NPS Pharmaceuticals, Inc. Message Board

dcaf7 94 posts  |  Last Activity: Jun 22, 2016 9:06 AM Member since: Apr 24, 2010
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  • Reply to

    Merrill Lynch Presentation

    by tartiaboy May 10, 2016 1:06 PM
    dcaf7 dcaf7 May 10, 2016 2:53 PM Flag

    For Europe, a separate Phase 3 trials with SPI-2012 will be required. No need to wait.

  • Reply to

    Apaziquone lecture

    by dcaf7 May 9, 2016 10:52 AM
    dcaf7 dcaf7 May 9, 2016 2:19 PM Flag

    This article describes several hypoxia activated prodrugs including Apaziquone . There you can find a short history of Apaz development, which is not long enough for entire lecture. I would like to hear about the mechanism of Apaz inactivation by blood.

  • Anti-cancer drugs: trials and tribulations in their development

    Wednesday 18 May 2016, 7.00PM

    Speaker: Professor Roger Phillips, University of Huddersfield

    An evening lecture organised jointly by the Royal Society of Chemistry (Central Yorkshire Section) and the Royal Society of Biology (Yorkshire Branch)

    The discovery and development of new anti-cancer drugs is a difficult, time consuming and expensive process. The field is littered with disappointment but these failures provide an opportunity to learn and apply this knowledge to the search for new drugs. This lecture will focus on one such example called EO9 (Apaziquone), a drug that is now in phase III clinical trials for non-muscle invasive bladder cancer despite a history of failure in other clinical trials

    Light refreshments will be available from 18.00

    Location: C/A102

    Admission: There is no charge for admission or refreshments but prior registration is requested. Further details from Dr Brian Grievson, Department of Chemistry, University of York, Heslington, York, YO10 5DD. Tel: (01904) 324543 e-mail: brian. grievson@york. ac. uk

    wwwDOTyorkDOTacDOTuk/chemistry/events/seminars/2016/rogerphillips18-05-2016/

    Wonder if it will be published.

  • Reply to

    SPI-2012 / part B drugs

    by ville_9 May 6, 2016 12:30 PM
    dcaf7 dcaf7 May 6, 2016 2:00 PM Flag

    Improving Incentives for the Best Clinical Care

    Today, Medicare Part B generally pays physicians and hospital outpatient departments the average sales price of a drug, plus a 6 percent add-on. The proposed model would test whether changing the add-on payment to 2.5 percent plus a flat fee payment of $16.80 per drug per day changes prescribing incentives and leads to improved quality and value. CMS would update the flat fee at the beginning of each year by the percentage increase in the consumer price index for medical care for the most recent 12-month period. This test would begin in late 2016 (no earlier than 60 days after the rule is finalized).

    The independent Medicare Payment Advisory Commission (MedPAC) described a similar approach in its June 2015 report to Congress.

    CMS expects that the add-on payment of 2.5 percent plus a flat $16.80 fee will cover the cost of any drug paid under Medicare Part B. The flat fee is calculated such that it is budget neutral in aggregate. CMS intends for the test to result in savings through changes in prescribers’ behavior.

    Physicians often can choose among several drugs to treat a patient, and the current Medicare Part B drug payment methodology can penalize doctors for selecting lower-cost drugs, even when these drugs are as good or better for patients based on the evidence. To illustrate the effect of this change, consider two drugs each prescribed for a similar condition, with similar patient outcomes, but with widely varying prices. The average sales price for Drug A is $5, and for Drug B it’s $100. Today, Drug A is paid at $0.30 above the price of the drug and Drug B at $6.00. But under this proposal, Medicare would pay Drug A at $16.93 above the average sales price and Drug B at $19.30.

    wwwDOTcmsDOTgov/Newsroom/MediaReleaseDatabase/Fact-sheets/2016-Fact-sheets-items/2016-03-08DOThtml

  • dcaf7 dcaf7 May 6, 2016 8:10 AM Flag

    It is GAAP (65.5M) vs non-GAAP (80.6M) reporting.

  • Potentially, it is 25% dilution. It is serious.

  • Reply to

    AZ bought 2 biotech firms last year

    by nptimothy May 2, 2016 11:38 AM
    dcaf7 dcaf7 May 3, 2016 1:20 PM Flag

    May be MEK inhibition in cell lines showed dismal responses but MEK inhibition with selumetinib in KRAS mutation-positive patients demonstrated 37% response rate (vs 0%) and prolonged PFS. Perhaps inhibition of both EGFR and MEK is a better strategy and will be explored in future but Phase 2 data indicate that inhibition of MEK only could be beneficial for patients.

  • Reply to

    AZ bought 2 biotech firms last year

    by nptimothy May 2, 2016 11:38 AM
    dcaf7 dcaf7 May 3, 2016 9:11 AM Flag

    It has a good rationale. Trial's population is KRAS mutation-positive patients. How can you say "No "driver" mutations in the MAPK pathway"? What do you know?

