Avid Bioservices Inc (CDMO)

[biopharm]

Is this Xencor Xmab5871 infringing upon PS Targeting IP rights? I say YES and this is why we must ask the new BODs to make damn sure they protect the IP assets and KNOWING the details of Steve Demattos departure, his confidentiality agreement, his deposition in relation to the sabotage by CSM who had CEO Gerald Finken and his sidekick Jeanette Bleecker that we know already admitted swapping and sabotaging the Peregrine trial....is critical to realizing the true value of the PS Targeting IP at Peregrine, now called Avid Bioservices.

Ask the new BODs why they are not getting all this information and making it known to the public and all shareholders.....as they can't keep it a secret when they get requests via certified letters.

XmAb5871 is a first-in-class monoclonal antibody that targets CD19 with its variable domain and uses the XmAb immune inhibitory Fc domain to target Fc?RIIb, a receptor that inhibits B cell function. XmAb5871 is the first drug candidate to our knowledge that targets Fc?RIIb inhibition.

Yes, Xencor to their knowledge MAY now know PS Targeting rights are being infringed upon....

If everyone does not resend certified letters and question EVERYTHING ....then we will see breadcrumb nothing in return for the sale or license of the PS Targeting platform

Seek the answers

Now

What happens first, the targeting of flipped PS, THEN the downstream changes ....and the new BODs are 100% responsible for Fiduciary Duties in the handling and protection of our assets, including their #1 assets of PS Targeting, which includes much of the sealed records past.....where it would be inconceivable that they could possibly make a rational decision on any true value of PS Targeting till all questions are answered and if that makes no sense to them....well then, maybe we have more than enough mentally unstable minds in charge of the PS Targeting IP rights, that may need to be removed from their duties??

This is simple re: that PS Targeting is upstream....global.....and just because it was difficult to realize the power of PS Targeting in the past does not mean one has to hand it over for breadcrumbs if promised a well funded CDMO operation. What would a jury say once all sealed records were read to them....once all depositions become public knowledge.....once all certified letters become public ? Once email after email was disclosed .....and it begins to become a bit mind boggling in how the new BODs would not take this more seriously than it seems, as Dr Roger Lias thinks it will blow over or maybe he was told that....

p85a recruitment by the CD300f phosphatidylserine receptor mediates apoptotic cell clearance required for autoimmunity suppression.

p85a recruitment by the CD300f phosphatidylserine receptor mediates apoptotic cell clearance required for autoimmunity suppression.
Linjie Tian, Seung-Chul Choi, +5 authors John E. ColiganNature communications2014

View on PubMed

Abstract
Apoptotic cell (AC) clearance is essential for immune homeostasis. Here we show that mouse CD300f (CLM-1) recognizes outer membrane-exposed phosphatidylserine, and regulates the phagocytosis of ACs. CD300f accumulates in phagocytic cups at AC contact sites. Phosphorylation within CD300f cytoplasmic tail tyrosine-based motifs initiates signals that positively or negatively regulate AC phagocytosis. Y276 phosphorylation is necessary for enhanced CD300f-mediated phagocytosis through the recruitment of the p85a regulatory subunit of phosphatidylinositol-3-kinase (PI3K). CD300f-PI3K association leads to activation of downstream Rac/Cdc42 GTPase and mediates changes of F-actin that drive AC engulfment. Importantly, primary macrophages from CD300f-deficient mice have impaired phagocytosis of ACs. The biological consequence of CD300f deficiency is predisposition to autoimmune disease development, as Fc?RIIB-deficient mice develop a systemic lupus erythematosus-like disease at a markedly accelerated rate if CD300f is absent. In this report we identify the mechanism and role of CD300f in AC phagocytosis and maintenance of immune homeostasis.
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https://www.semanticscholar.org/paper/p85a-recruitment-by-the-CD300f-phosphatidylserine-Tian-Choi/0cf029bab0d343bf988266b9bb33861454159c99

The Biology and Disease Relevance of CD300a, an Inhibitory Receptor for Phosphatidylserine and Phosphatidylethanolamine
Olatz Zenarruzabeitia, Joana Vitallé, Cristina Eguizabal, Venkateswara R. Simhadri and Francisco Borrego
J Immunol June 1, 2015, 194 (11) 5053-5060; DOI: https://doi.org/10.4049/jimmunol.1500304
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A recent study reported that the interaction between CD300a and PS inhibits tumor cell killing by NK cells (11). Several studies showed that, in the tumor microenvironment, there is a significant stress imposed on the tumor endothelium by acidity, reactive oxygen species, and transient hypoxia, which result in the redistribution and exposure of PS and PE (84). Indeed, expression of PS was detected in gastric carcinoma (85), ovarian carcinoma (86), and melanoma (87). Recent data support that the binding of CD300a-Ig to tumor cells is reduced when PS is blocked and that the blocking of PS enhances NK cell–mediated cytotoxicity. Blocking of PS partially restored NK cell cytotoxicity, indicating that tumor cells express an additional ligand for CD300a (11). This additional ligand might be PE, which also was shown to be a ligand for CD300a (13, 38). Therefore, a new tumor immune-evasion mechanism was suggested to be mediated through the interaction between PS and PE on tumor cells and CD300a on cytotoxic lymphocytes.
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http://www.jimmunol.org/content/194/11/5053