関: fenofibrate

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/16 15:59:45」(JST)

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Fenofibrate (INN), marketed as Tricor and under several other brand names, is a drug of the fibrate class. It is mainly used to reduce cholesterol levels in patients at risk of cardiovascular disease. Like other fibrates, it reduces both low-density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels, as well as increasing high-density lipoprotein (HDL) levels and reducing triglyceride levels.^[1] It is used alone or along with statins in the treatment of hypercholesterolemia and hypertriglyceridemia.

Fenofibrate has been used since 1975, is one of the most commonly prescribed fibrates, and has a well known efficacy and tolerability profile.^[1]

Medical uses

Fenofibrate is mainly used for primary hypercholesterolemia or mixed dyslipidemia. Fenofibrate appears to decrease the risk of cardiovascular disease and possibly diabetic retinopathy in those with diabetes mellitus.^[2] It also appears to be helpful in decreasing amputations of the lower legs in this same group of people.^[3] Fenofibrate also has an unlabeled use as an added therapy of high blood uric acid levels in people who have gout.^[4]

It is used in addition to diet to reduce elevated low-density lipoprotein cholesterol (LDL), total cholesterol, triglycerides (TG), and apolipoprotein B (Apo B), and to increase high-density lipoprotein cholesterol (HDL) in adults with primary hypercholesterolemia or mixed dyslipidemia.^[5]

Severe hypertriglyceridemia type IV or V

It is used in addition to diet for treatment of adults with severe hypertriglyceridemia. Improving glycemic control in diabetics showing fasting chylomicronemia will usually decrease the need for pharmacologic intervention.^[5]

Statins remain first line for treatment of blood cholesterol. AHA Guidelines from 2013 did not find evidence for routine use of additional medications.^[6]

Contraindications

Fenofibrate is contraindicated in:^[5]

Patients with severe renal impairment, including those receiving dialysis (2.7-fold increase in exposure, and increased accumulation during chronic dosing in patients with estimated glomerular filtration rate (eGFR)<30mL/min)
Patients with active liver disease, including those with primary biliary cirrhosis and unexplained persistent liver function test (LFT) abnormalities
Patients with preexisting gallbladder disease
Nursing mothers
Patients with known hypersensitivity to fenofibrate or fenofibric acid

Adverse effects

The most common adverse events (>3% of patients with coadministered statins) are^[7]

Headache
Back pain
Nasopharyngitis
Nausea
Myalgia
Joint pain or arthralgia
Diarrhea
Upper respiratory tract infection

Precautions

Musculoskeletal

Myopathy and rhabdomyolysis; increased risk when coadminstered with a statin, particularly in the elderly and patients with diabetes, renal failure, hypothyroidism^[7]

Hepatotoxicity

Can increase serum transaminases; liver tests should be monitored periodically^[7]

Nephrotoxicity

Can increase serum creatinine levels; renal function should be monitored periodically in patients with renal insufficiency^[7]

Biliary

Can increase cholesterol excretion into the bile, leading to risk of cholelithiasis; if suspected gallbladder studies are indicated. See "Interaction" section under Bile Acid Sequestrant^[7]

Coagulation/Bleeding

Exercise caution in concomitant treatment with oral coumarin anticoagulants (e.g. Warfarin). Adjust the dosage of coumarin to maintain the prothrombin time/INR at desired level to prevent bleeding complications^[7]

Overdose

“There is no specific treatment for overdose with fenofibric acid delayed-release capsules. General supportive care Is indicated, including monitoring of vital signs and observation of clinical status”. Additionally, hemodialysis should not be considered as an overdose treatment option because fenofibrate heavily binds to plasma proteins and does not dialyze well.^[7]

Interactions

The following drug interactions with fenofibrate is considered major and may need therapy modifications:

Bile acid sequestrants (e.g. cholestyramine, colestipol, etc.): If taken together, bile acid resins may bind to fenofibrate, resulting in a decrease in fenofibrate absorption. In order to maximize absorption, patients need to separate administration by at least 1 hour before or 4–6 hours after taking the bile acid sequestrant.^[7]^[8]
Immunosuppressants (e.g. cyclosporine or tacrolimus): There is an increased risk of renal dysfunction with concomitant use of immunosuppressants and fenofibrate. Please approach with caution when coadministering additional medications that decrease renal function.^[9]
Vitamin K antagonists (e.g. warfarin): As previously mentioned, fenofibrate interacts with coumarin anticoagulants to increase the risk of bleeding. Dosage adjustment of Vitamin K antagonist may be necessary.^[7]
Statins: Combination of statins and fenofibrate may increase the risk of rhabdomyolysis or myopathy.^[10]

