Bioactive lipid LPA mediates fibrogenesis in bleomycin mouse model of scleroderma

Amira Pharmaceuticals, Inc. announced today that their collaborators, Andrew Tager, M.D. and Flavia V. Castelino, M.D. of Massachusetts General Hospital, Harvard Medical School, will present a preclinical proof-of-concept study which demonstrates that the bioactive lipid lysophosphatidic acid (LPA), through its high affinity LPA1 receptor, is an important mediator of fibrogenesis in the bleomycin mouse model of scleroderma.  Data will be presented as part of a poster session for the 1st Systemic Sclerosis World Congress to be held in Florence, Italy, February 11 to 13, 2010.

"Our data shows that in mice deficient for the LPA1 receptor, there is dramatic protection from the bleomycin-induced skin fibrosis seen in normal mice," said Dr. Tager, a member of Amira's Scientific Advisory Board.  "In addition, similar protection from fibrosis was observed in normal mice treated with Amira's LPA1 receptor antagonist, AM095."

Peppi Prasit, Ph.D., Chief Scientific Officer, said, "AM095 is an orally available, potent and selective antagonist of the LPA1 receptor.  We are currently moving AM095 and AM152, another LPA1 antagonist, through GLP toxicology testing and expect to initiate human clinical studies in the second half of 2010."

Bob Baltera, Chief Executive Officer, added, "So far we have seen compelling data in numerous preclinical models of fibrosis.  We are excited by the possibility of eventually exploring efficacy in human disease settings, such as idiopathic pulmonary fibrosis, scleroderma, kidney and liver fibrosis, and various metastatic cancers. There is a lot of work to be done, and we are up to the challenge."