Diabetes-induced break down of the blood-retinal barrier outcomes in leaky blood vessels in the eye.
The pharmacological activity of ASP-440 in reducing the extreme retinal albumin leakage in diabetic and hypertensive rats suggests that the serine protease plasma kallikrein has a key role in blood-retinal barrier breakdown caused by hyperglycemia and hypertension, therefore inhibition of this enzyme might provide a new therapeutic approach to the treatment of DME , commented Tamie J. Chilcote, Ph.D., chief operating officer of ActiveSite, and a co-author of the scholarly study. Also, because ASP-440 works well via a systemic route of administration, without need for intraocular delivery, targeting plasma kallikrein opens up the chance of an orally-administered therapeutic method of DME. .. ActiveSite’s ASP-440 plasma kallikrein inhibitor effective in reducing diabetes-induced blood-retinal barrier breakdown ActiveSite Pharmaceuticals, Inc., announced today the web publication of a report in the journal Diabetes that describes the potency of its novel plasma kallikrein inhibitor ASP-440 in reducing blood-retinal barrier breakdown in a rodent style of diabetes.However, the mechanism where corticosteroids stabilize or appear to accelerate regression of this tumor is unknown. We recently isolated and identified hemangioma-derived multipotential stem cells from specimens of proliferating infantile hemangiomas.5 These cells screen a mesenchymal morphology, robust proliferation, and multilineage differentiation in vitro and form human arteries with features of infantile hemangioma when injected subcutaneously into nude mice.5 This vasculogenic activity is unique to hemangioma-derived stem cells; hemangioma-derived endothelial cells6 and hemangioma-derived endothelial progenitor cells,7 which are phenotypically much like normal individual endothelial cells when cultured in vitro, do not form arteries in this murine model.