CAMBRIDGE, Mass.--()--Stromedix, Inc., a biotechnology company focused on innovative therapies for fibrosis and organ failure, announced today that it has exclusively licensed the rights to a monoclonal antibody to integrin αvβ5 from the University of California. This compound is the second Stromedix pipeline asset to be sourced from the laboratory of Dean Sheppard, M.D., at University of California, San Francisco (UCSF). Preclinical research suggests that αvβ5 plays an important role in a variety of acute and chronic organ failure settings.
“Our research indicates that the αvβ5 antibody might have value in treating acute and chronic organ failure. We’re excited to see whether it can help patients suffering from these debilitating conditions.”
"I am pleased to continue our long-term collaboration with the Stromedix team," said Dean Sheppard, M.D., Chief of the UCSF Division of Pulmonary, Critical Care, Allergy and Sleep Medicine. “Our research indicates that the αvβ5 antibody might have value in treating acute and chronic organ failure. We’re excited to see whether it can help patients suffering from these debilitating conditions.”
Research in Dr. Sheppard’s lab has identified a critical role for αvβ5 in regulating endothelial barrier function, suggesting that an antibody to αvβ5 may have value in acute organ failure settings associated with vascular leakage. Other studies suggest a role in for αvβ5 in activating the pro-fibrotic cytokine TGFβ and promoting fibrosis.
“The Stromedix team has made significant progress in tackling the challenges of clinical development in fibrotic diseases,” said Michael Gilman, Ph.D., Founder and Chief Executive Officer of Stromedix. “Our clinical development strategy uses a proprietary biomarker database to discover the biologically active dose of an anti-fibrotic agent in the context of a small, short-term trial. We are excited to be able to leverage what we’ve learned in the STX-100 program to the αvβ5 antibody and to build a pipeline of valuable biologic drugs to treat chronic and acute organ failure.”
About Fibrosis and Organ Failure
Fibrosis results from the body’s attempt to repair chronic tissue injury. Ongoing cycles of injury and repair, often playing out over decades, lead to accumulation of scar tissue in affected organs and disruption of normal tissue architecture and function. Ultimately the organ fails. Fibrosis is the final common pathway in virtually all forms of chronic organ failure, whether in kidney, liver, lung, or other organs, conditions affecting tens of millions of patients in the United States. Moreover, the biology of fibrosis is similar regardless of cause – viral, chemical, physical or inflammatory. Fibrosis results from the excessive activity of fibroblasts, in particular a differentiated form known as the myofibroblast. The biology of these cells is well understood and there is consensus among experts that pharmacological attenuation of myofibroblast activity ought to slow or perhaps even reverse disease progression, thereby preserving organ function and prolonging healthy life.
Stromedix is a privately held biotechnology company based in Cambridge, Massachusetts, focused on innovative therapies for fibrosis organ failure. The company’s lead compound, STX-100, has completed a Phase 1 clinical trial, and Phase 2 trials in idiopathic pulmonary fibrosis and chronic allograft nephropathy are currently being planned. The FDA has granted orphan drug designation to STX-100 for both indications. Investors in Stromedix include Atlas Venture, New Leaf Venture Partners, Frazier Healthcare Ventures, Bessemer Venture Partners and Red Abbey Venture Partners. Biogen Idec is also a shareholder. For more information on Stromedix, please visit http://www.stromedix.com.
The information stated above was prepared by Stromedix, Inc. and reflects solely the opinion of the corporation. Nothing in this statement shall be construed to imply any support or endorsement of Stromedix, or any of its products, by The Regents of the University of California, its officers, agents and employees.