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Why Stay If Quick Dollars Are Desired?
I marvel at the several (well, many) posters lamenting every sort of development and non-development that putatively keeps the AVXL share price suppressed. The vast majority of postings lay out these concerns.
Why so? What, perchance, causes otherwise astute small-cap investors to think any very promising start-up biotech is somehow going to cause ever-increasing share purchases — before the company has any approved drug or device to sell? Not a penny of sales revenues; yet so many think that, somehow, the AVXL share price should, right now, be on a steep, continuing, ascending curve.
Why hold positions that will be going nowhere at least until Anavex Life Sciences Corp has a drug that it can sell?
Of course, that’s a question only for the momentum, day-trading types. DOLLARS NOW is the guiding theme. But how many such dollars have been gained in the last year? Best of luck to those playing that game. I wish you well, indeed. But so far, not too rewarding.
But many AVXL share holders took market positions only as long-term investments. Personally, I’m not (much) anticipating any new dollars in my bank account until at least 2023. Dead money, as it were, until then.
But I understand the foundational, revolutionizing Anavex science, with enough confidence to have allowed me to confidently expend several thousand dollars to purchase shares.
Only two possible outcomes. Bad; the company fails to gain permission to sell any of its several breakthrough drugs. With that, I lose my money (which, carefully, was money I could afford to lose). Or, good; by 2023 Anavex Life Sciences Corp sells treatment drugs for millions of people, worldwide, with a variety of central nervous system and other diseases. At $500 to $1000 per share, I’ll be very satisfied. Dividends, alone, will be my reward. The equity position remains in my estate, to be passed on to beneficiaries at my demise.
Let’s watch. In time (not this year or next), Anavex science will prevail; big time.
Indications of the Anavex Future
As a biologist, I’ve scrutinized any number of otherwise obscure research reports dealing with Anavex sigma-1 receptor agonists. The most revealing and indicative are the many reports of the Anavex molecules acting in murines, lab rats or mice, against a range of diseases and conditions.
Those reports, coupled with Anavex researchers laying out various molecular and cytological mechanisms of action of their sigma-1 receptor agonists, prompted me several years ago to take a position in AVXL equities. I didn’t bet my ranch; used only discretionary funds whose loss would not impact my financial status in any way. As with all continuing to maintain a strong AVXL position, I’ll either lose my investment, or, in time (a few years, at least) it will be handsomely rewarding. Here is my analysis and perspective of the most recent Anavex information, at this URL:
https://www.anavex.com/wp-content/uploads/2018/07/Anavex-AAIC-2018-DT-01-Presentation.pdf
More so than ever before, I’m convinced my investment in Anavex Life Sciences Corp was a good one. Here are my thoughts on the matter.
Could an Anavex molecule actually stop or reverse the universal progression of Alzheimer’s dementia? This was indicated by a number of murine studies. The unique abilities of the Anavex drugs (orally administered) to ably cross the blood/brain barrier and become incorporated inside neurons (nerve cells), and thereafter restore previously lost nerve functions was both demonstrated in murines, and the mechanisms of these actions were graphically described.
But all of that was only in animals. In humans? Yes, there, too; but only in a small population of Australians, in a clinical trial whose goal was merely safety and tolerability, not efficacy. Wonderful results for a significant portion of those trial participants. Safe (no disqualifying side effects), and tolerable (dosages effectively determined).
The larger question, now, is what fraction of a large, generalized Alzheimer’s population might favorably respond to Anavex 2-73 treatment. That small Phase 1 clinical trial was insufficient for this determination.
Now, plans are underway for a full-scale double-blind, well-controlled clinical trial of Anavex 2-73 against Alzheimer’s disease. I’m eager to learn how that trial turns out. But with the new information just released, it's almost certain that clinical trial will yield data allowing (well, forcing) FDA approval.
Now, Anavex has discovered genomic factors that predispose Alzheimer’s patients to favorable treatment by Anavex 2-73. Those with the disease and the favorable genes will have their Alzheimer’s symptom prevented from progressing, or have them suppressed. Either outcome exceeds any existing standard of care.
The genomic factors were anticipated; now known, and they will be used to select participants in the up-coming Phase 3 clinical trial. In effect, Anavex now gets to include only those who will favorably respond to treatment; having the pre-tested genes for such.
Wonderfully, the recent Anavex announcement indicates that about 80% of Alzheimer’s patients have Anavex-favorable genes. Until this was announced, the number of Alzheimer’s patients that could be treated was unknown. Now, it’s known — four out of five. Moreover, genetic testing can pre-select patients, so the 20% that are not open to Anavex treatment will not be unsuccessfully subjected to it.
