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But I think OHM the son of a gun has done it again and is highlighting that MVC with MK – 2006 actually suppresses the expression of PDL one and I’m not sure if that’s in hot or cold tumors. Our data suggests we increase the expression of PDL one in cold tumors, allowing our molecule through immuno modulation to work and possibly checkpoint inhibitors to also work. Is there a need for Checkpoint inhibitors OHM?

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The difference between cold tumors and hot tumors is that in cold tumors there is little immune activity acting against the tumors in hot tumors the immune system is highly active and is trying to kill the tumors. In cold tumors you're going to see very low levels of PD-L1 because the rise in PD-L1 is a response to high immune activity. Maraviroc would decrease PD-L1 very little on cold tumors because there is very little there. But maraviroc like leronlimab would turn the tumor hot by the M2 to M1 macrophage switch but undoubtedly not as much as leronlimab. Then unlike leronlimab it would decrease PD-L1 levels

If the PD-L1 levels are increasing you definitely want a PD-L1 inhibitor. Because the PD-L1 would still be trying to protect the tumor and you want to strip away that protection.