Olmesartan is an angiotensin II type 1 (AT1) receptor blocker (ARB). In vitro studies cited indicate that Olmesartan does not enhance PPAR-γ-mediated transcriptional activity.

In vitro activity: Olmesartan (0.7-5 mM; 24, 48 and 72 h) inhibits the growth of HeLa cells in a concentration- and time-dependent manner[3].

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Under the condition without additional albumin, Olmesartan at 10 µM did not significantly elevate the mRNA expression of adipose protein 2 (aP2) or adiponectin (adipogenic marker genes reflecting PPAR-γ activity) in differentiating 3T3-L1 mouse preadipocytes. This indicates a lack of PPAR-γ agonistic action under these experimental conditions.

Olmesartan (1 mg/kg, 2 mg/kg, p.o.) is dose-dependently lowered in SHR after repeated administration, with no discernible effects on body weight or food consumption over a 10-week period[1]. Mice treated with Hyd and olemesartan (5 mg/kg/d, p.o.) exhibit comparable reductions in systolic blood pressure. Treatment with olmesartan prevents cardiac hypertrophy as determined by gene expression, heart weight, cardiomyocyte cross-sectional area, and echocardiography. Treatment with omesartan reverses the downregulation of Ren-Tg mice's ACE2 and Mas receptor gene expressions, and it prevents the upregulation of NADPH oxidase (Nox)4 expression and reactive oxygen species[2].

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In spontaneously hypertensive rats (SHR) fed a high-fat diet (HFD), once-daily oral administration of Olmesartan at 2 mg/kg for 11 weeks significantly reduced systolic blood pressure compared to the HFD-vehicle group.
Olmesartan (2 mg/kg) treatment ameliorated insulin resistance in HFD-fed SHR, as evidenced by a reduction in the homeostasis model assessment for insulin resistance (HOMA-IR) value.
Olmesartan (2 mg/kg) corrected hypertriglyceridemia in HFD-fed SHR, significantly lowering plasma triglyceride concentration.
Olmesartan (2 mg/kg) improved the decreased plasma adiponectin concentration caused by HFD in SHR.
Olmesartan (2 mg/kg) provided renal protection in HFD-fed SHR. It significantly reduced urinary albumin excretion.
It also significantly decreased urinary excretion of monocyte chemoattractant protein-1 (MCP-1) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), markers of renal inflammation and oxidative stress, respectively.
Histopathological analysis showed that Olmesartan (2 mg/kg) ameliorated HFD-induced glomerular injury, significantly lowering the glomerular injury score.
The beneficial effects of Olmesartan (2 mg/kg) on insulin resistance, hypertriglyceridemia, and renal damage did not significantly differ from those of telmisartan (2 mg/kg).

Olmesartan medoxomil, with an IC50 of 66.2 μM, is a strong and specific inhibitor of the angiotensin AT1 receptor.

Cell Line: Human cervical cancer cell line (HeLa)
Concentration: 0.7- 5 mM
Incubation Time: 24, 48 and 72 h
Result: IC50s against HeLa cell line are 4.685 and 1.651 mM for 48 and 72 h, respectively

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For the adipocyte differentiation assay, 3T3-L1 mouse preadipocytes were seeded and grown to confluence. Differentiation was induced using a standard cocktail (dexamethasone, isobutyl methylxanthine, insulin). The terminal differentiation medium contained insulin. Olmesartan (10 µM) was added continuously to the culture media from the initiation of differentiation until sample collection on day 8. Total RNA was extracted, and mRNA expression levels of aP2 and adiponectin were quantified by real-time PCR. Gene expression levels were normalized to Ribosomal protein S18.

Male db/db diabetic mice aged 10 to 12 weeks, using background strain C57BL/KsJ, are employed, along with age-matched non-diabetic lean control mice (C57BL).For a period of 12 weeks, ten diabetic mice and ten non-diabetic control mice were given a placebo (0.5% sodium CMC/saline solution), while the other ten diabetic mice received daily gavages of 20 mg/kg Olmesartan (MB5704). Every two weeks, the blood glucose, body weight, and urine output of the mice are observed. Following therapy, mice are put to sleep, and trunk blood is taken, centrifuged, and then aliquoted and kept at -80°C to extract plasma. Mice's kidney tissues are extracted. Kidney tissue slices are frozen in liquid nitrogen and kept at -80°C in order to extract proteins. The remaining kidney tissue is embedded in paraffin and fixed with 4% paraformaldehyde in order to be immunostained.Mice

