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Gentium's Defibrotide Highlighted in Two Poster Presentations at,American Association for Cancer Research Annual Meeting

ase gene expression, but also decreases its enzymatic activity in MM cell lines. Thus, Defibrotide may suppress tumor-associated angiogenesis and tumor dissemination through suppression of heparanase with a subsequent reduction in the release of stores of growth factors from the extra-cellular matrix. This, in part, may explain Defibrotide's anti-MM activity both in vitro and in vivo."

On Tuesday, April 17, 2007, from 1:00 p.m. to 5:00 p.m. (Pacific Time), Dr. Gunther Eissner, Ph.D., Gentium's Chief of Biology, will present a poster entitled "Defibrotide: an endothelium stabilizing drug prevents angiogenesis in vitro and in vivo." (Poster session 21, Tumor Biology 29, Abstract #4627, Board #30)

The anti-angiogenic potential of Defibrotide was tested in vitro using a kit with human micro-vascular endothelial cells forming vessel structures across a layer of dermal fibroblasts. The results demonstrated that Defibrotide at concentrations corresponding to pharmacological Defibrotide blood levels (100 (mu)g/mL) reduced vessel formation, which could be confirmed by two classical in vitro angiogenesis assays (tube formation in matrigel, rat aortic ring sprouting).

In vivo, tumor angiogenesis was assessed in the murine dorsal skin-fold chamber model using the inoculation of human gastric adenocarcinoma (TMK-1) cells. Intravenous application of Defibrotide (450 mg/kg daily) significantly reduced tumor angiogenesis, as measured by micro-vascular density at day 7 (p=0.035).

The signal transduction mechanism of Defibrotide as demonstrated by Western blotting results show that Defibrotide reduces phosphorylation-activation of p70S6 kinase, which is a key target in the PI3K/Akt/mTOR signaling pathway linked to angiogenesis. Additional in vitro data show that Defibrotide does not influence proliferation of vascular, perivascular or tumor cells, and that it might selectively act through a migration and tube formation inhibition of endothelial cells.


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