CHAMGAP
APPROVEDReviewed and approved by the Chamgap Editorial Team (2026-07-24). The draft was written by AI, the existence of all 4 cited sources was verified at the original page, and the verdict passed blind grading and adversarial audit. Methodology v0.6.
Verdict No. 1646 · Search date 2026-07-24 · Methodology v0.6

Obeticholic acid,
does it really help with Prevention of clinical progression, including death, transplantation, and hepatic decompensation, in primary biliary cholangitis with inadequate response to UDCA?

30-Second Summary
D
Evidence Grade D · 25 · Safety unknown
Liver tests improved, but the confirmatory trial did not show slower clinical progression
What the
research shows
Obeticholic acid is rated D because it improved liver-test surrogate outcomes in primary biliary cholangitis but did not confirm prevention of patient-important clinical progression. The peer-reviewed POISE original report succeeded on its ALP-and-bilirubin primary surrogate endpoint in the actual ITT population of 216. The peer-reviewed confirmatory COBALT trial then failed its composite primary clinical-event endpoint in the actual randomized ITT analysis of 334 participants: HR 1.01 (95% CI 0.68 to 1.51). In plain terms, liver tests improved, but patient outcomes did not. European Union authorization was revoked, and the FDA warns about serious liver injury.
What the
ads claim
Marketing can convert reductions in ALP and bilirubin directly into prevention of decompensation, transplantation, and death. The evidence instead shows that liver tests improved while patient outcomes did not, and the randomized clinical-event confirmatory primary endpoint failed.
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Useful facts when choosing a product

  • Obeticholic acid is an FXR agonist and has commonly been started at 5 mg orally once daily in PBC, with adjustment according to response and tolerability.
  • POISE established a biochemical surrogate response involving ALP and bilirubin, not reductions in death, liver transplantation, or hepatic decompensation.
  • The conditional European Union marketing authorization was revoked in 2024 because clinical benefit remained unconfirmed; current national authorization and availability require separate checking.
  • Liver function requires close monitoring, and the medicine is contraindicated in advanced cirrhosis, current or previous hepatic decompensation, or evidence of portal hypertension.
Gap Measurement · Verdict 1646 · D 25
What advertising claims
What independent, higher-quality research supports
△ GAP
01

What the research actually shows

POISE was a peer-reviewed 12-month phase 3 randomized double-blind placebo-controlled original report; its actual 216-participant ITT analysis met the biochemical primary endpoint. COBALT was the peer-reviewed postmarketing clinical-event confirmatory trial; its actual randomized 334-participant ITT primary analysis failed, with event rates of 28.6% and 28.9% and HR 1.01. The trial ended early amid crossover, and the external-control analysis remains vulnerable to observational bias. EMA revoked the conditional European Union authorization in 2024 for unconfirmed clinical benefit, while the FDA warned in 2024 of serious liver injury even in patients without cirrhosis.

02

Why this is classified as D (25)

POISE met a surrogate primary endpoint, whereas the COBALT clinical-event composite primary endpoint failed in the actual 334-participant randomized ITT analysis with HR 1.01. Surrogate-based accelerated or conditional approval followed by confirmatory failure gives D with 25 points. Elafibranor in verdict 1605, which is C with 50 points, is in the same indication but still lacks a clinical-event confirmatory trial; obeticholic acid differs because its confirmatory trial was conducted and failed.

Counterpoint. The biochemical response is real and clinical value may remain possible for some patients. Serious liver risk and authorization status make this a specialist decision rather than a self-treatment option.

Rejudgment record. New verdict — Accepted POISE surrogate-primary success but prioritized failure of the clinical-event composite primary endpoint in the 334-participant randomized ITT COBALT analysis under rule ①-ⓐ and the confirmatory-failure criterion

Sub-claim grades by effect

This ingredient is marketed for several effects. A single overall grade blends strong and weak claims together, so each effect is graded separately here. The overall grade reflects the strongest disconfirming or core claim.

