OlmesartanCAS# 144689-24-7 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 144689-24-7 | SDF | Download SDF |
PubChem ID | 158781 | Appearance | Powder |
Formula | C24H26N6O3 | M.Wt | 446.5 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | RNH 6270; CS 088 | ||
Solubility | DMSO : 50 mg/mL (111.98 mM; Need ultrasonic) | ||
Chemical Name | 5-(2-hydroxypropan-2-yl)-2-propyl-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]imidazole-4-carboxylic acid | ||
SMILES | CCCC1=NC(=C(N1CC2=CC=C(C=C2)C3=CC=CC=C3C4=NNN=N4)C(=O)O)C(C)(C)O | ||
Standard InChIKey | VTRAEEWXHOVJFV-UHFFFAOYSA-N | ||
Standard InChI | 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) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Potent angiotensin II type I (AT1) receptor antagonist (IC50 = 6.7 nM at hAT1 receptors). Improves cognitive function in a mouse model of hypertension- and hyperlipidemia-associated cognitive decline; ameliorates arterial stiffness in a rat model of chronic renal failure. Metabolite of Olmesartan medoxomil. |
Olmesartan Dilution Calculator
Olmesartan Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.2396 mL | 11.1982 mL | 22.3964 mL | 44.7928 mL | 55.991 mL |
5 mM | 0.4479 mL | 2.2396 mL | 4.4793 mL | 8.9586 mL | 11.1982 mL |
10 mM | 0.224 mL | 1.1198 mL | 2.2396 mL | 4.4793 mL | 5.5991 mL |
50 mM | 0.0448 mL | 0.224 mL | 0.4479 mL | 0.8959 mL | 1.1198 mL |
100 mM | 0.0224 mL | 0.112 mL | 0.224 mL | 0.4479 mL | 0.5599 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Olmesartan(RNH 6270; CS 088) is an angiotensin II receptor antagonist which is used as an anti-hypertensive.
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Pharmacovigilance database search discloses ClC-K channels as a novel target of the AT1 receptor blockers valsartan and olmesartan.[Pubmed:28334417]
Br J Pharmacol. 2017 Jul;174(13):1972-1983.
BACKGROUND AND PURPOSE: Human ClC-K chloride channels are highly attractive targets for drug discovery as they have a variety of important physiological functions and are associated with genetic disorders. These channels are crucial in the kidney as they control chloride reabsorption and water diuresis. In addition, loss-of-function mutations of CLCNKB and BSND genes cause Bartter's syndrome (BS), whereas CLCNKA and CLCNKB gain-of-function polymorphisms predispose to a rare form of salt sensitive hypertension. Both disorders lack a personalized therapy that is in most cases only symptomatic. The aim of this study was to identify novel ClC-K ligands from drugs already on the market, by exploiting the pharmacological side activity of drug molecules available from the FDA Adverse Effects Reporting System database. EXPERIMENTAL APPROACH: We searched for drugs having a Bartter-like syndrome as a reported side effect, with the assumption that BS could be causatively related to the block of ClC-K channels. The ability of the selected BS-causing drugs to bind and block ClC-K channels was then validated through an integrated experimental and computational approach based on patch clamp electrophysiology in HEK293 cells and molecular docking simulations. KEY RESULTS: Valsartan and Olmesartan were able to block ClC-Ka channels and the molecular requirements for effective inhibition of these channels have been identified. CONCLUSION AND IMPLICATIONS: These results suggest additional mechanisms of action for these sartans further to their primary AT1 receptor antagonism and propose these compounds as leads for designing new potent ClC-K ligands.
Circulating progenitor cells in hypertensive subjects: Effectiveness of a treatment with olmesartan in improving cell number and miR profile in addition to expected pharmacological effects.[Pubmed:28301500]
PLoS One. 2017 Mar 16;12(3):e0173030.
