Obeticholic acid 5mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
5mg
Oral
Drugs affecting intestinal secretions
Active ingredients:
Obeticholic acid
No active safety alerts
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
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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 Obeticholic acid
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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.
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Suspected adverse reactions reported for Obeticholic acid
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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.
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1 products
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Ocaliva 5mg tablets
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WHO defined daily dose (DDD)
10 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 NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Show details
Ursodeoxycholic acid 500mg capsules
Capsule
500mg
Same therapeutic group
Obeticholic acid 10mg tablets
Tablet
10mg
Same therapeutic group
Ursodeoxycholic acid 250mg tablets
Tablet
250mg
Same therapeutic group
Cholic acid 50mg capsules
Capsule
50mg
Same therapeutic group
Cholic acid 250mg capsules
Capsule
250mg
Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Obeticholic acid
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(2)
Obeticholic acid for treating primary biliary cholangitis (TA443)
TA443
Technology appraisal
Updated Apr 2017Elafibranor for previously treated primary biliary cholangitis (TA1016)
TA1016
Technology appraisal
Updated Nov 2024Source: 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 & product information
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Codes for healthcare professionals and prescribing systems
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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 codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
24 hours
Mechanism
Primary biliary cirrhosis is an autoimmune process by which the bile ducts and l…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.5 hours
Obeticholic acid is absorbed in the gastrointestinal tract. The Cmax of obeticholic acid occurs at approximately 1.5…
Half-life
24 hours
The biological half-life of obeticholic acid is reported to be 24 hours.
[L12738]
[L12738]
Protein binding
99%
Obeticholic acid and its metabolic conjugates are >99% plasma protein-bound.
[L12633][L12720]
[L12633][L12720]
Volume of distribution
618 L
The volume of distribution of obeticholic acid is 618 L.
[L12633][L12720]
[L12633][L12720]
Metabolism
13.8%
The metabolism of obeticholic acid occurs in the liver. Obeticholic acid is conjugated with glycine or taurine, followed by secretion into bile.…
Elimination
87%
About 87% of an orally administered dose is accounted for in the feces. Less than 3% of the dose can be recovered in the urine.
[L12633][L12720]
[L12633][L12720]
Clearance
Clearance information for obeticholic acid is not readily available in the literature.
[L12633][L12720]
[L12633][L12720]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Primary biliary cirrhosis, or PBC, is a progressive and chronic condition that leads to hepatic injury often resulting in end-stage liver failure that requires liver transplantation.[A192786]
Obeticholic acid is a farnesoid-X receptor (FXR) agonist used to treat this condition, possibly allowing for increased survival.[A18696] In 2016, it was granted approval to treat primary biliary cholangitis in combination with [ursodeoxycholic acid], which was previously the mainstay treatment for this condition.[A18696][L12633] In May 2021, the FDA updated its prescribing information to contraindicate the use of obeticholic acid in patients with PBC and advanced cirrhosis (e.g. those with portal hypertension or hepatic decompensation) due to a risk of liver failure, in some cases requiring liver transplantation.[L34650]
Obeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH). The NDA from Intercept Pharmaceuticals was approved in November 2019 and obeticholic acid is expected to be granted full approval for this indication in 2020.[L12636]
Obeticholic acid is a farnesoid-X receptor (FXR) agonist used to treat this condition, possibly allowing for increased survival.[A18696] In 2016, it was granted approval to treat primary biliary cholangitis in combination with [ursodeoxycholic acid], which was previously the mainstay treatment for this condition.[A18696][L12633] In May 2021, the FDA updated its prescribing information to contraindicate the use of obeticholic acid in patients with PBC and advanced cirrhosis (e.g. those with portal hypertension or hepatic decompensation) due to a risk of liver failure, in some cases requiring liver transplantation.[L34650]
Obeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH). The NDA from Intercept Pharmaceuticals was approved in November 2019 and obeticholic acid is expected to be granted full approval for this indication in 2020.[L12636]
Properties:
View FDA drug labelsolid
Avg. mass: 420.63 Da
DrugBank indication
Obeticholic acid is indicated for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate response to UDCA. It is also used as a monotherapy in adults with PBC that are unable to tolerate UDCA.
