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Azilsartan (TAK-536)

Alias: TAK-536;TAK-536; TAK-536;Edarbi
Cat No.:V1790 Purity: ≥98%
Azilsartan(TAK-536; TAK536;Edarbi;Ipreziv) is a potent andorally bioavailable angiotensin II type 1 (AT1) receptor antagonist with antihypertensive effects.
Azilsartan (TAK-536)
Azilsartan (TAK-536) Chemical Structure CAS No.: 147403-03-0
Product category: RAAS
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Azilsartan (TAK-536):

  • Azilsartan Medoxomil (TAK 491)
  • Azilsartan D5
  • Azilsartan-d4 (TAK-536-d4)
  • Azilsartan medoxomil monopotassium (TAK 491)
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Azilsartan (TAK-536; TAK536; Edarbi; Ipreziv) is a potent and orally bioavailable angiotensin II type 1 (AT1) receptor antagonist with antihypertensive effects. It inhibit the RAAS pathway with an IC50 of 2.6 nM and has been approved for use in the treatment of hypertension. Azilsartan was developed by Takeda Pharmaceuticals for the treatment of hypertension. Azilsartan lowers blood pressure by blocking the action of angiotensin II, a vasopressor hormone. Azilsartan inhibits the specific binding of 125I-Sar1-Ile8-AII to human angiotensin type 1 receptors. Azilsartan also inhibits the accumulation of AII-induced inositol 1-phosphate (IP1) in the cell-based assay with an IC50 value of 9.2 nM. Azilsartan medoxomil is a useful and attractive new option for lowering BP in patients with essential hypertension, particularly for those not able to tolerate other antihypertensive drugs.

Biological Activity I Assay Protocols (From Reference)
ln Vitro
Azilsartan (0-200 μM, 0-72 hours) decreases HepG2 cell viability [5]. In HepG2 cells, azilartan (100 μM) causes apoptosis during a 24-hour period [5]. With an IC50 of 2.6 nM, acilestan prevents the particular binding of 125I-Sar1-Ile8-AII to the human angiotensin type 1 receptor[3]. Azilsartan efficiently suppresses aortic endothelial and vascular cell proliferation in the absence of exogenous Ang II supplementation [5]. Compared to valsartan, azilartan has a larger influence on adipogenesis and the expression of genes encoding leptin, adiponectin, PPARδ, and peroxisome proliferator-activated receptor-alpha (PPARα). Influence [1].
ln Vivo
In obese Koletsky rats, azilstaran (0–3 mg/kg) administered orally once daily for five days lowers systolic blood pressure (SBP) at a dose of 2 mg/kg[2]. Azilsartan (0–2 mg/kg, orally administered, once daily for 21 days) reduces basal plasma insulin levels and blood pressure[2]. Azilsartan (2 and 4 mg/kg; PO, daily for 9 days) provides defense against secondary brain injury caused by ischemia[4].
Cell Assay
Cell proliferation assay [5]
Cell Types: HepG2 and KDR Cell
Tested Concentrations: 5, 25, 50, 100 and 200 μM
Incubation Duration: 24, 48 and 72 hrs (hours)
Experimental Results: The viability of HepG2 cells gradually diminished by increasing the incubation time and duration. At the same dose, the inhibitory concentration (IC 50%) of azilsartan on HepG2 cells at the 24-hour treatment time point was 100 μM, and under similar treatment conditions, no obvious cytotoxic effect was observed in KDR epithelial normal cells.

Apoptosis analysis [5]
Cell Types: HepG2 Cell
Tested Concentrations: 100 μM
Incubation Duration: 24 hrs (hours)
Experimental Results: 57.2% early and 0.52% late apoptosis were induced after 24 hrs (hours).
Animal Protocol
Animal/Disease Models: Male Wistar-Kyoto (WKY) rats, obese Koletsky rats (n=6 per group)[2]
Doses: 0, 1, 2 and 3 mg/kg
Route of Administration: po (oral gavage), one time/day (9:00-10:00 hrs (hours)) for 5 days
Experimental Results: diminished SBP (systolic blood pressure) in obese Koletsky rats to that of normal rats at 2 mg/kg, whereas the 3 mg/kg dose elicited hypotension.