CD34+ circulating progenitor cells (CD34+CPCs) are a population of multipotent cells which can delay the development of atherosclerosis and cardiovascular disease (CVD) in conditions of increased CV risk. MicroRNAs (miRs) 221 and 222 modulate different genes regulating angiogenesis and inflammation; moreover, miR221/22 have beenshown to participate in differentiation and proliferation of CD34+CPCs, inhibiting cell migration and homing. miR221/222 in CD34+CPCs from hypertensive subjects are also increased and associated with CD34+cell number and reactive oxygen species (ROS). We evaluated CD34+CPC number, intracellular miR221/222 and ROS levels, arterial stiffness (AS)and echocardiography indices at baseline (T0).Then, after a six-month treatment with Olmesartan, 20 mg/day (T1), in 57 hypertensive patients with left ventricular hypertrophy (LVH) and with no additional risk factor for CVD, and in 29 healthy controls (baseline),fibrinogen, C-reactive protein (CRP), glucose and lipid profiles were also evaluated.At T1, blood pressure values, CRP and fibrinogen levels, ROS and miR221/222 were significantly decreased (all p <0.001), as were AS indices and LV mass index (p<0.001), while cell number was increased (p<0.001). Olmesartan is effective in reducing miR and ROS levels in CD34+CPCs from hypertensive subjects, as well as in increasing CD34+CPC number, providing multilevel CV protection, in addition to its expected pharmacological effects.
miR-205 mediates the inhibition of cervical cancer cell proliferation using olmesartan.[Pubmed:28304186]
J Renin Angiotensin Aldosterone Syst. 2016 Jul-Sep;17(3):1470320316663327.
OBJECTIVE: The renin-angiotensin-aldosterone system has become known as a prerequisite for tumor angiogenesis that is now recognized as a crucial step in the development of tumors, including cervical cancer. The Ang II-AT1R pathway is known to play an important role in tumor angiogenesis. MicroRNAs (miRNAs) are a class of small, regulating RNAs that participate in tumor genesis, differentiation and proliferation. The current study focused on the anti-tumor mechanism of Olmesartan, a novel angiotensin II antagonist, on cervical cancer cells. MATERIALS AND METHODS: qRT-PCR and Western blot were used to demonstrate the effect of Olmesartan on miR-205 and VEGF-A expression. miR-205 mimics and VEGF-A shRNA plasmid were separately transfected into HeLa and Siha cells to further validate the function of miR-205 and VEGF-A in cervical cancer cell proliferation. RESULTS: It was found that Olmesartan could upregulate miR-205 and inhibit VEGF-A expression in HeLa and Siha cells. In addition, VEGF-A was proven to be a target gene of miR-205. CONCLUSION: This result provides a new idea on the anti-tumor mechanism of Olmesartan, which may be used as a novel therapeutic target of cervical cancer.
Effects of olmesartan on arterial stiffness in rats with chronic renal failure.[Pubmed:22694778]
Cardiovasc Diabetol. 2012 Jun 13;11:66.
BACKGROUND: It has been suggested that the antioxidant properties of Olmesartan (OLM), an angiotensin II type 1 receptor (AT(1)R) blocker, contribute to renal protection rather than blood pressure lowering effects despite the fact that causal relationships between hypertension and renal artery disease exist. This study aimed to examine the hypothesis whether the antioxidative activities of OLM were correlated to arterial stiffness, reactive oxygen species and advanced glycation end products (AGEs) formation in rats with chronic renal failure (CRF). METHODS: CRF rats were induced by 5/6 nephrectomy and randomly assigned to an OLM (10 mg/day) group or a control group. Hemodynamic states, oxidative stress, renal function and AGEs were measured after 8 weeks of OLM treatment. RESULTS: All the hemodynamic derangements associated with renal and cardiovascular dysfunctions were abrogated in CRF rats receiving OLM. Decreased cardiac output was normalized compared to control (p <0.05). Mean aortic pressure, total peripheral resistance and left ventricular weight/body weight ratio were reduced by 21.6% (p <0.05), 28.2% (p <0.05) and 27.2% ((p <0.05). OLM also showed beneficial effects on the oscillatory components of the ventricular after-load, including 39% reduction in aortic characteristic impedance (p < 0.05), 75.3% increase in aortic compliance (p <0.05) and 50.3% increase in wave transit time (p < 0.05). These results implied that OLM attenuated the increased systolic load of the left ventricle and prevented cardiac hypertrophy in CRF rats. Improved renal function was also reflected by increases in the clearances of BUN (28.7%) and serum creatinine (SCr, 38.8%). In addition to these functional improvements, OLM specifically reduced the levels of malondialdehyde (MDA) equivalents in aorta and serum by 14.3% and 25.1%, as well as the amount of AGEs in the aortic wall by 32% (p < 0.05) of CRF rats. CONCLUSION: OLM treatment could ameliorate arterial stiffness in CRF rats with concomitant inhibition of MDA and AGEs levels through the reduction of oxidative stress in aortic wall.