[L12633]
Obeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH), and is likely to be approved for this indication in 2020.
[L12636]
[L12633]
Obeticholic acid is currently being considered for FDA approval to treat fibrosis caused by non-alcoholic liver steatohepatitis (NASH), and is likely to be approved for this indication in 2020.
[L12636]
Also known as(27)
(3α,5β,6α,7α)-6-ethyl-3,7-dihydroxycholan-24-oic acid
6-alpha-ethylchenodeoxycholic acid
6-ECDCA
6-Ethyl-CDCA
6-ethylchenodeoxycholic acid
6alpha-Ethyl-chenodeoxycholic acid
6α-ethylchenodeoxycholic acid
Obeticholic acid
Dosage forms(6)
Tablet (Oral) — 10 mg
Tablet (Oral) — 5 mg
Tablet, film coated (Oral) — 10 mg/1
Tablet, film coated (Oral) — 10 MG
Tablet, film coated (Oral) — 5 MG
Tablet, film coated (Oral) — 5 mg/1
Molecular properties(19)
Drug interactions(374)
Known interactions with other medications. Always consult a healthcare professional.
The risk or severity of bleeding and bruising can be increased when Lepirudin is combined with Obeticholic acid.
Bivalirudin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Bivalirudin is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Alteplase is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Urokinase is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Reteplase is combined with Obeticholic acid.
Anistreplase
Unknown severity
The risk or severity of bleeding and bruising can be increased when Anistreplase is combined with Obeticholic acid.
Tenecteplase
Unknown severity
The risk or severity of bleeding and bruising can be increased when Tenecteplase is combined with Obeticholic acid.
Drotrecogin alfa
Unknown severity
The risk or severity of bleeding and bruising can be increased when Drotrecogin alfa is combined with Obeticholic acid.
Streptokinase
Unknown severity
The risk or severity of bleeding and bruising can be increased when Streptokinase is combined with Obeticholic acid.
Dicoumarol
Unknown severity
The risk or severity of bleeding and bruising can be increased when Dicoumarol is combined with Obeticholic acid.
Argatroban
Unknown severity
The risk or severity of bleeding and bruising can be increased when Argatroban is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Ardeparin is combined with Obeticholic acid.
Phenindione
Unknown severity
The risk or severity of bleeding and bruising can be increased when Phenindione is combined with Obeticholic acid.
Fondaparinux
Unknown severity
The risk or severity of bleeding and bruising can be increased when Fondaparinux is combined with Obeticholic acid.
Pentosan polysulfate
Unknown severity
The risk or severity of bleeding and bruising can be increased when Pentosan polysulfate is combined with Obeticholic acid.
Phenprocoumon
Unknown severity
The risk or severity of bleeding and bruising can be increased when Phenprocoumon is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Heparin is combined with Obeticholic acid.
Enoxaparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Enoxaparin is combined with Obeticholic acid.
4-hydroxycoumarin
Unknown severity
The risk or severity of bleeding and bruising can be increased when 4-hydroxycoumarin is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Coumarin is combined with Obeticholic acid.
Ximelagatran
Unknown severity
The risk or severity of bleeding and bruising can be increased when Ximelagatran is combined with Obeticholic acid.
Desmoteplase
Unknown severity
The risk or severity of bleeding and bruising can be increased when Desmoteplase is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Ancrod is combined with Obeticholic acid.
Rivaroxaban
Unknown severity
The risk or severity of bleeding and bruising can be increased when Rivaroxaban is combined with Obeticholic acid.
Sulodexide
Unknown severity
The risk or severity of bleeding and bruising can be increased when Sulodexide is combined with Obeticholic acid.
Semuloparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Semuloparin is combined with Obeticholic acid.
Idraparinux
Unknown severity
The risk or severity of bleeding and bruising can be increased when Idraparinux is combined with Obeticholic acid.
Astaxanthin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Astaxanthin is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Apixaban is combined with Obeticholic acid.
Otamixaban
Unknown severity
The risk or severity of bleeding and bruising can be increased when Otamixaban is combined with Obeticholic acid.
Amediplase
Unknown severity
The risk or severity of bleeding and bruising can be increased when Amediplase is combined with Obeticholic acid.
Dabigatran etexilate
Unknown severity
The risk or severity of bleeding and bruising can be increased when Dabigatran etexilate is combined with Obeticholic acid.
Danaparoid
Unknown severity
The risk or severity of bleeding and bruising can be increased when Danaparoid is combined with Obeticholic acid.
Dalteparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Dalteparin is combined with Obeticholic acid.
Tinzaparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Tinzaparin is combined with Obeticholic acid.
Ethyl biscoumacetate
Unknown severity
The risk or severity of bleeding and bruising can be increased when Ethyl biscoumacetate is combined with Obeticholic acid.
Nadroparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Nadroparin is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Ditazole is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Edoxaban is combined with Obeticholic acid.
Sodium citrate
Unknown severity
The risk or severity of bleeding and bruising can be increased when Sodium citrate is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Dextran is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Bemiparin is combined with Obeticholic acid.
Parnaparin
Unknown severity
The risk or severity of bleeding and bruising can be increased when Parnaparin is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Desirudin is combined with Obeticholic acid.
Antithrombin Alfa
Unknown severity
The risk or severity of bleeding and bruising can be increased when Antithrombin Alfa is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Protein C is combined with Obeticholic acid.
Antithrombin III human
Unknown severity
The risk or severity of bleeding and bruising can be increased when Antithrombin III human is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Letaxaban is combined with Obeticholic acid.
The risk or severity of bleeding and bruising can be increased when Darexaban is combined with Obeticholic acid.
Betrixaban
Unknown severity
The risk or severity of bleeding and bruising can be increased when Betrixaban is combined with Obeticholic acid.
Showing 50 of 374 interactions
Food & lifestyle interactions
Advice
Take with or without food.
Toxicity & overdose
LD50 information for obeticholic acid is not readily available in the literature.
[L12633]
The maximum documented exposure to obeticholic acid was 500 mg in healthy research volunteers. Doses of 250 mg have been administered to healthy volunteers for 12 consecutive days. Pruritus and reversible transaminase liver elevations were observed.
In PBC patients who received 25mg daily to 50mg daily (2.5 to 5 times the maximum recommended dose), dose-dependent transaminase and bilirubin elevations, ascites, primary biliary cholangitis aggravation, and new-onset jaundice were reported.
[L12720]
In the case of an overdose with obeticholic acid, clinical monitoring and supportive care should be offered as they are required.
[L12720]
[L12633]
The maximum documented exposure to obeticholic acid was 500 mg in healthy research volunteers. Doses of 250 mg have been administered to healthy volunteers for 12 consecutive days. Pruritus and reversible transaminase liver elevations were observed.
In PBC patients who received 25mg daily to 50mg daily (2.5 to 5 times the maximum recommended dose), dose-dependent transaminase and bilirubin elevations, ascites, primary biliary cholangitis aggravation, and new-onset jaundice were reported.
[L12720]
In the case of an overdose with obeticholic acid, clinical monitoring and supportive care should be offered as they are required.