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Seven-week-old male spontaneously hypertensive rats (SHR) were used. The animals were fed either a control diet or a high-fat diet (HFD). Olmesartan was suspended in 1% tragacanth gum solution (vehicle) and administered orally by gastric gavage once daily at doses of 1 mg/kg or 2 mg/kg for varying durations (4 to 11 weeks) depending on the experiment.
In Experiment 1, SHR fed HFD received vehicle, Olmesartan (1 mg/kg), or Olmesartan (2 mg/kg) for >4 weeks to assess effects on mean arterial blood pressure (MAP), which was measured continuously via an implanted carotid artery catheter under conscious, unrestrained conditions.
In Experiment 2, SHR were divided into groups: control diet + vehicle, HFD + vehicle, HFD + Olmesartan (2 mg/kg), and HFD + telmisartan (2 mg/kg). Drugs were administered once daily for 11 weeks. Systolic blood pressure was measured every 5 weeks using a tail-cuff sphygmomanometer in awake rats. An insulin tolerance test (intraperitoneal injection of 0.75 U/kg regular insulin) was performed on week 9. A 24-hour urine sample was collected in metabolic cages on week 11. At the end of the study (week 11), after a 12-hour fast, animals were anesthetized, and blood and kidney samples were collected for biochemical and histopathological analysis.

Absorption, Distribution and Excretion
Following oral administration, the prodrug olmesartan medoxomil is rapidly absorbed and metabolized to olmesartan in the gastrointestinal tract. Esterification aims to increase the bioavailability of olmesartan from 4.5% to 28.6%. After oral administration of 10-160 mg olmesartan, peak plasma concentrations are reached at 0.22-2.1 mg/L within 1-3 hours, with an AUC of 1.6-19.9 mg/L. Within the therapeutic dose range, the pharmacokinetic profile of olmesartan is nearly linear and positively correlated with dose. Steady-state plasma concentrations of olmesartan are reached after 3-5 days with once-daily dosing. The primary route of excretion for olmesartan is unchanged in feces. Approximately 10-16% of the systemic bioavailable dose is excreted in the urine. The total plasma clearance is 1.3 L/h, and the renal clearance is 0.6 L/h. In rats, olmesartan barely crosses the blood-brain barrier. Olmesartan crosses the rat placental barrier and distributes to the fetus. The volume of distribution of olmesartan is approximately 17 L. Olmesartan is highly bound to plasma proteins (99%) and does not penetrate erythrocytes. Protein binding remains constant even at plasma olmesartan concentrations well above the recommended dose range. During gastrointestinal absorption, olmesartan ester is rapidly and completely bioactivated to olmesartan via ester hydrolysis. Benicar and suspensions prepared from Benicar are bioequivalent. The absolute bioavailability of olmesartan is approximately 26%. Peak plasma concentration (Cmax) of olmesartan is reached 1 to 2 hours after oral administration. Food does not affect the bioavailability of olmesartan. The total plasma clearance of olmesartan is 1.3 L/hr, and the renal clearance is 0.6 L/hr. Approximately 35% to 50% of the absorbed dose is excreted in the urine, with the remainder excreted in the feces via bile. Olmesartan exhibits linear pharmacokinetic characteristics after a single oral dose up to 320 mg and multiple oral doses up to 80 mg. Steady-state plasma concentrations of olmesartan are reached within 3 to 5 days, and once-daily dosing does not lead to plasma accumulation. Olmesartan is distributed in rat milk; it is currently unknown whether the drug is distributed in human milk. Metabolites/Metabolites: During gastrointestinal absorption, olmesartan medoxomil is rapidly and completely bioactivated to olmesartan via ester hydrolysis. Measurable amounts of olmesartan medoxomil were not detected in plasma or excrement, confirming this rapid first-pass metabolism. This first-pass metabolism is not driven by cytochrome enzymes, therefore, no interactions with other drugs are expected through this mechanism. The pharmacologically active portion does not appear to undergo further metabolism. After rapid and complete conversion to olmesartan during absorption, olmesartan undergoes almost no further metabolism.

