Not sure where you got 9.85 ms cT1 from. I misr

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Not sure where you got 9.85 ms cT1 from.

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I misread that that was the PDFF number. It was 27.64 in haplotype group the same as no n- haplotype. Although you'd still expect an increase.

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In the 350mg >950ms cT1 group we achieved -68.86. That's 25x what the 700mg did.

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So ask yourself why there was no breakout of cT1 levels in 700mg. Could it be because there were few with >950ms? With higher CCR5 expression higher ms may have only been in the haplotype group. Wouldn't you think that would affect the numbers between haplotype and non-haplotype.

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Looking at PDFF, The 700mg normal did horribly even worse than Placebo if you look at the highs but considering only the average, there was a slight benefit of 6.1% loss in fat.

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+3.75 is better than +9.85. But once again what were the baseline numbers between 350mg and 700mg. Knowing that baseline is important.

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The 700mg HM did the best with a loss of 28% fat or 38% better than placebo.
The 350mg >950 ms cT1 group did about 19% better than placebo.

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The difference in PDFF in all 350 mg was 15.79%. The difference in PDFF for the total 700mg group was only 6.1%. White fat to Brown fat transposition is correlated to CCR5 expression and thus blockade. A novel idea but do you think it's possible that the 700mg group outside of the haplotypes had less severe NASH. Which means less CCR5 expression. Which means lower cytokine expression. Which means less fat and less scarring. Which means you will see a lesser change and lower percentages.

It is not due to normal 700mg being less effective, but due to the level of NASH. Without the baseline and end of trial raw numbers you can't make a proper comparison.

Oh wait that's not so novel, I already posted about it.

https://investorshangout.com/post/view?id=6427476