Mechanism of action

"In summary, enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL underlie the hypotriglyceridemic effect of fibrates, whereas their effect on HDL metabolism is associated with changes in HDL apolipoprotein expression."^[11]

Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. It lowers lipid levels by activating Peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII, which increases lipolysis and elimination of triglyceride-rich particles from plasma.^[11]

PPARα also increases apoproteins AI and AII, reduces very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) containing apoprotein B, and increases high-density lipoprotein (HDL) containing apoprotein AI and AII.

Formulations

Fenofibrate is available in several formulations and is sold under several brand names, including Tricor by AbbVie, Lipofen by Kowa Pharmaceuticals America Inc, Lofibra by Teva, Lipanthyl, Lipidil, and Supralip by Abbott Laboratories, Fenocor-67 by Ordain Health Care, Fenogal by SMB Laboratories, Antara by Oscient Pharmaceuticals, Tricheck by Zydus (CND), Atorva TG by Zydus Medica, Golip by GolgiUSA and Storfib by Ranbaxy (India). Different formulations may differ in terms of pharmacokinetic properties, particularly bioavailability; some must be taken with meals, whereas others may be taken without regard to food.^[12]

The active form of fenofibrate, fenofibric acid, is also available in the United States, sold as Trilipix. Fenofibric acid may be taken without regard to the timing of meals.^[7]^[13]

When fenofibrate and a statin are given as combination therapy, it is recommended that fenofibrate be given in the morning and the statin at night, so that the peak dosages do not overlap.^[14]

Controversy

In the United States, Tricor was reformulated in 2005. This reformulation is controversial, as it is seen as an attempt to stifle competition from generic equivalents of the drug,^[15] and is the subject of antitrust litigation by generic drug manufacturer Teva.^[15] Also available in the United States, Lofibra is available in 54 and 160 mg tablets, as well as 67, 134, and 200;mg micronized capsules.^[16] Generic equivalents of Lofibra capsules are currently available in all three strengths in the United States. In Europe, it is available in either coated tablet or capsule; the strength range includes 67, 145, 160 and 200 mg. The differences among strengths are a result of altered bioavailability (the fraction absorbed by the body) due to particle size. For example, 200 mg can be replaced by 160 mg micronized fenofibrate. The 145 mg strength is a new strength that appeared in 2005-2006 which also replaces 200 or 160 mg as the fenofibrate is nanonised (i.e. the particle size is below 400 nm).

History

Fenofibrate was first synthesized in 1974 as a derivative of clofibrate, and was launched on the French market shortly thereafter. It was initially known as procetofen, and was later renamed fenofibrate to comply with World Health Organization International Nonproprietary Name guidelines.^[17]

Fenofibrate was developed by Groupe Fournier SA of France, which was acquired in 2005 by Solvay Pharmaceuticals, a business unit of the Belgian corporation Solvay S.A.. In 2009, Solvay was in turn acquired by Abbott Laboratories (now AbbVie).

Research

In adult rat studies using pentylenetetrazol and lithium-pilocarpine models, Fenofibrate exhibits anticonvulsant properties comparable to the ketogenic diet potentially via agonism of PPAR-a. These findings may be useful for future ketogenic diet study protocols. ^[18]

