Kevetrin Demonstrates Signifcant Results in the Treatment of Multi-Drug Resistant Cancer Cells

BEVERLY, MA–(Marketwire – June 21, 2010) – Cellceutix Corporation (OTCBB: CTIX) is pleased to announce that they have concluded more pre-clinical cell studies for Kevetrin, their flagship compound for the treatment of multi-drug resistant strains of lung, breast and colon cancers. The research was conducted on drug resistant non-small cell lung carcinoma cells by the Cellceutix research team at a world-renown cancer hospital in Boston.

The studies were focused on the methods of action with Kevetrin pertaining to the cell life cycle process. Efficient elimination of carcinoma cells requires identifying multi-pathways to treat the affected cells. This research had the purpose of identifying another pathway that Kevetrin may be effective against multi-drug resistant cancer cells. The data compiled from the research showed that Kevetrin had a 78% effective rate of G2/M arrest. The data also showed that cells treated with Kevetrin also demonstrated a 66% increase in apoptosis, defined as a form of cell death, as compared to non-treated cells.

“The G2/M portion of a cancer cell’s cycle is critical as it the stage before a cell enters mitosis, the time when the cell divides into 2 identical nuclei. Kevetrin is proving once again to slow or stop the growth of carcinoma cells,” stated Cellceutix Chief Scientific Officer Dr. Krishna Menon. ”The increased apoptosis is very significant because it shows that the cancer cells are being destroyed without damaging any of the healthy cells around it.”

George Evans, CEO of Cellceutix, commented, “This data provides important insight into how Kevetrin is working to attack resistant cancer cells and significant because when dealing with drug-resistant cancers it is imperative to find multiple pathways to destroy the cells.” Mr. Evans continued, “We are very excited about the potential Kevetrin is presenting to the value of our company as all pre-clinical data has been extremely promising.”