BerGenBio commences preclinical development of BGB324 anti-cancer drug

BerGenBio AS, an emerging oncology biopharma, today announced it has initiated preclinical development of its proprietary lead compound, BGB324. This compound will be a first-in-class inhibitor of AXL kinase.

Richard Godfrey, BerGenBio's CEO, explained that BGB324 is the result of BerGenBio's focus on therapeutics that target the epithelial-mesenchymal transition (EMT) in cancer, considered to play a critical role in tumor metastasis and escape from chemotherapy. "Interest in EMT has increased dramatically; leading researchers in the field now believe that inhibition of the EMT process has the potential to delay or prevent metastasis, overcome and even reverse drug resistance and prevent cancer recurrence" said Mr. Godfrey.

Professor James Lorens, cofounder of BerGenBio noted that "the vast majority of cancer-related deaths are attributable to secondary or metastatic tumors, which tend to be resistant to current therapies and difficult to treat." BerGenBio's drug development strategy builds on an understanding of the fundamental biological mechanisms that drive tumor metastasis and drug resistance. AXL represents a novel target in this area and this has provided a unique opportunity for clinical translation. Christopher Molineaux, Executive VP of Drug Development at BerGenBio explains that "BGB324 is an orally bioavailable and highly selective AXL inhibitor which we anticipate will be well tolerated. Our preclinical results suggest that BGB324 can be highly effective in the right clinical setting."

Mr. Godfrey said: "Having completed a successful fundraising, we have assembled a highly experienced international team to accelerate the development of BGB234. We have in-licensed BGB324 from South San Francisco-based Rigel Pharmaceuticals (Nasdaq: RIGL), where substantial preclinical characterization has already been completed. Our development plan for BGB324 aims to initiate Phase I clinical studies by the end of 2012."

Source:

: BerGenBio AS

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