Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
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.
Made my final, completing AVXL purchase this morning.
Will now just sit back and watch share pricing trends; anticipating eventually handsome rewards (years from now; not days or months, and in the form of dividends, not share sales).
Far more important and significant will be the getting of Anavex 2-73 into the treatment regimens of literally millions of Alzheimer's and other neurodegenerating disease victims.
Yes, perhaps elsewhere.
Because of Anavex 2-73's safety and efficacy, there is a good likelihood that it might be approved for medical use in some “backward” country somewhere else in the world; say, India, or even Australia. “Backward” because of less stringent drug approval strictures. “If it works, and it’s safe, we use it.”
Won’t that be a marvel? Anavex 2-73 gets approved in numerous foreign countries, and their Alzheimer’s (and other neurodegenerative disease) cases vanish — while the FDA continues to question the statistical significance of the most recent Anavex 2-73 clinical data.
Status of Alzheimer’s Research and Anavex 2-73
By now, it’s clear that for most government agencies, (FDA, et al.), pharmaceutical company officers, and neurological researchers, the only acceptable explanation for the cause of Alzheimer’s is amyloid plaque and tau-tangle accumulations. The targeting for treatment of any other cellular processes or functions is an on-going professional anathema.
Decades of exemplary careers and billions of research dollars have been committed to the protein waste explanation for Alzheimer’s treatment. Presently, any other plausible approach, particularly in the form of an easily-synthesized small protein that can be orally administered, effectively crossing the blood/brain barrier, evoking no serious adverse events, and demonstrably stabilizing or reducing Alzheimer’s symptoms is arrogantly rejected. Too simple. It is a profound threat to entire neurology research careers. Anavex’s 2-73 molecule flies in the face and intellect of the most brilliant neurology scientists on the planet. They, of all people, know that such a molecule just can’t work; that sooner or later, it will be further proven that the only way to effectively treat Alzheimer’s is to, some how, remove the disease’s waste proteins. Period.
Of course, the profound multitude of failures in that approach in the last quarter-century will have no bearing on future Alzheimer’s research. Researchers will persist. That’s all they know. Work harder, longer, with greater expenditures, and, somehow, a solution will appear.
But, quietly, that’s not what clinical neurologists tell their Alzheimer’s patients and their care givers (and bill-payers). “I’m sorry. Right now there really isn’t much we can do for your Alzheimer’s, other than to monitor its progression. We’ll try to make things as comfortable as possible. But we have no magic pill. Please consider donating for more Alzheimer’s research.”
The implications of all of this?
External forces must come into play. In order for ossified Alzheimer’s treatment research structures to be broken, external parties must exert useful, new pressures on researchers and their legal governing body, the FDA. Two major power communities must come into play: widespread public opinion expressions, and well-articulated legislative mandates. Articulate letters of opinion from citizens need to appear in all of the usual media, and particularly, federal senators and representatives need to be forcing the issue. The words “Anavex 2-73" needs to be heard, understood, and discussed by a broad band of Americans.
Congressional hearings may need to be held, letting all parties understand the cogent issues. New legislation may be required.
Without any of this, things, clearly, will continue as they have.
Denial of Service
I apologize if, perhaps, my postings here might have caused certain parties to engage in any sort of ihub denial of service. (Sarcasm)
Thanks to those who have been forwarding all of my cogent info to appropriate parties. Sooner or later, no matter what, the Anavex story will become widely known.
The sooner the better.
“@Alz_Gal Don't try to reason with the Anavex crowd. They are profoundly stupid.”
Would love to sit down with Mr. Feuerstein and have a brief discussion of the primary, secondary, and tertiary structures of enzyme proteins, and just how those get mis-folded in dysfunctional rough endoplasmic reticula, disjointed from neuron mitochondria.
Profoundly stupid, am I?
Check back in a year. Neuron cytology and biochemistry will be the same. The status of Anavez — and it’s shareholders — will not be.
Tom,
Thanks so much.
I know enough about technical analysis only to be dangerous to myself.
But from my naive, inexperienced scan of the price lines, I saw $3.50 as a (for me) favorable buy point target. The 50-day moving average pointed toward that, as far as I could tell.
Likewise, the 200-day moving average, around $4.30 looks to be a higher get-in target, should that hold.
From the Anavex science (for which I know almost as much about as you do TA), I’m certain that in months or a year or two the AVXL shareprice will be solidly in double, perhaps even triple digits. Therefore, whether I wait and luck out around $3.50, or, the trendline ascends and pierces $4.30 and I buy up there, I’ll be rewarded. More shares are better, of course. Would like to make my trade less than $4.00, approaching $3.50.
But if I have to chaise it and grab shares going away at $4.50, so be it. I’ll be happy — even if it retraces after that down to sub-$3.00 for a time. Ain’t gonna stay there, I’m certain. Too many have Alzheimer’s and need a working, workable treatment. The biochemistry of A2-73 provides that (at eventually sharply-ascending AVXL shareprices).
Again, thanks for your detailed discourse.
"The Geometric Fibonacci picture now.... "
Ok, fine.
But for us simple add and subtract retail investors, what does this mean?
I sent some funds to my brokerage and want to purchase some more AVXL shares and they have the dollars and I can trade. When might you suggest I do this?
Take the time to read and consider the details of the molecules in the Anavex pipeline, pp 1 - 5, http://ih.advfn.com/p.php?pid=nmona&article=73142440
Too detailed for me to recount here; but Anavex is not just A2-73. It's other existing and to-be-discovered analogues will have massive applications, far beyond just Alzheimer's.
Medical science will not be the same in the next few years.
Moderators, I’m open to the posting of my post 84054 on the yellow sticky notes section. The information complements and expands on what’s presented in my previous sticky notes posting already on the sticky notes section.
Posting of the newer message might allow a broader presentation and recognition of the information to a wider audience, should people link to it in external emailings (as I would hope and encourage).
The Anavex story is still hidden. Let’s get it out into the world.
Feel free to copy and convert my message below (84054) to a PDF or other document and distribute to whomever appropriate.
(Try to maintain the boldfaces, underlines, and italics, as they facilitate reader attention to crucial points.)
The Anavex 2-73 data need to be learned by so many.
Things to Know
A Promising New Alzheimer’s Treatment Drug
The Problem. Alzheimer’s disease debilitates and kills ever-increasing numbers of aging Americans. The Alzheimer’s Foundation of America estimates that as many as 5.1 million Americans may have the disease, and the number is increasing with our large, aging population. The disease is devastating to both its victims and their care givers. Treatments and care-giving costs are massive, stretching collectively into the many billions of dollars.
