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Sanofi Message Board

biotech_invest 91 posts  |  Last Activity: Sep 29, 2016 3:51 PM Member since: Mar 5, 1998
  • Reply to

    What I'm watching out for at the AAIC 7/26/16.

    by imtom9930 Jul 25, 2016 11:57 PM
    biotech_invest biotech_invest Jul 26, 2016 9:03 PM Flag

    so, pps spike should be tomorrow? after all newspapers publish Tanzi breakthrough presentation about new AD drug PBT2 that cure AD in Petri dish?
    And what will be a next hope that PRAN pumpers are going to seed? Of course, they still have PCH lift "any day from now" but pps trend shows that this "hope" is very weak.
    Staring of Phase I for PD? Also too weak to keep pps from declining to $4, $3 and below...
    Indeed, it will be difficult challenge for PRAN pumpers to generate "new hope" :-)

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 26, 2016 12:32 PM Flag

    sure, I never say that AD is a simple disease. I know, you and other PRAN pumpers always doubt in my brain abilities :-) And always ignore 100% proof: top solver of InnoCentive starting 2013 and to present (will be included soon in 2016 list of top solvers because already have 3 awarded solutions in 2016) with 18 awarded solutions.
    Most likely that AD is just one of forms of Tauopathies (a class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles in the human brain). In case of tauopathies (that includes numeous diseases like Frontotemporal dementia, Huntington's disease, Progressive supranuclear palsy etc) there is no Abeta plaques formation. In case of AD we have both p-tau tangles and Abeta plaques. Abeta plaques can be just a collateral product of neuronal degeneration when too many APP is delivered to axons that "dying back" because of microtubules disintegration.
    If TauRx drug is effective for AD and FTD in Phase III trials it means that tau is a main player in AD (no Abeta in case of FTD). But if LMTX® is effective only in case of behavioural
    variant frontotemporal dementia (bvFTD) but fail in AD trial it means that Abeta can be main player in AD.
    Just wait for tomorrow Wischik presentation :-)

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 26, 2016 9:10 AM Flag

    They can publish everything but everybody knows that it's just BS :-) Nobody will pay attention to presentations of those ugly liars after tomorrow TauRx presentation. PBT2 is a fake AD/HD drug that failed in Ph2 and will fail in Ph3 trial.

    Sentiment: Strong Sell

  • Reply to

    What I'm watching out for at the AAIC 7/26/16.

    by imtom9930 Jul 25, 2016 11:57 PM
    biotech_invest biotech_invest Jul 26, 2016 8:54 AM Flag

    and what is your prediction about PRAN pps spike after Tanzi presentation? up to $10?
    Once again for people who never work in science: meeting and conference presentation mean NOTHING. You can present any results at meeting but then never publish it. Nobody pay real attention to presented results before publication. Tanzi postdocs did everything that their boss asked and PBT2 now is the best AD drug in the world :-) But it works only in Petri dish and in one lab. Nobody can reproduce those "phenomenal results" :-) And nobody will even try before publication.

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 25, 2016 11:17 AM Flag

    Looks like that the results for Phase III FTD will be presented later. But they also promised "to make an initial announcement of the results of the first two trials to complete at two presentations at the Alzheimer's Association International Conference (AAIC) in Toronto, Canada on 27th July."

    "ABERDEEN, Scotland and Singapore, 22nd July 2016 – TauRx Therapeutics Ltd recently completed its
    Phase 3 clinical trial of the company’s second generation tau aggregation inhibitor, LMTX®, in behavioural
    variant frontotemporal dementia (bvFTD), believed to be the largest Phase 3 study ever undertaken in
    patients with this rare neurodegenerative disorder. Public disclosure of the study results will be delayed for
    a few weeks in order to permit the company to protect intellectual property arising from the on-going
    analysis of the patient data. The results of this trial, originally planned for presentation at the 2016
    Alzheimer’s Association International Conference (AAIC) in Toronto, will now be reported for the first time
    at the 10th International Conference on Frontotemporal Dementias (ICFTD) in Munich on 31 August-2
    September 2016."

