So how your hypothesis explain the higher effectiv

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So how your hypothesis explain the higher effectiveness of 700 ml dozing in mTNBC and Covid trials?

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100% receptor occupancy with 700mg, not quite 100% occupancy with lower doses. The higher the immune and inflammatory response the more of an increase you'll see in CCR5 expression, expression of other receptors that bind the same ligands as CCR5 and the inflammatory chemokines. With CCR5 being the predominate receptor for immune/inflammatory response you want to shut that down 100% and let the weaker but more prolific than normal receptors take over that response.

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Also what would you say about this hypothesis by Jay from YMB?

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CXCR3 is like an immune system backup for the CCR5 receptor. CXCR3 and it's ligands activate many if not all of the same downstream pathways as CCR5. From what I've seen of the effects of CXCR3 agonists blocking, CXCR3 has a lesser effect than blocking CCR5. So CCR5 is most likely the biggest influencer on the immune system.

Shutting down both CCR5 and CXCR3 may mean you have immunosuppression. In out of control situations like critical Covid-19 but in other instances it might be too much. Before you try blocking both they'd have to start with pre-clinical studies.

CCR5 is not RANTES, CCL5 is RANTES. CCL5 binds to CCR5.