Liège-based Convert Pharmaceuticals SA has been granted a total of €13.6m in equity and non-dilutive funding by investors Droia Oncology Ventures, Meusinvest and Spinventure, with non-dilutive support by the Walloon region and funds from the European Eurostars programme.
The proceeds will be used to prepare and conduct Phase I clinical studies with Convert's nitroaromatic lead anti-cancer drug CP-506, which may bring a novel approach to tackling certain aggressive and resistant tumours. Co-founders Prof. Dr. Philippe Lambin, Paul Tulcinsky, and Nicolas Geûens licenced the compound from Professors Jeffrey Smaill and Adam Patterson from University of Auckland (NZ) to leverage tumour hypoxia.
Tumour hypoxia, which occurs wherever tumour cells are deprived of oxygen, has been shown to promote the development of aggressive tumours, which resist to chemo-, immuno-, and radiotherapy, and is strongly associated with a poor clinical outcome. Preclinical studies have confirmed the outstanding anti-cancer potential of CP-506.
Chief Scientific Advisor of Convert, Prof. Dr. Philippe Lambin from Maastricht University, said: "Convert was founded to develop next-generation tumor-microenvironment modulated prodrugs. These prodrugs are inactive by themselves, but transform into potent anti-cancer agents when entering tumors. Many tumors contain areas that are insufficiently oxygenated. These areas are hard to treat with radio-, chemo- and immunotherapies. However, Convert's lead drug becomes active in these areas and eradicates them very efficiently."
Janwillem Naesens, Managing Partner at Droia and CEO of Convert, added: "We are currently completing the team, which is already working hard on bringing the first drug to cancer patients. In the meantime we are evaluating other drug candidates, based on Convert's innovative insights in both the tumor-microenvironment and specific biomarkers (for hypoxia) as well as in the chemical design of prodrugs."
The hypoxia-activated cytotoxin improves the activity, specificity and safety relative to older hypoxia-activated prodrugs that target the HIF signal pathway. The company said in a press release that tumor sensitivity to CP-506 is not only driven by hypoxia, but also enhanced by other factors that are developed to allow selection of potential responders to CP-506.