Animal/Disease Models: Obese Koletsky rats (16, n = 8 per group)[2]
Doses: 0 and 2 mg/kg
Route of Administration: po (oral gavage), one time/day (9:00-10:00 hrs (hours)) for 21 days
Experimental Results: Lowered blood pressure, basal plasma insulin concentration and the homeostasis model assessment of insulin resistance index, and inhibited over-increase of plasma glucose and insulin concentrations during oral glucose tolerance test.

Animal/Disease Models: Male Wistar Rats (240–280 g)[4]
Doses: 0, 2, and 4 mg/kg
Route of Administration: Orally, daily for 9 days, starting 7 days before the day of surgery
Experimental Results: Individual treatments with Azilsartan (2 & 4 mg/kg) and Coenzyme Q10 (20 & 40 mg/kg) Dramatically attenuate
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
In rats, minimal azilsartan-associated radioactivity crossed the blood-brain barrier. Azilsartan passed across the placental barrier in pregnant rats and was distributed to the fetus.
The volume of distribution of azilsartan is approximately 16 L. Azilsartan is highly bound to human plasma proteins (>99%), mainly serum albumin. Protein binding is constant at azilsartan plasma concentrations well above the range achieved with recommended doses.
Following an oral dose of C-labeled azilsartan medoxomil, approximately 55% of radioactivity was recovered in feces and approximately 42% in urine, with 15% of the dose excreted in urine as azilsartan. The elimination half-life of azilsartan is approximately 11 hours and renal clearance is approximately 2.3 mL/min. Steady-state levels of azilsartan are achieved within five days, and no accumulation in plasma occurs with repeated once-daily dosing.
Azilsartan medoxomil is hydrolyzed to azilsartan, the active metabolite, in the gastrointestinal tract during absorption. Azilsartan medoxomil is not detected in plasma after oral administration. Dose proportionality in exposure was established for azilsartan in the azilsartan medoxomil dose range of 20 mg to 320 mg after single or multiple dosing. The estimated absolute bioavailability of azilsartan following administration of azilsartan medoxomil is approximately 60%. After oral administration of azilsartan medoxomil, peak plasma concentrations (Cmax) of azilsartan are reached within 1.5 to 3 hours. Food does not affect the bioavailability of azilsartan.
For more Absorption, Distribution and Excretion (Complete) data for Azilsartan (8 total), please visit the HSDB record page.
Metabolism / Metabolites
Azilsartan medoxomil is rapidly hydrolysed to the active moiety azilsartan by esterases in the gastrointestinal tract and/or during drug absorption. Based on vitro studies, the enzymes involved in the hydrolysis of azilsartan medoxomil to azilsartan in human plasma, and in human liver and small intestinal cytosol seem to be similar to those involved in the hydrolysis of olmesartan medoxomil. Currently, no drug interactions are listed for the hydrolysis of azilsartan medoxomil. The enzyme carboxymethylenebutenolidase is a recently discovered hydrolysis mechanism for azilsartan medoxomi in the intestine and liver, but no interactions with other drugs have been reported for this enzyme in the Metabolism and Transport Drug Interaction Database (DIDB). Also no interactions have been reported for human serum albumin or arylesterases. Since there are multiple esterase pathways involved in the conversion of azilsartan medoxomil to azilsartan, the potential for interactions via this pathway is considered to be minimal. The metabolites M-I and M-II were formed by decarboxylation and dealkylation of azilsartan, respectively, and are pharmacologically inactive. CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 are all capable of metabolising azilsartan. However, CYP2C9 showed the highest activity in metabolising azilsartan to M-II and CYP2C8 in metabolising azilsartan to M-I.
Azilsartan is metabolized to two primary metabolites. The major metabolite in plasma is formed by O-dealkylation, referred to as metabolite M-II, and the minor metabolite is formed by decarboxylation, referred to as metabolite M-I. Systemic exposures to the major and minor metabolites in humans were approximately 50% and less than 1% of azilsartan, respectively. M-I and M-II do not contribute to the pharmacologic activity of Edarbi. The major enzyme responsible for azilsartan metabolism is CYP2C9.
Biological Half-Life
The half-life of azilsartan in plasma was between 4 and 6 hr in rats and dogs and approximately 12 hr in humans.
The elimination half-life of azilsartan is approximately 11 hours ... .
