ReviewDrug design, development and therapy2015
Idiopathic pulmonary fibrosis: current treatment options and critical appraisal of nintedanib.
Review in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 53 citations in OpenAlex.
- Nintedanib Attenuates Epidural Fibrosis after Laminectomy in Rats.Journal of Korean Neurosurgical Society · 2026Article
- Idiopathic Pulmonary Fibrosis, Today and Tomorrow: Certainties and New Therapeutic Horizons.Pulmonary therapy · 2025Review
- Early pirfenidone treatment enhances lung function in idiopathic pulmonary fibrosis patients.World journal of clinical cases · 2024Article
- Single-cell combined with transcriptome sequencing to explore the molecular mechanism of cell communication in idiopathic pulmonary fibrosis.Journal of cellular and molecular medicine · 2024Article
- DAB2 promotes pulmonary fibrosis and may act as an intermediate between IGF‑1R and PI3K/AKT signaling pathways.Experimental and therapeutic medicine · 2023Article
- Targeting the lung epithelium after intravenous delivery by directed evolution of underexplored sites on the AAV capsid.Molecular therapy. Methods & clinical development · 2022Article
- The Inflammasome NLR Family Pyrin Domain-Containing Protein 3 (NLRP3) as a Novel Therapeutic Target for Idiopathic Pulmonary Fibrosis.The American journal of pathology · 2022Review
- Blockade of the pro-fibrotic reaction mediated by the miR-143/-145 cluster enhances the responses to targeted therapy in melanoma.EMBO molecular medicine · 2022Article
- Antifibrotic drugs as therapeutic tools in resistant melanoma.EMBO molecular medicine · 2022Article
- Analysis of the safety and efficacy of different plasma concentrations of pirfenidone in patients with idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2022Article
- The Anti-Fibrotic Effect of Cold Atmospheric Plasma on Localized Scleroderma In Vitro and In Vivo.Biomedicines · 2021Article
- Age-Related Dynamics of Lung-Resident Memory CD8Frontiers in immunology · 2021Review
- Article
- Cyclic Stretching of Fibrotic Microtissue Array for Evaluation of Anti-Fibrosis Drugs.Cellular and molecular bioengineering · 2019Article
- Role of fibroblast growth factor 23 and klotho cross talk in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Hydrogel-based delivery of Il-10 improves treatment of bleomycin-induced lung fibrosis in mice.Biomaterials · 2019Article
- Idiopathic and immune-related pulmonary fibrosis: diagnostic and therapeutic challenges.Clinical & translational immunology · 2019Review
- Human microvasculature-on-a chip: anti-neovasculogenic effect of nintedanib in vitro.Angiogenesis · 2018Article
- Small Molecule Tyrosine Kinase Inhibitor Nintedanib Reduces Development of Cardiac Allograft Vasculopathy in Murine Aortic Allografts.Transplantation direct · 2018Article
- Anti-fibrotic nintedanib-a new opportunity for systemic sclerosis patients?Clinical rheumatology · 2018Review
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is the most common type of idiopathic interstitial pneumonia and is characterized by a poor prognosis, with an estimated 5-year survival of approximately 20%. Progressive and irreversible lung functional impairment leads to chronic respiratory insufficiency with a severely impaired quality of life. In the last 2 decades, novel treatments for IPF have been developed as a consequence of an increasing understanding of disease pathogenesis and pathobiology. In IPF, injured dysfunctional alveolar epithelial cells promote fibroblast recruitment and proliferation, resulting in scarring of the lung tissue. Recently, pirfenidone and nintedanib have been approved for the treatment of IPF, having shown efficacy to slow functional decline and disease progression. This article focuses on the pharmacologic characteristics and clinical evidence supporting the use of nintedanib, a potent small-molecule tyrosine kinase inhibitor, as therapy for IPF. After introducing the mechanism of action and pharmacokinetics, an overview of the safety and efficacy results from the most recent clinical trials of nintedanib in IPF is presented.
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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.