To gain FDA approval for a new drug, it must be a) safe (few side effects), b) be efficacious, yield positive treatment outcomes, and c) equal or eclipse existing standard of care drugs.
The new information raises no safety issues. As in both murines and humans, the Anavex molecules are safe.
The big Phase 3 clinical trial will reveal significant, positive treatment outcomes for the vast majority, or universal fractions of trail participants. Anavex has everything stacked in it’s favor: include in the trial only those with treatment-favorable genes. Significant positive clinical outcomes are now assured.
Lastly, any of those treatment outcomes will eclipse the treatment outcomes of any existing Alzheimer’s drug. The standard of care is presently minimal; merely slowing for a moderate period the rate of symptomatic decline. Every shred of evidence, both murine and human, indicates Anavex 2-73 will either stop the progression of Alzheimer’s symptoms, or even reverse them. With either of those outcomes, FDA approval is mandated.
In summary, the biggest news is the determination that 80% of Alzheimer’s patients have Anavex-favorable genes. Clinical matters will progress more slowly than wished, but I have a five-year perspective on my AVXL investment. Today, I’m confident that in five years my Anavex holdings will be quite valuable, and more importantly, Alzheimer’s disease will, for at least 80% be wonderfully treatable.
The 80% Factor
A key finding revealed in the PDF:
Majority of AD population, about 80% has no variant SIGMAR1 gene, hence the majority of patients is expected to benefit from ANAVEX®2-73.
Anavex Anti-aging Factor?
One key insight for me was confirmation that endogenous S1R ligand depletes, in particular with age. Thus the need for 2-73 or other exogenous ligand.
Investment Public Gives Not a Hoot About MRIs
Yes, those of us who know are excited, encouraged about the (rather certain) probability that MRI or other new diagnostic methods will allow Anavex Life Sciences Corp to favorably select for any of its up-coming clinical trials patients with elevated, positive responses to Anavex 2-73. Keep out non-responders; test only on people who will respond favorably. With that, the clinical deck is stacked in Anavex’s favor. Test the drugs on populations of people pre-determined to have the genes or other factors that positively respond to Anavex treatment.
Still, for the vast majority of biotech investors, none of that will prompt new, higher-price AVXL buying. Those folks will wait until they see actual human, clinical trial outcomes. When any of those are positive, AVXL has a certain profitable future. Until then, before clinical results are learned, it’s all conjectural. The only thing that will drive AVXL prices significantly higher (say, >$10), will be real clinical results on real, diseased people.
Info That Will Elevate the AVXL Share Price
Personally, I’m not envisioning any dramatic share price change coming out of tomorrow’s conference.
After accumulating a few hundred shares of AVXL in the last several years, after following all of the message board postings, corporate announcements, and, as a biologist scrutinizing all of the related Anavex science (which is exceptional), experience reveals that “the market,” whether retail or institutional, simply isn’t going to commit to any elevated share price on the account of whatever is revealed at tomorrow’s conference. Whatever is mentioned, it will be dismissed, disregarded, or neglected. Everyone who knows “real stuff,” knows that Alzheimer’s and other central nervous system diseases are simply too hard for some start-up biotech firm to conquer. Out of hand, Anavex information of any sort is summarily disregarded. So, too, will be whatever is mentioned tomorrow, I think.
But, will I then be liquidating my small AVXL holding? Nope. In time, matters will progress importantly and successfully. Anavex science (for those who can understand it — very few, even among medical professionals) will eventually prevail.
Here are the things low-info biotech investors would, eventually, respond to:
1. A detailed account of the now multi-year symptomatic outcomes of the majority of the Australians in the original Phase 1 study; from the 50 or so who have elected to continue to take Anavex 2-73, telling how it has either stopped the progression of Alzheimer’s symptoms, or even reversed them.
2. An official Anavex or FDA announcement of favorable suppression of Rett syndrome symptoms, with few or absent side effects, after a short or moderate treatment period. That would irrefutably validated the treatment validity of Anavex drugs.
3. An announcement by Australian medical officials that for bioethical reasons the 450-patient double-blind Anavex 2-73 Phase 3 study is being terminated preliminarily. Virtually all of the Alzheimer’s patients blindly taking Anavex 2-73 had the progression of their dementias terminated, with many experiencing increased, normalized cognition. By the bioethics rules of double-blind clinical trials, it is unethical to continue the study with the placebo arm, 150 Alzheimer’s patients who would unnecessarily continue to degenerate.
4. Similarly, an announcement that the European clinical study of Anavex 2-73 against Pakinson’s is terminated for bioethical reasons of profound safety and efficacy.
5. Baring any of the above, announcement by either the FDA, Australian, or European medical authorities of marketing approval for any Anavex drug against any disease.
