Qureight has published a peer‑reviewed viewpoint arguing that fibrosis extent should become the principal structural imaging biomarker in antifibrotic clinical trials.
The Cambridge‑based imaging company said the paper sets out a scientific and regulatory case for positioning fibrosis burden as the leading candidate for FDA biomarker qualification.
In fibrotic interstitial lung disease, pulmonary fibrosis causes scar tissue to accumulate, distorting the lung and reducing functioning tissue. Forced vital capacity is currently the primary registrational endpoint in antifibrotic trials. It has supported the approval and adoption of several therapies. However, FVC is a downstream measure of lung function influenced by factors beyond fibrosis.
In the Viewpoint, titled ‘Fibrosis extent on HRCT: the principal structural imaging biomarker for antifibrotic trials’, Qureight CSO Dr Simon Walsh explained: “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.”
He added: “The opportunity now is to build the regulator-facing evidence needed to use fibrosis burden consistently and confidently across trials.”
The paper outlines how measuring fibrosis extent using imaging biomarkers for quantitative high‑resolution computed tomography can complement FVC by providing a more biologically proximate view of whether a therapy is slowing pulmonary fibrosis.
Qureight said that for fibrosis extent to become a surrogate endpoint, a more robust evidence base is required. This includes trial‑level data demonstrating a clear association between treatment‑driven changes in fibrosis accumulation and proof that slowing fibrosis progression predicts how patients feel, function or survive.