    AD Phase III trials:
    1) Study TRx-237-005 is assessing the safety and efficacy of LMTX® in up to 800 patients diagnosed with mild Alzheimer’s disease. The main measures of efficacy to be used in the study are:
    The change in study subjects’ performance at the beginning and the end of the study in two commonly used clinical assessments:
    The Alzheimer’s Disease Assessment Scale – Cognitive Subscale, known as ADAS-cog11
    The Modified Alzheimer’s Disease Cooperative Study – Activities of Daily Living, known as ADCS-ADL
    The safety and tolerability of LMTX® at 200mg per day given for up to 18 months
    2) Study TRx-237-015 is assessing the safety and efficacy of LMTX® in 890 patients diagnosed with mild to moderate Alzheimer’s. The main measures of efficacy to be used in the study are:

  • biotech_invest biotech_invest Jul 24, 2016 11:01 AM Flag

    Well, and again I'll repeat: looks like that Tanzi becomes senile idiot that even don't know that many metal chelators have antibiotic properties. Citations are below:

    J Food Prot. 2006 Jun;69(6):1460-2.
    Antimicrobial properties of the chelating agent EDTA on Streptococcal bovine mastitis isolates.
    Reidmiller JS1, Smith WL, Sawyer MM, Osburn BI, Stott JL, Cullor JS.
    To determine the efficacy of the chelating agent EDTA on microbial growth, separate cultures of two streptococcal bovine mastitis isolates, Streptococcus agalactiae and Streptococcus uberis, were exposed to known concentrations of EDTA. Bacterial cultures of 10(8) CFU/ml were exposed to concentrations of EDTA ranging from 30 to 100 mM in an in-vitro-milk environment. Multiple replications of cultures exposed to EDTA were plated during a two-hour time course. A concentration of 100 mM EDTA resulted in a 90% reduction of S. agalactiae and a 99% reduction of S. uberis. Under these experimental conditions, EDTA treatments in cultures of both isolates exhibited from 1 to 2 log reductions suggesting that EDTA is a potentially effective antimicrobial against streptococcal isolates implicated in causing bovine mastitis.

    The synergistic effect of EDTA/antimicrobial combinations on Pseudomonas aeruginosa
    R.J.W. LAMBERT, G.W. HANLON AND S.P. DENYER. 2004.
    Aims: To demonstrate that the nonlinear concentration-dependent inhibition of Pseudomonas aeruginosa to EDTA can be used to successfully model and predict the potentiation of antimicrobials by EDTA.
    Methods and Results: A model used successfully to describe the concentration-dependent inhibition of bacterialgrowth caused by many antimicrobials was unable to describe the inhibition of P. aeruginosa by EDTA.

    Sentiment: Strong Sell

  • Reply to

    What to watch for at AAIC 2016

    by interesting2me Jul 20, 2016 9:11 AM
    biotech_invest biotech_invest Jul 24, 2016 9:37 AM Flag

    "Maybe Tanzi has done it with LMTX or MBlue in his model" ?
    It must be head-to-head comparison of LMTX/MBlue and PBT2 in Tanzi so-called AD-in-dish model. If he not show this comparison all PBT2 results will be under big question. Sure, that Tanzi postdocs "did their best" to get "very impressive results" :-)
    We will know how LMTX works in humans next week. Just wait 3 days.

    Sentiment: Strong Sell

  • Reply to

    What to watch for at AAIC 2016

    by interesting2me Jul 20, 2016 9:11 AM
    biotech_invest biotech_invest Jul 23, 2016 2:52 PM Flag

