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QuickView for Fluvastatin (compound)

Name: fluvastatin
PubChem Compound ID: 10501876
Molecular formula: C24H26FNO4
Molecular weight: 413.459 g/mol
Name: fluvastatin
Name (isomeric): DB01095
Drug Type: small molecule
Fluindostatin; Fluvastatine [INN-French]; Fluvastatinum [INN-Latin]; Fluvastatin sodium; Fluvastatina [INN-Spanish]
Brand: Canef, Lescol, Lescol XL, Cranoc
Category: HMG-CoA Reductase Inhibitors, Anticholesteremic Agents, Hydroxymethylglutaryl-CoA Reductase Inhibitors
CAS number: 93957-54-1
Indication: 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.
Fluvastatin, the first synthetically-derived HMG-CoA reductase inhibitor, is a hydrophilic, acidic, antilipemic agent used to lower cholesterol and triglyceride levels associated with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb), to slow the progression of coronary atherosclerosis in patients with CHD and as s...
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Mechanism of Action:
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 re...
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Absorption: Rapidly and almost completely absorbed (> 90%), but undergoes extensive first pass metabolism. Bioavailability is 24% (range 9-50%).
Protein binding: 98% bound to plasma proteins
Biotransformation: Undergoes hepatic metabolism primarily via hydroxylation of the indole ring at the 5- and 6-positions to 5-hydroxy fluvastatin and 6-hydroxy fluvastatin, respectively. N-dealkylation to N-desisopropyl fluvastatin and beta-oxidation of the side chain also occurs. Metabolized primarily by the CYP2C9 isozyme system (75%), and to a lesser extent by CYP3A4 (~20%) and CYP2C8 (~5%). Hydroxylated metabolites retain some pharmcological activity, but are present as conjugates (glucuronides and sulfates) in the blood and are rapidly eliminated via bile into feces.
Route of elimination: Fluvastatin is metabolized in the liver, primarily via hydroxylation of the indole ring at the 5- and 6-positions. In vitro studies demonstrated that fluvastatin undergoes oxidative metabolism, predominantly via 2C9 isozyme systems (75%). No significant (<6%) renal excretion of fluvastatin occurs in humans.
Half Life: 1-3 hours
Clearance: 0.8 L/h/kg 107 +/- 38.1 L/h [Hypercholesterolemia patients receiving a single dose of 20 mg] 87.8 +/- 45 L/h [Hypercholesterolemia patients receiving 20 mg twice daily] 108 +/- 44.7 L/h [Hypercholesterolemia patients receiving 40 mg single] 64.2 +/- 21.1 L/h [Hypercholesterolemia patients receiving 40 mg twice daily]
Toxicity: Generally well-tolerated. May cause GI upset (diarrhea, nausea, constipation, gas, abdominal pain), myotoxicity (mypothy, myositis, rhabdomyolysis), and hepatotoxicity.
Affected organisms: Humans and other mammals
Food interaction:
May be taken with or without food, but should be taken consistently.
Drug interaction:
FenofibrateIncreased risk of myopathy/rhabdomyolysis
CholestyramineIncreased/decreased effect according to spacing
AnisindioneFluvastatin may increase the anticoagulant effect of anisindione. Monitor for changes in the therapeutic and adverse effects of anisindione if fluvastatin if initiated, discontinued or dose changed.
CyclosporinePossible myopathy and rhabdomyolysis
GemfibrozilIncreased risk of myopathy/rhabdomyolysis
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