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Vertex Pharmaceuticals Incorporated Message Board

gladpick 57 posts  |  Last Activity: 15 hours ago Member since: Jan 24, 2000
  • Reply to

    My Take

    by gladpick Apr 17, 2014 2:56 PM
    gladpick gladpick 15 hours ago Flag

    Papa,
    I hope I am wrong about my lower ($80 to 85) predicted upside. Nevertheless I will be elated even with $80 to 85. I just think the $100 target was doable before the 3 house of reps caused mayhem in biotech stocks. it will take time for the damage they caused to diminish. As I said I hope I am wrong with my guarded prediction.

  • gladpick by gladpick Apr 17, 2014 2:56 PM Flag

    PPS moves up and down with the biotech indexes until mid 2014 when CF phase 3 results are announced. If results are in line with what most of us longs expect I think we may hit mid 80's. if the results are mediocre or not good we will go down to low 40's or upper 30's basically because, unfortunately, the management's past decisions have turned us into a one drug company. In that case the company should be sold for maybe 50 to $55 if we are lucky.

  • Reply to

    Do you smell something

    by gladpick Apr 9, 2014 3:42 PM
    gladpick gladpick Apr 10, 2014 12:35 PM Flag

    Obviously I am sizzling into bacon. Obviously I misspoke.

  • Reply to

    Do you smell something

    by gladpick Apr 9, 2014 3:42 PM
    gladpick gladpick Apr 9, 2014 5:56 PM Flag

    Oh, a poor short gave me a thumb down vote. hehehehe

  • I am smelling sizzling bacon!

  • On Jan 9, VRTX announced VX-135 and Daclatasvir had achieved 91% (10 out of 11 -- one person from the original 12 dropped out early due to vomiting) SVR4 after 12 weeks of combination therapy. Apparently at that time they must not have had the SVR for the 12 week. Let us assume they wanted to wait for the final data at the end of 24 weeks to account for possible relapsers. According to my calculations April 3 was 12 weeks after Jan 9. This is now April 9. Why VRTX has not published any data about the efficacy of that trial?

    Anyone who cares to speculate?

  • Reply to

    shorts ratio

    by gladpick Apr 9, 2014 10:24 AM
    gladpick gladpick Apr 9, 2014 12:34 PM Flag

    "They may have already covered by now"

    Some may have covered but I doubt if most covered, since there was a relentless selling and not enough buyers which caused a downward spiral for the past several weeks. Of course all of this is just conjectures on our part. We will know for sure the short numbers which will be released soon.

  • gladpick by gladpick Apr 9, 2014 11:43 AM Flag

    here is a summary of the remainder of the article which eliminates some of words in the article to see if yahoo will allow it to go through.
    And in fact, a drug already exists that can block ........... Known as VX - 765, it was tested years ago by Vertex Pharmaceuticals as a treatment for chronic seizure disorder. A trial showed that it wasn't effective enough against seizures, but it was safe for humans.

    This is solid, interesting, useful science in the field of HIV ...........," Gallo says, although he questions whether blocking the cells' death might lead them to later replicate the virus. (Greene believes the cells will degrade the viral DNA and recover.)

    Greene envisions the drug, if it proves effective, as a stopgap for patients in developing countries who don't have easy access to antiretroviral drugs. It could also be an addition to such therapy. ........

