Redx has presented pre-clinical data for its newly nominated development candidate RXC006 at the Advances in Fibrosis Drug Discovery Conference in Cambridge, USA on 29 November 2018. RXC006, a novel inhibitor of the porcupine enzyme, will be developed as an orally administered, first-in-class treatment for the orphan disease, idiopathic pulmonary fibrosis (IPF). IPF is a severe and life-threatening chronic lung condition with very poor prognosis and limited treatment options. The company expects to commence first-in-man studies with RXC006 during 2020. In the first public disclosure of data on RXC006, Dr. Peter Bunyard, Head of Fibrosis at Redx, presented results from preclinical studies in a plenary session as well as a poster which showed that RXC006 was highly effective at suppressing the Wnt pathway (porcupine sits on the Wnt pathway) and that RXC006 was able to suppress lung fibrosis, in vivo. Suppression of fibrosis has also been shown in animal models of both liver and kidney fibrosis. More specifically, it was shown that RXC006 was able to suppress the release of Wnt-5a (another protein on the Wnt pathway) from human lung fibroblasts at nanomolar concentrations and reduce fibroblast activation. In two separate mouse models of disease, RXC006 strongly reduced collagen deposition and significantly impacted Ashcroft scores (a validated scale for estimating the severity of pulmonary fibrosis), when dosed therapeutically.