Does 93% Of Patients Going Into Open Label Extension Bode Well For Blarcamesine Or Not?

Do not trade this blog as 4 billion years of evolution is against me and possibly even God laughs at it, He has a great sense of humor!

Returning To My Old Friend…

I have found outside of any paywall a very usefull paper as it looked at about six years of following probable Alzheimer’s patients population of some 300 to 400 subjects. I derived many of my conclusions on Blarcamesine performance from this paper’s content. The many assertion this paper was making was that only after 3 years of following the subjects a watertight conclusion can be reached whether the drug truly makes a difference in the limiting the progress of the disease. I have plotted the probabilities of patient’s outcomes.

Link https://jamanetwork.com/journals/jamaneurology/fullarticle/775209

In year one about 25% patients show no decline, and the dropouts are just below 10%. Roughly 65% show some decline but the dropout rate is still very small. If Blarcamesine was to show its extraordinary therapeutic effect it would reverse the decline not just slow it just as it had done to the few patients in Phase2a AD. In another illustration from this reference I looked at the OLE dropout rate and the vague statement from Dr. Missling who said that number of patients remaing in the study after 5 years was between 10 and 21. To my reckoning there is a big difference between these two numbers in terms of the expected consequences for the strength of therapeutice effect. The 93% going into the OLE seems to be a number that should not raise an alarm or cause investors to doubt the efficay, especially in light of the importance and distribution of the genetic markers in the population.

The above illustration conveys the possible conclusion that for the population in Phase 2a AD Blarcamesine removes the morbidity due to Alzheimer’s disease. The above line represents the population of the spuses of the patients and works as controls against which the the morbidity due to Alzheimer’s can be measured. With 10 ptients, the morbidity is removed from the sample but with 21 patients it seems that life extansion has been achieved. The sample size is rather small but the signal is very strong. From the recent slew of news we gather that Dr Missling is actively pursuing this possibility. There was talk of murine model in which mice were dosed and then it was attempted to induce them to develop symptoms of Alzheimer’s by injecting them with amyloid plaque. The conclusion from the study was that Blarcamesine has protective effect and that the mice did not developed the symptoms. It seems that the direction in which the research by the company goes starts exploring the possibility of neuroprotection and hopefully can lead to life extension as I have presented the case for, here.

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