| 词条 | Fluvastatin |
| 释义 |
| verifiedrevid = 461102905 | IUPAC_name = (3R,5S,6E)-7-[3-(4-Fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid | image = Fluvastatin.svg | width = 250 | tradename = Lescol, others | Drugs.com = {{drugs.com|monograph|lescol}} | MedlinePlus = a694010 | pregnancy_AU = D | pregnancy_US = X | legal_AU = S4 | legal_CA = Rx-only | legal_UK = POM | legal_US = Rx-only | legal_status = Rx-only | routes_of_administration = By mouth (capsules, tablets) | bioavailability = 24–30%[1][1] | protein_bound = >98%[1] | metabolism = Hepatic: CYP2C9 (75%), CYP3A4 (20%), CYP2C8 (5%)[1][2] | elimination_half-life = 1–3 hours (capsule), 9 hours (XR formulations)[1][2] | excretion = Faeces (95%), urine (5%)[1] | IUPHAR_ligand = 2951 | CAS_number_Ref = {{cascite|correct|??}} | CAS_number = 93957-54-1 | ATC_prefix = C10 | ATC_suffix = AA04 | ATC_supplemental = | PubChem = 446155 | DrugBank_Ref = {{drugbankcite|correct|drugbank}} | DrugBank = DB01095 | ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}} | ChemSpiderID = 393587 | UNII_Ref = {{fdacite|correct|FDA}} | UNII = 4L066368AS | KEGG_Ref = {{keggcite|correct|kegg}} | KEGG = D07983 | ChEBI_Ref = {{ebicite|correct|EBI}} | ChEBI = 38565 | ChEMBL_Ref = {{ebicite|correct|EBI}} | ChEMBL = 1078 | C=24 | H=26 | F=1 | N=1 | O=4 | molecular_weight = 411.466 g/mol | smiles = O=C(O)C[C@H](O)C[C@H](O)/C=C/c2c(c1ccccc1n2C(C)C)c3ccc(F)cc3 | StdInChI_Ref = {{stdinchicite|correct|chemspider}} | StdInChI = 1S/C24H26FNO4/c1-15(2)26-21-6-4-3-5-20(21)24(16-7-9-17(25)10-8-16)22(26)12-11-18(27)13-19(28)14-23(29)30/h3-12,15,18-19,27-28H,13-14H2,1-2H3,(H,29,30)/b12-11+/t18-,19-/m1/s1 | StdInChIKey_Ref = {{stdinchicite|correct|chemspider}} | StdInChIKey = FJLGEFLZQAZZCD-MCBHFWOFSA-N }} Fluvastatin is a member of the statin drug class, used to treat hypercholesterolemia and to prevent cardiovascular disease. It was patented in 1982 and approved for medical use in 1994.[3] Adverse effectsAdverse effects are comparable to other statins. Common are nausea, indigestion, insomnia and headache. Myalgia (muscle pain), and rarely rhabdomyolysis, characteristic side effects for statins, can also occur.[4] InteractionsContrary to lovastatin, simvastatin and atorvastatin, fluvastatin has no relevant interactions with drugs that inhibit the liver enzyme CYP3A4, and a generally lower potential for interactions than most other statins. Fluconazole, a potent inhibitor of CYP2C9, does increase fluvastatin levels.[4] PharmacologyMechanism of action{{main|Statin}}Fluvastatin works by blocking the liver enzyme HMG-CoA reductase, which facilitates an important step in cholesterol synthesis.[5] PharmacodynamicsIn a Cochrane systematic review the dose-related magnitudes of fluvastatin on blood lipids was determined. Over the dose range of 10 to 80 mg/day total cholesterol was reduced by 10.7% to 24.9%, LDL cholesterol by 15.2% to 34.9%, and triglycerides by 3% to 17.5%.[6] PharmacokineticsThe drug is quickly and almost completely (98%) absorbed from the gut. Food intake slows down absorption, but does not decrease it. Due to its first-pass effect, bioavailability is lower: about 24–30%[1][5] according to different sources. Over 98% of the substance is bound to plasma proteins.[5] Several cytochrome P450 enzymes (mainly CYP2C9, but also CYP3A4 and CYP2C8)[7] are involved in the metabolism of fluvastatin, which makes is less liable to interactions than most other statins. The main metabolite is inactive and is called "N-desisopropyl propionic acid" in the literature.[5][4] 93–95% of the drug is excreted via the feces, less than 2% of which in form of the original substance.