Redx (AIM: REDX), the drug discovery and development company focused on cancer and fibrosis, announces that it 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. 

Dr Jörg Distler, Professor of Internal Medicine, University of Erlangen-Nuremberg, Germany and a key opinion leader in the development of novel anti-fibrotic therapies, commented: "Wnt pathway inhibition presents a novel and exciting opportunity to treat fibrotic diseases, I truly support the idea of targeting the porcupine enzyme."

Dr Richard Armer, Chief Scientific Officer, Redx Pharma plc added: "The data suggests that RXC006 has great potential to treat fibrosis in human patients. Redx are progressing RXC006 towards the clinic for the treatment of Idiopathic Pulmonary Fibrosis and plan to initiate first in man clinical trials during 2020."

There is strong scientific evidence that the Wnt pathway is critically involved in the scarring process (fibrosis) in the lung that is the hallmark of IPF.¹ Over time, this leads to the lungs being unable to function effectively, ultimately resulting in suffocation and death. RXC006 represents a novel approach to treat this debilitating and progressive disease through targeting porcupine, a component enzyme of the Wnt pathway. Porcupine inhibition suppresses the release of all Wnt ligands and therefore should eliminate one of the major drivers of fibrosis in IPF.  The median survival from IPF diagnosis is 3 years and the annual incidence is between 6.8-16.3/100,000 population in the U.S.²