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Prana Biotechnology Limited Message Board

  • twosidestoapancake twosidestoapancake Jan 7, 2012 11:10 AM Flag

    Past Posts

    Posted Feb 18 2004
    by awonabee

    :::::::::: Tuesday December 16, 8:32 am ET :::::::::::::

    Prana Announces Positive Results Published for new Alzheimer's Disease Treatment

    MELBOURNE, Australia, Dec. 16 /PRNewswire-FirstCall/ -- Australian drug development company Prana Biotechnology Limited (Nasdaq: PRAN - News; ASX: PBT - News) today released the results of a pilot Phase 2 clinical trial showing that treatment with its drug PBT-1 (clioquinol) for Alzheimer's Disease slowed progression of cognitive decline in a group of patients with moderate to severe disease. The findings were published in Archives of Neurology on December 15, 2003

    When compared to patients treated with placebo, those receiving PBT-1 experienced improved cognitive performance, together with a significant lowering in plasma of the key marker of Alzheimer's disease, the amyloid beta protein. Treatment with PBT-1 was administered to patients and found to be well tolerated.

    The study, performed through the Mental Health Research Institute in Melbourne (MHRI), enrolled 36 patients who were assessed for indicators of cognitive performance such as memory, orientation, language, attention and reasoning using a cognitive score on the Alzheimer's Disease Assessment Scale, the so-called ADAS-cog score. The scores range from 0 to 70. A healthy normal adult has a very low score but as dementia progresses, the score increases.

    Eighteen of the patients were assigned to placebo and 18 received Prana's Alzheimer's Disease drug, PBT-1, the first of Prana's metal protein attenuating compounds (MPACs) to be developed for Alzheimer's Disease. PBT-1 is a chemical that binds zinc and copper, and has been shown to lower the levels of amyloid beta and the associated toxicity in the brains of transgenic mice used as a model of Alzheimer's Disease.

    The more affected patients entering Prana's pilot clinical trial (ie those with higher ADAS-cog scores) showed an average deterioration in score at 24 weeks of about 1.5 points on PBT-1 and about 8.9 on placebo, a difference of 7.4 in favour of PBT-1.

    Generally, untreated patients with mild to moderate disease could be expected to gain six to 12 points in their ADAS-cog score over 12 months. A panel convened by the Food and Drug Administration in the US deemed that an improvement of four points would be clinically significant.

    "It is extremely encouraging to see findings like this in a clinical setting," said Professor Colin Masters, a Director of Prana based at the University of Melbourne and the MHRI. Professor Masters jointly discovered the association between metals and aggregated proteins in the brains of patients with Alzheimer's Disease.

    "We designed the trial to detect only conspicuous effects on cognition, and that was exactly what we were able to show. In addition, we showed decreased blood levels of amyloid beta, the major protein associated with plaques in the brain. This is the first time any drug has been shown to lower blood levels of this indicator of Alzheimer's Disease," he said.

    Professor Masters added: "It is also heartening that the drug appears to be well tolerated. To date, ten patients who elected to continue taking PBT-1 at completion of the formal 36-week period of the trial have completed 18 months of treatment with no clinically significant adverse events attributable to the treatment."

    There is currently no cure for Alzheimer's Disease. It is estimated to affect between 80,000 and 120,000 Australians, a figure that is likely to increase significantly with the ageing of the population. The most widespread treatment is a drug called Aricept that acts by improving the transmission of a particular type of nerve in the brain. The clinical trials of Aricept showed a difference at 24 weeks of about three points between active treatment and placebo. <part1>

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    • cieloromano posted Nov2005

      The research groups around Ashley Bush, Rudi Tanzi and Colin Masters (who is one of the founders of the now widely accepted amyloid concept underlying Alzheimer's disease) are working for more than 10 years now on the potential therapeutic use of Cu/Zn chelators. Clioquinol (PBT1) works in the transgenic Alzheimer mice model (50% reduction of amyloid plaques) and showed a therapeutic effect in Alzheimer patients (even if observation time and patient numbers were too small to draw final conlcusions). Clinical research on PBT1 has then been stopped for safety concerns. Hope is on the similar PBT2 which has a capacity to enter the brain and may be therefore given at lower dosage to be effective (there could be also patent reasons to prefer PBT2, PBT1 is an old drug which had been already commercialized in the past as an antibiotic).

      In my expierence as a former researcher in the Alzheimer field, PBT2 has tremendous potential if successful in Phase II and III. There are currently no drugs that reduce amyloid plaque load. In my feeling, Bush and Tanzi would not have continued with PBT2 development and would not have wasted their time if they were not personally convinced that the molecule works (their persuasion is supported by a large number of experimental studies). Whatever works and will have an even moderate benefit in the still hopeless area of Alzheimer's disease, will become a number 1 blockbuster (see Pfizer with their relatively little effective donepezil blockbuster, a therapy that does not even tackle the pathology, but gives just a slight improvement of symptoms).

      It is a mixture between solid evidence, hope and tremendous potential. And it justifies an investment.


