ReviewCore evidence2015
Nintedanib: evidence for its therapeutic potential in idiopathic pulmonary fibrosis.
Review in Core evidence, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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.
Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Beyond scarring: a next-generation vision for pulmonary fibrosis management.Molecular biology reports · 2026Review
- Baseline neutrophil-to-lymphocyte ratio predicts survival time after the initiation of nintedanib in patients with interstitial lung disease.BMC pulmonary medicine · 2026Article
- Prognostic factors in patients with interstitial lung disease treated with nintedanib: a multicenter retrospective study in Japan.Scientific reports · 2025Article
- In Vivo Target Engagement Assessment of Nintedanib in a Double-Hit Bleomycin Lung Fibrosis Rat Model.International journal of molecular sciences · 2025Article
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- Circulating biomarkers in patients with progressive fibrosing interstitial lung disease treated with nintedanib: a pilot study.Scientific reports · 2025Article
- Perioperative nintedanib for lung resection in patients with idiopathic pulmonary fibrosis.Molecular and clinical oncology · 2025Article
- Nintedanib administration after the onset of acute exacerbation of interstitial lung disease in the real world.Scientific reports · 2023Article
- Effect of a novel tyrosine kinase inhibitor nintedanib on bFGF and VEGF concentrations in a rabbit retinal vein occlusion model.International journal of ophthalmology · 2023Article
- Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Novel oxindole/benzofuran hybrids as potential dual CDK2/GSK-3β inhibitors targeting breast cancer: design, synthesis, biological evaluation, andJournal of enzyme inhibition and medicinal chemistry · 2021Article
- Clinical Significance of Continuable Treatment with Nintedanib Over 12 Months for Idiopathic Pulmonary Fibrosis in a Real-World Setting.Drug design, development and therapy · 2021Article
- Scarred Lung. An Update on Radiation-Induced Pulmonary Fibrosis.Frontiers in medicine · 2020Review
- Nintedanib ameliorates tracheal stenosis by activating HDAC2 and suppressing IL-8 and VEGF in rabbit.American journal of translational research · 2020Article
- Article
- Effects of PARP-1 Deficiency and Histamine HFrontiers in pharmacology · 2019Article
- Protective Effects of Nintedanib against Polyhexamethylene Guanidine Phosphate-Induced Lung Fibrosis in Mice.Molecules (Basel, Switzerland) · 2018Article
- Nintedanib reduces pulmonary fibrosis in a model of rheumatoid arthritis-associated interstitial lung disease.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Anti-fibrotic efficacy of nintedanib in pulmonary fibrosis via the inhibition of fibrocyte activity.Respiratory research · 2017Article
- Aliskiren attenuates bleomycin-induced pulmonary fibrosis in rats: focus on oxidative stress, advanced glycation end products, and matrix metalloproteinase-9.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive disease with poor prognosis. The molecular mechanisms involved in the progression of IPF are not fully understood; however, the platelet-derived growth factor (PDGF)/PDGF receptor pathway is thought to play a critical role in fibrogenesis of the lungs. Other growth factors, including fibroblast growth factor and vascular endothelial growth factor, are also thought to contribute to the pathogenesis of pulmonary fibrosis. Nintedanib is an inhibitor of multiple tyrosine kinases, including receptors for PDGF, fibroblast growth factor, and vascular endothelial growth factor. In the Phase II TOMORROW trial, treatment with 150 mg of nintedanib twice daily showed a trend to slow the decline in lung function and significantly decrease acute exacerbations in patients with IPF, while showing an acceptable safety profile. The Phase III INPULSIS trials demonstrated a significant decrease in the annual rate of decline in forced vital capacity in IPF patients treated with 150 mg nintedanib twice daily. In the INPULSIS-2 trial, the time to the first acute exacerbation significantly increased in IPF patients who were treated with 150 mg of nintedanib twice daily. Pirfenidone, another antifibrotic drug, was shown to limit the decline in pulmonary function in patients with IPF in the ASCEND trial. Combination therapy with nintedanib and pirfenidone is anticipated, although further evaluation of its long-term safety is needed. There is limited evidence for the safety of the combination therapy although a Phase II trial conducted in Japan demonstrated that combination therapy with nintedanib and pirfenidone was tolerable for 1 month. Available antifibrotic agents (ie, pirfenidone and N-acetylcysteine) have limited efficacy as single therapies for IPF; therefore, further study of combination therapy with antifibrotic agents is needed.
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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.