Perioperative Rosuvastatin in Cardiac Surgery — NEJM
A novel asymmetric synthesis of a (3,5)-dihydroxyhexanoic ester is described. The ester, which serves as the precursor for generating the side chain of rosuvastatin, is synthesized from -glucose and subsequently coupled, under Wittig olefination conditions, with a phosphonium ylide derived from an appropriately substituted pyrimidine moiety. The coupling results in the formation of a precursor containing all the structural features of rosuvastatin. This precursor is converted into rosuvastatin calcium following a well-established procedure.
Rosuvastatin to Prevent Vascular Events in Men and …
● reduce LDL-C, Total-C, non-HDL-C and Apo-B in children and adolescents 7 to 17 years of age with homozygous familial hypercholesterolemia, either alone or with other lipid-lowering treatments (e.g., LDL apheresis).
1. Levy, RI. A quarter century of drug treatment of dyslipoproteinemia, with a focus on the new HMG-CoA reductase inhibitor fluvastatin. Circulation 1993; 87(4 Suppl):III45.
2. Jones, P, Kafonek, S, Laurora, I, et al for the CURVES Investigators. Comparative dose efficacy study of atorvastatin versus simvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol 1998; 81:582.
3. Rosenson, RS. Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia. Expert Rev Cardiovasc Ther 2003; 1:495.
4. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344:1383.
5. Knopp, RH. Drug Treatment of lipid disorders. N Engl J Med 1999; 341: 498-511.
6. Parker, TS, McNamara, DJ, Brown, C, Garrigan, O, Kolb, R, Batwin, H, Ahrens, EH Jr. Mevalonic acid in human plasma: relationship of concentration and circadian rhythm to cholesterol synthesis rates in man. Proc Natl Acad Sci USA 1982; 79: 3037–3041.
7. Jones, PJ, Schoeller, DA. Evidence for diurnal periodicity in human cholesterol synthesis. J Lipid Res 1990; 31: 667–673. 8. Mevacor (lovastatin) package insert. Whitehouse Station, NJ: Merck Pharmaceuticals; 2004.
9. Lescol (fluvastatin) package insert. East Hanover, NJ: Novartis Pharmaceuticals; 2004.
10. Zocor (simvastatin) package insert. Whitehouse Station, NJ: Merck Pharmaceuticals; 2004.
11. Saito, Y, Yoshida, S, Nakaya, N, Hata, Y, Goto, Y. Comparison between morning and evening doses of simvastatin in hyperlipidemic subjects. A double-blind comparative study. Arterioscler Thromb. 1991; 11:816-26.
12. Lipitor (atorvastatin calcium) package insert. Morris Plains, NJ: Pfizer Pharmaceuticals; 2003.
13. Crestor (rosuvastatin) package insert. Wilmington, DE: AstraZeneca; 2003.
14. Cilla, DD Jr, Gibson, DM, Whitfield, LR, Sedman, AJ. Pharmacodynamic effects and pharmacokinetics of atorvastatin after administration to normocholesterolemic subjects in the morning and evening. J Clin Pharmacol. 1996; 36:604-9.
15. Plakogiannis, R, Cohen, H, Taft, D. Effects of morning versus evening administration of atorvastatin in patients with hyperlipidemia. Am J Health Syst Pharm. 2005; 62(23):2491-4.
16. Martin, PD, Mitchell, PD, Schneck, DW. Pharmacodynamic effects and pharmacokinetics of a new HMG-CoA reductase inhibitor, rosuvastatin, after morning or evening administration in healthy volunteers. Br J Clin Pharmacol. 2002; 54:472-7.
17. Fauler, G, Abletshauser, C, Erwa, W, Loser, R, Witschital, K, Marz, W. Time-of-intake (morning versus evening) of extended-release fluvastatin in hyperlipemic patients is without influence on the pharmacodynamics (mevalonic acid excretion) and pharmacokinetics. Int J Clin Pharmacol Ther. 2007; 45(6): 328-34.
18. Report of the National Cholesterol Education Program on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel. Arch Intern Med. 1988; 148(1): 36-69.
19. Greenberg, RN. Overview of patient compliance with medication dosing: a literature review. Clin Ther. 1984; 6(5):592-9.
rosuvastatin , Crestor: Side Effects & Dosage of Statins
Patients have traditionally been instructed by their physicians to take statins in the evening for maximal effect.(5) The rationale for this recommendation comes from evidence that hepatic HMG-CoA reductase activity6 and cholesterol biosynthesis(7) are greatest at night, while the half-lives of many statins are relatively short. For example, Lovastatin, (8) Fluvastatin, (9) and Simvastatin (10) all have half-lives less than six hours. Thus, in order to achieve maximal LDL lowering, it has been advised to administer statins in the evening in order to inhibit the enzyme while it is most active. Indeed, early studies with simvastatin found that evening administration resulted in significantly greater reductions in LDL cholesterol when compared to daytime administration (21% versus 15% reduction, respectively).(11)
Rosuvastatin - National Institutes of Health
Rosuvastatin is contraindicated for use in pregnant women since safety in pregnant women has not been established and there is no apparent benefit to therapy with rosuvastatin during pregnancy. Because HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, rosuvastatin may cause fetal harm when administered to pregnant women. Rosuvastatin should be discontinued as soon as pregnancy is recognized . Limited published data on the use of rosuvastatin are insufficient to determine a drug-associated risk of major congenital malformations or miscarriage. In animal reproduction studies, there were no adverse developmental effects with oral administration of rosuvastatin during organogenesis at systemic exposures equivalent to a maximum recommended human dose (MRHD) of 40 mg/day in rats or rabbits (based on AUC and body surface area, respectively). In rats and rabbits, decreased pup/fetal survival occurred at 12 times and equivalent, respectively, to the MRHD of 40 mg/day .
16/10/2017 · Rosuvastatin is a commonly used ..
CRESTOR is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of cholesterol. studies in animals, and studies in cultured animal and human cells have shown rosuvastatin to have a high uptake into, and selectivity for, action in the liver, the target organ for cholesterol lowering. In and studies, rosuvastatin produces its lipid-modifying effects in two ways. First, it increases the number of hepatic LDL receptors on the cell-surface to enhance uptake and catabolism of LDL. Second, rosuvastatin inhibits hepatic synthesis of VLDL, which reduces the total number of VLDL and LDL particles.