Notes

^ ^a ^b Yang LP, Keating GM (2009). "Fenofibric acid: in combination therapy in the treatment of mixed dyslipidemia". Am J Cardiovasc Drugs 9 (6): 401–9. doi:10.2165/11203920-000000000-00000. PMID 19929038.
^ Fazio S (2009). "More clinical lessons from the FIELD study". Cardiovasc Drugs Ther 23 (3): 235–41. doi:10.1007/s10557-008-6160-5. PMID 19160032.
^ Steiner G (2009). "How can we improve the management of vascular risk in type 2 diabetes: insights from FIELD". Cardiovasc Drugs Ther 23 (5): 403–8. doi:10.1007/s10557-009-6190-7. PMID 19757004.
^ Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T et al. (2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care Res (Hoboken) 64 (10): 1431–46. doi:10.1002/acr.21772. PMC 3683400. PMID 23024028.
^ ^a ^b ^c Package Insert: Abbot Laboratories (October 2010)
^ Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH et al. (2014). "2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation 129 (25 Suppl 2): S1–45. doi:10.1161/01.cir.0000437738.63853.7a. PMID 24222016.
^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j Fenofibric Acid FDA Label Prescribing Information"FDA Label Information" (PDF). FDA.
^ Product Information: TriCor(TM), fenofibrate. Abbott Laboratories, North Chicago, IL, 1998.
^ Product Information: Sandimmune(R) oral capsules, oral solution, intravenous injection, cyclosporine oral capsules, oral solution, intravenous injection. Novartis Pharmaceuticals Corporation, East Hanover, NJ, 2010.
^ Product Information: TRICOR(R) oral tablets, fenofibrate oral tablets. Abbott Laboratories, North Chicago, IL, 2007.
^ ^a ^b Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC (1998). "Mechanism of action of fibrates on lipid and lipoprotein metabolism". Circulation 98 (19): 2088–93. doi:10.1161/01.cir.98.19.2088. PMID 9808609.
^ Ling H, Luoma JT, Hilleman D (2013). "A review of currently available fenofibrate and fenofibric acid formulations". Cardiol Res 4 (2): 47–55. doi:10.4021/cr270w.
^ Alagona P (2010). "Fenofibric acid: a new fibrate approved for use in combination with statin for the treatment of mixed dyslipidemia". Vasc Health Risk Manag 6: 351–62. doi:10.2147/vhrm.s6714. PMC 2879297. PMID 20531954.
^ Wierzbicki AS, Mikhailidis DP, Wray R, Schacter M, Cramb R, Simpson WG et al. (2003). "Statin-fibrate combination: therapy for hyperlipidemia: a review". Curr Med Res Opin 19 (3): 155–68. doi:10.1185/030079903125001668. PMID 12814127.
^ ^a ^b Abbott's request to dismiss the antitrust charge over Tricor was rejected. FDANews, Drug Daily Bulletin, (June 1, 2006) [1]
^ TEVA Pharmartsau6i8mkst7oceutical Lofibra Product Site
^ Lalloyer F, Staels B (2010). "Fibrates, glitazones, and peroxisome proliferator-activated receptors". Arterioscler. Thromb. Vasc. Biol. 30 (5): 894–9. doi:10.1161/ATVBAHA.108.179689. PMC 2997800. PMID 20393155.
^ Porta N, Vallée L, Lecointe C, Bouchaert E, Staels B, Bordet R et al. (2009). "Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, exerts anticonvulsive properties". Epilepsia 50 (4): 943–8. doi:10.1111/j.1528-1167.2008.01901.x. PMID 19054409.

External links

U.S. National Library of Medicine: Drug Information Portal - Fenofibrate

UpToDate Contents

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1. フィブラート系薬剤による脂質低下 lipid lowering with fibric acid derivatives
2. スタチン系およびフィブラート系以外の薬剤による脂質低下 lipid lowering with drugs other than statins and fibrates
3. スタチン誘発性ミオパチー statin myopathy
4. スタチン：作用、副作用、および投与 statins actions side effects and administration
5. 高トリグリセリド血症患者に対するアプローチ approach to the patient with hypertriglyceridemia

English Journal

Investigating the correlation between in vivo absorption and in vitro release of fenofibrate from lipid matrix particles in biorelevant medium.

