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Farnesoid X nuclear receptor ligand obeticholic acid for non-cirrhotic, non-alcoholic steatohepatitis (FLINT): a multicentre, randomised, placebo-controlled trial
Open accessAbstract
Background The bile acid derivative 6-ethylchenodeoxycholic acid (obeticholic acid) is a potent activator of the farnesoid X nuclear receptor that reduces liver fat and fibrosis in animal models of fatty liver disease. We assessed the efficacy of obeticholic acid in adult patients with non-alcoholic steatohepatitis.Methods We did a multicentre, double-blind, placebo-controlled, parallel group, randomised clinical trial at medical centres in the USA in patients with non-cirrhotic, non-alcoholic steatohepatitis to assess treatment with obeticholic acid given orally (25 mg daily) or placebo for 72 weeks. Patients were randomly assigned 1:1 using a computer-generated, centrally administered procedure, stratified by clinical centre and diabetes status. The primary outcome measure was improvement in centrally scored liver histology defined as a decrease in non-alcoholic fatty liver disease activity score by at least 2 points without worsening of fibrosis from baseline to the end of treatment. A planned interim analysis of change in alanine aminotransferase at 24 weeks undertaken before end-of-treatment (72 weeks) biopsies supported the decision to continue the trial (relative change in alanine aminotransferase -24%, 95% CI -45 to -3). A planned interim analysis of the primary outcome showed improved efficacy of obeticholic acid (p=0·0024) and supported a decision not to do end-of-treatment biopsies and end treatment early in 64 patients, but to continue the trial to obtain the 24-week post-treatment measures. Analyses were done by intention-to-treat. This trial was registered with ClinicalTrials.gov, number NCT01265498.Findings Between March 16, 2011, and Dec 3, 2012, 141 patients were randomly assigned to receive obeticholic acid and 142 to placebo. 50 (45%) of 110 patients in the obeticholic acid group who were meant to have biopsies at baseline and 72 weeks had improved liver histology compared with 23 (21%) of 109 such patients in the placebo group (relative risk 1·9, 95% CI 1·3 to 2·8; p=0·0002). 33 (23%) of 141 patients in the obeticholic acid developed pruritus compared with nine (6%) of 142 in the placebo group.Interpretation Obeticholic acid improved the histological features of non-alcoholic steatohepatitis, but its long-term benefits and safety need further clarification.Funding National Institute of Diabetes and Digestive and Kidney Diseases, Intercept Pharmaceuticals.
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“In addition, FXR regulates other pathways with direct antiinflammatory and antifibrotic effects. 13-15”
From A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis (2016) · cites this paper as [14]
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Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Although OCA was generally well tolerated, concerns were raised by the occurrence of side effects such as pruritus, which developed in 23% of patients on OCA without leading to drug discontinuation, increased total serum cholesterol and low-density lipoprotein (LDL)-cholesterol levels and a modest, but significant, reduction in high-density lipoprotein (HDL)-cholesterol [83].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Pruritus was the main side effect of obeticholic acid (33% vs. 6% placebo) [46].”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Importantly however obeticholic acid improved fibrosis in 35% of patients versus only 19% in the placebo arm (p = 0.004) [46].”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Significantly more patients in the obeticholic acid arm (45%) versus placebo (21%) showed improved liver histology [46] (defined as decrease in NAS ≥2 points without worsening of fibrosis).”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [46]
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“Nevertheless, while the primary endpoint was reached, no statistically significant effect on the resolution of NASH was seen, which could limit direct clinical usefulness.”
From Current treatment of non‐alcoholic fatty liver disease (2022) · cites this paper as [46]
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“The drug is approved at a 5 or 10 mg daily dose for second-line therapy in primary biliary cholangitis 379 and was developed for MASH at a higher dose (25 mg daily), based on a phase II placebo-controlled trial showing improvement in fi brosis and liver enzymes after 18 months of treatment.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [380]
In the citing paper
“Although patients treated with OCA showed a significant improvement in the NAFLD activity score (i.e., the primary histological outcome) and a significant decrease in liver fibrosis, NASH resolution occurred in only 22% of patients treated with OCA (without a statically significant effect compared to placebo), and no effect was observed in patients with advanced fibrosis.”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although OCA was generally well tolerated, concerns were raised by the occurrence of side effects such as pruritus, which developed in 23% of patients on OCA without leading to drug discontinuation, increased total serum cholesterol and low-density lipoprotein (LDL)-cholesterol levels and a modest, but significant, reduction in high-density lipoprotein (HDL)-cholesterol [83].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although OCA was generally well tolerated, concerns were raised by the occurrence of side effects such as pruritus, which developed in 23% of patients on OCA without leading to drug discontinuation, increased total serum cholesterol and low-density lipoprotein (LDL)-cholesterol levels and a modest, but significant, reduction in high-density lipoprotein (HDL)-cholesterol [83].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although patients treated with OCA showed a significant improvement in the NAFLD activity score (i.e., the primary histological outcome) and a significant decrease in liver fibrosis, NASH resolution occurred in only 22% of patients treated with OCA (without a statically significant effect compared to placebo), and no effect was observed in patients with advanced fibrosis.”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although patients treated with OCA showed a significant improvement in the NAFLD activity score (i.e., the primary histological outcome) and a significant decrease in liver fibrosis, NASH resolution occurred in only 22% of patients treated with OCA (without a statically significant effect compared to placebo), and no effect was observed in patients with advanced fibrosis.”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although patients treated with OCA showed a significant improvement in the NAFLD activity score (i.e., the primary histological outcome) and a significant decrease in liver fibrosis, NASH resolution occurred in only 22% of patients treated with OCA (without a statically significant effect compared to placebo), and no effect was observed in patients with advanced fibrosis.”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“Although OCA was generally well tolerated, concerns were raised by the occurrence of side effects such as pruritus, which developed in 23% of patients on OCA without leading to drug discontinuation, increased total serum cholesterol and low-density lipoprotein (LDL)-cholesterol levels and a modest, but significant, reduction in high-density lipoprotein (HDL)-cholesterol [83].”
