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Alba Therapeutics Announces IND for Beta Cell Preservation in Type 1 Diabetes Using AT-1001
Date:9/5/2007

BALTIMORE, Sept. 5 /PRNewswire/ -- Alba Therapeutics Corporation today announced that its Investigational New Drug Application for oral AT-1001 for the preservation of endogenous insulin production capacity in new-onset type 1 diabetes (T1D) patients, has cleared the 30 day deliberation period by the U.S. Food and Drug Administration (FDA). The Company plans to initiate an exploratory diabetes study in 2008 while focusing the majority of its development resources for oral AT-1001, its lead compound, in gastrointestinal diseases such as Celiac and Crohn's disease.

"Acceptance by the FDA of this application emphasizes the safety of the drug and the vast potential that inhibitors of barrier dysfunction, such as AT-1001, have in the treatment of a wide variety of immune-related diseases. The data we plan to generate from the initial Phase II study in diabetics will educate us about the therapeutic potential of inhibiting intestinal permeability in patients suffering from T1D," said Dr. Blake Paterson, CEO of Alba. "We are preparing an IND for AT-1001 as a treatment for Crohn's disease, and look forward to advancing other molecules within our pipeline towards the clinic," said Dr. Paterson.

About Type I Diabetes

Type 1 diabetes is an autoimmune disease in which the body's immune system attacks and destroys the insulin-producing beta cells of the pancreas. The symptoms associated with T1D can appear suddenly and leave a person dependent on injected insulin for life. The disease carries the constant threat of devastating complications such as heart and kidney disease, nerve damage and blindness. Like other autoimmune diseases, T1D is triggered by an environmental agent in genetically susceptible individuals. The entry of the environmental trigger into the body is thought to be through the intestinal tract.

About AT-1001

AT-1001 is an inhibitor of barrier dysfunction that has been shown to block intestinal permeability and the genesis of
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SOURCE Alba Therapeutics Corporation
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