Medicine · Pulmonology (Asthma, COPD, Tuberculosis, Pneumonia, ILD, Pleural Diseases)

A 62-year-old woman with IPF has been on nintedanib for 8 months. Her FVC decline over 12 months was 180 mL (>100 mL decline = clinically significant). Which statement about nintedanib's mechanism in IPF is correct?

  • A Nintedanib is an antifibrotic that blocks TGF-β receptor directly
  • B Nintedanib inhibits tyrosine kinases including VEGFR, PDGFR, and FGFR, slowing FVC decline
  • C Nintedanib reverses existing fibrosis by activating matrix metalloproteinases
  • D Nintedanib acts by blocking IL-13 signalling in alveolar macrophages
Correct answer: B. Nintedanib inhibits tyrosine kinases including VEGFR, PDGFR, and FGFR, slowing FVC decline

Explanation

Nintedanib is a triple angiokinase tyrosine kinase inhibitor (VEGFR-1/2/3, PDGFR-α/β, FGFR-1/2/3) that slows IPF progression by inhibiting fibroblast proliferation and differentiation. In the INPULSIS trials, nintedanib reduced annual FVC decline by ~125 mL compared to placebo. It does not reverse fibrosis. Pirfenidone acts via TGF-β modulation; anti-IL-13 therapies (e.g., tralokinumab) were investigated but not established for IPF.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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