (10(-12) to 10(-7) mol/kg) increase of diastolic blood pressure in pithed rats treated with tubocurarine, propranolol, and atropine."( Reduction of vascular noradrenaline sensitivity by AT1 antagonists depends on functional sympathetic innervation.
Dendorfer, A; Dominiak, P; Raasch, W; Ziegler, A, 2004
)
0.32
" Dosage was doubled at week 4 and hydrochlorothiazide was added at week 12 if blood pressure response was inadequate."( Olmesartan compared with other angiotensin II receptor antagonists: head-to-head trials.
Stumpe, KO, 2004
)
0.32
"Angiotensin II type 1 receptor blockade with a therapeutic dosage of candesartan maintains significant control of blood pressure and may improve QOL-scores, especially when combined with a reducing sodium diet."( Assessment of quality of life in a randomized clinical trial of candesartan only or in combination with DASH diet for hypertensive patients.
Geleris, P; Kirpizidis, H; Stavrati, A, 2005
)
0.8
" Furthermore, because of the notorious subtarget dosing of such agents in clinical practice, we explored the influence of a modest dosing of an angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blockers, and the combination on common biologic markers of coronary atherosclerotic disease."( Lack of effect on coronary atherosclerotic disease biomarkers with modest dosing of an angiotensin-converting enzyme inhibitor, angiotensin II type-1 receptor blocker, and the combination.
Cox, CD; Meyerrose, GE; Peek, MC; Seifert, CF; Simoni, JS; Tsikouris, JP, 2006
)
0.33
"This study of various methods of the renin-angiotensin system inhibition in stable coronary atherosclerotic disease patients demonstrates negligible effects of a modest dosing of ramipril and the combination of ramipril plus candesartan on common biologic markers of coronary atherosclerotic disease."( Lack of effect on coronary atherosclerotic disease biomarkers with modest dosing of an angiotensin-converting enzyme inhibitor, angiotensin II type-1 receptor blocker, and the combination.
Cox, CD; Meyerrose, GE; Peek, MC; Seifert, CF; Simoni, JS; Tsikouris, JP, 2006
)
0.52
" Patients' dosing histories were compiled electronically (MEMS, AARDEX)."( Management of patients with uncontrolled arterial hypertension--the role of electronic compliance monitoring, 24-h ambulatory blood pressure monitoring and Candesartan/HCTZ.
Mengden, T; Tousset, E; Uen, S; Vetter, H, 2006
)
0.53
" Beginning 8 wk after birth, SHR underwent unilateral nephrectomy and were given vehicle (control), or candesartan at a standard 5 mg/kg per d (T5), high 25 mg/kg per d (T25), or ultrahigh 75 mg/kg per d dosage (T75)."( Long-term, high-dosage candesartan suppresses inflammation and injury in chronic kidney disease: nonhemodynamic renal protection.
Dworkin, LD; Gong, R; Rifai, A; Tolbert, EM; Yu, C, 2007
)
0.87
" Models were adjusted for demographic, clinical, physician, and hospital characteristics; models were also adjusted for dosage categories, which were represented by time-dependent variables."( Angiotensin II receptor blockers for the treatment of heart failure: a class effect?
Behlouli, H; Hudson, M; Humphries, K; Pilote, L; Sheppard, R; Tu, JV, 2007
)
0.34
" It compared the antihypertensive effect between increasing ARB dosage and the addition of controlled-release nifedipine."( [NICE-Combi study: effect of nifedipine in combination with an angiotensin II receptor blocker on BP control and renal protection].
Hasebe, N, 2006
)
0.33
" The authors randomly assigned 269 patients who had persistent proteinuria (> or =1 g/d) despite 7 wk of treatment with the highest approved dosage of candesartan (16 mg/d) to 16, 64, or 128 mg/d candesartan for 30 wk."( Supramaximal dose of candesartan in proteinuric renal disease.
Burgess, E; Chiu, A; Muirhead, N; Pichette, V; Rene de Cotret, P; Tobe, S, 2009
)
0.87
"To describe the antihypertensive dose-response of combination therapy with candesartan and hydrochlorothiazide (HCT)."( A dose-response analysis of candesartan-hydrochlorothiazide combination therapy in patients with hypertension.
Elmfeldt, D; Karlson, BW; Olofsson, B; Zetterstrand, S, 2009
)
0.88
" An E(max) model was used to describe the placebo-adjusted dose-response surface for systolic and diastolic blood pressure (BP) reductions."( A dose-response analysis of candesartan-hydrochlorothiazide combination therapy in patients with hypertension.
Elmfeldt, D; Karlson, BW; Olofsson, B; Zetterstrand, S, 2009
)
0.65
" At baseline and after each dosing period, blood pressure measurements and 24-hour urine collections were obtained."( Modulation of advanced glycation end products by candesartan in patients with diabetic kidney disease--a dose-response relationship study.
Clifton, GD; LaSalle, BK; Saha, SA; Short, RA; Tuttle, KR,
)
0.39
" Because administration of candesartan at appropriate dosage (4-12 mg/day) significantly decreased self-measured morning home BP, candesartan might possess the property to maintain a sustained BP reduction for up to 24 hours after dosing, and might be able to prevent early morning cardiovascular events."( [Evaluation of antihypertensive effect of angiotensin II receptor blockers in patients with essential hypertension by self-measured home blood pressure--HACARARE 300 study].
Msanobu, T, 2009
)
0.65
"To study the impact of the dosing time of an angiotensin II receptor blocker (ARB) titrated by self-measured home blood pressure (HBP) on cardiorenal damage in hypertensives."( Effect of dosing time of angiotensin II receptor blockade titrated by self-measured blood pressure recordings on cardiorenal protection in hypertensives: the Japan Morning Surge-Target Organ Protection (J-TOP) study.
Eguchi, K; Hoshide, S; Ishikawa, J; Ishikawa, S; Kario, K; Shimada, K; Shimizu, M; Yano, Y, 2010
)
0.36
" Individuals were then randomly allocated to receive bedtime dosing or awakening dosing of candesartan (+/- diuretic as needed) titrated to achieve a target systolic HBP less than 135 mmHg."( Effect of dosing time of angiotensin II receptor blockade titrated by self-measured blood pressure recordings on cardiorenal protection in hypertensives: the Japan Morning Surge-Target Organ Protection (J-TOP) study.
Eguchi, K; Hoshide, S; Ishikawa, J; Ishikawa, S; Kario, K; Shimada, K; Shimizu, M; Yano, Y, 2010
)
0.58
"In HBP-guided antihypertensive treatment in hypertensives, bedtime dosing of an ARB may be superior to awakening dosing for reducing microalbuminuria."( Effect of dosing time of angiotensin II receptor blockade titrated by self-measured blood pressure recordings on cardiorenal protection in hypertensives: the Japan Morning Surge-Target Organ Protection (J-TOP) study.
Eguchi, K; Hoshide, S; Ishikawa, J; Ishikawa, S; Kario, K; Shimada, K; Shimizu, M; Yano, Y, 2010
)
0.36
"The regular dose of an angiotensin II type-1 receptor blocker (ARB) in renal transplant patients for hypertension is shown to be safe and effective; however, information on the appropriate dosing of ARBs in renal transplant patients is limited."( Safety and efficacy of administering the maximal dose of candesartan in renal transplant recipients.
Abe, T; Ichimaru, N; Imamura, R; Isaka, Y; Kawada, N; Kitamura, H; Kojima, Y; Kokado, Y; Moriyama, T; Nonomura, N; Okumi, M; Rakugi, H; Takahara, S, 2011
)
0.61
"In the Japan Morning Surge-Target Organ Protection (J-TOP) study, which was an open-label multicenter trial to compare bedtime or awakening dosing of candesartan (+ diuretics as needed) among individuals with home SBP higher than 135  mmHg, we evaluated 254 hypertensive patients who underwent ambulatory BP monitoring, and measured their BNP at baseline and after 6th month of treatment."( Association between asleep blood pressure and brain natriuretic peptide during antihypertensive treatment: the Japan Morning Surge-Target Organ Protection (J-TOP) study.
Eguchi, K; Hoshide, S; Ishikawa, J; Ishikawa, S; Kario, K; Shimada, K; Shimizu, M; Yano, Y, 2012
)
0.58
" In view of these findings, we should lower dosage and prolong dosing interval for nephrotic patients in the combination of enalapril and candesartan."( The effect of candesartan on the pharmacokinetics of enalaprilat in nephrotic rats.
Bi, BT; Lin, HB; Lin, T; Ma, AD; Xu, JP; Yang, XM; Yang, YB, 2012
)
0.94
" The purpose of this research was to inform selection of an appropriate pre-specified primary dose-response analysis to demonstrate drug efficacy in a registration trial."( Improper selection of a pre-specified primary dose-response analysis delays regulatory drug approval.
Gobburu, J; Jadhav, P; Liu, J; Wang, Y, 2013
)
0.39
"49 healthy, white, male subjects received: 60 mg nifedipine and 32 mg candesartan FDC, the loose combination of 60 mg nifedipine GITS and 32 mg candesartan, 60 mg nifedipine GITS alone, or 32 mg candesartan alone in a randomized, non-blinded, 4-period, 4-way crossover design with each dosing following overnight fasting."( Investigation of bioequivalence of a new fixed-dose combination of nifedipine and candesartan with the corresponding loose combination as well as the drug-drug interaction potential between both drugs under fasting conditions.
Brendel, E; Dietrich, H; Froede, C; Thomas, D; Weimann, B, 2013
)
0.85
" When comparing AUC(0-tlast) and Cmax of nifedipine and candesartan after dosing with the loose combination vs."( Investigation of bioequivalence of a new fixed-dose combination of nifedipine and candesartan with the corresponding loose combination as well as the drug-drug interaction potential between both drugs under fasting conditions.
Brendel, E; Dietrich, H; Froede, C; Thomas, D; Weimann, B, 2013
)
0.86
" Individual-level linkage of nationwide registries of hospitalization and drug dispensing in Denmark was used to describe patterns of ARB prescriptions and estimate dosage before and after November 2010."( Dosage of angiotensin-II receptor blockers in heart failure patients following changes in Danish drug reimbursement policies.
Gislason, GH; Kristensen, SL; Køber, L; Lamberts, M; Selmer, C; Torp-Pedersen, C; von Kappelgaard, LM, 2014
)
0.4
"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
)
0.97
" 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
)
0.75
"In the Japan Morning Surge-Target Organ Protection (J-TOP) study, which compared bedtime or awakening dosing of candesartan (+diuretics as needed) among subjects with home systolic BP (SBP) higher than 135 mm Hg, we evaluated 180 hypertensive patients who successfully underwent pulse wave analysis by HEM-9000AI and measured their urinary albumin/creatinine ratio (UACR) and left ventricular mass index (LVMI) (n = 144) at baseline and after 6 months of treatment."( Correlation of Central Blood Pressure to Hypertensive Target Organ Damages During Antihypertensive Treatment: The J-TOP Study.
Eguchi, K; Hoshide, S; Ishikawa, J; Kario, K; Shimizu, M; Yano, Y, 2015
)
0.63
" The methods were successfully determined the three components in bulk powder, laboratory-prepared mixtures, and combined dosage forms."( Mean centering of ratio spectra and concentration augmented classical least squares in a comparative approach for quantitation of spectrally overlapped bands of antihypertensives in formulations.
Abdel Monem Hegazy, M; Fayez, YM, 2015
)
0.42
" Treatments were administered for 12 weeks without dosage adjustment."( A Randomized, Double-blind, Candesartan-controlled, Parallel Group Comparison Clinical Trial to Evaluate the Antihypertensive Efficacy and Safety of Fimasartan in Patients with Mild to Moderate Essential Hypertension.
Cha, GS; Cha, TJ; Chae, SC; Chun, KJ; Hong, GR; Hur, SH; Hwang, JY; Kim, DI; Kim, DS; Kim, KS; Kim, MH; Lee, JH; Lee, SG; Yang, DH, 2016
)
0.73
" Although the pharmacology of ROMK channels is still being developed, channel inhibitors have been identified and shown to cause natriuresis and diuresis, in the absence of any significant kaliuresis, on acute oral dosing to rats or dogs."( The Renal Outer Medullary Potassium Channel Inhibitor, MK-7145, Lowers Blood Pressure, and Manifests Features of Bartter's Syndrome Type II Phenotype.
Alonso-Galicia, M; Corona, A; Felix, JP; Garcia, ML; Gill, C; Hampton, C; Kaczorowski, GJ; Kohler, M; Liu, J; Metzger, JM; Ormes, J; Owens, K; Pai, LY; Pasternak, A; Price, O; Priest, BT; Rasa, C; Roy, S; Shah, K; Sullivan, KA; Tang, H; Thomas-Fowlkes, B; Tong, V; Xiao, J; Zhou, X, 2016
)
0.43
"For both candesartan and amlodipine, the 90% confidence intervals for the geometric mean ratios of area under the concentration-time curve from time zero to the time of dosing interval of 24 hours and maximum concentration after drug administration fell within the bioequivalence acceptance criteria."( No pharmacokinetic interactions between candesartan and amlodipine following multiple oral administrations in healthy subjects.
Huh, W; Kim, JR; Kim, S; Ko, JW, 2018
)
1.17
"Three breastfeeding mothers, all stabilized on candesartan (8-32 mg/d), provided milk and plasma samples over one dosing interval (24 hours)."( Transfer of Candesartan Into Human Breast Milk.
Coberger, ED; Dalrymple, JM; Jensen, BP, 2019
)
1.15
" Once weekly oral dosing of nano-FDC of amlodipine, CNDT and hydrochlorothiazide provided adequate antihypertensive effect which was not statistically different from daily dosing of free drugs in dexamethasone-induced animal model."( Pharmacokinetic and pharmacodynamic evaluation of nano-fixed dose combination for hypertension.
Bhandari, RK; Bhatia, A; Kaur, N; Malhotra, S; Pandey, AK; Rather, IIG; Shafiq, N; Sharma, S, 2020
)
0.56
"Once weekly oral dosing of nano-FDC of amlodipine, CNDT and hydrochlorothiazide provided adequate antihypertensive effect and was not statistically different from daily dosing of free drugs in dexamethasone-induced animal model."( Pharmacokinetic and pharmacodynamic evaluation of nano-fixed dose combination for hypertension.
Bhandari, RK; Bhatia, A; Kaur, N; Malhotra, S; Pandey, AK; Rather, IIG; Shafiq, N; Sharma, S, 2020
)
0.56
" Considering these factors, a more individualized approach of candesartan dosing should be investigated in patients with HF."( Population Pharmacokinetics of Candesartan in Patients with Chronic Heart Failure.
Bonnefois, G; de Denus, S; Dubé, MP; Kassem, I; Li, J; Nekka, F; Rouleau, JL; Sanche, S; Tardif, JC; Turgeon, J; White, M, 2021
)
1.15
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
antihypertensive agentAny drug used in the treatment of acute or chronic vascular hypertension regardless of pharmacological mechanism.
angiotensin receptor antagonistA hormone antagonist that blocks angiotensin receptors.
environmental contaminantAny minor or unwanted substance introduced into the environment that can have undesired effects.
xenobioticA xenobiotic (Greek, xenos "foreign"; bios "life") is a compound that is foreign to a living organism. Principal xenobiotics include: drugs, carcinogens and various compounds that have been introduced into the environment by artificial means.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (2)

