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Sanofi Message Board

scistats 194 posts  |  Last Activity: Apr 13, 2014 2:43 AM Member since: Apr 5, 2009
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  • Verified December 2013 by Children's Oncology Group

    It is totally bizarre that this trial is seemingly moving forward while Chip denies any Imetelstat solid tumor activity. When will this trial be withdrawn???

    Sentiment: Strong Buy

  • So, I would expect a few more drop-outs as Rochester Minnesota is in sub-zero conditions this time of year, and most folks do not live in Rochester.

    Factor in the fact that dosing is still being determined with the goal of extending the time between treatments, mom and pop from Iowa simply might not be able to keep up with the demands of the trial at this time.

    Furthermore, the trial has enrolled some very sick people with more than one health issue to worry about.

    The real question is how many CR's and for how long.

    Sentiment: Strong Buy

  • Imetelstat is not a "cure all".
    It looks like it works for a sub-population of myelofibrosis patients.
    Once the markers are determined, I think we are looking at a possible orphan status as Biomarin is doing in "breast cancer", a broad name for a what is in reality a group of diseases. From a financial perspective, orphan indications garner more pay per patient, and Geron can establish this with markers. Similarly, Imetelstat may be effective for subsets of solid tumors, but unless there is a targeted approach, the trials will washed out by patient mismatches. Fortunately CR's are almost unheard of for myelofibrosis, so this binary outcome is saving Geron's hide from what would otherwise be a total p-value hangman's noose. They dodged a bullet.

    Sentiment: Strong Buy

  • Int J Biochem Cell Biol. 2010 Oct;42(10):1602-5. doi: 10.1016/j.biocel.2010.06.010. Epub 2010 Jun 15.
    Casein Kinase II: an attractive target for anti-cancer drug design.
    Hanif IM, Hanif IM, Shazib MA, Ahmad KA, Pervaiz S.
    Author information
    Casein Kinase II (CK2) is a ubiquitous serine/threonine kinase that is highly conserved in eukaryotic cells. CK2 has been shown to impact cell growth and proliferation, as numerous growth-related proteins are substrates of CK2. More importantly, experimental evidence linking increased expression and activity of CK2 to human cancers underscores the relevance of CK2 biology to cellular transformation and carcinogenesis. Due to the critical regulatory role CK2 plays in cell fate determination in cancer cells, there is a tremendous interest in the development of CK2-specific therapies. Supporting this, recent reports have demonstrated that genetic manipulation of CK2 expression as well as pharmacological inhibition of its enzymatic activity sensitizes cancers to apoptotic stimuli. Here we provide a succinct account of the biology of CK2, its cellular substrates, its pro-survival and pro-proliferation activity, and highlight evidence for its involvement in human cancer.

    Abstract Number: A56
    Presentation Title: The telomerase inhibitor imetelstat exhibits anti-tumor and anti-cancer stem cell effects through perturbation of Casein Kinase-2 signaling.
    Location: West Hall, Level One, Moscone Center West
    Poster Board Number: A56
    Author Block: Ryan T. Nitta, Christopher O'Sullivan, Amrita Ramiya, Tong Lin, Hooman Kashani, Immanual S. Joseph. Geron Corp., Menlo Park, CA
    Abstract Body: Imetelstat treatment (2 weeks at 3uM) resulted in decreased expression of casein kinase 2 (CK2) subunits alpha and beta, and a reduction in phosphorylation of downstream CK2 substrates such as the DNA repair protein XRCC1. In addition, imetelstat reduced the transcriptional activity of beta-catenin, which is regulated by member

    Sentiment: Strong Buy

  • scistats scistats Feb 3, 2014 12:08 PM Flag

    Indeed, the next step is to definitely correlate genetic and biochemical markers with imetelstat success.

    If patients have the marker(s) correlating with myelofibrosis vulnerability to imetelstat, you treat them.

    With this strategy, Geron MAY completely cure ~20% of myelofibrosis cases. So, imetelstat is good for 20% of cases. Good news for these patients!

    In terms of finances. Geron charges a premium, and the PPS is worth what? 10 PPS or 20 PPS?

    Sentiment: Strong Buy

  • How do you START a phase 2 without first having markers to guide its success?

    So, Geron's phase 2 patient selection criteria is going to be VERY interesting.

