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Hi Chris…. Good to hear from you again… Been awhile…. AVXL was Always high up on my ALZ list… Bill had discussed it before… Hope this tidbit helps… *** I’ll get more from the article later… “Summary
Anavex Life Sciences’ OLE study demonstrates that its Alzheimer’s drug works for years beyond the clinical study. The OLE expands efficacy to include patients’ behavioral abilities.
The Anavex drug may offer years of extra mental lucidity and greater self-sufficiency among Alzheimer’s patients.
The EU’s approval of Blarcamesine could increase Anavex’s market value from $ 800 million to $ 8 billion “

This is lengthy…. I would recommend highly that those truly interested in unbiased biotech analysis subscribe to SA……..

“Does Anavex’s Alzheimer’s Drug Actually Confer Benefit Over Three Years
May 15, 2025 8:49 PM

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$8.44
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Summary
Anavex Life Sciences’ OLE study demonstrates that its Alzheimer’s drug works for years beyond the clinical study. The OLE expands efficacy to include patients’ behavioral abilities.
The Anavex drug may offer years of extra mental lucidity and greater self-sufficiency among Alzheimer’s patients.
The EU’s approval of Blarcamesine could increase Anavex’s market value from $800 million to $8 billion.

akinbostanci/iStock via Getty Images

Last year, top researchers in Alzheimer’s Disease treatments published a scientific journal article describing how a new drug can slow the cognitive decline of Alzheimer’s patients by 36%, and by nearly 50% for people with a particular genotype. About 70% of humans have that particular genotype, so an enormous portion of the population would likely gain years of mental lucidity if they used this new drug.

The new drug is called Blarcamesine, and it was invented by Anavex Life Sciences (NASDAQ:AVXL). The European Medicines Agency has accepted Anavex’s application to market Blarcamesine as a daily pill for Alzheimer’s treatment. By the end of the year, Alzheimer’s patients around the world will know if the EU has ushered in a new hope for them.

The Phase 2b/3 clinical trial demonstrated that taking Blarcamesine over the course of 48 weeks slows cognitive-behavioral decline by 27% as measured by the CDR-SB. This performance equals that of the leading FDA-approved drug: Biogen’s Lecanemab.

Plus, Blarcamesine does not cause brain-bleeding, while Lecanemab does. And Blarcamesine took about thirty weeks less than Lecanemab to produce the impressive results.

And yet, for many whose family members suffer from Alzheimer’s Disease, a lingering question remains. Would Blarcamesine work beyond the first 48 weeks of treatment? A prolonged effect could mean the difference between months of extra mental lucidity and years of extra mental lucidity.

An Open-Label Extension (OLE) study of Blarcamesine attempted to answer that question.

The OLE Study
The Open Label Extension Study for Anavex’s Blarcamesine drug went on for 144 weeks. It started after the original 48-week, double-blind Phase 2b/3 clinical trial ended.

In an early April presentation at the AD/PDTM 2025 Conference in Vienna, Austria, Dr. Timo Grimmer presented the results in a paper entitled, “Phase IIb/III ATTENTION-AD Study: Over Three Years of Continuous Treatment with Oral Blarcamesine Continues to Significantly Benefit Early Alzheimer’s Disease Patients.”

I agree that the OLE provided crucial evidence that Blarcamesine confers clinical benefits for three years or possibly close to four years.

Let me describe the OLE. Both the treatment group and the placebo group patients of the clinical trial were offered an opportunity to take Blarcamesine as a daily pill as part of the extension study.

The OLE patients were not unblinded, meaning, they were not told which group they belonged to in the original study — the placebo group or the treatment group. This means that the patients could not draw any definitive conclusions about whether the drug had an effect on them in the original drug trial. In this way, a proper comparison could be made between the two groups in the OLE study.

The OLE compared two groups: the early starters (the group who had taken the drug during the clinical trial) and the late starters (the former placebo group, who started taking the drug only at the start of the OLE).

How will the rate of cognitive decline of the early starters compare to that of the late starters after 144 weeks? Will the late starters “catch up” to the early starters in their cognitive abilities?

And can any conclusions be drawn about the performance of the drug in slowing cognitive decline in general?

Better to Start Taking Blarcamesine Earlier than Later
All participants of the original clinical trial were composed of people diagnosed with Alzheimer’s Disease. They were in the earlier stages of disease progression — some suffered from Mild Cognitive Impairment (MCI) and some from Mild Dementia due to Alzheimer’s. Among the trial participants there were a disproportionate number of people who carry the APOE4 gene, a gene variant that causes earlier and more severe Alzheimer’s symptoms.

