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INTRODUCTION Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease often managed with Nintedanib, a tyrosine kinase inhibitor targeting several profibrotic pathways. Although clotting processes are involved in wound healing and repair in the lung, there is no data on the role of antithrombin III on in IPF patients treated with Nintedanib. A previous proteomic analysis of serum of IPF patients before and after one year of Nintedanib treatment showed differential protein expression of antithrombin III. AIMS Here we used quant