In experiments described in the paper, Fallon's team showed that biglycan delivered to the bloodstream draws utrophin to the cellular membranes of muscle cells.
In more recent tests using an improved formulation of biglycan, Fallon said the team has seen that figure rise to 50 percent in some muscles, meaning that mice treated with biglycan are holding on to more of their function for a longer time.
The absence of a chemically identifiable interterritorial matrix was confirmed by the immunoreactivity of the epiphyseal cartilage for biglycan and decorin (Figure 3).
Previous studies have shown that biglycan and decorin are expressed in normal epiphyseal chondrocytes, but they are distributed in the cartilaginous matrix in a mutually exclusive pattern.
This award provides funding and support for the accelerated preclinical development of biglycan as a novel disease-modifying therapeutic for Duchenne Muscular Dystrophy (DMD).
NIH's continued support of biglycan is only the most recent accomplishment originating from Dr.
21, 2012 /PRNewswire-USNewswire/ --Parent Project Muscular Dystrophy (PPMD) announced today that it will award Tivorsan Pharmaceuticals (Tivorsan) a $500,000 grant to develop the company's biglycan therapeutic candidate for Duchenne muscular dystrophy.
Building on that work, the Tivorsan team seeks to use recombinant human biglycan (rh-BGN) to increase utrophin at the muscle cell membrane, resulting in reduced muscle damage and improved function.
Tivorsan's Biglycan is a proprietary form of a naturally-occurring protein that works through a compensatory pathway to restore muscle health in dystrophin-deficient muscles.
This method, using recombinant human biglycan, is based on 25 years of basic science work in the Fallon laboratory at Brown University, Providence, RI.
In the standard mouse model of DMD, biglycan
reduced muscle damage, reduced muscle degeneration and improved muscle function.
The company is actively working towards human clinical studies with a proprietary form of the natural biglycan
protein, which appears to have a unique mechanism of action that may apply to all genetic forms of DMD.