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ONYX Pharmaceuticals, AŞ Message Board

  • latishajones latishajones Jul 27, 1998 1:57 AM Flag


    onxx is going to have a great quarter and mr. Hollings who is an insider knows about it already!!

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    • IT's was a good price 7 $

    • >>I received a package from the Clinical
      Coordinator at Onyx, that had a lot of imformation in
      reprints of clinical test of O15. I was impressed with
      success of O15 in all of the case studies. But most
      importantly, many of the case studies and press stories are
      recent. This would tend to tell me that Onyx is not
      standing still. <<

      Due some homework. Onyx quit all their virus work years ago. They don't own O15 anymore. A Chinese company does.


    • Interresting to read!

    • Remember July 1998


    • Three important issues are at stake here and
      yet none are answered. The first is how (and

      why) does adenovirus kill cells? This is of

      fundamental interest but also of critical importance to the
      clinical effect of ONYX-015. It makes sense
      viruses of this type should exert fine control
      cell death mechanisms because arguably
      they wish
      to suppress such pathways early in
      infection to
      allow maximium virus reproduction,
      and then to
      stimulate these pathways late in
      infection to aid viral
      dispersal. To determine the
      role of p53 in this process
      will require normal
      permissive primary cell lines
      with inducible p53

      The second
      question is the host range of
      ONYX-015. One might
      argue that it does not
      matter clinically if this
      mutant adenovirus can
      replicate in all tumor cells
      as long as it does not
      replicate in normal
      cells. However, from a strictly
      scientific point of
      view one absolutely wants to
      know how the host
      range of the virus is
      determined. Perhaps the virus
      may be telling us
      something very novel about
      cancer cells. If it is
      not p53 status, what is it?
      Again the clue to
      explain the host range of the
      deletion mutant will
      come from the normal virus and a
      understanding of the role of the E1B 55 kDa

      protein in its lytic cycle6. Already it is clear that

      the 55 kDa protein has striking similarities to
      host mdm2 protein, with both competing for
      same binding site on p53 and targeting p53
      ubiquitin-dependent degradation. Importantly,
      effect of E1B depends on another viral
      called E4 orf 6. In the absence of this protein,
      is stabilized by E1B whereas in its presence
      is degraded at an enhanced rate.

      do these concerns raise any questions
      about the
      future of selective replication-competent
      viruses in
      human clinical trials? Perhaps not at this
      because notably missing from the new
      study is any
      analysis of wild-type versus
      E1B-deletion mutant virus
      activity in normal human
      cells. Yet it is just here
      that the ONYX-015 virus
      shows such promising
      selectivity. At the moment
      we have two incompletely
      phenomena: the exact regulation of the p53

      pathway and its control in tumor cells that express

      wild-type p53 (as opposed to normal cells), and
      precise function of the E1B 55 kDa protein.
      new studies will resolve these disputes,
      already one can anticipate subtle answers.

    • ... for me, it was options (This was back when I
      was younger and invulnerable.) <g>

      Actually my margin call was triggered by a stupid, long
      move I made on both the Nasdaq and the NYSE recently
      (in a sector I know nothing about in a very volatile
      market). I had to dump about 1/3 of my ONXX at a fairly
      big loss (and it wasn't easy to sell either). Hope
      none of the other Onyx longs here got hurt too

    • Actually my margin call was triggered by a
      stupid, long move I made on both the Nasdaq and the NYSE
      recently (in a sector I know nothing about in a very
      volatile market). I had to dump about 1/3 of my ONXX at a
      fairly big loss (and it wasn't easy to sell either).
      Hope none of the other Onyx longs here got hurt too

      The short-term loss aside, it's too bad I
      had to sell, 'cause I still believe in the promise of
      015 and am not as cynical about Onyx's other projects
      as some "insiders" who post here. Some reasons: The
      Warner-Lambert re-signing this past year for inflammation
      screens wasn't done on a whim; WLA isn't going to throw
      millions of dollars at a small biotech for kicks. They
      expect a return on their investment, which now extends
      into 2001 I believe. Also, although Lilly is slow to
      pull out of a deal going bad, I've heard no rumors in
      that regard here or elsewhere, so I assume the BRCA1
      project is still alive. The Bayer deal was set to end
      this year anyway. If it does, that doesn't mean Onyx
      is falling apart at the seams, it just mean the
      project wasn't fruitful enough for Bayer to justify
      renewing. Bayer has been through some rough financial times
      recently; they're not going to be reckless in their Onyx
      dealings. Again, I'm not saying Onyx shareholders should
      count on a strong pipeline to be there in case 015
      fails ('cause the pipeline won't sustain the company
      for very long in that event), but I'm not convinced
      by anything I've seen here that the pipeline won't
      contribute to Onyx's future growth if 015 can advance into
      phase 2b/3.

      I subscribe to "Nature Medicine",
      and will share my thoughts on the adenovirus paper
      after I get this month's issue. Should be soon.

    • block trade 200.000 !? any news in the air ?

    • this is probably relevant. you can get the whole
      10k by pulling up onxx using yahoo quotes and then
      clicking on the sec link. good

      "...To inactivate p53, the virus makes a protein called
      E1B 55k, which binds directly to p53 and blocks its
      function. Once p53
      has been inactivated, the virus can
      replicate its DNA and proceed through its growth cycle

      ONYX-015 has been modified so that it cannot make E1B 55k.
      As a result, it should not disarm the p53 system
      when it infects normal cells and should not complete
      its growth cycle. However, in the majority of cancer
      cells, p53 is already disarmed through mutation of the
      p53 gene or other mechanisms. When ONYX-015 infects
      cells lacking p53 function, the virus growth cycle
      should proceed unchecked. It is expected that the cancer
      cells will be killed, new virus particles will be
      produced, and neighboring cancer cells will be infected and

      IN VITRO and IN VIVO animal tests by the Company
      have shown that ONYX-015 replicates in and kills tumor
      cells with mutant p53 gene sequence. In addition, the
      Company has shown that tumor cells with normal p53 gene
      sequence but lacking p53 function are also destroyed by
      ONYX-015. The ONYX-015 replication and cell
      effect is markedly reduced (100 to 1000 fold) in
      numerous normal cell types. However, certain normal skin
      cells, when tested IN VITRO, appeared to be more
      sensitive to ONYX-015 than normal cells of other types
      tested, despite the
      presence of p53 in these cells.
      This, however, has not been seen in patients enrolled
      in the clinical trials. The p53 program includes a
      research program which studies ONYX-015, and other viruses
      as well, to learn more about their impact on normal
      cells and cells deficient in p53 tumor suppressor

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