Pathfinder cell-based therapy reverses diabetes in mouse model

Mar 30 2011

Pathfinder, LLC, a private biotechnology company focused on the treatment of diseases characterized by organ-specific cell damage ("Pathfinder"), today announced publication of promising preclinical data demonstrating that the Company's unique cell-based therapy is able to completely reverse diabetes in a mouse model.  The results of the study, which will be printed in the April issue of Rejuvenation Research and available currently online, are the first to describe the Company's proprietary Pathfinder Cells ("PCs"), which stimulate regeneration of damaged tissues without the cells themselves being incorporated into the newly generated tissue.

"Though preliminary, the robustness of these results is very encouraging," stated Paul G. Shiels, Ph.D., University of Glasgow, Glasgow, United Kingdom. "With only two treatments with PCs, just days after induction of diabetes, we were able to quickly regenerate critically damaged pancreatic tissue, restoring and maintaining normal glucose levels and healthy body weight.  Importantly, these results enhance our understanding of the mechanisms of self-repair elicited by PCs, which may represent a novel cell therapy-based approach to treating diseases marked by tissue damage and loss of organ function."

Richard L. Franklin, M.D., Ph.D., Founder, CEO and President of Pathfinder said, "We are pleased to share our preliminary findings for this exciting new cell-based technology.  We will continue to focus our efforts on elucidating the mechanism by which PCs stimulate tissue regeneration, as well as explore the potential use of such therapy in treating diseases with high unmet need such as diabetes, cardiac ischemia, and renal reperfusion injury."

The efficacy of PC treatment was examined using the common streptozotocin (STZ)-induced diabetic mouse model.  At three and ten days following administration of STZ, which destroys insulin-producing beta-cells, 1.5 million human or rat pancreas-derived PCs were injected into mice intravenously.  As early as day nine, animals treated with rat or human PCs had significantly lower blood glucose than control animals (p<0.01).  Animals in the control group became profoundly diabetic within one week following STZ administration, while PC-treated mice showed a progressive reduction in blood glucose, achieving normal levels by day 39 and maintaining these levels with no further treatment through day 89, at which point the study was terminated.  Concurrent with the restoration of normal glucose levels, PC-treated animals recovered from an initial loss of body mass and maintained normal body weight for the remainder of the study.

Immunohistochemical analyses of animal tissues confirmed that PC treatment lead to regeneration of pancreatic beta-cells and formation of functional islets, which displayed normal architecture.  Further examination determined that the regenerated islets consisted overwhelmingly of mouse cells, and to a much lesser extent, donor PCs (0.05-0.18%).  The few PCs present in the islet tissue were diffused throughout sections, indicating that the PCs themselves do not form islet-like structures in vivo.  Importantly, this strongly suggests that PCs activate mechanism(s) in the host that drive pancreatic islet regeneration, but which are not capable of initiating such repair in the absence of PCs.

Dr. Franklin concluded, "These data indicate the feasibility of using PCs to stimulate the regeneration of critically damaged adult tissue.  The further development of PCs as a vehicle for regenerative medicine offers exciting prospects for future therapies."