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Prana Biotechnology Limited Message Board

kadaicher1 745 posts  |  Last Activity: 7 hours ago Member since: Jan 23, 2004
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  • Reply to

    Prospects

    by kadaicher1 20 hours ago
    kadaicher1 kadaicher1 7 hours ago Flag

    Either would make me very happy as a shareholder ITM.

  • kadaicher1 kadaicher1 7 hours ago Flag

    Wow, Blue have about 4 drugs in development, negligible income 6m and a pharma development deal. SP$123 I think I have miscalculated how far Pran can run on a good trial result.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 8 hours ago Flag

    What makes you think anyone cares about tour list Bio. I sure don't. I love this, so you are assuming when PBT2 goes into a pivotal phase 3 trial the price will remain the same 55 M market cap, and on approval it will rocket to a billion or so. Too funny.
    I imagine Prana are all hands on deck to resolve the FDA concerns and when they have something, we will hear from them. I am fine with that, and I own stock.

    Sentiment: Strong Buy

  • kadaicher1 by kadaicher1 20 hours ago Flag

    Firstly the market was sold a red herring by non involved commentators that the Reach2HD trial did not work. Peer review has now corrected that misconception, yet no value has been added yet. I guess that will be when the pivotal phase3 gets the go ahead.
    On top of that trial result it has emerged that PBT2 did have an effect on an important biomarker in the blood from the HD trial.
    PBT434 should be ready for the clinic now, but it looks like it is being delayed till work can be completed around several orphan indications related to Parkinson's. So even though PBT434 has already reversed Parkinson's in several animal models during independent testing in the UK, it looks like Prana will be going after the orphan indications rather than Parkinson's. That is a very smart way to go and when PBT434 gets into the clinic as early as later this year, with model work to report on the orphan indications, PBT434 should have a very positive effect on the SP.
    The HD trial will be done in several countries and with a trial that size and the expenses involved, even if it is run by HSG, I would not be broken hearted if they go after the PBT434 orphan indications first, because I think they have the potential to add value faster.
    They have been doing work and registering MPACs I have not seen before, so there could be news there.
    The ongoing AD development work for PBT2 will probably be announced after the extension trial results. It will be interesting to see if there is any talk of raising the dose. For now what we need are the 2 yr safety data. Also if the crossovers from placebo say any change in hippocampus atrophy rates.
    I would like to hear something on MS but I don't know if they have time or resources.

    Sentiment: Strong Buy

  • Reply to

    Bottomed

    by schieboutz Mar 27, 2015 3:12 PM
    kadaicher1 kadaicher1 22 hours ago Flag

    Nice strategy schieboutz.

    Sentiment: Strong Buy

  • Reply to

    Realistic possibility of an 80 bagger here

    by kadaicher1 Feb 17, 2015 4:12 PM
    kadaicher1 kadaicher1 22 hours ago Flag

    Looking at those tiny ph1 and ph2 trial sizes for the already approved orphan indications above, when Prana gets PBT434 into the clinic they could do the early trial work for several indications very quickly and any efficacy seen could send the SP wild IMHO.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 22 hours ago Flag

    In IMAGINE Prana were looking for plaque reduction as evidence of target engagement. I would say they saw that.
    Amazingly, now the patents have run out for those statins, their effectiveness is being seriously questioned. [with the patent expiration of Lipitor in November 2011, its best-selling drug with $9.6B sales] That is a lot of annual earnings since it was approved in Dec 96:-)

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 22 hours ago Flag

    I have not seen it. Maybe injectable amounts of pure AB are not easy to get hold of.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 22 hours ago Flag

