CEO Explains Why Cellceutix's Leading Drug Candidate May Be a Major Breakthrough in Cancer Rese

CEO Explains Why Cellceutix's Leading Drug Candidate May Be a Major Breakthrough in Cancer Research

ID: 37599

(firmenpresse) - LOS ANGELES, CA -- (Marketwire) -- 07/26/11 -- The CEO of Cellceutix Corporation (OTCQB: CTIX) (PINKSHEETS: CTIX), a preclinical cancer, anti-inflammatory and autism drug developer says his company's leading drug candidate, Kevetrin, is a new class of chemistry in medicine which has proven to this point to restore p53 (also known as the "Guardian Angel" gene ) back to a normal status so it can do its job as master regulator and see to it that the cancer cells are destroyed without damaging any DNA.

Cellceutix has been in the news and attracting investor attention lately as developments with Kevetrin as a novel indication for a variety of drug-resistant cancers nears clinical trials after producing strong pre-clinical data.

Leo Ehrlich, CEO of Cellceutix, tells BioMedReports in an exclusive interview that p53 is a key component in regulating the cell cycle.

"In more than half of all cancers, the p53 has lost all or a portion of its function which allows cancer cells to run rampant," explains Ehrlich. "Researchers have known about the p53 correlation to carcinomas, but have yet been able to come-up with a solution to restore the function of p53. There was a class of drugs called 'Nutlins' a few years ago that believed to hold promise, but proved to be genotoxic -- meaning that the drug damaged the host's DNA -- so that quickly was realized as not a viable option. Kevetrin has proven to this point to restore p53 back to a normal status so it can do its job as master regulator and see to it that the cancer cells are destroyed without damaging any DNA."

The full exclusive interview with Ehrlich on the significance of his company's drug compound, including more details about the drug candidate's clinical trial at a major cancer center is available now at:



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Datum: 26.07.2011 - 11:01 Uhr
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News-ID 37599
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