I wanted to apologize if I inadvertently pumped the stock up 11 cents to have a nice end to the week he he - TGIF! I'll try to be more pessimistic next time LOL
Actually, I don't think anything I could say means squat, but I also do not I believe in the efficient market theory either. Especially in a market held up by QEx as we flush our economic future away.
Not much, however, 1 week closer, PLUS:
Novartis wants in the Neuro-degenerative disease space and is openly shopping for a seat at the table. Wasn't the earlier 12 week human study of PBT2 performed in Sweden? (I'm not sure, but I think so). Also, a shake-up in the long-standing leadership at Novartis and Roche, where you are likely to see some interesting moves from these two players according to Jeffries analyst.
Merck perhaps purveying the field looking for opportunities too, discontinuing further development of a Parkinson's candidate and we have PBT434 having met pre-clinical milestones so far in the MJFF pipleline, yet they are not further developing their Parkinson's drug. My best guess is a follow-on grant from MJFF in August around the two year mark.
FDA relaxed guidelines coming any time now , plus other legislation also pushing for other exceptional circumstances to market.
AD a G8 priority. Australia and France are now being held up as models, with already a national funding effort in place to address this issue.
Shift to early detection, and new AD blood plasma screening discovery announce by CSIRO, with Prana Biotech mentioned as un-confirmed beneficiary.
I don't think investors realize what a hot sector AD is becoming, or really believe the possibility that PBT2 could actually be in the market prior to 2016, but the possibility does exists without the shareprice reflecting it at all. The chances of a partnership announcement have never been greater if you look at the regulatory approval environment surrounding Alzheimer's.
We have been mentioned many times in financial news as being among the top 5 in this race, right alongside big Pharma.
Disease modifying results on PBT2 would completely rock the Biotech markets, and analysts do not even pick up on the this sector as a serious opportunity because of all the casualties lying about the battlefield. The risk/reward is off the charts for any winning candidate showing a disease-modifying result.
I agree on reading the entire article. I saw this posted on hotcopper, and of course there are no limits to the size of your post their so the entire article was copied and referenced with a link - like the good old days on YMB. The recent changes to YMB are terrible. I think they have severely limited the quality of their own boards in some of the extreme limits they have placed on postings.
I can see such limits on trailing comments to news article, but to so severely limit an investors message board really cuts into the quality and value of their message boards. just my opinion...
Griffith, Peters, McCaul Introduce the Patient Choice Act
H.R.2090 - To amend chapter V of the Federal Food, Drug, and Cosmetic Act to permit provisional approval of fast track products.
Three US legislators have moved to introduce legislation they say would accelerate US Food and Drug Administration (FDA) approvals while giving patients the option to obtain therapies outside of clinical trials.
A New Bill
A statement from the co-sponsors of the bill—Reps. Morgan Griffith (R-VA), Scott Peters (D-CA) and Michael McCaul (R-TX)—however, indicate that as quickly as FDA might be moving, it's not quick enough for the estimated 500,000 patients who die each year from cancer. "For diseases like melanoma, Lou Gehrig’s disease, and Parkinson’s disease, either very few drugs are available or those in the pipeline cannot make it through FDA’s delays and regulations," they said.
The solution, they said, lies in their new bill, the Patient Choice Act of 2013, which allows patients to purchase access to experimental treatment options, giving them an additional chance at a life-saving therapy.
“There are research facilities in San Diego developing potentially life-saving medicines and therapies, which have been proven safe after rigorous testing. Unfortunately, because of the lengthy FDA approval process, patients with the most urgent need aren’t able to access them,” Peters wrote in a statement. “We should be doing more to promote research and innovation here in the United States, and this bill is a way to incentivize researchers to stay here while getting patients remedies that they need.”
another one bites the dust...
Merck & Co. (MRK) said it will end development of the experimental drug preladenant for Parkinson’s disease because a preliminary review of the data from late-stage clinical trials suggests it doesn’t work.