    kad, your statement that "PBT2 prevents and clears tangles" is an ugly lie :-) Especially second part about "clears tangles". LMTX can do it (i.e. dissolve tangles) even in vitro when tau tangles were formed artificially. But nobody showed that PBT2 can dissolve tau tangles in vitro or in vivo.
    Wischik published it in PNAS (1996). Where is Tanzi published that PBT2 can "clear tau tangles?
    Selective inhibition of Alzheimer disease-like tau aggregation by phenothiazines
    C M Wischik, P C Edwards, R Y Lai, M Roth, and C R Harrington
    In Alzheimer disease (AD) the microtubule-associated protein tau is redistributed exponentially into paired helical filaments (PHFs) forming neurofibrillary tangles, which correlate with pyramidal cell destruction and dementia. Amorphous neuronal deposits and PHFs in AD are characterized by aggregation through the repeat domain and C-terminal truncation at Glu-391 by endogenous proteases. We show that a similar proteolytically stable complex can be generated in vitro following the self-aggregation of tau protein through a high-affinity binding site in the repeat domain. Once started, tau capture can be propagated by seeding the further accumulation of truncated tau in the presence of proteases. We have identified a nonneuroleptic phenothiazine previously used in man (methylene blue, MB), which reverses the proteolytic stability of protease-resistant PHFs by blocking the tau-tau binding interaction through the repeat domain. Although MB is inhibitory at a higher concentration than may be achieved clinically, the tau-tau binding assay was used to identify desmethyl derivatives of MB that have Ki values in the nanomolar range. Neuroleptic phenothiazines are inactive. Tau aggregation inhibitors do not affect the tau-tubulin interaction, which also occurs through the repeat domain. Our findings demonstrate that biologically selective pharmaceutical agents could be developed to facilitate the proteolytic degradation of tau aggregates..."

    Sentiment: Strong Sell

  • Reply to

    What to watch for at AAIC 2016

    by interesting2me Jul 20, 2016 9:11 AM
    biotech_invest biotech_invest Jul 22, 2016 6:46 PM Flag

    Well, we will know it after 5 days from today.
    BTW, why this analysts forgot about PRAN and it's co-founder Tanzi who practically cured AD in Petri dish with metal chelator PBT2?
    However, she is right about Phase II trial results vs. Phase III ones. LMTX can also fail in Phase III. In this case we will not see any effective AD DMT drugs during next 10-15 years. It will be very sad news for AD patients and their relatives.

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 18, 2016 11:00 PM Flag

    sure, why not :-) Question is wait for what?
    We will know how effective anti-tau AD therapy vs. anti-amyloid one in July 27th. But if you are waiting for PCH lift that can happen "any day from now" (prophetic prediction of one of PRAN's pumpers) I'm not sure that I can join you in this infinite waiting :-)
    This time AAIC might be very interesting: amyloid theory of AD vs. tau one. Tanzi, Masters, Bush and other cronies vs. just one guy Prof. Claude M. Wischik. Idiotic "metal theory of AD" vs. simple tau-based AD etiology.
    So, let's wait and see who was right.

    Sentiment: Strong Sell

  • Reply to

    Metallo-pathways to AD

    by pivalde Jul 12, 2016 10:07 AM
    biotech_invest biotech_invest Jul 18, 2016 4:56 PM Flag

    Wow! Looks like that PBT2 is practically a panacea: even can prevent tau tangles formation :-) When this legend was born? And who is a father? Again Tanzi?
    If anti-tau AD therapy is effective in Phase III everybody will forget about PBT2 and other anti-amyloid drugs. Just wait 9 days and you can also move on... Success of anti-tau AD therapy will easy crash amyloid paradigm of AD etiology. Switch PBT2 to anti-tau function is laughable. Only idiots like you believes in this Tanzi fairy tale for stupid investors.

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 18, 2016 10:50 AM Flag

    Are you seriously waiting for pps spike after Tanzi, Masters etc presentations at AAIC? In this case you are just a naive idiot. Prana can stop pps decline only by lift of PCH for Phase III HD with PBT2 250 mg daily dosing. They have PCH during almost 1.5 year and still "working with FDA". Looks like that PRAN wants to have a world record for longest PCH :-) Not sure that any biotech had 2 years of PCH so in Feb 2017 Prana will get it :-)

    Sentiment: Strong Sell

  • Reply to

    APOe4 in Children

    by tb00tb00a Jul 13, 2016 10:52 PM
    biotech_invest biotech_invest Jul 18, 2016 10:42 AM Flag

    Why you are so sure that Masters will say something interesting? Work with him? Or prepare presentation for him? Most likely it will be just empty talk about some almost undetectable trend in PBT2 treated patients. Nobody will pay attention to this BS (especially Big Pharma). Everybody who will be at AAIC is waiting for presentation of Professor Claude M. Wischik, co-founder and Executive Chairman of TauRx Therapeutics (27th July).

