That P2a paper is the best reference we have and with a very simple calculation that data yield 16 P2b/3 super responders.
I went further than that compensating also for the fact that in the P2b/3 trial only mild AD patient were enrolled. Also considering that APOE3 alleles were the differentiating feature between analysis subgroups 1 and 2, plus a few other thing to land at 20’ish patients potentially improving over baseline.
Altogether though such simple calculations are futile as they use as the reference the really small P2a open label trial data. The n = 21 contains bias from 32 to 31 (misdiagnosis), then a few drop outs and lack dna sampling.
New factors and combinations thereof may be / have been found in the much larger P2b/3 data etc. The strongly non linear relationship between concentration and response, we just have no basis to extrapolate on either.
Yes a silly leap from < 10% in the P2a data to about 4 times more in the P2b/3 trial based on what?
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