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Prana Biotechnology Limited Message Board

kadaicher1 206 posts  |  Last Activity: 3 hours ago Member since: Jan 23, 2004
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  • kadaicher1 kadaicher1 3 hours ago Flag

    I am just making that assumption based on the statement that he will be using quarterly reports to update on the PCH, which Bob posted above. Close to the halfway point of the year it is not exactly what I wanted to hear. Lets hope I am wrong and it is the next report. Maybe I am just being too negative.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 16 hours ago Flag

    It took longer than anticipated for Kempler to let us know Prana would miss the original guidelines by a wide margin. The result of that is the very low SP we now see.

    Sentiment: Strong Buy

  • Reply to

    Iron promotes Abeta aggregation

    by pivalde May 25, 2016 7:00 AM
    kadaicher1 kadaicher1 17 hours ago Flag

    With a stronger affinity to iron and nearly equal in copper, it would seem pbt434 would be a useful combination drug with the zinc effects of PBT2 in AD.
    [The synergy among 8-OHQs and the rescue of each model by multiple, functionally distinct 8-OHQs establish that each model can benefit from at least two metal chelation-dependent protective pathways.] (Tartiff,Lindquist 2011)
    This will be the first time Prana have had two MPAC drugs to combine against a neurodegenerative condition.

    Sentiment: Strong Buy

  • Reply to

    any explanation?

    by pvretire May 27, 2016 10:46 AM
    kadaicher1 kadaicher1 May 28, 2016 1:50 AM Flag

    Or you could assume that PBT2 is not on the market and therefore not available to continue after a trial.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 27, 2016 12:16 PM Flag

    No he did not like your MAB, Bapi. And he was right.

    Sentiment: Strong Buy

  • Reply to

    any explanation?

    by pvretire May 27, 2016 10:46 AM
    kadaicher1 kadaicher1 May 27, 2016 12:02 PM Flag

    I agree about that trials center. To me it looks like he is using Lawler to attract volunteers. It is pretty sloppy work. Remember Lawler was introduced as a Sola AD patient, but the cameraman filmed a PBT2 container in front of Lawler. It made the trials doc look like he did not know who was on what. That trials center may be effective at executing trials, but I think they spend less on PR than Prana.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 27, 2016 11:30 AM Flag

    I think that is fair comment. In the AIBL they have observed a slow buildup of plaques over time. That is not to say pathogens are not part of the problem, but there is, as Tanzi said, more work to be done.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 27, 2016 10:56 AM Flag

    Yea right Bio. You believed in MABs as I recall. Try to recall Prana's preclinical work on Tau was with a model which produced no AB. Prana is running preclinical work on both Parkinsonian and tauopathy orphans to identify the best orphan to tackle with PBT434. Being head of Prana's scientific team Tanzi probably knows that:-)
    It looks to me like Tanzi and the old farters are streets ahead of any young scientists I know about.
    Tanzi has always said that there are multiple causes of AD and he is still backing the Metals Theory as part of a multi faceted treatment for AD.
    That said the upcoming trial is HD.

    Sentiment: Strong Buy

  • Reply to

    Progress

    by copper725 May 27, 2016 7:52 AM
    kadaicher1 kadaicher1 May 27, 2016 10:41 AM Flag

    Are you that thick. Prana is in the track they identified before the Reach2HD trial. Now they are looking to do a registration trial once their data is complete. Sure they are a little behind the time line. In case you don't understand how things work, a small biotech working in a complex neuro field would probably take a year to plan and start a registration trial. The delay caused by the FDA PCH has sure hit the SP, but it is not as bad as it looks, and when it comes off there is an opportunity to take a nice profit from here.
    I am an investor here. I guess you are short, or a paid basher, or just unbalanced enough to just keep coming back for no reason.

    Sentiment: Strong Buy

  • Reply to

    Progress

    by copper725 May 27, 2016 7:52 AM
    kadaicher1 kadaicher1 May 27, 2016 9:29 AM Flag

    Copper you know that Prana are working on a safety data pack which will clear the way for the entire mpac class of drugs. I am only quoting Prana's annual reports. What is your problem? That is right, you are just a basher troll.

