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EntreMed Commences Continuous Dosing Clinical Trial For MKC-1
Date:4/2/2008

shown to induce apoptosis, inhibit mitotic spindle formation, and prevent chromosome segregation in the M-phase (mitosis) of the cell cycle. Furthermore, MKC-1 inhibits the PI3K-Akt-mTOR signaling pathways, which may occur through inhibition of the mTOR/rictor pathway. The PI3K-Akt- mTOR pathway is the most frequently mutated pathway in human tumors. Mutations in this pathway have been shown to promote tumor progression and decrease survival in cancer patients.

"The potential of increasing drug activity by exploiting its inhibitory effects on the PI3K-Akt-mTOR pathway is exciting and we hope to define this effect with novel molecular imaging techniques," commented Dr. Glenn Liu.

EntreMed Vice President and Chief Medical Officer, Carolyn F. Sidor, M.D., M.B.A., commented on the study, "This will be our first continuous dosing study for MKC-1 in patients with solid tumors. We believe that a continuous dosing schedule has the potential to improve tolerability and enhance MKC-1 activity in cancer patients, similar to increased antitumor activity that sustained exposure has demonstrated in preclinical studies. Through this Phase 1 study, we expect to determine not only the maximum tolerated dose of MKC-1 when administered orally twice a day on a continuous basis, but the pharmacodynamic changes using imaging techniques as proof of drug effect and assessment of toxicity."

About EntreMed

EntreMed, Inc. is a clinical-stage pharmaceutical company developing therapeutic candidates primarily for the treatment of cancer and inflammation. MKC-1 is currently in multiple Phase 2 clinical trials for cancer. MKC-1 is an oral cell-cycle regulator with activity against the mTOR pathway. ENMD-1198, a novel antimitotic agent, is in a Phase 1 study in advanced cancer patients and ENMD-2076, a selective kinase inhibitor, is expected to begin a Phase 1 study in 2Q08. The Company also has an approved IND application for Panzem(R) in rheumatoid arthritis. EntreMe
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