Treatments. Effectively, there are none presently. A few, very expensive drugs can temporarily, for just a few weeks or months, merely slow the aggravating progression of symptoms. No treatment drug or protocol either stops or cures the inevitable progression to profound disability and ultimate death from the disease. A diagnosis of Alzheimer’s disease is a curse for which modern medicine offers no hope.
Treatment Research. The cause of Alzheimer’s symptoms is almost universally perceived to be the accumulation in or near nerve cells (neurons) of two waste proteins, agglomerations of beta-amyloid plaque, and neurofibrillary tangles, insoluble twisted fibers composed largely of the protein tau, composing the tau tangles.
Current research has strived to remove these neuron wastes that complicate normal brain nerve functions. Plainly, and tragically, all of these efforts have failed. The research drugs targeted at waste proteins have either failed to reduce their presence, or have concomitantly caused serious, even lethal side effects.
The other approach has been to prompt the immune system to chemically destroy and remove the waste proteins. These efforts, too, have failed in every case.
Until now, there have been no drugs that have demonstrated any safe, effective potential to successfully treat Alzheimer’s in any useful way. The disease continues to be an un-treatable curse.
Until now.
A Successful New Drug in Development. A different treatment approach is required. Instead to attempting to pharmaceutically remove beta-amyloid plaques and tau tangles, one company’s researchers have intelligently targeted — successfully — the root cause of those waste protein agglomerations. Instead of attempting to remove them after their formation, after they persist and continue to cause nerve dysfunction, the new approach is to keep them from ever forming, or facilitate their removal by natural, innate cellular processes (as occurs in normal, non-diseased neurons). This approach will revolutionize Alzheimer’s treatment (along with a number of other neurodegenerative diseases).
Children and young adults virtually never get Alzheimer’s. It appears in middle to older aged individuals; after earlier years of mental normalcy. With age, neurons in many people fail to work normally. The new drug restores youthful “homeostasis,” consistent, normal cell status or function, in a powerfully unique and successful way.
The proper function of two structures, organelles, in the neuron are essential. Mitochondria are tiny cellular structures that extract energy from digested food molecules and store that energy in adenosine triphosphate, ATP. ATP is then used in virtually all cellular reactions and processes to power them. ATP is the cell’s energy resource. Without adequate ATP, cellular processes are diminished or inhibited, and disease ensues.
The other essential organelle is the endoplasmic reticulum. Endoplasmic reticula (among other things) take ATP from adjacent, connected mitochondria and use its energy to properly fold and lock together complex proteins, primarily essential enzymes. Virtually all cellular chemistry is mediated by controlling enzymes, much as a key unlocks a lock. If a key, in this case an enzyme in a neuron, is bent or misfolded, the lock, or the life-supporting chemical reaction cannot occur.
In most neurodegenerative conditions, especially Alzheimer’s, endoplamic reticula become separated from the mitochondria. They no longer can receive sufficient ATP to properly fold proteins into normal reaction-controlling enzymes. The cell fails to function properly, or even dies (as in the case of advanced Alzheimer’s neurons).
The solution? Find a molecule that re-connects and maintains the mitochondrion-endoplasmic reticulum connection. Keep the two organelles connected, so proper, healthful enzymes can be normally synthesized — as was the case before Alzheimer’s struck.
The Revolutionizing Molecule. Wonderfully, such a molecule has been found, and has been tested in early trials on humans, with extremely positive results. The molecule is Anavex 2-73, a patented proprietary chemical of Anavex Life Sciences Corp. (AVXL:NASDAQ).
Early clinical trials of Anavex 2-73 have established the following facts.
1. Few or No Side Effects. After a year of administration to people with mid to moderate levels of Alzheimer’s, no serious, debilitating, or disqualifying side effects appeared. For drugs treating nerve or brain conditions, this is exceptionally rare.
2. Stops or Improves Alzheimer’s Symptoms. Remarkably, Anavex 2-73 in dosing ranges between 10 to 50 mg (very small amounts) in a one-year clinical trial period, either a) stopped the progression of symptoms, keeping them at the initial dosing level; or b) remarkably reversed the severity of symptoms, trending at the end of the 52-week trial toward mental and functional normalcy.
Larger, substantiating clinical trials of Anavex 2-73 for Alzheimer’s should be forthcoming. But preliminary lab data in animals, followed by the profound findings of the recently-reported clinical trial in humans are revolutionary. Now, there is profound hope for a) successful treatment of Alzheimer’s, and b) termination of the progression of the disease at its earliest, mildest degrees.
The Future. Anavex 2-73 holds the promise of solving the expanding Alzheimer’s problem, first in America, and then in the rest of the world. The sooner Food and Drug Administration (FDA) approval is attained for this safe and effective drug, the sooner millions will no longer be medically and financially ruined by this frightful disease.
*******************
Study Data. Scrutinize the clinical results of an early 52-week trial of Anavex 2-73 here:
http://www.anavex.com/wp-content/uploads/CTAD-Anavex-December-2016-2.pdf
Notice the minimal and insignificant adverse events (side effects) on page 18.
The data plot on page 25 (the yellow doted line) shows cognition results.
Page 33 enumerates the positive results of Anavex 2-73
Nothing scientifically substantial. All is well.
Importantly, nothing mentioned in the conference call session negated the now-substantiated, solid science of A2-73. The lateral and ascending trendlines of the seminal graphs of the study released earlier this week, showing stabilized or improved cognitive and functional outcomes with A2-73 administration, coupled with the reports of absent or insignificant adverse events (side effects) in virtually all study participants, continue to show that A2-73 can successfully treat Alzheimer’s like no other drug or molecule.
Simply, it works. For many, it stops the progression of Alzheimer’s symptoms; for some, it actually reduces symptoms, causing patients to revert to higher levels of mental and functional normalcy.
And earlier dosings, at the earliest stages or presentations of Alzheimer’s, perhaps for longer periods, might actually restore full, normal mental health. Later studies I expect will show this.
And, as I’ve mentioned before, A2-73's greatest use might eventually be for universal prophylaxis, prevention, where virtually everyone at the age of 40 or 50 is prescribed to take it, to prevent Alzheimer’s, Parkinson’s, ALS, and any number of other geriatric CNS diseases — not to mention cancers, et al.
When approved for used by the FDA (who knows when that might be), Anavex 2-73 will instantly become the SOC (standard of care) for Alzheimer’s presentations. Nothing now, nor anything in any other drug company’s pipeline has any demonstrated potential to match A2-73's results. Existing SOC drugs (there are just a very few) never reduce symptoms, nor even stop their progression. The acetylcholinesterase inhibitors merely slow, for a short time (a few weeks or months), the adverse progression of symptoms. That’s a low standard of comparison for A2-73 to eclipse.