ClassDescription
benzimidazolecarboxylic acidA member of the class of benzimidazoles carrying a carboxy group at unspecified position.
biphenylyltetrazoleA member of the class of biphenyls that consists of a biphenyl ring system substituted by a tetrazole ring at an unspecified position.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathways (1)

PathwayProteinsCompounds
Candesartan Action Pathway74

Protein Targets (39)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
acetylcholinesteraseHomo sapiens (human)Potency13.80290.002541.796015,848.9004AID1347398
USP1 protein, partialHomo sapiens (human)Potency22.38720.031637.5844354.8130AID504865
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency13.80290.01237.983543.2770AID1645841
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency27.31890.000214.376460.0339AID720691; AID720692; AID720719
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency0.01910.003041.611522,387.1992AID1159552; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency25.37350.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency0.10640.001530.607315,848.9004AID1224841; AID1224842; AID1259401
pregnane X nuclear receptorHomo sapiens (human)Potency15.84890.005428.02631,258.9301AID1346985
estrogen nuclear receptor alphaHomo sapiens (human)Potency1.15090.000229.305416,493.5996AID743069; AID743078; AID743079; AID743080; AID743091
cytochrome P450 2D6Homo sapiens (human)Potency0.01950.00108.379861.1304AID1645840
potassium voltage-gated channel subfamily H member 2 isoform dHomo sapiens (human)Potency35.48130.01789.637444.6684AID588834
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency31.03990.000323.4451159.6830AID743065; AID743067
gemininHomo sapiens (human)Potency13.33590.004611.374133.4983AID624296
peripheral myelin protein 22Rattus norvegicus (Norway rat)Potency36.12540.005612.367736.1254AID624032
Cellular tumor antigen p53Homo sapiens (human)Potency33.49150.002319.595674.0614AID651631; AID720552
[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)
Epidermal growth factor receptorHomo sapiens (human)IC50 (µMol)3.27690.00000.536910.0000AID625184
Receptor tyrosine-protein kinase erbB-2Homo sapiens (human)IC50 (µMol)5.94720.00010.545310.0000AID625186
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)IC50 (µMol)3.06520.00041.877310.0000AID625207
Aldo-keto reductase family 1 member B1Rattus norvegicus (Norway rat)Ki3.03980.00322.28879.3160AID625207
Cytochrome P450 3A4Homo sapiens (human)IC50 (µMol)9.00000.00011.753610.0000AID625251
Adenosine receptor A3Homo sapiens (human)IC50 (µMol)1.21990.00001.89408.5470AID625196
Adenosine receptor A3Homo sapiens (human)Ki0.68950.00000.930610.0000AID625196
60 kDa heat shock protein, mitochondrialHomo sapiens (human)IC50 (µMol)100.00000.17004.559010.0000AID1594139
Cytochrome P450 2C9 Homo sapiens (human)IC50 (µMol)3.00000.00002.800510.0000AID625248
Beta-3 adrenergic receptorHomo sapiens (human)IC50 (µMol)4.30000.00233.24158.0600AID625206
Beta-3 adrenergic receptorHomo sapiens (human)Ki3.20000.00302.30986.0450AID625206
Alpha-1B adrenergic receptorRattus norvegicus (Norway rat)IC50 (µMol)1.21990.00021.874210.0000AID625196
Alpha-1B adrenergic receptorRattus norvegicus (Norway rat)Ki0.68950.00010.949010.0000AID625196
Alpha-2B adrenergic receptorHomo sapiens (human)IC50 (µMol)3.84300.00001.23808.1590AID625202
Alpha-2B adrenergic receptorHomo sapiens (human)Ki1.75440.00020.725710.0000AID625202
5-hydroxytryptamine receptor 1ARattus norvegicus (Norway rat)Ki0.00060.00010.739610.0000AID37529
Sodium-dependent noradrenaline transporter Homo sapiens (human)IC50 (µMol)3.06520.00081.541620.0000AID625207
Sodium-dependent noradrenaline transporter Homo sapiens (human)Ki3.03980.00031.465610.0000AID625207
Thromboxane-A synthase Homo sapiens (human)IC50 (µMol)3.05940.00091.230410.0000AID625229
Type-1 angiotensin II receptorHomo sapiens (human)IC50 (µMol)0.04050.00020.09323.6000AID1289936; AID1289942; AID568897
Type-1 angiotensin II receptorHomo sapiens (human)Ki0.00700.00020.18374.7000AID1289936; AID1352010
Type-1 angiotensin II receptorOryctolagus cuniculus (rabbit)Ki0.00060.00021.18284.7000AID37529
Alpha-1A adrenergic receptorRattus norvegicus (Norway rat)IC50 (µMol)1.21990.00001.819410.0000AID625196
Alpha-1A adrenergic receptorRattus norvegicus (Norway rat)Ki0.68950.00000.965010.0000AID625196
Type-2 angiotensin II receptorHomo sapiens (human)Ki10.00000.00020.56507.7790AID1277889
10 kDa heat shock protein, mitochondrialHomo sapiens (human)IC50 (µMol)100.00000.17004.559010.0000AID1594139
Thiosulfate sulfurtransferaseHomo sapiens (human)IC50 (µMol)100.00000.06003.96319.7000AID1594135
60 kDa chaperonin Escherichia coliIC50 (µMol)175.00000.03903.55529.8000AID1594140; AID1594141
10 kDa chaperonin Escherichia coliIC50 (µMol)175.00000.03903.55529.8000AID1594140; AID1594141
[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)
Type-1A angiotensin II receptor Rattus norvegicus (Norway rat)Kd0.00320.00000.00270.0100AID412478
Leukotriene B4 receptor 2Homo sapiens (human)EC50 (µMol)15.00000.07001.93756.8000AID1779666
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Type-1 angiotensin II receptorHomo sapiens (human)Affinity0.00010.00050.03150.2300AID243379
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (398)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell population proliferationEpidermal growth factor receptorHomo sapiens (human)
MAPK cascadeEpidermal growth factor receptorHomo sapiens (human)
ossificationEpidermal growth factor receptorHomo sapiens (human)
embryonic placenta developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein phosphorylationEpidermal growth factor receptorHomo sapiens (human)
hair follicle developmentEpidermal growth factor receptorHomo sapiens (human)
translationEpidermal growth factor receptorHomo sapiens (human)
signal transductionEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
activation of phospholipase C activityEpidermal growth factor receptorHomo sapiens (human)
salivary gland morphogenesisEpidermal growth factor receptorHomo sapiens (human)
midgut developmentEpidermal growth factor receptorHomo sapiens (human)
learning or memoryEpidermal growth factor receptorHomo sapiens (human)
circadian rhythmEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell population proliferationEpidermal growth factor receptorHomo sapiens (human)
diterpenoid metabolic processEpidermal growth factor receptorHomo sapiens (human)
peptidyl-tyrosine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
cerebral cortex cell migrationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell growthEpidermal growth factor receptorHomo sapiens (human)
lung developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cell migrationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of superoxide anion generationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
response to cobalaminEpidermal growth factor receptorHomo sapiens (human)
response to hydroxyisoflavoneEpidermal growth factor receptorHomo sapiens (human)
cellular response to reactive oxygen speciesEpidermal growth factor receptorHomo sapiens (human)
peptidyl-tyrosine autophosphorylationEpidermal growth factor receptorHomo sapiens (human)
ERBB2-EGFR signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
negative regulation of epidermal growth factor receptor signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
negative regulation of protein catabolic processEpidermal growth factor receptorHomo sapiens (human)
vasodilationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of phosphorylationEpidermal growth factor receptorHomo sapiens (human)
ovulation cycleEpidermal growth factor receptorHomo sapiens (human)
hydrogen peroxide metabolic processEpidermal growth factor receptorHomo sapiens (human)
negative regulation of apoptotic processEpidermal growth factor receptorHomo sapiens (human)
positive regulation of MAP kinase activityEpidermal growth factor receptorHomo sapiens (human)
tongue developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA repairEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA replicationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of bone resorptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of DNA-templated transcriptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of vasoconstrictionEpidermal growth factor receptorHomo sapiens (human)
negative regulation of mitotic cell cycleEpidermal growth factor receptorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIEpidermal growth factor receptorHomo sapiens (human)
regulation of JNK cascadeEpidermal growth factor receptorHomo sapiens (human)
symbiont entry into host cellEpidermal growth factor receptorHomo sapiens (human)
protein autophosphorylationEpidermal growth factor receptorHomo sapiens (human)
astrocyte activationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of fibroblast proliferationEpidermal growth factor receptorHomo sapiens (human)
digestive tract morphogenesisEpidermal growth factor receptorHomo sapiens (human)
positive regulation of smooth muscle cell proliferationEpidermal growth factor receptorHomo sapiens (human)
neuron projection morphogenesisEpidermal growth factor receptorHomo sapiens (human)
epithelial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
positive regulation of epithelial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
regulation of peptidyl-tyrosine phosphorylationEpidermal growth factor receptorHomo sapiens (human)
protein insertion into membraneEpidermal growth factor receptorHomo sapiens (human)
response to calcium ionEpidermal growth factor receptorHomo sapiens (human)
regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of synaptic transmission, glutamatergicEpidermal growth factor receptorHomo sapiens (human)
positive regulation of glial cell proliferationEpidermal growth factor receptorHomo sapiens (human)
morphogenesis of an epithelial foldEpidermal growth factor receptorHomo sapiens (human)
eyelid development in camera-type eyeEpidermal growth factor receptorHomo sapiens (human)
response to UV-AEpidermal growth factor receptorHomo sapiens (human)
positive regulation of mucus secretionEpidermal growth factor receptorHomo sapiens (human)
regulation of ERK1 and ERK2 cascadeEpidermal growth factor receptorHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeEpidermal growth factor receptorHomo sapiens (human)
cellular response to amino acid stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to mechanical stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to cadmium ionEpidermal growth factor receptorHomo sapiens (human)
cellular response to epidermal growth factor stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to estradiol stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to xenobiotic stimulusEpidermal growth factor receptorHomo sapiens (human)
cellular response to dexamethasone stimulusEpidermal growth factor receptorHomo sapiens (human)
positive regulation of canonical Wnt signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
liver regenerationEpidermal growth factor receptorHomo sapiens (human)
cell-cell adhesionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein kinase C activityEpidermal growth factor receptorHomo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleEpidermal growth factor receptorHomo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of prolactin secretionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of miRNA transcriptionEpidermal growth factor receptorHomo sapiens (human)
positive regulation of protein localization to plasma membraneEpidermal growth factor receptorHomo sapiens (human)
negative regulation of cardiocyte differentiationEpidermal growth factor receptorHomo sapiens (human)
neurogenesisEpidermal growth factor receptorHomo sapiens (human)
multicellular organism developmentEpidermal growth factor receptorHomo sapiens (human)
positive regulation of kinase activityEpidermal growth factor receptorHomo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayEpidermal growth factor receptorHomo sapiens (human)
cell surface receptor signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of protein phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
enzyme-linked receptor protein signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
heart developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuromuscular junction developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
motor neuron axon guidanceReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
Schwann cell developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
peptidyl-tyrosine phosphorylationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell growthReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of microtubule-based processReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
immature T cell proliferation in thymusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
negative regulation of immature T cell proliferation in thymusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of Rho protein signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
intracellular signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-ERBB3 signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-EGFR signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB2-ERBB4 signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
wound healingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
myelinationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of MAP kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transductionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of translationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of angiogenesisReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell adhesionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of transcription by RNA polymerase IReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
oligodendrocyte differentiationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of epithelial cell proliferationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
regulation of ERK1 and ERK2 cascadeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cellular response to growth factor stimulusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cellular response to epidermal growth factor stimulusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
semaphorin-plexin signaling pathwayReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of protein targeting to membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neurotransmitter receptor localization to postsynaptic specialization membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neurogenesisReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of MAPK cascadeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
negative regulation of apoptotic processReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
multicellular organism developmentReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
positive regulation of cell population proliferationReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuron differentiationReceptor tyrosine-protein kinase erbB-2Homo 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)
lipid hydroxylationCytochrome P450 3A4Homo sapiens (human)
lipid metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid catabolic processCytochrome P450 3A4Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid metabolic processCytochrome P450 3A4Homo sapiens (human)
cholesterol metabolic processCytochrome P450 3A4Homo sapiens (human)
androgen metabolic processCytochrome P450 3A4Homo sapiens (human)
estrogen metabolic processCytochrome P450 3A4Homo sapiens (human)
alkaloid catabolic processCytochrome P450 3A4Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 3A4Homo sapiens (human)
