Elafibranor 80mg tablets
Requires a prescription from a doctor or prescriber
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Safety monitoring data
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Suspected adverse reactions reported for Elafibranor
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1 branded products available
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Iqirvo 80mg tablets
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(2)
Elafibranor for previously treated primary biliary cholangitis (TA1016)
Seladelpar for previously treated primary biliary cholangitis (TA1171)
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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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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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 the 50 most relevant studies.
Reviews & meta-analyses: 10 · Randomised trials: 5 · 2016–2026
Showing the 50 most relevant studies, sorted by most relevant.
Jörn M. Schattenberg, Albert Parés, Kris V. Kowdley, et al.
Journal of Hepatology, 2021
- Alkaline Phosphatase
- Bilirubin
- Liver Cirrhosis, Biliary
Kris V. Kowdley, Christopher L. Bowlus, Cynthia Levy, et al.
New England Journal of Medicine, 2023
- Cholestasis
- Alkaline Phosphatase
- Bilirubin
Naren Nallapeta, Shayan Mahapatra, Bharadwaj Jilakaraju, et al.
Journal of Hepatology, 2026
David Jones, Emily Combe, Harun Knight, et al.
Journal of Comparative Effectiveness Research, 2026
- Liver Cirrhosis, Biliary
- Alkaline Phosphatase
- Bayes Theorem
Aim: To indirectly compare the efficacy and safety of elafibranor and seladelpar, as second-line treatments for primary biliary cholangitis. Materials & methods: Bayesian network meta-analyses compared data from randomized-controlled studies of elafibranor and seladelpar identified by a systematic literature review up to June 2024: (a) elafibranor (n = 108) versus placebo (n = 53; ELATIVE [NCT04526665]) and (b) seladelpar (n = 128) versus placebo (n = 65; RESPONSE [NCT03301506]). Patients from ELATIVE not meeting the RESPONSE upper limit of normal (ULN) criteria for alkaline phosphatase (ALP) and total bilirubin were excluded (n = 16); summary statistics for ELATIVE were recalculated using the new dataset. Randomeffects models assessed the outcomes of cholestasis response (ALP <1.67 × ULN, ALP reduction ≥15% from baseline and total bilirubin ≤ULN), ALP normalization, change from baseline in ALP and pruritus, pruritus as a treatment-emergent adverse event and all-cause discontinuation. Results: Elafibranortreated patients had greater odds of achieving cholestasis response than placebo- (median odds ratio [95% credible interval]: 84.79 [12.49, 2513.00]) or seladelpar-treated patients (13.02 [1.45, 420.20]), with posterior probabilities ≥99% that odds were higher with elafibranor than seladelpar or placebo. Among patients with ALP ≥350 U/l, the median odds ratio [95% credible interval] of cholestasis response for elafibranor-treated patients versus seladelpar-treated patients was 18.71 [0.65, 10,610.00], with a 95.2% posterior probability that odds were higher with elafibranor than seladelpar. For all other outcomes, there was no strong evidence of a difference between treatments. Conclusion: Bayesian network metaanalyses found strong probabilistic evidence supporting the treatment benefit of elafibranor compared with seladelpar for the achievement of cholestasis response at 52 weeks, while the treatment effect on other outcomes was uncertain. Head-to-head studies are needed to validate results of these indirect comparisons.
Abstract licence: CC BY
E Combe, D Jones, H Knight, et al.
Value in Health, 2024
Adnan Malik, Mahum Nadeem, Muhammad Imran Malik
Clinical Journal of Gastroenterology, 2021
- Chalcones
- Non-alcoholic Fatty Liver Disease
- Propionates
Vlad Ratziu, Stephen A. Harrison, Sven Francque, et al.
Gastroenterology, 2016
- Biopsy
- Europe
- Gastrointestinal Agents
Cynthia Levy, George Abouda, Bahri M. Bilir, et al.
Journal of Hepatology, 2025
- Pentanoic Acids
- Propionates
- Cholangitis, Sclerosing
Cynthia Levy, George Abouda, Bahri M. Bilir, et al.
Journal of Hepatology, 2025
C. Bowlus, K. Kowdley, C. Levy, et al.
P23 Efficacy of elafibranor in primary biliary cholangitis: results from the variable double-blind period of ELATIVE®, a randomised, placebo-controlled phase III trial, 2024
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
70.2 hours
Mechanism
Proliferator-activated receptor (PPAR) is a nuclear receptor that regulates nume…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
80 mg
[L50768]…
Half-life
80 mg
Protein binding
99.7%
[L50768]
Volume of distribution
4731 L
[L50768]…
Metabolism
Elimination
120 mg
Clearance
50.0 L/h
[L50768]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L50768][L51873]
In the US, this indication is approved under accelerated approval and is subject to change based on the determined clinical benefit of the drug in future confirmatory trials.
[L50768]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 230 interactions
While the exact mechanism of action has not been fully elucidated, elafibranor and its active metabolite (GFT1007) are dual α and β/δ agonists.[A263833][L50768] The signalling pathway for PPARδ was reported to include Fibroblast Growth Factor 21 (FGF21)-dependent downregulation of CYP7A1, the key enzyme for the synthesis of bile acids from cholesterol.[L50768]
An in vitro PPAR functional assay showed that both elafibranor and GFT1007 produced activation of PPARalpha (EC50 = 46 nM and 14 nM, respectively, and Emax = 56% and 61%, respectively, relative to reference agonists). The potency of elafibranor and GFT1007 for PPAR-alpha activation exceeded the respective potencies for PPAR-gamma and PPAR-delta activation by approximately 3- to 8-fold.[L50768]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L50768]
The mean (SD) Cmax at steady state was 802 (443) ng/mL for elafibranor and 2058 (459) ng/mL for GFT1007.
