Angiotensin II type 1 receptor (AT1R); the Ki value of Azilsartan (TAK-536) for human AT1R in competitive binding assays was 0.6 nM, and it had no significant binding to AT2R (Ki > 10,000 nM) [3]

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].

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1. AT1R binding and functional inhibition: In human AT1R-expressing CHO cells, Azilsartan (TAK-536) competitively inhibited [³H]-angiotensin II binding with a Ki of 0.6 nM. In rat aortic smooth muscle cells, it dose-dependently inhibited angiotensin II-induced intracellular Ca²⁺ elevation (IC50 = 1.2 nM) and angiotensin II-induced cell contraction (IC50 = 0.9 nM) [3]
2. Anticancer activity in HepG2 cells: Treatment of human hepatocellular carcinoma HepG2 cells with Azilsartan (TAK-536) (10–80 μM) for 48 hours reduced cell viability (IC50 = 35 μM), increased apoptotic rate (from 3.2% ± 0.5% to 28.6% ± 2.3% at 60 μM), and upregulated cleaved caspase-3/9 and Bax expression (by 2.8-fold and 2.1-fold, respectively) via inducing oxidative stress (intracellular ROS increased by 3.5-fold at 60 μM) and activating NF-κB (p65 nuclear translocation increased by 2.4-fold) [5]
3. Neuroprotective effects on cerebral ischemic cells: In oxygen-glucose deprivation (OGD)-treated PC12 cells (neuronal-like cells), Azilsartan (TAK-536) (1–10 μM) increased cell viability (from 42% ± 3% to 78% ± 4% at 10 μM), reduced mitochondrial ROS production (by 45% ± 5% at 10 μM), and restored mitochondrial membrane potential (by 52% ± 6% at 10 μM) by upregulating SIRT3 and PGC-1α expression (by 1.8-fold and 2.0-fold, respectively) [4]
4. Vascular cell protection: In human aortic endothelial cells (HAECs) treated with angiotensin II, Azilsartan (TAK-536) (1 μM) upregulated eNOS expression (by 1.6-fold) and NO production (by 40% ± 4%), and downregulated TNF-α and IL-6 secretion (by 35% ± 3% and 30% ± 2%, respectively) [1]

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].

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1. Improvement of insulin sensitivity in Koletsky rats: In obese spontaneously hypertensive Koletsky rats (fa/fa), oral administration of Azilsartan (TAK-536) (10 mg/kg/day) for 4 weeks reduced systolic blood pressure (from 165 ± 8 mmHg to 132 ± 6 mmHg), decreased fasting blood glucose (from 185 ± 12 mg/dL to 142 ± 8 mg/dL), and improved insulin sensitivity (homeostasis model assessment-insulin resistance, HOMA-IR, decreased from 7.8 ± 0.6 to 4.2 ± 0.4). It also increased adipose tissue GLUT4 expression (by 1.7-fold) and skeletal muscle insulin receptor phosphorylation (by 1.5-fold) [2]
2. Neuroprotection in cerebral ischemia: In a rat model of middle cerebral artery occlusion (MCAO, 2 hours of occlusion followed by 24 hours of reperfusion), intraperitoneal injection of Azilsartan (TAK-536) (5 mg/kg) immediately after reperfusion reduced cerebral infarct volume (from 38% ± 4% to 15% ± 3%), improved neurological deficit scores (from 3.2 ± 0.3 to 1.1 ± 0.2), and increased cerebral cortex SIRT3/PGC-1α expression (by 2.1-fold and 2.3-fold, respectively). It also reduced cerebral mitochondrial ROS (by 50% ± 5%) and lipid peroxidation (MDA decreased by 42% ± 4%) [4]
3. Vascular function improvement in hypertensive rats: In spontaneously hypertensive rats (SHRs), oral Azilsartan (TAK-536) (5 mg/kg/day) for 8 weeks improved aortic endothelium-dependent vasodilation (acetylcholine-induced dilation increased from 30% ± 3% to 65% ± 4%) and reduced aortic media thickness (by 28% ± 3%) via inhibiting AT1R-mediated oxidative stress (NADPH oxidase activity decreased by 40% ± 4%) [1]