calcitriol biosynthetic process from calciolCytochrome P450 3A4Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D metabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D catabolic processCytochrome P450 3A4Homo sapiens (human)
retinol metabolic processCytochrome P450 3A4Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 3A4Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 3A4Homo sapiens (human)
aflatoxin metabolic processCytochrome P450 3A4Homo sapiens (human)
oxidative demethylationCytochrome P450 3A4Homo sapiens (human)
protein folding60 kDa chaperoninEscherichia coli K-12
response to radiation60 kDa chaperoninEscherichia coli K-12
response to heat60 kDa chaperoninEscherichia coli K-12
virion assembly60 kDa chaperoninEscherichia coli K-12
chaperone cofactor-dependent protein refolding60 kDa chaperoninEscherichia coli K-12
protein refolding60 kDa chaperoninEscherichia coli K-12
chaperone cofactor-dependent protein refolding60 kDa chaperoninEscherichia coli K-12
response to heat60 kDa chaperoninEscherichia coli K-12
inflammatory responseAdenosine receptor A3Homo sapiens (human)
signal transductionAdenosine receptor A3Homo sapiens (human)
activation of adenylate cyclase activityAdenosine receptor A3Homo sapiens (human)
regulation of heart contractionAdenosine receptor A3Homo sapiens (human)
negative regulation of cell population proliferationAdenosine receptor A3Homo sapiens (human)
response to woundingAdenosine receptor A3Homo sapiens (human)
regulation of norepinephrine secretionAdenosine receptor A3Homo sapiens (human)
negative regulation of cell migrationAdenosine receptor A3Homo sapiens (human)
negative regulation of NF-kappaB transcription factor activityAdenosine receptor A3Homo sapiens (human)
presynaptic modulation of chemical synaptic transmissionAdenosine receptor A3Homo sapiens (human)
G protein-coupled adenosine receptor signaling pathwayAdenosine receptor A3Homo sapiens (human)
adhesion of symbiont to host60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of type II interferon production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
T cell activation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
MyD88-dependent toll-like receptor signaling pathway60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of T cell mediated immune response to tumor cell60 kDa heat shock protein, mitochondrialHomo sapiens (human)
'de novo' protein folding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic process60 kDa heat shock protein, mitochondrialHomo sapiens (human)
response to unfolded protein60 kDa heat shock protein, mitochondrialHomo sapiens (human)
response to cold60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of interferon-alpha production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of type II interferon production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of interleukin-10 production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of interleukin-12 production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of interleukin-6 production60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein refolding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
B cell proliferation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
B cell activation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of macrophage activation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of apoptotic process60 kDa heat shock protein, mitochondrialHomo sapiens (human)
negative regulation of apoptotic process60 kDa heat shock protein, mitochondrialHomo sapiens (human)
isotype switching to IgG isotypes60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein stabilization60 kDa heat shock protein, mitochondrialHomo sapiens (human)
positive regulation of T cell activation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
chaperone-mediated protein complex assembly60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein maturation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
biological process involved in interaction with symbiont60 kDa heat shock protein, mitochondrialHomo sapiens (human)
cellular response to interleukin-760 kDa heat shock protein, mitochondrialHomo sapiens (human)
T cell activation60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein import into mitochondrial intermembrane space60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein folding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrial unfolded protein response60 kDa heat shock protein, mitochondrialHomo sapiens (human)
apoptotic mitochondrial changes60 kDa heat shock protein, mitochondrialHomo sapiens (human)
xenobiotic metabolic processCytochrome P450 2C9 Homo sapiens (human)
steroid metabolic processCytochrome P450 2C9 Homo sapiens (human)
cholesterol metabolic processCytochrome P450 2C9 Homo sapiens (human)
estrogen metabolic processCytochrome P450 2C9 Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 2C9 Homo sapiens (human)
epoxygenase P450 pathwayCytochrome P450 2C9 Homo sapiens (human)
urea metabolic processCytochrome P450 2C9 Homo sapiens (human)
monocarboxylic acid metabolic processCytochrome P450 2C9 Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 2C9 Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 2C9 Homo sapiens (human)
amide metabolic processCytochrome P450 2C9 Homo sapiens (human)
icosanoid biosynthetic processCytochrome P450 2C9 Homo sapiens (human)
oxidative demethylationCytochrome P450 2C9 Homo sapiens (human)
omega-hydroxylase P450 pathwayCytochrome P450 2C9 Homo sapiens (human)
receptor-mediated endocytosisBeta-3 adrenergic receptorHomo sapiens (human)
negative regulation of G protein-coupled receptor signaling pathwayBeta-3 adrenergic receptorHomo sapiens (human)
diet induced thermogenesisBeta-3 adrenergic receptorHomo sapiens (human)
carbohydrate metabolic processBeta-3 adrenergic receptorHomo sapiens (human)
generation of precursor metabolites and energyBeta-3 adrenergic receptorHomo sapiens (human)
energy reserve metabolic processBeta-3 adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messengerBeta-3 adrenergic receptorHomo sapiens (human)
adenylate cyclase-modulating G protein-coupled receptor signaling pathwayBeta-3 adrenergic receptorHomo sapiens (human)
response to coldBeta-3 adrenergic receptorHomo sapiens (human)
heat generationBeta-3 adrenergic receptorHomo sapiens (human)
negative regulation of multicellular organism growthBeta-3 adrenergic receptorHomo sapiens (human)
eating behaviorBeta-3 adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeBeta-3 adrenergic receptorHomo sapiens (human)
brown fat cell differentiationBeta-3 adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayBeta-3 adrenergic receptorHomo sapiens (human)
positive regulation of cold-induced thermogenesisBeta-3 adrenergic receptorHomo sapiens (human)
norepinephrine-epinephrine-mediated vasodilation involved in regulation of systemic arterial blood pressureBeta-3 adrenergic receptorHomo sapiens (human)
MAPK cascadeAlpha-2B adrenergic receptorHomo sapiens (human)
angiogenesisAlpha-2B adrenergic receptorHomo sapiens (human)
regulation of vascular associated smooth muscle contractionAlpha-2B adrenergic receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
cell-cell signalingAlpha-2B adrenergic receptorHomo sapiens (human)
female pregnancyAlpha-2B adrenergic receptorHomo sapiens (human)
negative regulation of norepinephrine secretionAlpha-2B adrenergic receptorHomo sapiens (human)
platelet activationAlpha-2B adrenergic receptorHomo sapiens (human)
activation of protein kinase B activityAlpha-2B adrenergic receptorHomo sapiens (human)
negative regulation of epinephrine secretionAlpha-2B adrenergic receptorHomo sapiens (human)
receptor transactivationAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of MAPK cascadeAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of neuron differentiationAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of blood pressureAlpha-2B adrenergic receptorHomo sapiens (human)
positive regulation of uterine smooth muscle contractionAlpha-2B adrenergic receptorHomo sapiens (human)
adrenergic receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
adenylate cyclase-activating adrenergic receptor signaling pathwayAlpha-2B adrenergic receptorHomo sapiens (human)
monoamine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transportSodium-dependent noradrenaline transporter Homo sapiens (human)
chemical synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
response to xenobiotic stimulusSodium-dependent noradrenaline transporter Homo sapiens (human)
response to painSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine uptakeSodium-dependent noradrenaline transporter Homo sapiens (human)
neuron cellular homeostasisSodium-dependent noradrenaline transporter Homo sapiens (human)
amino acid transportSodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine transportSodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine uptake involved in synaptic transmissionSodium-dependent noradrenaline transporter Homo sapiens (human)
sodium ion transmembrane transportSodium-dependent noradrenaline transporter Homo sapiens (human)
prostaglandin biosynthetic processThromboxane-A synthase Homo sapiens (human)
icosanoid metabolic processThromboxane-A synthase Homo sapiens (human)
cyclooxygenase pathwayThromboxane-A synthase Homo sapiens (human)
intracellular chloride ion homeostasisThromboxane-A synthase Homo sapiens (human)
response to ethanolThromboxane-A synthase Homo sapiens (human)
positive regulation of vasoconstrictionThromboxane-A synthase Homo sapiens (human)
response to fatty acidThromboxane-A synthase Homo sapiens (human)
regulation of cell growthType-1 angiotensin II receptorHomo sapiens (human)
kidney developmentType-1 angiotensin II receptorHomo sapiens (human)
renin-angiotensin regulation of aldosterone productionType-1 angiotensin II receptorHomo sapiens (human)
maintenance of blood vessel diameter homeostasis by renin-angiotensinType-1 angiotensin II receptorHomo sapiens (human)
regulation of systemic arterial blood pressure by renin-angiotensinType-1 angiotensin II receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayType-1 angiotensin II receptorHomo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathwayType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of cytosolic calcium ion concentrationType-1 angiotensin II receptorHomo sapiens (human)
Rho protein signal transductionType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of macrophage derived foam cell differentiationType-1 angiotensin II receptorHomo sapiens (human)
regulation of vasoconstrictionType-1 angiotensin II receptorHomo sapiens (human)
calcium-mediated signalingType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of phospholipase A2 activityType-1 angiotensin II receptorHomo sapiens (human)
low-density lipoprotein particle remodelingType-1 angiotensin II receptorHomo sapiens (human)
regulation of renal sodium excretionType-1 angiotensin II receptorHomo sapiens (human)
angiotensin-activated signaling pathwayType-1 angiotensin II receptorHomo sapiens (human)
regulation of cell population proliferationType-1 angiotensin II receptorHomo sapiens (human)
symbiont entry into host cellType-1 angiotensin II receptorHomo sapiens (human)
regulation of inflammatory responseType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of inflammatory responseType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of protein metabolic processType-1 angiotensin II receptorHomo sapiens (human)
cell chemotaxisType-1 angiotensin II receptorHomo sapiens (human)
phospholipase C-activating angiotensin-activated signaling pathwayType-1 angiotensin II receptorHomo sapiens (human)
blood vessel diameter maintenanceType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of blood vessel endothelial cell proliferation involved in sprouting angiogenesisType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of CoA-transferase activityType-1 angiotensin II receptorHomo sapiens (human)
positive regulation of reactive oxygen species metabolic processType-1 angiotensin II receptorHomo sapiens (human)
inflammatory responseType-1 angiotensin II receptorHomo sapiens (human)
blood vessel remodelingType-2 angiotensin II receptorHomo sapiens (human)
regulation of systemic arterial blood pressure by circulatory renin-angiotensinType-2 angiotensin II receptorHomo sapiens (human)
angiotensin-mediated vasodilation involved in regulation of systemic arterial blood pressureType-2 angiotensin II receptorHomo sapiens (human)
brain renin-angiotensin systemType-2 angiotensin II receptorHomo sapiens (human)
cell surface receptor signaling pathwayType-2 angiotensin II receptorHomo sapiens (human)
G protein-coupled receptor signaling pathwayType-2 angiotensin II receptorHomo sapiens (human)
G protein-coupled receptor signaling pathway coupled to cGMP nucleotide second messengerType-2 angiotensin II receptorHomo sapiens (human)
brain developmentType-2 angiotensin II receptorHomo sapiens (human)
regulation of blood pressureType-2 angiotensin II receptorHomo sapiens (human)
negative regulation of heart rateType-2 angiotensin II receptorHomo sapiens (human)
negative regulation of cell growthType-2 angiotensin II receptorHomo sapiens (human)
positive regulation of phosphoprotein phosphatase activityType-2 angiotensin II receptorHomo sapiens (human)
regulation of metanephros sizeType-2 angiotensin II receptorHomo sapiens (human)
exploration behaviorType-2 angiotensin II receptorHomo sapiens (human)
nitric oxide-cGMP-mediated signalingType-2 angiotensin II receptorHomo sapiens (human)
angiotensin-activated signaling pathwayType-2 angiotensin II receptorHomo sapiens (human)
vasodilationType-2 angiotensin II receptorHomo sapiens (human)
negative regulation of blood vessel endothelial cell migrationType-2 angiotensin II receptorHomo sapiens (human)
positive regulation of DNA-templated transcriptionType-2 angiotensin II receptorHomo sapiens (human)
negative regulation of neurotrophin TRK receptor signaling pathwayType-2 angiotensin II receptorHomo sapiens (human)
neuron apoptotic processType-2 angiotensin II receptorHomo sapiens (human)
positive regulation of metanephric glomerulus developmentType-2 angiotensin II receptorHomo sapiens (human)
positive regulation of branching involved in ureteric bud morphogenesisType-2 angiotensin II receptorHomo sapiens (human)
positive regulation of extrinsic apoptotic signaling pathwayType-2 angiotensin II receptorHomo sapiens (human)
inflammatory responseType-2 angiotensin II receptorHomo sapiens (human)
osteoblast differentiation10 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein folding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic process10 kDa heat shock protein, mitochondrialHomo sapiens (human)
response to unfolded protein10 kDa heat shock protein, mitochondrialHomo sapiens (human)
chaperone cofactor-dependent protein refolding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
sulfur amino acid catabolic processThiosulfate sulfurtransferaseHomo sapiens (human)
cyanate catabolic processThiosulfate sulfurtransferaseHomo sapiens (human)
epithelial cell differentiationThiosulfate sulfurtransferaseHomo sapiens (human)
rRNA import into mitochondrionThiosulfate sulfurtransferaseHomo sapiens (human)
rRNA transportThiosulfate sulfurtransferaseHomo sapiens (human)
chemotaxisLeukotriene B4 receptor 2Homo sapiens (human)
negative regulation of adenylate cyclase activityLeukotriene B4 receptor 2Homo sapiens (human)
keratinocyte migrationLeukotriene B4 receptor 2Homo sapiens (human)
leukotriene signaling pathwayLeukotriene B4 receptor 2Homo sapiens (human)
neuropeptide signaling pathwayLeukotriene B4 receptor 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (131)