      Some reference:

    • Very interesting. Back in "the day" (2004)PRAN rallied from $4 to $10 on those reports. Here we are after seven years with "much improved prospects" trying to move higher from $1.50. Is PRAN a mirage?

    • neoe111 posted apr2005 (concerning PB1)

      Prana doesn´t approach the problem by blocking Beta-Amyloid production the target are the metals that bind with it, that is unique:

      Prana's platform technology has been developed over many years at several internationally recognised research facilities:

      The University of Melbourne, Department of Pathology; Melbourne, Australia
      The Massachusetts General Hospital, Genetics and Aging Unit; Boston, USA
      The Mental Health Research Institute of Victoria; Melbourne Australia
      In Alzheimer's disease the consensus is that the most relevant protein is beta-amyloid. In 1984 Professors Masters and Beyreuther, and the late Dr Glenner, sequenced the chemistry of the protein that has since become the dominant focus world wide of Alzheimer's disease research.

      In 1987 Professors Masters, Beyreuther and Tanzi discovered the way beta-amyloid was produced and in 1994 Dr Bush discovered the interaction between metals and beta-amyloid, causing toxicity in Alzheimer's disease. This work paved the way for the development of therapeutic drugs to treat the disease.

      Based on these fundamental theories and supporting evidence, a known compound (PBT-1) was identified as having significant potential as a therapeutic agent. In June 2001, the scientific journal Neuron published a study conducted by Prana sponsored scientists Dr. Robert Cherny and Dr Bush reporting that PBT-1, a copper/zinc-binding drug, given orally to transgenic mice markedly reduced their Alzheimer brain pathology within nine weeks. Beta-amyloid accumulation decreased by 50 percent during that period. This breakthrough provides a viable explanation for the abnormal binding of these metals with beta-amyloid that is commonplace in Alzheimer's disease. The reaction ultimately leads to the corruption of the protein and its ensuing toxicity. Copper and Zinc are normally present at high concentrations in the regions of the brain that are most affected by Alzheimer's disease damage.

      Prana believes that the "metal theory" may best explain many inconsistencies in the current standard theories.

      These include:

      The reason why even though beta-amyloid is produced throughout the body, plaques only form in certain brain regions.
      The source of much of the oxidative damage in Alzheimer brains and the reason why plaques are toxic to neurons.
      Why genetic mutations in beta-amyloid can predispose people to developing Alzheimer's disease.
      Why apolipoprotein E4 is a risk factor for developing Alzheimer's disease.
      The reason why the disease is species specific and even gender specific.
      Why strategies that simply attempt to block beta-amyloid production such as vaccines and secretase inhibition may cause unacceptable toxicities and side-effects.
      In December 2003, promising PBT-1 PII results were published in Archives of Neurology demonstrating a statistically significant difference at several time points between the treated and untreated Alzheimer's disease patients. Based on these results and the resolution of a patent dispute with P.N. Gerolymatos, S.A. in August 2004, Prana can now consider taking PBT-1 into further clinical development

    • costamosta Oct2004

      "The Extension Study data demonstrates that PBT-1 treatment for Alzheimer's appears to slow the expected disease progression by about half,"

    • ellie1890 posted in Aug2004

      Melbourne, Australia – August 9, 2004: Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT) today announced that Prana and Massachusetts General Hospital have agreed to settle all outstanding litigation with P.N Gerolymatos S.A. (P.N.G.) regarding the exploitation rights to certain patents relating to pharmaceutical compositions and uses of clioquinol (also known as PBT-1). Accordingly, all patent oppositions in Europe and Australia are being withdrawn and the law suits pending before the U.S. District Court for the District of Columbia and the Court of Athens in Greece are being dismissed.

      As a result of the settlement, Prana and P.N.G. have agreed to recognize the rights of each other to develop clioquinol in their respective territories. Prana will hold the rights to clioquinol in the United States and Japan, while P.N.G. will hold the rights for European and other territories. Prana has agreed to allot 1.35 million shares which will be held in escrow for twelve months and pay a royalty to P.N.G. on sales in the USA and Japan, Prana will receive a percentage of PNG’s income for the other territories.

      Mr. Geoffrey Kempler, Executive Chairman of Prana commented, “Prana now holds issued patents in the US on clioquinol (PBT-1), a drug which has already demonstrated that it can slow down the progression of the disease in a group of moderate to severe Alzheimer’s disease patients. In December 2003, promising Phase II clinical trial results evaluating clioquinol in Alzheimer’s disease were published in the Archives of Neurology. This settlement heralds a very important opportunity for Prana, its an important part of our drug pipeline and allows Prana to undertake further clinical development of clioquinol.”

      Commenting on the settlement, Mr. Panayotis Gerolymatos, President and Chief Executive Officer of P.N. Gerolymatos S.A. stated: “We are pleased to put this litigation behind us. The amicable settlement makes possible the further development of clioquinol and we look forward to working jointly with Prana in this regard.”

      Unlike current approved Alzheimer’s therapies that largely treat the symptoms of the disease, clioquinol, PBT-2 and Prana’s other MPAC’s (Metal Protein Attenuating Compound) hold promise to help prevent the progression of the disease.

      of Melbourne and Massachusetts General Hospital as a teaching hospital of Harvard Medical School discovered Prana’s technology.