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Azilsartan is a white crystalline powder formulated into oral tablets. Azilsartan is an angiotensin II type 1 (AT1) receptor antagonist. It is used alone or in combination with other classes of antihypertensive agents in the management of hypertension. Azilsartan medoxomil, a prodrug, which is hydrolyzed to azilsartan in the gastrointestinal tract during absorption. HUMAN EXPOSURE AND TOXICITY: Limited data are available related to overdosage in humans. During controlled clinical trials in healthy subjects, once-daily doses up to 320 mg of azilsartan were administered for seven days and were well tolerated. The use of azilsartan during pregnancy is contraindicated. Drugs that act directly on the renin-angiotensin system (e.g., ACE inhibitors, angiotensin II receptor antagonists) reduce fetal renal function and increase fetal and neonatal morbidity and mortality when used in pregnancy during the second and third trimesters. ACE inhibitors also may increase the risk of major congenital malformations when administered during the first trimester of pregnancy. Azilsartan should be discontinued as soon as possible when pregnancy is detected, unless continued use is considered life-saving. ANIMAL STUDIES: There was no evidence of carcinogenicity when azilsartan was administered in the diet to mice and rats for up to two years. Also, azilsartan had no adverse effects on fertility of male or female rats at oral doses of up to 1,000 mg/kg/day. Azilsartan was not teratogenic when administered at oral doses up to 1,000 mg/kg/day to pregnant rats or up to 50 mg/kg/day to pregnant rabbits. However, embryo-fetal toxicity occurred at azilsartan doses of 1,000 mg/kg/day in rats (dilated renal pelvis and short supernumerary ribs) and 50 mg/kg/day in rabbits (increased post-implantation loss, embryo-fetal deaths, and decreased number of live fetuses). Embryo-fetal toxicity was also reported in rats with azilsartan doses as low as 30 mg/kg/day (delayed ossification in the caudal vertebrae) and 100 mg/kg/day (lower male fetal body weight) and at 500 mg/kg/day in rabbits (increased post-implantation loss). Azilsartan medoxomil, azilsartan, and the M-II metabolite were positive for structural aberrations in the Chinese Hamster Lung Cytogenetic Assay. In this assay, structural chromosomal aberrations were observed with the prodrug, azilsartan medoxomil, without metabolic activation. The active moiety, azilsartan was also positive in this assay both with and without metabolic activation. The major human metabolite, M-II was positive in this assay during a 24-hour assay without metabolic activation. Azilsartan medoxomil, azilsartan, and M-II were devoid of genotoxic potential in the Ames reverse mutation assay with Salmonella typhimurium and Escherichia coli, the in vitro Chinese Hamster Ovary Cell forward mutation assay, the in vitro mouse lymphoma (tk) gene mutation test, the ex vivo unscheduled DNA synthesis test, and the in vivo mouse and/or rat bone marrow micronucleus assay.
Hepatotoxicity
Azilsartan has been associated with a low rate of serum aminotransferase elevations that, in controlled trials, was no higher than with placebo therapy. These elevations were transient and rarely required dose modification. No specific instances of clinically apparent acute liver injury have been reported in association with azilsartan therapy, but it has been available for a limited time. Other ARBs have been linked to rare instances of symptomatic hepatotoxicity. The onset of liver injury is usually within 1 to 8 weeks of starting therapy and the serum enzyme pattern is typically hepatocellular with an acute hepatitis-like clinical syndrome. In some instances, cholestasis has developed which can be prolonged and relapsing, but ARB therapy has not been associated with vanishing bile duct syndrome or chronic liver injury. Immunoallergic manifestations (rash, fever, eosinophilia) are not common, nor is autoantibody formation.
Likelihood score: E* (Unproved but suspected rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because no information is available on the use of azilsartan during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Interactions
Since the use of potassium supplements and potassium-containing salt substitutes with an angiotensin II receptor antagonist (e.g., azilsartan medoxomil) can increase the potential for hyperkalemia, some clinicians have suggested that concomitant administration of these agents with azilsartan medoxomil should be avoided.
Since the use of potassium-sparing diuretics (i.e., amiloride, spironolactone, triamterene) with an angiotensin II receptor antagonist (i.e., azilsartan medoxomil) can increase the potential for hyperkalemia, some clinicians have suggested that concomitant administration of these drugs with azilsartan medoxomil should be avoided.
Concomitant treatment with nonsteroidal anti-inflammatory agents (NSAIAs), including selective cyclooxygenase-2 (COX-2) inhibitors, and angiotensin II receptor antagonists may result in deterioration of renal function, including possible acute renal failure, in patients who are geriatric, volume-depleted (including those on diuretic therapy), or have compromised renal function. These effects usually are reversible. Renal function should be periodically monitored in patients receiving azilsartan and NSAIA therapy. The antihypertensive effect of azilsartan may be attenuated in patients receiving NSAIAs, including selective COX-2 inhibitors.
Reversible increases in serum creatinine, which may occur in patients receiving azilsartan medoxomil, may be larger in patients also receiving hydrochlorothiazide.
References

