The media don’t and can’t get it.
The media (in all forms and perspectives) have a number inherent barriers or impediments keeping a full Anavex story from being presently told or understood by them.
They neither know how to, nor wish to parse out the profound data underlying Anavex 2-73's future. The presenters are journalists, or advertising types, with little or no scientific training and minimal understanding of neuron chemistry or molecular function. All of that is for “brain scientists,” beyond anything they could understand or independently analyze syntactically. It’s beyond them. They don’t know a mitochondrion from an endoplasmic reticulum, nor a sigma-one receptor or a facilitating agonist.
They are convinced that the only possible way to know if a new drug is safe and effective is to have it undergo, in the end, a Phase 3 FDA double-blind clinical test. Until data from such a study are published, drug-reporting journalists are going to retreat from any alternative, premature (to them) detailing of profound safety and efficacy. Too many previous new drug stories have been foisted upon them, only to prove to have been hype-the-stock promotions, with Phase 3 results eventually proving the new drugs’ failures.
Standard, best practice. No other way. Say nothing. Post nothing. Until double-blind Phase 3 results are released. Any premature (pre-Phase 3) presentations could end a journalist’s career.
On the contrary, every biologist (as with myself) with even a moderate and recollected understanding of second-level undergraduate cellular biology and human physiology perceives the most recent Anavex clinical details completely. Important things are evident to the knowledgeable: the presented data thoroughly affirm Anavex 2-73's efficacy against Alzheimer’s symptoms (the ascending plot of mental function is stunning, unprecedented, and not a placebo effect nor inordinate happenstance), and the absence of serious adverse events is revelatory. Lastly, for those who understand the seminal (but often mysterious) role of energized endoplasmic reticula in the proper folding and function of essential reaction-controlling enzymes, the entire Alzheimer’s puzzle begins to be revealed. In summary, A2-73 re-connects mitochondria with rough ER, from which proper enzymes then are synthesized. With those, neurons revert to normalized function (“homeostasis”). Waste proteins (amyloid plaques nor tau-tangles) are no longer produced, even cleared. Neurons then work normally, and over time Alzheimer’s symptoms abate.
Here, we know all of this. And be assured, so do all of the corporate pharmaceutical principals, both the white-coat lab types and corporate executives. Not a one of them is waiting for some distant and lengthy double-blind Phase 3 data set to confirm Anavex’s profound future. In defense of their expensive in-house failures, a few of the white-coat types may be throwing all sorts of lab materials against Board of Directors’ conference room walls. None of it is sticking. The old, last-century approaches to drug treatments for Alzheimer’s have all been expensive dead-end failures. With Anavex, it’s a new century, a new era regarding Alzheimer’s.
Those who ponder Anavex — and there a many, in every laboratory or corporate office building — know full well the future is with Anavex’s unique, proprietary chemistry. They won’t be waiting for some Phase 3 data to emerge before taking, in whatever they can, appropriate new measures.
It’s going to be interesting to follow those developments.
AI
