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Author Notes:

Corresponding author: Bashar S Staitieh, MD, 615 Michael Street, Suite 205, Atlanta, GA 30322, TEL: 404-712-2970, FAX: 404-712-2974, bashar.staitieh@emory.edu.

Disclosures: ER has received speaker’s fees from AstraZeneca, Intermune and Takeda. SV has received consultancy fees from Intermune.

Subjects:

Research Funding:

BSS is supported by a training grant from the National Institutes of Health (T32 HL 076118-09).

ER is supported by the NIHR Respiratory Disease Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College London.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Medicine, General & Internal
  • General & Internal Medicine
  • Idiopathic pulmonary fibrosis
  • N-acetylcysteine
  • nintedanib
  • pirfenidone
  • prednisone
  • PLACEBO-CONTROLLED TRIAL
  • TUMOR-NECROSIS-FACTOR
  • INTERSTITIAL LUNG-DISEASES
  • RANDOMIZED-TRIAL
  • RECEPTOR ANTAGONIST
  • N-ACETYLCYSTEINE
  • INTERFERON-GAMMA
  • GENE-EXPRESSION
  • CLINICAL-COURSE
  • MESSENGER-RNA

Pharmacologic therapies for idiopathic pulmonary fibrosis, past and future

Tools:

Journal Title:

Annals of Medicine

Volume:

Volume 47, Number 2

Publisher:

, Pages 100-105

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Idiopathic pulmonary fibrosis (IPF) is a severe, progressive fibrotic disease of the lung of unknown etiology that affects approximately 150,000 patients in the United States. It carries a median survival of two to three years, but clinical course can vary markedly from patient to patient. There has been no established treatment for IPF, but recent advances in coordinated clinical trials through groups such as IPFnet and academia-industry partnerships have allowed this relatively rare disease to be studied in much greater depth. Historically, the default therapy for IPF was a combination of prednisone, N-acetylcysteine, and azathioprine, but recent trials have shown that this regimen actually increases mortality. An enormous body of work in recent years, spanning the bench to the bedside, has radically altered our understanding of the molecular mechanisms underlying IPF. Newer modalities, particularly those involving monoclonal antibodies targeted at specific pathways known to contribute to the fibrotic process, have generated a great deal of excitement in the field, and recent clinical trials on therapies such as pirfenidone and nintedanib herald a new era in targeted IPF therapies.

Copyright information:

© 2015 Informa UK, Ltd.

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