    Sentiment: Strong Buy

  • Reply to

    Progress

    by copper725 May 27, 2016 7:52 AM
    kadaicher1 kadaicher1 May 27, 2016 8:54 AM Flag

    It is from the 2014 annual report. How obvious is that?
    [Accounting for the limitations of conducting a small trial, the unusual and unexpected response of the placebo group, and the body of scientific evidence contained in peer reviewed journals and previous trials, we believe a
    larger trial of PBT2 powered to test cognitive benefit may deliver positive results. We remain committed to
    developing PBT2 for Alzheimer’s Disease alongside Huntington Disease. ]
    You know HD is going to be first. Why keep repeating those stupid questions when you know what is planned from a few years back.I would guess a Parkinsonian orphan may preceed the AD trial as well, but at this point that is just a guess.
    From the 2011 annual report
    [ the World Congress on Huntington’s Disease was held in Melbourne, September 11-14. Prana was a sponsor of the Congress and showcased PBT2 as a promising treatment for Huntington’s Disease, a devastating genetic disease that causes losses in motor functioning and cognition. The Board decided to advance PBT2 in Huntington’s in parallel with Alzheimer’s Disease because it provides a much faster path to market.]
    Now that Reach2HD provided good results in cognition improvement, good enough to base a P3 registration trial on, there is no doubt the HD trial will be first. Hope that clears any doubts you have on the order, and how long that plan has been in place, again.

    Sentiment: Strong Buy

  • Reply to

    Current monoclonal antibody (mab) in AD study

    by copper725 May 26, 2016 11:33 AM
    kadaicher1 kadaicher1 May 27, 2016 7:12 AM Flag

    Ha, I could get dragged into an AD discussion, but the truth is the cost of a full on AD efficacy trial a little beyond Prana right now. They did run the little IMAGINE AD study to try to get some partner interest, but it proved too small for a result either way.
    What has come out of the AD studies is the stat sig executive function gain from the EURO trial in TMTB. That is exactly the same cognition gain demonstrated in Reach2HD, so those results over two diseases are hardly by chance.HD is the lead for PBT2, not AD. My guess is a parkinsonian orphan will also make it to market with PBT434 before a PBT2 registration trial in AD.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 27, 2016 3:38 AM Flag

    PBT2 is an antibiotic with excellent BBB penetrating ability. Zn analog the antibiotic clioquinol, but it was chosen for its attraction to metals.
    From a Tanzi interview this month
    [I also have two drugs in clinical trials. One, that stops the amyloid from aggregating, is called PBT2, from Prana Biotechnology, a company I founded in my lab. That drug aims to stop the aggregation of the amyloid in the brain so it can clear out. And then we have another drug that is just getting into clinical trials that stops the amyloid from being made, that’s called GSM, which stands for gamma-secretase modulator. So one of them basically turns off the spigot, the other unclogs the drain.]
    Of course brain damage which causes excess AB to build can be from other sources, for instance AB build is seen around traumatic brain injury. AB increase has even been noted right after lumbar puncture for no apparent reason.
    Obviously Prof Tanzi does not think PBT2 is finished as an AD treatment. Which is what Prana have stated also.

    Sentiment: Strong Buy

  • Reply to

    Amyloid beta Homeostasis

    by copper725 May 26, 2016 11:16 AM
    kadaicher1 kadaicher1 May 26, 2016 12:58 PM Flag

    It is metal homeostasis with PBT2, mainly inside the neurons. What is homeostasis of AB? Please explain. AB is produced as needed. It has an affinity to metals just a little lower than PBT2.
    No Tanzi was not in on that, but he did speak out against that direction of research, and even provided evidence that AB is a component of the brain's innate immune system.

    Sentiment: Strong Buy

  • Reply to

    Inhibiting AB Aggregation

    by tb00tb00a May 26, 2016 12:00 PM
    kadaicher1 kadaicher1 May 26, 2016 12:21 PM Flag

    An independent opinion from Merz and the Planck Institute when they tested the MOA. [The data indicates that it may be most beneficial for neuroprotective agents such as PBT2, that can interrupt Aβ self-assembly into aggregates, to be administered to early stage patients to best maintain synaptic plasticity and function as an effective treatment for Alzheimer's Disease (AD).]

    Sentiment: Strong Buy

  • Reply to

    Current monoclonal antibody (mab) in AD study

    by copper725 May 26, 2016 11:33 AM
    kadaicher1 kadaicher1 May 26, 2016 12:15 PM Flag

    Considering no disease modifying AD trials have succeeded, that last sentence is not something everybody here needed to read, and they were rushed in with poor P2 or failed P2 results.

