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Gastroenterology · Clinical trials

Primary Biliary Cholangitis Clinical Trials

Approved therapies, the pivotal-trial endpoints they were judged on, the magnitude of benefit — and the drugs that failed their endpoints, and why.

Indication overview

About primary biliary cholangitis — and why its trials are hard

Primary biliary cholangitis (PBC) is a chronic autoimmune cholestatic liver disease in which progressive destruction of small intrahepatic bile ducts leads to cholestasis, fibrosis, and potentially cirrhosis; it predominantly affects women and often presents with fatigue and pruritus and a raised alkaline phosphatase (ALP). Ursodeoxycholic acid (UDCA) is first-line and improves survival, but a substantial minority have an inadequate biochemical response and need second-line therapy. Obeticholic acid, an FXR agonist, gained accelerated approval in 2016 based on ALP reduction, but subsequent safety concerns led the FDA to restrict its use in 2024 and the drug was ultimately withdrawn from the US market after its confirmatory trial failed to verify clinical benefit. Two PPAR agonists received accelerated approval in 2024: elafibranor (a PPAR alpha/delta agonist) and seladelpar (a PPAR delta agonist), both used with or without UDCA. Regulatory endpoints use a composite biochemical response built on ALP and bilirubin, with pruritus increasingly assessed as a key patient-reported outcome.

Indication
Primary Biliary Cholangitis
ICD-10-CM
K74.3 — Primary biliary cholangitis

Approved therapies & pivotal evidence

What's been approved — and by how much it moved the endpoint

Drug (brand)ApprovedSettingPivotal trialPrimary endpointMagnitude of benefit
Ursodeoxycholic acid (Actigall/URSO)1997First-line PBC; hydrophilic bile acidPooled analyses of randomized trials and long-term cohortsBiochemical response (ALP/bilirubin) and transplant-free survivalImproves biochemistry and survival; ~30-40% have inadequate response requiring add-on therapy
Obeticholic acid (Ocaliva)2016Second-line PBC (accelerated approval); FXR agonist. FDA restricted use in advanced cirrhosis in 2024 and the drug was subsequently withdrawn from the US marketPOISE (Phase 3)Composite: ALP <1.67x ULN with >=15% reduction and normal total bilirubin at 12 months~46-47% vs ~10% placebo (dose-dependent pruritus a major issue)
Elafibranor (Iqirvo)2024Second-line PBC with UDCA or as monotherapy if UDCA-intolerant (accelerated approval); PPAR alpha/delta agonistELATIVE (Phase 3)Composite biochemical response at week 52 (ALP <1.67x ULN, >=15% ALP decrease, normal total bilirubin)~51% vs ~4% placebo
Seladelpar (Livdelzi)2024Second-line PBC with UDCA or as monotherapy if UDCA-intolerant (accelerated approval); PPAR delta agonistRESPONSE (Phase 3, NEJM 2024)Composite biochemical response at month 12; key secondaries ALP normalization and pruritus (NRS) changeComposite ~61.7% vs 20% placebo; ALP normalization ~25% vs 0%; significant pruritus improvement

Where trials have failed

Drugs that missed their endpoint — and what contributed

The most instructive lessons in primary biliary cholangitis development come from programmes that failed the endpoint that mattered.

Drug / trialEndpoint outcomeWhat contributed
Obeticholic acid (confirmatory) — COBALT confirmatory outcomes trialDid not verify the predicted clinical benefit required to confirm accelerated approval; combined with hepatotoxicity signals this led to 2024 FDA restrictions and US market withdrawalReliance on an ALP-based surrogate, confounding from off-study therapy, and serious liver-injury reports in the post-marketing period
Setanaxib (GKT831) — Phase 2 in PBC (NADPH oxidase 1/4 inhibitor)Did not clearly meet its primary biochemical endpoint across the overall population; further PBC development was not advanced on those resultsModest and subgroup-limited effect on cholestatic markers (exact magnitude unverified)

Choosing the right endpoint

Primary endpoints that matter in primary biliary cholangitis trials

  • Composite biochemical response — ALP threshold (e.g., <1.67x ULN with >=15% reduction) plus normal bilirubin at 12 months; the standard accelerated-approval endpoint.
  • ALP normalization — Return of alkaline phosphatase to the normal range, a more stringent secondary marker associated with better prognosis.
  • Pruritus (NRS) — Patient-reported itch severity; a key symptom endpoint where PPAR agonists showed benefit and FXR agonists worsened it.
  • Transplant-free survival — Long-term clinical outcome underpinning UDCA's benefit and the goal that surrogate endpoints aim to predict.

How iNGENū runs primary biliary cholangitis trials

Physician-led design, built for FDA submission

Endpoint & biomarker strategy

Board-certified specialists design endpoints and patient selection aligned to current FDA guidance for this indication.

FDA-ready data

Built to ICH-GCP and 21 CFR 312.120, with direct FDA submission — data accepted by the FDA, EMA and MHRA.

Faster, lower-cost delivery

~4-week ethics via the TGA CTN scheme, up to 43.5% R&D rebate, and 80–90% below US CRO cost.

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Frequently asked questions

Primary Biliary Cholangitis clinical trials — FAQs

What is the first-line treatment for PBC?
Ursodeoxycholic acid (UDCA) is first-line and improves biochemistry and transplant-free survival. Roughly a third of patients respond inadequately and need a second-line agent.
What changed for obeticholic acid?
After 2016 accelerated approval based on ALP reduction, its confirmatory trial failed to verify clinical benefit and serious liver-injury signals emerged, leading to 2024 FDA restrictions and eventual US market withdrawal.
How do the 2024 PPAR agonists differ from obeticholic acid on itch?
Elafibranor and seladelpar tended to improve or not worsen pruritus, whereas obeticholic acid frequently caused dose-dependent itching, a meaningful tolerability advantage for the newer agents.

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