Febuxostat 120mg tablets
Requires a prescription from a doctor or prescriber
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Official medicine documents
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Drug safety updates
MHRA alerts for Febuxostat
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 Febuxostat
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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 Febuxostat
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22 branded products available
MHRA licensed products
View all licensed products for Febuxostat on the MHRA register
Adenuric 120mg tablets
Elstabya 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
Febuxostat 120mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
80 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 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.
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Supply & safety information
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Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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. 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 the 50 most relevant studies.
Reviews & meta-analyses: 27 · Randomised trials: 17 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
I. Mackenzie, I. Ford, G. Nuki, et al.
Lancet, 2020
K. Kimura, T. Hosoya, S. Uchida, et al.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2018
Fan Wu, Lvyi Chen, Yimei Du
Clinical Rheumatology, 2024
Jianhao Deng, Peng-Hui Lai, Li Xie, et al.
Clinical and Translational Science, 2024
Jiaojiao Chen, Yanyun Zhang, Yinglin Wang, et al.
Renal Failure, 2025
Abstract Objective This study evaluates and compares the effectiveness and safety of febuxostat and allopurinol in chronic kidney disease (CKD) stages 3–5 patients with asymptomatic hyperuricemia using a network meta-analysis. Methods A systematic review and network meta-analysis were conducted, adhering to PRISMA-NMA guidelines. Searches included PubMed, Embase, Cochrane Library, and Chinese databases up to June 2024. Randomized controlled trials (RCTs) and cohort studies were assessed for methodological rigor using GRADE. Results A total of 12 RCTs and 4 cohort studies (n = 2,423 participants) were included. Febuxostat was associated with greater improvements in estimated glomerular filtration rate compared to allopurinol (MD, 4.99 mL/min/1.73 m2; 95%CI −0.65 to 10.78; certainty: low) and placebo (MD, 4.72 mL/min/1.73 m2; 95%CI 0.67 to 8.82; low). Serum uric acid reduction was also more pronounced with febuxostat (MD, −0.61 mg/dL; 95%CI −1.15 to −0.05; moderate). Safety outcomes, including major cardiovascular events and adverse events, showed no significant differences between febuxostat and allopurinol. Subgroup analyses revealed enhanced effectiveness of febuxostat at six months of treatment. Conclusions This analysis provides robust evidence that febuxostat might offers greater improvements in kidney function and uric acid levels compared to allopurinol or placebo in asymptomatic hyperuricemia with CKD stage 3–5 patients, without compromising safety. These findings can guide clinical decision-making and treatment optimization.
Abstract licence: CC BY
Lin TS, Lin YL, Hsu CH, et al.
2025
BackgroundGout is caused by hyperuricemia and is associated with cardiovascular diseases. Treatment for hyperuricemia primarily involves urate-lowering medications. Some trials showed higher cardiovascular mortality rates with febuxostat compared to allopurinol in gout patients. However, data on the cardiovascular safety of benzbromarone compared to allopurinol is limited, and there is no data comparing benzbromarone to febuxostat. This study aims to assess the cardiovascular safety of benzbromarone, febuxostat, and allopurinol in gout patients.MethodsA comprehensive search was conducted across PubMed and EMBASE from their inception to August 2024. Inclusion criteria were randomized controlled trials (RCTs) and cohort studies including adult patients with the diagnosis of gout, with urate-lowering medications. The outcome was the incidence of major adverse cardiovascular events. This systematic review and network meta-analysis were recorded in INPLASY with the ID INPLASY202460049.ResultsA total of 176 studies were identified through the database search. There were 119 articles identified in EMBASE and 57 articles identified in PubMed. Following screening and review, 17 qualified studies (5 RCTs) were included in the network meta-analysis. The relative cardiovascular event risk (risk ratio, RR) for benzbromarone compared to febuxostat is 0.82 (95% CI 0.61-1.09), and for benzbromarone compared to allopurinol, the RR is 0.87 (95% CI 0.75-1.01). The RR for febuxostat compared to allopurinol is 1.08 (95% CI 0.97-1.20).ConclusionOur network meta-analysis suggests a subtle trend indicating a lower risk of cardiovascular events for benzbromarone compared to both febuxostat and allopurinol in gout patients, although not statistically significant.Systematic review registrationhttps://inplasy.com/inplasy-2024-6-0049/, identifier INPLASY202460049.
Abstract licence: CC BY
Sheng Chao, Kejing Zhu, Lei Jia, et al.
Frontiers in Pharmacology, 2026
Dewi C, Puspita F, Insani WN, et al.
