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Novogen Announces Establishment of Global Collaboration to Drive The Development of Drugs to Treat Brain Cancer
Date:12/20/2013

therapy.

The program is based on the high potency of Trilexium against GBM cells, with both GBM stem cells and somatic cells being killed at equivalent dosages.

Progression of GBM following radiotherapy and chemotherapy is believed to result from the regrowth of cancer stem cells that are chemo-resistant. Recurrent tumor cells, like their parent GBM stem cells, are highly drug-resistant and with increased aggression, accounting for the poor prognosis associated with GBM.

Dr David Brown, Novogen Group CSO, said, "The collaborative effort to date has focused on bringing Trilexium into the clinic for the treatment of GBM, and that goal will continue with the aim of bringing that agent into the clinic in early 2015."

"The expansion of the collaboration to include Cornell takes the program to the next level, which is to achieve personalized chemotherapy for patients with GBM. The objective is to identify a panel of Trx analogs that target individual GBM mutations within the genotype spectrum that characterises GBM malignancies. That data then will inform our clinical objective which is to match the best drug candidate to an individual tumor genotype."  

"WCMC has particular skills in identifying the genotype of explants from fresh biopsies of GBM tumors. We will be utilizing this ability to screen Trilexium analogs for activity against a wide range of individual tumors," Brown added.

About Glioblastoma

Glioblastoma multiforme is the most common and aggressive form of primary brain tumor. Worldwide, in developed countries, an estimated 3.5 cases per 100,000 people are diagnosed per year. Glioblastoma is one of the cancers most resistant to treatments and is associated with extremely poor prognosis. Despite therapeutic intervention (surgery/radiation/chemotherapy), glioblastoma remains a devastating disease with a median 2-year survival rate in the range of 10–25%.

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SOURCE Novogen Limited
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