Yes, I am not sure how to interpret that information right now given, we don’t know exactly the mechanism of action that Leronlimab has in NASH. Certainly we know that it is a CCR5 blockade, however we do not know exactly how blocking CCR5 reduces fibrotic scar tissue in NAFLD and Nash liver patients.
All I can think of is that the molecule itself while bound to CCR5, may interfere with other cytokines and chemokine activity which would be necessary to remove scar tissue when all of the CCR5 receptors are bound which would happen in 700mg in contrast to what would happen in 350. Where I would think, less than 100% receptor occupancy is achieved.
Possibly, with all the scar tissue and fibrotic tissue in that environment, you’re adding more substance in monoclonal antibody form to the mix of things and therefore are in a way constricting the environment thereby pressing on inadvertently at least, the receptors of other cytokines and chemokines that would need to be activated to reduce the fibrotic inflammatory scar tissue. That is only a hypothesis