1. AT1R competitive binding assay:
- Reagent preparation: Human AT1R-expressing CHO cell membranes were prepared by homogenization and centrifugation. [³H]-angiotensin II (radioactive ligand) and Azilsartan (TAK-536) (serial concentrations: 0.01–100 nM) were dissolved in binding buffer (50 mM Tris-HCl, pH 7.4, containing 10 mM MgCl₂).
- Experimental procedure: The reaction system (200 μL) contained cell membranes (10 μg protein), [³H]-angiotensin II (0.5 nM), and different concentrations of Azilsartan (TAK-536). It was incubated at 25°C for 60 minutes, then filtered through glass fiber filters to separate bound and free ligands. The filters were washed with cold binding buffer, and radioactivity was measured with a liquid scintillation counter.
- Data analysis: The Ki value was calculated using the Cheng-Prusoff equation based on the inhibition rate of [³H]-angiotensin II binding at each Azilsartan (TAK-536) concentration [3]
2. Angiotensin II-induced Ca²⁺ elevation assay:
- Rat aortic smooth muscle cells were loaded with Fluo-4 AM (a Ca²⁺ fluorescent probe) for 30 minutes at 37°C. After washing, cells were treated with Azilsartan (TAK-536) (0.1–10 nM) for 15 minutes, then stimulated with angiotensin II (100 nM). Fluorescence intensity (excitation 488 nm, emission 525 nm) was measured in real time to assess intracellular Ca²⁺ changes. The IC50 was calculated from the dose-response curve [3]

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.

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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).

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1. HepG2 cell anticancer assay:
- HepG2 cells were seeded in 96-well plates (5×10³ cells/well) and cultured for 24 hours. They were then treated with Azilsartan (TAK-536) (10–80 μM) for 48 hours. Cell viability was measured using the MTT assay. For apoptosis detection, cells were stained with Annexin V-FITC/PI and analyzed by flow cytometry. Western blot was used to detect cleaved caspase-3/9, Bax, and NF-κB p65 (nuclear/cytoplasmic fractions). Intracellular ROS was measured with DCFH-DA fluorescent probe [5]
2. OGD-induced PC12 cell neuroprotection assay:
- PC12 cells were cultured in glucose-free DMEM and placed in a hypoxic chamber (1% O₂, 5% CO₂, 37°C) for 4 hours (OGD model). After OGD, cells were treated with Azilsartan (TAK-536) (1–10 μM) for 24 hours. Cell viability was detected by CCK-8 assay. Mitochondrial ROS was measured with MitoSOX Red, and mitochondrial membrane potential with JC-1 staining. SIRT3/PGC-1α expression was detected by Western blot [4]
3. HAECs vascular protection assay:
- Human aortic endothelial cells (HAECs) were treated with angiotensin II (100 nM) and Azilsartan (TAK-536) (1 μM) for 24 hours. NO production was measured with Griess reagent. eNOS expression was detected by Western blot, and TNF-α/IL-6 secretion by ELISA [1]

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.

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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.

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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

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1. Koletsky rat insulin sensitivity model:
- Male obese spontaneously hypertensive Koletsky rats (fa/fa, 12–14 weeks old, 300–350 g) were randomly divided into 2 groups (n=8):
- Model group: Oral gavage of normal saline (1 mL/kg/day).
- Azilsartan (TAK-536) group: Oral gavage of Azilsartan (TAK-536) (10 mg/kg/day, dissolved in normal saline).
- Treatment duration: 4 weeks, with free access to food and water. Blood pressure was measured weekly using a tail-cuff plethysmograph. At the end of treatment, fasting blood glucose and insulin were measured to calculate HOMA-IR. Adipose tissue and skeletal muscle were collected for Western blot (GLUT4, insulin receptor phosphorylation) [2]
2. Rat MCAO cerebral ischemia model:
- Male Sprague-Dawley rats (250–300 g) were subjected to MCAO by inserting a nylon suture into the middle cerebral artery for 2 hours, followed by reperfusion. Rats were divided into 2 groups (n=8):
- MCAO group: Intraperitoneal injection of normal saline (1 mL/kg) immediately after reperfusion.
- Azilsartan (TAK-536) group: Intraperitoneal injection of Azilsartan (TAK-536) (5 mg/kg, dissolved in normal saline) immediately after reperfusion.
- After 24 hours of reperfusion, neurological deficit scores were evaluated (0–4 scale). Brains were collected to measure infarct volume (TTC staining). Cerebral cortex was used to detect SIRT3/PGC-1α (Western blot) and mitochondrial ROS/MDA (biochemical kits) [4]
3. SHR vascular function model:
- Male spontaneously hypertensive rats (SHRs, 10 weeks old, 220–250 g) were divided into 2 groups (n=8):
- SHR control group: Oral normal saline (1 mL/kg/day).
- Azilsartan (TAK-536) group: Oral Azilsartan (TAK-536) (5 mg/kg/day, dissolved in normal saline).
- Treatment duration: 8 weeks. Aortic rings were isolated to measure endothelium-dependent vasodilation (myograph system). Aortic media thickness was analyzed by HE staining. NADPH oxidase activity was measured by lucigenin chemiluminescence [1]

