FLUVASTATIN

Details

Stereochemistry	RACEMIC
Molecular Formula	C24H26FNO4
Molecular Weight	411.4659
Optical Activity	( + / - )
Defined Stereocenters	2 / 2
E/Z Centers	1
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

CC(C)N1C(\C=C\[C@H](O)C[C@H](O)CC(O)=O)=C(C2=C1C=CC=C2)C3=CC=C(F)C=C3

InChI

InChIKey=FJLGEFLZQAZZCD-JUFISIKESA-N

InChI=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-/m0/s1

HIDE SMILES / InChI

Molecular Formula	C24H26FNO4
Molecular Weight	411.4659
Charge	0
Count

Stereochemistry	ABSOLUTE
Additional Stereochemistry	No
Defined Stereocenters	2 / 2
E/Z Centers	1
Optical Activity	UNSPECIFIED

Description
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021192s019lbl.pdf | https://www.drugbank.ca/drugs/DB01095

Fluvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. Fluvastatin is marketed under the trade names Lescol, Canef, Vastin. LESCOL/LESCOL XL is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce elevated TC, LDL-C, Apo B, and TG, and to increase HDL-C in adult patients with primary hypercholesterolemia and mixed dyslipidemia Reduce elevated TC, LDL-C, and Apo B levels in boys and post-menarchal girls, 10 to 16 years of age, with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy Reduce the risk of undergoing revascularization procedures in patients with clinically evident CHD Slow the progression of atherosclerosis in patients with CHD. 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.

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
HMG-CoA reductase 49 Target ID: CHEMBL402 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021192s019lbl.pdf \| https://www.ncbi.nlm.nih.gov/pubmed/10965989	Inhibitor 8504		28.0 nM [IC50]
Oligopeptide transporter small intestine isoform 6 Target ID: CHEMBL4605 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15846457	Inhibitor 8504		337.0 µM [IC50]

Conditions

Condition	Modality	Highest Phase	Product
Hypercholesterolemia 51 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021192s019lbl.pdf	Primary	Approved 8583	LESCOL Approved Use LESCOL/LESCOL XL is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce elevated TC, LDL-C, Apo B, and TG, and to increase HDL-C in adult patients with primary hypercholesterolemia and mixed dyslipidemia (1.1) Reduce elevated TC, LDL-C, and Apo B levels in boys and post-menarchal girls, 10 to 16 years of age, with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy (1.1) Reduce the risk of undergoing revascularization procedures in patients with clinically evident CHD (1.2) Slow the progression of atherosclerosis in patients with CHD (1.2) Launch Date 1993
Atherosclerosis 76 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021192s019lbl.pdf	Primary	Approved 8583	LESCOL Approved Use LESCOL/LESCOL XL is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce elevated TC, LDL-C, Apo B, and TG, and to increase HDL-C in adult patients with primary hypercholesterolemia and mixed dyslipidemia (1.1) Reduce elevated TC, LDL-C, and Apo B levels in boys and post-menarchal girls, 10 to 16 years of age, with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy (1.1) Reduce the risk of undergoing revascularization procedures in patients with clinically evident CHD (1.2) Slow the progression of atherosclerosis in patients with CHD (1.2) Launch Date 1993
Dyslipidemia 34 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/021192s019lbl.pdf	Primary	Approved 8583	LESCOL Approved Use LESCOL/LESCOL XL is an HMG-CoA reductase inhibitor (statin) indicated as an adjunctive therapy to diet to: Reduce elevated TC, LDL-C, Apo B, and TG, and to increase HDL-C in adult patients with primary hypercholesterolemia and mixed dyslipidemia (1.1) Reduce elevated TC, LDL-C, and Apo B levels in boys and post-menarchal girls, 10 to 16 years of age, with heterozygous familial hypercholesterolemia after failing an adequate trial of diet therapy (1.1) Reduce the risk of undergoing revascularization procedures in patients with clinically evident CHD (1.2) Slow the progression of atherosclerosis in patients with CHD (1.2) Launch Date 1993

C_max

Value	Dose	Co-administered	Analyte	Population
205 μg/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29368187	20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered:		FLUVASTATIN plasma	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED

AUC

Value	Dose	Co-administered	Analyte	Population
206.2 μg × h/mL EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29368187	20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered:		FLUVASTATIN plasma	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED

T_1/2

Value	Dose	Co-administered	Analyte	Population
0.54 h EXPERIMENT https://www.ncbi.nlm.nih.gov/pubmed/29368187	20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered:		FLUVASTATIN plasma	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED

Doses

Dose	Population	Adverse events
640 mg 1 times / day multiple, oral Highest studied dose Dose: 640 mg, 1 times / day Route: oral Route: multiple Dose: 640 mg, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/11336101	unhealthy, ADULT Health Status: unhealthy Age Group: ADULT Sex: M+F Food Status: FED Sources: https://pubmed.ncbi.nlm.nih.gov/11336101	Sources: https://pubmed.ncbi.nlm.nih.gov/11336101

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
substrate 1946 inhibitor 2252	substrate 1193 inhibitor 2438	substrate 1388 inhibitor 2507

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP1A2 2153 CYP2C19 2057 CYP3A 227 CYP2C8 1057 P-gp 1741 BCRP 910 OAT3 747 OAT1 725	CYP1A2 1197 CYP2A6 626 CYP2B6 776 CYP2C19 1119 CYP2E1 729 CYP3A5 446 CYP1A1 389 CYP2C8 810 P-gp 2052 BCRP 697 OATP1B1 503 OATP2B1 122 OATP1B3 435	CYP1A1 151

Drug as perpetrator

Target	Modality	Activity
CYP2D6 2546	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/8737761/ Page: 3.0	moderate [IC50 100 uM]
CYP1A2 2333	inhibitor 4027 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP2C19 2141	inhibitor 4027 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP3A 317	inhibitor 4027 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
P-gp 1932	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/17064205/	not significant
CYP3A4 2633	inhibitor 4027 Sources: https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2044.2005.04110.x	weak [Ki 94.3 uM]
CYP2C8 1117	inhibitor 4027 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	yes [IC50 20 uM]
OAT1 730	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/14729100/	yes [IC50 26.3 uM]
OAT3 749	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/14729100/	yes [IC50 5.79 uM]
CYP2C9 2497	inhibitor 4027 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	yes [Ki 0.3 uM]
BCRP 985	inhibitor 4027 Sources: https://pubmed.ncbi.nlm.nih.gov/15955871/ Page: 5.0	yes [Ki 5.43 uM]
CYP1A1 272	inducer 1966 Sources: https://pubmed.ncbi.nlm.nih.gov/8937853/	yes

Drug as victim

Target	Modality	Activity	Clinical evidence
CYP2C9 1193	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	major	yes (co-administration study) Comment: Coadministration with rifampicin (CYP2C9 inducer) increased the CL/F of fluvastatin by 95% and to reduce AUC by 50%. Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract
CYP1A1 389	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	minor
CYP2C8 810	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	minor
CYP2D6 1388	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	minor
CYP3A4 1946	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract; https://pubmed.ncbi.nlm.nih.gov/17064205/	minor	unknown (co-administration study) Comment: Coadministration with cyclocporine resulted in 3.1-fold increase in AUC; however, cannot be explained through these mechanisms, since neither pravastatin nor fluvastatin has been shown to be a substrate for either P-gp or CYP3A4; coadministration with itraconazole had no significant impact on Cmax and AUC of fluvastatin Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract; https://pubmed.ncbi.nlm.nih.gov/17064205/
CYP1A2 1197	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP2A6 626	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP2B6 776	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP2C19 1119	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP2E1 729	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
CYP3A5 446	substrate 4014 Sources: https://dmd.aspetjournals.org/content/27/3/410.abstract	no
P-gp 2052	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/11368292/ Page: 14.0	no	unknown (co-administration study) Comment: Coadministration with cyclocporine resulted in 3.1-fold increase in AUC; however, cannot be explained through these mechanisms, since neither pravastatin nor fluvastatin has been shown to be a substrate for either P-gp or CYP3A4 Sources: https://pubmed.ncbi.nlm.nih.gov/11368292/ Page: 14.0
OATP1B3 435	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/17470528/	yes
OATP2B1 122	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/17470528/	yes
OATP1B1 503	substrate 4014 Sources: https://pubmed.ncbi.nlm.nih.gov/17470528/	yes	unlikely (co-administration study) Comment: coadministered with rifampin. See https://pubmed.ncbi.nlm.nih.gov/29768081/. Pharmacogenomic study also performed. Not significant: see https://www.lipidjournal.com/article/S1933-2874(14)00072-5/pdf Sources: https://pubmed.ncbi.nlm.nih.gov/17470528/
BCRP 697	substrate 4014 Sources: https://www.jpharmsci.org/article/S0022-3549(16)30083-1/pdf	yes	yes (pharmacogenomic study) Comment: AUC of drug increased by 72% Sources: https://www.jpharmsci.org/article/S0022-3549(16)30083-1/pdf