    Trouble is AD presents will multiple pathologies and probably multiple causes. Amyloid could have a hand in triggering the AD prion like cascade. In TBI the amyloid at the damage site tend to lead to AD, but I guess no one is able to look at what is happening with tau in that case.
    Some of the normal memory loss work was done in old wild type mice, ie not genetically modified models. That MPACs can reverse cognition loss in the old mice, but do not have any effect on young mice clearly demonstrate an effect on the ageing process and the life extension could be as a result of better brain health or a specific effect on the ageing gene CLK1 as one researcher suggested.
    A more natural amyloid reduction by removal of the toxic transition metals I think has got to be a better means to combat any toxicity caused by excess plaque.
    It is interesting to note that in monoclonal antibody trials which directly attacked the amyloid wherever it was, demonstrated an increase in CSF AB42, and it was claimed as evidence of success. In the Euro trial, there was a stat sig reduction of AB42 and that was claimed as evidence of success.
    I think it is safe to assume that as PBT2 does not attack plaques directly, and assuming AB42 is generated as a secretase modulated response to adverse conditions and pathogens, then by removing the toxic condition, secretase is self regulated lower as the threat is diminished.
    From China
    " By means of autometallographic analysis, we show for the first time that both the number and size of the zinc-containing plaques were significantly reduced in the brain of amyloid-β protein precursor (AβPP)/presenilin 1 (PS1) double transgenic mice treated with CQ (30 mg/kg/day) orally for 2 months. This was accompanied by a reduction in Aβ burden in the CQ-treated mouse brain. Furthermore, CQ treatment markedly reduced the expression levels of AβPP protein, the β-site of AβPP cleaving enzyme 1 (BACE1), PS1, and the secreted β-secretase-derived fragments of AβPP (s"

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 29, 2015 6:42 PM Flag

    I guess all this should not be such a surprise. Tanzi and Moir demonstrated AB was part of the brain's innate immune system back in 2010.
    The Alzheimer's disease-associated amyloid beta-protein is an antimicrobial peptide.
    Soscia SJ1, Kirby JE, Washicosky KJ, Tucker SM, Ingelsson M, Hyman B, Burton MA, Goldstein LE, Duong S, Tanzi RE, Moir RD.
    METHODOLOGY/PRINCIPAL FINDINGS:
    Here, we provide data supporting an in vivo function for Abeta as an antimicrobial peptide (AMP). Experiments used established in vitro assays to compare antimicrobial activities of Abeta and LL-37, an archetypical human AMP. Findings reveal that Abeta exerts antimicrobial activity against eight common and clinically relevant microorganisms with a potency equivalent to, and in some cases greater than, LL-37. Furthermore, we show that AD whole brain homogenates have significantly higher antimicrobial activity than aged matched non-AD samples and that AMP action correlates with tissue Abeta levels. Consistent with Abeta-mediated activity, the increased antimicrobial action was ablated by immunodepletion of AD brain homogenates with anti-Abeta antibodies.
    CONCLUSIONS/SIGNIFICANCE:
    Our findings suggest Abeta is a hitherto unrecognized AMP that may normally function in the innate immune system. This finding stands in stark contrast to current models of Abeta-mediated pathology and has important implications for ongoing and future AD treatment strategies.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 29, 2015 5:59 PM Flag

    GY, cling to that if it makes you feel good.

    Sentiment: Strong Buy

  • Reply to

    Tau paper from Mayo Clinic

    by pivalde Mar 29, 2015 3:42 AM
    kadaicher1 kadaicher1 Mar 29, 2015 7:19 AM Flag

    I am not sure you can rule out one or the other till the trigger is proved. PBT2 effects both AB and tau.
    "The majority of the Alzheimer's research field has really focused on amyloid over the last 25 years," Dr. Murray says. "Initially, patients who were discovered to have mutations or changes in the amyloid gene were found to have severe Alzheimer's pathology—particularly in increased levels of amyloid. Brain scans performed over the last decade revealed that amyloid accumulated as people progressed, so most Alzheimer's models were based on amyloid toxicity. In this way, the Alzheimer's field became myopic."

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 29, 2015 7:07 AM Flag

    We will have to agree to disagree on that. Biotechs raise into results all the time. Kempler must have had about $20M on the line, and has not sold any.
    There were lawyers trying to raise a case and usually is. Revlins did resign. Most of the current capital was raised during the trial with an at market facility they had in place. For the last months there was no use of the at market facility. I still think that was a mistake. The price would not have dropped so far. Even another 20m would have been handy with the number of programs possible with this MPAC platform.
    Look at a couple of Canadian examples. Neurochem raised 60m before results and is still operating as Bellus Health. No comment on the direction.
    Allon only raised enough for the trial and went belly up within 6 months with holders getting zero compensation as their stock was cancelled and Palladin took it all.
    Point of interest, Allon was going after PSP with a market they estimated at $700m. That is one of the orphan indications being targeted by Prana.
    Prana have a lot of possible directions in play and it should be the fiduciary duty of a CFO to raise cash when the opportunity arrives IMHO. It does make you appreciate the Prana management when you see other companies like Allon. Unbelievable Allon won some gongs as the best biotech. To me that looked like a big roll of the dice with holders money, but obviously could have been smelling like a rose if they pulled it off. To get to that point Allon had raised about $100m. I was intending to invest there but the CEO didn't look right when asked why there was no ongoing research on Davunitide. Just dodged a bullet there:-)

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 29, 2015 5:45 AM Flag

    AB clumps around TBI and can lead to AD. Ability of MPACs to capture free metals could reduce the AB build as well as preventing the excitotoxicity. The potential is there that it could prevent the AD risk from TBI if the amyloid build could be reduced at the TBI site.

