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Sanofi Message Board

biotech_invest 143 posts  |  Last Activity: 2 hours 53 minutes ago Member since: Mar 5, 1998
  • because if shorts borrow and Sell-to-short more shares they "know something" :-)
    BTW what they "knew" when shorted 4.5M SIAL at average $100 just before SIAL buyout for $140? $1.8B losses just in one moment.
    For MNKD with 131M shorted sales pps spike to $10 will bring at least $400-500M losses.
    Everybody asks just one question: why shorts are not covering? The answer may be very simple: they don't care about potential huge losses because they put under risk their clients money. In simple words these losses are already "priced in" as potential in portfolio of short-trading funds. When shorted MNKD the portfolio managers have trusted to wrong predictions of own analysts: Afrezza sales will be very low, at some point several Afrezza users will get lung cancer and MNKD pps will be crashed to $1 and below. Average gain from 131M shorted stock (at average $8-9) will be almost $1B. Not bad. If they still believe in this "prediction" they will never cover and may be even add more 10-20M shares.
    Time will tell who was right here: Mann who sold successfully several biotechs or shorts that are thinking that this time Mann bet on wrong technology and put under risk $1B of his own money.

    Sentiment: Strong Buy

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 22, 2015 5:20 PM Flag

    kad, I understand your point here: you are believing in Prana science and investing in what you are believe. But I "invest in what I know. PD is not my area but I have some experience in AD research. When I firstly saw that Prana has claimed to cure AD with PBT2 I was LOL. Never think that serious investors will put money on table and buy this fake biotech. But they did and lost big money. I was betting on PBT2 failure in AD trial and my gain was doubled. BTW I also played against Dimebon and short MDVN before phase III trial results.
    My credo in investment is simple: if I think that some biotech is scam I never hide my opinion but share it. In 80% cases I'm right and it bring me good profit. In 20% I mistaken and got some losses. You can follow my opinions or not , it's your business.
    Yes, I don't believe in PRAN science and Tanzi ideas to cure AD with metal chelator. AD is very hard puzzle that can't be solved so simply. Good luck with you investments that based on "believing" in science in small-cap biotechs. Add ORMP, XOMA, AXON, CTIX, BIOD and etc (all i my Fake biotech list).

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 22, 2015 4:30 PM Flag

    "my accusations about lies in peer-reviewed journal papers is astounding" ? Are you seriously? Just read this paper "In science, irreproducible research is a quiet crisis"
    "EVEN WHEN NO one’s done anything obviously wrong, scientific experiments sometimes yield results that turn out to be incorrect. When Doug Melton’s team at Harvard University discovered betatrophin, a hormone that could trigger the pancreas to make beta cells lost in diabetes, their 2013 paper was touted as a breakthrough. But when they redid the experiment and increased the number of animals, the original result didn’t quite hold up. The hormone’s effect was far weaker than first reported...."
    You will see that "my accusations" are nothing in comparison with real problem in science. I even completely stop my attempts to reproduce any results because it's just waste of time and money. Authors always answer like this:
    "As Olsen recalled, the scientist seemed surprised to hear from him and said that the technique was very difficult and that he would not recommend that people do it. It became clear to Olsen that it was something that the original research team had tried and failed to do many times, and then had gone and published a paper based on the few times it worked."
    PBT2 is safe compound but it can't solve AD puzzle :-)

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 22, 2015 2:47 PM Flag

    thanks for the link, it was interesting to I read this paper. BTW the correspondent author Susan Lindquist was published at least one paper with Tanzi as co-author. The paper was published in Science and sure it gave them both very good opportunity to get funds (money)
    Science. 2011 Dec 2;334(6060):1241-5. doi: 10.1126/science.1213210. Epub 2011 Oct 27.
    Functional links between Aβ toxicity, endocytic trafficking, and Alzheimer's disease risk factors in yeast.
    Treusch S1, Hamamichi S, Goodman JL, Matlack KE, Chung CY, Baru V, Shulman JM, Parrado A, Bevis BJ, Valastyan JS, Han H, Lindhagen-Persson M, Reiman EM, Evans DA, Bennett DA, Olofsson A, DeJager PL, Tanzi RE, Caldwell KA, Caldwell GA, Lindquist S.

