Reducing lung function decline in patients with idiopathic pulmonary fibrosis: potential of nintedanib
Hannah V Woodcock,1,2 Philip L Molyneaux,1,3 Toby M Maher1–3
1Interstitial Lung Disease Unit, Royal Brompton Hospital, 2Centre for Respiratory Research, University College London, 3National Heart and Lung Institute, Imperial College London, London, UK
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.
Keywords: interstitial lung disease, BIBF 1120, clinical trials, usual interstitial pneumonia, acute exacerbation
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