As a biologist and small-position retail AVXL shareholder I’ll let others comment and prognosticate on progressing share prices, new study fundings, etc. All of those are irrelevant if the underlying, foundational science of Anavex 2-73 is flawed. Be assured, it is not.
Feel free to copy, post, and distribute my brief comments on the recent CDAT presentation. It's in the public domain. I posted it here so as to clearly lay out the implications of the new study data.
I’m a retired biologist and have done a good deal of technical writing, primarily in the presentation of complex biological and ecological topics to lay, public audiences. Many (well, most) of my professional colleagues are inexperienced and not always artful in presenting complex scientific topics to lay audiences. My teaching and publishing experiences have allowed a good degree of success in such endeavors. I hope the posting can be of use.
Yes, the several (not just 2-73) Anavex stories need to rise to public awareness. Out of curiosity, I just did a Bing websearch on “Anavex 2-73.” Merely some old, out-of-date URLs. Not a word on the revolutionizing new data, nor their profound implications for a) Alzheimer’s patients, b) medical care and cost systems, c) insurance implications, nor d) corporate or personal investment implications. Nothing. Not a word.
I’m certain it won’t be just A2-73 against Alzheimer’s. Very strong preliminary evidence of similar or exceeding outcomes will be forthcoming for Parkinson’s disease. Add amyotrophic lateral sclerosis (Lou Gehrig’s disease) and multiple sclerosis (and even others; cancers, epilepsy, psychiatrics), and the Anavex story will actually exceed the penicillin and modern antibiotics stories of the last century.
Hope I might be able to assist in getting the new stories out. I note with a bit of a chuckle that one of my similar postings a few months ago, after the earlier Anavex study announcement went out, got posted in the highlights section, but then quickly disappeared as the market did not respond as aggressively as my conjectures suggested they might. I was not premature in those; they were merely not fully understood at the time. The data for lay readers were insufficient. No longer. The recent data plottings, showing stable or increased cognition trends validate my earlier notions on Anavex.
Let me know how I can help in getting the stories and messages to the right people and places.
"...scientists do understand it but are too biased to give it respect?"
No, they understand it completely. Nothing mysterious about Anavex 2-73. It's just different from anything they ever imagined might work against the neuron deficiencies that underly the root cause(s)of Alzheimer's.
After spending years and years in the lab striving for useful applications and efficacies of the approaches one has believed in, Anavex's revolutionary approach requires a complete re-thinking of the solutions to the Alzheimer's problem.
Medicine has historically been confounded by this sort of thing. It took many decades for conventional, highly-regarded medical people to believe Pasteur and Lister and Semmelweis that "germs" actually caused disease.
As with the antibiotic revolution in the late 1940s, modern physicians will much more quickly embrace an Anevex understanding and treatment of Alzheimer's and other CNS diseases. The clinical data (as they were with antibiotics) will be too overwhelming to discount.
We (and they) have just seen the first of those affirming data. Lots more to come, I'm certain.
"Any thoughts why AVXL isn't being more talked about?"
Yes. Anavex technology is utterly revolutionary. It is in no neurobiology textbook. It was never even remotely imagined by any of the world-class researchers in the room (except for the Anavex principals).
It rubs harshly against all of the pre-conceived Alzheimer’s pharmaceutical treatment options, of which there are only two: administer an acetylcholinesterase inhibitor (to, for only a period, facilitate otherwise diminishing thought processes), or, find a safe, effective drug that causes the removal of protein wastes (amyloid plaques, tau-protein tangles) in the neuron, either immunologically or by extraneous molecules.
None of these treatment approaches have shown any useful efficacy. Immunological approaches have had severe, debilitating side effects, and waste protein-clearing molecules, too, have all sorts of untoward outcomes (or simply don’t work at all).
Billions (yes, billions) of research dollars have been expended in these efforts — primarily by the researchers and corporate officials listening to the Anavex presentation at the conference. We can conjecture on the internal thoughts a number of the Anavex slides evoked: “Oh, feces, look at that! Symptomatic stabilization — even IMPROVEMENT. And no side effects, and orally administered. How am I gonna explain this to my Board of Directors? How am I now gonna get another million dollars for the new drug tests I want to work on?”
Don’t say a thing. Keep this all very quiet. Maybe it’l all just go away and everyone can go back to his lab and spend lots more on new immunology or waste-clearing drugs. “Otherwise, I got no future with my Big Pharma company. Say, where is that Anavex guy? Maybe he needs a new lab technician?”
The presented data are in line with what I expected — and very favorable.
Will Anavex 2-73 be a “cure” for Alzheimer’s? No indication of that from the presented data.
But the trend lines of cognition and awareness and other Alzheimer’s disability markers are all favorable. Over the longer periods of the studies, those quantified and measured factors either remained lateral (little changed), or improved. They didn't decline (unique).
Nothing like this in any pharmacy’s drug shelves. No existing (or even experimental) drug other then A-2-73 has been able to stabilize or improve Alzheimer’s mental factors. Current Standard of Care (SOC) drugs give merely a few weeks or months of reduced symptoms, merely slowing for a period the ever steeper descent into disability and death.
Anavex has no competition. These early clinical data show conclusively that Anavex 2-73 is both safe (absent, few, or inconsequential side effects; compared to symptoms being suppressed), and chronically effective — favorable trend lines continued throughout therapy periods; even becoming more favorable toward dosing end-periods for some factors.
What might all of this mean?
1. Because A2-73 demonstrates efficacy, stabilized or increased cognitive factors, current SOC drugs no longer could be considered “standard.” There is not a shred of evidence indicating Anavex 2-73 won’t, soon enough (sooner will be better) become the worldwide Standard of Care for Alzheimer’s. Unlike anything available today, it doesn’t merely slow for a time the progression of Alzheimer’s symptoms, it stabilizes or improves them.
2. Because A2-73 has no side effects of consideration, its demonstrated safety will allow its approval by the FDA. It demonstrably treats Alzheimer’s, with safety.
3. The data strongly suggest that administration of Anavex 2-73 at the very first symptomatic indications of Alzheimer’s would keep symptoms from developing to further, more debilitating stages of the disease. With this, A2-73 could be prescribed for every middle-aged or older person showing any preliminary Alzheimer’s symptom (“Hey, what’s our neighbor’s name again?”). No, Anavex 2-73 will not be an Alzheimer’s cure. But it very strongly (to me) appears to be a powerful prophylactic, a preventative treatment that can keep millions from descending into the cognitive hell of the full-blown disease.