    Couple comments about paper that you had cited as an evidence that PBT2 can be a neuroprotective compound and even cure some neurodegenerative diseases. I agree that both PBT2 and 8-OHQ have ionophoric and intracellular chelation activities. And this intracellular metal chelation may change activity of metal-dependent proteins like cytochrome cooxidase, aconitase, alkaline phosphatase, malate dehydrogenase, SOD1 and many other enzymes.
    And authors admitted that "metal chelators are frequently dismissed as therapeutic agents because of the expectation that they lack mechanistic specificity." But other conclusion that "PBT2 is both well tolerated and effective in AD patients (31, 34)." is a lie. PBT2 is safe at 250 mg daily doses but it's not effective in AD patients.
    So, may be both mentioned compounds are bioactive ones but they are not cures for AD, HD, PD and etc. May be they even have some neuroprotective effects in such models as yeast and C. elegans but they are absolutely useless to cure human neurodegenerative diseases.

    Sentiment: Strong Sell

  • and it costed them at least 10-15M more shorted shares. At the same time daily volume is so low that short can't cover any significant portion of their positions (may be 1-2M per day).
    140-145M (35% outstanding shares) short interest is very attractive number for Big Players that want to initiate short squeeze event without any risk: they can just put Limited order on 10M MNKD shares ($6 and up to $8) and get price spike to $15.

    Sentiment: Strong Buy

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 19, 2015 12:21 AM Flag

    Well, it's zero because of wrong paradigm. Dimebone, Alzhemed, PBT2 and other fake AD were failed because they were designed to fight with amyloid. AD drugs were never designed to fight with tau aggregation in axons. TauRx drug is now in phase III trial and results will be released in 2016.
    You said that these morons are not investing in AD drugs? But look at AXON scam: cap $1.44B pps $19. I shorted this scam at $26 and will cover below $10. But some idiots were buying it at $29.

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 18, 2015 5:44 PM Flag

    Well, you can use this cellular model for tau aggregation and test PBT2 efficacy:
    J Biol Chem. 2015 Apr 24;290(17):10862-75. doi: 10.1074/jbc.M114.616029. Epub 2015 Mar 10.
    Cellular Models of Aggregation-dependent Template-directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer Disease.
    Harrington CR1, Storey JM2, Clunas S3, Harrington KA4, Horsley D4, Ishaq A3, Kemp SJ3, Larch CP3, Marshall C3, Nicoll SL3, Rickard JE4, Simpson M3, Sinclair JP3, Storey LJ3, Wischik CM5.

    Alzheimer disease (AD) is a degenerative tauopathy characterized by aggregation of Tau protein through the repeat domain to form intraneuronal paired helical filaments (PHFs). We report two cell models in which we control the inherent toxicity of the core Tau fragment. These models demonstrate the properties of prion-like recruitment of full-length Tau into an aggregation pathway in which template-directed, endogenous truncation propagates aggregation through the core Tau binding domain. We use these in combination with dissolution of native PHFs to quantify the activity of Tau aggregation inhibitors (TAIs). We report the synthesis of novel stable crystalline leucomethylthioninium salts (LMTX®), which overcome the pharmacokinetic limitations of methylthioninium chloride. LMTX®, as either a dihydromesylate or a dihydrobromide salt, retains TAI activity in vitro and disrupts PHFs isolated from AD brain tissues at 0.16 μm. The Ki value for intracellular TAI activity, which we have been able to determine for the first time, is 0.12 μm. These values are close to the steady state trough brain concentration of methylthioninium ion (0.18 μm) that is required to arrest progression of AD on clinical and imaging end points and the minimum brain concentration (0.13 μm) required to reverse behavioral deficits and pathology in Tau transgenic mice.

