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CEL-SCI Presents Data at American College of Rheumatology Conference Which Suggests that CEL-2000 Has Potential to Slow Damage Caused by Rheumatoid Arthritis
Date:10/19/2009

VIENNA, Va., Oct. 19 /PRNewswire-FirstCall/ -- CEL-SCI Corporation (NYSE Amex: CVM) announced today the presentation of new rheumatoid arthritis data at the American College of Rheumatology's annual meeting in Philadelphia, PA. The data, presented by Dr. Daniel Zimmerman in conjunction with the Company's collaborators from Washington Biotech, Northeastern Ohio Universities College of Medicine and BolderBiopath, indicate that CEL-SCI's rheumatoid arthritis treatment vaccine CEL-2000 acts to prevent or retard the permanent tissue damage caused by rheumatoid arthritis in animals. These statistically significant results were demonstrated by the measurement of four different parameters, suggesting that CEL-2000 appears to block the immune response that causes the autoimmunity which leads to rheumatoid arthritis. The long term results obtained with fewer doses of CEL-2000 vaccine were comparable or better than those seen with Enbrel®, a leading treatment for people with rheumatoid arthritis.

Geert Kersten, Chief Executive Officer of CEL-SCI said, "These results were achieved through a reduction of the inflammatory response that attacks the patient's joints. The goal for our new H1N1 therapy for H1N1 hospitalized patients is not dissimilar. Many of these patients die from the excessive inflammatory response. We feel that this new data is encouraging both for this rheumatoid arthritis vaccine as well as supportive of our H1N1 treatment."

In these studies, mice were injected with collagen to induce the autoimmune disease. Therapy with Enbrel or CEL-2000 was initiated and continued for 28 days after the initiation of a significant, uniform, and measurable level of arthritic disease in groups of mice. CEL-2000 was administered only twice, but Enbrel was administered every other day for the first 28 days. The extent of disease
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SOURCE CEL-SCI Corporation
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