Oxford Biomedica. 2005 to see 'Huge value creation' (Panmure Gordon)

Followers of the science may recall the paper in Nature in 2004, showing that vascular endothelial growth factor (VEGF), delivered via a lentiviral vector (which one not stated in abstract) expressing VEGF, prolonged survival in a pre-clinical model of ALS (the major form of motor neurone disease, MND). This is the basis of MoNuDin.




In July this year a paper in Neurobiol Dis from Boulis in USA - collaborator with OXB and including several OXB names - has shown that the insulin-like growth factor-1, IGF-1, again delivered by lentivirus vector (specifically EIAV, modified with a rabies protein which gets it taken up well by motor neurones (MN)), produced enhanced survival of MNs (in cell culture; not tested in intact animals) compared to controls and caused the MN axons to elongate greatly. The abstract concludes : “The enhanced motor neuron tropism of RabG.EIAV previously demonstrated in vivo, together with the trophic effects of RabG.EIAV-IGF-I MN gene expression may lend this vector to therapeutic application in motor neuron disease.”



The first study reported:
“VEGF treatment increased the life expectancy of ALS mice by 30 per cent without causing toxic side effects, thereby achieving one of the most effective therapies reported in the field so far.”

There may be a second string to the MND bow too.

rrr