    Sentiment: Strong Buy

  • Cancer is a broad name for many different diseases that often require personalized medicine.

    Using genetic markers, Dr. Ayalew Tefferi's "i-Harmony" system matches Geron's imetelstat therapy with patients for which it will be most effective.

    Intermediate or high-risk myelofibrosis is an orphan indication for which Jakafi is indicated. Imetelstat offers a CR whereas Jakafi does not.

    To make orphan indications viable, drug companies are allowed to charge a premium so that relatively fewer patients numbers do not diminish their chance of benefiting from the development of novel therapies.

    If you doubt the success or viability of targeting orphan diseases, review the history of Genzyme and Biomarin. Then, reconsider the valuation of Dr. Ayalew Tefferi's "i-Harmony" system. Coming soon, for solid tumors in mono and combination therapy!

    __♥ .____ ♥__

    Sentiment: Strong Buy

  • Reply to

    phase II imetelstat results

    by hayflicklim Feb 4, 2014 6:52 PM
    scistats scistats Feb 4, 2014 10:45 PM Flag

    Flick, the Geron study that you are referring to determined that imetelstat, in its current form and for the patients selected, does not work for non-small-cell lung cancer (NSCLC).

    Geron is now focusing on myelofibrosis, not lung cancer or breast cancer.

    The success reported by Mayo Clinic is for meylofibrosis, and they are working on matching patients for this indication.

    The next attempt at solid tumors is supposedly coming up in a trials called:

    "Imetelstat Sodium in Treating Younger Patients With Relapsed or Refractory Solid Tumors" Identifier:

    However, this trial may be cancelled out because Geron CEO "Chip" said the focus is on myelofibrosis.


    Sentiment: Strong Buy

  • This study is moving forward.

    Sentiment: Strong Buy

  • Reply to

    Be advised: Changes to NCT02011126 on 2014_01_30

    by scistats Feb 6, 2014 2:25 PM
    scistats scistats Feb 6, 2014 9:54 PM Flag

    This is the pediatric solid tumor trial for imetelstat being run by Texas Children's et al. Based on Chip's comments about solid tumors, we thought this trial might be cancelled, but as recently as January 30th, 2014, posted protocol changes suggesting this trial is going to happen. It will be interesting to see how imetelstat performs in the pediatric setting and establish the groundwork for what will most likely be combination therapies down the road. Imetelstat causes rapid shortening of telomeres but we need a chemotherapy to push these cells forward toward death and avoid "long delays incurred before cells succumb to crisis". So, expect a host of combination therapies.

    Sentiment: Strong Buy

  • Reply to

    2014 Published Findings by Tefferi and Team

    by irishtrader52 Feb 8, 2014 12:08 PM
    scistats scistats Feb 8, 2014 2:24 PM Flag

    Yes, Dr. Tefferi is definitely going to correlate genetic markers with imetelstat efficacy and identify the myelofibrosis patients for which it will work to achieve complete or partial remission.

    To this extent, it is personalized medicine, and effective for a subset of myelofibrosis patients.

    Imetelstat is also effective for essential thrombocythemia, and it may prove effective in combination with other drugs for solid tumors.

    Imetelstat is not a "cure all" or "one size fits all" medicine, but it is a valuable therapy that will saves the lives of people for which it is effective. I look forward to it being on the shelf as soon as possible.

    Sentiment: Strong Buy

  • A case of, "We don't know exactly how imetelstat works beyond telomerase inhibition. We know the mechanism involves multiple pathways, in part directed by the telomere itself, and we know imetelstat decreases expression of casein kinase 2 (CK2) subunits alpha and beta, and it does cause a reduction in phosphorylation of downstream CK2 substrates such as the DNA repair protein XRCC1. Importantly for patients, for myelofibrosis, it does work in certain patients to cause complete and partial remissions for which we are seeing genetic correlations. But the long-term durability and effects are not yet known."

    Sentiment: Strong Buy

  • Reply to

    Tom Brokaw Blood Cancer / Mayo Treatment

    by hoosier_investor Feb 11, 2014 6:25 PM
    scistats scistats Feb 11, 2014 6:54 PM Flag

    In other words, the exact mechanism of how it works is unclear and why it works in some genetic backgrounds better than other is not entirely known but progress in understanding these mechanisms of imetelstat are being made. More important is the fact that for some patients, so far, complete and partial remission is observed. The same could be said about the lack of perfect clarity of the mechanism for most, if not all, drugs on the market today for which new insight even after decades on the market is the rule rather than the exception. If we can accept this as investors and the FDA can accept this as a regulatory body, with added long-term safety data, acceptance is hopefully likely here, at least for myelofibrosis.

