Evidence map›Paper›PMID 41736725›Full record

ArticleERJ open research2026

Circulating biomarkers in subjects with progressive pulmonary fibrosis: data from the INBUILD trial.

Toby M Maher, R Gisli Jenkins, Francesco Bonella, Shervin Assassi, Claudia Diefenbach, Carina Ittrich, Klaus B Rohr, Martin Kolb

Abstract read
In one paragraph

Article in ERJ open research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Prevalence and Prognostic Impact of Progressive Pulmonary Fibrosis.Tuberculosis and respiratory diseases · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Toby M MaherNational Heart and Lung Institute, Imperial College London, London, UK.ORCID https://orcid.org/0000-0001-7192-9149
R Gisli JenkinsNational Heart and Lung Institute, Imperial College London, London, UK.
Francesco BonellaCenter for Interstitial and Rare Lung Diseases, Ruhrlandklinik University Hospital, Duisburg-Essen University, Essen, Germany.ORCID https://orcid.org/0000-0001-7579-9767
Shervin AssassiDivision of Rheumatology, University of Texas McGovern Medical School, Houston, TX, USA.ORCID https://orcid.org/0000-0002-8059-9978
Claudia DiefenbachBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Carina IttrichBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Klaus B RohrBoehringer Ingelheim International GmbH, Ingelheim am Rhein, Germany.
Martin KolbMcMaster University and St Joseph's Healthcare, Hamilton, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: We investigated the prognostic potential of circulating biomarkers at baseline and the effects of nintedanib on changes in these biomarkers in subjects with progressive pulmonary fibrosis (PPF). Methods: In the INBUILD trial, subjects with PPF received nintedanib (n=332) or placebo (n=331). Associations between biomarker levels at baseline and the rate of forced vital capacity (FVC) decline (mL·year Results: Baseline level of s-ICAM was significantly associated with rate of FVC decline and time to ILD progression or death over 52 weeks in the placebo group. No biomarker was significantly associated with time to first acute exacerbation or death or time to death. Decreases in Krebs von den Lungen-6 (KL-6), surfactant protein D (SP-D), CA-125 and CA19-9 were observed in subjects who received nintedanib Conclusions: In subjects with PPF, nintedanib reduced circulating CA-125 and, to a lesser extent, other markers of epithelial dysfunction.

Identifiers

PMID41736725
PMCPMC12926820

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.