[1]. Molecular and cellular effects of azilsartan: a new generation angiotensin II receptor blocker. J Hypertens. 2011 Dec;29(12):2476-83.

[2]. Azilsartan treatment improves insulin sensitivity in obese spontaneously hypertensive Koletsky rats. Diabetes Obes Metab. 2011 Dec;13(12):1123-9.

[3]. In vitro antagonistic properties of a new angiotensin type 1 receptor blocker, azilsartan, in receptor binding and function studies. J Pharmacol Exp Ther. 2011 Mar;336(3):801-8.

[4]. Neuroprotective potential of azilsartan against cerebral ischemic injury: Possible involvement of mitochondrial mechanisms. Neurochem Int. 2020 Jan;132:104604.

[5]. Novel angiotensin receptor blocker, azilsartan induces oxidative stress and NFkB-mediated apoptosis in hepatocellular carcinoma cell line HepG2. Biomed Pharmacother. 2018 Mar;99:939-946.

Additional Infomation
Therapeutic Uses
Edarbi is an angiotensin II receptor blocker (ARB) indicated for the treatment of hypertension to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. These benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes, including the class to which this drug principally belongs. /Included in US product label/
Edarbi may be used alone or in combination with other antihypertensive agents.
Both angiotensin II receptor antagonists /eg, azilsartan/ and ACE inhibitors have been shown to slow the rate of progression of renal disease in hypertensive patients with diabetes mellitus and microalbuminuria or overt nephropathy, and use of a drug from either class is recommended in such patients. /NOT included in US product label/
Drug Warnings
/BOXED WARNING/ WARNING: FETAL TOXICITY. When pregnancy is detected, discontinue Edarbi as soon as possibl. Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus
Drugs that act directly on the renin-angiotensin system (e.g., ACE inhibitors, angiotensin II receptor antagonists) reduce fetal renal function and increase fetal and neonatal morbidity and mortality when used in pregnancy during the second and third trimesters. ACE inhibitors also may increase the risk of major congenital malformations when administered during the first trimester of pregnancy. Azilsartan should be discontinued as soon as possible when pregnancy is detected, unless continued use is considered life-saving. Nearly all women can be transferred successfully to alternative therapy for the remainder of their pregnancy.
Use of drugs that affect the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue Edarbi as soon as possible. These adverse outcomes are usually associated with use of these drugs in the second and third trimester of pregnancy. Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. Appropriate management of maternal hypertension during pregnancy is important to optimize outcomes for both mother and fetus.
Because symptomatic hypotension may occur in patients with an activated renin-angiotensin system (e.g., patients with volume or salt depletion secondary to high doses of diuretics), azilsartan should be initiated in such patients after volume or salt depletion is corrected, or a lower initial dose of the drug should be used. If hypotension occurs in patients receiving azilsartan medoxomil, the patient should be placed in the supine position and, if necessary, an IV infusion of 0.9% sodium chloride injection should be administered. Transient hypotension is not a contraindication to additional doses of azilsartan, and therapy with the drug can be cautiously reinstated after blood pressure has been stabilized (e.g., with volume expansion).
For more Drug Warnings (Complete) data for Azilsartan (14 total), please visit the HSDB record page.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C25H20N4O5
Molecular Weight
456.45
Exact Mass
456.143
CAS #
147403-03-0
Related CAS #
Azilsartan medoxomil;863031-21-4;Azilsartan-d5;1346599-45-8;Azilsartan-d4;1794817-45-0;Azilsartan medoxomil monopotassium;863031-24-7
PubChem CID
135415867
Appearance
White to off-white solid powder
Density
1.4±0.1 g/cm3
Melting Point
212-214 °C
Index of Refraction
1.695
LogP
4.21
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
7
Rotatable Bond Count
7
Heavy Atom Count
34
Complexity
783
Defined Atom Stereocenter Count
0
InChi Key
KGSXMPPBFPAXLY-UHFFFAOYSA-N
InChi Code
InChI=1S/C25H20N4O5/c1-2-33-24-26-20-9-5-8-19(23(30)31)21(20)29(24)14-15-10-12-16(13-11-15)17-6-3-4-7-18(17)22-27-25(32)34-28-22/h3-13H,2,14H2,1H3,(H,30,31)(H,27,28,32)
Chemical Name
2-ethoxy-3-[[4-[2-(5-oxo-4H-1,2,4-oxadiazol-3-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid
Synonyms
TAK-536;TAK-536; TAK-536;Edarbi
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO:91 mg/mL (199.3 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.48 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (5.48 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 3: 30% PEG400+0.5% Tween80+5% Propylene glycol :30mg/mL


