Fenofibrate 160mg/5ml oral solution
Requires a prescription from a doctor or prescriber
Drug of the fibrate class, mainly used to reduce cholesterol levels
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Fenofibrate
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Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Fenofibrate
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
WHO defined daily dose (DDD)
200 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & safety information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing all 30 studies.
Reviews & meta-analyses: 7 · Randomised trials: 3 · 2001–2026
Showing all 30 studies, sorted by most relevant.
A. Keech, R. Simes, P. Barter, et al.
Lancet, 2005
- Hypolipidemic Agents
- Cardiovascular Diseases
- Cholesterol
Yansheng Liu, G. Guo, Lin-hua Zheng, et al.
The American Journal of Gastroenterology, 2023
- Liver Cirrhosis, Biliary
- Fenofibrate
- Cholagogues and Choleretics
Gi Eun Kim, Mariam Imran, Sherif Mostafa, et al.
Case Reports in Hepatology, 2025
Primary biliary cholangitis is a progressive disease with complications such as liver cirrhosis and hepatocellular carcinoma, and the treatment goal is to delay its progression. One of the markers for treatment response is alkaline phosphatase levels. Baricitinib has been used in one randomized controlled trial involving two patients to improve outcomes in unresponsive primary biliary cholangitis. We present a case of primary biliary cholangitis who had incomplete response to ursodeoxycholic acid, obeticholic acid, and fenofibrate but showed complete response to baricitinib in terms of sustained normalized alkaline phosphatase levels.
Abstract licence: CC BY
Lv Jin, H. Hua, Yong Ji, et al.
Biomolecules and Biomedicine, 2023
- Hyperlipidemias
- Fenofibrate
- Anti-Inflammatory Agents
Inflammation contributes to the pathogenesis of several diseases. Fenofibrate, known as a peroxisome proliferator-activated receptor - α (PPAR-α) agonist, is a classic drug for treating hyperlipidemia. In addition to its lipid-lowering effect, fenofibrate has also been reported to exert anti-inflammatory effects with complicated underlying mechanisms of action. In general, the anti-inflammatory effect of fenofibrate is secondary to its lipid-lowering effect, especially for the inflammation caused by hyperlipidemia in the circulatory system. Some anti-inflammatory actions may also come from its regulatory effects on intracellular lipid metabolism by activating PPAR-α. In addition, some roles in anti-inflammation might be mediated by its direct regulation of inflammatory signaling pathways. In order to understand anti-inflammatory activities and the underlying mechanisms of fenofibrate action in disease better, we herein reviewed and discussed the anti-inflammatory roles and its subserving mechanisms in various diseases of different organ systems. Thus, this review offers insights into the optimal use of fenofibrate in the clinical setting.
Abstract licence: CC BY
Ahmad A. Abulaban, H. Al-kuraishy, A. Al-Gareeb, et al.
European Journal of Medical Research, 2024
- Multiple Sclerosis
- Fenofibrate
- Central Nervous System
Multiple sclerosis (MS) is the most frequent inflammatory and demyelinating disease of the central nervous system (CNS). The underlying pathophysiology of MS is the destruction of myelin sheath by immune cells. The formation of myelin plaques, inflammation, and injury of neuronal myelin sheath characterizes its neuropathology. MS plaques are multiple focal regions of demyelination disseminated in the brain's white matter, spinal cords, deep grey matter, and cerebral cortex. Fenofibrate is a peroxisome proliferative activated receptor alpha (PPAR-α) that attenuates the inflammatory reactions in MS. Fenofibrate inhibits differentiation of Th17 by inhibiting the expression of pro-inflammatory signaling. According to these findings, this review intended to illuminate the mechanistic immunoinflammatory role of fenofibrate in mitigating MS neuropathology. In conclusion, fenofibrate can attenuate MS neuropathology by modulating different pathways, including oxidative stress, autophagy, mitochondrial dysfunction, inflammatory-signaling pathways, and neuroinflammation.