The market for Alzheimer’s prophylaxis and treatment is gigantic. Presently, there is no reason Anavex won’t be the sole, successful factor in addressing the problem.
I await similar studies and results for other central nervous system (CNS) diseases, such as Parkinson’s disease, multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s Disease). The are in vitro (test tube) and in vivo (in cells, mostly in lab animals) that Anavex 2-73 will be profoundly therapeutic for these conditions, too. (It already works for Rett’s Syndrome and some forms of epilepsy.)
Lastly, there are very preliminary lab indications that Anavex 2-73, or similar analogues in the Anavex pipeline, can treat cancers and a number of other human diseases.
All of that is more distantly in the future. The Anavex 2-73 clinical data presented at the CTAD conference validate its profound efficacy for Alzheimer’s. I await FDA approval of the drug. I can find no reason for that not to occur.
Xena,
Thanks.
Gratefully, my HSP is confined to my legs and I retain full mental facility. I can no longer walk in wild habitats for field studies, but I'm in quasi-retirement anyway.
More importantly, Anavex molecules have the promise of effectively treating and preventing just a multitude of 21st-century diseases; with greater results than antibiotics in the last century.
Well then, "thousands of millions"
A billion is a thousand million.
Observations of a small retail AVXL shareholder.
I thank everyone for their postings on this board. Varying viewpoints and perspectives, to be carefully read and considered by those of us with an interest or position in Anavex.
I’m a field biologist and biology instructor, reasonably familiar with the cellular biochemistry of the neuron. None of what I relate here should be construed as investment advice or encouragement; merely the perspectives of an informed small-time retail AVXL investor.
First, I believe and understand that Anavex’s Alzheimer’s treatment approach is unique and wholly different from any drug on the market or under development by any other company. This sets Anavex apart. Its story and future are entirely different from those of any other drug development or sales company. Comparisons with existing Alzheimer’s treatment drugs, about a dozen, with only three or four in common usage, are invalid. None of these have been able to effectively stop or reverse Alzheimer’s symptoms. They merely slow disease progression for a period (often only for a few weeks or months).
As I interpret the available clinical data, Anavex 2-73, in fact, stops symptomatic progression, keeping the disease from progressing to ever more debilitating stages. Yes, the clinical population sizes from which these results are derived are small; but statistically significant, and consistent across the populations. I’m convinced that any future clinical trials of Anavex 2-73 will merely further substantiate the molecule’s unique biochemistry, restoring defective neurons to “homeostasis,” a normalized, fully functioning status. This is accomplished by 2-73's ability to re-connect dislodged or poorly-connected endoplasmic reticula to mitochondria. This restores normalized protein folding in the endoplasmic reticula, creating fully- and normally-functioning reaction-controlling enzymes. With those, neurons will operate healthfully.
All of that is crucial. Other Alzheimer’s drugs attempt to remove A-beta plaques, or tau-tangles, waste protein accumulations found in all Alzheimer’s-affected neurons (but also, incongruously, often in fully healthy people, too). Millions of research dollars have been spent in perfecting and testing waste protein removal drugs; with no success. Many pharmaceutical companies and neurologists persist in this evermore useless pursuit. Anavex has a much better, cheaper, and effective approach. Cause neurons to synthesize functioning enzymes by facilitating normalized endoplasmic reticulum-mitochondria connections.
Another crucial clinical finding. Anavex 2-73 easily crosses the blood-brain barrier, efficiently diffusing into neurons. Few other drugs do this. This allows minimal dosages, in posted clinical trials between 10 and 50 milligrams per day, administered orally (not by injection). Ease of administration, effective in low doses. Extremely useful.
Then, on top of all of this — and it is crucial for FDA approval — Anavex 2-73 has had few or no adverse events in the posted clinical trials. No disqualifying side effects. This is exceptionally rare for any drug or chemical acting inside nerves and neurons. Anavex 2-73 easily gets into neurons, re-connects disconnected endoplasmic reticula with their associated mitochondria, and the neuron then functions normally — without untoward results.
With an understanding all of this I’m convinced the Food and Drug Administration will sooner or later authorize widespread clinical use of Anavex 2-73, at least at the start, for this seminal reason: Anavex 2-73 exceeds any Standard of Care (SOC) results for any existing Alzheimer’s treatment drug. They merely slow for a time (at best) the progression of symptoms. Anavx 2-73 stops symptomatic progression; meaning that if administered at the start of (or before) symptoms, the disease can be chronically suppressed and the patient maintained in a normal mental state. Anavex will become the new Standard of Care drug for Alzheimer’s. No competition.
Eventually, I see widespread prophylactic (preventative) use of 2-73. It may eventually be commonly administered to virtually everyone at the age of 50 or 60, keeping Alzheimer’s from ever developing. No side effects. A small, cheap protein, easily administered.
And, for an expanded story, consider 2-73's eventual treatment or prevention of Parkinson’s disease and other geriatric neurodegenerative diseases. Animal tests indicate equivalent efficacies.
In fact, I suffer (not badly) from hereditary spastic paraplegia (HSP), where the motor neurons of my spine are hyperactive, causing adductor muscles in my thighs to remain tight. I walk with difficulty (but no pain). There is a French report where transgenic rats, with the inserted genetic defect of my disease, were treated with Anavex 2-73 and their spasticity was resolved. Yes, I’m hoping that can eventually happen with me.
I won’t elaborate on the expansive pipeline of other molecules Anavex owns and is developing for other diseases. If only Anavex 2-73 comes to market the company will be a giant success (especially for those of us with equity positions). But I think Anavex 2-73 is the subject of only a few of the early chapters in the eventually more gigantic Anavex story.
Acronyms appearing in AVXL postings (incomplete — feel free to amend):
__________________________
AD — Alzheimer’s Disease
ADCS-ADL — Alzheimer's Disease Cooperative Study - Activities of Daily Living; measures the ability to independently perform daily activities such as eating, bathing, and using the telephone; [unable to discover the meaning of scoring data; presumably higher is favorable]
BIIB — Biogen, Inc.; a major pharmaceutical company, apparently in discussion with Anavex concerning Anavex 2-73 development, testing, and perhaps marketing
BP – Big Pharma, or Big Pharmaceuticals; any of the established, giant drug development and drug sales companies.