Absorption, Distribution and Excretion
In rats, very little of the radioactive material associated with azilsartan crosses the blood-brain barrier. Azilsartan can cross the placental barrier in pregnant rats and distribute to the fetus. The volume of distribution of azilsartan is approximately 16 liters. Azilsartan binds very well to human plasma proteins (>99%), primarily to serum albumin. Even at plasma azilsartan concentrations well above the recommended dose range, protein binding remains constant. Following oral administration of 14C-labeled azilsartan ester, approximately 55% of the radioactive material is recovered in feces, and approximately 42% in urine, of which 15% is excreted in the urine as azilsartan. The elimination half-life of azilsartan is approximately 11 hours, and renal clearance is approximately 2.3 mL/min. Steady-state plasma concentrations of azilsartan are achieved within five days, and repeated once-daily dosing does not lead to plasma drug accumulation.
Azilsartan medoxomil is hydrolyzed in the gastrointestinal tract to the active metabolite azilsartan during absorption. Azilsartan medoxomil is undetectable in plasma after oral administration. Following single or multiple doses, azilsartan exposure is dose-dependent within the azilsartan medoxomil dose range of 20 mg to 320 mg. The estimated absolute bioavailability of azilsartan after administration of azilsartan medoxomil is approximately 60%. Peak plasma concentrations (Cmax) of azilsartan are reached within 1.5 to 3 hours after oral administration of azilsartan medoxomil. Food does not affect the bioavailability of azilsartan.
For more complete data on the absorption, distribution, and excretion of azilsartan (8 items in total), please visit the HSDB record page.
Metabolism/Metabolites

Azilsartan medoxomil is rapidly hydrolyzed by esterases to the active ingredient azilsartan during gastrointestinal and/or drug absorption. In vitro studies have shown that the enzymes involved in the hydrolysis of azilsartan cilexetil to azilsartan in human plasma, liver, and small intestinal cytosol appear to be similar to those involved in the hydrolysis of olmesartan cilexetil. Currently, no drug interactions related to the hydrolysis of azilsartan cilexetil have been reported. Carboxymethylbutenolactonease is a recently discovered hydrolytic mechanism of azilsartan cilexetil in the intestine and liver, but interactions between this enzyme and other drugs have not been reported in the Drug Interactions in Metabolism and Transport Database (DIDB). Furthermore, interactions with human serum albumin or aryl esterases have not been reported. Since the conversion of azilsartan cilexetil to azilsartan involves multiple esterase pathways, the likelihood of interactions occurring through these pathways is extremely low. The metabolites MI and M-II are generated from the decarboxylation and dealkylation of azilsartan, respectively, and are pharmacologically inactive. CYP1A1, CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 all metabolize azilsartan. However, CYP2C9 exhibits the highest activity in metabolizing azilsartan to M-II, while CYP2C8 shows the highest activity in metabolizing azilsartan to MI. Azilsartan is metabolized into two major metabolites. The major metabolite in plasma is formed via O-dealkylation and is called metabolite M-II; the minor metabolite is formed via decarboxylation and is called metabolite MI. The systemic exposure to the major and minor metabolites in humans is approximately 50% and less than 1% of the total azilsartan, respectively. MI and M-II do not contribute to the pharmacological activity of edabide. The main enzyme responsible for azilsartan metabolism is CYP2C9.

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Biological Half-Life
The half-life of azilsartan in rat and dog plasma is 4 to 6 hours, and approximately 12 hours in humans.
The elimination half-life of azilsartan is approximately 11 hours…