    Sentiment: Strong Buy

  • Reply to

    Didn't I just see a quick: $5.14 on my screen?

    by markkrag Feb 13, 2014 11:19 AM
    scistats scistats Feb 13, 2014 11:37 AM Flag

    I just saw the same thing after reloading the page.
    $5.14 appeared in green.
    I reloaded again and the PPS flashed back to the previous value.

    Sentiment: Strong Buy

  • Imetelstat achieves complete and partial remission in this subset of patients.

    For these patients, imetelstat is "personalized" because its efficacy is expected to be correlated with markers that these patients have. These markers, the treatment frequency and duration, and the durability of imetelstat will be defined in a company sponsored, focused phase 2 or larger size and longer duration as Geron has already stated.

    In the meantime, we wait for Dr. Tefferi to release additional information about his trial, specifically the exact number of PR, CR, and durability. He is likely to publish these final results in a meeting abstract or journal, but Geron will be synchronized for any material news announcements. Unless Geron announces something, Scripps will not release news per the agreement.

    Sentiment: Strong Buy

  • He is referring to the pathway beyond what is known about JAK2, and yes genetic mutations linked with imetelstat success are associated, but this is not going to be an imetelstat talk per se. CR and PR results will come later when the trial wraps up, but we are without a doubt focusing imetelstat on a subset of myelofibrosis patients. Imetelstat will be a premium "orphan indication like" medicine that will be profitable but not a multi-billion blockbuster. PPS target for a buyout ~12 to 15 PPS if the CR and PR's hold. Have a nice day.

    Myeloproliferative Disorders: JAK2 and Beyond (MD Anderson, Srdan Verstovsek)

    Overview: The classic myeloproliferative neoplasms (MPNs)—
    essential thrombocythemia (ET), polycythemia vera (PV), and
    primary myelofibrosis (PMF)—are distinct clonal disorders of
    multipotent hematopoietic progenitor cells with common
    pathobiologic characteristics. The discovery that a somatic
    point mutation (JAK2V617F) in the Janus kinase 2 (JAK2) is
    highly prevalent in patients with MPNs has been a crucial
    breakthrough in our understanding of the underlying molecular
    mechanisms of these diseases, and therefore, preclinical
    and clinical research in recent years has focused intensely on
    the development of new therapies targeted to JAK2. Clinical
    results so far suggest that JAK2 inhibitors may provide
    valuable clinical benefits in reducing splenomegaly, improving
    disease-related signs and symptoms, and normalizing elevated
    blood cell counts in patients with MPNs. Since JAK2
    inhibitors are not specific for JAK2V617F mutation (they inhibit
    normal and mutated JAK2 tyrosine kinase) and the dysregulated
    JAK signal transducers and activators of transcription
    (STAT) pathway appears to be a common underlying pathophysiologic
    abnormality in all patients with classic MPN regardless
    of the presence or absence of a JAK2V617F mutation,
    current JAK2 inhibitors are effective in all patients with MPN
    regardless of their mutation status. The JAK1/2-sele

    Sentiment: Strong Buy

  • sunday, february 16, 2014
    Morning Moderator: Marin Xavier, MD
    7 a.m. Breakfast & View Exhibits
    8 a.m. Management of Acute Leukemia in the Elderly
    Hagop Kantarjian, MD
    8:45 a.m. New Agents in the Treatment of CLL
    Susan O’Brien, MD
    9:30 a.m. Break & View Exhibits
    10 a.m. The Economics of Cancer Care
    Hagop Kantarjian, MD
    10:45 a.m. T-cell Lymphomas
    Jasmine Zain, MD
    11:30 a.m. Extranodal Presentations of Lymphomas -
    Special Considerations
    Sunita Nasta, MD
    12:15 p.m. Lunch
    Afternoon Moderator: James Mason, MD
    1:15 p.m. New Agents for Myeloma - Is there an
    Optimal Approach?
    Morie Gertz, MD
    2 p.m. Myeloproliferative Disorders: JAK2 and Beyond
    Ayalew Tefferi, MD
    2:45 p.m. Management of Refractory, Indolent
    B-cell Malignancies
    Leo Gordon, MD
    3:30 p.m. Break & View Exhibits
    4 p.m. WORKSHOPS (repeat from Saturday)
    A. Clinical Challenges in Coagulation
    Stephan Moll, MD
    B. Clinical Challenges in Hematology
    Alice Ma, MD
    C. Interesting Cases in Hematology
    Rajiv Pruthi, MBBS
    D. Advanced Diagnostics in Hemostasis
    and Thrombosis II
    Craig Kitchens, MD
    5 p.m. Adjourn

