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?

Yes, the binding affinities, the difference between a monoclonal antibody and a small molecule and the toxicities all differentiate the molecules. But this PDL one suppression and enhancement could really give us a nice look at the moa’s and another reason why we “kick their ass”.

I’m now wondering if With MVC and MK-2006 PDL one suppression only happens in hot tumors because it’s not really a factor in cold tumors because PDL one isn’t really a factor in cold tumors. If right, this appears to suggest we are the only CCR five antagonist that can convert cold tumors to hot tumors. And not many other molecules in any classcan suggest they turn cold tumors into hot tumors. This is truly remarkable.