Toxicity Summary
Identification and Uses: Azilsartan is a white crystalline powder formulated as oral tablets. Azilsartan is an angiotensin II type 1 (AT1) receptor antagonist. It can be used alone or in combination with other classes of antihypertensive drugs to treat hypertension. Azilsartan ester is a prodrug that is hydrolyzed to azilsartan in the gastrointestinal tract during absorption. Human Exposure and Toxicity: Data on human overdose of azilsartan are limited. In controlled clinical trials in healthy subjects, up to 320 mg of azilsartan once daily for 7 days was well tolerated. Azilsartan is contraindicated during pregnancy. Drugs that act directly on the renin-angiotensin system (e.g., ACE inhibitors, angiotensin II receptor antagonists) used in the second or third trimester can impair fetal renal function and increase fetal and neonatal morbidity and mortality. ACE inhibitors used in early pregnancy may also increase the risk of serious congenital malformations in the fetus. Azilsartan should be discontinued as soon as pregnancy is discovered unless continued use is considered life-saving. Animal studies: Adding azilsartan to the diet of mice and rats for up to two years did not reveal evidence of carcinogenicity. Furthermore, oral doses of azilsartan up to 1000 mg/kg/day had no adverse effects on the fertility of male or female rats. Oral doses of azilsartan up to 1000 mg/kg/day in pregnant rats, or up to 50 mg/kg/day in pregnant rabbits, did not show teratogenicity. However, in rats, azilsartan at 1000 mg/kg/day caused embryo-fetal toxicity (manifested as renal pelvis dilation and shortness of extra ribs); in rabbits, azilsartan at 50 mg/kg/day caused embryo-fetal toxicity (manifested as increased post-implantation loss, embryo-fetal death, and reduced live birth count). Furthermore, in rats, azilsartan at doses as low as 30 mg/kg/day (resulting in delayed caudal vertebral ossification) and 100 mg/kg/day (resulting in reduced male fetal weight); and in rabbits, embryo-fetal toxicity was observed at a dose of 500 mg/kg/day (resulting in increased post-implantation loss). Azilsartan cilexetil, azilsartan, and its metabolite M-II all showed structural abnormalities in Chinese hamster lung cell genetic analysis. In this assay, chromosomal structural abnormalities were observed in the prodrug azilsartan cilexetil even without metabolic activation. The active ingredient azilsartan was positive in this assay regardless of metabolic activation. The major human metabolite M-II was also positive in the 24-hour assay without metabolic activation. Azilsartan medoxomil, azilsartan, and M-II showed no genotoxicity in the Ames reverse mutation assay for Salmonella and Escherichia coli, the in vitro forward mutation assay for Chinese hamster ovary cells, the in vitro mouse lymphoma (tk) gene mutation assay, the in vitro unprogrammed DNA synthesis assay, and the in vivo mouse and/or rat bone marrow micronucleus assay.

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Hepatotoxicity
Azilsartan was associated with a low incidence of elevated serum transaminases, which was no higher than in the placebo group in controlled trials. These elevations were transient and rarely required dose adjustment. Although there have been no reports of clinically significant acute liver injury associated with azilsartan treatment, the drug has a limited time on the market. Other angiotensin II receptor antagonists (ARBs) have been associated with rare cases of symptomatic hepatotoxicity. Liver injury typically occurs within 1 to 8 weeks after the start of treatment, with serum enzyme profiles usually showing hepatocellularity and accompanied by clinical syndromes similar to acute hepatitis. In some cases, cholestasis may occur and may persist and recur, but angiotensin receptor blocker (ARB) treatment is not associated with disappearance of bile duct syndrome or chronic liver injury. Immune allergic reactions (rash, fever, eosinophilia) are uncommon, as is the formation of autoantibodies. Probability score: E (Unproven, but suspected as a rare cause of clinically significant liver injury).

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Effects during pregnancy and lactation
◉ Overview of medication use during lactation
Because there is no information on the use of azisartan during lactation, alternative medications may be preferred, especially in breastfed newborns or preterm infants.
◉ Effects on breastfed infants
No relevant published information found as of the revision date.
◉ Effects on lactation and breast milk
No relevant published information found as of the revision date.

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Drug Interactions
Drug interactions may occur when potassium supplements and potassium-containing salt substitutes are used in combination with angiotensin II receptor antagonists (such as azilsartan). Because the combined use of potassium-sparing diuretics (such as amiloride, spironolactone, and triamterene) with angiotensin II receptor antagonists (such as azilsartan medoxomil) increases the risk of hyperkalemia, some clinicians recommend avoiding the combined use of these drugs with azilsartan medoxomil.

For elderly patients, patients with low blood volume (including those receiving diuretics), or patients with impaired renal function, concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs, including selective cyclooxygenase-2 (COX-2) inhibitors) and angiotensin II receptor antagonists may lead to worsening of renal function and even acute renal failure. These effects are usually reversible. Patients receiving azilsartan and NSAIDs should have their renal function monitored regularly. The antihypertensive effect of azilsartan may be diminished in patients receiving NSAIDs, including selective COX-2 inhibitors.
Patients receiving azilsartan medoxomil may experience a reversible increase in serum creatinine, while patients receiving hydrochlorothiazide may experience a greater increase in serum creatinine.