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Biological Half-Life
It has been reported that the mean plasma half-life of olmesartan is 10-15 hours after multiple oral administrations.
The elimination of olmesartan appears to be biphasic, with a terminal elimination half-life of approximately 13 hours.

Toxicity Summary
Identification and Use: Olmesartan is a white to pale yellow powder or crystalline powder, formulated as oral tablets. Olmesartan is an angiotensin II type 1 (AT1) receptor antagonist. It can be used alone or in combination with other classes of antihypertensive drugs (such as thiazide diuretics) to treat hypertension. Human Exposure and Toxicity: Data on human overdose are limited. The most likely manifestations of olmesartan overdose include hypotension and tachycardia; bradycardia may occur if parasympathetic (vagus nerve) excitation occurs. While olmesartan can be used in children with hypertension, it is not approved for use in children under 1 year of age. Drugs that act directly on the renin-angiotensin system (RAS) may affect the development of immature kidneys. Olmesartan is contraindicated during pregnancy. While use of olmesartan in early pregnancy does not cause serious malformations, use in mid-to-late pregnancy may lead to teratogenicity and serious fetal and neonatal toxicity. Fetal toxicity may include anuria, oligohydramnios, fetal craniofacial dysplasia, intrauterine growth restriction, preterm birth, and patent ductus arteriosus. Anuria-associated oligohydramnios may lead to fetal limb contractures, craniofacial deformities, and pulmonary dysplasia. Intrauterine exposure of the fetus to olmesartan may result in severe anuria and hypotension in newborns unresponsive to vasopressors and volume expansion therapy. Animal studies: Olmesartan did not show carcinogenicity in rats administered via diet for up to 2 years. Furthermore, olmesartan administration had no effect on fertility in either male or female rats. No teratogenic effects were observed in pregnant rats with oral doses up to 1000 mg/kg/day, or in pregnant rabbits with oral doses up to 1 mg/kg/day. However, significantly reduced birth weight and weight gain were observed in rats. Additionally, a dose-dependent increase in developmental milestone delays (delayed auricular separation, delayed eruption of lower incisors, delayed appearance of abdominal hair, delayed testicular descent, and delayed eyelid separation) and the incidence of renal pelvis dilatation were observed in rats. Olmesartan was negative in the in vitro Syrian hamster embryonic cell transformation assay and showed no genotoxicity in the Ames (bacterial mutagenesis) assay. However, in vitro experiments showed that the drug could induce chromosomal aberrations in cultured cells (Chinese hamster lungs) and was positive for thymidine kinase mutation in the in vitro mouse lymphoma assay. Olmesartan was negative in in vivo mutagenesis assays of the intestines and kidneys of MutaMouse mice and in the chromosome breakage assay (micronucleus assay) of mouse bone marrow at oral doses up to 2000 mg/kg.

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Hepatotoxicity
Olmesartan was associated with a low incidence of elevated serum transaminases (
Probability score: D (likely a rare cause of clinically significant liver injury)).

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Use during pregnancy and lactation
◉ Overview of use during lactation
Aside from one case of adverse reaction in a breastfed infant, there is no information regarding the use of olmesartan during lactation. Alternative medications are recommended, especially for breastfed newborns or preterm infants.
◉ Effects on Breastfed Infants
A healthy, full-term newborn, aged 6 days, was exposed to olmesartan via breast milk. The mother did not report the olmesartan dosage or breastfeeding. Weight gain was normal for the first two weeks postpartum, but a sudden weight loss was recorded during a pediatric check-up on day 17 postpartum. He was admitted to the hospital on day 21 and began mixed feeding (milk and formula). Biochemical tests showed an aspartate aminotransferase (AST) level of 250 mg/dL, and urinalysis was normal. Virological and metabolic transaminase elevations were ruled out. The infant's weight began to recover, and AST gradually returned to normal, decreasing to 50 mg/dL by day 24. Olmesartan was discontinued, and the infant was discharged on day 24 postpartum.
◉ Effects on Breastfeeding and Breast Milk
As of the revision date, no relevant published information was found.

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Protein Binding
Olmesartan is highly bound to plasma proteins. 99% of the administered dose remains in a bound state and cannot penetrate red blood cells.

