Pravastatin sodium - CAS 81131-70-6
Catalog number: B0084-303838
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
HMG-CoA Reductase (HMGCR)
Pravastatin sodium is an HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM.
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B0084-303838 500 mg $168 In stock
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Related CAS:
81093-37-0 (free acid)
White to Off-white Solid
Mevalotin; Selektine; Elisor; (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6-hydroxy-2-methyl-8-[(2S)-2-methylbutanoyl]oxy-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoate sodium
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1.Electrochemical properties and square-wave voltammetric determination of pravastatin
Biljana Nigovi. Anal Bioanal Chem (2006) 384: 431–437
Electrochemical assays have been extensively used for pharmaceutical analysis and have been proven to be fast, precise and to produce low-cost results with minimum interference from the drug excipients. Preliminary studies on the differential pulse polarographic reduction of pravastatin sodium have been reported , but other electroanalytical and adsorption properties of this compound have not yet been investigated. Adsorptive stripping voltammetry has been shown to be a sensitive analytical method for a wide range of organic compounds that are adsorbed in a submonomolecular layer on the electrode surface. It has been successfully applied to the analysis of atorvastatin in pharmaceutical products and spiked human plasma. The stripping technique is based on a two-step approach consisting of the initial pre-concentration step, during which the analyte is accumulated on the electrode surface under carefully controlled conditions, and subsequent measurement in which the accumulated analyte is stripped off and determined by a voltammetric method. Square-wave voltammetry is one of the most advanced methods in the family of pulse voltammetric techniques applied to the stripping of the deposit. The sensitivity of the technique depends primarily on the kinetics of the redox reaction in the stripping phase.
2.The HMG-CoA reductase inhibitor, pravastatin, prevents the development of monocrotaline-induced pulmonary hypertension in the rat through reduction of endothelial cell apoptosis and overexpression of eNOS
Pascal Guerard & Zo Rakotoniaina & Françoise Goirand. Naunyn-Schmiedeberg’s Arch Pharmacol (2006) 373:401–414
In conclusion, administration of pravastatin showed a trend toward reduction in mortality of hypertensive rats, and attenuates pulmonary hypertension and cardiac hypertrophy induced by monocrotaline. In our model, protective effects of pravastatin involve mainly an improvement in endothelial dysfunction, as shown by the increased endothelial-dependent relaxation of pulmonary artery. This is likely to be related to the increased eNOS expression and the decreased apoptosis observed in endothelial cells of monocrotaline rats treated with pravastatin. Nevertheless, mechanisms other than improvement of endothelial cells function might be involved, as suggested by the apparent discrepancy of the influence of L-NAME according to the outcome assessed. These results strongly support the development of further studies within the field of pulmonary hypertension prevention and treatment (Girgis et al. 2003; Kao 2005; Nishimura et al. 2002, 2003).
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CAS 81131-70-6 Pravastatin sodium

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