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.1908 mL 10.9541 mL 21.9082 mL
5 mM 0.4382 mL 2.1908 mL 4.3816 mL
10 mM 0.2191 mL 1.0954 mL 2.1908 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
Comparison of efficacy and safety of azilsartan and olmesartan in patients with essential hypertension
CTID: UMIN000016249
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2015-01-17
Depressor and anti-inflammatory effects of angiotensin II receptor blockers in metabolic and/or hypertensive patients with coronary artery disease
CTID: UMIN000016247
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2015-01-17
Effects of Olmesartan and Azilsartan on biomarkers of progression of CKD and arteriosclerosis in CKD patients
CTID: UMIN000015671
Phase:    Status: Complete: follow-up complete
Date: 2014-12-01
A randomized clinical trial to evaluate the efficacy of catecholamine surge supression by oral azilsartan in patients with hypertensive intracerebral hemorrhage
CTID: UMIN000014323
Phase: Phase I,II    Status: Complete: follow-up complete
Date: 2014-07-01
Potency of antihypertensive therapy with Azilsartan on Walking Activity among Peripheral Artery Disease Patients With hypertention and Intermittent Claudication
CTID: UMIN000013670
Phase:    Status: Complete: follow-up complete
Date: 2014-04-08
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None
CTID: jRCT1080222416
Phase:    Status:
Date: 2014-03-05