      This press release contains “forward looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 regarding the Company’s business strategy and future plans of operation. Forward-looking statements involve known and unknown risks and uncertainties; both general and specific to the matters discussed in this press release. These and other important factors, including those mentioned in various Securities and Exchange Commission filings made by the Company, may cause the Company’s actual results and performance to differ materially from the future results and performance expressed in or implied by such forward-looking statements. The forward-looking statements contained in this press release speak only as of the date hereof and the Company expressly disclaims any obligation to provide public updates, revisions or amendments to any forward-looking statements made herein to reflect changes in the Company’s expectations or future events.


    • posted 16April2004 by egmons2003

      Arch Neurol. 2003 Dec;60(12):1685-91. Related Articles, Links

      Comment in:
      Arch Neurol. 2003 Dec;60(12):1678-9.

      Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial.

      Ritchie CW, Bush AI, Mackinnon A, Macfarlane S, Mastwyk M, MacGregor L, Kiers L, Cherny R, Li QX, Tammer A, Carrington D, Mavros C, Volitakis I, Xilinas M, Ames D, Davis S, Beyreuther K, Tanzi RE, Masters CL.

      Departments of Pathology, The University of Melbourne, The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia.

      BACKGROUND: Alzheimer disease (AD) may be caused by the toxic accumulation of beta-amyloid (Abeta). OBJECTIVE: To test this theory, we developed a clinical intervention using clioquinol, a metal-protein-attenuating compound (MPAC) that inhibits zinc and copper ions from binding to Abeta, thereby promoting Abeta dissolution and diminishing its toxic properties. METHODS: A pilot phase 2 clinical trial in patients with moderately severe Alzheimer disease. RESULTS: Thirty-six subjects were randomized. The effect of treatment was significant in the more severely affected group (baseline cognitive subscale score of the Alzheimer's Disease Assessment Scale, >/=25), due to a substantial worsening of scores in those taking placebo compared with minimal deterioration for the clioquinol group. Plasma Abeta42 levels declined in the clioquinol group and increased in the placebo group. Plasma zinc levels rose in the clioquinol-treated group. The drug was well tolerated. CONCLUSION: Subject to the usual caveats inherent in studies with small sample size, this pilot phase 2 study supports further investigation of this novel treatment strategy using a metal-protein-attenuating compound.

    • posted 15Apr2004 by saravgbaby

      "Prana’s Alzheimer’s drug shows continued promise in extended clinical trial
      Melbourne, Australia – Friday April 16, 2004: Professor Colin Masters, a Director of Prana Biotechnology Limited (NASDAQ: PRAN, ASX: PBT) and Chairman of the Company's Scientific Advisory Board, today will present data from the extended Phase II trial of Prana’s drug, PBT-1, at the 8th International Springfield/Montreal Symposium on Advances in Alzheimer's Disease.
      At a session devoted to novel treatments of Alzheimer’s disease, Professor Masters will report that the use of PBT-1 for 18 months markedly slowed the decline in cognitive function associated with Alzheimer's disease compared with the predicted level of decline available from the scientific literature. In addition the longer term treatment was well tolerated.
      The extension study was conducted over 48 weeks following the formal trial period of the trial of 36 weeks. Nine of the original 18 patients completed the extension.
      Speaking from Montreal, Professor Masters stated that the outcome for patients in the extension study provided confirmatory and new evidence that MPACs such as PBT-1 may form the next generation of agents for the treatment of Alzheimer’s by slowing or stopping the disease rather than just dealing with the symptoms.
      Dr Sam Gandy, Director of the Farber Institute for Neurosciences at Thomas Jefferson University, Philadelphia, commented: “This PBT-1 (clioquinol) extension study reaffirms the safety and possible efficacy of this new class of drug for Alzheimer's disease. It will now be important to confirm the trend toward benefit in a larger trial with sufficient numbers of subjects to establish statistical significance.
      “Overall, anti-amyloid, “plaque-busting” drugs such as PBT-1 (clioquinol) provide a powerful approach toward proof of principle regarding the relationship between amyloid and cognitive decline in Alzheimer's disease," said Dr Gandy.
      The biannual Symposium on Advances in Alzheimer's Disease is organized by the Southern Illinois University (SIU) School of Medicine in Springfield, Illinois, the Department of Geriatrics at the Hopitaux Universitaires de Geneve, Switzerland, and the McGill University Faculty of Medicine in Montreal, Quebec.
      Recently (March 26) Prana announced that had added PBT-1 to its list of “neurological drugs to watch”, highlighting the most promising experimental drugs to treat diseases of the brain and nervous system.
      Prana also recently announced (7 April) that a publication in the Journal of Neuroscience added further support to Prana’s theory that metals in the brain, rather than proteins on their own, are responsible for the pathology of Alzheimer’s Disease and that attenuating the action of these metals, with drugs like PBT-1, may hold the key to effective therapeutic intervention."


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