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Drug Interactions
Alisartan and benicarpases are contraindicated in diabetic patients. Alisartan and benicarpases should be avoided in patients with renal insufficiency (glomerular filtration rate <60 mL/min).
Dual blocking of the renin-angiotensin system (RAS) with angiotensin receptor blockers, ACE inhibitors, or alisartan increases the risk of hypotension, hyperkalemia, and altered renal function (including acute renal failure) compared to monotherapy. Most patients receiving combination therapy with two RAS inhibitors do not experience additional benefit compared to monotherapy. Combination therapy with RAS inhibitors should generally be avoided. Blood pressure, renal function, and electrolytes should be closely monitored in patients taking benicarpases and other drugs that affect the RAS.
Elevated serum lithium levels and lithium toxicity have been reported when lithium is used in combination with angiotensin II receptor antagonists, including benicarpases. Serum lithium levels should be monitored during concomitant use.
Drug interactions (reduced antihypertensive effect) may occur when angiotensin II receptor antagonists are used in combination with nonsteroidal anti-inflammatory drugs (NSAIDs), including selective cyclooxygenase-2 (COX-2) inhibitors. Renal function deterioration, including acute renal failure, may occur in elderly patients, patients with hypovolemia (including those receiving concurrent diuretics), or patients with impaired renal function. Patients receiving olmesartan in combination with NSAIDs (including selective COX-2 inhibitors) should have their renal function monitored regularly.
For more complete data on olmesartan interactions (10 items in total), please visit the HSDB record page.

[1]. Effects of telmisartan and olmesartan on insulin sensitivity and renal function in spontaneously hypertensive rats fed a high fat diet. J Pharmacol Sci. 2016 Jul;131(3):190-7.

[2]. Olmesartan Inhibits Cardiac Hypertrophy in Mice Overexpressing Renin Independently of Blood Pressure: Its Beneficial Effects on ACE2/Ang(1-7)/Mas Axis and NADPH Oxidase Expression. J Cardiovasc Pharmacol. 2016 Jun;67(6):503-9.

[3]. Synergistic, cytotoxic and apoptotic activities of olmesartan with NF-κB inhibitor against HeLa human cell line. Toxicol Mech Methods. 2015;25(8):614-21.