Borkar N, Xia D, Holm R, Gan Y, Müllertz A, Yang M, Mu H.Author information Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2, 2100 Copenhagen, Denmark.AbstractLipid matrix particles (LMP) may be used as better carriers for poorly water-soluble drugs than liquid lipid carriers because of reduced drug mobilization in the formulations. However, the digestion process of solid lipid particles and their effect on the absorption of poorly water-soluble drugs are not fully understood. This study aimed at investigating the effect of particle size of LMP on drug release in vitro as well as absorption in vivo in order to get a better understanding on the effect of degradation of lipid particles on drug solubilisation and absorption. Fenofibrate, a model poorly water-soluble drug, was incorporated into LMP in this study using probe ultrasound sonication. The resultant LMP were characterised in terms of particle size, size distribution, zeta potential, entrapment efficiency, in vitro lipolysis and in vivo absorption in rat model. LMP of three different particle sizes i.e. approximately 100 nm, 400 nm, and 10 μm (microparticles) were produced with high entrapment efficiencies. The in vitro lipolysis study showed that the recovery of fenofibrate in the aqueous phase for 100 nm and 400 nm LMP was significantly higher (p<0.05) than that of microparticles after 30 min of lipolysis, suggesting that nano-sized LMP were digested to a larger extent due to greater specific surface area. The 100 nm LMP showed faster initial digestion followed by 400 nm LMP and microparticles. The area under the plasma concentration-time curve (AUC) following oral administration of 100 nm LMP was significantly higher (p<0.01) than that of microparticles and fenofibrate crystalline suspension (control). However, no significant difference was observed between the AUCs of 100 nm and 400 nm LMP. The same rank order on the in vivo absorption and the in vitro response was observed. The recovery (%) of fenofibrate partitioning into the aqueous phase during in vitro lipolysis and the AUC of plasma concentration-time curve of fenofibric acid was in the order of 100 nm LMP>microparticles>control. In summary, the present study demonstrated the particle size dependence of bioavailability of fenofibrate loaded LMP in rat model which correlates well with the in vitro drug release performed in the biorelevant medium.
European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences.Eur J Pharm Sci.2014 Jan 23;51:204-10. doi: 10.1016/j.ejps.2013.09.022. Epub 2013 Oct 14.
Lipid matrix particles (LMP) may be used as better carriers for poorly water-soluble drugs than liquid lipid carriers because of reduced drug mobilization in the formulations. However, the digestion process of solid lipid particles and their effect on the absorption of poorly water-soluble drugs are
PMID 24134899

PPAR agonist-mediated protection against HIV Tat-induced cerebrovascular toxicity is enhanced in MMP-9-deficient mice.

Huang W1, Chen L2, Zhang B3, Park M4, Toborek M4.Author information 1Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.2Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, USA.3Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, Kentucky, USA.4Department of Biochemistry and Molecular Biology, University of Miami School of Medicine, Miami, Florida, USA.AbstractThe strategies to protect against the disrupted blood-brain barrier (BBB) in HIV-1 infection are not well developed. Therefore, we investigated the potential of peroxisome proliferator-activated receptor (PPAR) agonists to prevent enhanced BBB permeability induced by HIV-1-specific protein Tat. Exposure to Tat via the internal carotid artery (ICA) disrupted permeability across the BBB; however, this effect was attenuated in mice treated with fenofibrate (PPARα agonist) or rosiglitazone (PPARγ agonist). In contrast, exposure to GW9662 (PPARγ antagonist) exacerbated Tat-induced disruption of the BBB integrity. Increased BBB permeability was associated with decreased tight junction (TJ) protein expression and activation of ERK1/2 and Akt in brain microvessels; these effects were attenuated by cotreatment with fenofibrate but not with rosiglitazone. Importantly, both PPAR agonists also protected against Tat-induced astrogliosis and neuronal loss. Because disruption of TJ integrity has been linked to matrix metalloproteinase (MMP) activity, we also evaluated Tat-induced effects in MMP-9-deficient mice. Tat-induced cerebrovascular toxicity, astrogliosis, and neuronal loss were less pronounced in MMP-9-deficient mice as compared with wild-type controls and were further attenuated by PPAR agonists. These results indicate that enhancing PPAR activity combined with targeting MMPs may provide effective therapeutic strategies in brain infection by HIV-1.Journal of Cerebral Blood Flow & Metabolism advance online publication, 15 January 2014; doi:10.1038/jcbfm.2013.240.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.J Cereb Blood Flow Metab.2014 Jan 15. doi: 10.1038/jcbfm.2013.240. [Epub ahead of print]
The strategies to protect against the disrupted blood-brain barrier (BBB) in HIV-1 infection are not well developed. Therefore, we investigated the potential of peroxisome proliferator-activated receptor (PPAR) agonists to prevent enhanced BBB permeability induced by HIV-1-specific protein Tat. Expo
PMID 24424383

Effects of the PPAR-α agonist fenofibrate on acute and short-term consequences of brain ischemia.