[5] NamesFluvastatin is the INN.[8] Brandnames include Lescol, Canef, Vastin. ResearchData from the Cholesterol Treatment Trialists’ (CTT) publication[9] was used to determine the effects of fluvastatin, atorvastatin and rosuvastatin on LDL cholesterol lowering and reduction of myocardial infarction. In two RCTs an average dose of 72 mg/day fluvastatin reduced LDL cholesterol by 31.9%, and reduced myocardial infarction, relative risk, 0.68 (95% CI 0.55 to 0.85) as compared to placebo. In five RCTs a mean atorvastatin dose of 26 mg/day reduced LDL cholesterol by 44.0% and reduced myocardial infarction, relative risk, 0.67 (95% CI 0.58 to 0.77) as compared to placebo. In four RCTs a mean rosuvastatin dose of 16 mg/day reduced LDL cholesterol by 48.8% and reduced myocardial infarction, relative risk, 0.82 (95% CI 0.73 to 0.93) as compared to placebo. Thus despite reducing LDL cholesterol by a much lesser amount with fluvastatin than atorvastatin and rosuvastatin, fluvastatin reduced myocardial infarction similarly to atorvastatin and to a greater degree than rosuvastatin.[6] References1. ^1 2 3 4 5 {{cite journal|last=Neuvonen|first=PJ|author2=Backman, JT|author3=Niemi, M|title=Pharmacokinetic comparison of the potential over-the-counter statins simvastatin, lovastatin, fluvastatin and pravastatin.|journal=Clinical Pharmacokinetics|date=2008|volume=47|issue=7|pages=463–74|doi=10.2165/00003088-200847070-00003|pmid=18563955}} {{Statins}}2. ^1 {{cite web|title=Lescol, Lescol XR (fluvastatin) dosing, indications, interactions, adverse effects, and more|work=Medscape Reference|publisher=WebMD|accessdate=18 March 2014|url=http://reference.medscape.com/drug/lescol-xl-fluvastatin-342456#showall}} 3. ^{{cite book |last1=Fischer |first1=Jnos |last2=Ganellin |first2=C. Robin |title=Analogue-based Drug Discovery |date=2006 |publisher=John Wiley & Sons |isbn=9783527607495 |page=472 |url=https://books.google.ca/books?id=FjKfqkaKkAAC&pg=PA472 |language=en}} 4. ^1 2 {{cite journal|title=Arzneistoff-Profile|veditors=Dinnendahl, V, Fricke, U|publisher=Govi Pharmazeutischer Verlag|location=Eschborn, Germany|date=2012|edition=26|volume=2|isbn=978-3-7741-9846-3|language=German}} 5. ^1 2 3 4 5 {{cite book|title=Austria-Codex|editor=Haberfeld, H|publisher=Österreichischer Apothekerverlag|location=Vienna|year=2015|language=German}} 6. ^1 {{Cite book|url=http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD012282.pub2/full|title=Fluvastatin for lowering lipids. Cochrane Database of Systematic Reviews|last=Adams|first=Stephen P.|last2=Sekhon|first2=Sarpreet S.|last3=Tsang|first3=Michael|last4=Wright|first4=James M.|date=2018-03-06|publisher=John Wiley & Sons, Ltd|year=|isbn=|location=|pages=|language=en|doi=10.1002/14651858.cd012282.pub2}} 7. ^Lescol {{drugs.com|monograph|lescol}} on Drugs.com. 8. ^{{cite web | title = International Nonproprietary Names for Pharmaceutical Substances (INN). Recommended International Nonproprietary Names (Rec. INN): List 30 | url = http://www.who.int/medicines/publications/druginformation/innlists/RL30.pdf | publisher = World Health Organization | accessdate = 29 November 2016 | date = 1990}} 9. ^{{Cite journal|last=Cholesterol Treatment Trialists’ (CTT).|first=|date=2005|title=Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90 056 participants in 14 randomised trials of statins|url=http://linkinghub.elsevier.com/retrieve/pii/S0140673605673941|journal=Lancet|volume=366|issue=9493|pages=1267–1278|doi=10.1016/s0140-6736(05)67394-1|issn=0140-6736|via=}} 7 : Carboxylic acids|Diols|Indoles|Fluoroarenes|Statins|Isopropyl compounds|Novartis brands |
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