Therapeutic Uses
Angiotensin II type 1 receptor blocker; antihypertensive drug. Benicar is 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 observed in controlled trials of antihypertensive drugs across various pharmacological classes, including the class to which Benicar belongs. Currently, no controlled trials have demonstrated that Benicar reduces risk. Controlling hypertension should be part of comprehensive cardiovascular risk management, which should include, where applicable, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and sodium restriction. Many patients require more than one medication to achieve their blood pressure targets. For specific recommendations on targets and management, please refer to published guidelines, such as those from the Joint National Hypertension Education Program and the Joint Committee on Prevention, Detection, Evaluation, and Treatment of Hypertension (JNC). Randomized controlled trials have shown that various antihypertensive drugs with different pharmacological classes and mechanisms of action reduce cardiovascular disease morbidity and mortality. Therefore, it can be concluded that the reduction in blood pressure, rather than the pharmacological properties of the drug, is the primary source of these benefits. The greatest and most significant benefit of antihypertensive drugs for cardiovascular outcomes is the reduction of stroke risk, but their effects on reducing myocardial infarction and cardiovascular mortality are also frequently observed. Elevated systolic or diastolic blood pressure increases cardiovascular risk, and the higher the blood pressure, the greater the absolute risk increase for every 1 mmHg increase. Therefore, even a slight reduction in severe hypertension can bring significant benefits. The relative risk reduction from blood pressure reduction is similar across different absolute risk populations; therefore, the absolute benefit is greater for patients with pre-existing high risk (but not hypertension) (e.g., diabetes or hyperlipidemia). For these patients, a more aggressive treatment regimen and a lower blood pressure target are expected to yield more significant benefits. Some antihypertensive drugs (monotherapy) have weaker antihypertensive effects in Black patients, and many antihypertensive drugs also have other approved indications and effects (e.g., treatment of angina, heart failure, or diabetic nephropathy). These factors can guide the choice of treatment regimen. The drug can be used alone or in combination with other antihypertensive drugs. /Included on US Product Label/
Angiotensin II receptor blockers (including olmesartan) and ACE inhibitors have been shown to delay the progression of kidney disease in hypertensive patients with diabetes and microalbuminuria or overt nephropathy, and one of these classes of drugs is recommended for such patients. /Not Included on US Product Label/
The efficacy of angiotensin II receptor blockers (including olmesartan) in the treatment of congestive heart failure is unclear. Although angiotensin II receptor blockers appear to have similar hemodynamic effects to ACE inhibitors, some clinicians have noted that, in the absence of data demonstrating comparable long-term cardiovascular and/or renal benefits, angiotensin II receptor blockers should primarily be reserved for patients who require ACE inhibitors but cannot tolerate them (e.g., due to cough). /Not Included on US Product Label/
A randomized, double-blind study evaluated the antihypertensive effects of benicar in a pediatric population, including 302 hypertensive patients aged 6 to 16 years. The study population included a cohort of 112 Black patients and a cohort of 190 mixed-race patients (38 of whom were Black). The predominant cause of hypertension was essential hypertension (87% in the Black cohort and 67% in the mixed-race cohort). Patients weighing 20 to <35 kg were randomized to receive 2.5 mg or 20 mg of benicar once daily, while patients weighing ≥35 kg were randomized to receive 5 mg or 40 mg of benicar once daily. After 3 weeks, patients were again randomized to continue benicar or receive a placebo, with a maximum treatment duration of 2 weeks. During the initial dose-response phase, benicar significantly reduced systolic and diastolic blood pressure in a weight-adjusted dose-dependent manner. Overall, both dose levels of benicar (low and high doses) significantly reduced systolic blood pressure by 6.6 mmHg and 11.9 mmHg from baseline, respectively. These reductions in systolic blood pressure included both the drug and placebo effects. During the randomization to placebo phase, patients continuing benicarca had a mean trough systolic blood pressure that was 3.2 mmHg lower and a mean trough diastolic blood pressure that was 2.8 mmHg lower than those who switched to placebo. These differences were statistically significant. Consistent with observations in the adult population, the decrease in blood pressure was smaller in Black patients. In the same study, 59 patients aged 1 to 5 years and weighing ≥5 kg received 0.3 mg/kg benicarca once daily for three weeks in an open-label phase, and were then randomized in a double-blind phase to receive benicarca or placebo. At the end of the second week of discontinuation, patients randomized to the benicarca group had a mean trough systolic/diastolic blood pressure that was 3/3 mmHg lower than those in the placebo group. The difference in blood pressure was not statistically significant (95% CI -2 to 7/-1 to 7).

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Drug Warning
/Black Box Warning/ Warning: Fetal toxicity. Benicarca should be discontinued as soon as pregnancy is discovered. Drugs that act directly on the renin-angiotensin system can cause injury or even death to the developing fetus.
Use of medications acting on the renin-angiotensin system in the mid-to-late stages of pregnancy 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 deformities. Potential neonatal adverse reactions include craniosynostosis, anuria, hypotension, renal failure, and death. Benicar should be discontinued as soon as pregnancy is confirmed. These adverse consequences are often associated with the use of these medications in the mid-to-late stages of pregnancy. Most epidemiological studies investigating fetal malformations following early pregnancy use of antihypertensive drugs have not differentiated between medications affecting the renin-angiotensin system and other antihypertensive drugs. Appropriate management of maternal hypertension during pregnancy is crucial for optimizing maternal and infant outcomes. In rare cases where no suitable alternative medication is available for a particular patient and medications affecting the renin-angiotensin system must be used, the pregnant woman should be informed of the potential risks to the fetus. A series of ultrasound examinations should be performed to assess the amniotic environment. If oligohydramnios is detected, benicar should be discontinued unless deemed essential to the mother's life. Fetal monitoring may be required depending on gestational age. However, patients and physicians should note that oligohydramnios may only occur after irreversible damage to the fetus. Newborns with a history of intrauterine exposure to benicardium: If oliguria or hypotension occurs, focus should be placed on maintaining blood pressure and renal perfusion. Exchange transfusion or dialysis may be necessary to reverse hypotension and/or replace impaired kidney function. FDA Pregnancy Risk Classification: D/Clear evidence of risk. Human studies, trial data, or post-marketing data have confirmed fetal risk. Nevertheless, the potential benefits of using this drug may outweigh the potential risks. For example, this drug may be appropriate in life-threatening situations or when other safer medications are unavailable or ineffective. /
For more complete data on drug warnings for olmesartan (19 total), please visit the HSDB records page.

