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Amarantus BioSciences Announces MANF Demonstrates Superiority Over GDNF In Neurorestoration Behavioural Animal Model Of Parkinson's Disease

SUNNYVALE, Calif., Oct. 25, 2012 /PRNewswire/ -- Amarantus BioSciences, Inc. (OTCQB: AMBS), a biotechnology company developing new disease-modifying treatments and diagnostics for Parkinson's disease and Traumatic Brain Injury centred on its proprietary anti-apoptosis therapeutic protein MANF, today announced that the Company has received positive behavioural efficacy data for MANF in a neurorestoration 6-hydroxydopamine (6-OHDA) rat model of Parkinson's disease. The data shows superiority of MANF over GDNF, a neurotrophic factor currently in a Phase 2 clinical trial as a disease-modifying treatment for Parkinson's disease, by demonstrating that when MANF is delivered directly to the primary brain region associated with Parkinson's called the substantia nigra, MANF significantly reduced behavioural deficits in the model, whereas GDNF did not. 

In Parkinson's disease, the nigro-striatal network (substantia nigra – striatum) is compromised due to the degeneration of dopaminergic neurons in the substantia nigra, which results in dopaminergic nerve terminal retraction from the striatum towards the substantia nigra. This leaves the striatum with inadequate dopamine levels, which in turn causes motor function deficits and other symptoms. Currently approved drugs that relieve symptoms focus on replacing the dopamine lost in the striatum; however, the symptom relief is temporary and the drugs typically lose their ability to abate symptoms roughly 7-10 years after the initiation of drug therapy. There are no approved therapies that focus on re-innervating the striatum by protecting dopaminergic neuron cell bodies in the substantia nigra while restoring dopaminergic innervation in the striatum.

In rat studies conducted by an independent academic laboratory contracted by Amarantus, 6-OHDA was injected directly into the striatum on one side of each rat's brain, causing their dopaminergic terminals to retract from the striatum towards the substantia nigra, and creating Parkinson's-like behavioural symptoms that were quantified by counting the number of times the rats turned in a circle in the same direction (behavioural deficits) in a given 120 minute period of time. MANF and GDNF were delivered directly into the substantia nigra of separate groups of rats 2 weeks following the administration of the 6-OHDA, in order to mimic as closely as possible in rats the treatment setting in humans where treatment would be administered after an extended timeframe following the initiation of dopaminergic nerve terminal retraction, each at the optimal dosing level of 10 micrograms. Four weeks following MANF treatment into the substantia nigra, behavioural deficits were reduced by ~43%, and six weeks following MANF treatment, behavioural deficits were reduced by ~53%; four weeks following GDNF treatment into the substantia nigra, behavioural deficits were reduced by ~16%, and six weeks following GDNF treatment, behavioural deficits actually increased by ~20%. 

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