How Blarcamesine May Prove Out in Alzheimer’s Therapy
As readers know, the validity and significance of the announced clinical results for blarcamesine treating Alzheimer’s are in contention. Many see the clinical metrics as only slightly positive, for a moderate portion of those in the 50mg dosing arm of the study. For those in the placebo and 30mg arms, clinical outcomes were not impressive.
Of course, we all await the release of new clinical data from Anavex, where the results of each of the three arms are distinctly separate: with no pooling of data. With that, it should be clear that blarcamesine in 50mg dosings does, indeed, at least for some, provide clinical outcomes where a) the progression of Alzheimer’s symptoms is stopped and mental capacities continue at a new, non-declining baseline, or b) compromised mental capacities are actually restored toward a normal, non-Alzheimer’s level.
Right now, from the announced clinical results, it would appear that blarcamesine might be able to help only a percentage of people with Alzheimer’s. A good number appear not to have been helped.
In this regard, first consider Aricept, a standard of care (SOC) FDA-approved drug for Alzheimer’s. It neither stops, delays, nor reverses the symptomatic progression of Alzheimer’s; it merely slows, for a period, the lethal progression of symptoms.
On the basis of what has been announced from the placebo-controlled, three-arm clinical study of blarcamesine, for those who would take blarcamesine and notice termination of symptomatic progression, it will be far better than Aricept. The same for those where the Anavex drug stopped symptomatic progression, creating a new, non-accelerating symptomatic baseline. With Aricept, the patient eventually (in a few weeks or months) resumes the lethal progression of symptoms. At least for some, blarcamesine stops that progression; may even restore normalized cognition and mental functions.
That, alone, should prompt the FDA to approve blarcamesine.
But there is this distinctive other blarcamesine therapy. It is very probable that for those for whom the drug does not reverse symptoms, it may actually markedly slow their progression, perhaps for many years. Not a cure, but able to add additional years of low-symptom conditions.
Many cancer drugs have a similar action. They do not cure the targeted cancer, but for some time they suppress its progression.
The first blarcamesine question is, “What percentage of those with Alzheimer’s taking 50mg actually have their symptoms reversed or reduced?”
But the second question would be, “For those who don’t gain symptomatic suppression (restoration of normalized cognition), can the drug at least favorably slow it; especially if administered at the disease’s earliest stages?”
Finally, of course, is the question of a potential Aricept synergy. Aricept does, indeed, slow the intensification of Alzheimer’s symptoms, at least for a period. Might a dual Aricept/blarcamesine therapeutic protocol be successful to some useful degree in patients who don’t respond to a blarcamesine monotherapy?