I see nothing else that could turn the investment public’s perspectives on Anavex Life Sciences Corp. I’m willing to wait. It'll be a few years, perhaps.
Alzheimer’s Genetics Database To Be Available
The National Institute on Aging Genetics of Alzheimer's Disease Data Storage Site (NIAGADS) will begin making large-scale DNA sequence data available to investigators.
...
"Genetic findings for Alzheimer's disease are critical for identifying targets for therapeutic development," Wang said. "Making these data available is particularly important since there is currently no treatment available that prevents or alters the course of this common and devastating disease."
Aging A Mitochondrial Dysfunction?
A new report, on mice, shows that when mitochondrial function was chemically disrupted, the mice aged extremely fast, promptly having hair fall out and skin wrinkling.
Then, the factors disrupting mitochondrial function were withdrawn, and the mice promptly resumed normalized hair and skin morphologies. Systemically (related to skin and hair) the chemically-aged mice were rejuvenated, because of restored mitochondrial function.
https://www.nature.com/articles/s41419-018-0765-9
The Sleep/Alzheimer’s/Anavex Connection
A new report lays out details of how poor sleep may induce, cause Alzheimer’s disease. Lot’s of details here:
https://www.sciencenews.org/article/sleep-brain-alzheimers-plaques-protein?utm_source=email&utm_medium=email&utm_campaign=latest-newsletter-v2
We note that improved sleep was an outcome of the first, short Anavex 2-73 clinical trial, in Australia. Sleep problems, deficiencies, are a typical symptom of Alzheimer’s disease, markedly and negatively affecting patient well-being.
Might the following scenario eventually be discovered? Anavex 2-73 is prescribed to middle aged or older people when the very first, very minor symptoms of Alzheimer’s appear. These folks are still in good health, fully functional in every mental capacity. But memory is starting to slip. And, these folks are no longer sleeping well.
After taking the Anavex 2-73, healthful sleep resumes, and continues with Anavex dosing. Then, it is discovered that full, fast-acting memory has been restored.
In this case, the Anavex drug functions because it allows the body to sleep normally, thereby allowing it to also clear the protein wastes that inhibit nerve functions.
Anavex causes, allows proper sleep. The resulting healthful sleep then allows the body to normally clear toxic protein wastes. Alzheimer’s disease onset and progression are therefore thwarted.
Might the Anavex/good sleep connection be at least one reason the Australians in the early Anavex 2-73 have almost universally elected to continue with the drug?
Alzheimer Drug Failures Taint Consideration of Anavex 2-73
A report tells how the people who really know about Alzheimer’s treatments, Alzheimer’s drug researchers, come right out and say that there is nothing, now, that can be a breakthrough Alzheimer’s drug:
Sixteen years ago they projected the impact of a breakthrough drug for AD with two scenarios: one in which this hypothetical drug delayed disease onset and the other in which the new drug slowed disease progression. Unfortunately neither scenario has come to pass. Since 2002 over 100 promising drugs for AD have entered clinical trials but not one has proved sufficiently effective to be approved for patient use.
Implications, Revelations of Continued Australian Post-trial Dosing
Whether for physical or mental reasons, it seems the phase 2 participants have no desire to do without.
Yes, Early Thinking About Two Anavex Questions
Two significant clinical determinations must be made.
1. Will Anavex 2-73 restoration of neuron architecture and function persist after a reviving initial treatment period without continued dosings?
If treatment must be chronic, continuing, that has economic implications for health insurance companies and patients; along with persisting revenue streams to Anavex Life Sciences Corp.
2. Will Anavex 2-73 demonstrate central nervous system disease prophylaxis, prevention before major disease symptoms occur?
If so, there would likely be widespread, perhaps universal prescription of the drug to people when they attain late middle age. Profound financial implications for all health care stakeholders (and for Anavex Life Sciences Corp).
The greater question is the latter, the prospect of Anavex prophylactic use against any number of CNS diseases and conditions.
We’ll all be watching these things in the coming years.
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.
Extrapolate, Then, To Alzheimer's, Parkinson's?
Thank you.
Would someone competent in the use of a simple calculator be able to extrapolate those numbers over to an eventual FDA approval for either Alzheimer's or Parkinson's? Of course. And those numbers will need a lot of zeros. Orders of magnitude (means, "times 10"), with more Alzheimer's and Parkinson's patients in the world.
Shall all of us, then, await the results from the Australian clinical trial? In the mean time, learn to calculate big numbers by counting columns of zeros. Will be some useful 7th-grade arithmetic in a few years.
All depends, of course, on how the people in the Australian trial turn out; if symptoms are either stabilized, suppressed, or reversed. With any of those outcomes, start counting lots of zeros behind Anavex dollar signs.
