Replies to post #280167 on Avid Bioservices Inc (CDMO)

[Protector]

biopharm, hasn't PPHM been there and didn't they have the T-shirt?

In the very beginning we had that story of cutting of bloodvessels to tumours.

Now with VEGF one seems to forget that it has TWO functions and not ONE. If someone will act on VEGF then it must be done in a way that angiogenesis is stopped but vascologenesis is NOT affected. Certainly in people (children to young adults till the age of about 21) that have non full grown vascular systems need vascologenesis for the formation of their vascular system.

And if angiogenesis is a feature of our bodies then that means it is NEEDED for something. It grows blood vessels starting from a vascular ancker-point. Hence one sees it start in the endothelial and make its way from there to form a network of blood-vessels of which the tumour can feed.

So VEGF therapies may PREVENT further extension (probably that wood have the good effect of slowing down or even stop tumour growth) but it would NOT clean up existing blood-vessels. However, if those existing blood-vessels would not get any oxygen anymore (and die off as a consequence because their oxygen supply is not restored) then blocking VEGF can help them OVERCOME absence of oxygen. Blocking that would indeed cut of supplies to the tumour.

NOW, why would I NOT be surprised that there is a PS-Receptor (one of the at least 10 identified on different cell types) that PREVENTS this blocking mechanisme as intended by Gabrilovich, from working? Very simply, in apoptosys our body would not want this effort to be done because the cells are dying. No need for further attention or fire-brigade services to keep them alive.

And I must start to think bio that doing lawns is a good preparation for biologists because you sited exactly the ONE sentence that supports that:

Phosphatidylserine inhibited the production of inflammatory mediators IL-6; IL-8; vascular endothelial growth factor [this is VEGF]; and, in particular, prostaglandin E(2) in IL-1ß-stimulated RA-FLS.

And that is WHY Gabrilovich is actively involved with PS-targetting/Bavituximab (and CD4/CD8+ helper cells levels and penetration in the tumour).

His VEGF approach COULD (as in not sure, not proven and PURE SPECULATION, but potentially possible and not far fetched) when combined with Bavituximab be a COMPLETE solution that does NOT NEED other combo drugs.


Some will say, hey that is not possible because what does replace the role that chemo/radio or IO drugs play in combo's and that makes Bavituximab work - namely cell damage with related PS-exposure?

The answer is VERY SIMPLE. With the described VEGF approach the affected vascular cells are actually KILLED, as with chemo/radio/IO; but by deprivation in this case and they ALSO start to expose PS more massively then in an apoptotic cycle. CELL-DEATH-->NO MORE FLIPASE->Phosphatidylserine (PS) Bi-Layer FLIPS inside out-->PS is exposed. And Bavituximab NEEDS that because if there is NO binding to PS then the Fc-Gamma binding CANNOT take place. Fc-Gamma binding with MDSC/M2 Macrophage receptors for Fc-Gamma is what activates the IL-12 and TGF-Alpha secretion that are the cytokines that STIMULATE the immune system (activate it) and make it possible for the auto-immune system that is activated with it the LEARN the condition and prevent RELAPSE.

Ofcourse if one can ALSO stop the CTLA-4 (T-Cell suppression) and PD-1 (programmed cell death), etc then the process may be sped up PROVIDED this doesn't MORE harm then good. Better a slow cure over several months with low or no side effects then a quick one that cures you and let side effects kill you.

[asmarterwookie]

Phosphatidylserine inhibited the production of inflammatory mediators IL-6; IL-8; vascular endothelial growth factor; and, in particular, prostaglandin E(2) in IL-1ß-stimulated RA-FLS.

IL-10... Superful hopeful that this truly knocks out F-18 Coagulation Driver as well. The brain is an interesting organ target.

Human IL-10 may be used for a variety of applications, including:
In vitro inhibition of inflammatory cytokine production by T?1 cells, macrophages, and monocytes.
In vitro induction of proliferation, differentiation, and antibody production by B cells, in synergy with IL-4.
Dendritic cell-mediated in vitro activation of type 1 regulatory T cells (Tr1).
In vitro co-stimulation of mast cells proliferation in the presence of IL-3 and IL-4

Further examination of immunosuppression associated cytokines, including IL-4, IL-9, IL-10, IL-13, IL-17, and TGFß, revealed the complex changes associated within each of our treatment groups

however, anti-PD-1 therapy alone increased levels the most, with the addition of PS antibody to anti-PD-1 therapy reducing IL-10 levels.

http://www.miltenyibiotec.com/en/products-and-services/macs-cell-culture-and-stimulation/cytokines-and-growth-factors/premium-and-research-grade/human-il-10.aspx?gclid=CNn9n7Gr2NACFcKNswodRNQGww


Seems we have people in some pretty important places in the coming weeks...

I wonder what Pres Don talked to Dr. Soon about?

https://www.statnews.com/2016/11/21/trump-soon-shiong/


One could even refer to Steve King as the Dr. of Soon....LOL

OR better yet...

Dr. Imminent..........hmmmm copyright 2016

Myeloid Deprived Suppressor Cells is what I thought I read when I 1st saw the info on MDSCs. Deprived of the correct signaling....Targeting and attaching to PS relieves that depravity and starts the proper cytokine storm. A protaganistic storm.

When the final puzzle picture is finally seen the Peregrine will either rise like a Phoenix or flop like a bad wookie joke.....



wook