From Gut-pancreas-liver Axis as a target for treatment of NAFLD/NASH (2020) · cites this paper as [83]
In the citing paper
“OCA is a semisynthetic bile acid analogue that improved histological features of NASH and fibrosis in phase IIb clinical trials (35).”
From Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis (2016) · cites this paper as [35]
In the citing paper
“FLINT (phase 2b)77: 25 mg OCA for 18 months improved NAFLD activity score (predefined primary endpoint) and its individual components, but did not result in significantly higher NASH resolution (22 vs 13% compared with placebo); however, a higher proportion of patients (35 vs 19%) showed improved fibrosis (by at least one stage).”
From Novel therapeutic targets for cholestatic and fatty liver disease (2022) · cites this paper as [77]
In the citing paper
“Although OCA was validated in several clinical trials for its benefit in ameliorating NASH-induced liver fibrosis51,52, the response rate was 23%, far from satisfactory19,20.”
From SUMOylation inhibitors synergize with FXR agonists in combating liver fibrosis (2020) · cites this paper as [52]
In the citing paper
“OCA has a high safety profile in patients with NASH as demonstrated in the FLINT trial, with the major adverse effects being pruritus and alterations of serum lipid profiles144.”
From The gut microbiome and liver cancer: mechanisms and clinical translation (2017) · cites this paper as [144]
In the citing paper
“Given the potential for NF-kB to cause cardiac hypertrophy independent of processes such as hypertension, this presents indirect evidence for the potential of FXR-targeted therapies to improve heart failure144,145.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [144]
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Shamseddeen, H., Vilar-Gomez, E., Chalasani, N., Myers, R. P., Subramanian, G. M., Shlevin, H. H., Allgood, A. E., & Orman, E. S. (2020) · Drug Safety · doi:10.1007/s40264-019-00896-1 · Cited by 6
Self-citationJayabalan, D., Dhakal, S., Chandra, J., Fasser, D. A., Jeffrey, G. P., Garas, G., Vilar-Gomez, E., Calzadilla-Bertot, L., & Adams, L. A. (2026) · American Journal of Gastroenterology · doi:10.14309/ajg.0000000000003918 · Cited by 3
Advances and Emerging Therapies in the Treatment of Non-alcoholic Steatohepatitis
Brennan, P. N., The University of Edinburgh, C. F. R. M., NHS Tayside, N. H. A. M. S., The University of Dundee, D. O. M. A. C. M., Dillon, J. F., NHS Tayside, N. H. A. M. S., The University of Dundee, D. O. M. A. C. M., McCrimmon, R., NHS Tayside, N. H. A. M. S., & The University of Dundee, D. O. M. A. C. M. (2022) · European Endocrinology · doi:10.17925/ee.2022.18.2.148 · Cited by 3
Metadata
- Authors
- Neuschwander-Tetri, B. A., Loomba, R., Sanyal, A. J., Lavine, J. E., Van Natta, M. L., Abdelmalek, M. F., Chalasani, N., Dasarathy, S., Diehl, A. M., Hameed, B., Kowdley, K. V., McCullough, A., Terrault, N., Clark, J. M., Tonascia, J., Brunt, E. M., Kleiner, D. E., & Doo, E.
- Affiliations
- University of California San Diego (US)
- Virginia Commonwealth University (US)
- Columbia University (US)
- Duke University (US)
- Indiana University Indianapolis (US)
- Case Western Reserve University (US)
- University of California, San Francisco (US)
- Virginia Mason Medical Center (US)
- Cleveland Clinic (US)
- Johns Hopkins University (US)
- Washington University in St. Louis (US)
- National Cancer Institute (US)
- National Institute of Diabetes and Digestive and Kidney Diseases (US)
- ORCID
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 385
- Issue
- 9972
- Pages
- 956-965
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC4447192
- OpenAlex
- W2106768039
- Cited by
- 2,237
- References
- 30
- Citations by year
- 2026: 89 · 2025: 111 · 2024: 145 · 2023: 159 · 2022: 192 · 2021: 236 · 2020: 264 · 2019: 245 · 2018: 234 · 2017: 229 · 2016: 190 · 2015: 130
- FWCI
- 139.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (grants U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734, U01DK061737, U01DK061738, U01DK061730, U01DK061713)
- National Center for Advancing Translational Sciences (NCATS) for NASH CRN Studies (grants UL1TR000439, UL1TR000436, UL1TR000006, UL1TR000448, UL1TR000100, UL1TR000004, UL1TR000423, and UL1TR000058)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- obeticholic acid, nonalcoholic steatohepatitis, non-cirrhotic liver disease, bile acid derivatives, liver histopathology, liver fibrosis, alanine aminotransferase, treatment discontinuation
- MeSH terms
- Receptor, Farnesoid X-Activated, Administration, Oral, Chenodeoxycholic Acid, Double-Blind Method, Female, Humans, Cholesterol, HDL, Cholesterol, LDL, Liver, Liver Cirrhosis, Male, Middle Aged, Weight Loss, Treatment Outcome, Receptors, Cytoplasmic and Nuclear, Non-alcoholic Fatty Liver Disease
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