Avid Bioservices Inc (CDMO)

[aikifredicist]

Ok, I've been busy today too. Went to aikido this morning and got tossed around and slammed to the mat time and again for two hours. (Ok, I was out there tossing around other guys too.) Had errands to run this afternoon, etc.

Regarding the seminar last night:
1) Birge was the first speaker and led off discussing ps exposure on apoptic (sp?) cells and cancer. And introduced TAM receptors and mentioned PD-1 and PD-L1 signaling. It seems that one variant of TAM can be neutralized by vitamin K or worfran !
In general the speakers before Brekken reviewed the action of various receptors and cells in immune inhibition -- TIM, TAM, Mer, MDSC's, etc. The discussion was rapid and addressed to researchers conversant in the field so much flew over my head.

2)Graham emphasized Mer: a dual taget for cancer. Mer inhibition polarized Macrophages from M2 to M1 and showed results in mice.

3)Gabrilovich spoke of the presence of MDSC's in the tumor environment as predictors of clinical outcome in cancer.

It was shown that clinically addressing each factor in turn by current treatment could improve survival but none resulted in acquired immunity and flat line long term survival.

Some slides (Birges) showed how TAM / TIM bind to ps resulting in immune inhibition.

4) Brekken's talk was a relief, much easier to understand -- then again I am very familiar with the topic and action of bavi.

So the seminar presented a summary of the various known mechanisms of immune inhibition in cancer and their relation to ps exposure and then the reversal of these effects when ps is cloaked by the binding with Bavi.

I'm sure that the conference attendees who sat in on the seminar got much more out of the presentations than I.

During the discussion period, the question of the danger of auto-immunity came up. Ever since investing in PPHM that has worried me. Could bavi attaching to ps in apoptic (ugh sp again???) cause an auto-immune response? Clearly experience with Bavi shown no such effect. But nobody had a clear understanding of just why. (So its not just me ) Brekken suggested that this may be due to the relatively low clinical doses of Bavi and that such an effect might only begin to show up at much higher dosages.

Also a question was asked regarding ps exposure on platelets and whether Bavi might affect clotting. It was pointed out that no clinical evidence of this has been shown. There was no one willing to venture a reason why but it clearly was not a problem at current clinical dosages.

North asked a question regarding fully human vs chimeric Bavi. Brekken saw no problem with the chimeric version. Once again at the clinical dose levels the body does not seem to mount a defense against chimeric Bavi.

This is just my understanding of the seminar but cancer immunology is definitely not my area of expertise so take it with a grain of salt.