Ann: Prana's PBT2 Directly Restores Neurons C, page-30

re: Ann: Prana's PBT2 Directly Restores N... OK tumesy, again sorry for the late reply. I have been away from the computer again. Normally if a world leading scientist like Melbourne University laureate professor Colin Masters puts his name on an abstract, then that abstract has been peer reviewed, as an investor I would take them at their word. I don't think anyone would disagree with that. I am sure you would agree.

Prana demonstrated the metal chaperone ability of PBT2, and the break down the plaques, and use the Western blot to show increased levels of phosphorylated GSK-3 a & b in the cells. "These data demonstrate PBT2 can decrease Ab levels by sequestering the Zn that promotes extracellular formation of protease resistant Ab:Zn aggregates, and that subsequent intracellular translocation of the Zn by PBT2 induces cellular responses with synapto-trophic potential."

Prana have strong evidence of an effect in the cell through observation of the increased of phosphorylated GSK-3. (OK not proof of cell repair, but evidence) As I understand it, they were not trying to call this a new mode of action, they had previously made that claim in the original paper and even before that. They had demonstrated the cell and dendritic spine repair/re-growth in the original paper.

A point that makes all this research more convincing, is that it was initiated to investigate cognition loss reversal, already demonstrated in a human clinical proof of concept trial.
What makes this research of such vital importance, is doubt that has been leveled at the results, regarding the durability of the response beyond 12 weeks, and the fact it is a genuine disease modifying treatment.
Some cite those two concerns and disregard the results of that trial. This new research, combined with the PBT1 85week results, suggests to me the chance of not being a durable response is remote.
Evotec made this assertion on their info sheet regarding their recent $830 million Roche deal just a few days ago.

"To date, no drug has demonstrated the ability to slow the progress of Alzheimer's disease, with all Phase III trials that have reported to date failing, Lanthaler noted. Meanwhile, drugs targeting the beta-amyloid pathway are yet to achieve proof of concept."
http://www.bioworld.com/servlet/com.accumedia.web.Dispatcher?next=bioWorldHeadlines_article&forceid=59411

None yet even achieved proof of concept. A proof of concept trial starts after the safety trial (phase1) is over. It can be a phase2a or 2b. I would call reversing some Alzheimer's cognition loss in just 12 weeks a very good proof of concept. That detail suggesting how the cell is repaired, is a very strong indication that the response will be durable and that PBT2 is indeed a disease modifying treatment. We need news like this when a CEO feels he can make a statement like the above.


This new evidence provides even more validation of the 2a human trial result, and added value is reasonable.
For a Pharma, it may or may not be enough to swing a deal.

For this investor,
It tells me that the chance for cognition improvement in the Huntington's trial is very good, considering that MOA has already worked on Alzheimers patients
It tells me to expect that the next Alzheimer's trial will demonstrate a durable response, and an increasing response. We already had that evidence from the original weaker PBT1 trial, which demonstrated an increasing response, although not reversal, in an open label trial out to about 85weeks. To see this evidence pointing to actual cell repair from PBT2 is very reassuring.


All the above is just my opinion. Please do your own research.

Abstract
http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2011.07402.x/abstract