[L50768]
The mean (SD) AUC was 3758 (1749) ng x h/mL for elafibranor and 11985 (7149) ng x h/mL for GFT1007.
[L50768]
Following once-daily dosing of 80 mg in patients with PBC, the median time to peak plasma concentrations (Tmax) of elafibranor and GFT1007 was 1.25 hours (range: 0.5-2 hours).
[L50768]
When administered with a high-fat and high-calorie meal, Tmax was delayed by 30 minutes for elafibranor and by 1-hour for GFT1007 compared to in fasted conditions. Under fed condition, mean Cmax and AUC of elafibranor decreased by 50% and 15% respectively and mean Cmax of GFT1007 decreased by 30%, but the AUC was not affected compared to fasted conditions. The difference was not clinically meaningful.
[L50768]
[L50768]
[L50768]
[L50768]
In vitro studies showed that elafibranor was metabolized by 15-ketoprostaglandin 13-Δ reductase (PTGR1), a cytosolic enzyme, to form GFT1007. Elafibranor was also metabolized by CYP2J2, UGT1A3, UGT1A4, and UGT2B7. GFT1007 was further metabolized by CYP2C8, UGT1A3, and UGT2B7.
[L50768]
Biliary excretion of elafibranor in humans was suggested by the excretion of 60% of orally administered elafibranor in the bile of rats.
[L50768]
[L50768]
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
PMID:35675826
Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Has a preference for poly-unsaturated fatty acids, such as gamma-linoleic acid and eicosapentanoic acid. Once activated by a ligand, the receptor binds to promoter elements of target genes.
Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as transcription activator for the acyl-CoA oxidase gene. Decreases expression of NPC1L1 once activated by a ligand
Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated pro-inflammatory responses.
Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of BMAL1 in the blood vessels (By similarity)
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
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
PMID:10220572 PMID:10421658 PMID:11500505 PMID:16332456
Mediates hepatobiliary excretion of mono- and bis-glucuronidated bilirubin molecules and therefore play an important role in bilirubin detoxification .
PMID:10421658
Also mediates hepatobiliary excretion of others glucuronide conjugates such as 17beta-estradiol 17-glucosiduronic acid and leukotriene C4 .
PMID:11500505
Transports sulfated bile salt such as taurolithocholate sulfate .
PMID:16332456
Transports various anticancer drugs, such as anthracycline, vinca alkaloid and methotrexate and HIV-drugs such as protease inhibitors .
PMID:10220572 PMID:11500505 PMID:12441801
Confers resistance to several anti-cancer drugs including cisplatin, doxorubicin, epirubicin, methotrexate, etoposide and vincristine PMID:10220572 PMID:11500505
PMID:10359813 PMID:11581266 PMID:15083066
Transports glucuronide conjugates such as bilirubin diglucuronide, estradiol-17-beta-o-glucuronide and GSH conjugates such as leukotriene C4 (LTC4) .
PMID:11581266 PMID:15083066
Transports also various bile salts (taurocholate, glycocholate, taurochenodeoxycholate-3-sulfate, taurolithocholate- 3-sulfate) (By similarity). Does not contribute substantially to bile salt physiology but provides an alternative route for the export of bile acids and glucuronides from cholestatic hepatocytes (By similarity). May contribute to regulate the transport of organic compounds in testes across the blood-testis-barrier (Probable).
Can confer resistance to various anticancer drugs, methotrexate, tenoposide and etoposide, by decreasing accumulation of these drugs in cells PMID:10359813 PMID:11581266
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 A05AX06
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)
Elafibranor
Additional database identifiers
Drugs Product Database (DPD)
27008
ChemSpider
8040573
BindingDB
50502541
PDB
MUO
ZINC
ZINC000114643710
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:9235
GenAtlas
PPARD
GeneCards
PPARD
GenBank Gene Database
L07592
GenBank Protein Database
190230
Guide to Pharmacology
594
UniProt Accession
PPARD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9236
GenAtlas
PPARG
GeneCards
PPARG
GenBank Gene Database
U79012
GenBank Protein Database
1711117
Guide to Pharmacology
595
UniProt Accession
PPARG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:18429
GeneCards
PTGR1
GenBank Gene Database
BC035228
GenBank Protein Database
23271371
UniProt Accession
PTGR1_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:12536
GeneCards
UGT1A4
GenBank Gene Database
M57951
GenBank Protein Database
184475
UniProt Accession
UD14_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12538
GeneCards
UGT1A6
UniProt Accession
UD16_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:2634
GeneCards
CYP2J2
GenBank Gene Database
U37143
GenBank Protein Database
18254513
Guide to Pharmacology
1332
UniProt Accession
CP2J2_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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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
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
HUGO Gene Nomenclature Committee (HGNC)
HGNC:53
GenAtlas
ABCC2
GeneCards
ABCC2
GenBank Gene Database
U63970
GenBank Protein Database
1764162
Guide to Pharmacology
780
UniProt Accession
MRP2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:54
GenAtlas
ABCC3
GeneCards
ABCC3
GenBank Gene Database
AB010887
GenBank Protein Database
3132270
UniProt Accession
MRP3_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
Linked open data from Wikidata (Q15409440), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.