Available Technology
Use of neamine for treating prostate cancer
Technology:
Small molecule that inhibits nuclear translocation of angiogenin (ANG)
Markets Addressed
ANG has been shown to stimulate rRNA transcription and induce angiogenesis via nuclear translocation. The dual role of ANG in prostate cancer progression suggests that ANG translocation is a molecular target for the development of cancer drugs. Inhibitors of ANG nuclear translocation would combine the benefits of both anti-angiogenesis and chemotherapy, due to the fact that both angiogenesis and cell proliferation are mediated, at least in part, by ANG activity. It is thought that targeting ANG translocation would be more efficacious than targeting ANG directly because of the high plasma concentration of ANG in the plasma.
Innovations and Advantages
Mechanistic studies have shown that ANG undergoes nuclear translocation in both endothelial and cancer cells where it up-regulates ribosomal RNA transcription, stimulating cell proliferation. Therefore, nuclear translocation of ANG is essential to cancer pathogenesis and is an interesting target for cancer drug development. We report a small molecule with low nephro- and ototoxicity that inhibits nuclear translocation of ANG.
Our small molecule has been shown to block ANG nuclear translocation and inhibit xenograft growth of human prostate cancer cells in athymic mice. The molecule not only prevents prostate intraepithelial neoplasias (PINs), but has been shown to fully reverse developed PIN in AKT transgenic mice.
Treatment with our compound decreased interluminal angiogenesis in AKT-induced prostate luminal cell proliferation. It also decreased cell proliferation in the ventral prostate, shrank established PIN and restored normal luminal architectures of the ventral prostate in AKT over-expressing mice.
Additional Information
Intellectual Property Status: Patent(s) pending
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Inventor(s):
Hu, Guofu
Categories:
For further information, please contact:
Michal Preminger, Director of Business Development
(617) 432-0920
Reference Harvard Case #3289