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Peregrine Pharmaceuticals, Inc. Message Board

  • laujhawj laujhawj Jan 26, 2013 8:09 PM Flag

    Review & Recap on my Previous Thoughts on Bevacizumab & Bavituximab

    The reason why Bevacizumab (Avastin) had, for the last decade plus, been used so ubiquitously (generating in 2010 around $7B)... has been its ability --- as a monoclonal antibody --- to deal with, to very good degrees, the protein VEGF that promotes the growth and proliferation of blood vessels in areas of tumor, outside of the CELLS.... thus allowing tumor/cancer to spread and proliferate, once the infected cells go APOPTOSIS, spreading their cancerous agent via said proliferation blood vessels.

    So, as you can see, Bavituximab can be looked at as working in a PARALLEL, "next door" parameter to Bevacizumab:

    And, thus, if Bavituximab (Bavi) should be proven to do as it is theorized, IT would also have SIMILAR, FAR REACHING impact to Bevacizumab... but works as the next generation of chemeric monoclonal antibody.

    The prefix or adjective "CHEMERIC" before the "monoclonal antibody" BAVITUXIMAB indicated that it is a GENETICALLY ENGINEERED anti-body from a set of protein molecules, for selective and specific binding affinity...

    In this case, Bavituximab's AFFINITY is for the "flipped" amino-phospholipids called Phosphatidylserine that are, IN NORMAL CELLS, usually kept inside the CELL (in a CYTOPLASMIC arrangement) & kept there by transport enzymes called "FLIPPASE"... that have been "flipped" (from a Cytoplasmic facing manner into an Exoplasmic facing manner)... DUE TO CANCER CELLS going through APOPTOSIS...

    (.... "Flippases," "floppases," "scramblases," etc. are a class of lipid transporters or amino-phospholipid translocase dealing with the movement of proteins & other enties within the cell as well as across cellular membranes: each class works on a specific place or task --- dealing with transport and cellular membrane polarity --- to make sure "things" get moved,from A to B, to C, etc: .... HERE we are only interested in the general "flippases" that "flip-flop" at the site of the bi-layer of amino-phospholipids of PHOSPHATIDYLSERINES comprising the bi-layered cell membrane, hither and thither, Cytoplasmically and Exoplasmically....)

    One of the theories, at this point, seems to be that the "flipping" of these Phosphatidylserine, PS, to the outside of an APOPOTOTIC cell is a result of the LOSS of --- or the loss of activities in --- the special class of enzyme "flippase" that NORMALLY keeps PS turning Cytoplasmically. In NORMAL, healthy cwells, these "flippase" preserve the polar region between the two-molecular thick bi-layered cell membrane, keeping PS from "flipping."

    There still SEEMS to be debates as to whether non-Apoptotic cells also allowing PS to "flip"... but most researchers seem to agree that in cancerous cells going through a cell death, APOPTOTIC phase, the PSs are exposed very ubiquitously.

    That's number #1: and if it is true, PPHM is in good shape, IF number #2 is also as they said...

    And #2 is: that their MONOCLONAL ANTI-BODY actually has a specific binding affinity to these "flipped" PS's.

    The general literature SEEMS to suggest that the reason for a cance cells going through apoptotic activities, with the "flipped" PS, is to send or broadcast chemical signals to surrounding cells --- which normally communicate with each other --- as well as to professional cancer cell killers like PHAGOCYTES (part of our immune), saying to them: "We are OK and normal... don't kill us, despite the little flippin' of these Phosphatidylserine amino-phospholipids from the inside of us cells!"

    Why do cancerous cells do these chemical signalling "tricks"? Obvious: they don't want to be identified and engulfed or killed (the word is normally phagocytosis) by their healthy, neighboring cells, as well as by professionally aggressive tumor-cell killers like White Blood Cells, which are always coursing through the highways and freeways of blood vessels nearby and which could stop any time, anywhere, and inspect suspecious activities outside of cell surfaces everywhere...

    Cancerous cells objectives, therefore, is to fool the healthy, phagocyotic cells for as long as possible, to give them time to multiply and infect other cells by invading them, going into the cells's nucleus, hijacking the normal cells DNA, and making it do the Cancerous cells bidding... and that's to manufacture the proteins, hormones, and chemicals that would fool the body NOT to attack them.... with the process keeping going and going until the Cancerous cells overwhelm their host, us... or other animals...

    Per the Company, BAVITUXIMAB is patentedly created to BIND to the exposed PS due to cancerous cells going through OPOPTOSIS (trying to do what I just went over)... thus, allowing other cells and White Blood Cells to know immediately, "Hey, you guys can't fool us via you chemical signals, via these suspciously flipped PS's... even if you're broadcasting at "normal frequencies"... We know whom you really are... and you ain't no friends of ours... So, prepared for REAL Death through our Phagocytosis magical activities!"

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    • It is painful to read such BS being spouted.

      ""The reason why Bevacizumab (Avastin) had, for the last decade plus, been used so ubiquitously (generating in 2010 around $7B)... has been its ability --- as a monoclonal antibody --- to deal with, to very good degrees, the protein VEGF that promotes the growth and proliferation of blood vessels in areas of tumor, outside of the CELLS....""

      VEGF promotes vascular growth in general. It isn't restricted to tumors. Of course the newly formed blood vessels induced by VEGF will be outside tumor cells, they are blood vessels, not some intracellular structures.

      ""thus allowing tumor/cancer to spread and proliferate, once the infected cells go APOPTOSIS, spreading their cancerous agent via said proliferation blood vessels.""

      No, the new vasculature provides increased access to nutrients and oxygen, which enables larger tumor size. Tumor spreading, or more precisely, metastasis, requires far more than increased blood flow provided by new blood vessels. There are genetic changes in tumor cells that promote metastasis. This person actually said infected cells go apoptosis? Is this some kind of a joke? What the hell infection is he or she talking about? These are transformed cells not virally infected cells producing large quantities of virus then undergoing in lysis to spread viral particles. Apoptosis is programmed cell death. If a tumor cell undergoes apoptosis, it dies, so it sure as hell can't spread.

      ""The prefix or adjective "CHEMERIC" before the "monoclonal antibody" BAVITUXIMAB indicated that it is a GENETICALLY ENGINEERED anti-body from a set of protein molecules, for selective and specific binding affinity..""

      It isn't CHEMERIC", it is CHIMERIC. Chimeric antibodies are almost always where the original antibody was made in mice. One can't use such antibody repeatedly in humans (or other non-mouse vertebrates) because the human immune system would recognize the mouse (murine) antibodies as foreign, and thus mount an immune response against the murine antibody and rapidly clear it from the blood stream, and do so with increasing vigor with each subsequent treatment. This response could also generate serious complications for the patient. Antibodies have constant and variable regions. The variable region provides the antigenic specificity as well as avidity. The constant region is species specific, so this is the part that generates the immune response when placed in a different species. What is done is that the murine constant region is replaced by the human constant region but they keep the murine variable region. The antibody in now chimeric as it has the human constant region fused to the original to murine variable region. This chimeric antibody is now invisible to the human immune system but still has the original murine variable region to provide antigenic specificity and avidity.

    • You don't know the basics so stop lecturing people.

 
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