  • Reply to

    ARRY at ASCO 2016

    by dcaf7 Apr 20, 2016 3:11 PM
    dcaf7 dcaf7 May 3, 2016 8:47 AM Flag

    One more abstract
    Abstract 3544
    Phase 2 results: encorafenib (ENCO) and cetuximab (CETUX) with or without alpelisib (ALP) in patients with advanced BRAF-mutant colorectal cancer (BRAFm CRC).

  • dcaf7 dcaf7 May 2, 2016 6:47 PM Flag

    He is correct. PFS in a single arm study cannot be used for any approval, including accelerated approval. Marqibo, Folotyn and Belinostat were all approved based on response rates. When you see a response, you know that it is a drug's effect. When you see a PFS curve with no control, what do you know? Placebo will also produce a curve.

  • dcaf7 dcaf7 May 2, 2016 2:46 PM Flag

    I would pay attention to what is going on with Neratinib. Compare titles for Poziotinob and Neratinib trials: "Poziotinib in Patients With HER2+ Recurrent Stage IV BC Who Have Received at Least 2 Prior HER2-directed Regimens" and "A Study of Neratinib Plus Capecitabine Versus Lapatinib Plus Capecitabine in Patients With HER2+ Metastatic Breast Cancer Who Have Received Two or More Prior HER2 Directed Regimens in the Metastatic Setting". Same patient population and Puma runs a 600-patient Phase 3 study with PFS and OS as primary endpoints. I don't see how Spectrum is able to negotiate accelerated approval, especially, if the results of Neratinib trial are positive.

  • dcaf7 dcaf7 May 2, 2016 10:22 AM Flag

    ASH is American Society of Hematology. Why should they accept any abstract on breast cancer? And I don't understand why everybody is so excited about Raj's excitement. He is a specialist in hematologic oncology and does not have any experience in breast cancer and HER inhibitors. We need to hear about how exciting is a new Korean data from more knowledgeable person.‎

  • Immunotherapy Puts 93 Percent of Advanced Leukemia Patients in Remission
    Friday, 29 Apr 2016 12:20 PM

    An astounding 93 percent of patients with advanced leukemia that was resistant to multiple other forms of therapy went into remission after their T-cells were genetically engineered to fight their cancers.

    Researchers at Fred Hutchinson Cancer Research Center worked with the University of Washington Cancer Consortium to enroll patients with B-cell acute lymphoblastic leukemia. All of the patients had advanced disease that had relapsed and were immune to other therapies.

    The patients received genetically engineered versions of their own T-cells — disease-fighting immune cells — with a synthetic receptor molecule called a CAR (chimeric antigen receptor) that allows T-cells to recognize and kill cancer cells that carry a specific marker called CD19.

    T-cells were extracted from patients, and a specialized virus delivered the DNA instructions for making the CAR into the cells. Then, the cells were multiplied to the billions in the lab.

    After chemotherapy, the reengineered cells were infused back into the patients they came from about two weeks after they were first extracted.

    A few weeks after the infusion, highly sensitive tests could find no trace of cancer in the bone marrow of 27 of 29 patients. CAR T-cells eliminated cancers anywhere in the body they appeared.

    wwwDOTnewsmaxDOTcom/Health/Health-News/immunotherapy-leukemia-patients-remission/2016/04/29/id/726461/

    Great results, do not bode well for Marqibo.

  • Reply to

    The Fool on the hill is back

    by wilderguide Apr 27, 2016 5:41 PM
    dcaf7 dcaf7 Apr 28, 2016 9:21 AM Flag

    Read the comment from Barry H Kaplan to this article. It is an oncologist view on Cobi, Cabo and Opdivo. He said that "Opdivo's benefits have been outrageously overstated".

  • $16.7M, 10% higher than in 1stQ15

  • It was $7.6 on Aug 28, 2015 but other closing prices were lower.

  • Reply to

    Apaziquone trial update

    by dcaf7 Apr 21, 2016 10:15 AM
    dcaf7 dcaf7 Apr 22, 2016 3:11 PM Flag

    I think that the logic for the second instillation was following: although the difference between placebo and Apaz groups after 90 min was not significant, it was in favor of Apaz. You may need more patients to reach lower p value. It is possible that Apaz works on floating cells better, but it still works on attached cells. Therefore, you may expect an additive effect from two instillations.

  • Reply to

    Apaziquone trial update

    by dcaf7 Apr 21, 2016 10:15 AM
    dcaf7 dcaf7 Apr 21, 2016 12:54 PM Flag

    My question was rhetorical.

  • Reply to

    Apaziquone trial update

    by dcaf7 Apr 21, 2016 10:15 AM
    dcaf7 dcaf7 Apr 21, 2016 11:51 AM Flag

    Do we know from whom?

  • Reply to

    Apaziquone trial update

    by dcaf7 Apr 21, 2016 10:15 AM
    dcaf7 dcaf7 Apr 21, 2016 11:27 AM Flag

    It could be an error. I don't want to think about other possibilities.

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