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:38561	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:38561
ChemicalBook	CB03386396	https://www.chemicalbook.com/ChemicalProductProperty_EN_CB03386396
eMolecules	10141252	https://www.emolecules.com/cgi-bin/more?vid=10141252
MolPort	MolPort-006-167-704	https://www.molport.com/shop/molecule-link/MolPort-006-167-704
ZINC	ZINC000001530639	http://zinc15.docking.org/substances/ZINC000001530639

PubMed

Title	Date	PubMed
Systems pharmacological analysis of drugs inducing stevens-johnson syndrome and toxic epidermal necrolysis.	2015-05-18	25811541
Statins alter the hepatobiliary transport of unconjugated and conjugated bilirubin in sandwich-cultured rat hepatocytes.	2014-09	24909372
Statin-induced inhibition of breast cancer proliferation and invasion involves attenuation of iron transport: intermediacy of nitric oxide and antioxidant defence mechanisms.	2014-08	24964743
Drug-Induced Acute Liver Injury Within 12 Hours After Fluvastatin Therapy.	2014-01-24	24451297
Detection of statin cytotoxicity is increased in cells expressing the OATP1B1 transporter.	2013-07	23564645
ATP-dependent transport of statins by human and rat MRP2/Mrp2.	2013-06-01	23562342
Identification of old drugs as potential inhibitors of HIV-1 integrase - human LEDGF/p75 interaction via molecular docking.	2012-12	22733274
Interference with bile salt export pump function is a susceptibility factor for human liver injury in drug development.	2010-12	20829430
Effects of add-on fluvastatin therapy in patients with chronic proteinuric nephropathy on dual renin-angiotensin system blockade: the ESPLANADE trial.	2010-11	20671225
The phototoxicity of fluvastatin, an HMG-CoA reductase inhibitor, is mediated by the formation of a benzocarbazole-like photoproduct.	2010-11	20668001
Effect of an antimicrobial agent on atherosclerotic plaques: assessment of metalloproteinase activity by molecular imaging.	2010-03-23	20298932
A gene score of nine LDL and HDL regulating genes is associated with fluvastatin-induced cholesterol changes in women.	2010-03	19773416
In vitro interactions between primycin and different statins in their effects against some clinically important fungi.	2010-02	19875509
Roles of different CYP enzymes in the formation of specific fluvastatin metabolites by human liver microsomes.	2009-11	19663817
Application of a 3,3-diphenylpentane skeleton as a multi-template for creation of HMG-CoA reductase inhibitors.	2009-08-01	19502059
Enantioselectivity in the pharmacokinetic interaction between fluvastatin and lercanidipine in healthy volunteers.	2009-02	19033449
Pretreatment with statin attenuates the cardiotoxicity of Doxorubicin in mice.	2009-01-15	19147586
Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat.	2008-05-31	18384769
Comprehensive analysis of the effects of ordinary nutrients on hepatitis C virus RNA replication in cell culture.	2007-06	17420205
Inhibitors of the mevalonate pathway as potential therapeutic agents in multiple myeloma.	2007-03	16996129
Effects of chronic treatment with statins and fenofibrate on rat skeletal muscle: a biochemical, histological and electrophysiological study.	2006-12	17031388
Effect of low-density lipoprotein cholesterol on angiotensin II sensitivity: a randomized trial with fluvastatin.	2006-06	16618834
Chiral evaluation of fluvastatin in human plasma by high-performance liquid chromatography electrospray mass spectrometry.	2006-03-07	16480934
Fluvastatin ameliorates podocyte injury in proteinuric rats via modulation of excessive Rho signaling.	2006-03	16452496
Muscle symptoms associated with statins: a series of twenty patients.	2006-01	16433891
[Fluvastatin-induced dermatomyositis].	2005-12	16446645
Focal seizures after treatment with fluvastatin in a patient with a history of catastrophic antiphospholipid syndrome.	2005-11-15	16111706
Prediction of CYP2C9-mediated drug-drug interactions: a comparison using data from recombinant enzymes and human hepatocytes.	2005-11	16081671
Evaluation of the anti-HIV activity of statins.	2005-10-14	16184043
Human hepatobiliary transport of organic anions analyzed by quadruple-transfected cells.	2005-10	16046661
Binding thermodynamics of statins to HMG-CoA reductase.	2005-09-06	16128575
Effect of atorvastatin and fluvastatin on the metabolism of midazolam by cytochrome P450 in vitro.	2005-08	16029222
Bile salt export pump (BSEP/ABCB11) can transport a nonbile acid substrate, pravastatin.	2005-08	15901796
Regional intestinal absorption and biliary excretion of fluvastatin in the rat: possible involvement of mrp2.	2005-07-20	16026004
Immediate effects of fluvastain on circulating soluble endothelial protein C and free tissue factor pathway inhibitor in acute coronary syndromes.	2005-05	16142594
In vitro and pharmacophore-based discovery of novel hPEPT1 inhibitors.	2005-04	15846457
Expression of serum and glucocorticoid-inducible kinase1 in diabetic rats and its modulation by fluvastatin.	2005	16696316
[Cardiology in 1997].	1998-10-05	9818470
Troglitazone upregulates LDL receptor activity in HepG2 cells.	1998-08	9703316
Postural hypotension induced by paroxetine.	1998-02-21	9518913
A head-to-head comparison of the cost effectiveness of HMG-CoA reductase inhibitors and fibrates in different types of primary hyperlipidemia.	1997-01	9110123
Effect of fluvastatin or bezafibrate on the distribution of high density lipoprotein subpopulations in patients with familial hypercholesterolemia.	1996-09	8876936
Fluvastatin in combination with other lipid-lowering agents.	1996-01	8729588
Currently available hypolipidaemic drugs and future therapeutic developments.	1995-10	8593127
Efficacy and safety of triple therapy (fluvastatin-bezafibrate-cholestyramine) for severe familial hypercholesterolemia.	1995-07-13	7604807
Fluvastatin in combination with other lipid-lowering agents.	1994-12	19496270
Treatment of primary hypercholesterolemia: fluvastatin versus bezafibrate.	1994-06-06	8017468
Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination.	1994-05	8192170
HMG-CoA reductase inhibitors: design, synthesis, and biological activity of tetrahydroindazole-substituted 3,5-dihydroxy-6-heptenoic acid sodium salts.	1993-11-12	8246237
Synthesis and biological activity of new HMG-CoA reductase inhibitors. 3. Lactones of 6-phenoxy-3,5-dihydroxyhexanoic acids.	1991-10	1656041

