ReNeuron Group PLC (LON:RENE) said new positive data relating to its CTX cell therapy candidate have been published in the peer-reviewed scientific journal Stem Cells.
The developer of cell-based therapeutics said the data was included in a paper entitled "Implantation of the clinical-grade human neural stem cell line, CTX0E03, rescues the behavioural and pathological deficits in the quinolinic acid-lesioned rodent model of Huntington's disease".
It said the new data show for the first time that ReNeuron's CTX human neural stem cell line can rescue deficits associated with an accepted animal model of Huntington's disease, a progressive genetic brain disorder.
ReNeuron has previously presented data demonstrating that its CTX stem cell line, currently undergoing clinical evaluation for the treatment of stroke disability, can cause functional and behavioural recovery in animal models of ischemic (restriction of blood supply) injury.
The new data published today show that implantation of CTX cells into a model of Huntington's disease can reduce inflammation, glial scar formation and induce host neurogenesis (the generation of new brain cells) leading to a recovery in behavioural deficits.
ReNeuron said the results are particularly encouraging as they also demonstrate that CTX, a well-characterised neural stem cell line that has been evaluated in multiple pre-clinical and clinical studies, can differentiate into medium spiny neurons, engraft into the host tissue and form functional connections with the surrounding tissue.
"The data being published today represent a significant advance in the potential use of human allogeneic stem cell lines as therapeutic candidates for the treatment of Huntington's disease,” Dr Randolph Corteling, the head of research at ReNeuron said in a statement.
“Importantly, the immortalisation technology found within ReNeuron's CTX cell line allows for the scaled production of 'off the shelf' human neural stem cells, with the potential to treat a variety of different neurological disorders," he added.