Processvia Protein(s)Taxonomy
epidermal growth factor receptor activityEpidermal growth factor receptorHomo sapiens (human)
virus receptor activityEpidermal growth factor receptorHomo sapiens (human)
chromatin bindingEpidermal growth factor receptorHomo sapiens (human)
double-stranded DNA bindingEpidermal growth factor receptorHomo sapiens (human)
MAP kinase kinase kinase activityEpidermal growth factor receptorHomo sapiens (human)
protein tyrosine kinase activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane signaling receptor activityEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor receptor activityEpidermal growth factor receptorHomo sapiens (human)
integrin bindingEpidermal growth factor receptorHomo sapiens (human)
protein bindingEpidermal growth factor receptorHomo sapiens (human)
calmodulin bindingEpidermal growth factor receptorHomo sapiens (human)
ATP bindingEpidermal growth factor receptorHomo sapiens (human)
enzyme bindingEpidermal growth factor receptorHomo sapiens (human)
kinase bindingEpidermal growth factor receptorHomo sapiens (human)
protein kinase bindingEpidermal growth factor receptorHomo sapiens (human)
protein phosphatase bindingEpidermal growth factor receptorHomo sapiens (human)
protein tyrosine kinase activator activityEpidermal growth factor receptorHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activator activityEpidermal growth factor receptorHomo sapiens (human)
ubiquitin protein ligase bindingEpidermal growth factor receptorHomo sapiens (human)
identical protein bindingEpidermal growth factor receptorHomo sapiens (human)
cadherin bindingEpidermal growth factor receptorHomo sapiens (human)
actin filament bindingEpidermal growth factor receptorHomo sapiens (human)
ATPase bindingEpidermal growth factor receptorHomo sapiens (human)
epidermal growth factor bindingEpidermal growth factor receptorHomo sapiens (human)
growth factor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
RNA polymerase I core bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein tyrosine kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
transmembrane receptor protein tyrosine kinase activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
transmembrane signaling receptor activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
signaling receptor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ATP bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
coreceptor activityReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
receptor tyrosine kinase bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
identical protein bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ErbB-3 class receptor bindingReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
protein heterodimerization activityReceptor tyrosine-protein kinase erbB-2Homo 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)
monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
steroid bindingCytochrome P450 3A4Homo sapiens (human)
iron ion bindingCytochrome P450 3A4Homo sapiens (human)
protein bindingCytochrome P450 3A4Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
oxidoreductase activityCytochrome P450 3A4Homo sapiens (human)
oxygen bindingCytochrome P450 3A4Homo sapiens (human)
enzyme bindingCytochrome P450 3A4Homo sapiens (human)
heme bindingCytochrome P450 3A4Homo sapiens (human)
vitamin D3 25-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
caffeine oxidase activityCytochrome P450 3A4Homo sapiens (human)
quinine 3-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
testosterone 6-beta-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1-alpha,25-dihydroxyvitamin D3 23-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
aromatase activityCytochrome P450 3A4Homo sapiens (human)
vitamin D 24-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 2-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1,8-cineole 2-exo-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
magnesium ion binding60 kDa chaperoninEscherichia coli K-12
protein binding60 kDa chaperoninEscherichia coli K-12
ATP binding60 kDa chaperoninEscherichia coli K-12
isomerase activity60 kDa chaperoninEscherichia coli K-12
ATP hydrolysis activity60 kDa chaperoninEscherichia coli K-12
identical protein binding60 kDa chaperoninEscherichia coli K-12
unfolded protein binding60 kDa chaperoninEscherichia coli K-12
ATP-dependent protein folding chaperone60 kDa chaperoninEscherichia coli K-12
G protein-coupled adenosine receptor activityAdenosine receptor A3Homo sapiens (human)
lipopolysaccharide binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
p53 binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
DNA replication origin binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
single-stranded DNA binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
RNA binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
double-stranded RNA binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
ATP binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
high-density lipoprotein particle binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
isomerase activity60 kDa heat shock protein, mitochondrialHomo sapiens (human)
ATP hydrolysis activity60 kDa heat shock protein, mitochondrialHomo sapiens (human)
enzyme binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
ubiquitin protein ligase binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
apolipoprotein binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
apolipoprotein A-I binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
unfolded protein binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein-folding chaperone binding60 kDa heat shock protein, mitochondrialHomo sapiens (human)
ATP-dependent protein folding chaperone60 kDa heat shock protein, mitochondrialHomo sapiens (human)
monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
iron ion bindingCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid 14,15-epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid 11,12-epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
oxidoreductase activityCytochrome P450 2C9 Homo sapiens (human)
(S)-limonene 6-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
(S)-limonene 7-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
caffeine oxidase activityCytochrome P450 2C9 Homo sapiens (human)
(R)-limonene 6-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
aromatase activityCytochrome P450 2C9 Homo sapiens (human)
heme bindingCytochrome P450 2C9 Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygenCytochrome P450 2C9 Homo sapiens (human)
norepinephrine bindingBeta-3 adrenergic receptorHomo sapiens (human)
beta-adrenergic receptor activityBeta-3 adrenergic receptorHomo sapiens (human)
protein bindingBeta-3 adrenergic receptorHomo sapiens (human)
beta3-adrenergic receptor activityBeta-3 adrenergic receptorHomo sapiens (human)
beta-3 adrenergic receptor bindingBeta-3 adrenergic receptorHomo sapiens (human)
protein homodimerization activityBeta-3 adrenergic receptorHomo sapiens (human)
epinephrine bindingBeta-3 adrenergic receptorHomo sapiens (human)
alpha2-adrenergic receptor activityAlpha-2B adrenergic receptorHomo sapiens (human)
protein bindingAlpha-2B adrenergic receptorHomo sapiens (human)
epinephrine bindingAlpha-2B adrenergic receptorHomo sapiens (human)
actin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
neurotransmitter:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
dopamine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
norepinephrine:sodium symporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
protein bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
monoamine transmembrane transporter activitySodium-dependent noradrenaline transporter Homo sapiens (human)
alpha-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
metal ion bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
beta-tubulin bindingSodium-dependent noradrenaline transporter Homo sapiens (human)
monooxygenase activityThromboxane-A synthase Homo sapiens (human)
thromboxane-A synthase activityThromboxane-A synthase Homo sapiens (human)
iron ion bindingThromboxane-A synthase Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygenThromboxane-A synthase Homo sapiens (human)
heme bindingThromboxane-A synthase Homo sapiens (human)
12-hydroxyheptadecatrienoic acid synthase activityThromboxane-A synthase Homo sapiens (human)
hydroperoxy icosatetraenoate dehydratase activityThromboxane-A synthase Homo sapiens (human)
angiotensin type I receptor activityType-1 angiotensin II receptorHomo sapiens (human)
angiotensin type II receptor activityType-1 angiotensin II receptorHomo sapiens (human)
protein bindingType-1 angiotensin II receptorHomo sapiens (human)
bradykinin receptor bindingType-1 angiotensin II receptorHomo sapiens (human)
protein heterodimerization activityType-1 angiotensin II receptorHomo sapiens (human)
angiotensin type II receptor activityType-2 angiotensin II receptorHomo sapiens (human)
protein bindingType-2 angiotensin II receptorHomo sapiens (human)
receptor antagonist activityType-2 angiotensin II receptorHomo sapiens (human)
RNA binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
ATP binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein folding chaperone10 kDa heat shock protein, mitochondrialHomo sapiens (human)
unfolded protein binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein-folding chaperone binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
metal ion binding10 kDa heat shock protein, mitochondrialHomo sapiens (human)
thiosulfate sulfurtransferase activityThiosulfate sulfurtransferaseHomo sapiens (human)
5S rRNA bindingThiosulfate sulfurtransferaseHomo sapiens (human)
3-mercaptopyruvate sulfurtransferase activityThiosulfate sulfurtransferaseHomo sapiens (human)
leukotriene receptor activityLeukotriene B4 receptor 2Homo sapiens (human)
leukotriene B4 receptor activityLeukotriene B4 receptor 2Homo sapiens (human)
G protein-coupled peptide receptor activityLeukotriene B4 receptor 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (64)

