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Posted On: 06/12/2022 1:33:50 PM
Post# of 148894
Given what I just learned from the picture I just posted, I agree with you.
I originally based that statement on my thinking that it worked better being less saturated because 350 worked better than 700. But, less saturation had nothing to do with it. It makes sense that it would work best when fully saturated, but CCR5 was not even present in the non haplotype group at the early stages of NAFLD.
As the disease progressed, CCR5 levels began to increase, thereby driving inflammation up and fibrosis increased. Introducing LL only makes sense when CCR5 levels are upregulated.
Would you tend to think that with the 350mg LL dosing, 100% RO was achieved or do you think that had 700mg been dosed in those same patients, LL would have achieved the same, better or worse outcomes than it achieved dosed at 350mg?
I originally based that statement on my thinking that it worked better being less saturated because 350 worked better than 700. But, less saturation had nothing to do with it. It makes sense that it would work best when fully saturated, but CCR5 was not even present in the non haplotype group at the early stages of NAFLD.
As the disease progressed, CCR5 levels began to increase, thereby driving inflammation up and fibrosis increased. Introducing LL only makes sense when CCR5 levels are upregulated.
Would you tend to think that with the 350mg LL dosing, 100% RO was achieved or do you think that had 700mg been dosed in those same patients, LL would have achieved the same, better or worse outcomes than it achieved dosed at 350mg?
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