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Posted On: 06/12/2022 11:19:53 AM
Post# of 145875
The fact that the 700mg dose was so effective ONLY in the increased CCR5 haplotype speaks to the fact that even that doubled dose did not fully saturate all of the CCR5 which were expressed.
And in the rest of the trial, where CCR5 was distributed in lesser quantities than in the haplotype, then the 350mg dose did better.
Comparing the NAFLD group (less than 950 msec) to the NASH group (greater than 950 msec), dosing remaining the same at 350mg LL, we had a better overall response in the NASH group where it was about twice as effective than in the NAFLD group. Dosing was constant, 350 mg, so Receptor Occupancy probably remained constant as well. The only factor changing was the fat/fibrosis ratio where in the NASH group, it was lower, since fibrosis was increased. And in the NAFLD group, fat was increased, where LL performance was less optimal.
In general, doubling dose to 700mg led to furthered attenuation of efficacy with same and here with the increased dosing, Receptor Occupancy was likely saturated. But not with the haplotype, where RO was likely under 100%.
And in the rest of the trial, where CCR5 was distributed in lesser quantities than in the haplotype, then the 350mg dose did better.
Comparing the NAFLD group (less than 950 msec) to the NASH group (greater than 950 msec), dosing remaining the same at 350mg LL, we had a better overall response in the NASH group where it was about twice as effective than in the NAFLD group. Dosing was constant, 350 mg, so Receptor Occupancy probably remained constant as well. The only factor changing was the fat/fibrosis ratio where in the NASH group, it was lower, since fibrosis was increased. And in the NAFLD group, fat was increased, where LL performance was less optimal.
In general, doubling dose to 700mg led to furthered attenuation of efficacy with same and here with the increased dosing, Receptor Occupancy was likely saturated. But not with the haplotype, where RO was likely under 100%.
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