Article Text

Download PDFPDF

Repositioning compounds from cancer drug discovery to IPF: PI3K inhibition
  1. Claudia A Staab-Weijnitz,
  2. Oliver Eickelberg
  1. Comprehensive Pneumology Center, University Hospital, Ludwig-Maximilians-University and Helmholtz Zentrum München, Munich, Germany
  1. Correspondence to Professor Oliver Eickelberg, Comprehensive Pneumology Center, University Hospital, Ludwig-Maximilians-University and Helmholtz Zentrum München, Munich 81377, Germany; oliver.eickelberg{at}

Statistics from

Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease that presents with a 5-year survival of 20–30%, hence with a mortality rate as high as many aggressive cancer types.1 According to a current analysis by the British Lung Foundation, the incidence of IPF in the UK has long been underestimated ( In addition, a recent systematic review shows that IPF incidence rates have increased worldwide.2 Two recently approved treatments for IPF, pirfenidone and nintedanib, have been shown to decelerate lung function decline in IPF, but do not halt disease progression or cure the disease.3 ,4 Hence, there is a clear need for novel therapeutic strategies, which manifests in (at time of writing) 46 registered interventional clinical studies for IPF ( and a continued quest for novel drug targets by the scientific community, fuelled by an increased understanding of IPF pathogenesis.5 Considering the substantial pathological heterogeneity of IPF and the multitude of dysregulated signalling pathways,6 it is likely that a successful cure of IPF will involve not a single, but several active agents, specifically targeting different pathomechanistic aspects of IPF.

With de novo drug development being an expensive and time-consuming process, it seems highly sensible to examine whether effective treatment for other disease entities with significant pathomechanistic overlap with IPF is suitable for IPF therapy as well. Notably, repositioning of drugs can shorten drug development time by >50% as phases like chemical optimisation, safety assessment or pharmacokinetic (PK) profiling can be bypassed. …

View Full Text

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Linked Articles

  • Interstitial lung disease
    Paul F Mercer Hannah V Woodcock Jessica D Eley Manuela Platé Michal G Sulikowski Pascal F Durrenberger Linda Franklin Carmel B Nanthakumar Yim Man Federica Genovese Robin J McAnulty Shuying Yang Toby M Maher Andrew G Nicholson Andy D Blanchard Richard P Marshall Pauline T Lukey Rachel C Chambers
  • Airwaves
    BMJ Publishing Group Ltd and British Thoracic Society