Then, Tell Us, Please
Well, then, if Anavex Life Sciences Corp gets FDA approval to sell Anavex 2-73 to treat little girls with Rett syndrome, what will be the revenue stream to the company? Tell us, where will that send the AVXL share price?
Any special knowledge on the matter?
Rett Start May Be Totally Disregarded
It’s quite feasible that an announced start of the Anavex 2-73 clinical trial for little girls with Rett syndrome will affect the AVXL share price in no way whatsoever. How many stock investors, retail or institutional, have ever even heard of “Rett syndrome.” Like some here, it will be confused with some “Rhett” guy in a 1930s movie.
Then, there will be biotech investment experts (we have a number here) who will turn around and say that even if Anavex 2-73 gets FDA approval to treat Rett syndrome, with only a few thousand girls with the malady Anavex Life Science Corp could never make enough funds to even try to make and sell it for this “rare” disease. “There are other biotechs, fully established and profitable, that should be bought. Stay away from little Anavex. No future.”
The general investment public, retail and institutional, is unable to comprehend or appreciate the unique, proprietary, game-changing outcomes that will occur when – perhaps in a few years — Anavex Life Science Corp gets to sell any of the drugs in its pipeline.
Very good chance that will be in Australia, or perhaps Spain. AVXL share prices can’t take off until the general public reads stories about people (not the drug itself) that have gained suppression of CNS disease degeneration, or, even, had symptoms reversed.
When millions of families of American Alzheimer’s victims read of profound treatment and prevention outcomes with Anavex 2-73 in some foreign country, news media will write “interesting” stories on the phenomenon; asking what keeps that drug from being sold in the US. FDA: “Too dangerous, not tested enough to know if it’s safe or effective.”
Till all of that starts, two or three years from now, I’m just sitting back, stupidly holding my few hundred AVXLs. Dead money, for now.
But, then....!
“Homeostasis” Isn’t the Word
Understandably, a few posters have suggested that once the investing public learns of Anavex 2-73's ability to restore homeostasis in dysfunctional neurons, the resulting interest in Anavex Life Sciences Corp will push share prices higher. No doubt.
But “homeostasis” is a generalized biological term, with a multitude of accurate applications and involvements, not just neurons, by any means. The maintenance of normal body temperature is a homeostatic process. One sweats in hot weather to help return body temps to a normal, narrow range. You put on a coat in winter to maintain body temperatures; to maintain thermal homeostasis.
Homeostasis, in its classic understandings, is any body process that is maintained by the sensing of things moving too far from normal, followed by a responsive feedback that forces things back to within a normal range, as with body temperature, as mentioned.
Because a multitude of processes, cellular or systemic, involve some sort of homeostasis, the term is not really accurate, even useful in describing the therapeutic function of Anavex 2-73.
Yes, the molecule does restore the homeostatic interactions between the mitochondria and endoplasmic reticula in neurons, thereby restoring normalized neuron functions. Very healthful, indeed.
But it’s not useful to claim Anavex 2-73 “works by homeostasis.” The word, for those familiar with biological terms, is too generalized. Some other word or phrase, more descriptive and accurate, is needed.
Instead of “homeostasis” when referring to Anavex 2-73, I suggest “neural rejuvenation.” Anavex 2-73, by neural rejuvenation, restores neuron or nerve functions to a more juvenile, less diminished, more healthful state.
Of course, this will be objected to by those who are certain that there simply can’t be any drug that reverses the processes of aging, whether typical or pathogenic. For them, it would be bad form to even entertain the notion that some molecule might effectively restore diminished cellular functions that result from aging. A “fountain of youth” chemical is simply not looked for; is held to be not a possibility. Again, very bad form.
But, of course, virtually every major advancement in medicine for the last four centuries at its start, assailed and confronted accepted knowledge; was regarded at the time to be “bad form.” William Harvey; and blood circulation (arterial and venous functions). Semmelweis, Pasteur, and Lister; and the germ theory of pathogenesis. Alexander Flemming; and antibiotics. Many others.
Now (well, in a few years), Anavex? With neural rejuvenation?
The Cascading Perception of Diverse Anavex Solutions
Ponder the potential public perceptions of three positive Anavex clinical trial results, likely to appear within a year or two.
First, the new trial with 300 Australians with Anavex-favorable Alzheimer’s genes taking Anavex 2-73. I contend it won’t take the entire 48 weeks of that trial for the public to learn of the drug’s efficacy. Last time, word got out that a few Alzheimer’s patients resumed playing the piano well, painted pictures again, etc. That was in a trial with only 32 random, un-selected folks. How Anavex or Australian medical people will keep positive results hidden for the entire 48 months will be interesting. Doubt that it can be done.
