Scientific Insights Into IBIO-CFB03 Presented at American College of Rheumatology Annual Meeting

iBio, Inc. (NYSE MKT:

), a leader in plant-based biotechnology for developing and manufacturing biological products, announced the presentation at the annual meeting on November 10 of the American College of Rheumatology (ACR) in San Francisco, CA of new information on the mechanism of action of iBio's proprietary product candidate for the treatment of fibrotic diseases, IBIO-CFB03. Dr. Tetsuya Nishimoto, a post-doctoral fellow in the laboratory of Dr. Carol Feghali-Bostwick, the SmartState® and Kitty Trask Holt Endowed Chair and Professor of Medicine at the Medical University of South Carolina, in an ACR-invited oral presentation, described recent new and unpublished data and insights about how peptides derived from endostatin can block or reduce fibrosis in a variety of tissues. In summary, proteolytic pathways (proteolysis being the breakdown of proteins into smaller polypeptides or amino acids) induced by endostatin-related peptides contained within IBIO-CFB03 stimulate the production of enzymes which degrade the extracellular matrix that is produced in excess in fibrotic diseases such as scleroderma. This enables IBIO-CFB03 to not only arrest fibrosis, but to potentially reverse ongoing fibrotic pathology. iBio owns exclusive worldwide rights to IBIO-CFB03 and patents covering endostatin-derived peptides for the treatment of fibrotic diseases. Dr. Feghali-Bostwick's laboratory is collaborating with iBio for the development of products against fibrotic diseases. Support for its work has recently been supplemented by the award of an STTR grant from the National Institutes of Health to aid the development of IBIO-CFB03 as a treatment for fibrotic disease. "Research teams at the Medical University of South Carolina, Novici Biotech, and iBio have been working diligently and successfully to decipher the mechanism by which endostatin-derived peptides improve fibrosis," said Terence Ryan, Ph.D., iBio's Chief Scientific Officer. "Data on this mechanism of action have been confidentially disclosed to the FDA and details will be publicly disclosed in an upcoming peer-reviewed scientific publication." In addition to the ACR-selected oral presentation by Dr. Nishimoto, an additional oral presentation, based on Dr. Feghali-Bostwick's research, discussed epigenetic differences in identical twins which may modulate scleroderma disease, and a poster describing the role of lysyl oxidase in promoting fibrosis was also presented by the Feghali-Bostwick lab.