Ouk T1, Gautier S1, Pétrault M1, Montaigne D2, Maréchal X3, Masse I1, Devedjian JC4, Deplanque D1, Bastide M1, Nevière R3, Duriez P1, Staels B5, Pasquier F6, Leys D7, Bordet R1.Author information 1EA 1046-Département de Pharmacologie médicale, University Lille Nord de France; Université de Lille 2-Faculté de Médecine; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.21] EA 1046-Département de Pharmacologie médicale, University Lille Nord de France; Université de Lille 2-Faculté de Médecine; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France [2] EA 4484-Département de Physiologie, University Lille Nord de France; Université de Lille 2-Faculté de Médecine; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.3EA 4484-Département de Physiologie, University Lille Nord de France; Université de Lille 2-Faculté de Médecine; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.4EA 1046-Département de Pharmacologie médicale, University Lille Nord de France; Université du Littoral; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.5U 1011 Inserm, University Lille Nord de France; Institut Pasteur de Lille; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.6EA 1046-Centre de la Mémoire, Clinique Neurologique-Hôpital Roger Salengro; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.7EA 1046-Service de Neurologie et Pathologie Neurovasculaire, Clinique Neurologique-Hôpital Roger Salengro; Centre Hospitalier Universitaire; Institut de Médecine Prédictive et de Recherche Thérapeutique, Lille, France.AbstractIn stroke, there is an imperative need to develop disease-modifying drugs able to (1) induce neuroprotection and vasculoprotection, (2) modulate recovery and brain plasticity, and (3) limit the short-term motor and cognitive consequences. We hypothesized that fenofibrate, a peroxisome proliferator-activated receptor-α (PPAR-α) agonist, could exert a beneficial effect on immediate and short-term poststroke consequences related to its pleiotropic mechanisms. Rats or mice were subjected to focal ischemia to determine the effects of acute treatment by fenofibrate on (i) motor and memory impairment, (2) both cerebral and vascular compartments, (3) inflammation, (4) neurogenesis, and (5) amyloid cascade. We show that fenofibrate administration results in both neuronal and vascular protection and prevents the short-term motor and cognitive poststroke consequences by interaction with several mechanisms. Modulation of PPAR-α generates beneficial effects in the immediate poststroke consequences by mechanisms involving the interactions between polynuclear neutrophils and the vessel wall, and microglial activation. Fenofibrate modulates mechanisms involved in neurorepair and amyloid cascade. Our results suggest that PPAR-α agonists could check the key points of a potential disease-modifying effect in stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 8 January 2014; doi:10.1038/jcbfm.2013.233.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.J Cereb Blood Flow Metab.2014 Jan 8. doi: 10.1038/jcbfm.2013.233. [Epub ahead of print]
In stroke, there is an imperative need to develop disease-modifying drugs able to (1) induce neuroprotection and vasculoprotection, (2) modulate recovery and brain plasticity, and (3) limit the short-term motor and cognitive consequences. We hypothesized that fenofibrate, a peroxisome proliferator-a
PMID 24398933

Japanese Journal

Influence of procetofen on lipid metabolism in normocholesteremic rats

KRITCHEVSKY D
Pharmacol Res Commun 11, 635-641, 1979
NAID 30013166834

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Fenofibrate
Systematic (IUPAC) name
	propan-2-yl 2-{4-[(4-chlorophenyl)carbonyl]phenoxy}-2-methylpropanoate
Clinical data
Trade names	Fenoglide, Lipofen
AHFS/Drugs.com	monograph
MedlinePlus	a601052
Pregnancy; category	US: C (Risk not ruled out);
Legal status	Legend;
Routes of; administration	Oral
Pharmacokinetic data
Protein binding	99%
Metabolism	glucuronidation
Half-life	20 hours
Excretion	urine (60%), feces (25%)
Identifiers
CAS Registry Number	49562-28-9
ATC code	C10AB05
PubChem	CID: 3339
DrugBank	DB01039
ChemSpider	3222
UNII	U202363UOS
KEGG	D00565
ChEBI	CHEBI:5001
ChEMBL	CHEMBL672
Chemical data
Formula	C20H21ClO4
Molecular mass	360.831 g/mol
	SMILES O=C(c1ccc(Cl)cc1)c2ccc(OC(C(=O)OC(C)C)(C)C)cc2;
	InChI InChI=1S/C20H21ClO4/c1-13(2)24-19(23)20(3,4)25-17-11-7-15(8-12-17)18(22)14-5-9-16(21)10-6-14/h5-13H,1-4H3 ; Key:YMTINGFKWWXKFG-UHFFFAOYSA-N ;
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英: procetofen
関: フェノフィブラート

