Guildford, UK, 12 July 2010: ReNeuron Group plc (LSE: RENE.L) today announces important new data regarding the mechanisms of action of its lead CTX stem cell line in pre-clinical models of brain damage. The results of these studies will be presented in two posters1 at the UK National Stem Cell Network Annual Scientific Conference, taking place on 12 – 14 July, 2010 at the University of Nottingham, East Midlands Conference Centre, Nottingham, UK.
In one series of studies, the angiogenic potential of the CTX stem cell line was tested, both in vitro and in rodent models of stroke damage. Angiogenesis is a multiple-step process whereby new blood vessels develop from pre-existing vasculature, potentially contributing to the functional recovery of the brain from damage such as that caused by ischaemic stroke. The results of these studies showed that the CTX cells express several trophic and pro-angiogenic factors in culture and also induce endothelial cell markers associated with blood vessel formation in the host at both 72 hours and 7 days post-implantation of the cells into the brain. Taken together, these results suggest that the CTX cells may play a role in promoting the functional recovery of stroke patients through up-regulation of angiogenesis in the region of ischaemic brain damage.
In a series of further studies, the CTX cells were seen to inhibit T cell activation. This immunosuppressive activity was in part attributed to the up-regulation of the ligand CD274, a regulator of T cell function. T cells are a type of white blood cell associated with the mediation of immune responses in the body. These results suggest that the CTX cells may act to suppress the inflammatory response associated with brain damage, thereby aiding the natural healing processes in the brain. This anti-inflammatory characteristic opens up a number of exciting new potential applications for the CTX cell line as a cell-based therapy for certain inflammatory diseases both within and beyond the brain.
ReNeuron recently announced the commencement of a UK Phase I clinical trial of its lead ReN001 stem cell therapy for disabled stroke patients. The ReN001 therapy represents the initial therapeutic application of the Company’s CTX stem cell line. Due in part to the anti-inflammatory properties of the CTX cells, patients in this clinical trial will not require immunosuppressive drug treatments alongside their cell therapy.
Further information concerning the conference can be found at: www.uknscn.org/meetings/meetings10.html.
John Sinden, Chief Scientific Officer of ReNeuron, said:
“We are excited by the results of these new pre-clinical studies. They build on previously presented research findings regarding the way in which our CTX cell line may effect repair in the brain, and suggest that a number of repair mechanisms may be at work, post-implantation of the cells. These latest findings further illustrate and potentially explain the potency of the CTX cells in assisting the body’s own repair mechanisms in vascular conditions such as stroke and peripheral arterial disease, and suggest the potential utility of the cells to treat a much wider range of inflammatory diseases.”
1. Human neural stem cells promote angiogenesis in vitro and in vivo following intracerebral implantation Hicks C, Stevenato L, Richardson S, Stroemer P, Corteling R, Miljan E, Sinden J.
Involvement of CD274 in neural stem cell line mediated suppression of T cell activation Corteling R, Stevenato L, Hicks C, Miljan E, Sinden J.
Michael Hunt, Chief Executive Officer – ReNeuron +44 (0) 1483 302560
Dr John Sinden, Chief Scientific Officer – ReNeuron
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ReNeuron is a leading, clinical-stage stem cell business. Its primary objective is the development of novel stem cell therapies targeting areas of significant unmet or poorly met medical need.
ReNeuron has used its unique stem cell technologies to develop cell-based therapies for significant disease conditions where the cells can be readily administered “off-the-shelf” to any eligible patient without the need for additional immunosuppressive drug treatments. ReNeuron’s lead candidate is its ReN001 stem cell therapy for the treatment of patients left disabled by the effects of a stroke. A ground-breaking first-in-man clinical trial of ReN001 has recently commenced in the UK. ReNeuron’s ReN009 stem cell therapy is being developed as a treatment for peripheral arterial disease, a serious and common side-effect of diabetes. The Company is also developing stem cell therapies for other conditions such as blindness-causing diseases of the retina.
ReNeuron has also developed a range of stem cell lines for non-therapeutic applications – its ReNcell® products for use in academic and commercial research. The Company’s ReNcell®CX and ReNcell®VM neural cell lines are marketed worldwide under license by USA-based Millipore Corporation.
ReNeuron’s shares are traded on the London AIM market under the symbol RENE.L. Further information on ReNeuron and its products can be found at www.reneuron.com.
This announcement contains forward-looking statements with respect to the financial condition, results of operations and business achievements/performance of ReNeuron and certain of the plans and objectives of management of ReNeuron with respect thereto. These statements may generally, but not always, be identified by the use of words such as “should”, “expects”, “estimates”, “believes” or similar expressions. This announcement also contains forward-looking statements attributed to certain third parties relating to their estimates regarding the growth of markets and demand for products. By their nature, forward-looking statements involve risk and uncertainty because they reflect ReNeuron’s current expectations and assumptions as to future events and circumstances that may not prove accurate. A number of factors could cause ReNeuron’s actual financial condition, results of operations and business achievements/performance to differ materially from the estimates made or implied in such forward-looking statements and, accordingly, reliance should not be placed on such statements.