Rostafuroxin - CAS 156722-18-8
Catalog number: B0084-474617
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Na+/K+ ATPase
Rostafuroxin is a Na+/K+ ATPase modulator that treats hypertension by normalizing renal Na+/K+ ATPase pump function.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-474617 50 mg $399 In stock
B0084-474617 100 mg $599 In stock
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Brife Description:
Na+/K+ ATPase antagonist
White Solid
PST-2238; PST 2238; (3S,5R,8R,9S,10S,13S,14S,17S)-17-(furan-3-yl)-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,15,16-dodecahydro-1H-cyclopenta[a]phenanthrene-3,14,17-triol
Soluble in DMSO.
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -20℃ for long term (months to years).
Shelf Life:
2 years
Boiling Point:
451.3±45.0°C at 760 mmHg
1.226±0.06 g/cm3
Canonical SMILES:
1.Endogenous and exogenous cardiac glycosides: their roles in hypertension, salt metabolism, and cell growth.
Schoner W;Scheiner-Bobis G Am J Physiol Cell Physiol. 2007 Aug;293(2):C509-36. Epub 2007 May 9.
Cardiotonic steroids (CTS), long used to treat heart failure, are endogenously produced in mammals. Among them are the hydrophilic cardenolide ouabain and the more hydrophobic cardenolide digoxin, as well as the bufadienolides marinobufagenin and telecinobufagin. The physiological effects of endogenous ouabain on blood pressure and cardiac activity are consistent with the "Na(+)-lag" hypothesis. This hypothesis assumes that, in cardiac and arterial myocytes, a CTS-induced local increase of Na(+) concentration due to inhibition of Na(+)/K(+)-ATPase leads to an increase of intracellular Ca(2+) concentration ([Ca(2+)](i)) via a backward-running Na(+)/Ca(2+) exchanger. The increase in [Ca(2+)](i) then activates muscle contraction. The Na(+)-lag hypothesis may best explain short-term and inotropic actions of CTS. Yet all data on the CTS-induced alteration of gene expression are consistent with another hypothesis, based on the Na(+)/K(+)-ATPase "signalosome," that describes the interaction of cardiac glycosides with the Na(+) pump as machinery activating various signaling pathways via intramembrane and cytosolic protein-protein interactions. These pathways, which may be activated simultaneously or selectively, elevate [Ca(2+)](i), activate Src and the ERK1/2 kinase pathways, and activate phosphoinositide 3-kinase and protein kinase B (Akt), NF-kappaB, and reactive oxygen species.
2.OASIS-HT: design of a pharmacogenomic dose-finding study.
Staessen JA;Kuznetsova T;Acceto R;Bacchieri A;Brand E;Burnier M;Celis H;Citterio L;de Leeuw PW;Filipovský J;Fournier A;Kawecka-Jaszcz K;Manunta P;Nikitin Y;O'Brien ET;Redón J;Thijs L;Ferrari P;Valentini G;Bianchi G Pharmacogenomics. 2005 Oct;6(7):755-75.
Experimental evidence and observations in humans strongly support an interactive role of mutated alpha-adducin, sodium (Na(+))/potassium (K(+))-adenosine triphosphatase (ATPase) activity and endogenous ouabain in Na(+) homeostasis and the pathogenesis of hypertension. The Ouabain and Adducin for Specific Intervention on Sodium in HyperTension (OASIS-HT) trial is an early Phase II dose-finding study, which will be conducted across 39 European centers. Following a run-in period of 4 weeks without treatment, eligible patients will be randomized to one of five oral doses of rostafuroxin consisting of 0.05, 0.15, 0.5, 1.5, or 5.0 mg/day. Each dose will be compared to a placebo in a double-blind crossover experiment with balanced randomization. Treatment will be initiated with the active drug and continued with placebo or vice versa. Each double-blind period will last 5 weeks. The primary end point is the reduction in systolic blood pressure defined as the average of three clinic readings with the patient in the sitting position. Secondary end points include the reduction in diastolic blood pressure on clinic measurement, the decrease in the 24-h blood pressure, and the incidence of end points related to safety.
3.Targeting Ouabain- and Adducin-dependent mechanisms of hypertension and cardiovascular remodeling as a novel pharmacological approach.
Ferrari P;Ferrandi M;Valentini G;Manunta P;Bianchi G Med Hypotheses. 2007;68(6):1307-14. Epub 2006 Nov 9.
Essential hypertension is a heterogeneous multifactorial syndrome associated with a high cardiovascular risk. A multiple choice of antihypertensive drugs is available; however, a high individual variability to the antihypertensive therapy is still responsible for a modest reduction of the CV risk and not satisfactory control of blood pressure levels. The success of future hypertension treatment will depend upon the understanding of the genetic molecular mechanisms operating in subsets of patients, and the ability of new drugs to specifically correct such alterations. Two mechanisms, among others, are involved in determining the abnormalities of tubular Na(+) reabsorption observed in essential hypertension: the polymorphism of the cytoskeletal protein alpha-adducin and the increased circulating levels of endogenous ouabain (EO). Both lead to increased activity and expression of the renal Na-K pump, the driving force for tubular Na transport. Morphological and functional cardiovascular alterations have also been associated with adducin and EO. Rostafuroxin is a new oral antihypertensive agent able to selectively antagonize adducin and EO hypertensive and molecular effects. It is endowed with high potency and efficacy in reducing blood pressure and preventing organ hypertrophy in animal models representative of both adducin and EO mechanisms.
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