  • gladpick by gladpick Apr 9, 2014 11:16 AM Flag

    It won't let me post the last part of the article about Greene's work

  • Reply to

    VX-765 and HIV

    by gladpick Apr 7, 2014 12:11 PM
    gladpick gladpick Apr 9, 2014 11:05 AM Flag

    "The response is a self-destruct protocol called pyroptosis. In contrast to the better-known apoptosis, in which cells die quietly without triggering inflammation, pyroptosis is "not a bland, but a fiery death," Greene says. These cells spew inflammation-causing chemicals as they die, attracting more T-cells that can then become infected themselves by the newly freed HIV. "In a bacterial infection, recruiting all these cells might be a good strategy for containing the infection," Greene says, but with HIV a vicious cycle of infection results. Pyroptosis also explains why AIDS is associated with high levels of inflammation.
    Experiments by Greene's team showed that blocking a key component of pyroptosis could stop the cell death entirely; they also identified the protein that senses viral DNA to kick off the process. After studying the pathway in cultured spleen and tonsil tissue, they had an opportunity to confirm the findings in a patient's freshly removed lymph node, stained for their target proteins and viewed under the microscope. It showed the traditional virus replication happening in cells at the center of the node and resting cells dying all around. To Greene, the sight was unbelievable: "We could see this pyroptotic pathway playing out like nobody's business. In this one snapshot, we could see what we had been working on for eight years."
    There's good news though: Greene estimates 95 percent of the cells that die in HIV infections are killed through pyroptosis, so the findings raise hope for a new type of treatment that could prevent HIV from progressing into AIDS. "Inhibiting activation of the immune system is not a new concept, but this gives us a new pathway to target," says Robert Gallo, director of the Institute of Human Virology at the University of Maryland School of Medicine, who was not involved in the study. He warns that other pathways may be at work that are still unknown but that this one is promising if it truly accounts forlarge%ofTcell deaths

  • Reply to

    VX-765 and HIV

    by gladpick Apr 7, 2014 12:11 PM
    gladpick gladpick Apr 9, 2014 10:58 AM Flag

    Below may may be old info and in case some have not been exposed to it i like to post it here and in subsequent posts(too long for one post).

    "Cells' Fiery Suicide in HIV Provides New Treatment Hope
    Most T cells are not killed by the HIV virus itself, but by the body’s defense mechanism. Stopping this process could prevent a patient’s progression to AIDS
    Dec 19, 2013 |By Beth Skwarecki
    Advances against AIDS
    The difference between HIV infection and full-blown AIDS is, in large part, the massive die-off of the immune system’s CD4 T-cells. But researchers have only observed the virus killing a small portion of those cells, leading to a longstanding question: What makes the other cells disappear? New research shows that the body is killing its own cells in a little-known process. What’s more, an existing, safe drug could interrupt that self-destruction, thereby offering a way to treat AIDS.

    The destructive process has caught scientists by surprise. "We thought HIV infects a cell, sets up a virus production factory and then the cell dies as a consequence of being overwhelmed by virus. But there are not enough factories to explain the massive losses," says Warner Greene, director of virology and immunology at the Gladstone Institutes, whose team published two papers today in Science and Nature describing the work. (Scientific American is part of Nature Publishing Group.)

    Greene suspects that researchers in the past failed to notice the process because they were looking in the wrong place. Instead of studying active CD4 T cells in the blood, his team examined spleen and tonsil tissue, where most cells are in a resting state. When HIV enters a resting cell, it transcribes its genes into DNA, but then hits a dead end: the cell's machinery isn't available to finish the replication process. This part of the story had been known for years, but Greene's team discovered that something very surprising happens next. "Instead of that being the end of the story, cells detect that DNA in their cytoplasm and launch an immune response against it, and that immune response results in the death of those cells."

  • Reply to

    VX-765 and HIV

    by gladpick Apr 7, 2014 12:11 PM
    gladpick gladpick Apr 9, 2014 10:39 AM Flag

    I looked up the definition of PDUFA whch is " FDA date for approval." I wonder if that means the date the FDA's internal committee meets and decides for approval/non-approval and then it takes time for them to draft the letter of approval, etc.

    Or could it be possible that PDUFA date was changed to a later date and VRTX did not bother to announce that? I say that because in my book It is not unusual for this management not to bother informing its investors.

  • gladpick by gladpick Apr 9, 2014 10:24 AM Flag

    As of 14th of march 9.10% of float was short as opposed to 7.06% the month before.

    I can't wait to see these shorts sizzle into bacon.

  • Reply to

    NKTR102 and 214 is why I am here

    by kklausbeckerman Apr 9, 2014 9:55 AM
    gladpick gladpick Apr 9, 2014 10:20 AM Flag

    Timely news announcement by NKTR!

  • Reply to

    VX-765 and HIV

    by gladpick Apr 7, 2014 12:11 PM
    gladpick gladpick Apr 9, 2014 8:51 AM Flag

    Good news. To my knowledge VRTX management has not said any thing about a plan for a phase 2a proof of concept. It seems to me a bit of publicity may help the stock.

  • It is about time for the insiders to show confidence and value in the stock by buying in the open market!!!