Patents

Sample Use Guides

In Vivo Use Guide

Usual Adult Dose for Hyperlipidemia Immediate Release Capsules: -Low-density lipoprotein cholesterol (LDL-C) reduction to a goal of 25% or greater: Initial dose of 40 mg orally once a day in the evening or 40 mg orally twice a day -LDL-C reduction to a goal of less than 25%: Initial dose of 20 mg orally once a day -Maintenance dose: 20 mg to 80 mg per day Usual Adult Dose for Hyperlipoproteinemia Type IIa (Elevated LDL) Immediate Release Capsules: -Low-density lipoprotein cholesterol (LDL-C) reduction to a goal of 25% or greater: Initial dose of 40 mg orally once a day in the evening or 40 mg orally twice a day -LDL-C reduction to a goal of less than 25%: Initial dose of 20 mg orally once a day -Maintenance dose: 20 mg to 80 mg per day

Route of Administration: Oral

In Vitro Use Guide

Fluvastatin markedly inhibits the formation of thiobarbituric acid reactive substances in iron (II)-supported peroxidation of liposomes with IC50 of 12 uM. Fluvastatin ranging from 1 uM to 100 uM inhibits peroxyl radical-mediated peroxidation of liposomes induced by water-soluble and lipid-soluble radical generators, 2,2'-azobis (2-amidinopropane) dihydro-chloride and 2,2'-azobis (2,4-dimethylvaleronitrile), respectively.

Substance Class	Chemical Created by `admin` on `Mon Mar 31 18:21:19 GMT 2025` Edited by `admin` on `Mon Mar 31 18:21:19 GMT 2025`
Record UNII	4L066368AS
Record Status	`Validated (UNII)`
Record Version

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Name

Type

Language

FLUVASTATIN

Official Name

English

FLUVAS

Preferred Name

English

FLUVASTATIN [VANDF]

Common Name

English

FLUVASTATIN [MI]

Common Name

English

NSC-758896

Code

English

Fluvastatin [WHO-DD]

Common Name

English

fluvastatin [INN]

Common Name

English

6-HEPTENOIC ACID, 7-(3-(4-FLUOROPHENYL)-1-(1-METHYLETHYL)-1H-INDOL-2-YL)-3,5-DIHYDROXY-, (3R,5S,6E)-REL-

Systematic Name

English

Classification Tree Code System Code

WHO-VATC

QC10AA04