eso, it is very likely and I would say that it does not take so long because the discussions most likely have started by now.
But IMO before that Prana needs to have a manufacturer and a marketer. IMO the manufacturer does not bring any money to the table but the marketer ( a Big Pharma) needs to pay a lot of money to get PBT2. I am waiting that there will be soon a manufacturer and a marketer. Both of these need to be ready on that very day of approval. Both of these need time to be ready on the approval day, IMO at least some 6 months. This is why I am waiting news every day.
The extension study has still possibilities to demonstrate stronger efficacy in essential measurements. If PBT2 stops the cognition decline and hippocampus artophy during the second year on PBT2 , Prana could get also PBT2 for AD to accelerated approval because of the bad nature of AD (??). But it is still very hypothetical but also possible. Those results are ready in 6 months.
A company is increasing their sales over 30% / quarter and increasing their sales force correspondingly. You need to have some inventory and you need to increase also the production.
There is plenty of work for all 9 people Prana has. They are not marketing people neither drug manufacturers but smart to find new indications for their 1500 MPACs. But Big Pharama has these missing skills. That is why I think that one of Big pharmas will get enough interested in PBT2 to make a deal with Kempler. But I agree, Prana does not need a comercial partner for the ph3 HD study. It has now FDA and most like HD organisations will again come and help in the next phase. But to get PBT2 to the market all over the globe is a very big marketing effort and there it is good to have a big pharma partner.
That is my prediction but let us see. So the case would be " Accelerated review- approval with post approval conditional studies" . It could well be something else but I think we will hear soon about it more.
To me it looks like discussions are ongoing and that also ph3 study will be done for HD. I assume that PBT2 could get to the market as an investigational drug.
J Alzheimers Dis. 2014 Sep 26. [Epub ahead of print]
Towards a Unified Vision of Copper Involvement in Alzheimer's Disease: A Review Connecting Basic, Experimental, and Clinical Research.
Pal A1, Siotto M2, Prasad R1, Squitti R3.
Copper is an essential micronutrient for physiological cell functioning and central nervous system (CNS) development. Indeed, it is a cofactor of many proteins and enzymes in a number of molecular pathways, including energy generation, oxygen transportation, hematopoiesis, cellular growth and metabolism, and signal transduction. This is because it serves as a catalyst of reduction-oxidation (redox) reactions in these processes. When copper is kept under control, bound to special proteins, it yields key properties. However, when it spirals out of control, it is exchanged among small compounds (it is loosely bound to them), and its redox activity makes it dangerous for cell viability, promoting oxidative stress. Copper homeostasis in the CNS is securely synchronized, and perturbations in brain copper levels are known to underlie the pathoetiology of wide a spectrum of common neurodegenerative disorders, including Alzheimer's disease. The main objective of this review is to provide some of the most relevant evidence gleaned from recent studies conducted on animal models and humans, and to discuss the evidence as it pertains to a new concept: Aberrant copper metabolism, which appears to have a genetic basis, is a modifiable risk factor accelerating Alzheimer's disease and initiation/progression of cognitive deficits in a percentage of susceptible persons.
Yes, this is just the way how the hedge fund managers do, they do it in both ways ! They can use a few millions to get the pps up and down, what ever they want. Cremer told it all few years ago in a video interview ( it was posted again on the HC board) They give misinformation to some who distribute it further etc.
So I think that they only took the info from the safety monitoring board (perhaps a bit old report) and what they had used when filling the forms for PBT2 to be an Orphan drug. In that application safety is a big thing, they had to inform exactly how long the patients had been on the drug. If anyone reports something only about the progress of extension study he will not tell in this quite a complex way as was in this July announcement. Only my opinion once again.
Linda, in the preliminary annual report they say " study is on going and will be compleated at the end of 2014/early 2015".
I think they reported in July safety info, how many people had been checked by the safety monitoring board and how long each of them had been on PBT2. But this has been informed very poorly.
It would not be according to the protocol if one single person had been not taken the drug for several months and then started on it again. At this point I believe the preliminary annual report "the end of 2014/early 2014".
This is a free paper but unfortunately in Japanese language. There are however also nice pictures about plaque formation and about the role of metals in synapses. In any case this is a good demonstration that metal theory is widely accepted in the world and in fact it is not anymore a theory.
Nihon Eiseigaku Zasshi. 2014;69(3):155-65.
Crosstalk between Metals and Neurodegenerative Diseases.
Kawahara M1, Mizuno D.
Trace elements including iron, zinc, copper, and manganese play essential roles in the maintenance of brain functions. Accumulating evidence suggests that dyshomeostasis of trace elements is implicated in the pathogenesis of neurodegenerative diseases including Alzheimer's disease, vascular type of dementia, prion diseases, and dementia with Lewy bodies. These diseases share similarity in the formation of β-sheets containing amyloid fibrils from disease-associated proteins, including the β-amyloid protein (AβP), the prion protein, α-synuclein, and polyglutamine, and the introduction of apoptotic degeneration. Trace elements can bind to these proteins and cause their conformational changes. Furthermore, these proteins reportedly play crucial roles in the regulation of trace elements. Considering that these proteins colocalize in synapses, it is possible that the interactions between the disease-associated proteins and trace elements are based on the physiological roles of these proteins. We review here the current understanding of the pathology of neurodegenerative diseases based on metal binding to disease-associated proteins and on the disruption of metal homeostasis.
I think that the daily numbers are better than the ones reported twice a month because they inform the daily shorts bought and it is easy to remember what happened on that day. What we should still need to know how much shorts have sold each day and so we would know the daily balance of shorts. Big picture is more valuable and so small accuracy problems do not matter. One day we will have it and so more clear picture can be seen about the short activity. With Prana the short activity is not so important at all because all that really matters is the progress of PBT2 to the market.
Yesterday it was 27% ( 303277) of the total vol of 1129080. This could indicate again some pressure on the PPS but it could be that the total vol of shorts has gone down during the past few weeks.
This is a crossectional study, but looks like it would be beneficial to do exercises and control your wight.
Neurobiol Aging. 2014 Aug 27. pii: S0197-4580(14)00541-7. doi: 10.1016/j.neurobiolaging.2014.05.036. [Epub ahead of print]
Physical activity, body mass index, and brain atrophy in Alzheimer's disease.
Boyle CP1, Raji CA2, Erickson KI3, Lopez OL4, Becker JT5, Gach HM6, Longstreth WT Jr7, Teverovskiy L8, Kuller LH9, Carmichael OT10, Thompson PM11.
The purpose of this study was to use a novel imaging biomarker to assess associations between physical activity (PA), body mass index (BMI), and brain structure in normal aging, mild cognitive impairment, and Alzheimer's dementia. We studied 963 participants (mean age: 74.1 ± 4.4 years) from the multisite Cardiovascular Health Study including healthy controls (n = 724), Alzheimer's dementia patients (n = 104), and people with mild cognitive impairment (n = 135). Volumetric brain images were processed using tensor-based morphometry to analyze regional brain volumes. We regressed the local brain tissue volume on reported PA and computed BMI, and performed conjunction analyses using both variables. Covariates included age, sex, and study site. PA was independently associated with greater whole brain and regional brain volumes and reduced ventricular dilation. People with higher BMI had lower whole brain and regional brain volumes. A PA-BMI conjunction analysis showed brain preservation with PA and volume loss with increased BMI in overlapping brain regions. In one of the largest voxel-based cross-sectional studies to date, PA and lower BMI may be beneficial to the brain across the spectrum of aging and neurodegeneration.