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 18, 2015 2:48 PM Flag

    forget to cite paper about tau aggregation model

    J Biol Chem. 2015 Apr 24;290(17):10862-75. doi: 10.1074/jbc.M114.616029. Epub 2015 Mar 10.
    Cellular Models of Aggregation-dependent Template-directed Proteolysis to Characterize Tau Aggregation Inhibitors for Treatment of Alzheimer Disease.
    Harrington CR1, Storey JM2, Clunas S3, Harrington KA4, Horsley D4, Ishaq A3, Kemp SJ3, Larch CP3, Marshall C3, Nicoll SL3, Rickard JE4, Simpson M3, Sinclair JP3, Storey LJ3, Wischik CM5.

    Tanzi can use this model and prove that PBT2 can destroy tau aggregates in cell model.

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 18, 2015 2:32 PM Flag

    just citing, citing and citing papers about how good PBT2 as AD cure :-) You remember me guys that were citing published papers about other failed AD drug - Dimebon. But Dimebon even showed good results in AD phase II before complete failure in phase III. Same about Alzhemed and other fake drugs. Looks like even Tanzi has already admitted that PBT2 is not cure for AD but you continue to cite papers that were published by Tanzi as..kissers :-)
    If you know how easy to do falsification in science you will never believe so blindly in published results. So-called "metal theory of AD" is baloney invented by Tanzi to earn good money for his retirement (may be to buy yacht , nice bungalow and etc.).
    "Invest in what you know" but never invest in what you believe.
    About simple model where you can observe PBT2 in action: express GFP-tau in neurons, add inhibitor of PP2A or PBT2 (maximum concentration) and you will see that PBT2 can't prevent tau hyperphosporylation. Easy-to-do experiment and I'm sure that scientists in Big Pharma already did it. The results for Prana: no partner, no funds/institutions holding.
    Also there are no partners for HD, PD and etc.

    Sentiment: Strong Sell

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 18, 2015 1:09 PM Flag

    "Scientists at Bayer HealthCare reported that when they tried to reproduce 67 published discoveries in oncology, women’s health, and cardiovascular disease, only a quarter of the time were their in-house results completely consistent with what had been reported. A scientist at Amgen disclosed that, despite concerted effort, the company had successfully repeated only six of 53 major cancer findings."
    Most likely that Tanzi, Adlard and etc works are irreproducible and time will reveal the truth.
    BTW I didn't shorted PRAN yet (too low pps now) and even will buy it if run up happen (HD phase III or other positive events). But most likely Prana management will postpone HD phase III trial and agree to do animal tox studies. They will have more time to enjoy their good salaries and happy life. PRAN holders (at current pps) will have 50% losses and dead money for next 2-3 years.
    Good luck with pumping PRAN-scam :-) Will you continue to pump it if pps drop to cash/outstanding level ($0.75)?

    Sentiment: Strong Sell

  • Reply to

    Hey Bio

    by kadaicher1 Jun 17, 2015 6:09 PM
    biotech_invest biotech_invest Jun 18, 2015 11:11 AM Flag

    I see that you carefully read Wiki about tau and now know that just "removing" from neuron's axon will kill them very soon :-)
    BTW tau is always phosphorylated but the most important which sites (i.e. amino acids) are phosphorylated. GSK3 is not single kinase that work with tau:
    "The stress-activated protein (SAP) kinases SAPK1γ (also called JNK1), SAPK2a (also called p38, RK, CSBPs, Mpk2 and Mxi2), SAPK2b (also called p38β), SAPK3 (also called ERK6 and p38γ) and SAPK4 phosphorylate tau at many serine/threonine-prolines, Based on initial rates of phosphorylation, tau was found to be a good substrate for SAPK4 and SAPK3, a reasonable substrate for SAPK2b and a relatively poor substrate for SAPK2a and SAPK1γ. Phosphorylation of tau by SAPK3 and SAPK4 resulted in a marked reduction in its ability to promote microtubule assembly."
    Your hypothesis that PBT2 removes copper/zinc trapped in tangles and it disaggregates the tau tangles is just repeating of stupid statements of Tanzi and his as..kissers. Nobody (except Dr. Wishnik) show directly that tau aggregates can be destroyed. It's so easy to get them in vitro, add PBT2 and show that the aggregates disappeared. Can you cite such publication with PBT2?
    About "exact objections to Adlards paper"... To object it I need to repeat/reproduce experimental data. During my life I was trying to do it many times and in 80-90% I got negative results - just waste of time.
    Citation: "As a junior researcher, Olsen spent a year trying to repeat an experiment he had seen published in a prestigious journal. The technique in question supposedly could be used to track molecules within cells. At wits’ end, he contacted the scientist who had led the research to ask what he was doing wrong. As Olsen recalled, the scientist seemed surprised to hear from him and said that to hear from him and said that the technique was very difficult and that he would not recommend that people do it." In simple words he has admitted that they published false.

