ReNeuron Group plc has announced that it has taken a major step forward with its ReN002 diabetes programme with the generation of new data concerning its pancreatic cell lines for the treatment of Type 1 (juvenile) diabetes.
ReNeuron scientists have generated stable human pancreatic cell lines that form islet-like cell clusters. These clusters were shown to secrete insulin in response to glucose concentrations, demonstrating their potential as a cell therapy candidate for Type 1, insulin-dependent, diabetes patients.
The cell lines were generated using ReNeuron's patented c-mycER stem cell expansion technology, and can be continuously grown in culture. The cell lines were pre-screened for both genetic stability and their ability to express the appropriate phenotypic markers for insulin-producing beta cells, such as the islet cell transcription factor PDX1 and the functional beta cell receptor GLP1R.
These results will be presented at the JDRF Center for Beta Cell Therapy in Diabetes' 2007 Training Course in Bath, UK on 26-28 June. The ReN002 cells are currently being taken forward into pre-clinical models of diabetes.
The Company believes that its ability to efficiently expand well-characterised ReN002 cells using its c-mycER technology may offer a solution to the current problem facing experimental islet cell transplantation – the limited availability of donated pancreas tissue from which to derive purified islets.
Commenting on the announcement, Dr John Sinden, Chief Scientific Officer of ReNeuron, said: "We are excited by these results with our ReN002 programme, not least because having already demonstrated the ability of our c-mycER stem cell expansion platform to generate viable cell lines for neurological disorders, these new data indicate the potential of the technology to work in other significant disease areas. We now have the basis of a scalable cell therapy approach to Type 1 diabetes, a major disease target and one in which we believe cell therapy will play an important role in addressing in the future."