    Sentiment: Strong Buy

  • Reply to

    opps! - Rudy has a new theory

    by pvretire May 26, 2016 8:21 AM
    kadaicher1 kadaicher1 May 26, 2016 10:19 AM Flag

    Nothing new there that I can see, it was Tanzi and Moir who proposed this several years ago. Maybe the new development is that the theory is now being taken seriously.
    FYI PBT2 does not directly attack the AB system, which I think is a big advantage over MAB's.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 26, 2016 7:19 AM Flag

    Sounds like PBT2 is a candidate to fit right in there. That work he and Moir did was a few years before the IMAGINE and Reach2HD trials. They published it before the big monoclonal antibody failures from PFE, JNJ, ELN, LLY etc were complete. Big development dollars were wasted. Pharmas can ignore scientists like Tanzi at their own financial risk. I have seen opinion from Tanzi years back talking about multiple causes for AD. What is new here is that Tanzi has now been able to again demonstrate the amyloid effect on pathogens, this time with live human cells in a petri dish.
    Now we know AD is a reaction to various threats to the brain I see no reason to be optimistic that even an adjustable secretase inhibitor or direct removal antibody will do the job, where pathogens are concerned. An anti aggregation treatment like PBT2 will more likely fit the bill, with control through metal binding and not in any way a direct attack on the AB system, which is part of the brains immune system which may be in a fight with a pathogen.
    [The broad therapeutic potential of 8-OHQs has considerable implications because of the heterogeneous nature of neurodegenerative diseases. Brains of patients often present diverse, overlapping pathologies.](Lindquist)
    Considering his position it is not a surprise Tanzi is working on several directions of neurodegeneration research.
    [Dr. Rudolph Tanzi is a Professor of Neurology and holder of the Joseph P. and Rose F. Kennedy Endowed Chair in Neurology at Harvard University. At the Massachusetts General Hospital (MGH), Dr. Tanzi serves as the Vice-Chair of Neurology (Research) and Director of the Genetics and Aging Research Unit, which consists of eight laboratories investigating the genetic causes of Alzheimer’s disease. ]

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 May 26, 2016 4:45 AM Flag

    The emergence of PBT434 in ther clinic will be a good addition. Looking at the chart of attraction strength in the Prana World Orphan Drug Congress presentation Prana will now have the capability of combining in a much better iron attraction with their zinc and copper ionaphore PBT2. That could be great news in HD. Reach2HD did not reduce iron as I recall.
    [Alterations in Brain Transition Metals in Huntington Disease
    An Evolving and Intricate Story
    H. Diana Rosas, MD, Y. Iris Chen, PhD, Gheorghe Doros, PhD, David H. Salat, PhD, Nan-kuei Chen, PhD, Ken K. Kwong, PhD, Ashley Bush, MD, PhD, Jonathan Fox, PhD, and Steven M. Hersch, MD, PhD
    Results
    In the basal ganglia, progressive increases in the phase evolution were found in HD, beginning in pre-manifest individuals who were far from expected onset and increasing with proximity to expected onset and thereafter. Increases in the cerebral cortex were regionally selective and present only in symptomatic HD. Increases were verified by excessive deposition of brain iron, but a complex alteration in other transition metals was found.]

    Sentiment: Strong Buy

  • Reply to

    What now?

    by copper725 May 25, 2016 7:14 AM
    kadaicher1 kadaicher1 May 25, 2016 1:02 PM Flag

    Prana have been working to get PBT2 through trials since 2005. They started the first AD P2 trials in 2006 and the results came in at the peak of the global financial crisis towards the end of 2008. The ranking analysis was published in 2009. In 2011(I think) Prana indicated they would lead to market with PBT2 in HD because much smaller trials would be required. The HD trial was a success, as the first ever HD trial in HD for PBT2 the trial primary endpoint had to be safety. A hit in a cognition endpoint was a very encouraging and will be the focus of the coming P3 registration trial. There is no drug for cognition and at a recent conference cognition was voted as the main concern amongst people with HD risk. Right now Prana are upgrading the toxicology package at the request of the FDA before a P3 is done in the USA.

    Sentiment: Strong Buy

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