CNS — Central Nervous System; the brain and spinal cord; the bodily location of central nervous system disorders, such as Alzheimer’s disease and Parkinson’s disease
CTAD — Clinical Trials on Alzheimer's Disease; a current or recent meeting of neuroscience researchers where neuroscience reports are posted and presented
EEG — Electroencephalogram; observes electrical activity in the brain; abnormal activity associated with neurological diseases and conditions
ERG — Electroretinography — measures electrical responses of cells in the retina; can reveal neurological problems
HAM-D — Hamilton Rating Scale for Depression; rates the severity of depression
MMSE — Mini-Mental Status Examination; 30-point questionnaire in clinical and research settings to measure cognitive impairment; higher scores indicate higher cognition (thinking) skills.
MTD — Maximum Tolerated Dose; the highest dose of a radiological or pharmacological treatment that will produce the desired effect without unacceptable toxicity
PD — Parkinson’s Disease
Phase 1 – Initial clinical study of a new drug; to determine dose range toleration and pharmacokinetics
Phase 2a: — Pilot clinical trial to evaluate efficacy (and safety) in selected populations
of patients with the disease or condition to be treated, diagnosed, or prevented.
Objectives may focus on dose-response, type of patient, frequency of dosing, or
numerous other characteristics of safety and efficacy.
PK — “pharmacokinetics;” the progression and fate of an administered chemical or drug in the body
Merriam-Webster:
data — noun, plural, but singular or plural in construction, often attributive
https://www.merriam-webster.com/dictionary/data
The proliferated acronyms appearing in company PR’s (that’s “press releases”) and postings on this board are confusing, obscuring the meaning and significance of the associated numbers (the data).
Several post frequently and usefully here. Would someone take the time to list out all of the appearing acronyms (meaning, the sequences of letters that stand for specific worded phrases or concepts), followed by a) the actual, full worded phrase or concept, and b) most importantly, describe the significance and applicability of the phrase or concept.
With this, new viewers might more accurately perceive what the plethora capital letter sequences and their numerical data actually mean.
Presently, we have acronymic confusion, obscuring the value of the terms and associated data.
By the way, “data” is plural, a set of quantities or information. The singular is "datum." One datum, many data. We have lots of data. They — properly, not “it” — need clear presentation and understanding.
Yes, the Anavex pipeline is not a narrow tube only of 2-73.
A number of analogues and distinct new chemistries targeting more than Alzheimer's.
As a biologist, I continue to be impressed with the unique cellular chemistry of these molecules, restoring defective neurons (and others) to normal function ("homeostasis") unlike any other drugs.
Anavex has the potential to revolutionize 21st century medicine as antibiotics did in the middle of the last century (or better).
Not interested in a share-for-share collaboration with Biogen.
As always, none of these comments are intended as buy or sell guidance for AVXL shares. Just my personal perspectives.
I just purchased another small number of AVXL, around $3.80. I’m confident this will, in a year or more, be a very rewarding investment.
But I’ve punched a few numbers on this, in conjectured speculation of both future AVXL share prices and potential dividends, should Anavex 2-73 prove to be a viable, successful Alzheimer’s treatment and/or prophylactic (as the data presently so strongly suggest).
I will not post my spreadsheet here. Each, should you wish, needs to punch his own numbers. Here, as I’ve seen it, are the figures to play with.
First, what might be the potential market for A2-73, starting purely with Alzheimer’s patients who could be treated? One authoritative source states that presently — with greatly increasing numbers in years ahead — 5.3 million Americans suffer with the disease. Worldwide, 44 million are affected.
Next, what would annual A2-73 treatment costs be? How many dollars will come to Anevex from each treated patient each year? What revenues might Anavex yield from A2-73 sales in a few years for Alzheimer’s?
Lastly, then, how much of those A2-73 corporate revenues would drop down into distributed dividends? What would be the annual per-dividend payout?
Then, consider Parkinson’s disease, for which A2-73 is very likely to show efficacy. An authoritative source claims about 500,000 Americans have this disease presently, with approximately 50,000 new diagnoses each year. Run the same calculation ranges with these numbers.
A2-73 and other molecules in the Anavex pipeline will have expanded applications for other chronic and debilitating diseases. What might revenue and dividend outcomes be for those?
And, these conjectures are solely American; but all of the indicated conditions exist in the rest of the Western, even entire world. What will be the elevating revenue factors with worldwide A-73 sales and applications?
It is not useful for me to reveal my calculations. Do your own. Clearly, a one-for-one share trade with a Biogen, yielding a new share price between $100 and $300 or so looks enticing. But when considering longer-term, continuing, multi-disease revenue streams, those numbers are minute. I want Anavex to expand to a full-sized, self-contained pharmaceutical, collaborating only as initially necessary. With such, continuing shareholder payouts will be orders of magnitude greater than the single share exhange.
No, Anavex has not specifically mentioned enzymes, misfolded or otherwise. That’s a molecular chemistry detail that is not specifically characterized in any of the 2-73 studies. But cellular biologists know of this well. No need to mention it. Enzymes are complex proteins, with three structures: primary structure, the simple sequence of constituent amino acids; secondary structure, the twisted or bend arrangements of the amino acid sequences; and lastly the tertiary structure, the complex folding of the coils and other structures of the secondary structure.
Virtually all chemical reactions in any cell occur because of the presence of specific reaction-controlling enzymes, of which there are thousands. Those enzymes are made in ribosomes, which are attached during protein synthesis to the rough endoplasmic reticulum (RER), which is attached to the mitochondria, where ATP’s are available to power the protein-synthesizing reactions. Disconnect the RER from the mitochondria and the attached ribosomes have a difficulty producing well-formed, functioning enzyme proteins. Here’s where 2-73 uniquely works; it functionally reconnects the RER with mitochondria, allowing normalized and fully-functioning enzymes to be made. No other drug does this. With 2-73, no excessive waste proteins are made to clog up and suppress normal neuron function.
No, amyloid plaque proteins are not “misfolded.” They are chemical wastes the neuron failed to discard or dysfunctionally produced. Yes, amyloid plaques lead to neuron dysfunction, resulting in Alzheimer’s symptoms. Presently, most drug companies have been targeting the plaques, presuming their prevention or elimination would be an Alzheimer’s cure. Problem is, no drug effectively does this. Any drug capable of dissolving or disintegrating the plaques is too big and too delicate to cross the blood-brain barrier (and it probably would mess with other good proteins – side effects).
This is crucial. Anavex does not target either amyloid plaques nor A-beta tangles (other protein waste accumulations). Both are seen in virtually every Alzheimer’s case. But Anavex’s approach attacks the problem at its start, even before protein wastes can accumulate; by reconnecting and maintaining (“homeostasis”) proper mitochondrial-RER connections.