Anavex reported that the early starters declined cognitively at a slower pace than the late starters. The benefit of starting just 48 weeks earlier on Blarcamesine was rather great.

All of the findings were statistically significant at 192 weeks (the end of the study). The original study found that use of Blarcamesine slowed cognitive decline as measured by the ADAS-Cog13 by 36% over the course of 48 weeks. Of course, slowing decline by such a degree was extremely encouraging. The fact that the originally medicated patients widened its cognitive “lead” over the original placebo group over the course of an additional 144 weeks is meaningful.

Exactly how meaningful?

In the original clinical trial, the treatment group scored over 2 points “better” (a lower score) than the placebo on the ADAS-Cog13. That was after 48 weeks of treatment for the treatment group and 48 weeks of a placebo for the placebo group.

Then, during the OLE, both groups were treated daily with Blarcamesine. After an additional 144 weeks, the early starters extended their “lead” from 2.0 points to 3.83 points over the late starters. Even though the late starters had been treated for 144 weeks, the early starters nearly doubled their original “lead” over the late starters. The late starters not only did not catch up to the early starters, but they actually fell behind much further.

Anavex described the results in this manner:

The delayed-start analysis for ADAS-Cog13 showed a significant difference between early start and late start treatment groups up to Week 192 (LS mean difference -3.83, P = 0.0165), favoring the early start group. Together these results suggest that participants who initiated treatment with blarcamesine earlier in their disease progression showed greater stability of cognitive function compared to those who did not initiate blarcamesine until ~1 year later.

To put it another way, the group of patients who took Blarcamesine for 192 weeks scored a good deal better on the ADAS-Cog13 than the group of patients who took Blarcamesine for only 144 weeks. This way of looking at it makes it sound like taking Blarcamesine for just 48 weeks longer makes a huge difference. And that may very well be true.

It may also be true that taking Blarcamesine 48 weeks earlier in one’s disease progression is of vast importance. That is the conclusion that Anavex drew from the OLE study, except without the “vast” descriptor.

What is very interesting is that the graph in Anavex’s presentation shows that the late starters did indeed “catch up” to the early starters at “Week 96” on the graph (Week 48 of the OLE). So, after just 48 weeks of treatment during the OLE, the late-starters were approximately equal to the early-starters in their ADAS-Cog13 scores, despite the late starters having taken the drug for 48 weeks fewer than the early starters. What does this mean? It might mean that the first 48 weeks of treatment are quite powerful and that the second 48 weeks of treatment are not as powerful.

Over the next 96 weeks (Week 96 to Week 192 on the graph), the early starters pulled ahead by a great deal, speeding nearly 4 points “ahead” of the late-starters on the ADAS-Cog13 scores.

Interestingly, there was a subset of patients who had a much smaller delay between the original trial study and the OLE, specifically less than 19 days. This group, which enjoyed almost continuous access to Blarcamesine, actually sped ahead to a 4.2 point lead over the late-starters. So, those who had little or no interruption in their treatment opened up a 4.2 point lead over the late-starters, versus a 3.8 point lead for the entire group of early-starters. This indicates that uninterrupted intake of Blarcamesine has benefits over interrupting one’s intake of the drug. To characterize the degree of the “lead,” those who took Blarcamesine with little or no interruption more than doubled their already-large lead over the late starters.

All of the above-mentioned findings further demonstrate the efficacy of Blarcamesine to slow cognitive decline.

ADCS-ADL Results
The participants in the original trial took the ADCS-ADL test to measure their behavioral habits — how well were they taking care of themselves and doing daily activities. The ADCS is based on caretaker interviews.

In the placebo-controlled original trial, the treatment group slowed their behavioral deterioration by 0.775 points compared to the placebo group. This 10% slowing of behavioral decline was not statistically significant. However, during the OLE, this 0.775 point “lead” that the treatment group held over the placebo group ballooned to 4.3 points. This was statistically significant, and represents a 5.5X multiplication of the original “gap” of .775 points.

For those who suffered little or no interruption in treatment, the multiple was 7.4X! The gap or “lead” was 5.75 points. To give some context, the original placebo group deteriorated by over 7.5 points during the 48-week clinical trial, and the treatment group deteriorated by over 6.7 points during that period. So, the gap that opened up between the two groups over 196 weeks (5.75 points) represents a major slowdown in behavioral decline for the early starters. It represents something like a 9-month delay in behavioral decline for the late-starters.

For further context, a typical Alzheimer’s patient loses about 4 points per year on the ADCS-ADL, according to one journal article.

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