Potential Dosing Durations of Anavex 2-73
The following conjectures are of no importance regarding any investment in AVXL securities, or near-term share prices of such. Offered are merely conjectures of how long patients taking Anavex 2-73 (once approved by the FDA) might be taking the drug.
Conventional perspectives would presume that once diagnosed with a central nervous system disease or condition allowed to be treated by Anavex 2-73 by the FDA, such treatment, such dosing, would be continuous, without interruption or termination.
This is reasonable, considering the targeted CNS diseases. All of them are chronic (continuing) in duration. Therefore, treatment dosings, once started, would be presumed to be likewise chronic, continuing.
In the case of Alzheimer’s, it could be reasonably presumed that Anavex 2-73 dosings, once started, will need to be continued, without interruption. The disease persists; therefore continuing treatment will be required. Understandable, unless....
Unless Anavex 2-73 not only temporally (for a time) restores normalized neuron function, but also restores normalized neuron architecture and biochemical function. It is already known that a primary mechanism of action of Anavex 2-73 is to more functionally reconnect endoplasmic reticula with their associated, energy-supplying mitochondria, thereby allowing normalized protein folding. Properly folded proteins, in most cases, are functioning enzymes, which control normalized cell chemical pathways. Normalized cellular function and health result.
Here’s the yet unanswered question. If dissembled endoplasmic reticula and their associated mitochondria are chemically re-connected by the Anavex sigma-1 receptor agonist, allowing restored, normalized enzyme production, how long do those re-connections last? Do both of those organelles rather quickly dis-connect upon the immediate absence of the Anavex molecule; or, does the molecule cause a more permanent, lasting re-connection?
It is not unreasonable for a more permanent, lasting re-connection to occur. It can take many years, even decades, for the endoplasmic reticula to disconnect from the mitochondria. Alzheimer’s, except for a few, rare genetic forms, seldom occurs until subjects are at least in their forties or fifties. Sixties and seventies are more common ages of typical Alzheimer’s onset. For all of those earlier years, neuron organelles remained functionally intact.
Therefore, if Anavex 2-73 re-connects them, will they quickly dis-connect in the absence of the drug; or will the restoration of normalized neuron architecture — properly connected ERs with mitochondria — continue for substantial periods of time? That might, indeed, prove to be the case. After a few months, say, of Anavex 2-73 dosing (at optimized levels), restored neuron functions may well persist, with no continuing need for the presence of sigma-1 receptor agonists.
How well will those organelles remain connected? Will Alzheimer’s patients have to take persisting doses of Anavex 2-73 chronically? Or, for shorter, defined start-of-treatment periods only?
Perhaps treatment will require ample start-of-treatment dosings, then tailored down to smaller chronic maintenance doses.
Conversely, will effective prophylactic (preventional) dosings be very small, before any gross, frank symptoms appear? Will small initial dosings prevent either the onset or the progression of Alzheimer’s, if started early enough?
None of this can be presently known; will need extensive clinical determinations.
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