Was a short note on 2-73 results.
But entirely misstated how 2-73 stops the progression of Alzheimer's symptoms. The article stated that it re-myelinates nerves cells; restores the normal myelin sheath of neurons.
Nice thought. That might work for multiple schlerosis, where demyelination, loss of the insultating myelin sheath of the neuron, is the primary cause of the disease's symptoms.
Alzheimer's has little or no demyelination. 2-73 restores disrupted mitochondrial-endoplasmic reticular connections so as to allow the neuron to synthesize complex folded proteins, fully functioning enzymes, that control and direct normal cell functions.
A Conjecture or Two
None of the following is to be regarded by anyone as either good investment advice, nor a depiction of what will happen in the future with Anavex 2-73. It is merely a conjecture; based upon existing, albeit incomplete or not fully developed or released information.
Two significant facts (not conjectures) have just been posted. Anavex 2-73, for a 41-week dosing period, at doses ranging from 10 to 50 mgs, produces no appreciable or disqualifying side effects. None of the patients in the 41-week dosing period elected or were forced out because of side effects. For neurological drugs, that is remarkable.
Secondly, and extremely important, the drug simply stopped the progression of Alzheimer’s symptoms during the entire 41-week study period. Nothing else has been shown to do this.
From all of that, here are my conjectures.
After 2-73 gains FDA approval for Alzheimer’s patients, it becomes widely prescribed, both for early-stage presentations, where it will prevent progression to later debilitating stages, and also to those with more advanced symptoms, where, as in this present study, symptomatic progression is terminated.
All well and good, both for Anavex and for patients. Here, then, is the greater conjecture.
Because of 2-73's safety, lack of side effects, and probably as a result of new studies, it becomes prescribed as the preferred treatment for Parkinson’s, amyotrophic lateral sclerosis (Lou Gerhig’s Disease), and perhaps other geriatric neurodegenerative diseases.
If any of this occurs (quite likely, I think), it will revolutionize modern medicine, to the degree or greater than antibiotics did in the late 40's and early 50's.
But here’s a panoptic conjecture. It soon becomes apparent that 2-73 should simply be prescribed, prophylactically (solely for prevention), for everyone at the age of 50. Just as so many now take statins to prevent heart disease, many, many more (well, everyone) could take a daily 10mg of Anavex 2-73 to prevent the onset of Alzheimer’s, ALS, Parkinson’s and who know what other diseases afflicting people in the last half of their lives.
Then, when millions are taking preventative doses of 2-73, for the diseases for which it is known or presumed to be efficacious or preventative, this might be discovered. Presently, there are fragmentary indications that 2-73 prevents or treats various cardiovascular conditions, and perhaps, even forms of cancer.
What happens if it is discovered that those taking 2-73 chronically simply have reduced or absent other diseases, without side effects? Prescribe it then for everyone.
Others can conjecture on the revenue streams chronic administration of 2-73 to virtually everyone at the age of 50 or so would generate.
Now, is there any legitimate biological basis for these conjectures, particularly 2-73's prevention of a multitude of geriatric diseases? Very much. Uniquely, 2-73 restores the connection and mutual, normal function of mitochondria and endoplasmic reticula. Mitochondria synthesize adenosine triphosphate, ATP, the energy source for most cellular reactions. Endoplasmic reticula, when attached to the mitochondria, use the ATP’s energy to properly fold genetically-directed proteins into precise, folded structures; in most cases reaction-controlling enzymes. Mis-folded proteins; poorly-functioning enzymes, cannot efficiently and completely control and promote cellular chemical reactions. Hence, disease. The tertiary, 3-D structure of enzymes is intensely studied. Mis-folded enzyme proteins simply fail to properly promote or control cellular chemistry. Disease or death results. Anavex 2-73 restores a more youthful, full-functioning mitochondrion-endoplasmic reticulum arrangement. Fully functioning enzymes can then be synthesized, with proper cellular health restored.
Lets’ watch and see what happens.
Perfect. Then disregard the posting. Like so much here, it's irrelevant.
What, per chance, do you see as the connection? Elaborate.
Let us strive for factual accuracy.
The IHUB Detailed Quote page indicates that there are 91,240,000 outstanding Freestone shares. The insider holdings just posted by RedShoulder indicate a total of 38,616,442 shares.
That accounts for 42.3% of the outstanding shares, not the majority I stated in my previous post.
Nonetheless, it’s a substantial fraction of outstanding shares, and does not include undisclosed “insider” shares owned by family members and informed friends of the company officials.
Most likely, those additional shares total more than 50% of those outstanding.
No sales into the 100,000 bid.
The notion that no one is selling, in the murky light of some forthcoming foreclosure (predicted in some posts here) because they would lose money is incredulous.
Clear fact. The majority of shares are held by company insiders, who know the company’s future. They have not and are not liquidating their positions. No one is.
Clearly, if a company is going bust, with no future, it’s best to sell as many shares as soon as possible. Recover whatever remaining value one’s position in an equity presents itself. Why wait until the price is sub-penny. Sell soon. Sell quick. Before the worst times come.
There is not a bit of anticipated “bad times” sales by FSNR insiders who, for so long, have retained their positions.
And, someone wants to buy 100,000 shares at a reduced price. Why wouldn’t those with knowledge that the company were going bust, the insiders, not act on this? Why no sales into the 100,000 bid?
2-73 will not be a “cure,” by any means; BUT....
No, a course of 2-73, causing endoplasmic reticula to physiologically reconnect with mitochondria and restore normal neuron function in Alzheimer’s, Parkinson’s, or other neurodegenerative diseases, will not be a cure. Stop the 2-73 therapy, and whatever originally caused the ER/mitochondrial dysfunction will resume.
Same way with diabetes. Insulin injections can control blood sugar levels, approaching normalcy. But stop taking the insulin and diabetic symptoms will resume.
The implications? Those for whom 2-73 is efficacious will not be taking the drug for a restricted period of time. It must be administered for the rest of their (then) longer lives.
In fact, this is exactly the sort of drug profile Big Pharma want to concentrate on; on drugs that require continuing, long-term administration — yielding continuing, long-term revenues.
Case in point. Multiple drug resistant bacteria are proliferating. But Big Pharma conducts very little or no research on finding new antibiotics. Takes lots of resources and time to find and synthesize the new antibiotics, but if they are effective, the simply kill off the bacteria in a restricted period of time. No long-term, continuing revenues from those being treated.