The drugmaker said it will stop the extension portions of the trials and no longer plans to file for marketing approval of the medicine. There were two studies that added preladenant to levodopa, the standard treatment for Parkinson’s disease, and one that tested it as stand-alone care, Whitehouse Station, New Jersey-based Merck said in a statement.
CHICAGO (Reuters) - U.S. scientists say a dramatic result last year suggesting that a cancer drug already approved by U.S. regulators could quickly clear out Alzheimer's plaques in mice was too good to be true.
The study, published last year in the journal Science, showed the skin cancer drug bexarotene cut the amount of an Alzheimer's-linked protein called beta amyloid by half in three days. It also reversed Alzheimer's symptoms, restoring a sense of smell in treated mice and allowing them to resume nest building activities.
"People were clamoring for this drug after he went on TV and was pushing it."
Sisodia said he and fellow Alzheimer's colleagues, who included Dr. Rudolph Tanzi of Massachusetts General Hospital in Boston and Dr. David Holtzman of Washington University School of Medicine, wanted to see if the stunning results could be replicated in their own labs, a standard part of the scientific process.
Researchers failed to see any effects on Alzheimer's plaques in three strains of mice that were treated with bexarotene.
As I recall, in the original treatments of the earlier PBT1, that it lead to a severe vitamin B12 deficiency, and I even thought that at some point w/PBT1 or PBT2 that it was intended to administer vitamin B12. Not saying there is a link with these standalone study findings, just a curious association of recall that came to mind. My hope is for PBT2 to be a disease-modifying piece of the puzzle toward a cure. Maybe B complex vitamins have their place too.
Kad, Prana has apparently has a framework agreement in place with the CSIRO. It seems not so transparent, or else I am simply clueless about it which is as likely - could this be a stumbling block to a deal? I wish I knew more. I still consider the positives to outweigh negatives, such as the recent multi-million dollar refund Prana recently received, allegedly being a financial beneficiary of this new blood-plasma based panel for A-beta burden/load, etc.,
It's perhaps old news to LT holders, but I never quite got up to speed on it.
It is thought that their primary mechanism of action is to redistribute extracellular metal ions to intracellular stores where they are required for biochemical function.19
 While these reports are encouraging for the further development of metal-targeted compounds for neurodegenerative disease, concerns remain for the unintended consequences of manipulating metal distribution in the brain. New reagents are needed that can function as metal-binding agents that mitigate the damaging effects of metals while preserving their beneficial effects.
SUMMARY OF THE INVENTION
 Herein, we disclose prochelators that are designed to bind metals only under conditions of oxidative stress. Given that elevated production of H2O2 by deviant Cu-Aβ interactions may be the trigger point for neurodegeneration, prochelators that are activated by H2O2 may be beneficial for managing a transition metal burden at locations of disease progression without stimulating widespread metal redistribution.
 Provided herein are prochelator compounds of Formula I or Formula II:
Other evidence, however, suggests that Aβ-Cu complexes are pro-oxidant and directly culpable of neurotoxicity. In vitro, Aβ in the presence of Cu or Fe and reducing agents like ascorbate produces H2O2, which can subsequently react with the reduced metal to produce hydroxyl radicals via the Fenton reaction.9-11 Metal-mediated H2O2 generation appears at an early stage during in vitro Aβ aggregation,11 which supports the notion that soluble Aβ-Cu species are responsible for the oxidative damage that is one of the earliest pathological events in AD.12 Furthermore, copper has been shown to intensify Aβ toxicity in primary cortical neurons.9, 10, 13 Like Cu2+, Zn2+ also promotes Aβ aggregation in vitro, but the Zn-induced aggregates appear to be neuroprotective, perhaps by displacing Cu2+ and thereby suppressing H2O2 generation.14-16
 An emerging hypothesis to reconcile the seemingly contradictory evidence related to metals, Aβ, and oxidative stress is that metal binding and Aβ aggregation may represent an initial, protective response to dampen ROS production. Excessive H2O2 production and an overburden of Cu could eventually push the system into a vicious cycle that switches Aβ-Cu activity from antioxidant to pro-oxidant.17 During this stage, metal exchange with Zn2+ could promote further Aβ aggregation as a defense against Cu-induced damage. While strong chelating agents are known to reverse metal-induced aggregates, this model suggests that disaggregating plaques alone could have the unintended consequence of exacerbating oxidative damage.17
 Metal chelating agents have appeared as a compelling strategy for Alzheimer's disease therapies.18 In particular, 8-hydroxyquinoline (8HQ) derivatives clioquinol and PBT2 have shown promising results in mouse models and in phase IIa clinical trials of Alzheimer's patients.19, 20 These compounds inhibit metal-induced Aβ aggregation and ROS generation.21
You failing to mention the last dilution that should have dropped the stock down to under 6.2 cents per share, and at the same the CEO promoting his WIFE to VP. Now, I am not implying anything sexist here - just implying the conflict of interest that exists with this company that any prudent investor would want to know this looks more like a family scam shell company existing of a guy and his wife, and pumping this QTMM sham company into something other than what is you should called out for it, and you are calling others thieves and derogatory?!!!
