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Re: Protector post# 267283

Saturday, 06/25/2016 1:06:47 PM

Saturday, June 25, 2016 1:06:47 PM

Post# of 345789

vinmantoo, it doesn't matter that a singled out drugs that addresses one specific PS receptor shows some (limited) clinical improvement.



Right, the clinical improvement from use of anti-PD-L1, or anti-CTL4 or anti-PD1 antibodies was so limited that the FDA approved multiple treatments as single agent in various cancers. In contrast, the magic all powerful, all purpose Bavi failed in single agent in in combo in trial after trial. Yes you have a real strong point there.


You need to bind them ALL (10+ receptor types) together and the only way to do that in a synchronised way is capping Phosphotidylserine (PS) and not mixing 10+ drugs to block Tim1, Tim3, Tim4, Axl, Mer, Tyro-3, CD300a, RAGE, BAI-1, Stabilin etc



I don't know where you are getting that idea from, but it has been clearly been proven wrong based on human clinical trials and FDA approval. Results have been even more promising when combining two such targets, either in the same pathway, (anti-PD-L1 + anti-PD1) or in different pathways (anti-PD-L1 and anti-CTL4). You need to stop with the nonsense that you need to bock all 10 or 12 receptors to get an effect.


The PS from APPOPTIC cells is NEGLIGIBLE compared to the PS exposed due to other therapy damage (CHEMO, RADIO, etc).



That is flat out wrong. The is an estimated 25 million PS molecules per cell and major amounts are expressed on apoptotic cells.

http://www.ncbi.nlm.nih.gov/pubmed/22858544

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