    Sentiment: Strong Sell

  • Reply to

    Metallo-pathways to AD

    by pivalde Jul 12, 2016 10:07 AM
    biotech_invest biotech_invest Jul 18, 2016 9:02 AM Flag

    so, by saying it you predict that TauRx AD will fail in Phase III trials? Well, if you are right (we will know it in less than 10 days) it will be a proof that your brain is still functional :-) But if TauRx LMTX® show 80% slowing of cognition decline (as it was in Phase 2 trial) it will be 100% proof that you are stupid and senile idiot that know nothing about AD.
    Indeed, PBT2 was USELESS approach and now EVERYBODY knows it. Only idiots like you still believes that metal chelators can cure AD, HD, PD etc. and continue as..kissing of Tanzi.

    Sentiment: Strong Sell

  • In first case just erase all cookies in web browser and you will get old version back. PRAN pumpers are so funny guys and MB becomes boring without them :-) Hope they have enough brains to return back and make us LOL :-)

  • Reply to

    APOe4 in Children

    by tb00tb00a Jul 13, 2016 10:52 PM
    biotech_invest biotech_invest Jul 15, 2016 8:43 AM Flag

    LOL! 'm not sure that you have even 10% of my brain abilities :-) You are just anonymous writer on YMB that has no any proof that your brain is functional. So, you are just NOTHING.
    Just shut up and go back to your stinky rat hole.

    Sentiment: Strong Sell

  • Reply to

    APOe4 in Children

    by tb00tb00a Jul 13, 2016 10:52 PM
    biotech_invest biotech_invest Jul 14, 2016 3:11 PM Flag

    and what is your point here? want to give them PBT2?

    Sentiment: Strong Sell

  • Reply to

    Metallo-pathways to AD

    by pivalde Jul 12, 2016 10:07 AM
    biotech_invest biotech_invest Jul 12, 2016 7:55 PM Flag

    Again this BS about "important role of metals" in AD etiology :-) Hope that Tanzi, Bush etc will never get grants after anti-tau AD therapy will be approved FDA. Well, I almost forgot that those liars can easy switch to "metal theory of tau disbalance of AD"

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 11, 2016 1:07 PM Flag

    Tau phosphorylation also can be abnormal and p-tau can't bind with microtubule's surface. In this case microtubule breaking down becomes abnormal so their rebuilding just can't compensate microtubules loss in AD axons. P-tau in PHF and tangles can't contact with phosphatases - enzymes that remove extra phosphate groups from p-tau. LMTX destroys tau tangles and solubilizes p-tau i.e. provides p-tau interaction with phosphatases. If you destroy tau tangles in axons most likely you cure AD and tauopathies (including Frontotemporal dementia and may be PD).
    That is my point. And what is your (or Tanzi) hypothesis about how metal chelator PBT2 destroys tau tangles? Any mechanisms?

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jul 11, 2016 11:48 AM Flag

    kad, your bluffing is so funny :-)
    you are citing now things known during 20-25 years but can't explain your BS statement "PBT2 MOA it also protects the microtubules from the hyperphosphorylation which leads to tau tangles" :-)
    And another bluff is also funny: "Tanzi has demonstrated with his 3D human AD cell model that both AB and tangles are important" - where is a link to publication?
    It's just infinite talks about "AD-in-dish" model but there is no any publications. Tanzi just talking and never publish any real papers. PBT2 in his model did practically everything: stopped amyloid plaques formation, decreases tau phosphorylation, destroys tau tangles inside of neurons.... Too many functions for one simple metal chelator :-) Looks like that Tanzi postdocs got practically all results that he asked them to get :-)
    BTW why amyloid plaques are not important (and even not exist) in case of
    tauopathies (class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles)?
    Patients have a neurodegeneration, cognition decline but there is no any amyloid plaques in their brains.

    Sentiment: Strong Sell

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