Processvia Protein(s)Taxonomy
endosomeEpidermal growth factor receptorHomo sapiens (human)
plasma membraneEpidermal growth factor receptorHomo sapiens (human)
ruffle membraneEpidermal growth factor receptorHomo sapiens (human)
Golgi membraneEpidermal growth factor receptorHomo sapiens (human)
extracellular spaceEpidermal growth factor receptorHomo sapiens (human)
nucleusEpidermal growth factor receptorHomo sapiens (human)
cytoplasmEpidermal growth factor receptorHomo sapiens (human)
endosomeEpidermal growth factor receptorHomo sapiens (human)
endoplasmic reticulum membraneEpidermal growth factor receptorHomo sapiens (human)
plasma membraneEpidermal growth factor receptorHomo sapiens (human)
focal adhesionEpidermal growth factor receptorHomo sapiens (human)
cell surfaceEpidermal growth factor receptorHomo sapiens (human)
endosome membraneEpidermal growth factor receptorHomo sapiens (human)
membraneEpidermal growth factor receptorHomo sapiens (human)
basolateral plasma membraneEpidermal growth factor receptorHomo sapiens (human)
apical plasma membraneEpidermal growth factor receptorHomo sapiens (human)
cell junctionEpidermal growth factor receptorHomo sapiens (human)
clathrin-coated endocytic vesicle membraneEpidermal growth factor receptorHomo sapiens (human)
early endosome membraneEpidermal growth factor receptorHomo sapiens (human)
nuclear membraneEpidermal growth factor receptorHomo sapiens (human)
membrane raftEpidermal growth factor receptorHomo sapiens (human)
perinuclear region of cytoplasmEpidermal growth factor receptorHomo sapiens (human)
multivesicular body, internal vesicle lumenEpidermal growth factor receptorHomo sapiens (human)
intracellular vesicleEpidermal growth factor receptorHomo sapiens (human)
protein-containing complexEpidermal growth factor receptorHomo sapiens (human)
receptor complexEpidermal growth factor receptorHomo sapiens (human)
Shc-EGFR complexEpidermal growth factor receptorHomo sapiens (human)
basal plasma membraneEpidermal growth factor receptorHomo sapiens (human)
semaphorin receptor complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
nucleusReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
nucleoplasmReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
early endosomeReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
cytosolReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
endosome membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
basolateral plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
apical plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
neuromuscular junctionReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ruffle membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
presynaptic membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
myelin sheathReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
perinuclear region of cytoplasmReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
ERBB3:ERBB2 complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
receptor complexReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
plasma membraneReceptor tyrosine-protein kinase erbB-2Homo sapiens (human)
basal plasma membraneReceptor tyrosine-protein kinase erbB-2Homo 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)
cytoplasmCytochrome P450 3A4Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 3A4Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 3A4Homo sapiens (human)
cytoplasm60 kDa chaperoninEscherichia coli K-12
cytosol60 kDa chaperoninEscherichia coli K-12
membrane60 kDa chaperoninEscherichia coli K-12
GroEL-GroES complex60 kDa chaperoninEscherichia coli K-12
plasma membraneAdenosine receptor A3Homo sapiens (human)
presynaptic membraneAdenosine receptor A3Homo sapiens (human)
Schaffer collateral - CA1 synapseAdenosine receptor A3Homo sapiens (human)
dendriteAdenosine receptor A3Homo sapiens (human)
plasma membraneAdenosine receptor A3Homo sapiens (human)
synapseAdenosine receptor A3Homo sapiens (human)
mitochondrial matrix60 kDa heat shock protein, mitochondrialHomo sapiens (human)
extracellular space60 kDa heat shock protein, mitochondrialHomo sapiens (human)
cytoplasm60 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrion60 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrial inner membrane60 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrial matrix60 kDa heat shock protein, mitochondrialHomo sapiens (human)
early endosome60 kDa heat shock protein, mitochondrialHomo sapiens (human)
cytosol60 kDa heat shock protein, mitochondrialHomo sapiens (human)
plasma membrane60 kDa heat shock protein, mitochondrialHomo sapiens (human)
clathrin-coated pit60 kDa heat shock protein, mitochondrialHomo sapiens (human)
cell surface60 kDa heat shock protein, mitochondrialHomo sapiens (human)
membrane60 kDa heat shock protein, mitochondrialHomo sapiens (human)
coated vesicle60 kDa heat shock protein, mitochondrialHomo sapiens (human)
secretory granule60 kDa heat shock protein, mitochondrialHomo sapiens (human)
extracellular exosome60 kDa heat shock protein, mitochondrialHomo sapiens (human)
sperm midpiece60 kDa heat shock protein, mitochondrialHomo sapiens (human)
sperm plasma membrane60 kDa heat shock protein, mitochondrialHomo sapiens (human)
migrasome60 kDa heat shock protein, mitochondrialHomo sapiens (human)
protein-containing complex60 kDa heat shock protein, mitochondrialHomo sapiens (human)
lipopolysaccharide receptor complex60 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrial inner membrane60 kDa heat shock protein, mitochondrialHomo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2C9 Homo sapiens (human)
plasma membraneCytochrome P450 2C9 Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C9 Homo sapiens (human)
cytoplasmCytochrome P450 2C9 Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C9 Homo sapiens (human)
plasma membraneBeta-3 adrenergic receptorHomo sapiens (human)
receptor complexBeta-3 adrenergic receptorHomo sapiens (human)
plasma membraneBeta-3 adrenergic receptorHomo sapiens (human)
cytosolAlpha-2B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2B adrenergic receptorHomo sapiens (human)
cell surfaceAlpha-2B adrenergic receptorHomo sapiens (human)
intracellular membrane-bounded organelleAlpha-2B adrenergic receptorHomo sapiens (human)
plasma membraneAlpha-2B adrenergic receptorHomo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
cell surfaceSodium-dependent noradrenaline transporter Homo sapiens (human)
membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
neuronal cell body membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
presynaptic membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
plasma membraneSodium-dependent noradrenaline transporter Homo sapiens (human)
axonSodium-dependent noradrenaline transporter Homo sapiens (human)
endoplasmic reticulumThromboxane-A synthase Homo sapiens (human)
endoplasmic reticulum membraneThromboxane-A synthase Homo sapiens (human)
cytosolThromboxane-A synthase Homo sapiens (human)
plasma membraneType-1 angiotensin II receptorHomo sapiens (human)
membraneType-1 angiotensin II receptorHomo sapiens (human)
plasma membraneType-1 angiotensin II receptorHomo sapiens (human)
plasma membraneType-2 angiotensin II receptorHomo sapiens (human)
plasma membraneType-2 angiotensin II receptorHomo sapiens (human)
mitochondrion10 kDa heat shock protein, mitochondrialHomo sapiens (human)
membrane10 kDa heat shock protein, mitochondrialHomo sapiens (human)
extracellular exosome10 kDa heat shock protein, mitochondrialHomo sapiens (human)
mitochondrial matrix10 kDa heat shock protein, mitochondrialHomo sapiens (human)
extracellular spaceThiosulfate sulfurtransferaseHomo sapiens (human)
mitochondrionThiosulfate sulfurtransferaseHomo sapiens (human)
mitochondrial matrixThiosulfate sulfurtransferaseHomo sapiens (human)
mitochondrionThiosulfate sulfurtransferaseHomo sapiens (human)
nucleoplasmLeukotriene B4 receptor 2Homo sapiens (human)
plasma membraneLeukotriene B4 receptor 2Homo sapiens (human)
membraneLeukotriene B4 receptor 2Homo sapiens (human)
plasma membraneLeukotriene B4 receptor 2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (208)