Not the case with Anavex 2-73. With, perhaps, 5 million Americans affected by Alzheimer’s, each patient will be taking 2-73 for the rest of their days. THAT’s long-term revenues.
Now, of course, astute minds will point out that we presently have no evidence that 2-73 will be continually effective, with no loss of efficacy over time. Will 2-73 lose efficacy after a certain period? Only long-term administration and monitoring will determine this.
This, generally, is why advanced, long-duration double-blind Phase 3 trials, with both experimental and control arms (some with the drug, others without, just a sugar pill) are usually preferred and required by the FDA.
But, in animal trials, and in the short human trials (to be announced tomorrow), it is expected that profound positive results will appear (they already have in the animal models). With the absence of adverse effects, in both murine (mouse) and human trials, there will be no reason for the FDA to require double-blind Phase 3 trials. Early “compassionate approval” will be justified.
Personally, I have every reason to believe, based upon (among other things) the 2-73 molecule’s ability to so easily cross the blood/brain barrier and enter dysfunctional neurons, uninhibited by normal toxin-clearing or immunosuppressive functions of the body, it will continue to work favorably for extended or continuing durations.
With all of that a) Anavex (or a collaborator) will reap gigantic and continuing revenues, b) shareholders will be richly rewarded, and most importantly, c) millions of patients will live normal lives.
How Anavex 2-73 is different from all the others.
An intelligent poster (above) asked me to tell the difference from Anavex 2-73 and all the previous Alzheimer’s drugs by other pharmaceuticals. One shouldn’t be investing in AVXL without knowing, at least superficially, those gigantic differences.
Presently, a lot of investment wags — who obviously couldn’t name off-hand three organelles (cellular components) — are ignorantly lumping 2-73 in with all of the several Alzheimer’s drug failures, along with the current acetylcholinesterase inhibitors (such as Aricept), which have minimal real usefulness. They improve cognition slightly for a short period of time, after which the disease continues on to to utter debility and death.
And that’s important to know. If, as it will, 2-73 exhibits even slightly better or longer cognition improvements, FDA will measure it against Aricept. No competition. Given 2-73's infrequent and minor adverse events — side effects — the FDA must approve it. It works better, and has fewer adverse events. Anavex has no real competition.
Why? Because all of the previous Alzheimer’s drugs have targeted different cellular functions, compared to the root-cause target of Anavex.
One big drug effort (don’t recall the name, offhand) attempted to prompt the immune system into clearing amyloid-Beta wastes. These protein waste clumps are microscopically diagnostic indicators of Alzheimer’s. And, clearly, they do disrupt proper and normal neuron function. It was thought that by clearing the a-Beta clumps, symptoms would resolve.
Except, no one was really able to prompt the immune system to only clear the a-Beta wastes. Other things in the brain were also affected, very severely. Immunotherapy approaches to treating Alzheimer’s have universally been a failure. I don’t believe any Big Pharma is current researching this any more.
A second approach, still targeting a-Beta wastes, is to find some molecule that a) crosses the blood/brain barrier (a difficult task), and then b) selectively enters affected neurons and somehow prompts the molecular clearing of a-Beta proteins. My understanding is that there might be several labs working in this arena. But the hurdles are high. Adverse effects will be obviating. I will stay clear of any such approach. Chances of therapeutic success extremely low, if not absent.
The current and only pharmaceutical treatment, such as Aricept, involves the administration of acetylcholinesterase inhibitors. These work outside the neuron, at the inter-neuron gaps, the synapses. The normal enzyme acetylcholinesterase breaks down an essential nerve signal chemical. By doing so, nerve impulses are facilitated across the synapses of Alzheimer’s neurons. But only for a few weeks or months. Acetylcholinesterase inhibitors soon lose their ability to keep things functioning. The disease then progresses degeneratively.
I know about this, as my father died of Alzheimer’s, and was a test patient in a clinical test for an acetylcholinesterase inhibitor drug. We had about three weeks of mild cognitive improvement, with no long-term good results.
Now, how is 2-73 different and so much better? On the face of it simple (but at the molecular level, rather complicated; I won’t attempt to present the deep molecular biology).
In virtually all neurodegenerative diseases, including Alzheimer’s, Parkinson’s, and others, neurons fail to function properly because reaction-controlling enzymes become mis-folded or physically distorted. Virtually all chemical reactions in cells are controlled by moderating enzymes. If any of those go wrong, disease ensues. In the case of Alzheimer’s normal nerve cell wastes don’t get cleared, and the diagnostic a-Beta waste protein clumps, along with Tau-tangles, accumulate. With all of that, nerves don’t function well.
Unlike all the others, Anavex targets the root cause of these debilities: misfolded or inadequate enzymes. And those are caused when the endoplasmic reticulum, responsible for protein folding, among other things, becomes physically or chemically detached from the cell’s power plant, the mitochondrion. Cells, with normal ER/mitochondrial connections function well. Disconnect the ER from the power-providing mitochondrion, and all sorts of cellular things will go awry.
In the simplest terms, 2-73 re-connects the endoplasmic reticula to the associated mitochondria. The cell then resumes normal function. Proper enzymes are made, wastes are cleared, and nerve impulses are transmitted unhindered.
And, remarkably, all of that happens at very low concentrations (doses between 30 and 50 mg), after the molecule rather magically jumps the blood/brain barrier and easily enters the neuron.
That, alone, is wonderful. But, most importantly, 2-73 appears to restrict its activities to the ER/mitochondrion connection, yielding few adverse events, none of which will obviate clinical use of the drug.
Almost too good to be true. But the biology is now known and demonstrated. It’s all up to the FDA to approve the drug. It has no competition. Nothing comes close.
Bud,
I thank you for your comment.
I’m a biologist. I understand the essentials of the unique biochemistry of 2-73 and cellular physiology. I’m not any sort of investment guru, and have no comments (even interest in) the many chart and trends postings here. Plenty of experts on those topics. (But, of course, I do hold a number of AVXL shares, and don’t intend to reap any profits for several years, when appreciation will have added one or two digits to the share price.)
But the molecular and cellular functions of Anavex drugs are far more complicated than the multi-colored share price charts so frequently posted (and, by me, misunderstood). I’m a retired biology teacher, with a certain ability to present complicated biological concepts to interested audiences, whether to students interested for a good grade, or, here, for audiences trying to do due diligence on the arcane topics of neurological drugs.
With Anavex, we have a winner.
Glad to be of some help.
I’m not impressed with this new drug. For the few (and it will be a few — it only works [maybe] for a small fraction of Alzheimer’s patients who have an uncommon genotype), this could be a useful drug.