Abstract licence: CC BY
C. Deerochanawong, Sin Gon Kim, Yu-Cheng Chang
Diabetes & Metabolism Journal, 2024
- Diabetes Mellitus, Type 2
- Fenofibrate
- Hypertriglyceridemia
Hypertriglyceridemia and decreased high-density lipoprotein cholesterol (HDL-C) persist despite statin therapy, contributing to residual atherosclerotic cardiovascular disease (ASCVD) risk. Asian subjects are metabolically more susceptible to hypertriglyceridemia than other ethnicities. Fenofibrate regulates hypertriglyceridemia, raises HDL-C levels, and is a recommended treatment for dyslipidemia. However, data on fenofibrate use across different Asian regions are limited. This narrative review summarizes the efficacy and safety data of fenofibrate in Asian subjects with dyslipidemia and related comorbidities (diabetes, metabolic syndrome, diabetic retinopathy, and diabetic nephropathy). Long-term fenofibrate use resulted in fewer cardiovascular (CV) events and reduced the composite of heart failure hospitalizations or CV mortality in type 2 diabetes mellitus. Fenofibrate plays a significant role in improving irisin resistance and microalbuminuria, inhibiting inflammatory responses, and reducing retinopathy incidence. Fenofibrate plus statin combination significantly reduced composite CV events risk in patients with metabolic syndrome and demonstrated decreased triglyceride and increased HDL-C levels with an acceptable safety profile in those with high CV or ASCVD risk. Nevertheless, care is necessary with fenofibrate use due to possible hepatic and renal toxicities in vulnerable individuals. Long-term trials and real-world studies are needed to confirm the clinical benefits of fenofibrate in the heterogeneous Asian population with dyslipidemia.
Abstract licence: CC BY-NC
Ronak Lakhia, Matanel Yheskel, Andrea Flaten, et al.
American journal of physiology. Renal physiology, 2018
- Cysts
- Fatty Acids
- Fatty Liver
Jin Yoo, In-Kyung Jeong, K. Ahn, et al.
Metabolism: clinical and experimental, 2021
- Autophagy
- Cells, Cultured
- HeLa Cells
F. Qiu, Tuo Meng, Qian Chen, et al.
Molecular pharmaceutics, 2019
- Polylactic Acid-Polyglycolic Acid Copolymer
- Hypolipidemic Agents
- Capillary Permeability
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
62 found
Half-life
23 hours
Mechanism
Fenofibrate activates peroxisome proliferator activated receptor alpha (PPARα),…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
300mg
[A185954]
Half-life
23 hours
[L8588][L8591]…
Protein binding
99%
[A185936]
Volume of distribution
0.89L/kg
[A36366]
Metabolism
[A185972][L8588][L8591]…
Elimination
5-25%
[A185936][L8588][L8591]…
Clearance
1.1L/h
[L8588][L8591]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Fenofibrate was granted FDA approval on 31 December 1993.[L8585]
- To reduce triglyceride (TG) levels in adults with severe hypertriglyceridemia (TG greater than or equal to 500 mg/dL)
- To reduce elevated low-density lipoprotein cholesterol (LDL-C) in adults with primary hyperlipidemia when the use of recommended LDL-C lowering therapy is not possible
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1385 interactions
[L8651]
The oral TDLO in rats is 9mg/kg.
[L8651]
Treat patients with supportive care including monitoring of vital signs and observing clinical status.
[L8588][L8591]
Recent overdose may be treated with inducing vomiting or gastric lavage.
[L8588][L8591]
Due to fenofibrate's extensive protein binding, hemodialysis is not expected to be useful.
[A185936][L8588][L8591]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A185954]
[L8588][L8591]
Fenofibrate has a half life of 19-27 hours in healthy subjects and up to 143 hours in patients with renal failure.
[A36366]
[A185936]
[A36366]
[A185972][L8588][L8591]
Fenofibric acid is either glucuronidated or has its carbonyl group reduced to a benzhydrol that is then glucuronidated.
[L8588][L8591]
Glucuronidation of fenofibrate metabolites is mediated by UGT1A9.
[A17495]
Reduction of the carbonyl group is primarily mediated by CBR1 and minorly by AKR1C1, AKR1C2, AKR1C3, and AKR1B1.
[A185984]
[A185936][L8588][L8591]
70-75% of the dose recovered in the urine is in the form of fenofibryl glucuronide and 16% as fenofibric acid.
