RXC006, an oral treatment candidate for idiopathic pulmonary fibrosis (IPF) and other types of fibrosis, was seen to ease lung scarring in a mouse model of IPF, its developer, Redx Pharma, has announced.
The investigative inhibitor is also reported to work favorably in human lung fibroblasts grown in the laboratory. Based on these results, Redx Pharma plans to start clinical trials testing RXC006 in 2020.
These preclinical results were disclosed at the 2nd Anti-Fibrotic Drug Development Summit, recently held in Cambridge, Massachusetts. The findings were presented by Peter Bunyard, PhD, head of fibrosis for the company, in an oral session and a poster titled “Wnt Pathway Suppression and Fibrosis.“
RXC006 is being developed as an inhibitor of an enzyme called porcupine. This enzyme is important for the activation of a cellular pathway known as Wnt signaling — a group of molecules that work together to control tissue remodeling processes involved in fibrosis, autoimmune diseases, and cancer.
By blocking Wnt signaling, RXC006 aims to suppress several underpinnings of fibrosis, including inflammation, cell death, epithelial-mesenchymal transition, and fibroblast activation. The goal is to prevent fibrosis progression, and possibly reverse fibrosis, in patients.
Targeting the Wnt pathway is “a novel and exciting opportunity to treat fibrotic diseases. I truly support the idea of targeting the porcupine enzyme,” Jörg Distler, MD, a professor at the University of Erlangen-Nuremberg in Germany and a researcher who specializes in fibrosis and fibroblast activation, said in a Redx press release.
Preclinical data showed that RXC006 at very low concentrations was highly effective in blocking the Wnt pathway, and in reducing the activation of human lung fibroblasts — cells involved in lung repair, inflammation, and scarring (fibrosis).
Importantly, RXC006 was also able to suppress lung fibrosis in vivo (within a living being). In two separate mouse models of IPF, oral treatment with RXC006 strongly reduced signs of lung fibrosis; its use significantly lessened lung weight, collagen deposition, and the activation of a number of pro-fibrotic genes.
RXC006’s anti-fibrotic effects were also seen in animal models of liver and kidney fibrosis.
“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” with plans to request trials in people beginning in 2020, said Richard Armer, chief scientific officer at Redx Pharma.
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