    Sentiment: Strong Sell

  • biotech_invest biotech_invest Jun 17, 2015 6:50 PM Flag

    "Invest in What You Know"
    MNKD is 30% of my biotech portfolio and I'm going to increase positions. Guess why? Because I know how TS technology works and can predict what kind of drugs can be delivered if combined with DKP carrier. There are a huge portfolio of drugs that need faster PK/PD than SC injections or tablets. Proteins, peptides and even small molecules can be mixed with DKP and will have Tmax = 10-15 minutes after inhalation. When Big Pharma finally realize this fact there will a long line to partner with MNKD. For example Adasuve (first inhalable antipsychotic drug) can be mixed with DKP and it's PK will be even better than current form.
    Inhalation of chemotherapeutic drugs mixed with DKP will help treat lung cancer (drugs including siRNA) will be delivered inside of cancer cells and kill them.
    I invest only in what I know.

    Sentiment: Strong Buy

  • Mann sold several companies with huge profit and Sanofi didn't mistake when initiated a collaboration with Regeneron and paid REGN upfront
    November 29, 2007
    Regeneron Initiates Major Global Collaboration with Sanofi-aventis to Develop and Commercialize Fully-Human Therapeutic Antibodies
    Sanofi-aventis plans to increase its stake in Regeneron to approximately 19%
    TARRYTOWN, N.Y.--(BUSINESS WIRE)--Nov. 29, 2007--Regeneron Pharmaceuticals, Inc. (Nasdaq: REGN) and sanofi-aventis (Euronext: SAN and NYSE: SNY) announced today that they have entered into a global, strategic collaboration agreement to discover, develop, and commercialize fully-human therapeutic antibodies utilizing Regeneron's proprietary VelociSuite of technologies (including VelocImmune®).

    Sanofi-aventis will also increase its ownership of Regeneron's outstanding common stock from approximately 4 percent to approximately 19 percent by purchasing 12 million newly issued shares of Regeneron common stock at a price of $26.00 per share, subject to customary closing conditions including antitrust clearance.

    As part of the research agreement, sanofi-aventis will make an $85 million upfront payment to Regeneron and will fund up to $475 million of research over the next five years. Sanofi-aventis will have an option to extend the research agreement for up to an additional three years.
    For any new product successfully developed as part of the collaboration, sanofi-aventis will take the lead in commercialization activities and will consolidate the sales. Regeneron will have the right to co-promote any and all collaboration products worldwide. In the United States, profits will be shared equally. Outside the United States, profits will be split on a pre-determined sliding scale with sanofi-aventis' share ranging from 65 percent to 55 percent. In addition, Regeneron will be entitled to receive up to a total of $250 million of sales milestone payments when the collaboration achieves certain aggregate annual ex-U.S. sales levels, starting at $1 billion.

