SB 611812

Urotensin-II (UT) antagonist; attenuates cardiac dysfunction CAS# 345892-71-9

SB 611812

Catalog No. BCC6257----Order now to get a substantial discount!

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Quality Control of SB 611812

Number of papers citing our products

Chemical structure

SB 611812

3D structure

Chemical Properties of SB 611812

Cas No. 345892-71-9 SDF Download SDF
PubChem ID 10278166 Appearance Powder
Formula C17H16Cl3F3N2O3S M.Wt 491.74
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 10 mM in DMSO
Chemical Name 2,6-dichloro-N-[4-chloro-3-[2-(dimethylamino)ethoxy]phenyl]-4-(trifluoromethyl)benzenesulfonamide
SMILES CN(C)CCOC1=C(C=CC(=C1)NS(=O)(=O)C2=C(C=C(C=C2Cl)C(F)(F)F)Cl)Cl
Standard InChIKey UIZHOFJFIOCYLH-UHFFFAOYSA-N
Standard InChI InChI=1S/C17H16Cl3F3N2O3S/c1-25(2)5-6-28-15-9-11(3-4-12(15)18)24-29(26,27)16-13(19)7-10(8-14(16)20)17(21,22)23/h3-4,7-9,24H,5-6H2,1-2H3
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.
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.
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.

Biological Activity of SB 611812

DescriptionUrotensin-II (UT) antagonist. Inhibits urotensin-II-induced proliferation of neonatal cardiac fibroblasts. Attenuates cardiac dysfunction in a rat model of coronary artery ligation; decreases cardiomyocyte hypertrophy, ventricular dilatation and cardiac remodeling.

SB 611812 Dilution Calculator

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Preparing Stock Solutions of SB 611812

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.0336 mL 10.168 mL 20.3359 mL 40.6719 mL 50.8399 mL
5 mM 0.4067 mL 2.0336 mL 4.0672 mL 8.1344 mL 10.168 mL
10 mM 0.2034 mL 1.0168 mL 2.0336 mL 4.0672 mL 5.084 mL
50 mM 0.0407 mL 0.2034 mL 0.4067 mL 0.8134 mL 1.0168 mL
100 mM 0.0203 mL 0.1017 mL 0.2034 mL 0.4067 mL 0.5084 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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References on SB 611812

Urotensin-II receptor blockade with SB-611812 attenuates cardiac remodeling in experimental ischemic heart disease.[Pubmed:16919371]

Peptides. 2006 Nov;27(11):2919-26.

It is now well established that urotensin-II (UII) levels are increased in several cardiovascular diseases. We previously demonstrated that UII and the UII receptor (UT) protein levels are significantly increased in the hearts of both humans and rats with congestive heart failure (CHF). We have also recently demonstrated that UII blockade, with a selective UII antagonist, improves heart function in a rat model of ischemic CHF. Here, we evaluated the attenuation of cardiac remodeling associated with UII antagonism in the same rat model of ischemic CHF. Animals were administered a specific UT receptor antagonist, SB-611812 (30 mg/kg/day, gavage), or vehicle 30 min prior to coronary artery ligation followed by daily treatment for 8 weeks. Myocardial interstitial fibrosis was analyzed by Masson's trichrome and picrosirius red staining. RT-PCR analysis was utilized for mRNA expression studies. We used Western blotting to assess levels of collagen types I and III. Mitogenic activity of UII on cultured neonatal cardiac fibroblasts was also evaluated. Following coronary ligation, SB-611812 significantly attenuated both myocardial and endocardial interstitial fibrosis, and reduced collagen type I:III ratio (P<0.01). UII induced proliferation of cardiac fibroblasts and this mitogenic effect was significantly inhibited with 1 microM of SB-611218 (P<0.05). We demonstrate here that selective blockade of UT reduces diastolic dysfunction by decreasing myocardial fibrosis post-coronary ligation in vivo, and inhibits UII-mediated fibroblast proliferation in vitro.

Urotensin-II blockade with SB-611812 attenuates cardiac dysfunction in a rat model of coronary artery ligation.[Pubmed:16797584]

J Mol Cell Cardiol. 2006 Aug;41(2):285-95.

Expression of urotensin II (UII) is significantly elevated in the hearts of patients with congestive heart failure (CHF). Recent reports have also shown increased plasma levels of UII in patients with CHF, and these levels correlated with the severity of disease. We therefore hypothesized that blockade of UII signaling would improve cardiac function in a rat model of CHF. CHF was induced in rats by ligating the left coronary artery. Animals were randomized to either treatment with a specific UT receptor antagonist, SB-611812 (30 mg/kg/day, UID by gavage), or vehicle, starting either 30 min prior to coronary ligation (early treatment) or 10 days after ligation (delayed treatment). Treatment drug or vehicle was administered daily thereafter for 8 weeks. We measured cardiac function and evaluated the levels of mRNA expression for mediators of CHF. In addition, we evaluated UII and UT protein levels using immunohistochemistry and Western blotting. Cardiomyocyte hypertrophy was evaluated by measuring cardiomyocyte cross-sectional area. Animals with CHF showed increased UII and UT expression as evidenced by immunohistochemistry and Western blotting. Treatment with the SB-611812 significantly reduced overall mortality, left ventricular end-diastolic pressure by 72%, lung edema by 71%, right ventricular systolic pressure by 92%, central venous pressure by 59%, cardiomyocyte hypertrophy by 54%, and ventricular dilatation by 79% (P < 0.05). Therefore, blockade of the UT receptor reduced mortality and improved cardiac function in this model of myocardial infarction and CHF, suggesting an important role for UII in the pathogenesis of this condition.

Urotensin-II and cardiovascular remodeling.[Pubmed:17988761]

Peptides. 2008 May;29(5):764-9.

Urotensin-II (U-II), a cyclic undecapeptide, and its receptor, UT, have been linked to vascular and cardiac remodeling. In patients with coronary artery disease (CAD), it has been shown that U-II plasma levels are significantly greater than in normal patients and the severity of the disease is increased proportionally to the U-II plasma levels. We showed that U-II protein and mRNA levels were significantly elevated in the arteries of patients with coronary atherosclerosis in comparison to healthy arteries. We observed U-II expression in endothelial cells, foam cells, and myointimal and medial vSMCs of atherosclerotic human coronary arteries. Recent studies have demonstrated that U-II acts in synergy with mildly oxidized LDL inducing vascular smooth muscle cell (vSMC) proliferation. Additionally, U-II has been shown to induce cardiac fibrosis and cardiomyocyte hypertrophy leading to cardiac remodeling. When using a selective U-II antagonist, SB-611812, we demonstrated a decrease in cardiac dysfunction including a reduction in cardiomyocyte hypertrophy and cardiac fibrosis. These findings suggest that U-II is undoubtedly a potential therapeutic target in treating cardiovascular remodeling.

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