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InterMune, Inc. Message Board

biotech_invest 133 posts  |  Last Activity: Dec 20, 2014 1:07 PM Member since: Mar 5, 1998
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  • Reply to

    Tau

    by kadaicher1 Dec 19, 2014 10:13 AM
    biotech_invest biotech_invest Dec 20, 2014 1:07 PM Flag

    Conclusion
    In summary, we present evidence that human wild type tau phosphorylation can be modulated by copper, and a copper-modulating strategy suitable for human use is effective in an animal model of tau expression. Translation to human subjects is consequently possible, but justification for such a trial depends on the demonstration that this intervention is functionally important for brain neurons, and will require careful monitoring to avoid adverse effects from copper deficiency.

    So, if Tanzi can prove that PBT2 can modulate cooper and in such way to decrease tau phosphorylation level in human brains Big Pharma will be interesting in collaboration with Prana. Measuring of pTau in CSF (CSF-PHFtau) is possible and Prana must include it in next AD trial.
    HD is caused by aggregation of HTT mutant forms that create intranuclear inclusions bodies and cytoplasmic aggregates in neurons. There is a big difference with AD where tau protein is not mutated (if mutated it's not AD but tauopathy). The cure for HD might some selective inhibitors that reduce the aggregation and toxicity of HTT.
    Again Prana scientist must show that PBT2 is an inhibitor of HTT aggregation.

  • Reply to

    Tau

    by kadaicher1 Dec 19, 2014 10:13 AM
    biotech_invest biotech_invest Dec 20, 2014 12:41 PM Flag

    Removing of aggregated tau from axons is a big challenge (may be TauRx Rember is the only one drug that can do it). Simpler approach is to prevent excessive tau phosphorylation.
    Since PBT2 is a chelating agent it can change an equilibrium of Cu2+ and Zn2+ ions in brains. Recently published paper showed that the rate of tau phosphorylation in neurons depends on both copper and zinc.
    Modulation of tau phosphorylation by environmental copper
    Kellen Voss, Christopher Harris, Martina Ralle, Megan Duffy, Charles Murchison and Joseph F Quinn

    The transition metal copper enhances amyloid β aggregation and neurotoxicity, and in models of concomitant amyloid and tau pathology, copper also promotes tau aggregation. Since it is not clear if the effects of environmental copper upon tau pathology are dependent on the presence of pathological amyloid β, we tested the effects of copper overload and complexing in disease models which lack pathological amyloid β.
    Methods
    We used cell culture and transgenic murine models to test the effects of environmental copper on tau phosphorylation. We used oral zinc acetate as a copper lowering agent in mice and examined changes in blood and brain metals through inductively coupled plasma mass spectroscopy. Behavioral effects of copper lowering were assessed with Morris water maze and novel object recognition tasks. Changes in tau phosphorylation were examined by phosphorylation specific antibodies on Western blots.
    Results
    In human neuroblastoma cells, excess copper promoted tau phosphorylation and a copper complexing agent, tetrathiomolybdate, attenuated tau phosphorylation. In a transgenic mouse model expressing wild type human tau, copper-lowering by oral zinc suppressed plasma and brain levels of copper, and resulted in a marked attenuation of tau phosphorylation. No significant changes in behavior were observed with copper lowering, but a trend to improved recognition of the novel object was observed in zinc acetate treated mice.

  • Reply to

    Tau

    by kadaicher1 Dec 19, 2014 10:13 AM
    biotech_invest biotech_invest Dec 19, 2014 4:30 PM Flag

    so kad, now you are in tauists camp? and state that PBT2 can remove tau tangles from dying neurons?
    Good tactic :-)

  • biotech_invest biotech_invest Dec 19, 2014 3:48 PM Flag

    in your dreams?
    looks like you have a lot of PRAN shares that you bought at $10 and now you are waiting for a miracle :-)

  • biotech_invest biotech_invest Dec 19, 2014 3:44 PM Flag

    Why you answer? Are you stinky rfk? Or just forgot to change YMB ID?
    We are waiting for HD phase IIb trail start and don't care about commentary of so-called "independent" scientist on the HD trial.