[L12720]
How it works
Mechanism of action
Primary biliary cirrhosis is an autoimmune process by which the bile ducts and liver are damaged progressively, leading to fibrosis and cirrhosis. Bile acids increase the risk of damage and fibrosis to the damaged bile ducts.[A192786][A192795]
Obeticholic acid is a potent agonist of the farnesoid X receptor, which serves to regulate the hepatic metabolism of bile and cholesterol. This drug acts by binding to the farnesoid X receptor (FXR), found in the nucleus of liver and intestinal cells, which in turn increases liver bile flow, suppressing its production and decreasing hepatocyte exposure to excess levels of bile with cholestasis. Cholestasis is a process that normally causes inflammation and cirrhosis of the liver.[A192792][L12633]
Obeticholic acid is a potent agonist of the farnesoid X receptor, which serves to regulate the hepatic metabolism of bile and cholesterol. This drug acts by binding to the farnesoid X receptor (FXR), found in the nucleus of liver and intestinal cells, which in turn increases liver bile flow, suppressing its production and decreasing hepatocyte exposure to excess levels of bile with cholestasis. Cholestasis is a process that normally causes inflammation and cirrhosis of the liver.[A192792][L12633]
Pharmacodynamics
The activation of the FXR by obeticholic acid acts to reduce the synthesis of bile acids, inflammation, and the resulting hepatic fibrosis. This may increase the survival of patients with PBC, but to date, an association between obeticholic acid and survival in PBC has not been established.[A192786][L12633]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Obeticholic acid is absorbed in the gastrointestinal tract. The Cmax of obeticholic acid occurs at approximately 1.5 hours after an oral dose and ranges from 28.8-53.7 ng/mL at doses of 5-10mg.
[L12735]
The median Tmax for both the conjugates of obeticholic acid is about 10 hours.
[L12633]
One product monograph reports a Tmax of 4.5h for both 5 and 10mg doses. The AUC ranged from 236.6-568.1 ng/h/mL with 5mg to 10 mg doses.
[L12735]
[L12735]
The median Tmax for both the conjugates of obeticholic acid is about 10 hours.
[L12633]
One product monograph reports a Tmax of 4.5h for both 5 and 10mg doses. The AUC ranged from 236.6-568.1 ng/h/mL with 5mg to 10 mg doses.
[L12735]
Half-life
The biological half-life of obeticholic acid is reported to be 24 hours.
[L12738]
[L12738]
Protein binding
Obeticholic acid and its metabolic conjugates are >99% plasma protein-bound.
[L12633][L12720]
[L12633][L12720]
Volume of distribution
The volume of distribution of obeticholic acid is 618 L.
[L12633][L12720]
[L12633][L12720]
Metabolism
The metabolism of obeticholic acid occurs in the liver. Obeticholic acid is conjugated with glycine or taurine, followed by secretion into bile. The conjugates are then absorbed in the small intestine and then re-enter the liver via enterohepatic circulation.
The intestinal microbiota in the ileum converts conjugated obeticholic acid in a deconjugated form that may be either reabsorbed or eliminated. Glycine conjugates account for 13.8% of the metabolites and taurine conjugates account for 12.3%. Another metabolite, 3-glucuronide, may also be formed, but displays little pharmacological activity.
[L12633]
The intestinal microbiota in the ileum converts conjugated obeticholic acid in a deconjugated form that may be either reabsorbed or eliminated. Glycine conjugates account for 13.8% of the metabolites and taurine conjugates account for 12.3%. Another metabolite, 3-glucuronide, may also be formed, but displays little pharmacological activity.
[L12633]
Route of elimination
About 87% of an orally administered dose is accounted for in the feces. Less than 3% of the dose can be recovered in the urine.
[L12633][L12720]
[L12633][L12720]
Clearance
Clearance information for obeticholic acid is not readily available in the literature.
[L12633][L12720]
[L12633][L12720]
Drug targets(1)
Proteins and enzymes this drug interacts with in the body
Bile acid receptor
NR1H4
agonist
Specific functionbile acid binding
Cellular location
Nucleus
General function & pharmacology
Ligand-activated transcription factor. Receptor for bile acids (BAs) such as chenodeoxycholic acid (CDCA), lithocholic acid, deoxycholic acid (DCA) and allocholic acid (ACA). Plays a essential role in BA homeostasis through the regulation of genes involved in BA synthesis, conjugation and enterohepatic circulation.
