"Gustavo Frenkel, Eyal Gilboa, \"Process for the preparation of fluvastatin sodium crystal form XIV.\" U.S. Patent US20050119342, issued June 02, 2005."@en . . . . . "* 0.35 L/kg"@en . "Rapidly and almost completely absorbed (> 90%), but undergoes extensive first pass metabolism. Bioavailability is 24% (range 9-50%) when a 10 mg dose is given. The mean relative bioavailability of the extended-release tablet is 29% (range: 9% to 66%) compared to an immediate-release capsule administered under fasting conditions. When given orally, fluvastatin reaches peak concentrations (Tmax) in less than one hour. Taking the extended release tablet with a high-fat meal will delay absorption (Tmax = 6 hours) and increase bioavailability by approximately 50%. However, the maximum concentration of fluvastatin sodium extended-release tablets seen after a high fat meal is less than the peak concentration following a single dose or twice daily dose of the 40 mg fluvastatin capsule."@en . "* 0.8 L/h/kg * 107 \u00B1 38.1 L/h [Hypercholesterolemia patients receiving a single dose of 20 mg] * 87.8 \u00B1 45 L/h [Hypercholesterolemia patients receiving 20 mg twice daily] * 108 \u00B1 44.7 L/h [Hypercholesterolemia patients receiving 40 mg single] * 64.2 \u00B1 21.1 L/h [Hypercholesterolemia patients receiving 40 mg twice daily]"@en . . "Humans and other mammals"@en . . . . "To be used as an adjunct to dietary therapy to prevent cardiovascular events. May be used as secondary prevention in patients with coronary heart disease (CHD) to reduce the risk of requiring coronary revascularization procedures, for reducing progression of coronary atherosclerosis in hypercholesterolemic patients with CHD, and for the treatment of primary hypercholesterolemia and mixed dyslidipidemia. "@en . . . . . "When orally administered, fluvastatin is primarily excreted in the faces ( ~90%) as metabolites, with less than 2% present as unchanged drug. Approximately 5% was recovered in the urine. "@en . . . . . . . . . . "Fluvastatin selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis. Inhibition results in a decrease in hepatic cholesterol levels which stimulates the synthesis of LDL receptors and increases hepatic uptake of LDL cholesterol. The end result is decreased levels of plasma total and LDL cholesterol. "@en . . . "Generally well-tolerated. May cause gastrointestinal upset (diarrhea, nausea, constipation, gas, abdominal pain), myotoxicity (mypothy, myositis, rhabdomyolysis), and hepatotoxicity."@en . "# FDA label # Toda T, Eliasson E, Ask B, Inotsume N, Rane A: Roles of different CYP enzymes in the formation of specific fluvastatin metabolites by human liver microsomes. Basic Clin Pharmacol Toxicol. 2009 Nov;105(5):327-32. doi: 10.1111/j.1742-7843.2009.00453.x. Epub 2009 Aug 6. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/19663817"@en . . . . . "approved"@en . . "3 hours "@en . . . . . . . . . . " "@en . . . "Fluvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Fluvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease. It is also the first entirely synthetic HMG-CoA reductase inhibitor and is structurally distinct from the fungal derivatives of this therapeutic class. "@en . "May be taken with or without food, but should be taken consistently."@en . . . . . . . . . . . . "Fluvastatin"@en . . "98% bound to plasma proteins. At therapeutic concentrations, the protein binding of fluvastatin is not affected by warfarin, salicylic acid and glyburide."@en . . . . . . . . . . . . . "When given with an evening meal, Cmax and AUC decreased while Tmax increased 2-fold"@en . . . . . "93957-54-1"@en . . " "@en .