AI
Sunday, November 16, 2025 1:31:05 PM
But on the A/T/N biomarker spectrum (Aß42/40, p-tau181, p-tau231, NfL), Blarcamesine still has no reported p-tau181, p-tau231, or NfL data.
So:
Can they really claim “disease-modifying” or “upstream to amyloid and tau” if the tau markers don’t show any convincing correlation?
If CHMP is benchmarking against donanemab/lecanemab on A/T/N, how big a hole is that for Blar?
There are still folks hoping the post-hoc ABCLEAR3 genetics can rescue the re-exam. I’m curious how you view that in light of how rare post-hoc biomarkers actually move the needle at EMA.
I don't think the AB42/40 data will save the day. As you have pointed out pTau181 and NfL were not significant in the entire population. I had previously pointed out the very low N for the biomarkers. For some unknown reason, many patients who stayed in the entire 48 week trial never got the biomarker blood-work (simple blood test can get all 3 biomarkers in one panel from Labcorp and pTau 231 from Quest or other labs). Compared to the ADAS-Cog N of 313 patients completing 48 weeks - only 197 did the 'significant' AB42/40 biomarker at week 48. Because only baseline and 48 weeks, Anavex cannot use MMRM/LSM to finesse this dataset -- what happened to these patients and are they representative. Now imagine if you were to cut N down a further 30% for ABCLEAR1 or 50% for ABCLEAR 3. pTau231 has even fewer patients.
Although higher N, there were still an unexplained reduction of N for NfL and pTau181 - and these biomarkers failed - likely due to very large variance. Was the test even done at the same lab?
See the n values below