Then, perhaps even before the 48 weeks of the Alzheimer’s trial is completed, some mothers with Rett Syndrome little girls (disease happens only in females) may begin to exclaim how their children are sleeping normally, have reduced fits and increased, normalized motor control. That will make front page news stories with about the third mother telling about the successes of her little girl taking “that new, wonderful drug.”
Then, from across the pond, reports begin to appear that Anavex 2-73 is bringing symptomatic relief to Europeans with Parkinson’s.
At that point, the contentions that I and a few others have made — who understand the biochemistry of the Anavex sigma-1 receptor agonist and it’s ability to restore normalized neuron functions, applicable to a diversity of central nervous system diseases — will be then regarded not as hypothetical or dreamy; rather, as real and applicable. Imagine for yourself the news articles that will begin to appear on the topic. Imagine the article titles. (You can do that yourself.)
At its start, Had some retired high school biology teacher claimed that Alexander Fleming’s work with a culture-contaminating mold would eventually result in a totally new class of antibiotic therapies, which would save millions upon millions of lives, that bloke would have been about as highly regarded as a more contemporary retired biology teacher (me) who has proclaimed that Anavex sigma-1 receptor agonists will decidedly change 21st century medicine.
It took a decade of work, and the onset of a world war to get Fleming’s work into commercial production of millions of doses of penicillin. Anavex needs neither. Just the results from one or two of the upcoming clinical trials. Everything will be different and fall into place, then.
Will be fun to watch.
$$ First
The Science doesn't seem to break through until there is a guarantee of money associated with it.
Let me clarity.
For Anavex, it'll be market psychology, alone, UNTIL it has a drug it can sell, whether in Australia, the US, or elsewhere.
When a drug can be sold, equity investors will then look at drug market sizes, potential profit margins, corporate revenues, etc. Those, of course, will depend on the validity of the drug's science, as demonstrated in the clinical trials that allowed authorized drug sales approval.
I'm not an active investor, buying and selling multiple positions. I have two buy and hold long positions, both biotechs — for which I expect no returns for five years or so. Then, my patience will be rewarded. AVXL will pay off big for me. I have an even smaller position in LXGTF. The profit-making science underlying both of these is extremely strong, allowing each company to meet un-met medical needs.
But neither are for the buy-and-sell types. Buy, hold, and wait. Dead money, as it were, for the “make it big now” types. I’m not trying in any way to compete with the day-traders, momentum riders, etc. In that regard, I’m not an “investor.” I’m merely a dumb shareholder, with patience. Check back with me in, say, 2023.
No Attention To The Science. Not A Factor
For several years, now, I’ve tried to find the correlations between biotech share prices and the science that underlies each biotech firm. For biotechs addressing CNS diseases, such as Biogen and Anavex, there appears to be virtually no correlation. I conclude that the majority of biotech investors, both retail and institutional, either don’t understand the basal science of the firms they invest in, or, for whatever reasons, elect to look at other extraneous factors to control their buy and sell decisions.
Biogen announces that their Alzheimer’s drug, a monoclonal antibody, for the first time actually caused an undisclosed degree of amyloid reduction in Alzheimer’s patients. Also, the drug slowed the progression of the severity of the disease’s symptoms. Consequently, Biogen share prices elevated rather sharply.
Of course, the drug had to be administered intravenously, at doses high enough that for some it caused brain swelling. The actual degree to which it slowed the progression of Alzheimer’s was not clearly told.
I won’t lay out the science of Anavex Life Sciences Corp, demonstrated in both murine and human subjects. Were I to do that, my point would be strongly affirmed by the Anavex critics who would then quickly lay out — as they have over the last several years — their noted deficiencies in Anavex science.
It’s clear, very few invest in Anavex (or Biogen, et al.) because they believe the underlying science is sound and will yield marketable drugs. Instead, they “read the market” and figure out how the majority of science-ignorant investors will respond to their hazy perceptions of a company’s future.
Presently, “the market” thinks Biogen has a big future; that it finally has a new, big treatment for millions of Alzheimer’s patients. Shareholders are going to get rich, for sure, now.
“The market” also knows with full confidence that little Anavex can’t possibly have a future. The company could show that some people taking their drug had an almost complete reversal of their severe Alzheimer’s symptoms, and no one would pay any attention. Wait......? (Point proven.)
A few of us, on the “outside,” with small to moderate long-term AVXL positions, will continue to watch the Anavex story develop; fully expecting overwhelming pronouncements of Anavex deficiency and decline until some national medical authority grants marketing permission for an Anavex drug. Then, against all that the really smart biotech investors know, a few might buy in, thinking the company, at last, might be somewhat profitable.
