Evidence map›Paper›PMID 25745043›Full record

ReviewThe European respiratory journal2015

Mode of action of nintedanib in the treatment of idiopathic pulmonary fibrosis.

Lutz Wollin, Eva Wex, Alexander Pautsch, Gisela Schnapp, Katrin E Hostettler, Susanne Stowasser, Martin Kolb

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in The European respiratory journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03562416 (Nintedanib Plus Usual Transplant Care Compared to Usual Transplant Care Alone After Single Lung Transplantation in Patients With Idiopathic Pulmonary Fibrosis), which is not on this map. Cited by 523 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
523citing papers in PubMed, 3 pooled it
39.7field-weighted citation impact, top 1% of its field
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.

NCT03562416 phase2terminatednot on this mapstarted 2019, after this paper: background citation

Nintedanib Plus Usual Transplant Care Compared to Usual Transplant Care Alone After Single Lung Transplantation in Patients With Idiopathic Pulmonary Fibrosis: a Pilot Randomized Controlled Trial

TypeinterventionalSponsorTemple UniversityRan2019 to 2021Enrolled1ConditionsIdiopathic Pulmonary Fibrosis, Lung Transplant, ComplicationsArmsNintedanib, Placebo Oral Tablet
3 · Its place in the literature

Who cites it

523 citing papers in PubMed, 3 syntheses or guidelines pooled it, 957 citations in OpenAlex.

  1. Pooled it
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  8. Biomarkers associated with pulmonary exacerbations in a randomized trial of nintedanib for radiation pneumonitis.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2024
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463 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 3 countries.

Lutz WollinBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany Stefan-lutz.wollin@boehringer-ingelheim.com.
Eva WexBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany.
Alexander PautschBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany.
Gisela SchnappBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach, Germany.
Katrin E HostettlerUniversity Hospital Basel, Basel, Switzerland.
Susanne StowasserBoehringer Ingelheim Pharma GmbH & Co. KG, Ingelheim am Rhein, Germany.
Martin KolbMcMaster University, Hamilton, ON, Canada.
Boehringer Ingelheim (Germany) · DEMcMaster University · CAUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal disease characterised by fibrosis of the lung parenchyma and loss of lung function. Although the pathogenic pathways involved in IPF have not been fully elucidated, IPF is believed to be caused by repetitive alveolar epithelial cell injury and dysregulated repair, in which there is uncontrolled proliferation of lung fibroblasts and differentiation of fibroblasts into myofibroblasts, which excessively deposit extracellular matrix (ECM) proteins in the interstitial space. A number of profibrotic mediators including platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and transforming growth factor-β are believed to play important roles in the pathogenesis of IPF. Nintedanib is a potent small molecule inhibitor of the receptor tyrosine kinases PDGF receptor, FGF receptor and vascular endothelial growth factor receptor. Data from in vitro studies have shown that nintedanib interferes with processes active in fibrosis such as fibroblast proliferation, migration and differentiation, and the secretion of ECM. In addition, nintedanib has shown consistent anti-fibrotic and anti-inflammatory activity in animal models of lung fibrosis. These data provide a strong rationale for the clinical efficacy of nintedanib in patients with IPF, which has recently been demonstrated in phase III clinical trials.

Indexed as

AnimalsApoptosisBleomycinCell DifferentiationCell ProliferationClinical Trials as TopicEnzyme InhibitorsExtracellular MatrixFibroblast Growth FactorsFibroblastsFibrosisHumansIdiopathic Pulmonary FibrosisIndolesLungLung DiseasesBleomycinEnzyme InhibitorsFibroblast Growth FactorsIndolesnintedanibPlatelet-Derived Growth FactorSilicon DioxideTransforming Growth Factor beta

Identifiers

PMID25745043
PMCPMC4416110
OpenAlexW2120791222

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.