[feno-1] Yang LP, Keating GM (2009). "Fenofibric acid: in combination therapy in the treatment of mixed dyslipidemia". Am J Cardiovasc Drugs 9 (6): 401–9. doi:10.2165/11203920-000000000-00000. PMID 19929038.

[2] Fazio S (2009). "More clinical lessons from the FIELD study". Cardiovasc Drugs Ther 23 (3): 235–41. doi:10.1007/s10557-008-6160-5. PMID 19160032.

[3] Steiner G (2009). "How can we improve the management of vascular risk in type 2 diabetes: insights from FIELD". Cardiovasc Drugs Ther 23 (5): 403–8. doi:10.1007/s10557-009-6190-7. PMID 19757004.

[4] Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T et al. (2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care Res (Hoboken) 64 (10): 1431–46. doi:10.1002/acr.21772. PMC 3683400. PMID 23024028.

[ReferenceB-5] Package Insert: Abbot Laboratories (October 2010)

[ATP4_Guidelines-6] Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH et al. (2014). "2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation 129 (25 Suppl 2): S1–45. doi:10.1161/01.cir.0000437738.63853.7a. PMID 24222016.

[Fenofibric_acid_label_information-7] ^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ ^j Fenofibric Acid FDA Label Prescribing Information"FDA Label Information" (PDF). FDA.

[8] Product Information: TriCor(TM), fenofibrate. Abbott Laboratories, North Chicago, IL, 1998.

[9] Product Information: Sandimmune(R) oral capsules, oral solution, intravenous injection, cyclosporine oral capsules, oral solution, intravenous injection. Novartis Pharmaceuticals Corporation, East Hanover, NJ, 2010.

[10] Product Information: TRICOR(R) oral tablets, fenofibrate oral tablets. Abbott Laboratories, North Chicago, IL, 2007.

[staels-11] Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC (1998). "Mechanism of action of fibrates on lipid and lipoprotein metabolism". Circulation 98 (19): 2088–93. doi:10.1161/01.cir.98.19.2088. PMID 9808609.

[12] Ling H, Luoma JT, Hilleman D (2013). "A review of currently available fenofibrate and fenofibric acid formulations". Cardiol Res 4 (2): 47–55. doi:10.4021/cr270w.

[13] Alagona P (2010). "Fenofibric acid: a new fibrate approved for use in combination with statin for the treatment of mixed dyslipidemia". Vasc Health Risk Manag 6: 351–62. doi:10.2147/vhrm.s6714. PMC 2879297. PMID 20531954.

[14] Wierzbicki AS, Mikhailidis DP, Wray R, Schacter M, Cramb R, Simpson WG et al. (2003). "Statin-fibrate combination: therapy for hyperlipidemia: a review". Curr Med Res Opin 19 (3): 155–68. doi:10.1185/030079903125001668. PMID 12814127.

[fdanews.com-15] Abbott's request to dismiss the antitrust charge over Tricor was rejected. FDANews, Drug Daily Bulletin, (June 1, 2006) [1]

[16] TEVA Pharmartsau6i8mkst7oceutical Lofibra Product Site

[17] Lalloyer F, Staels B (2010). "Fibrates, glitazones, and peroxisome proliferator-activated receptors". Arterioscler. Thromb. Vasc. Biol. 30 (5): 894–9. doi:10.1161/ATVBAHA.108.179689. PMC 2997800. PMID 20393155.

[Porta2009-18] Porta N, Vallée L, Lecointe C, Bouchaert E, Staels B, Bordet R et al. (2009). "Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, exerts anticonvulsive properties". Epilepsia 50 (4): 943–8. doi:10.1111/j.1528-1167.2008.01901.x. PMID 19054409.

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procetofen