But, like so many others, it attempts to clear amyloid wastes from affected neurons, on the presumption that the amyloid masses are the direct cause of Alzheimer’s. Get rid of the amyloid masses and all should be well.
That’s not Anavex’s approach whatsoever. It is more enlightened, presuming that amyloid accumulations occur because of mitochondrial/endoplasmic reticulum disconnection and the consequent mis-folding of essential intra-neuron proteins this causes. That’s the root cause of Alzheimer’s, Parkinson’s, and large number (if not all) neurodegenerative diseases.
Wonderfully, Anavex 2-73 properly connects endoplasmic reticula with the mitochondria, so both organelles function normally, creating no amyloid or tau-tangle wastes.
Moreover, 2-73 works at low dosages, easily crosses the blood/brain barrier, and has demonstrated no adverse events (“side effects”) of any obviating consequence.
My money stays with Anavex.
Implications for the medical insurance industry.
As a contravening position to my earlier post (where I claimed that approval and use of 2-73 will be a major threat to large segments of the medical care industry, and, therefore, early announcements of 2-73 efficacy will not be well-received by the “experts”), one must consider the implications for the medical insurance industry — which is burdened with ever-increasing costs to care for senile dementia (Alzheimer’s), Parkinson’s, and several other neurodegenerative diseases for which there is considerable animal and some human data showing profound treatment efficacy with 2-73.
What will be the results when medical insurance companies come to the realization that prescription of 2-73 to those showing the earliest, slightest Alzheimer’s or Parkinson’s symptoms will terminate the debilitating progression of those extremely costly diseases?
Insurance companies will be able to save billions of dollars. Might the medical insurance fraternity bring pressures to bear on FDA for “compassionate approval” of 2-73?
And, I’m certain the pricing wizards at Anavex will take all of this into consideration. Most of us have pondered what the company might charge for a daily or weekly dose of FDA-approved 2-73 (or any of the other in-the-pipeline drugs). I’d hope it will be minimal, say $3 to $5 a day (I could afford that). But, given the profound insurance savings, Anavex may charge much larger fees, which the medical insurance companies will still accept, resulting in reduced overall costs (no more institutional care costs, etc.).
For anyone who takes the time to discern the actual outcomes of currently available Alzheimer’s treatment drugs, this promotion of “more is better” is, on the face of it, laughable.
Unless one understands that current Alzheimer’s treatments are very ineffective, that they, at best, provide for slightly increased cognitive function for short initial periods (weeks or months), the announcement sounds good and reasonable.
The drugs are rather expensive, have lots of adverse events (“side effects”), don’t provide really useful cognitive restoration, and after the initial period of slightly-improved thinking, AD patients continue on their tragic mental decline, as though never having had the drug.
The only useful new treatment will be Anavex 2-73; of which there was no mention. Nor will there be, even after Wednesday’s favorable efficacy data are released. As I’ve posted before, the entire medical treatment and research community is certain that Alzheimer’s is directly caused by a-beta deposits and tau-tangles, and they’ve learned that several previous drugs aimed at clearing these waste neuron proteins have been utterly ineffective, with severe side effects. With that thinking, the only alternative is the called-for increase in the rather short-lived, ineffective acetylcholinesterase inhibitor drugs.
It took 19th-century physicians many decades to come to the realization that infectious diseases are caused by microbes, germs. Physicians are extremely resistant to any concepts or ideas not taught to them in med school.
The FDA approval and prescribed use of Anavex 2-73 is going to be a threat to conventional medicine for several reasons. First, it simply contradicts what is “clearly known” about Alzheimer’s (as mentioned above). Far worse (from the physicians’ personal viewpoint), will be the drug’s threat to medical practice services and fees. The treatment of Alzheimer’s and other neurodegenerative diseases (most of which will be markedly reduced by 2-73) will threaten the multi-billion dollar dementia and neurodegenerative medical sector. Instead of expensive, closely-monitored drugs and personal care requirements for contemporary Alzheimer’s patients, general practitioners (or nurse practitioners) will simply prescribe a daily dose of, say, 30mgs of 2-73, thereby terminating, even reversing the progression of the earliest Alzheimer’s symptoms. The only applicable medical term will then be, “Next patient, please.” Simple office visit stuff.
“Past presentations haven't caused much positive comment from any respected experts on Alzheimer's disease. I expect the same with this presentation.”
The “respected experts” are all Alzheimer’s researchers — who are entrenched in the idea that Alzheimer’s disease is caused by a-beta plaques and/or tau tangles, and therefore, the only viable treatment can be some agent that removes or inhibits the deposit of these neuron wastes. Or, worse, AD simply can’t be prevented and can only be treated by acetylcholinesterase inhibitors, to provide, for a short time, slightly increased cognition.
For the experts to comment positively on Anavex’s entirely different and unique approach is to effectively admit that the research they are getting paid for is rather worthless.
Consequently, they will stay quietly in the wings, letting things play out (hoping that FDA approval of 2-73 doesn’t — as it will — completely terminate their entire research careers).
The frequent posting of concern lumping 2-73 in with both existing and proposed new Alzheimer’s drugs, in regard to the multitude of side effects each of these has, is understandable. It is presumed that all such drugs, necessarily, must have untoward side effects; therefore, so will 2-73 when used in humans.
This is an error. There is not a scintilla of evidence, in either animal or human trials, at efficacious dosages, that 2-73 has any side effects of consideration. In fact, it virtually has none whatsoever.
The reason for this is that 2-73 works very differently from other AD drugs. They a) reduce acetylcholinesterase decay, facilitating inter-neuron signaling (but only for a time), b) target removal of a-beta waste protein clusters or tau-tangles, or c) attempt to prompt the immune system to target and clean up the neurological wastes that are presumed to be (incorrectly) the root cause of AD symptoms.
Anavex 2-73 works entirely differently. In extremely low concentrations, it both crosses the blood/brain barrier and enters neurons, where it then remarkably restores normal endoplasmic rectulum/mitochondrial connections, allowing mitochondria to provide the ER with adequate ATP so proteins are normally processed and folded. In all of the neurodegenerative conditions 2-73 has been shown to be efficacious, the endoplasmic reticula (ER) have become physically and chemically detached from the energy-supplying mitochondria.
To summarize, 2-73 at effective doses simply fails to disrupt or interfere with any normal cellular or systemic process. It therefore has no known side effects.
Those who wish to base their AVXL investment decisions on the dismal prior records of failed or weak AD drugs are free to do so. But, as a biologist, I understand 2-73's unique biochemistry. No comparison whatsoever to any other AD drug.