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Namespace Prefixes

PrefixIRI
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Statements

Subject Item
n2:DB01095
rdf:type
n3:Drug
n3:description
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.
n3:dosage
n24:271B6544-363D-11E5-9242-09173F13E4C5 n24:271B6545-363D-11E5-9242-09173F13E4C5 n24:271B6546-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# 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
n3:group
approved
n3:halfLife
3 hours
n3: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.
owl:sameAs
n16:DB01095 n23:DB01095
dcterms:title
Fluvastatin
adms:identifier
n6:Fluvastatin n7:D07983 n17:PA449688 n18:C07014 n19:0078-0176-05 n20:DB01095 n21:5136
n3:mechanismOfAction
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.
n3:packager
n9:271B6534-363D-11E5-9242-09173F13E4C5 n9:271B6535-363D-11E5-9242-09173F13E4C5 n9:271B6533-363D-11E5-9242-09173F13E4C5 n9:271B6538-363D-11E5-9242-09173F13E4C5 n9:271B6539-363D-11E5-9242-09173F13E4C5 n9:271B6536-363D-11E5-9242-09173F13E4C5 n9:271B6537-363D-11E5-9242-09173F13E4C5 n9:271B653A-363D-11E5-9242-09173F13E4C5 n9:271B653B-363D-11E5-9242-09173F13E4C5
n3:patent
n14:6242003 n14:2346868 n14:2085037 n14:5354772
n3:routeOfElimination
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.
n3:toxicity
Generally well-tolerated. May cause gastrointestinal upset (diarrhea, nausea, constipation, gas, abdominal pain), myotoxicity (mypothy, myositis, rhabdomyolysis), and hepatotoxicity.
n3:volumeOfDistribution
* 0.35 L/kg
n12:hasAHFSCode
n13:24-06-08
n3:foodInteraction
May be taken with or without food, but should be taken consistently. When given with an evening meal, Cmax and AUC decreased while Tmax increased 2-fold
n3:proteinBinding
98% bound to plasma proteins. At therapeutic concentrations, the protein binding of fluvastatin is not affected by warfarin, salicylic acid and glyburide.
n3:salt
n3:synthesisReference
Gustavo Frenkel, Eyal Gilboa, "Process for the preparation of fluvastatin sodium crystal form XIV." U.S. Patent US20050119342, issued June 02, 2005.
n26:hasConcept
n27:M0179302
foaf:page
n11:fluvastatin.html n28:fluvastatinxl.htm
n3:IUPAC-Name
n4:271B654B-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B6551-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B6550-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B654D-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B654E-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B654F-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B6561-363D-11E5-9242-09173F13E4C5 n4:271B6549-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B6563-363D-11E5-9242-09173F13E4C5 n4:271B6547-363D-11E5-9242-09173F13E4C5 n4:271B654A-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B6548-363D-11E5-9242-09173F13E4C5
n12:hasATCCode
n22:C10AA04
n3:H-Bond-Acceptor-Count
n4:271B6557-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B6558-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B6552-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B6553-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B6555-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B6554-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B6556-363D-11E5-9242-09173F13E4C5
n3:absorption
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.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
93957-54-1
n3:category
n3: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]
n3:containedIn
n8:271B6543-363D-11E5-9242-09173F13E4C5 n8:271B6541-363D-11E5-9242-09173F13E4C5 n8:271B6542-363D-11E5-9242-09173F13E4C5 n8:271B653C-363D-11E5-9242-09173F13E4C5 n8:271B653F-363D-11E5-9242-09173F13E4C5 n8:271B6540-363D-11E5-9242-09173F13E4C5 n8:271B653D-363D-11E5-9242-09173F13E4C5 n8:271B653E-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n4:271B655D-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B655F-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B6560-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n4:271B6562-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B655C-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B655B-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B655E-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B654C-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B6559-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B655A-363D-11E5-9242-09173F13E4C5