“The 350 tells the story of MOA in fibroinflamma

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“The 350 tells the story of MOA in fibroinflammation and deposition of fibrovascular tissue .. very impressive “

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To me, this sounds like if you have a patient with baseline cT1 > 950, treat him with 350mg LRM.

The 350mg dose bound to the CCR5 receptors of the HSCs, Hepatic Stellate Cells and put a halt to their intracellular communication which otherwise would lead to fibrosis and scarring. In fact, with a reduction of 68.86 cT1 in only 14 weeks, essentially, you are reducing your NAS stage by 2. So an NAS of 7 with 14 weeks of 350mg LRM treatment becomes an NAS of 5. NASH to NAFLD in 14 weeks. Very impressive.

Why didn't that happen in the sick patients using 700 mg LRM? Were there any sick patients using 700 mg LRM? Yes, but they were the 5 HM which also did very well on the fibrosis front, but not quite as well as the 350mg > 950 cT1 group. The 700 HM group achieved -45.4 cT1 where as the 350 > 950 cT1 achieved -68.86 cT1. Regarding Fibrosis only, even with increased CCR5 on the cell surfaces of the HSCs, the 700mg did not achieve what the 350mg LRM achieved. Why?