    Sentiment: Strong Buy

  • Reply to

    Q&A with Rudy Tanzi posted today

    by interestingtome1 Jun 12, 2015 2:27 PM
    biotech_invest biotech_invest Jun 17, 2015 3:26 PM Flag

    kad, each time when I read your comments and questions I see that you are just a naive dilettante in science :-)
    "why Rudy does not include PBT2 as a treatment to remove Tau?"
    Simple answer will be that Tanzi knows that PBT2 is useless for "removing" tau. Because tau can't be removed from axons - it's very important protein that protects axon microtubules. Hyperphosphorylated tau (p-tau) loses this very important function and aggregates but these aggregates are not dangerous for axons i.e. they are not interfere with fast axonal transport.

    "Prana have demonstrated that PBT2 can remove Tau in a model just like the leading so called tau drug has"
    Tanzi knows that these "results" are irreproducible and want other people forget about them. PBT2 can't fight with both excess of tau phosphorylation and tau aggregation. Tau drug Rember just destroys p-tau aggregates and may be slow down axon degeneration.

    Will not comment the statements of this idiot Adlard with his stupid presentation “Metal Chaperones are novel therapeutic agents for tauopathy”. Will just cite this guy:

    “When papers are written and data are presented in public it looks like everything is just perfect, and that is not what science is,” Olsen said. “Science is an imperfect human activity that we try to do as best we can.”

    Sentiment: Strong Sell

  • "Bloomberg reported Thursday that Regeneron shares dropped 20 percent, the most in five years, on the Nasdaq Stock Market after downgrades at Credit Suisse and Morgan Stanley.
    Credit Suisse analyst Michael Aberman stopped recommending that investors buy the shares, citing "increased caution" about aflibercept. Recent data suggested the drug may have more toxic side effects than Genentech's Avastin. Analyst Aberman said that he is modifying probability adjusted net present value model and lowering his price target. The analyst expects REGN to be range bound in the high teens to low-$20s over the next 6-12 months, hence downgrading the stock.
    Steven Harr of Morgan Stanley also abandoned his buy recommendation, however, both said investors should hold the stock.
    Meanwhile, four other analysts still recommend buying Regeneron, whose largest shareholder is sanofi-aventis."
    Currently, REGN is down $3.69 or 19.34% and trading at $15.39.

    MNKD was downgraded by

    5/11/2015 JPMorgan Downgrade Underweight (Neutral) N/A
    (N/A) 3.81 5.93 55.64%
    3/3/2015 Goldman Sachs Downgrade Sell (Neutral) 3.00
    (6.00) 6.64 5.93 -10.69%

    MNKD Price Target Summary

    Highest: $16.25 (Griffin Securities)
    Lowest: $3.00 (Goldman Sachs)

    If history repeat again we should see 30X MNKD pps ($200) in 2020-22.

    Sentiment: Strong Buy

  • Reply to

    why can't TS deliver long acting insulin?

    by musherga Jun 15, 2015 10:59 AM
    biotech_invest biotech_invest Jun 15, 2015 12:47 PM Flag

    "Insulin glargine has a substitution of glycine for asparagine at N21 (Asn21) and two arginines added to the carboxy terminal of B chain. The arginine amino acids shifts the isoelectric point from a pH of 5.4 to 6.7, making the molecule more soluble at an acidic pH and less soluble at physiological pH. The isoelectric shift also allows for the subcutaneous injection of a clear solution. The glycine substitution prevents deamidation of the acid-sensitive asparagine at acidic pH. In the neutral subcutaneous space, higher-order aggregates form, resulting in a slow, peakless dissolution and absorption of insulin from the site of injection.[14] It can achieve a peakless level for at least 24 hours."
    Definitely insulin glargine is not good candidate to mix with DKP: it can just precipitate in lungs and induce strong cough. Insulin detemir is better candidate: in systemic circulation it will bind with albumin and PK/PD will be the same as for SC injection.
    One cartridge for evening meal with both fast-acting insulin and basal one should be very convenient for diabetics.

