This paper below is an animal study but there could well be one of Prana's MPAC for MS.
Choi BY et al, Jan 26.2013 :
The present study aimed to evaluate the therapeutic potential of clioquinol (CQ), a metal chelator, on multiple sclerosis pathogenesis. Experimental autoimmune encephalomyelitis was induced by immunization with myelin oligodendrocyte glycoprotein (MOG(35-55)) in female mice. Three weeks after the initial immunization, demyelination and immune cell infiltration in the spinal cord were analyzed. CQ (30mg/kg) was given by gavage once per day for the entire experimental course. CQ profoundly reduced the daily clinical score and incidence rate of EAE mice. The CQ-mediated inhibition of the clinical course of EAE was accompanied by suppression of demyelination and reduced infiltration by encephalitogenic immune cells including CD4, CD8, CD20 and F4/80 positive cells. CQ also remarkably inhibited EAE-associated BBB disruption and MMP-9 activation. Autophagy contributes to clearance of aggregated proteins in astrocytes and neurons. The present study found that EAE increased the induction of autophagy and CQ further increased this expression. Furthermore, the present study found that post-treatment with CQ also reduced the clinical course of EAE and spinal cord demyelination. These results demonstrate that CQ inhibits the clinical features and neuropathological changes associated with EAE. The present study suggests that transition metals may be involved in several steps of multiple sclerosis pathogenesis. HIGHLIGHT: EAE mice spinal cord shows aberrant vesicular zinc staining in the white matter. Clioquinol inhibited the daily clinical score and incidence rate of EAE mice. Clioquinol suppressed demyelination and reduced infiltration of encephalitogenic immune cells. Clioquinol inhibited the EAE-associated BBB disruption and MMP-9 activation. Clioquinol increased the induction of autophagy in EAE mice.
We should savor these days when the share price remains in the $2 ballpark as we wait in anticipation of the clinical results for HD and AD. This is excitement at its best. If the results are as good as we hope they'll be, MPAC could suddenly become the new paradigm for treating neurodegenerative diseases and we could become rich from our humble shareholdings. If not, we'll remain poor and will have to lick our wounds. If the former scenario pans out and the share price rockets and Prana becomes a household name in pharmaceutical-investing circles, we'll be able to look back and relish the days when we could buy the stock for $2 instead of $50.
A friend of mine bought shares of Apple for $4 a number of years ago, and recalls the anxiety of wondering whether the stock was overpriced at the time.
Very good post regarding impact on Prana IP, amongst other things.
My understanding is that Prana has marketing rights to Clioquinol in the US. Correct?
The deepening foundation of promising pre-clinical research regarding their MPAC library should increase the company IP value - and continues to make the stock seem undervalued IMO.
I get the feeling that the current small group of Prana people are geared to complete the heavy tasks in moving on AD/HD - their research focus over 2 decades - and methodically progressing to a PD phase 1. But it doesn't appear that an MS agent, clioquinol or modification thereof, would seem to be on the radar screen. Perhaps this is underestimating the company.
Everybody is using Clioquinol, because it is available, but Prana probably have better in their library. In the split Prana got the USA and Japan for Clioquinol marketing, but by the time that was resolved Prana had already moved on to better MPACs with more BBB penetration, better safety profiles and worldwide marketing rights. I think the CSIRO owns 1% of PBT2. I wish they owned more for obvious reasons.The CSIRO seems to operate that way. When they won the case for WiFi rights, they could charge whatever they wanted, but just took the small percentage agreed to in the original agreement.
The CSIRO s running the AIBL longidudinal study into Alzheimer´s, as most on here will know, with 1000+ patients. Does anybody here know if the AIBL eventually decided to throw in with Reisa Sperling´s A4 trial? I doubt that would happen, but you never know.
Prana's home page: "The mission of the company is to develop disease modifying therapeutics for the treatment of common neurological disorders, with a focus upon Alzheimer's, Parkinson's and Huntington's diseases. Other potential applications for this platform technology include specific cancers and Age-related Macular Degeneration".
Prana has over 800 MPACs in it's library. It is self clear that it will develop these potential drugs to be used in many different diseases as in MS, ALS,essential tremor etc , but now at first AD, HD and PD. They have a lot of understanding the MPACs work and so later perhaps there are also MPACs for cardiomyopathy, cancers, strokes etc.