Assay IDTitleYearJournalArticle
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.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1214222Cmax in men plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214117Tmax in human plasma expressing CYP2C8*4 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
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.
AID237981Percentage modification of drug adsorbed after administration to human2005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
AID1594140Inhibition of Escherichia coli GroEL expressed in Escherichia coli DH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured rhodanese refolding by measuring rhodanese enzyme activity 2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1487370Binding affinity to human AT1 receptor expressed in CHO cells assessed as dissociation rate constant at 1.5 nM incubated for 60 mins followed by compound washout in presence of losartan2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID364008Antagonist activity at AT1 receptor in rat aorta2008European journal of medicinal chemistry, Sep, Volume: 43, Issue:9
Angiotensin II--AT1 receptor antagonists: design, synthesis and evaluation of substituted carboxamido benzimidazole derivatives.
AID1214133Clearance in human plasma expressing CYP2C9*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1594137Inhibition of ATPase activity of Escherichia coli GroEL expressed in Escherichia coliDH5alpha incubated for 60 mins using ATP by spectrometric analysis2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1487382Binding affinity to human AT1 receptor expressed in CHO cells assessed as residence time at 1.5 nM incubated for 60 mins followed by compound washout in presence of losartan2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID699539Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID181931Percent inhibition of angiotensin II (0.1 ug/kg iv) -induced pressor response 3h after administration of test compounds (1 mg/kg po) in conscious male Sprague-Dawley rats1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID247116Maximal effect against human Angiotensin II receptor type 12005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
AID37516Inhibitory activity against Angiotensin II receptor, type 1 in rabbit aorta1996Journal of medicinal chemistry, Feb-02, Volume: 39, Issue:3
Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy.
AID1487364Displacement of [3H]-candesartan from human AT1 receptor expressed in CHO cells assessed as dissociation rate constant at 1.5 nM pre-incubated with cells followed by compound washout and subsequent addition of [3H]-candesartan up to 60 mins2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID239885pKa value against human Angiotensin II receptor type 12005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
AID1214128Clearance in human plasma expressing CYP2C9*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214129AUC in human plasma expressing CYP2C9*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID699540Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1594145Inhibition of Escherichia coli GroEL expressed in Escherichia coli DH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured rhodanese refolding by measuring rhodanese enzyme activity 2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID243379Binding affinity for AT1 receptor2005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
AID1487362Antagonist activity at human AT1 receptor expressed in CHO cells assessed as reduction in angiotensin 2-induced inositol phosphate accumulation by measuring dissociation rate constant preincubated with cells followed by compound washout in presence of los2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1214111Half life in human plasma expressing CYP2C8*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID185269Percent inhibition of the Angiotensin-II (0.1ug/kg, iv) induced pressor response after 3 hours of administration (1 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1214099AUC in human plasma expressing CYP2C8*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1487375Antagonist activity at human AT1 receptor expressed in CHO cells assessed as reduction in angiotensin 2-induced inositol phosphate accumulation by measuring residence time constant preincubated with cells followed by compound washout in presence of losart2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1214118Clearance in human plasma expressing CYP2C8*4 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1214122Tmax in human plasma expressing CYP2C9*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1487380Binding affinity to human AT1 receptor expressed in CHO cells assessed as residence time at 1.5 nM incubated for 60 mins followed by compound washout2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1214104AUC in human plasma expressing CYP2C8*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID27862Total clearance value was evaluated2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID39791Relative 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.
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.
AID181935Percent inhibition of AII (0.1 ug/kg iv) -induced pressor response at 7 hr after administration of test compounds (0.1 mg/kg po) in conscious male Sprague-Dawley rats.1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID1214126Half life in human plasma expressing CYP2C9*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214127Tmax in human plasma expressing CYP2C9*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1214119AUC in human plasma expressing CYP2C9*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID185267Percent inhibition of the Angiotensin-II (0.1micro g/kg, iv) induced pressor response after 7 hours of administration (3 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1594141Inhibition of Escherichia coli GroEL expressed in Escherichia coliDH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured soluble pig heart MDH refolding by measuring MDH enzyme acti2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1487363Antagonist activity at human AT1 receptor expressed in CHO cells assessed as reduction in angiotensin 2-induced inositol phosphate accumulation by measuring dissociation rate constant preincubated with cells followed by compound washout and subsequent add2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID185264Percent inhibition of the Angiotensin-II (0.1micro g/kg, iv) induced pressor response after 7 hours of administration (10 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1214102Tmax in human plasma expressing CYP2C8*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1594134Inhibition of native soluble pig heart MDH assessed as reduction in MDH enzyme activity using sodium mesoxalate as substrate and NADH by malachite green dye based spectrometric analysis2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID167803Concentration required for inhibition of Angiotensin-II induced rabbit aorta strips contraction1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1352010Displacement of [125I-Sar1-Ile8]-Ang2 from human angiotensin 2 receptor type 1 receptor expressed in HEK293 cells after 1 hr by gamma counting analysis2018European journal of medicinal chemistry, Feb-10, Volume: 145Integration of multi-scale molecular modeling approaches with experiments for the in silico guided design and discovery of novel hERG-Neutral antihypertensive oxazalone and imidazolone derivatives and analysis of their potential restrictive effects on cel
AID1214131Half life in human plasma expressing CYP2C9*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1737440Modulation of cell death in imatinib-resistant human K562 cells assessed by increase in imatinib-mediated cell death in presence of presence of imatinib measured after 72 hrs by Propidium iodide stain based FACS assay (Rvb = 17%)2020European 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.
AID412478Antagonist activity at AT1 receptor in rat aortic rings2008Bioorganic & medicinal chemistry, Dec-15, Volume: 16, Issue:24
Design, synthesis, and evaluation of 5-sulfamoyl benzimidazole derivatives as novel angiotensin II receptor antagonists.
AID1214156Clearance in men plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214100Cmax in human plasma expressing CYP2C8*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1277889Binding affinity to type-2 angiotensin-2 receptor (unknown origin)2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Structural determinants of subtype selectivity and functional activity of angiotensin II receptors.
AID39038Inhibition of specific binding of [125 I ] Angiotensin-II (0.2 nM) to bovine adrenal cortex1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1487374Antagonist activity at human AT1 receptor expressed in CHO cells assessed as reduction in angiotensin 2-induced inositol phosphate accumulation by measuring residence time constant preincubated with cells followed by compound washout and subsequent additi2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID386623Inhibition of 4-(4-(dimethylamino)styryl)-N-methylpyridinium uptake at human OCT1 expressed in HEK293 cells at 100 uM by confocal microscopy2008Journal of medicinal chemistry, Oct-09, Volume: 51, Issue:19
Structural requirements for drug inhibition of the liver specific human organic cation transport protein 1.
AID1594135Inhibition of native rhodanese (unknown origin) assessed as reduction in rhodanese enzyme activity after 45 mins by Fe(SCN)3 dye based spectrometric analysis2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID679591TP_TRANSPORTER: inhibition of Digoxin transepithelial transport (basal to apical)(Digoxin: 0.1 uM, Candesartan: 50 uM) in MDR1-expressing LLC-PK1 cells2002Life sciences, Feb-15, Volume: 70, Issue:13
Interaction of digoxin with antihypertensive drugs via MDR1.
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID167359Inhibitory activity against angiotensin II type 1 induced contractions in rabbit aorta1996Journal of medicinal chemistry, Feb-02, Volume: 39, Issue:3
Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy.
AID1487376Displacement of [3H]-candesartan from human AT1 receptor expressed in CHO cells assessed as residence time at 1.5 nM pre-incubated with cells followed by compound washout and subsequent addition of [3H]-candesartan up to 60 mins2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID185393Percent inhibition of the Angiotensin-II (0.1ug/kg, iv) induced pressor response after 7 hours of administration (1 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1289936Displacement of [3H]-Asp-{Nomega-[N-(4-propanoylaminobutyl)aminocarbonyl]}Arg-ValTyr-Ile-His-Pro-Phe-OH Tris(hydrotrifluoroacetate) from human AT1 receptor transfected in CHO cells co-expressing Galpha16-mtAEQ after 2 hrs by liquid scintillation counting2016Journal of medicinal chemistry, Mar-10, Volume: 59, Issue:5
Mimicking of Arginine by Functionalized N(ω)-Carbamoylated Arginine As a New Broadly Applicable Approach to Labeled Bioactive Peptides: High Affinity Angiotensin, Neuropeptide Y, Neuropeptide FF, and Neurotensin Receptor Ligands As Examples.
AID1214109AUC in human plasma expressing CYP2C8*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID37529Inhibitory activity against Angiotensin II receptor, type 1 in rat adrenal membrane1996Journal of medicinal chemistry, Feb-02, Volume: 39, Issue:3
Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1214116Half life in human plasma expressing CYP2C8*4 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1214157Clearance in women plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214106Half life in human plasma expressing CYP2C8*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214110Cmax in human plasma expressing CYP2C8*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID237099Time required for elimination of 50% of the compound2005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