Until then? We’ll just read and watch. Biotech investors know their stuff. It’s virtually unrelated to any science, any mechanism of action, or actual therapeutic outcomes. It’s only what they think “the market” will perceive. Market sociology and investor psychology, only. Until Anavex gets formal approval to sell a drug somewhere, I’ll just sit back and watch. It will only be more of what we’ve been watching for three years now. The science is irrelevant. It’s market psychology, alone.
No, your interpretation of the intent of my posting is completely wrong.
Discerning readers will understand.
Well, Biogen, Someday, Might Compete With Donepezil (Aricept).
Important, defining excerpts from the Biogen new release:
The study achieved statistical significance on key predefined endpoints evaluating efficacy at 18 months on slowing progression in Alzheimer’s Disease Composite Score (ADCOMS) and on reduction of amyloid accumulated in the brain as measured using amyloid-PET (positron emission tomography).
This release discusses investigational uses of an agent in development and is not intended to convey conclusions about efficacy or safety. There is no guarantee that any investigational uses of such product will successfully complete clinical development or gain health authority approval.
Right to Try Not Likely
Use of new "right to try" provisions of anticipated or in-process legal maneuvers for Alzheimer's patients wanting to try Anavex 2-73 is not likely to be allowed. Anavex lawyers, most likely, will tell the company to not make the drug available outside of formal FDA approval of the drug, for anticipated (however minute) liability reasons. If even one person taking Anavex 2-73 under new "right to try" laws got any sort of untoward outcome, such as a heart attack, even if covered by the right to try law, Anavex Life Sciences Corp could be tied up in any number and sort of legal machinations and procedures it simply wouldn't wish to contend with.
Given the propensities of various portions of the legal profession to undertake actions against "big companies" for putatively altruistic purposes (ha), I seriously doubt Anavex Life Sciences Corp will ever allow its drugs to be sold or used in a "right to try" setting. Very quickly, that becomes a "right to try" for lawyers --- right to go to trial.
A Trial “Failure” Could Be A Great Success
Conduct of the announced clinical trial in Australia will yield incontrovertible results. It will be double-blind (no one knows who’s getting what), in three arms; approximately 150 Alzheimer’s patients taking a starch pill that looks and tastes exactly like the real ones (this, the control or placebo arm); then, two other arms of about 150 each, taking two different dosages of Anavex 2-73, the experimental arms. The trial is to run for 48 weeks.
In the earlier Australian clinical trial of Anavex 2-73, conducted only to assess dosing tolerability and safety (not actual efficacy against disease symptoms), only 32 patients were involved. Of those, six were apparent “super responders,” people for whom Alzheimer’s symptoms did significantly regress. It has been contended that those results cannot be relied upon, inasmuch as the clinical population was tiny; that such results could well have been mere chance, not a result of Anavex 2-73 per se.
Perhaps more significant, however, has been the request by trial participants in that study to continue to take the drug for an extended, continuing period after the formal trial ended. Readers will have to determine for themselves why those requests were a) made, and b) agreed to by Australian medical authorities.
Of course, Anavex has conducted precise genomic analyses on people in that first study, and have been able to discover statistical correlations between various genomic sequences (genes) and behavioral outcomes related to the Anavex 2-73 dosings in the study. With those data, participants in the new, much larger study are to include only those with Anavex-responsive genes. Of the 32 participants of the original study, six were “super responders,” about 18%.
This time, those exhibiting favorable treatment responses should be much higher, because they have been genomically pre-selected for favorable outcomes.
But, let’s imagine that the genomic selections were not accurate; that, in fact, genomic analysis was unable to accurately determine those Alzheimer’s patients most likely to respond well to Anavex 2-73 treatment. What if only 18% of the 300 people taking the drug get substantial relief, reversing debilitating symptoms so that a normal life could be once again lived? Would that be a clinical failure of Anavex 2-73? Let the reader discern.
But, here’s an alternative outcome that must be considered. There is a biochemical basis for it.
Let’s presume that, indeed, only 18% of the 300 people taking the drug in the upcoming Australian trial really gain, strong, discernable symptomatic relief. Good enough (or, not). The real issue is with the other 82% who did not show a strong, symptomatic turn around. How did the drug affect them? It clearly didn’t make them any better.
But what if, for the 48 weeks of the study, they all maintained the cognitive levels they had at the start of the trial? For 48 weeks, they didn’t get any better; just stayed the same? That would be a clinical failure of the drug?
What are the clinical implications if Anavex 2-73 turns out to be a drug that instead of reversing Alzheimer’s symptoms it merely stops their progression to ever-greater levels of severity?
What if the study determines that, at the least, symptoms will be maintained at the level of first administration of the drug? Would there be any market for a drug that might successfully prevent the progression of Alzheimer’s dementia at stages when it is first discovered, when patients could still live reasonably normal, non-institutionalized lives?