  • biotech_invest biotech_invest Dec 19, 2014 3:36 PM Flag

    wow, stinky rfk is always here to support his cronies pumpers :-)
    still waiting for $10 pps to recover your losses? no way for such high level... May be this run up will drive PRAN to $2.50 i.e. easy 20-30% gain.
    BTW why PRAN management keep silence about HD trial? If they not release info during next 2 weeks this run up will die again around $2

  • biotech_invest biotech_invest Dec 19, 2014 3:18 PM Flag

    for morons and idiots like you the reading of WIKI will be very useful: at least you will stop to use a term "METAL THEORY" in application to AD.
    Before we have a cure for AD there are only hypotheses: amyloid hypothesis, tau hypothesis and may be metal hypothesis...
    If you Google latest research you will find some mentions about so-called metal theory. But who is author?
    Bush who is co-author (2010) and very active as..kisser of Tanzi.
    So, my advice to stupid dilettante pierreluke77: read the Wiki and may you will finally understand the difference between theory and hypothesis.

    J Alzheimers Dis. 2013;33
    The metal theory of Alzheimer's disease.
    Bush AI
    Brain homeostasis of transition metals is severely perturbed in Alzheimer's disease (AD), with extracellular pooling of zinc and copper in amyloid, and intraneuronal accumulation of iron. Rapidly accumulating evidence indicates that these perturbances themselves may contribute significantly to the cognitive loss and neurodegeneration, even in the absence of AD proteopathy. There is now strong evidence that each of the major protein participants in AD pathology has physiologically important interactions with transition metals: AβPP is the neuronal iron export ferroxidase with a major interaction with ferroportin, presenilins are needed for the import of ≈ 50% of cellular copper and zinc, and tau promotes the export of neuronal iron by facilitating the trafficking of AβPP to the surface. Therefore, amyloid and tau pathology arise in a milieu of constitutively high metal flux, and the major components of AD pathology may contribute to the disease by failing in their metal transport roles.

    J Alzheimers Dis. 2010;20(2):509-16. doi: 10.3233/JAD-2010-1390.
    PBT2 rapidly improves cognition in Alzheimer's Disease: additional phase II analyses.
    Faux NG1, Ritchie CW, Gunn A, Rembach A, Tsatsanis A, Bedo J, Harrison J, Lannfelt L, Blennow K, Zetterberg H, Ingelsson M, Masters CL, Tanzi RE, Cummings JL, Herd CM, Bush AI.

  • Reply to

    Biotech_invest

    by whoskold Dec 18, 2014 2:46 PM
    biotech_invest biotech_invest Dec 18, 2014 4:22 PM Flag

    opposite? In this case you should sell PRAN short right now.
    Buying PRAN-scam right now is a good possibility to make some money. Why not? Pecunia non olet ("money does not stink") :-)

    BiotechInvest ‏@Biotech_Invest Dec 10
    12/10/14: PRAN run up is good for making easy money (20-30% gain in next 2-3 days).

  • Reply to

    Science Matters Here

    by tb00tb00a Oct 9, 2014 10:22 AM
    biotech_invest biotech_invest Dec 18, 2014 2:00 PM Flag

    usually never response to one day old PRAN pumpers like you... you are just a nit for me
    pcyc_2010
    5 posts | Last Activity: 29 minutes ago
    Member since: Dec 18, 2014

  • Reply to

    Science Matters Here

    by tb00tb00a Oct 9, 2014 10:22 AM
    biotech_invest biotech_invest Dec 18, 2014 12:43 PM Flag

    very pathetic and pompous statement :-) Looks like author wants to say that he is scientist.
    But I have liked one sentence from this statement:
    "If the metal theory is correct, then this company will be worth a fortune."
    I see some doubt here so the author is not completely despairing guy.
    Some correction: for AD etiology we have several HYPOTHESES and no one theory (read Wiki):
    "The cause for most Alzheimer's cases is still mostly unknown except for 1% to 5% of cases where genetic differences have been identified. Several competing hypotheses exist trying to explain the cause of the disease: 1) Genetics; 2) Cholinergic hypothesis; 3) Amyloid hypothesis; 4) Tau hypothesis; 5) Other hypotheses include HSV1 and
    "The cellular homeostasis of ionic copper, iron, and zinc is disrupted in AD, though it remains unclear whether this is produced by or causes the changes in proteins. These ions affect and are affected by tau, APP, and APOE. Some studies have shown an increased risk of developing AD with environmental factors such as the intake of metals, particularly aluminium.[66] The quality of some of these studies has been criticised,[67] and other studies have concluded that there is no relationship between these environmental factors and the development of AD.[68] Some have hypothesised that dietary copper may play a causal role."

    BUT THERE IS NO ANY METAL THEORY OF AD

    Conclusion: Everybody who is mentioning METAL THEORY is an idiot.

