Avid Bioservices Inc (CDMO)

[Protector]

goodJohn, you should have quoted the next sentence too because that sentence expresses the assumption that what you seem to aim for isn't the case, at least not in the current state of knowledge and understanding of things.

If we reasonably exclude that the immune system would produce B-cells to recognize whatever Bavi exposes with its non PS bound side, because we don’t even have the beginning of prove of that, and if we also exclude that the momentary presence of Bavi creates ‘learning grounds’ of something that could be learned and applied later in the absence of Bavi, because let alone we also do not have a beginning of prove of that we probably all together wouldn’t even be able to just name something that could qualify, we must look in another direction.

I think that with your quoted sentence below you describe a scenario within the scope of the exclusion of my quote above.

Maybe after exposure to Bavituximab, and an immune response is initiate for tumor-specific mutation or tumor specific antigen.

That's where FTM is going to ask you, and I ask you with him if he does, to advance more grounds. Possibly only a theory explaining a mechanism that can be understood, even one that Thorpe or others have not described, but that from a scientific point could possibly be a working theory where all forces are in balance, will pass. It must not in this stage be 100% water tight but it must at least offer a possibility of explanation of a mechanism that can be explained without sudden jumps loosing everybody in the process.

I made such description myself with the Bavi binding with PS through receptor approach while I know very well that this has never been seen or documented, neither for PS neither for any other substance, and that all receptor access is ruled by receptor chemical programming. Hence, a virus with its envelope is one well-know technique of using the receptor by fooling it.

So if I compare your theory, which I don't 100% get for now and I think neither do a couple of other posters by lack of sufficient well ordered and comprehensive information on your behalves, with what I advanced as a possibility, then I can point to A) A possible- possibly wrong but not excluded - mechanism and B) a precedent where it is proven that receptors do not discriminate on the molecule they let in as long as it chemically binds with the receptor's chemical setup. If a virus has an envelope that would be recognized as a vitamin, no matter what is attached to it at the other side it will pass together with the envelope.

So from there I have redefined the functional role of the chemical programming of the receptor as a means of selection and selective traction provider but not as a guarded/policed gate towards entrance of the cell. That is within the scope of the state of the art because although the current understanding may create the perception of it acting in a policing role of the receptor it has never been observed as active policing but always as passive inability of substances to pass. See it as a big ship that can only be pulled into the harbor by small ships and only by those it made a specific rendez-vous with. They provide traction into the harbor but they will not block other ships that have other ways to make it in. At the most they compete for passage space if both would want in at the same moment and the river is to small.

That is a BIG difference because in that definition you have selection by ability (the ability of a passing substance to get traction into the cell by its ability to bind with the bate, the chemical programming of the receptor). In what I advance I say Bavi manages to come sufficiently close into the receptor gate (eg: when the gate is setup to catch something that is very close, but no cigar, to the Bavi molecule arm and would therefore not receive the traction because it cannot fully accomplish the binding) and then being in that location finds a SECONDARY way of traction into the cell, not by binding with whatever the chemical programming of the receptor is at that moment BUT instead with the ALWAYS within proximity PS which is pierced by the receptor and sits very close to the position where the substances reside that that do the normal programming of the receptor. PS is more abundantly available which may compensate for some extra distance to cover as there is more binding potential.

Now I think it is such kind of detail you will have to provide for your theory, while I agree it is much more sophisticated then the quite straight forward theory I propose, and I follow KT in saying you should do an effort in writing that in a language we can all understand (composition build-up and vocabulary).

For now you didn't convince me that something is learned by the immune system when it is exposed to Bavi that results in later active workings after Bavi is no longer in the body. I stick with persistent Bavi presences in a cloaked way (inside the cell) as a readily on-incident deployable immune system suppressor-suppressor, a Kryptibody as I named it.

However, I am open to listen because if you are correct that would be nice for us in the long run and I've seen minds to come up with the most extraordinary things that nobody was willing to believe, or could understand, until suddenly proven or better explained.

I have to agree with posters on the board that in the short term it will not be much of a factor in Peregrine's pps/partnership UNLESS of course you are bringing something they already know and decided not to make public yet. In that case the BP's know it too or their partnership agreements will be VERY narrow, excluding an exploitation of such knowledge when it is made public by the agreement they hold.