My father, tragically, succumbed to Alzheimer’s. He was an accomplished pubic accountant, with a well-developed practice. In his mid-60s, he and the family noticed a slowing of his mind. He could still think and relate with people; but at a slower pace. After several years of the continuance of his cognitive decline, he gave up his accounting practice, and in five or so years he mentally decayed to utter social debility. Like so many with the disease, he died in utter mental decay in an institution.
Such would not have been the case, were Anavex 2-73 available, and prescribed to him in his 60s, when his mental capacities first started to slow. Holding his cognition at that only slightly-reduced level would have allowed him to live an otherwise very normal life in his last decades.
So, I contend that if the Australian trial of Anavex 2-73 merely stops the progression of Alzheimer’s cognition decline, it will be a great success. That would be far better than the few approved Alzheimer’s drugs presently on the market. They don’t reverse or stop the progression of symptoms; they merely slow, for a time, their progression.
The biochemistry and cellular biology that would account for Anavex 2-73's ability to hold neuron functions at start-of-dosing baselines is reasonable. Simply, the molecule prevents the progression of neuron organelle dysfunction at an early stage. Where neurons are rather completely disrupted, where mitochondria and the associated endoplasmic reticula are no longer in proper chemical and mechanical alignment, Anavex 2-73 may not be able to restore the chemical collaborations of those two essential organelles.
But the presence of the drug, before things become profoundly misaligned, may well prevent progression to neuron dysfunction. Which national health service or medical insurance company wouldn’t support, endorse, and use such a drug for Alzheimer’s patients at their earliest diagnosis? A great success.
Reversal of Alzheimer’s symptoms would be great. Hope it will happen. But the mere suppression of their progression would be significant — better than anything on any pharmacy shelf. I see a very high chance for this.
“Perhaps” No Longer the Controlling Word
Until now, everything about Anavex Life Science Corp and it’s untested drugs was stated or regarded with words such as “Perhaps.”
“Perhaps Anavex 2-73 might yield some unique, helpful CNS disease outcomes. But no way to know yet.”
“Perhaps the molecule does, indeed, re-connect neuron organelles, allowing the restoration of normalized function. But not known with any certainty.”
“Perhaps Anavex 2-73 will be therapeutic for Alzheimer’s patients. But no way to know that without a proper, large-number double-blind clinical test.”
Now, statements about Anavex Life Sciences Corp and its drug Anavex 2-73 will no longer include the words “perhaps” or “maybe.”
The conduct of a large-scale, double-blind clinical trial, authorized and monitored by a modern nation’s medical control agency (in Australia) removes a lot of “maybe’s.” Anavex skeptics can express each of their previous cautions and warnings about the company and the drug’s insufficiencies and information gaps. But many of those are no longer valid.
A 48 week clinical trial, double-blind and placebo-controlled, is the gold standard of clinical drug trials. No one, pro or con, will be able to persuasively argue against whatever results appear from the trial.
The mere fact that Australian medical authorities have authorized and will monitor the trial is extremely affirmative. They don’t have any “concerns” or mis-givings about either the drug itself, nor the conduct of the new trial. They’ve given the go-ahead; pulling the air out of the so-often posted statements, here, of inadequacies of multiple kinds.
In short, Anavex Life Sciences Corp, and Anavex 2-73 are legitimate; not conjectural, “maybe” or “perhaps” entities any more. Anavex is now playing on the big stage, with a full script, with the best critics in the opening night audience. The program tells the unfolding story: The new drug Anavex 2-73 will be precisely tested on precisely selected Alzheimer’s patients who have the highest chances of gaining degrees of symptomatic relief. 450 actors, in three concurrent acts. On stage left, those getting a low dose of the drug. On center stage, actors getting a high dose. On stage right, those getting a starch pill that looks and tastes like the real pills the other actors are getting.
Come Thursday morning, who will be at the box office clamoring for tickets? Surely, a bunch of back of the house retail types; those who have been following the Anavex story, but awaiting “real news.” They have it, now.
But shoving their ways to the front of the lines will be investment fund managers, and higher-ups in pharmaceutical companies. Both will be greatly affected by how the play ends, how the plot turns out.
Will be fun watching how the investment and pharmaceutical press communities tell the new Anavex story. “Perhaps” will be replaced with “Will be closely watched....”
Most of us, here, have our tickets (well, AVXL shares). Will be one of the best stage shows in a long time.
Population Fractions with Favorable Genetics Yet Unknown
I’ve seen no occurrence data, related to any of the various genomic traits associated with Anavex 2-73 efficacy. Study of the genes of the people in the early Australian study (just 32 people) revealed particular genetic tendencies toward Anavex 2-73 efficacy. In short, there are coordinated clinical and genetic data showing the drug works with particular efficacy in people with particular genes.