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Pharmacodynamics
Generally, the physiological effects of olmesartan include lowering blood pressure, lowering aldosterone levels, reducing cardiac activity, and increasing sodium excretion. Hypotension in patients with volume or salt insufficiency: Symptomatic hypotension may occur after initiating olmesartan treatment in patients with activated renin-angiotensin-aldosterone systems, such as those with volume and/or salt insufficiency (e.g., patients receiving high-dose diuretics). Treatment should be initiated under close medical supervision. If hypotension occurs, the patient should be placed in a supine position and intravenous saline infusion should be administered if necessary. Transient hypotensive reactions are not a contraindication to continued treatment, and treatment can usually be continued once blood pressure stabilizes. Valvular stenosis: Theoretically, patients with aortic stenosis may be at risk of reduced coronary perfusion due to their smaller reduction in afterload. Renal impairment: Because olmesartan inhibits the renin-angiotensin-aldosterone system, susceptible individuals may experience changes in renal function after olmesartan treatment. In patients whose renal function may depend on the activity of the renin-angiotensin-aldosterone system (e.g., patients with severe congestive heart failure), treatment with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor antagonists is associated with oliguria and/or progressive azotemia, and in rare cases, can lead to acute renal failure and/or death. Similar outcomes may occur in patients receiving olmesartan. Elevated serum creatinine or blood urea nitrogen (BUN) have been reported in studies of patients with unilateral or bilateral renal artery stenosis using ACE inhibitors. There are currently no studies on the long-term use of olmesartan medoxomil in patients with unilateral or bilateral renal artery stenosis, but similar results are expected. Celiac enteropathy: Severe chronic diarrhea with significant weight loss has been reported in patients after months to years of olmesartan treatment. Intestinal biopsy often shows villous atrophy. If these symptoms occur during olmesartan treatment, other causes should be ruled out. If no other cause is found, discontinuation of olmesartan medoxomil should be considered. Electrolyte Imbalance: Olmesartan medoxomil contains olmesartan, a drug that inhibits the renin-angiotensin system (RAS). RAS inhibitors can cause hyperkalemia. Monitor serum electrolytes regularly. Olmesartan is an angiotensin II receptor blocker (ARB) widely used to treat hypertension. In vitro studies cited in this article show that it does not enhance PPAR-γ-mediated transcriptional activity. Using a spontaneously hypertensive rat (SHR) model fed a high-fat diet, this study found that the beneficial effects of olmesartan (improved insulin sensitivity, correction of hypertriglyceridemia, and renal protection) are mediated through PPAR-γ-independent effects, most likely through AT1 receptor blockade.

C24H26N6O3

446.50

446.206

C, 64.56; H, 5.87; N, 18.82; O, 10.75

144689-24-7

Olmesartan-d4; 1420880-41-6; Olmesartan-d6; 1185144-74-4; Olmesartan medoxomil; 144689-63-4

158781

White to off-white solid powder

1.3±0.1 g/cm3

738.3±70.0 °C at 760 mmHg

186-188ºC

400.3±35.7 °C

0.0±2.6 mmHg at 25°C

1.671

3.72

3

7

8

33

656

0

O([H])C(C([H])([H])[H])(C([H])([H])[H])C1=C(C(=O)O[H])N(C([H])([H])C2C([H])=C([H])C(C3=C([H])C([H])=C([H])C([H])=C3C3N=NN([H])N=3)=C([H])C=2[H])C(C([H])([H])C([H])([H])C([H])([H])[H])=N1

VTRAEEWXHOVJFV-UHFFFAOYSA-N

InChI=1S/C24H26N6O3/c1-4-7-19-25-21(24(2,3)33)20(23(31)32)30(19)14-15-10-12-16(13-11-15)17-8-5-6-9-18(17)22-26-28-29-27-22/h5-6,8-13,33H,4,7,14H2,1-3H3,(H,31,32)(H,26,27,28,29)

5-(2-hydroxypropan-2-yl)-2-propyl-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]imidazole-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 (5.60 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 (5.60 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (5.60 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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 (Please use freshly prepared in vivo formulations for optimal results.)