None
CTID: jRCT1080222411
Phase:    Status:
Date: 2014-03-03
None
CTID: jRCT1080222391
Phase:    Status:
Date: 2014-02-10
clinical outcomes of Azilsartan, angiotensin receptor blocker on castration-resistant prostate cancer
CTID: UMIN000012656
Phase:    Status: Complete: follow-up complete
Date: 2014-02-01
The effect of azilsartan on excercise capacity in hypertensive patients with sarcopenia
CTID: UMIN000012816
Phase:    Status: Recruiting
Date: 2014-01-20
MULTICENTER PROBE STUDY-4; COMPARISON OF THE EFFECTS OF ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS
CTID: UMIN000012768
Phase:    Status: Complete: follow-up complete
Date: 2014-01-06
MULTICENTER PROBE STUDY-4; COMPARISON OF THE EFFECTS OF ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS
CTID: UMIN000012768
Phase:    Status: Complete: follow-up complete
Date: 2014-01-06
Comparison of effects of azilsartan and olmesartan in paitents with type 2 diabetes mellitus with hypertension: A crossover trial.
CTID: UMIN000012619
Phase:    Status: Pending
Date: 2013-12-18
Comparison of effects of azilsartan and olmesartan in paitents with type 2 diabetes mellitus with hypertension: A crossover trial.
CTID: UMIN000012619
Phase:    Status: Pending
Date: 2013-12-18
AziLsartan treatMent as a swItch strateGy for improvement of uncontrolled Hypertension and blood pressure variabiliTY
CTID: UMIN000012586
Phase:    Status: Complete: follow-up complete
Date: 2013-12-16
Switch from ARB Combination Tablets to Azilsartan: Clinical research on organ protective effect in hypertensive patients living in Okayama
CTID: UMIN000012587
Phase:    Status: Complete: follow-up complete
Date: 2013-12-16
AziLsartan treatMent as a swItch strateGy for improvement of uncontrolled Hypertension and blood pressure variabiliTY
CTID: UMIN000012586
Phase:    Status: Complete: follow-up complete
Date: 2013-12-16
Switch from ARB Combination Tablets to Azilsartan: Clinical research on organ protective effect in hypertensive patients living in Okayama
CTID: UMIN000012587
Phase:    Status: Complete: follow-up complete
Date: 2013-12-16
Ehime Study - Effect of Azilsartan on Home Blood Pressure
CTID: UMIN000011936
Phase:    Status: Complete: follow-up complete
Date: 2013-10-01
Ehime Study - Effect of Azilsartan on Home Blood Pressure
CTID: UMIN000011936
Phase:    Status: Complete: follow-up complete
Date: 2013-10-01
A clinical questing examination to verify vasculo-protective effect of azilsartan treatment in the uncontrolled hypertensive patients with diabetes mellitus.
CTID: UMIN000011892
Phase:    Status: Complete: follow-up complete
Date: 2013-09-27
A clinical questing examination to verify vasculo-protective effect of azilsartan treatment in the uncontrolled hypertensive patients with diabetes mellitus.
CTID: UMIN000011892
Phase:    Status: Complete: follow-up complete
Date: 2013-09-27
The hypertensive patients is RECOMMENDed for organ protection by ARB decreased early-morning blood pressure study
CTID: UMIN000011197
PhaseNot applicable    Status: Recruiting
Date: 2013-07-17
Influence of Azilsartan or Olmesartan on renin-angiotensin-aldosterone system.
CTID: UMIN000011006
Phase:    Status: Complete: follow-up complete
Date: 2013-06-19
The comparison of azilsartan and amlodipine for treatment of VEGF receptor-tyrosine kinase inhibitor-induced hypertension in advanced kidney cancer patients
CTID: UMIN000010940
Phase:    Status: Complete: follow-up continuing
Date: 2013-06-12
Effects of azilsartan in chronik kidney disease with hypertension
CTID: UMIN000010788
Phase: Phase IV    Status: Complete: follow-up complete
Date: 2013-05-23
Efficacy and safety of treatment with Azilsartan in type 2 diabetes mellitus patients with hypertension who did not show target blood pressure by telmisartan.
CTID: UMIN000010604
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2013-05-01
Medical effects of Azilsartan in patients with hypertension not controlled by other ARBs
CTID: UMIN000010610
Phase: Phase IV    Status: Complete: follow-up complete
Date: 2013-05-01
Antihypertensive effects of low-dose azilsartan in clinical practice
CTID: UMIN000009515
Phase:    Status: Complete: follow-up complete
Date: 2012-12-31
Azilsartan Circadian and Sleep pressure the 1st study
CTID: UMIN000009576
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2012-12-18
Azilsartan can restore circadian rhythm of the urinary sodium excretion
CTID: UMIN000009549
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2012-12-14
Effect and safety of conversion from Candesartan to Azilsartan in renal transplant recipeints
CTID: UMIN000008989
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2012-10-09
Efficacy and safety of treatment with new ARB Azilsartan in hypertension patients who did not show target blood pressure by other ARBs.
CTID: UMIN000008700
PhaseNot applicable    Status: Complete: follow-up complete
Date: 2012-08-20
Impact of azilsartan on proteinuria in patients with chronic kidney disease
CTID: UMIN000008597
PhaseNot applicable    Status: Recruiting
Date: 2012-08-05
Evaluation for Efficacy and Safety of Azilsartan in Patients with Hypertension
CTID: UMIN000008577
Phase:    Status: Recruiting
Date: 2012-08-01

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