Anavex Life Sciences Corp (AVXL)

[falconer66a]

Very different.

Are SAVA and AVXL on similar but different paths?

Here’s what Cassava Sciences claims about it’s new drug simufilam: “Simufilam is a proprietary, small molecule (oral) drug that restores the normal shape and function of altered filamin A (FLNA), a scaffolding protein, in the brain. Altered FLNA in the brain disrupts the normal function of neurons, leading to Alzheimer’s pathology, neurodegeneration and neuroinflammation.”

So, it restores the shape and function of filamin A, “a scaffolding protein, in the brain.” Well and good.

Next must be clinical trial results confirming both safety and efficacy. In the clinical trials required by the FDA for sales and use approval, will the drug be successful in both safety and efficacy? Yet to be determined or demonstrated.

I haven’t deigned to search out and scrutinize the pre-clinical studies on simufilam, so I can lend no understanding of how those data and outcomes might project the regulatory future of the drug. If it works, well and good.

But I don’t see this as a potentially negating competitor to either blarcamesine (Anavex 2-73) or Anavex 3-71. First, Cassava’s simufilam, as best as I can determine, is aimed solely at Alzheimer’s. The Anavex drugs are targeted, presently (more to come), at three CNS diseases, Rett syndrome, Parkinson’s disease dementia, and Alzheimer’s. Far broader applications, with far broader mechanisms of action. More "upstream," favorably fixing a diversity of "downstream" biochemical anomalies.

And, very different mechanisms of action. Cassava’s simufilam favorably reconfigures just one particular protein, filamin A, which may indeed help suppress Alzheimer’s. But for other CNS diseases, doubtful.

In summary, Cassava and Anavex, while both targeting Alzheimer’s, are on very differing “pathways.” I’ll go with Anavex. Their drug, blarcamesine, causes the cell (neurons) to properly configure, fold, a diversity of “downstream-acting” proteins (primarily, enzymes) which then healthfully normalize a diversity of cellular functions; not the least of which is autophagy, the ability of the cell to consume and reprocess chemical wastes (such as the protein wastes, beta-amyloid and tau clusters) that apparently cause or contribute to Alzheimer’s.