Friday, January 04, 2013 3:21:11 PM
Kevetrin acting through both major pathways of tumor suppression, Rb-E2F and MDM2-p53, has far reaching consequences. Due to the complexity of proapoptotic and antiapoptotic pathways with multiple players involved and redundant signaling networks, blocking only one antiapoptotic factor may not result in robust antitumor activity. However, Kevetrin acts via multiple targets to produce potent efficacy in various xenograft tumor models. We have also demonstrated that Kevetrin is non-genotoxic. DNA damaging drugs result in rapid phosphorylation of H2A.X at Ser 139 by PI3K-like kinases; however, Kevetrin did not induce phosphorylation of H2A.X. Since Kevetrin was well-tolerated in GLP safety pharmacology and toxicity studies, we have submitted an IND application for a Phase I clinical trial at Dana Farber / Harvard Cancer Center for 2012.
http://cancerres.aacrjournals.org/cgi/content/short/72/8_MeetingAbstracts/2874?rss=1
Leo discusses NYT article, 12/24/2012~
http://www.marketwire.com/press-release/cellceutix-comments-on-new-york-times-article-heralding-p53-drugs-as-new-age-cancer-otcbb-ctix-1740893.htm
Leo discusses plans for 2013, 12/31/2012~
http://www.marketwatch.com/story/cellceutix-ceo-discusses-corporate-developments-in-2012-and-plans-for-2013-2012-12-31?reflink=MW_news_stmp
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Cellceutix chief executive Leo Ehrlich issued a statement noting that Merck, Roche and Sanofi are not yet in the clinical trial stage.
“The New York Times may have overlooked Cellceutix and [its drug] Kevetrin, but the organizations that are contacting us to host and sponsor clinical trials certainly have not,” Ehrlich said.
All of the drug companies are working on cancer drugs that would reactivate a protein called p53, sometimes called “the angel of death” because it triggers the destruction of badly damaged cells. Cancer cells disable p53, allowing them to multiply.
http://www.boston.com/businessupdates/2012/12/26/cellceutix-stock-surging-optimism-about-new-cancer-drug/fhhKIUMYKrO4HuFS9VRmYP/story.html
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