Researchers claim phenoxodiol kills rapidly proliferating T-cells

Australian bio pharmaceutical company Novogen's subsidiary, Marshall Edwards, Inc today said that researchrs at its Malaghan Institute of Medical Research in Wellington, New Zealand, have found that abnormally proliferating human T-cells and rapidly dividing cancer cells such as primary myeloid and lymphoid leukemic blast cells undergo programmed cell death when exposed briefly to the investigational anti-tumour drug phenoxodiol.

The company said that the results make phenoxodiol a promising candidate for the treatment of pathologically-activated lymphocytes such as those in acute lymphoid leukaemia, or diseases driven by T-cell proliferation such as autoimmune diseases and graft-versus-host disease, according to an article published in the Haematologica Journal on 16 June, 2009, (available on ).

Marshall Edwards says the researchers demonstrated that phenoxodiol inhibited plasma membrane electron transport and cell proliferation and promoted apoptosis of rapidly proliferating human T-cells, induced to undergo rapid proliferation by exposure to cells from an incompatible donor, but at the same time it did not affect normal resting T-cells.

''These findings indicate that phenoxodiol may have utility against autoimmune diseases, such as rheumatoid arthritis and psoriasis, as well as having potential in management of graft rejection in transplantation patients'' said Prof. Alan Husband, group director of research, Marshall Edwards, Inc. ''We're appreciative of Dr Patries Herst and colleagues for undertaking this important research.''

Phenoxodiol is being developed by the US oncology company Marshall Edwards, Inc. as a chemosensitising agent in combination with platinum drugs for late stage, chemoresistant ovarian cancer and as a monotherapy for prostate and cervical cancers. It is said to have a unique mechanism of action, binding to cancer cells via a surface oxidase, disrupting membrane electron transport and causing major downstream disturbances in expression of proteins necessary for cancer cell survival and responsible for the development of drug resistance.

In cancer cells, phenoxodiol appears to inhibit selectively the pro-survival regulator known as S-1-P (sphingosine-1-phosphate) that is over-expressed in cancer cells. In response to phenoxodiol, the S-1-P content in cancer cells is decreased, rendering those cells more sensitive to chemotherapy.