ReviewDrug design, development and therapy2013
Reducing lung function decline in patients with idiopathic pulmonary fibrosis: potential of nintedanib.
Review in Drug design, development and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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
15 citing papers in PubMed, 46 citations in OpenAlex.
- Discovery of indolylchalcone benzenesulfonamides as selective inhibitors of tumor-associated carbonic anhydrase IX and XII.Scientific reports · 2026Article
- Article
- Nintedanib Ameliorates Bleomycin-Induced Pulmonary Fibrosis, Inflammation, Apoptosis, and Oxidative Stress by Modulating PI3K/Akt/mTOR Pathway in Mice.Inflammation · 2023Article
- Indole Antitumor Agents in Nanotechnology Formulations: An Overview.Pharmaceutics · 2023Review
- Preparation and Study of Folate Modified Albumin Targeting Microspheres.Journal of oncology · 2022Article
- Synergistic Inhibition of Renal Fibrosis by Nintedanib and Gefitinib in a Murine Model of Obstructive Nephropathy.Kidney diseases (Basel, Switzerland) · 2021Article
- Application of nintedanib and other potential anti-fibrotic agents in fibrotic diseases.Clinical science (London, England : 1979) · 2019Review
- Role of Receptor Tyrosine Kinase Signaling in Renal Fibrosis.International journal of molecular sciences · 2016Review
- Increased FGF1-FGFRc expression in idiopathic pulmonary fibrosis.Respiratory research · 2015Article
- Attenuating endogenous Fgfr2b ligands during bleomycin-induced lung fibrosis does not compromise murine lung repair.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Acute exacerbation of idiopathic pulmonary fibrosis-a review of current and novel pharmacotherapies.Journal of thoracic disease · 2015Review
- Nintedanib: first global approval.Drugs · 2015Article
- The treatment of idiopathic pulmonary fibrosis.F1000prime reports · 2014Review
- Protective role of andrographolide in bleomycin-induced pulmonary fibrosis in mice.International journal of molecular sciences · 2013Article
- Real-World Experience with Nintedanib in Patients with Idiopathic Pulmonary Fibrosis.Respiration; international review of thoracic diseasesArticle
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
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic lung disease with no clear etiology and a paucity of therapeutic options. Nintedanib (previously known as BIBF 1120) is a tyrosine kinase receptor antagonist which inhibits a number of key receptors, including those for platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF). These growth factors are profibrotic and each has been investigated as a potential standalone therapeutic target in IPF. Simultaneous inhibition of these receptors, with an analog of nintedanib, has proved to be effective in experimental animal models of pulmonary fibrosis. This observation, together with extensive safety and pharmacokinetic data from studies of nintedanib in malignancy, paved the way for the clinical development of this drug in IPF. The Phase IIb TOMORROW trial demonstrated that treatment with nintedanib may potentially slow decline in lung function, decrease the frequency of acute exacerbations, and improve quality of life in patients with IPF. While these observations are drawn from a single clinical trial, taken together with the preclinical data they suggest that nintedanib may yet become an important therapeutic option for individuals with IPF. The results of ongoing parallel, international, multicenter Phase III clinical trials are therefore eagerly awaited.
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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.