Effect (sub-claim)GradeBasis
Prevention of PBC clinical progression including death, transplantation, and hepatic decompensationDThe COBALT clinical-event composite primary endpoint failed in 334 randomized ITT participants with HR 1.01.
Improvement in biochemical ALP and bilirubin responseCPOISE succeeded in 216 participants, but this is a surrogate for clinical benefit.
Prevention of hospitalization for hepatic decompensationDThe prespecified COBALT primary composite containing this event was null.

Cross-check — Codex and Claude

This verdict was drafted by Codex through literature review and source-existence checks, cross-checked through blind grading and adversarial audit, and settled by reapplying the methodology boundary rules. Cases with split grades were resolved through rejudgment.
03

Evidence Table

StudyDesignSampleFundingEndpointResultWeight
Nevens F et al.; POISE Study Group. 2016Peer-reviewed phase 3 randomized double-blind placebo-controlled original report216Intercept PharmaceuticalsBiochemical composite primary endpoint of ALP and bilirubinThe primary endpoint succeeded; approximately 46% to 47% in active groups versus 10% with placebo. It was a surrogate, not a clinical event.Pivotal surrogate-efficacy trial
Kowdley KV et al. COBALT. 2025Peer-reviewed randomized placebo-controlled confirmatory original report166Intercept PharmaceuticalsPrimary composite of death, liver transplantation, MELD at least 15, uncontrolled ascites, or hospitalization for hepatic decompensationThe primary endpoint failed: 28.6% versus 28.9%, ITT HR 1.01 (95% CI 0.68 to 1.51).Decisive clinical confirmatory trial
EMA Ocaliva Article 20 procedure. 2024Regulatory review and final European Commission decisionEuropean Medicines AgencyVerification of clinical benefit required for conditional authorizationEuropean Union marketing authorization was revoked after confirmatory failure and insufficient supportive evidence.Regulatory context, not a substitute for trial results
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Receipt — 4 References

All 4 cited sources were verified for existence at the original page (as of 2026-07-24).

Nevens F, Andreone P, Mazzella G, et al.; POISE Study Group. A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis. N Engl J Med. 2016;375(7):631-643. PMID: 27532829. DOI: 10.1056/NEJMoa1509840.
checked
Kowdley KV, Hirschfield GM, Coombs C, et al. COBALT: A Confirmatory Trial of Obeticholic Acid in Primary Biliary Cholangitis With Placebo and External Controls. Am J Gastroenterol. 2025;120(2):390-400. PMID: 39140490. PMCID: PMC11774195. DOI: 10.14309/ajg.0000000000003029.
checked
European Medicines Agency. Ocaliva Article 20 procedure: Revocation of conditional marketing authorisation for Ocaliva. EMA/556104/2024. European Commission decision, 30 August 2024. PMID: none. DOI: none.
checked
U.S. Food and Drug Administration. Ocaliva (obeticholic acid): Drug Safety Communication—Serious Liver Injury Being Observed in Patients without Cirrhosis. 12 December 2024. PMID: none. DOI: none.
checked
Draft and rewrite: Codex (AI) · Verification: Codex blind grading and adversarial audit · Final adjudication: Claude
Reviewed and approved: Chamgap Editorial Team · Approval date: 2026-07-24 · Corrections: none

Cite this verdict

Obeticholic acid x prevention of clinical progression in PBC Evidence Grade D card
[Chamgap] Obeticholic acid x prevention of clinical progression in PBC — Evidence Grade D·25. 4 cited sources checked. Source: https://chamgap.com/en/verdicts/liver/obeticholic-acid-pbc-clinical-progression/ · CC BY 4.0

CC BY 4.0 — free to use with attribution; do not distort grades, numbers, or verdict meaning.

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Chamgap is an information source. It reports what research has and has not confirmed; it does not tell readers what to take or buy. That decision belongs to readers and, when needed, medical or legal professionals. This verdict reflects literature available up to the search date and may change as new research appears. Nothing here is medical advice.