The effect on the traditional biomarkers is bound to be stronger in a symptomatic drug like the mabs than an upstream, long term drug like blarcamesine.
The mabs immediately go to work attacking the plaques, while blarcamesine is instead permanently reducing the neurological degeneration that will create plaques months and years into the future.
You can see the delayed clinical effect in the 2b/3 ADAS-Cog13 graphs, and you can see blarcamesine's unique long range, disease modifying effects in the 144/192 weeks OLE analysis.
The time frames for the mabs is more immediate and of lesser duration, but its immediacy does result in stronger traditional biomarker results. Basically, that's because those biomarkers are set to efficiently detect plaque reduction (mabs) rather than long term disease modification (blarcamesine). This is another function of AD being defined as a plaque disease, and another reason why placing weight on these tests will tilt the playing field toward approving more ineffective AD drugs over better options. I can hope the EMA catches this, as well.
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