    Sentiment: Strong Buy

  • scistats scistats Feb 15, 2014 7:08 PM Flag

    Let's hope that the CR and PR's increase in number and duration Vette.
    Go to minute 6 of this YouTube video.
    "Myelofibrosis Update 2014 - Mayo Clinic"

    Sentiment: Strong Buy

  • Reply to

    New Data

    by irishtrader52 Feb 16, 2014 4:11 AM
    scistats scistats Feb 16, 2014 4:57 AM Flag

    Abstract Submission
    Gabriela Baerlocher 1,*Elisabeth Oppliger Leibundgut 1Gary Spitzer 2Oliver Ottmann 3Olatoyosi Odenike 4Alexander Röth 5Michael McDevitt 6Srdan Verstovsek 7Kevin Nishimoto 8Christina Ayran 8Ted Shih 8Xiaolin Wang 8Dianne Morfeld 8David Snyder 9
    1Hematology, University Hospital and University of Bern, Bern, Switzerland, 2Upstate Oncology Associates, Greenville, SC, United States, 3Hematology and Oncology, Johann Wolfgang Goethe Universität, Frankfurt, Germany, 4University of Chicago, Chicago, IL, United States, 5University of Duisburg-Essen, Essen, Germany, 6The Johns Hopkins University, Baltimore, MD, 7University of Texas MD Anderson Cancer Center, Houston, TX, 8Geron Corporation, Menlo Park, CA, 9Hematology and HCT, City of Hope, Duarte, CA, United States

    Please indicate your presentation preference: Oral Presentation
    Has the submitted material been published in a journal (printed or online)?: No
    Has the submitted material been presented or submitted to another event?: Yes

    Sentiment: Strong Buy

  • Reply to

    New Data

    by irishtrader52 Feb 16, 2014 4:11 AM
    scistats scistats Feb 16, 2014 4:58 AM Flag

    New information: Oral presentation at ASH 2012. Updated data on hematologic and molecular response for new pts and longer follow-up on exisiting ET pts. Rapid and durable molecular response by reduction of JAK2V617F allele burden in JAK2-positive pts is highlighted
    Do you wish to apply for a Travel grant?: No
    Background: Myeloproliferative neoplasms (MPNs), such as essential thrombocythemia (ET), are driven by neoplastic progenitor cells. Telomerase is upregulated in neoplastic progenitor cells and sustains indefinite replication. Imetelstat is a first in class, potent, specific inhibitor of telomerase. In vitro studies suggest that imetelstat selectively inhibits spontaneous CFU-megakaryocyte growth from the blood of pts with ET but not from healthy individuals. In addition, imetelstat inhibited the proliferation of neoplastic clonogenic cells in ET pts. An update of the ongoing phase 2 study is presented here.
    Aims: Primary endpoint was best overall hematologic response (HR) with complete response (CR) and partial response (PR) defined as platelet (plt) counts ≤400E3/µl and ≤600E3/µl (or 50% reduction from baseline), respectively, for ≥4 consecutive weeks (wks) in the absence of new thromboembolic events. A key secondary endpoint was molecular response (MR), which includes measurement of the JAK2V617F allele burden by allele-specific quantitative real-time PCR.
    Methods: This study enrolled pts with ET who had failed or were intolerant to ≥1 prior therapy, or refused standard therapy. During the induction phase, pts were treated with imetelstat 7.5 mg/kg or 9.4 mg/kg IV weekly until attainment of plt count approximately 250-300E3/µl. Maintenance phase was then commenced with dosing titrated to plt count.

    Sentiment: Strong Buy

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