In vitro antagonistic properties of a new angiotensin type 1 receptor blocker, azilsartan, in receptor binding and function studies.[Pubmed:21123673]
J Pharmacol Exp Ther. 2011 Mar;336(3):801-8.
The angiotensin II (AII) antagonistic action of azilsartan (AZL) [2-ethoxy-1-{[2'-(5-oxo-4,5-dihydro-1,2,4-oxadiazol-3-yl)biphenyl-4-yl]methyl}-1H -benzimidazole-7-carboxylic acid] was investigated in radioligand binding and function studies. AZL inhibited the specific binding of (1)(2)(5)I-Sar(1)-Ile(8)-AII to human angiotensin type 1 receptors with an IC(5)(0) of 2.6 nM. The inhibitory effect of AZL persisted after washout of the free compound (IC(50) value of 7.4 nM). Olmesartan, telmisartan, valsartan, and irbesartan also inhibited the specific binding with IC(5)(0) values of 6.7, 5.1, 44.9, and 15.8 nM, respectively. However, their inhibitory effects were markedly attenuated with washout (IC(5)(0) values of 242.5, 191.6, >10,000, and >10,000 nM). AZL also inhibited the accumulation of AII-induced inositol 1-phosphate (IP1) in the cell-based assay with an IC(5)(0) value of 9.2 nmol; this effect was resistant to washout (IC(5)(0) value of 81.3 nM). Olmesartan and valsartan inhibited IP1 accumulation with IC(5)(0) values of 12.2 and 59.8 nM, respectively. The activities of these compounds were markedly reduced after washout (IC(5)(0) value of 908.5 and 22,664.4 nM). AZL was defined as an inverse agonist in an experiment by using a constitutively active mutant of human angiotensin type 1 receptors. In isolated rabbit aortic strips, AZL reduced the maximal contractile response to AII with a pD'(2) value of 9.9. The inhibitory effects of AZL on contractile responses induced by AII persisted after the strips were washed; these inhibitory effects were more potent than those of Olmesartan. These results suggest that AZL is a highly potent and slowly dissociating AII receptor blocker. Its tight receptor binding might be expected to produce potent and long-lasting antihypertensive effects in preclinical and clinical settings.
Inhibition of cognitive decline in mice fed a high-salt and cholesterol diet by the angiotensin receptor blocker, olmesartan.[Pubmed:18028965]
Neuropharmacology. 2007 Dec;53(8):899-905.
The metabolic syndrome is closely related to dietary habits and seems to be associated with impairment of cognitive function in humans. Angiotensin receptor blockers are widely used with the expectation of preventing cardiovascular events and stroke and potential amelioration of the metabolic syndrome. We examined the diet-induced changes of cognitive function in mice treated with a high-salt and high-cholesterol diet. C57BL/6J mice were fed a high-salt (2% NaCl in drinking water) and high-cholesterol (1.25% cholesterol, 10% coconut oil) diet (HSCD) or a normal diet (ND), and subjected to 20 trials of a passive avoidance task every week from 8weeks of age. An age-dependent decline of the avoidance rate starting from 10weeks of age was observed in HSCD mice, whereas the avoidance rate gradually increased in the ND group. Oral administration of an angiotensin receptor blocker, Olmesartan, at a dose of 3mg/kg per day in drinking water from 8weeks of age prevents this decline of avoidance rate in HSCD mice (49% vs. 82% at 12weeks of age). Treatment with Olmesartan significantly decreased serum glucose and cholesterol levels in HSCD mice, with a slight decrease in blood pressure. Administration of Olmesartan in HSCD-fed mice showed a 1.6-fold increase in mRNA expression of a neuroprotective factor, MMS2, compared to HSCD-fed mice without Olmesartan. Olmesartan attenuated the increase in superoxide anion production detected by dihydroethidium staining in the brain of HSCD mice. Our results suggest that Olmesartan could be therapeutically effective in preventing the impairment of quality of life in persons on a high-fat and high-salt diet.