[A185936]
[L8588][L8591]
Proteins and enzymes this drug interacts with in the body
Activated by oleylethanolamide, a naturally occurring lipid that regulates satiety. Receptor for peroxisome proliferators such as hypolipidemic drugs and fatty acids. Regulates the peroxisomal beta-oxidation pathway of fatty acids.
Functions as a transcription activator for the ACOX1 and P450 genes. Transactivation activity requires heterodimerization with RXRA and is antagonized by NR2C2. May be required for the propagation of clock information to metabolic pathways regulated by PER2
Response to specific ligands is species-specific. Activated by naturally occurring steroids, such as pregnenolone and progesterone. Binds to a response element in the promoters of the CYP3A4 and ABCB1/MDR1 genes
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:15791618 PMID:16332456 PMID:18985798 PMID:19228692 PMID:20010382 PMID:20398791 PMID:22262466 PMID:24711118 PMID:29507376 PMID:32203132
Transports taurine-conjugated bile salts more rapidly than glycine-conjugated bile salts .
PMID:16332456
Also transports non-bile acid compounds, such as pravastatin and fexofenadine in an ATP-dependent manner and may be involved in their biliary excretion PMID:15901796 PMID:18245269
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC C10BA03
ATC C10BA12
ATC C10AB05
ATC C10BA09
ATC C10BA04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Fenofibrate
Additional database identifiers
Drugs Product Database (DPD)
1381
ChemSpider
3222
BindingDB
50085042
PDB
J3O
ZINC
ZINC000000584092
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9232
GenAtlas
PPARA
GeneCards
PPARA
GenBank Gene Database
L02932
GenBank Protein Database
307341
Guide to Pharmacology
593
UniProt Accession
PPARA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7968
GenAtlas
NR1I2
GeneCards
NR1I2
GenBank Gene Database
AF061056
GenBank Protein Database
3511138
Guide to Pharmacology
606
UniProt Accession
NR1I2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:14246
GeneCards
MMP25
Guide to Pharmacology
1647
UniProt Accession
MMP25_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12541
GeneCards
UGT1A9
GenBank Gene Database
S55985
GenBank Protein Database
7690346
UniProt Accession
UD19_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1863
GenAtlas
CES1
GeneCards
CES1
GenBank Gene Database
M73499
Guide to Pharmacology
2592
UniProt Accession
EST1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1548
GenAtlas
CBR1
GeneCards
CBR1
GenBank Gene Database
J04056
Guide to Pharmacology
1383
UniProt Accession
CBR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2621
GeneCards
CYP2C19
GenBank Gene Database
M61854
GenBank Protein Database
181344
Guide to Pharmacology
1328
UniProt Accession
CP2CJ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2610
GenAtlas
CYP2A6
GeneCards
CYP2A6
GenBank Gene Database
X13897
Guide to Pharmacology
1321
UniProt Accession
CP2A6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:384
GenAtlas
AKR1C1
GeneCards
AKR1C1
GenBank Gene Database
M86609
GenBank Protein Database
181549
UniProt Accession
AK1C1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:385
GenAtlas
AKR1C2
GeneCards
AKR1C2
GenBank Gene Database
U05598
GenBank Protein Database
531160
UniProt Accession
AK1C2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:386
GenAtlas
AKR1C3
GeneCards
AKR1C3
GenBank Gene Database
S68288
GenBank Protein Database
4261711
Guide to Pharmacology
1382
UniProt Accession
AK1C3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:381
GenAtlas
AKR1B1
GeneCards
AKR1B1
GenBank Gene Database
J04795
GenBank Protein Database
178487
Guide to Pharmacology
2768
UniProt Accession
ALDR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:42
GenAtlas
ABCB11
GeneCards
ABCB11
GenBank Gene Database
AF091582
GenBank Protein Database
3873243
Guide to Pharmacology
778
UniProt Accession
ABCBB_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Wikipedia article
drug of the fibrate class, mainly used to reduce cholesterol levels
Read on WikipediaATC classifications (Wikidata)
Linked open data from Wikidata (Q419724), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.