    "Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?
    Johnson VE1, Stewart W, Smith DH.
    Author information
    Abstract
    Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI."

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 29, 2015 5:34 AM Flag

    I have posted all this before. I just think it is very revealing regarding how MPACs would help AB do its job. I removed the date off the title because I know it upsets the trolls who have no current knowledge so don't know if it is new or not:-)

    Copper/zinc chelation by clioquinol reduces spinal cord white matter damage and behavioral deficits in a murine MOG-induced multiple sclerosis model.
    Choi BY1, Jang BG, Kim JH, Seo JN, Wu G, Sohn M, Chung TN, Suh SW.
    " 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 score 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."

    Sentiment: Strong Buy

  • Recent research has reinforced the fact that amyloid, when not trapped in plaques is good. It was found to reverse MS.
    "Though it has been well-documented that everyone is mesmerized by villains, we love converting foes into friends even more. Perhaps that is one part of why the news about the reformed beta-amyloid, a protein piece, is so exciting.

    Certain types of beta-amyloids, when incorrectly folded, have long been blamed by scientists for killing brain cells in Alzheimer's disease. But, when injected into mice with rodent models of multiple sclerosis, it reversed the damage of the disease, and in some cases even cured them.

    Multiple sclerosis is an autoimmune disorder that targets the brain and spine. It is caused by damage to the myelin sheath, the protective coating of nerve cells. The damage is caused by inflammation when the body's immune system cells attack the nervous system."

    Lawrence Steinman from California's Stanford University had expected the protein to exacerbate the damage caused by multiple sclerosis. After all, beta-amyloid is venomous to neurons and builds up where myelin sheaths are destroyed.

    But when PhD candidate Jacqueline Grant inserted the protein into mice's body cavities, they found just the opposite. In fact, the injection delayed or reversed the onset of paralysis.

    Researchers were stunned, and thought that the result must be a mistake. But when Grant injected mice again, she found the exact same results. The injections also seemed to reduce the level of inflammation."
    MPACs do not attack amyloid, but can mop up the free metals amyloid is also cleaning up. It works in MS and as AB groups around brain injuries, MPACs will probably be effective there also. Just my opinion.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 28, 2015 9:37 AM Flag

    It is a HD trial copper.
    PBT2 has shown plenty in AD. Stay tuned:-)

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 28, 2015 9:31 AM Flag

    Sure. You roaches would love open slather on this board. RKF is the roachbuster:-)
    Whats with that ID LC, are you 13yo

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 28, 2015 6:09 AM Flag

    I like your ideas. Regarding TBI. Several areas need to be addressed and is probably why no drugs have yet succeeded.
    Binding of free metals, anti inflammatory, anti oxidation and anti bacterial. The first three points fit for PBT2 and regarding the last point PBT2 is an analog of an antibiotic, so maybe scores there also. Worldwide market has been estimated as high as $10b. It sure is worth exploring considering the recent data on PBT2 and excitotoxicity. The main need is traffic accidents, then falls, then violence.

    Sentiment: Strong Buy

  • kadaicher1 kadaicher1 Mar 28, 2015 4:47 AM Flag

    Firstly, is it an AD trial waiting for the FDA green light? I direct your attention to the FACT it is a HD trial and that trial was a success. On that alone, the rational is that it is a pivotal trial for approval. It is near enough to a billion dollar market. Looking at other companies with similar orphan approvals a market cap around $4b could be a reasonable expectation.
    If it was a phase1, or phase2, these price levels may be justified, but this is an advanced p3 for approval.
    Success in HD will see pran not just go higher, more like ballistic.
    I know there are programs in AD, PD, Brain Cancer and several orphan needs in play, but the HD clarification is what I think you want.
    Why do you bother with the other fake IDs. They fool nobody.

    Sentiment: Strong Buy

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