Avid Bioservices Inc (CDMO)

[biopharm]

Dr. Brekken publicly, and with nodding authorisation of management - King, etc were present - at NYAS confirmed that the results of the 2nd ln NSCLC were BETTER then the conservative set filed with the FDA in order to get approved. I think that the case has been made more then sufficient times that the SUPER results announced on Sept 7th, 2012 have been obtained with a sabotage that was even in the DISADVANTAGE of Bavituximab and in the ADVANTAGE of the control arm.

I have heard this before and was told it is 100% truth, I believe my source 100%. I plan on making it to the next ASM and the next NYAS set of events, because just being there in person would probably be better than paying $7,000 for a research report with a few lines mentioning Bavituximab.

I extremely like what you said below, regarding Opdivo targeting T-cells and not cancer cells.

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I have more to say about this:

BTW: Opdivo targets T-cells, not cancer cells.

Yes, and that will place it in the disadvantage of anti-PD-L1 drugs who bind the PD-L1 marker expressed on the cell instead.

The T-Cells have a WIDER function. If you bind their PD-1 receptor to keep it from binding with the PD-L1 on the cell, then you are changing the T-cell's behaviour for the COMPLETE collection of cell's (cancer and other cells). And that has it's consequences for non-responders, which are the about 70% majority.

You must actually see it like this. The T-Cells have functions and then someone binds a few mushroom with their stem to the T-cell surface (BMY's molecule isn't exactly a mushroom but it is just as an illustration of the concept). Now that T-Cell is in general disabled from approaching other cells because the mushroom(s) on it's surface doesn't make that possible anymore. This means the T-cells become less effective for ALL receptor/marker expression activity in that area and that includes all interaction with:
- tumour cells (ok, that was intended, so good)
- healthy cells (bad and not intended)
- helper cells (CD-4, CD-8, etc not intended, kept from binding CD-4 glycoprotein on T-cell surface).

This last category makes the T-cell BLIND for substances in the blood stream (e.g. non-body own substance, damage residue part of some signalling, etc) that it cannot detect directly but which it detects via the helper cells such as CD-4 that express markers that bind with the T-cell's related CD4 glycoprotein.

More IMPORTANTLY for Bavituximab, the activation function FC-Gamma receptors on MDSC's, M2 Marcophages and immature dendritic cells (Bavi's immune stimulation process added to its immune suppression blocking process) as well as its workings on the adaptive and innate immune response system may be severely hindered by this. PD-L1 approaches don't have this problem because they target the immobile cell's, not those of the immune system floating in the bloodstream.

And we see what the above means in terms of side effects. Opdivo attacks a tumour at the cost of creating problems all over the place by disabling critical immune system functions.

Add Opdivo+Yervoy together and you reduce the number of responders (20% or below vs 30% for Opdivo alone). Let's not talk about the side effects because IHub's disk space would be insufficient to store them if listed. You need to take a holiday to read them all from BMY's own list.

Without Bavituximab (provided the pre-clinical results (200/300% improvement) and Dr. Brekken's enthusiasm are correct) the anti-PD-xyz alone have no future if combinations such as Docetaxel+Bavi and later anti-PD-xyz+Bavi come on the market.

Docetaxel+Bavi+Durvalumab could be an absolute MOS mover and has Earthquake potential in the Pharma/Biotech industry. Mark my words.

Docetaxel+Bavituximab will occupy the field in the mean time.