I am glad to see this. If you look at the patent filing I put forward and go read it, as I recall there is a discussion of the oxidation process, at what points it goes wrong, and it includes mention of PBT2 in the discussion. This patent claims that even under PBT2 treatment there can arise a trigger of oxidative stress for a period and the invention draws something away from the harmful, basically "hydrogen peroxide" structure of chemistry to prevent the harmful mechanism of oxidative stress. It is worth a read.
Sorry, but the most recent Proceedings of the National Academy of Sciences (PNAS) journal I could find available online was date 5/16, so I could not see the actual publication. Quite a few scientific newsfeeds are picking up on the news, so must be in some RSS feed, or something that goes out.
Yahoo recorded the session high at .245, which is USD 2.498, so if there is follow through today we should be bumping 2.50. Nice increasing volume. I am sure traders are taking notice so this type of trend can feed on itself a bit, but we've been a news driven stock for the most part.
Maybe the time to speculate on the trial outcome has finally arrived?
Perhaps someone can find the actual research that was published.
Molecular Trigger for Alzheimer's Disease Identified
May 20, 2013 — Researchers have pinpointed a catalytic trigger for the onset of Alzheimer’s disease – when the fundamental structure of a protein molecule changes to cause a chain reaction that leads to the death of neurons in the brain.
For the first time, scientists at Cambridge’s Department of Chemistry have been able to map in detail the pathway that generates “aberrant” forms of proteins which are at the root of neurodegenerative conditions such as Alzheimer’s.
They believe the breakthrough is a vital step closer to increased capabilities for earlier diagnosis of neurological disorders such as Alzheimer’s and Parkinson’s, and opens up possibilities for a new generation of targeted drugs, as scientists say they have uncovered the earliest stages of the development of Alzheimer’s that drugs could possibly target.
The study, published today in the Proceedings of the National Academy of Sciences, is a milestone in the long-term research established in Cambridge by Professor Christopher Dobson and his colleagues, following the realisation by Dobson of the underlying nature of protein ‘misfolding’ and its connection with disease over 15 years ago
Patent application title: PROCHELATORS USEFUL FOR INHIBITING METAL-ASSOCIATED TOXICITY
Inventors: Katherine J. Franz (Durham, NC, US) Marina G. D, Leed (Durham, NC, US)
IPC8 Class: AC07F504FI
USPC Class: 514 64
Class name: Drug, bio-affecting and body treating compositions designated organic active ingredient containing (doai) boron containing doai
Publication date: 2013-04-18
Patent application number: 20130096085
It is a given there will be an announcement of trial completion, so we are not within 40 days of receiving news of successful trial completion. Even without having results, it is somewhat of a safety & efficacy statement with the last formal dose duration being 12 weeks.
So announcement even of trial completion even without having results compiled is a positive news release for sure.
No comment was made by management that they will not raise additional funds before trial completion. I hope additional financing does not come before we have a double, triple or more, but for the record I did not read any statement by management that set any expectation as to future financing decisions or timing.