  • Reply to

    As a doc I have a question/concern

    by bandaidman44 Dec 18, 2014 11:28 AM
    biotech_invest biotech_invest Dec 18, 2014 11:44 AM Flag

    "as a "doc" you must know that measuring FEV1 is a simplest and cheapest procedure (may be only measuring of blood pressure is simpler).
    Just read this document: wwwDOTnlhepDOTorg/Documents/simple_office_spirometry.pdf

    Modern office spirometers process numeric results automatically and print out a report that
    includes data from each maneuver and a graph corresponding to those data points. Spirometer
    interpretations are based on widely recognized clinical practice guidelines and assume an accurate
    spirometer and good patient maneuver quality. Incorrect results or misleading interpretations
    may result if these conditions are not met. The degree of bronchodilator response may also be
    misinterpreted if either the baseline (pre-BD) or post-BD maneuver was of poor quality.
    In order to determine the severity of lung function impairment, the FEV1 is expressed as a
    percent of the predicted value.

    Coach the Patient. Ensure that the spirometer is ready to record the FVC maneuver. Coach
    the patient to take as deep a breath as possible. Watch to ensure that the patient inhales deeply.
    Encourage the patient to keep the chin up. Once he or she has sealed the lips around the
    mouthpiece, shout loudly, “BLAST out the air!” Then tell the patient more quietly to, “Keep
    going, keep going, blow out a little more air.” Some spirometers will help you by indicating
    with a graph or tone that the patient is continuing to exhale air toward the end of the maneuver.
    Step-by-Step Spirometry
    1. Explain the test and demonstrate the maneuver
    2. Coach for maximal inhalation, then have the patient BLAST out!
    3. Quietly encourage blowing out for at least 6 seconds
    4. If necessary, instruct the patient how to correct any problems
    5 Obtain three good maneuvers, two of which match closely

    Sentiment: Strong Buy

  • biotech_invest biotech_invest Dec 17, 2014 2:59 PM Flag

    gotcha :-) and put on ignore
    I know it's useless because you have multiple IDs generated by software. What is next? superbrainn008?

    goodbrainn007
    45 posts | Last Activity: 7 minutes ago
    Member since: Dec 15, 2014

    Sentiment: Strong Buy

  • biotech_invest biotech_invest Dec 17, 2014 2:52 PM Flag

    only insane investors will sell MNKD now. Be Neutral is OK: Afrezza is very unusual medication for diabetes patients and they need some time to accept the possibility of inhalable insulin. TV advertisement will be a key and the best comparison for Afrezza will be asthma inhalers: everybody use them in front of people and there are no any embarrassments. So plot when someone is using Afrezza in restaurant while you are waiting for his meal will be the best one.

    Sentiment: Strong Buy

  • you can try to use ignore button during all day or even during entire week but you will always see posts like:
    edward.drossman • Oct 27, 2014 11:06 AM Flag
    mark this
    MNKD will still be under 6 in Jan. 2015
    each time new ID and but same idiotic statement
    Bashers are desperate because even at pps $5 daily volume is too low for covering 79M short interest. Weak hands scared by bashers and corrupted analysts are already sold all MNKD shares. Wise investors are holding MNKD strong and adding at low (i.e. $5 and around). Funds are accumulating and waiting for big news. All MNKD holders know that MNKD cap will be at least $5B in 2015.
    Once again look at BLUE: their medication slightly improved conditions of 2 patients, they have diluted stock recently (sold shares for $200M), drug is early stage and investors will see FDA approval (if any) only after 4-5 years. But BLUE cap is $2.5B i.e. bigger than MNKD cap with FDA approved drug and launch date in Q1, 2015. Investomadness.
    Bahsers are calling MNKD longs stupid and predict pps below $6 in 2015. But their masters know the real price when 10% of diabetes patients will ask their doctors to prescribe Afrezza as meal time insulin.

    Sentiment: Strong Buy

  • Reply to

    ANTH vs SRNE

    by who_gnu_1235 Dec 16, 2014 11:24 AM
    biotech_invest biotech_invest Dec 17, 2014 10:47 AM Flag

    simple answer is Lupus medication. If Blisibimod is effective in subjects with systemic Lupus Erythematosus ANTH cap should at least similar to HGSI that was acquired by GSK for $3B. Main goal was HGSI lupus drug that received approval from the Food and Drug Administration, making it the first new treatment for the disease in about 50 years.
    Primary Outcome Measure in Phase III CHABLIS-SC1:
    Proportion of patients achieving an SLE Responder Index at week 52
    I think that ANTH drug has very high probability ( 70%) to meet primary goals. If I'm right we will see double digits pps in 2015.