Also regulates lipid and glucose homeostasis and is involved innate immune response .
PMID:10334992 PMID:10334993 PMID:21383957 PMID:22820415
The FXR-RXR heterodimer binds predominantly to farnesoid X receptor response elements (FXREs) containing two inverted repeats of the consensus sequence 5'-AGGTCA-3' in which the monomers are spaced by 1 nucleotide (IR-1) but also to tandem repeat DR1 sites with lower affinity, and can be activated by either FXR or RXR-specific ligands. It is proposed that monomeric nuclear receptors such as NR5A2/LRH-1 bound to coregulatory nuclear responsive element (NRE) halfsites located in close proximity to FXREs modulate transcriptional activity (By similarity). In the liver activates transcription of the corepressor NR0B2 thereby indirectly inhibiting CYP7A1 and CYP8B1 (involved in BA synthesis) implicating at least in part histone demethylase KDM1A resulting in epigenomic repression, and SLC10A1/NTCP (involved in hepatic uptake of conjugated BAs).
Activates transcription of the repressor MAFG (involved in regulation of BA synthesis) (By similarity). Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine) .
PMID:12754200 PMID:15471871 PMID:17895379
Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine) .
PMID:10514450 PMID:15239098 PMID:16269519
In the intestine activates FGF19 expression and secretion leading to hepatic CYP7A1 repression .
PMID:12815072 PMID:19085950
The function also involves the coordinated induction of hepatic KLB/beta-klotho expression (By similarity). Regulates transcription of liver UGT2B4 and SULT2A1 involved in BA detoxification; binding to the UGT2B4 promoter seems to imply a monomeric transactivation independent of RXRA .
PMID:12806625 PMID:16946559
Modulates lipid homeostasis by activating liver NR0B2/SHP-mediated repression of SREBF1 (involved in de novo lipogenesis), expression of PLTP (involved in HDL formation), SCARB1 (involved in HDL hepatic uptake), APOE, APOC1, APOC4, PPARA (involved in beta-oxidation of fatty acids), VLDLR and SDC1 (involved in the hepatic uptake of LDL and IDL remnants), and inhibiting expression of MTTP (involved in VLDL assembly .
PMID:12554753 PMID:12660231 PMID:15337761
Increases expression of APOC2 (promoting lipoprotein lipase activity implicated in triglyceride clearance) .
PMID:11579204
Transrepresses APOA1 involving a monomeric competition with NR2A1 for binding to a DR1 element .
PMID:11927623 PMID:21804189
Also reduces triglyceride clearance by inhibiting expression of ANGPTL3 and APOC3 (both involved in inhibition of lipoprotein lipase) .
PMID:12891557
Involved in glucose homeostasis by modulating hepatic gluconeogenesis through activation of NR0B2/SHP-mediated repression of respective genes.
Modulates glycogen synthesis (inducing phosphorylation of glycogen synthase kinase-3) (By similarity). Modulates glucose-stimulated insulin secretion and is involved in insulin resistance .
PMID:20447400
Involved in intestinal innate immunity. Plays a role in protecting the distal small intestine against bacterial overgrowth and preservation of the epithelial barrier (By similarity).
Down-regulates inflammatory cytokine expression in several types of immune cells including macrophages and mononuclear cells .
PMID:21242261
Mediates trans-repression of TLR4-induced cytokine expression; the function seems to require its sumoylation and prevents N-CoR nuclear receptor corepressor clearance from target genes such as IL1B and NOS2 .
PMID:19864602
Involved in the TLR9-mediated protective mechanism in intestinal inflammation. Plays an anti-inflammatory role in liver inflammation; proposed to inhibit pro-inflammatory (but not antiapoptotic) NF-kappa-B signaling) (By similarity)
Also regulates lipid and glucose homeostasis and is involved innate immune response .
