• Peer-reviewed Viewpoint ‘Fibrosis extent on HRCT: the principal structural imaging biomarker for antifibrotic trials’ presents argument for measuring both lung function and fibrosis extent in antifibrotic trials
• Evaluation of evidence from multiple studies positions fibrosis extent as the strongest candidate for a new defined structural imaging endpoint and for a staged FDA qualification programme

Cambridge, UK, 2 November 2026 – Qureight, an end-to-end imaging company providing enterprise-grade imaging and precision endpoints for clinical trials for lung and heart disease, today announced the publication of a peer-reviewed Viewpoint¹ in the European Respiratory Journal (ERJ). The paper provides a scientific and regulatory argument that fibrosis extent should be considered the principal structural imaging biomarker in antifibrotic clinical trials and the leading imaging candidate for FDA biomarker qualification. 

In fibrotic interstitial lung disease (ILD), pulmonary fibrosis is the build-up of scar tissue that distorts the lung and progressively removes functioning tissue. Forced vital capacity (FVC) is the current registrational primary endpoint in antifibrotic trials and has been central to the approval and adoption of several drugs in fibrotic ILD. However, FVC is a downstream measure of overall lung function, influenced by more than fibrosis alone. In the Viewpoint, titled ‘Fibrosis extent on HRCT: the principal structural imaging biomarker for antifibrotic trials’, Qureight CSO, Dr Simon Walsh explains how measuring the structural disease process directly by fibrosis extent, as determined using imaging biomarkers for quantitative high-resolution computed tomography (HRCT), can complement FVC, giving clinical trial sponsors a more biologically proximate view of whether a therapy is slowing pulmonary fibrosis.

For fibrosis extent to become a surrogate endpoint in antifibrotic trials, Qureight explains that a more robust body of evidence is required. This includes trial-level data showing a clear association between treatment-driven changes in the rate of fibrosis accumulation and evidence that treatment-induced attenuation of fibrosis progression predicts how patients feel, function, or survive.

Simon Walsh, MD, PhD, Chief Scientific Officer, Qureight, commented: “If an antifibrotic is designed to slow the accumulation of scar tissue, trials should measure that scar tissue directly. Quantitative HRCT can show structural disease change that lung-function testing alone cannot. The opportunity now is to build the regulator-facing evidence needed to use fibrosis burden consistently and confidently across trials.”

Walsh, SLF et al. (2026). Fibrosis extent on HRCT: the principal structural imaging biomarker for antifibrotic trials. European Respiratory Journal, 2601645. https://doi.org/10.1183/13993003.01645-2026