AID1214120Cmax in human plasma expressing CYP2C9*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1594139Inhibition of human N-terminal octa-His-tagged HSP60 expressed in Escherichia coli Rosetta(DE3) pLysS/human HSP10 expressed in Escherichia coli Rosetta(DE3) assessed as reduction in HSP60/HSP10-mediated denatured MDH refolding by measuring MDH enzyme acti2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID568897Binding affinity to angiotensin AT1 receptor2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID1214121Half life in human plasma expressing CYP2C9*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
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.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
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.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID26605pka value was determined1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID185270Percent inhibition of the Angiotensin-II (0.1ug/kg, iv) induced pressor response after 3 hours of administration (3 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
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.
AID1594144Inhibition of Escherichia coli GroEL expressed in Escherichia coliDH5alpha/Escherichia coli GroES expressed in Escherichia coli BL21 (DE3) assessed as reduction in GroEL/GroES-mediated denatured soluble pig heart MDH refolding by measuring MDH enzyme acti2019Bioorganic & medicinal chemistry letters, 05-01, Volume: 29, Issue:9
HSP60/10 chaperonin systems are inhibited by a variety of approved drugs, natural products, and known bioactive molecules.
AID568789Antagonist activity at angiotensin AT1 receptor2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1214224Half life in men plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214123Clearance in human plasma expressing CYP2C9*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
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.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID39652Inhibition against Angiotensin II receptor, type 12003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID1214107Tmax in human plasma expressing CYP2C8*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1214101Half life in human plasma expressing CYP2C8*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID27037Half life of compound was determined2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID1214124AUC in human plasma expressing CYP2C9*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214113Clearance in human plasma expressing CYP2C8*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
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.
AID311524Oral bioavailability in human2007Bioorganic & medicinal chemistry, Dec-15, Volume: 15, Issue:24
Hologram QSAR model for the prediction of human oral bioavailability.
AID1214221AUC in women plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1277888Displacement of 125I-[Sar1,Leu8] angiotensin-2 from rat type 1 angiotensin-2 receptor expressed in African green monkey COS7 cells after 24 hrs2016Bioorganic & medicinal chemistry letters, Feb-15, Volume: 26, Issue:4
Structural determinants of subtype selectivity and functional activity of angiotensin II receptors.
AID1214223Cmax in women plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214155Tmax in women plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214220AUC in men plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID588209Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset2010Chemical research in toxicology, Jul-19, Volume: 23, Issue:7
Developing structure-activity relationships for the prediction of hepatotoxicity.
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.
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.
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.
AID185262Percent inhibition of the Angiotensin-II (0.1micro g/kg, iv) induced pressor response after 3 hours of administration (10 mg/kg po) in rats1993Journal of medicinal chemistry, Jul-23, Volume: 36, Issue:15
Nonpeptide angiotensin II receptor antagonists. Synthesis and biological activity of benzimidazolecarboxylic acids.
AID1214125Cmax in human plasma expressing CYP2C9*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID568918Ratio of compound Ki to losartan Ki for angiotensin AT1 receptor2010Bioorganic & medicinal chemistry, Dec-15, Volume: 18, Issue:24
Angiotensin II receptor type 1 (AT1) selective nonpeptidic antagonists--a perspective.
AID364010Antihypertensive activity against desoxycortisone-induced hypertension in rat assessed as decrease in mean arterial blood pressure at 5 mg/kg, ip2008European journal of medicinal chemistry, Sep, Volume: 43, Issue:9
Angiotensin II--AT1 receptor antagonists: design, synthesis and evaluation of substituted carboxamido benzimidazole derivatives.
AID412480Antihypertensive effect in desoxycortisone acetate-induced hypertensive rat assessed as maximum decrease in mean arterial blood pressure at 5 mg/kg, ip after 6 hrs2008Bioorganic & medicinal chemistry, Dec-15, Volume: 16, Issue:24
Design, synthesis, and evaluation of 5-sulfamoyl benzimidazole derivatives as novel angiotensin II receptor antagonists.
AID1214153Half life in women plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1779666Agonist activity at human BLT2 overexpressed in CHO-K1 cells assessed as accumulation of inositol monophosphate measured after 90 mins by HTRF assay2021ACS medicinal chemistry letters, Aug-12, Volume: 12, Issue:8
Discovery of Irbesartan Derivatives as BLT2 Agonists by Virtual Screening.
AID1487369Binding affinity to human AT1 receptor expressed in CHO cells assessed as dissociation rate constant at 1.5 nM incubated for 60 mins followed by compound washout2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID699541Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1692293Inhibition of ADP-stimulated human platelet aggregation assessed as ADP light transmission at 50 uM preincubated for 5 min followed by ADP stimulation by light transmission aggregometry (Rvb = 62 +/- 3%)2020Journal of medicinal chemistry, 11-12, Volume: 63, Issue:21
Progress toward a Glycoprotein VI Modulator for the Treatment of Thrombosis.
AID1214103Clearance in human plasma expressing CYP2C8*1/*1 polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID239874Competitive antagonism of Angiotensin II receptor in endothelium removed isolated rat aortic ring; (n = 5)2005Bioorganic & medicinal chemistry letters, Sep-01, Volume: 15, Issue:17
Design, synthesis, and evaluation of novelly substituted benzimidazole compounds as angiotensin II receptor antagonists.
AID1289942Displacement of [3H]-Angiotensin 2 from human AT1 receptor transfected in CHOK1 cells preincubated for 30 mins with bovine serum albumin followed by radioligand addition by liquid scintillation counting2016Journal of medicinal chemistry, Mar-10, Volume: 59, Issue:5
Mimicking of Arginine by Functionalized N(ω)-Carbamoylated Arginine As a New Broadly Applicable Approach to Labeled Bioactive Peptides: High Affinity Angiotensin, Neuropeptide Y, Neuropeptide FF, and Neurotensin Receptor Ligands As Examples.
AID39039Inhibition of specific binding of [125I]angiotensin II (0.2 nM) to angiotensin II receptor in bovine adrenal cortex1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID23686Partition coefficient (logP)1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID1214114AUC in human plasma expressing CYP2C8*4 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214105Cmax in human plasma expressing CYP2C8*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID29138Acid dissociation value was evaluated2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID237841Oral bioavailability2005Journal of medicinal chemistry, Jun-30, Volume: 48, Issue:13
Pharmacophore, drug metabolism, and pharmacokinetics models on non-peptide AT1, AT2, and AT1/AT2 angiotensin II receptor antagonists.
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.
AID1214132Tmax in human plasma expressing CYP2C9*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
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.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1214154Tmax in men plasma at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1487372Binding affinity to human AT1 receptor expressed in CHO cells assessed as dissociation rate constant at 1.5 nM incubated for 60 mins measured after isotopic dilution2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID1216814Metabolic activation assessed as CYP2C9 activation-induced cytotoxicity in human HepG2 cells transfected with human AdCYP2C9 at MOI 10 for 2 days in presence of siNrf2 at 25 to 100 uM after 24 hrs by WST-8 assay2011Drug metabolism and disposition: the biological fate of chemicals, May, Volume: 39, Issue:5
CYP2C9-mediated metabolic activation of losartan detected by a highly sensitive cell-based screening assay.
AID16032Bioavailability1996Journal of medicinal chemistry, Dec-20, Volume: 39, Issue:26
Synthesis and angiotensin II receptor antagonistic activities of benzimidazole derivatives bearing acidic heterocycles as novel tetrazole bioisosteres.
AID1214130Cmax in human plasma expressing CYP2C9*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214108Clearance in human plasma expressing CYP2C8*2 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214115Cmax in human plasma expressing CYP2C8*4 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID1214112Tmax in human plasma expressing CYP2C8*3 allele carrier polymorphism at 25 to 32 mg by LC/MS/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Evaluation of the relationship between sex, polymorphisms in CYP2C8 and CYP2C9, and pharmacokinetics of angiotensin receptor blockers.
AID242919Competitive antagonism of Angiotensin II receptor in endothelium removed isolated rat aortic ring2005Bioorganic & medicinal chemistry letters, Sep-01, Volume: 15, Issue:17
Design, synthesis, and evaluation of novelly substituted benzimidazole compounds as angiotensin II receptor antagonists.
AID1487384Binding affinity to human AT1 receptor expressed in CHO cells assessed as residence time at 1.5 nM incubated for 60 mins measured after isotopic dilution2017Bioorganic & medicinal chemistry letters, 08-15, Volume: 27, Issue:16
Influence of the cellular environment on ligand binding kinetics at membrane-bound targets.
AID23918Renal clearance value was evaluated2003Journal of medicinal chemistry, Jun-05, Volume: 46, Issue:12
Angiotensin II AT1 receptor antagonists. Clinical implications of active metabolites.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1745854NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1745855NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346995Human AT1 receptor (Angiotensin receptors)1999British journal of pharmacology, Feb, Volume: 126, Issue:4
Distinction between surmountable and insurmountable selective AT1 receptor antagonists by use of CHO-K1 cells expressing human angiotensin II AT1 receptors.
AID1346995Human AT1 receptor (Angiotensin receptors)1999European journal of pharmacology, Feb-19, Volume: 367, Issue:2-3
Binding of the antagonist [3H]candesartan to angiotensin II AT1 receptor-transfected [correction of tranfected] Chinese hamster ovary cells.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (1,883)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's164 (8.71)18.2507
2000's1020 (54.17)29.6817
2010's601 (31.92)24.3611
2020's98 (5.20)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 122.63

