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Redx, Garvan Institute of Medical Research Partner to Advance Porcupine Inhibitor Program

NEW YORK – Redx on Tuesday said it is collaborating with the Garvan Institute of Medical Research in Sydney to screen small molecule targeted drug candidates using Garvan's preclinical cancer models.

Data produced from the collaboration will support Redx's Phase II trial of its porcupine inhibitor RXC004. In that study, Redx will assess the safety and efficacy of RXC004 in advanced microsatellite-stable metastatic colorectal cancer patients with aberrations in RING finger protein 43 (RNF43) or R-spondin (RSPO). An additional arm of the trial will test RXC004 with Bristol Myers Squibb's Opdivo (nivolumab).

The collaboration will explore treatments in the hopes of extending patient survival with highly fibrotic cancers like pancreatic cancer using patient-derived tumor tissue grown in mice. In addition to RXC004, the companies will use the platform to study UK-based Redx's other therapies in development for targets such as porcupine, ROCK2, and discoidin domain receptors (DDR). These targets are all implicated in cancer-associated fibrosis.

Garvan is currently testing RXC004 in its MoST-P clinical trial against RNF43-mutant pancreatic cancer. The MoST-P trial, carried out with the University of New South Wales, matches cancer patients to targeted therapies based on the genomic or fibrotic signature of the tumor. The study is part of Australia's Molecular Screening and Therapeutics (MoST) program, a framework protocol guiding multiple, parallel studies of targeted therapies for patients with advanced cancer.

The first set of data from the collaboration with Garvan using patient-derived mouse models on proprietary Redx molecules will be released in June. Then, further data from the collaboration in patient-derived pancreatic cancer models will be published later this year to improve Redx's understanding of RXC004's activity in Wnt-ligand driven tumors.

Therapeutic inhibition of porcupine has shown to diminish tumors with aberrations in RNF43 and RSPO through the Wnt pathway. Mutations in those genes increase Wnt-dependent signaling and are implicated in pancreatic and colorectal cancer. Redx presented in vitro and in vivo studies at the American Association for Cancer Research annual meeting in 2021, showing that RXC004 inhibited tumor proliferation, providing support for the proposed mechanism.