"In laboratory studies, triphendiol is more potent at apoptosis inductionin pancreatic and bile duct cancer cells compared to gemcitabine at up toten-fold lower concentrations," said Dr. Tytler.

There is an urgent need for new pancreatic cancer treatments because fewerthan 20 percent of patients are candidates for surgery. Current treatmentis limited to chemotherapy with gemcitabine, to which most patients areresistant or acquire resistance. This study assessed the potential oftriphendiol as a treatment for pancreatic adenocarcinoma using threerepresentative cell lines. Triphendiol-induced apoptosis (cell death) inall cell lines and pre-treatment with triphendiol increasedgemcitabine-dependent apoptosis. Animal model studies showed thattriphendiol in combination with gemcitabine inhibits tumor growth moreeffectively than each drug alone. Both triphendiol and gemcitabine induceapoptosis via a mitochondrial pathway.

Structurally, triphendiol is an analogue of phenoxodiol, both of which areinvestigational drugs that have been licensed by Novogen to MarshallEdwards, Inc. Phenoxodiol is currently in Phase III clinical developmentfor patients with late stage ovarian cancer under the OVATURE banner.Triphendiol has recently been granted orphan drug status by the FDA forpancreatic cancer, bile duct cancer and melanoma.

Like phenoxodiol, triphendiol is also able to induce apoptosis however,triphendiol-induced cell death is thought to proceed via bothcaspase-dependent and caspase-independent pathways. In pancreatic cancercells, triphendiol causes upregulation of p21 thereby arresting the cellcycle in G2M leading to apoptosis induction. Integral totriphendiol-induced apoptosis induction is mitochondrial depolarization dueto transitory changes is Bcl-2 and Bid expression. Like phenoxodiol,triphendiol also causes XIAP degradation. In bile-duct cancer cells,triphendiol induces apoptosis that is completely caspase-independent.Animal studies using nude mice bearing human pancreatic and bile ducttumors, demonstrated that oral triphendiol administration in combinationwith gemcitabine resulted in a mean reduction in tumor volume by 62 percentand 81 percent respectively compared with untreated tumors from controlanimals.

"With a lack of data from randomized Phase III studies, there is no currentevidence-based treatment recommendation for patients with advancedpancreatic cancer that have failed first-line gemcitabine," said WasifSaif, MD, Associate Professor and Director, Gastrointestinal CancersProgram, the Yale School of Medicine. "The ability of triphendiol tosensitize pancreatic cancer tumors to gemcitabine in animal studiesjustifies the continued development of triphendiol as a pancreatic cancertherapy, and would provide a welcome second-line therapeutic contingencyfor late stage gemcitabine refractory pancreatic cancer patients."

Professor Alan Husband, Group Director of Research for Marshall Edwards,Inc., said, "The commercial potential of the flavonoid technology platformfrom which these candidate molecules have been derived is now becomingevident. Through continued refinement of our proprietary molecularscaffold, we anticipate further enrichment of our pipeline with analogueswhose activity may be directed against a diverse array of cancer targets."

About Phenoxodiol and Triphendiol

Phenoxodiol is being developed as a therapy for late-stage, chemo-resistantprostate, ovarian and cervical cancers. It is a novel-acting drug thatinhibits key pro-survival signaling pathways operating viasphingosine-1-phosphate and Akt. Inhibition of these pathways leads toprevention of phosphorylation of key anti-apoptotic proteins such as XIAPand FLIPs. Loss of activity of these proteins restores the ability ofchemoresistant tumor cells to undergo apoptosis in response tochemotherapy. The molecular target for phenoxodiol is an oxidase enzymepresent on the surface of cancer cells, accounting for the highly selectivenature of the drug.

Triphendiol is being developed as a therapy for late state pancreatic andbile duct cancer and has recently been awarded orphan drug status.Triphendiol-induced apoptosis is initiated by mitochondrial depolarizationdue to transitory changes is Bcl-2 and Bid expression. Like phenoxodiol,triphendiol also causes XIAP degradation.

Multinational Trial Underway

Phenoxodiol in combination with carboplatin is currently being studied in amulti-national Phase III clinical trial called the OVATURE (OVArian TUmorREsponse) Trial, following positive findings of previous trials conductedin Australia and at Yale-New Haven Hospital. The OVATURE trial is takingplace at over 70 clinical sites in the United States, Europe, andAustralia. For more information on the trial, visit www.OVATUREtrial.com.

About Marshall Edwards, Inc.:

Marshall Edwards, Inc. (NASDAQ: MSHL) is a specialist oncology companyfocused on the clinical development of novel anti-cancer therapeutics.These derive from a flavonoid technology platform, which has generated anumber of novel compounds characterized by broad ranging activity against arange of cancer cell types with few side effects. The combination ofanti-tumor cell activity and low toxicity is believed to be a result of theability of these compounds to target an enzyme present on the surface ofcancer cells, thereby inhibiting the production of pro-survival proteinswithin the cell. Marshall Edwards, Inc. has licensed rights from NovogenLimited (NASDAQ: NVGN) to bring three oncology drugs -- phenoxodiol,triphendiol and NV-143 -- to market globally.

Marshall Edwards, Inc. is majority owned by Novogen, an Australianbiotechnology company that is specializing in the development oftherapeutics based on a flavonoid technology platform. Novogen, based inSydney, Australia, is developing a range of therapeutics across the fieldsof oncology, cardiovascular disease and inflammatory diseases. Moreinformation on phenoxodiol and on the Novogen group of companies can befound at www.marshalledwardsinc.com and www.novogen.com.

Under U.S. law, a new drug cannot be marketed until it has beeninvestigated in clinical trials and approved by the FDA as being safe andeffective for the intended use. Statements included in this press releasethat are not historical in nature are "forward-looking statements" withinthe meaning of the "safe harbor" provisions of the Private SecuritiesLitigation Reform Act of 1995. You should be aware that our actual resultscould differ materially from those contained in the forward-lookingstatements, which are based on management's current expectations and aresubject to a number of risks and uncertainties, including, but not limitedto, our failure to successfully commercialize our product candidates; costsand delays in the development and/or FDA approval, or the failure to obtainsuch approval, of our product candidates; uncertainties in clinical trialresults; our inability to maintain or enter into, and the risks resultingfrom our dependence upon, collaboration or contractual arrangementsnecessary for the development, manufacture, commercialization, marketing,sales and distribution of any products; competitive factors; our inabilityto protect our patents or proprietary rights and obtain necessary rights tothird party patents and intellectual property to operate our business; ourinability to operate our business without infringing the patents andproprietary rights of others; general economic conditions; the failure ofany products to gain market acceptance; our inability to obtain anyadditional required financing; technological changes; governmentregulation; changes in industry practice; and one-time events. We do notintend to update any of these factors or to publicly announce the resultsof any revisions to these forward-looking statements.

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