2025
Lin M, Zhang H, Wu H, et al.
2025
Wei Q, Shi Y, Hu R, et al.
2025
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
None known
Half-life
5 to 8 hours
Mechanism
Gout is a form of acute arthritis that is characterized by the accumulation of c…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
85%
[A230548]
…
Half-life
5 to 8 hours
[L32238]
Protein binding
99.2%
Volume of distribution
29 to 75 L
[A230598]
…
Metabolism
22–44%
Elimination
80 mg
Clearance
10 to 240 mg
[A230548]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
In February 2019, a black box warning for febuxostat was added, based on the findings of a post-market clinical study (the CARES trial) where there was an increased risk of cardiovascular (CV) fatal outcomes in patients with gout and known cardiovascular disease treated with febuxostat, when compared to those treated with allopurinol. The manufacturer and the FDA advise health professionals to limit the use of febuxostat to second-line therapy in patients who have inadequate response or intolerance to allopurinol, and to avoid the use of febuxostat in patients with cardiovascular diseases.[A2742][L13056]
[L46073]
It is not recommended for the treatment of asymptomatic hyperuricemia [L32238] or secondary hyperuricemia.
[A230583]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 211 interactions
[L13056]
Oral LD50 is 300 mg/kg in mice, 3200 mg/kg in rabbits, and 980 mg/kg in rats.
[L32273]
No dose-limiting toxicities were observed with febuxostat administered at doses up to 300 mg daily for seven days in healthy subjects. There are no reports of overdose of febuxostat in clinical studies and there is no known antidote. Overdose should be managed by symptomatic and supportive care.
[L32238]
XOR is mainly found in the dehydrogenase form under normal physiological conditions; however, in inflammatory conditions, XOR can be converted into the xanthine oxidase form, which catalyzes reactions that produce reactive oxygen species (ROS), such as peroxynitrite. ROS contribute to vascular inflammation and alterations in vascular function. As febuxostat can inhibit both forms of XOR, it can inhibit ROS formation, oxidative stress, and inflammation.[A2743] In a rat model, febuxostat suppressed renal ischemia-reperfusion injury by attenuating oxidative stress.[A2744]
Unlike [allopurinol] and [oxypurinol], febuxostat has no inhibitory actions against other enzymes involved in purine and pyrimidine synthesis and metabolism, because it does not structurally resemble purines or pyrimidines.[A230548]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A230548]
Tmax ranges from 1 to 1.5 hours. Following once-daily oral administration, Cmax was approximately 1.6 ± 0.6 mcg/mL at a dose of 40 mg febuxostat and 2.6 ± 1.7 mcg/mL at a dose of 80 mg febuxostat.
[L32238]
A high-fat meal decreased Cmax by 49% and AUC by 18%, but there were no clinically significant changes in the ability of febuxostat to decrease serum uric acid concentrations.
[L32238]
[L32238]
[L32238]
[A230598]
[A230548]
CYP1A2, CYP2C8, CYP2C9, and non-P450 enzymes are responsible for the oxidation reaction, which accounts for 2-8% of the metabolism of the dose.
[A230548]
Oxidation reaction produces 67M-1, 67M-2, and 67M-4, which are pharmacologically active metabolites. 67M-1, 67M-2, and 67M-4 can further undergo glucuronidation and sulfation.
[A230598]
Hydroxy metabolites are present in human plasma at much lower concentrations than the parent drug.
[L32238]
[L32238]
Approximately 45% of the total dose was recovered in the feces, where 12% of the dose accounted for the unchanged parent drug.
About 1% accounted for the acyl glucuronide metabolite, 25% accounted for oxidative metabolites and their conjugates, and 7% accounted for unidentified metabolites.
[L32238]
[A230548]
Proteins and enzymes this drug interacts with in the body
Contributes to the generation of reactive oxygen species. Has also low oxidase activity towards aldehydes (in vitro)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
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 M04AA03
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)
Febuxostat
Additional database identifiers
Drugs Product Database (DPD)
13271
ChemSpider
118173
BindingDB
50320491
PDB
TEI
ZINC
ZINC000000005423
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12805
GenAtlas
XDH
GeneCards
XDH
GenBank Gene Database
D11456
GenBank Protein Database
10336525
Guide to Pharmacology
2646
UniProt Accession
XDH_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12535
GeneCards
UGT1A3
GenBank Gene Database
M84127
GenBank Protein Database
340135
UniProt Accession
UD13_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:12554
GeneCards
UGT2B7
GenBank Gene Database
J05428
GenBank Protein Database
340080
UniProt Accession
UD2B7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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: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:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72