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 Index122.63 (24.57)
Research Supply Index7.76 (2.92)
Research Growth Index4.96 (4.65)
Search Engine Demand Index229.97 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (122.63)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials412 (21.36%)5.53%
Reviews180 (9.33%)6.00%
Case Studies67 (3.47%)4.05%
Observational6 (0.31%)0.25%
Other1,264 (65.53%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (161)

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
"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
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
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
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
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
Controlled evaLuation of Angiotensin Receptor Blockers for COVID-19 respIraTorY Disease [NCT04394117]Phase 4787 participants (Actual)Interventional2020-06-19Completed
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
A Randomised, Single Blind, Multicentre, 9-month, Phase IV Study, Comparing Treatment Guided by Clinical Symptoms and Signs and NT-proBNP vs Treatment Guided by Clinical Symptoms and Signs Alone, in Patients With Heart Failure (HF) and Left Ventricular Sy [NCT00391846]Phase 4252 participants (Actual)Interventional2006-10-31Completed
Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community- Acquired Pneumonia [NCT02735707]Phase 310,000 participants (Anticipated)Interventional2016-04-11Recruiting
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 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
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 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
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
NT-proBNP Selected PreventiOn of Cardiac eveNts in a populaTion of dIabetic Patients Without A History of Cardiac Disease: a Prospective Randomized Trial [NCT02817360]Phase 42,400 participants (Anticipated)Interventional2016-02-29Recruiting
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
Phase III Study of Irbersartan for the Early Treatment of Severe Sepsis Patients [NCT01992796]Phase 3300 participants (Anticipated)Interventional2014-01-31Not yet recruiting
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
[NCT00360763]Phase 4600 participants InterventionalRecruiting
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)
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
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
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
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
[NCT01629225]Phase 4500 participants (Anticipated)Interventional2013-07-31Recruiting
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
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
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
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.)
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
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
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)
[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, 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
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
Prospective Monitoring of Angiotensin Receptor Neprilysin Inhibitor in Older Adults With Heart Failure and Frailty [NCT04743063]40,000 participants (Anticipated)Observational2021-01-14Active, 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
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.)
The CORONAvirus Disease 2019 Angiotensin Converting Enzyme Inhibitor/Angiotensin Receptor Blocker InvestigatiON (CORONACION) Randomized Clinical Trial [NCT04330300]Phase 42,414 participants (Anticipated)Interventional2020-04-30Suspended(stopped due to Challenges with funding and very low incidence of COVID-19 at Irish study site)
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 ACE Inhibitor or an Angiotensin Receptor Blocker as a Treatment for Methamphetamine Dependence [NCT01062451]Phase 180 participants (Actual)Interventional2009-05-31Completed
"Early Treatment With Candesartan vs Placebo in Asymptomatic Genetic Carriers of Dilated Cardiomyopathy (EARLY-GENE Trial)" [NCT05321875]Phase 3320 participants (Anticipated)Interventional2022-06-02Recruiting
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)
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
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
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)
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
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
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
"Candesartan Cilexetil Tablets Specified Drug-use Survey Hypertension: Survey on Patients With Metabolic Syndrome" [NCT02166697]14,151 participants (Actual)Observational2006-06-30Completed
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]Stroke 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.
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)
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
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 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).
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
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 a Regression of Diabetic Retinopathy.
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]Change of Diastolic Blood Pressure (DBP)
NCT00348686 (6) [back to overview]Percent Change of proBNP(B Type Natriuretic Peptides) in Patients With Candesartan Plus Felodipine
NCT00348686 (6) [back to overview]Change of Systolic Blood Pressure (SBP)
NCT00348686 (6) [back to overview]LVH(Left Ventricular Hypertrophy) Regression by Echocardiac Parameter, Left Ventricular Mass Index
NCT00348686 (6) [back to overview]Percent Change of B Type Natriuretic Peptides (BNP) Level
NCT00348686 (6) [back to overview]Percent Change of proBNP(B Type Natriuretic Peptides) in Patients Treated With Candesartan Only
NCT00391846 (8) [back to overview]Number of CV Deaths
NCT00391846 (8) [back to overview]Changes in Health-related Quality of Life
NCT00391846 (8) [back to overview]Discontinuations
NCT00391846 (8) [back to overview]Total Number of Titration Steps in Prescribed Heart Failure Treatment
NCT00391846 (8) [back to overview]Changes in NT-proBNP Values Over Time in All Patients
NCT00391846 (8) [back to overview]Changes in Heart Failure Symptoms
NCT00391846 (8) [back to overview]Number of Days in Hospital for CV Reason
NCT00391846 (8) [back to overview]Composite Value of 3 Variables After 9 Months: Cardiovascular Death (Days Alive), Cardiovascular Hospitalization (Days Out of Hospital), Heart Failure Symptoms (Symptom Score Subset of the Kansas City Cardiomyopathy Questionnaire - Questions 3,5,7,9)
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).
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)
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
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)
NCT00605072 (5) [back to overview]Blood Pressure Outcome: Systolic BP
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]Cognitive Assessment: Trail Making Test Part B
NCT00605072 (5) [back to overview]Blood Flow Velocity, Sitting
NCT00607672 (13) [back to overview]Interleukin-6 (IL-6) Response
NCT00607672 (13) [back to overview]Plasminogen Activator Inhibitor-1 (PAI-1) Response
NCT00607672 (13) [back to overview]Interleukin-10 (IL-10) Response
NCT00607672 (13) [back to overview]Interleukin-8 (IL-8) Response
NCT00607672 (13) [back to overview]Tissue-type Plasminogen Activator (t-PA) Antigen Response
NCT00607672 (13) [back to overview]Vasopressor Drug Use
NCT00607672 (13) [back to overview]Stroke
NCT00607672 (13) [back to overview]Re-exploration for Bleeding
NCT00607672 (13) [back to overview]New Onset Atrial Fibrillation
NCT00607672 (13) [back to overview]Blood Loss
NCT00607672 (13) [back to overview]Acute Kidney Injury
NCT00607672 (13) [back to overview]Length of Hospital Stay
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 Systolic Blood Pressure (SBP).
NCT00690612 (2) [back to overview]Mean Change From Baseline to Final Visit in Diastolic Blood Pressure (DBP).
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 Glomerular Filtration Rate
NCT01678794 (2) [back to overview]Change in Urinary Sodium Excretion
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]Number of Subjects With Treatment-emergent Adverse Events (TEAEs) of Special Interest 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 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]Blood Pressure Control Rate at Weeks 28 and 52
NCT01788358 (9) [back to overview]Number of Subjects With Clinically Relevant Changes in Laboratory Parameters
NCT01794455 (2) [back to overview]Montgomery-Asberg Depression Rating Scale
NCT01794455 (2) [back to overview]Quick Inventory of Depressive Symptoms, Self-Rated (QIDS-SR16)
NCT01938664 (3) [back to overview]# of Participants Retained in Study
NCT01938664 (3) [back to overview]# of Participants With Adverse Events
NCT01938664 (3) [back to overview]# of Participants With Presence of Cocaine Metabolites Via Urinalysis
NCT01976572 (4) [back to overview]Tmax
NCT01976572 (4) [back to overview]T1/2
NCT01976572 (4) [back to overview]Cmax of Candesartan
NCT01976572 (4) [back to overview]AUC0-t of Candesartan
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]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]Executive Function
NCT01984164 (8) [back to overview]Language
NCT01984164 (8) [back to overview]Memory
NCT01984164 (8) [back to overview]White Matter Lesion Volume
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
NCT02016183 (4) [back to overview]Changes From Baseline in Systolic Blood Pressure (SBP) 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]Percentage of Participants Who Meet Targeted Blood Pressure Level at Baseline and Final Assessment
NCT02068495 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Events
NCT02068495 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Drug Reactions (ADRs)
NCT02068495 (6) [back to overview]Changes From Baseline in Systolic Blood Pressure (SBP) at Final Assessment
NCT02068495 (6) [back to overview]Changes From Baseline in Pulse Rate at Final Assessment
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
NCT02166697 (6) [back to overview]Number of Participants Reporting One or More Serious Adverse Drug Reactions (SADR)
NCT02166697 (6) [back to overview]Number of Participants Reporting One or More Adverse Drug Reactions (ADR)
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, or Lipid Abnormalities
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
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 ARB Combination Drug Therapy at Week 14
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
NCT02211638 (6) [back to overview]Number of Participants Who Experience at Least One Adverse Drug Reactions
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]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]Progression Rate From Early-Stage Nephropathy (Stage 2) to Overt Nephropathy (Stage 3) During the Treatment Period (Week 12)
NCT02332824 (5) [back to overview]Number of Participants Who Experience at Least One Treatment Emergent Adverse Event (TEAE)
NCT02646982 (22) [back to overview]Number of Participants With Elevated Serum Creatinine
NCT02646982 (22) [back to overview]Number of Participants With Hyperkalemia
NCT02646982 (22) [back to overview]Number of Participants With Hypotensive Episodes and Symptoms
NCT02646982 (22) [back to overview]Number of Participants With Symptoms of Hypotension
NCT02646982 (22) [back to overview]Vasoreactivity
NCT02646982 (22) [back to overview]Augmentation Index (AI)
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ40 Levels
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ42/Aβ40 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) Total Tau Levels
NCT02646982 (22) [back to overview]Clinical Dementia Rating (CDR) Score
NCT02646982 (22) [back to overview]Pulse Wave Velocity (PWV)
NCT02646982 (22) [back to overview]Number of Participants With a Hypotensive Episode
NCT02646982 (22) [back to overview]Hopkins Verbal Learning Test (HVLT) Delayed Recall Score
NCT02646982 (22) [back to overview]Cerebrospinal Fluid (CSF) Amyloid Aβ42 Levels
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]EXecutive Abilities: Measures and Instruments for Neurobehavioral Evaluation and Research (EXAMINER) Toolbox Composite Score
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]Trail Making Test (TMT) Part B - A
NCT02646982 (22) [back to overview]Number of Participants Discontinuing Study Medication
NCT02646982 (22) [back to overview]Trail Making Test (TMT) Part B
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]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 Change in Blood Urea Nitrogen
NCT03640312 (17) [back to overview]Change in Mean Systolic Blood Pressure
NCT03640312 (17) [back to overview]Mean Change in Serum Creatinine
NCT03640312 (17) [back to overview]Mean Change in Serum Potassium
NCT03640312 (17) [back to overview]Mean Change in Serum Sodium
NCT03640312 (17) [back to overview]Number of Patients Requiring Step up Treatment
NCT03640312 (17) [back to overview]Medication Adherence
NCT03640312 (17) [back to overview]Change in Mean Diastolic Blood Pressure
NCT03640312 (17) [back to overview]Change in Mean Systolic Blood Pressure
NCT03640312 (17) [back to overview]Mean Systolic 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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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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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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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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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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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 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 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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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 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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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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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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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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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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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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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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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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Number of CV Deaths

Number of deaths (NCT00391846)
Timeframe: 9 months

InterventionParticipants (Number)
Guided by NT-proBNP4
Not Guided by NT-proBNP5

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Discontinuations

Number of patients discontinued due to adverse events' (NCT00391846)
Timeframe: 9 months

InterventionParticipants (Number)
Guided by NT-proBNP8
Not Guided by NT-proBNP6

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Total Number of Titration Steps in Prescribed Heart Failure Treatment

Each titration step in prescribed medication is counted as one step, either up or down. One step up indicates an increase of dose in prescribed medication and one step down indicates a decrease of dose in prescribed medication. The sum of steps is given as a score. Score is given for each arm as a total number of titration steps for all patients in arm. (NCT00391846)
Timeframe: 9 months

InterventionTitration steps (Number)
Guided by NT-proBNP517
Not Guided by NT-proBNP485

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Changes in NT-proBNP Values Over Time in All Patients

The 95% confidential interval (CI) is given as measure of dispersion (NCT00391846)
Timeframe: 9 months and baseline

Interventionng/L (Geometric Mean)
Guided by NT-proBNP2332.1
Not Guided by NT-proBNP2063

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Changes in Heart Failure Symptoms

Changes from baseline in the symptom score subset (question 3, 5, 7 and 9) of KCCQ (swelling, fatigue, shortness of breath, shortness of breath night time). KCCQ is a self-administered by patient symptom score, where higher score reflect better health status. Scale scores are transformed to a 0 to 100 range by subtracting the lowest possible scale score, dividing by the range of the scale and multiplying by 100. This mean that the KCCQ scale is from 0 to 100 with the higher value showing a better health status. (NCT00391846)
Timeframe: 9 months and baseline

InterventionCategorial scale (Mean)
Guided by NT-proBNP3.67
Not Guided by NT-proBNP6.11

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Number of Days in Hospital for CV Reason

Each overnight stay is counted as one day. The lower the better (NCT00391846)
Timeframe: 9 months

InterventionDays in hospital (Mean)
Guided by NT-proBNP5.79
Not Guided by NT-proBNP5.94

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Composite Value of 3 Variables After 9 Months: Cardiovascular Death (Days Alive), Cardiovascular Hospitalization (Days Out of Hospital), Heart Failure Symptoms (Symptom Score Subset of the Kansas City Cardiomyopathy Questionnaire - Questions 3,5,7,9)

The non-parametric scale is constructed from 3 variables, modified after Cleland. Each patient receives a rank score from 1 to 246 (246-number of patients in the study). The lowest score receive patients who die (due to CV event), next patients still alive at end-of-study with the worst composite score, the best alive patients with 0 days in hospital and the largest improvement in the KCCQ (self-administered by patient symptom score, where the higher score reflect better health status). Scores will be summarized using non-parametric calculations. The mean of non-parametric scores is presented (NCT00391846)
Timeframe: 9 months

InterventionScores on a scale (Mean)
Guided by NT-proBNP118.6
Not Guided by NT-proBNP128.4

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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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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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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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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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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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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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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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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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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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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-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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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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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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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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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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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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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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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 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 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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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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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 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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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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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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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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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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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 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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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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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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# 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 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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# 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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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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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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"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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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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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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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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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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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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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 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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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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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 Who Experience at Least One Adverse Events

(NCT02068495)
Timeframe: Up to 12 Months

InterventionParticipants (Count of Participants)
Candesartan Cilexetil/Amlodipine286

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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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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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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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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

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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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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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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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, 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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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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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 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 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

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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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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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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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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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 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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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 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 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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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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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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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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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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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) 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) 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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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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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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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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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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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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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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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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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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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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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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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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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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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 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: 12 weeks

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

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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 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 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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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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Medication Adherence

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

InterventionParticipants (Count of Participants)
QUARTET LDQT21
Candesartan21

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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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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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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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