  • gladpick by gladpick Apr 7, 2014 12:11 PM Flag

    VX-765 "a cell permeable prodrug" is no longer mentioned anywhere on VRTX web site. I recall, it was briefly reported that Warner Greene's group had used it as one of the techniques to find alternative drugs for HIV. I do not recall Dr. Leiden saying much about it. Below is the section about the use of VX-765 in Greene's publication:

    "Extended Data Figure 9: Targeting caspase 1 via an orally bioavailable small molecule inhibitor prevents lymphoid CD4 T-cell death by HIV-1. (373 KB)
    a, VX-765 is a cell permeable pro-drug (1) that requires intracellular esterase cleavage in the cell to yield the aldehyde functionality (green) of the drug VRT-043298 (2b), which acts as a potent caspase 1 inhibitor. Adapted from ref. 38 with permission. b, VX-765 prevents CD4 T-cell death in a dose-dependent manner in HIV-infected lymphoid tissues. HLACs were either not infected or infected with HIV-1 in the absence of drugs or in the presence of efavirenz (100 nM), AMD3100 (250 nM) or VX-765 (0.05, 0.5 or 5 μM) as indicated. VX-765 was added to the cultures 4 hours before infection to allow absorption and processing by the cells. Flow cytometry plots depict gating on live cells based on the forward-scatter versus side-scatter profile of the complete culture. These results are representative of three independent experiments performed using tonsil cells from three different donors."

  • Reply to

    SEQUENCE OF EVENTS

    by gladpick Apr 6, 2014 11:20 AM
    gladpick gladpick Apr 6, 2014 11:25 AM Flag

    remainder of my previous post:

    SOMETIME IN 2015 –NKTR-102 for small cell lung cancer. Data is expected from a phase 2 trial conducted at U of PENN.

    SOMETIME IN 2015. NKTR_214 for immunotherapy may hit clinic “We remain very bulish on 214.” “It really looks quite revolutionary to us.” “It is the first home grown biologics for NKTR.”

  • gladpick by gladpick Apr 6, 2014 11:20 AM Flag

    SECOND QUARTER OF 2014– Phase 1 results of NKTR 171 to be announced.

    MIDDLE OF 2014 – Fast track NKTR 181 for pain. Plan to initiate the first phase 3. Late last year the FDA gave very good initial feedback for phase 3 plans. As we all know phase 2 provided effective pain relief with substantially fewer CNS side effects, however, due to the faulty design of the trial the placebo group did not have a pain rebound upon discontinuation of 181. Due to that faulty design, NKTR plans to “mitigate the key factors in phase 3” trial design.

    SEPT 16 OF 2014 – PDUFA date for Naloxegol. AstroZeneca is preparing for launch in Q1 of 2015. We get $35M in 2014 (if no safety issues). Then in early 2015 upon launch we get $100M in US and $40M in EU. Also “significant escalating double digits in global sales.” Any body knows the anticipated global sales for Naloxegol?
    As it has already been announced, Naloxegol in 2 phase 3 studies met the primary endpoint of responder rate and all the key secondary endpoints.

    THIRD Q OF 2014 – Top line data for BX-855 will be announced. FILING FOR APPROVAL BY END OF 2014.
    As it has already been announced, BX 855 was well tolerated and no safety issues so far. Estimated annual sales of $2B. “Royalties and sales milestones of over $70M” I assume per year.

    EARLY 2015 –Top line survival data for fast track NKTR 102 for breast cancer. “SUBMIT REGULATORY FILINGS IN US AND EU IN 2ND HALF OF 2015.”
    As it has been announced, the monitoring committee was apparently satisfied with the progress of phase 3 since it did not recommend any changes for its continuation.
    There was also good results from a separate study in Stanford which will be published in a major medical meeting in 2014.

    FIRST HALF OF 2015—Amikacin Inhale –BAYER. Phase 3 trial is expected to be completed. $700M annual sales. 30% flat royalty in US and 22% ex-US countries.

    SECOND HALF OF 2015 – CIPRO (BAYER). Phase 3 is ongoing. Annual sales $750M. Escalating royalties averaging 10%.

    SOMETIM

  • Capacity is expanding and we forecast $40 million in revenue for 2014. Importantly, 3D Systems remains overbooked for Phenix and can ship everything it builds. At this run rate, we see 3D Systems exiting 2014 with substantial market share for powder bed fusion systems.

VRTX
64.17-0.22(-0.34%)Apr 17 4:00 PMEDT

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