PMID:10334992 PMID:10334993 PMID:21383957 PMID:22820415
The FXR-RXR heterodimer binds predominantly to farnesoid X receptor response elements (FXREs) containing two inverted repeats of the consensus sequence 5'-AGGTCA-3' in which the monomers are spaced by 1 nucleotide (IR-1) but also to tandem repeat DR1 sites with lower affinity, and can be activated by either FXR or RXR-specific ligands. It is proposed that monomeric nuclear receptors such as NR5A2/LRH-1 bound to coregulatory nuclear responsive element (NRE) halfsites located in close proximity to FXREs modulate transcriptional activity (By similarity). In the liver activates transcription of the corepressor NR0B2 thereby indirectly inhibiting CYP7A1 and CYP8B1 (involved in BA synthesis) implicating at least in part histone demethylase KDM1A resulting in epigenomic repression, and SLC10A1/NTCP (involved in hepatic uptake of conjugated BAs).
Activates transcription of the repressor MAFG (involved in regulation of BA synthesis) (By similarity). Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine) .
PMID:12754200 PMID:15471871 PMID:17895379
Activates transcription of SLC27A5/BACS and BAAT (involved in BA conjugation), ABCB11/BSEP (involved in bile salt export) by directly recruiting histone methyltransferase CARM1, and ABCC2/MRP2 (involved in secretion of conjugated BAs) and ABCB4 (involved in secretion of phosphatidylcholine in the small intestine) .
PMID:10514450 PMID:15239098 PMID:16269519
In the intestine activates FGF19 expression and secretion leading to hepatic CYP7A1 repression .
PMID:12815072 PMID:19085950
The function also involves the coordinated induction of hepatic KLB/beta-klotho expression (By similarity). Regulates transcription of liver UGT2B4 and SULT2A1 involved in BA detoxification; binding to the UGT2B4 promoter seems to imply a monomeric transactivation independent of RXRA .
PMID:12806625 PMID:16946559
Modulates lipid homeostasis by activating liver NR0B2/SHP-mediated repression of SREBF1 (involved in de novo lipogenesis), expression of PLTP (involved in HDL formation), SCARB1 (involved in HDL hepatic uptake), APOE, APOC1, APOC4, PPARA (involved in beta-oxidation of fatty acids), VLDLR and SDC1 (involved in the hepatic uptake of LDL and IDL remnants), and inhibiting expression of MTTP (involved in VLDL assembly .
PMID:12554753 PMID:12660231 PMID:15337761
Increases expression of APOC2 (promoting lipoprotein lipase activity implicated in triglyceride clearance) .
PMID:11579204
Transrepresses APOA1 involving a monomeric competition with NR2A1 for binding to a DR1 element .
PMID:11927623 PMID:21804189
Also reduces triglyceride clearance by inhibiting expression of ANGPTL3 and APOC3 (both involved in inhibition of lipoprotein lipase) .
PMID:12891557
Involved in glucose homeostasis by modulating hepatic gluconeogenesis through activation of NR0B2/SHP-mediated repression of respective genes.
Modulates glycogen synthesis (inducing phosphorylation of glycogen synthase kinase-3) (By similarity). Modulates glucose-stimulated insulin secretion and is involved in insulin resistance .
PMID:20447400
Involved in intestinal innate immunity. Plays a role in protecting the distal small intestine against bacterial overgrowth and preservation of the epithelial barrier (By similarity).
Down-regulates inflammatory cytokine expression in several types of immune cells including macrophages and mononuclear cells .
PMID:21242261
Mediates trans-repression of TLR4-induced cytokine expression; the function seems to require its sumoylation and prevents N-CoR nuclear receptor corepressor clearance from target genes such as IL1B and NOS2 .