    Sentiment: Strong Buy

  • Reply to

    ANTH vs SRNE

    by who_gnu_1235 Dec 16, 2014 11:24 AM
    biotech_invest biotech_invest Dec 16, 2014 4:53 PM Flag

    don't worry. ANTH pps will grow in 2015 and may be we will see double digits pps next year.
    I'll add more ANTH positions at current pps (may be up to 10% of my portfolio).

    Interim analyses of CHABLIS-SC1 and BRIGHT-SC were planned for the third quarter of 2014 to confirm the clinical assumptions of the designs of these two studies. However, due to our on-going partnership negotiations for Asian rights for blisibimod for both lupus and IgA nephropathy, we elected to delay these analyses. We expect these discussions will be completed during the fourth quarter of 2014.

    Phase III CHABLIS-SC1: A Study of the Efficacy and Safety of Subcutaneous Blisibimod in Subjects With Systemic Lupus Erythematosus

    Estimated Enrollment: 400
    Study Start Date: February 2013
    Estimated Study Completion Date: December 2015
    Estimated Primary Completion Date: October 2015 (Final data collection date for primary outcome measure)

    BRIGHT-SC: Blisibimod Response in IgA Nephropathy Following At-Home Treatment by Subcutaneous Administration

    Estimated Enrollment: 200
    Study Start Date: July 2013
    Estimated Study Completion Date: December 2016
    Estimated Primary Completion Date: December 2015 (Final data collection date for primary outcome measure)

    Sentiment: Strong Buy

  • Reply to

    inhalable migraine medications in 2014

    by biotech_invest Dec 16, 2014 4:11 PM
    biotech_invest biotech_invest Dec 16, 2014 4:42 PM Flag

    FDA officers are stubborn and meticulous. But fortunately for MNKD FDA officers accepted an idea that MNKD active agent FDKP (fumaryl diketopiperazine) molecules are not damage lung epithelium cells i.e. "magically" transport insulin molecules through cells directly in systemic circulation.
    But now when MNKD got approval for "magic" trans-epithelial transport concept they must use it for all possible application (I have mentioned only a few) and make us rich during next 2-3 years. FDA will not worry about lung safety anymore. An efficacy, ultra-fast PK/PD, bioavailability of inhalable FDKP-based medications are out of distance if you compare with oral formulations.

    Sentiment: Strong Buy

  • in June 2014 FDA rejected Semprana, formerly known as Levadex, an inhalable treatment for migraines, because of problems with the drug’s delivery device (Levadex was developed by Map Pharmaceuticals Inc. (MAPP), which was acquired by Allergan earlier this year in a deal valued at $958 million)

    In November 2014 FDA has accepted Avanir's inhaled migraine treatment OptiNose's (inhaled, dry-powder sumatriptan).

    Looks like that MNKD was lucky to get FDA approval for inhalable diabetes medication. And they must use this advantage to develop inhalable migraine drug in combination with Technosphere technology. Allegran paid almost $1B for inhalable migraine medication and finally got FDA rejection.

    So future MNKD portfolio includes:
    1) $1B inhalable migraine medication;
    2) $3B inhalable diabetes medication GLP-1
    3) $300-500M inhalable fast-acting anti-psychotic medications like ADASUVE® (Staccato® loxapine)
    4) inhalable pain killer medications (good candidate is Cara Therapeutics' CR845 Peptide for Acute and Chronic Pain)
    Simple conclusion is: after 2-3 years from now MNKD cap should be at least $10B. And it's very modest prediction (look at REGN chart for last 2-3 years).
    GL

    Sentiment: Strong Buy

  • Reply to

    Vitamin B12 injections

    by willow917 Dec 12, 2014 11:04 AM
    biotech_invest biotech_invest Dec 12, 2014 12:20 PM Flag

    you should patent such good idea: a combination of Technosphere + B12 for lung delivery. I'm sure that one puff per month will be at least non-inferior (or may be even superior) to intramuscle (IM) injection. Of course, this formulation needs some simple clinical trials to prove be effective for B12 deficiency but insurance company will pay for such drug (less expensive than monthly IM at doctor office).
    GL

    Sentiment: Strong Buy

  • they just claimed "that the two patients who underwent the gene therapy treatment that the Cambridge, Mass.-based firm is developing are now experiencing robust production of hemoglobin and in a relatively short period of time, they're requiring minimal to no transfusion support"
    They are using lentivirus to delivery and integrate genes in human genome but this virus is too dangerous and can damage genes and induce cancer. When they will use it for big patient group they will get terrible side effects.

    Sentiment: Strong Buy

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