    Sentiment: Strong Buy

  • Reply to

    why can't TS deliver long acting insulin?

    by musherga Jun 15, 2015 10:59 AM
    biotech_invest biotech_invest Jun 15, 2015 12:31 PM Flag

    Well, insulin detemir is administrated once daily SC with evening meal or at bedtime.
    Initial dose
    Type 1 diabetes: Approximately one third of the total daily insulin requirements SC; rapid-acting or short-acting, premeal insulin should be used to satisfy the remainder of the daily insulin requirements; usual daily maintenance range is 0.5-1 unit/kg/day in divided doses; nonobese may require 0.4-0.6 unit/kg/day; obese may require 0.6-1.2 units/kg/day
    Type 2 diabetes inadequately controlled on oral medication: 10 units/day SC (or 0.1-0.2 unit/kg/day) in evening or divided q12hr
    Type 2 diabetes inadequately controlled on GLP-1 receptor agonist: 10 units/day SC given once daily in evening
    Since bioavailability of inhalable insulin is similar to SC, daily evening meal dosage 10-12 IU of detemir combined with diketopiperasine (co-dried microparticles) looks feasible. I don't see any technical obstacles to mix 4-8 IU of conventional insulin with 10-12 IU of detemir and co-dry them with DKP and load in one cartridge. MNKD or Sanofi can do it easy when detemir patent is expired (June 20, 2017).

    Sentiment: Strong Buy

  • Reply to

    why can't TS deliver long acting insulin?

    by musherga Jun 15, 2015 10:59 AM
    biotech_invest biotech_invest Jun 15, 2015 11:53 AM Flag

    come on, it's not correct question. TS technology can deliver even antibodies (high MW proteins) but the mechanisms of action of long acting (or basal) insulins are different: in one case it can be very slow sustained release from SC injection site because the insulin designed precipitate at this site (It consists of microcrystals that slowly release insulin, giving a long duration of action of 18 to 26 hours); in other case the basal insulin is modified: t is an insulin analogue in which a fatty acid (myristic acid) is bound to the lysine amino acid at position B29. It is quickly absorbed after which it binds to albumin in the blood through its fatty acid at position B29. It then slowly dissociates from this complex.
    If you combine first one with TS it will act as fast-acting insulin (no SR) but second one (Insulin detemir) is very good candidate for TS-mediated lung delivery. Moreover, ideally MNKD can combine fast-acting meal time insulin with basal one (like detemir) and recommend use it with first meal of day. In this case diabetics will avoid any injections.

    Sentiment: Strong Buy

  • Reply to

    Truly Amazed

    by jtsendence Jun 15, 2015 10:24 AM
    biotech_invest biotech_invest Jun 15, 2015 11:19 AM Flag

    don't forget that pending news also can send stock much lower :-)
    My prediction is that Prana management plan to go with animal toxicity studies for PBT2. These studies are not very expensive but they will take at least 2 years. During these 2 years of waiting PRAN pps will be around cash level: if they have $40M cash now and 53M total outstanding shares be ready for pps $0.75-0.8 (for PRAN buyers at $1.40 it will be -50% losses and dead money for next couple years).
    I hope I'm not right and phase III HD will finally start in 2015: run up should be nice and pps may jump to $3-4.

  • biotech_invest biotech_invest Jun 15, 2015 11:08 AM Flag

    WOW! Best news for last 3 months!
    Insulin lispro (marketed by Eli Lilly and Company as "Humalog") is a fast acting insulin analog. Engineered through recombinant DNA technology, the penultimate lysine and proline residues on the C-terminal end of the B-chain are reversed. This modification does not alter receptor binding, but blocks the formation of insulin dimers and hexamers. This allowed larger amounts of active monomeric insulin to be immediately available for postprandial injections.
    Sanofi wants to see what postprandial insulin is more effective to keep normal blood glucose level: Afrezza PD vs. insulin lispro PD. If Afrezza win this competition Sanofi will buy MNKD immediately.

    Primary Outcome Measures:
    Assessment of PD parameter: Area under the glucose infusion rate curve within 24 hours after administration of the investigational medicinal product or until administration of rescue insulin (GIR-AUC0-end) [ Time Frame: 24 hours ] [ Designated as safety issue: No ]

    Sentiment: Strong Buy

SNY
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