PMID:19864602
Involved in the TLR9-mediated protective mechanism in intestinal inflammation. Plays an anti-inflammatory role in liver inflammation; proposed to inhibit pro-inflammatory (but not antiapoptotic) NF-kappa-B signaling) (By similarity)
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP1A2Cytochrome P450 1A2
inhibitor
downregulator
Transporters(1)
Proteins that transport this drug across cell membranes
Bile salt export pump
ABCB11
inhibitor
inducer
Specific functionABC-type bile acid transporter activity
Cellular location
Apical cell membrane
General function & pharmacology
Catalyzes the transport of the major hydrophobic bile salts, such as taurine and glycine-conjugated cholic acid across the canalicular membrane of hepatocytes in an ATP-dependent manner, therefore participates in hepatic bile acid homeostasis and consequently to lipid homeostasis through regulation of biliary lipid secretion in a bile salts dependent manner .
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: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
Scientific references(7)
Markham A., Keam S.J.
Obeticholic Acid: First Global Approval.
Drugs
2016 Aug76(12):1221-6. doi: 10.1007/s40265-016-0616-x
Eslam M., Alvani R., Shiha G.
Obeticholic acid: towards first approval for NASH.
The Lancet
2019 Dec 14394(10215):2131-2133. doi: 10.1016/S0140-6736(19)32963-0. Epub 2019 Dec 5
Manne V., Kowdley K.V.
Obeticholic acid in primary biliary cholangitis: where we stand.
Curr Opinion Gastroenterol
2019 May35(3):191-196. doi: 10.1097/MOG.0000000000000525
Jones D.E.
Pathogenesis of primary biliary cirrhosis.
Gut
2007 Nov56(11):1615-24. doi: 10.1136/gut.2007.122150. Epub 2007 Jul 19
Onofrio F.Q., Hirschfield G.M., Gulamhusein A.F.
Primary biliary cholangitis: pathogenesis and therapeutic opportunities.
Nature Reviews Gastroenterology & Hepatology
202017(2):93-110. doi: 10.1038/s41575-019-0226-7
Bowlus C.L.
Obeticholic acid for the treatment of primary biliary cholangitis in adult patients: clinical utility and patient selection.
Hepat Medicine
2016 Sep 18:89-95. doi: 10.2147/HMER.S91709. eCollection 2016
Edwards J.E., LaCerte C., Peyret T., Gosselin N.H., Marier J.F., Hofmann A.F., Shapiro D.
Modeling and Experimental Studies of Obeticholic Acid Exposure and the Impact of Cirrhosis Stage.
Clinical Transl Science
2016 Dec9(6):328-336. doi: 10.1111/cts.12421. Epub 2016 Oct 15
ATC classification(1 code)
ATC A05AA04
International brands(1)
Experimental properties(4)
Commercial products(8)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Obeticholic acid
Additional database identifiers
Drugs Product Database (DPD)
22864
ChemSpider
394730
BindingDB
21675
PDB
CHC
ZINC
ZINC000014164617
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7967
GenAtlas
NR1H4
GeneCards
NR1H4
GenBank Gene Database
U68233
GenBank Protein Database
1546084
Guide to Pharmacology
603
UniProt Accession
NR1H4_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:42
GenAtlas
ABCB11
GeneCards
ABCB11
GenBank Gene Database
AF091582
GenBank Protein Database
3873243
Guide to Pharmacology
778
UniProt Accession
ABCBB_HUMAN
Patent information
7 active patents, 3 expired
10052337
United States
Approved 21 Aug 2018 · Expires 26 Apr 2036
10 years
10751349
United States
Approved 25 Aug 2020 · Expires 26 Apr 2036
10 years
10758549
United States
Approved 1 Sept 2020 · Expires 26 Apr 2036
10 years
10047117
United States
Approved 14 Aug 2018 · Expires 6 Sept 2033
7y 5m
9238673
United States
Approved 19 Jan 2016 · Expires 17 Jun 2033
7y 2m
The earliest active patent expires November 2027. Generic versions may become available after this date.
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)