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1. In vitro cytotoxicity: Azisartan (TAK-536) showed cytotoxicity to HepG2 cells with an IC50 of 35 μM (48-hour treatment), but showed no significant toxicity to normal human hepatocytes (L02 cells) at concentrations up to 80 μM [5]
2. Plasma protein binding: Azisartan (TAK-536) showed plasma protein binding in human, rat, and canine plasma >99% [1]
3. In vivo safety: In the 4-week Koletsky rat study and the 8-week SHR study, azisartan (TAK-536) (up to 10 mg/kg/day) did not cause significant changes in liver function (ALT/AST) or kidney function (creatinine/BUN) [1][2]

[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.

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 non-fatal cardiovascular events, primarily stroke and myocardial infarction. These benefits have been demonstrated in controlled trials across a wide range of pharmacological classes of antihypertensive drugs, including the primary class to which this drug belongs. /US Product Label Content/ Edarbi can be used alone or in combination with other antihypertensive drugs. Angiotensin II receptor antagonists (such as azilsartan) and ACE inhibitors have both been shown to slow the progression of kidney disease in hypertensive patients with diabetes and microalbuminuria or overt nephropathy; therefore, one of these classes of drugs is recommended for such patients. /Not Included in US Product Label/

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Drug Warnings /Black Box Warning/ Warning: Fetal toxicity. Edarbi should be discontinued as soon as pregnancy is discovered. Drugs that act directly on the renin-angiotensin system can cause damage or even death to the developing fetus.
Medications that act directly on the renin-angiotensin system (e.g., ACE inhibitors, angiotensin II receptor antagonists) can reduce fetal kidney function and increase fetal and neonatal morbidity and mortality when used in the second or third trimester. ACE inhibitors used in early pregnancy may also increase the risk of serious congenital malformations in the fetus. Azilsartan should be discontinued as soon as pregnancy is confirmed unless continued use is considered life-saving. Almost all women successfully switch to replacement therapy for the remainder of pregnancy.
Use of medications affecting the renin-angiotensin system in the second or third trimester can reduce fetal kidney function and increase fetal and neonatal morbidity and mortality. The resulting oligohydramnios may be associated with fetal lung malformation and skeletal malformations. Potential neonatal adverse reactions include craniosynostosis, anuria, hypotension, kidney failure, and death. Edarbi should be discontinued as soon as pregnancy is confirmed. These adverse consequences are often associated with the use of such medications in the second or third trimester. Most epidemiological studies investigating fetal abnormalities following the use of antihypertensive drugs in early pregnancy have not differentiated between drugs affecting the renin-angiotensin system and other antihypertensive drugs. Proper management of hypertension during pregnancy is crucial for optimizing maternal and infant outcomes. Because patients with activated renin-angiotensin systems (e.g., those experiencing volume or salt loss due to high-dose diuretics) may experience symptomatic hypotension, azilsartan should be started after correction of volume or salt loss, or at a lower initial dose, in such patients. If a patient taking azilsartan esters experiences hypotension, they should be placed in a supine position, and if necessary, receive an intravenous infusion of 0.9% sodium chloride. Transient hypotension is not a contraindication to increasing the dose of azilsartan; medication may be cautiously resumed once blood pressure stabilizes (e.g., through volume expansion). For more drug warnings about azilsartan (full version) (14 in total), please visit the HSDB record page.

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1. Azisartan (TAK-536) is a new generation of angiotensin II type 1 receptor blocker (ARB) with higher AT1R affinity and longer duration of action compared to conventional ARBs (e.g., losartan)[1][3].
2. Its pharmacological effects are not limited to lowering blood pressure: it can also improve insulin sensitivity (by upregulating GLUT4 and the insulin signaling pathway)[2], exert neuroprotective effects (through SIRT3/PGC-1α-mediated mitochondrial protection)[4], and inhibit HepG2 cell proliferation (through the ROS-NF-κB-apoptosis pathway)[5].
3. It is suitable for the treatment of essential hypertension, and preclinical studies have shown that it has potential applications in insulin-resistant obesity and ischemic stroke[1][2][4].

C25H20N4O5

456.45

456.143

147403-03-0

Azilsartan medoxomil;863031-21-4;Azilsartan-d5;1346599-45-8;Azilsartan-d4;1794817-45-0;Azilsartan medoxomil monopotassium;863031-24-7

135415867

White to off-white solid powder

1.4±0.1 g/cm3

212-214 °C

1.695

4.21

2

7

7

34

783

0

KGSXMPPBFPAXLY-UHFFFAOYSA-N

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)

2-ethoxy-3-[[4-[2-(5-oxo-4H-1,2,4-oxadiazol-3-yl)phenyl]phenyl]methyl]benzimidazole-4-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

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.

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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

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 (Please use freshly prepared in vivo formulations for optimal results.)