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Perhaps the body needs some of the CCR5 to be available (not 100% receptor occupancy) to perform it's normal function in order to help the liver deal with it's response to Leronlimab's effect on existing inflammation? Maybe a second or third downstream reaction to the increase in some of the positive Leronlimab effects? Seems like the only logical explanation. Although I have no idea why that would work or the MOA?

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If there were no other CCR receptors that bound the CCR5 ligands then you would definitely not want 100% occupancy because it would shut down the necessary functions of those ligands. But all ligands of CCR5 also bind to other CCR5 receptors. In an inflammatory or immune dysregulated state you will not only see an increase in CCR5 and it's ligands but also in those other CCR receptors. The combined effects of highly expressed CCR5 and the other receptors cause the overwheming state of response that exacerbates disease progression. With CCR5 blocked it brings things down to a more normal level (homeostasis).

In a past post I showed how the 700mg arm was biased towards those who might possibly have a CCR5 delta 32 single or double allele expression which could be the explanation for 700mg doing worse than 350mg.

https://investorshangout.com/post/view?id=6699694

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I'm curious to know why Bicarbonate increased in 350mg but not 700mg. This is definitely a riddle that needs to be figured out (350mg vs 700mg).

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A side effect of NASH and the inflammation is an impaired pancreas. The pancreas is partially responsible for bicarbonate levels. With NASH being resolved bicarbonate levels would be increased. The difference between the 700mg arm and the 350mg arm is explained above.