So, what if only 10% of people with Alzheimer’s have genetics that predispose them to effective treatment with Anavex 2-73? If that were the case (I don’t see that it will be), the drug would still gain rather immediate FDA approval, for those many millions with such genomic profiles. Anavex Life Sciences Corp would have a still large, profitable market for it’s new drug.
Anavex 2-73 re-connects and supports proper, normalized functions of mitochondria and the associated endoplasmic reticula. It may well be that those with advanced, chronic cases of Alzheimer’s have their neurons so diseased the Anavex 2-73 simply can’t put things back together again. Too far gone. It’s very reasonable to presume that Alzheimer’s progresses to states of such profound cellular dysfunction that the Anavex drug (or any other) simply cannot put things back together again.
Not yet tested (but may be revealed to some extent in the new Australian study) is the effect of early administration of Anavex 2-73. Most likely, earlier Anavex treatment is better treatment. Instead of waiting until patients have moderately advanced stages of the disease, prescribe and administer the drug just as soon as the first symptoms of dementia appear. Then, even at low intra-cellular concentrations, Anavex 2-73 can “fix things” before they become irreparable. Prophylaxis; prevention, at an early, even pre-symptomatic stage.
A number of dosing matters need to be determined. When should dosing begin? What symptoms should dictate when a physician prescribes the drug? What should be the dosing regimen: frequencies, dosing quantities? Might more advanced cases of Alzheimer’s best respond to IV dosings?
All, yet to be determined. No matter. With any clinical efficacies discovered in the upcoming Australian study, Anavex Life Science Corp has a great future, along with its shareholders and client patients.
A New Study, So Much More At Stake
Will clinical results of the new Australian trial of Anavex 2-73 be, in any appreciable way, different from those in the first Australian trial, which a) tested merely for tolerability and dosing levels (not efficacies, per se), and b) had but about 32 or so participants?
Here are differences to weigh.
The initial clinical trial in Australia had 32 mild-to-moderate Alzheimer’s patients. The new trial is to have approximately 450 patients, 14 times as many as the first study. One third (approx. 150) will receive one dosage level of the drug, another third will receive a second, different dosage, and a final third will receive a placebo dosage. The 48-week study will be double-blinded. Neither patients nor medical people will know who is getting which of the three dosages. All of the pills will look and taste the same. Only a computer code will know who gets what.
Anavex skeptics expressed the opinions that results from a mere 32 patients were insufficient to determine clinical efficacies. The few very positive clinical results were, it was claimed, merely happenstance. A larger clinical population, it was contended, would more accurately determine actual large-population efficacies that could be extrapolated to a large, national Alzheimer’s population.
So, this new trial has a statistically significant, large “n,” number of participants. And, the study is placebo-controlled. The placebo arm, of about 150 patients who think they are taking the drug (but are consuming a visually identical starch pill) will yield viable “results” against those from the other two, experimental arms; people taking the real drug.
The original study was a game played with but a single deck of 32 “cards.” Now, it will be three games: placebo, dosage 1, and dosage 2, each played with 150 “cards.” And, until the end of the trial, no one is to know which deck is being used in each “game.” Double-blind, in all three arms.
In the first Australian study of the initial 32 participants, the only clinical selection criterion was a medically-diagnosed Alzheimer’s condition.
But, this time, not only will there be three large dosage arms in the study, involving a total of 450 mid to mild Alzheimer’s patients, but each will include “genomic precision medicine biomarkers identified in the ANAVEX®2-73 Phase 2a study.” If participants are limited to those with both Alzheimer’s and the pre-determined genomic biomarkers associated with Anavex 2-73 efficacy, it’s a wholly different kind of study. This time, it will include only those with genomic tendencies known now to be favorable to Anavex 2-73 efficacy. People lacking those favorable genes will not be included. Anavex has stacked the deck, including only cards (well, real people) who have the highest chances of responding favorably.
First, let’s presume that no clinical results of any sort appear, or are released until the formal end of the study. Whatever those results will be, they will be altogether and in every respect definitive. Either Anavex 2-73 provides favorable outcomes as a treatment for early or mid-stage Alzheimer’s, or it does not. End of game; or start of a revolution in 21st century medical care.
But what if a good number of those in either of the experimental arms of the study, taking real Anavex 2-73, actually experience symptomatic reversal and relief in a few months of dosing? Just how might these frank (visually-discerned) results be concealed? Sure, doctors and nurses will not be allowed to relate any preliminary trial results, or personal observations. But how might Australian medical officials keep family members from sharing new, positive things they’ve noted in Aunt Matilda?
Will the efficacies of Anavex 2-73 require the entire 48-month study period to become evident to any interested public? Or, with two genomically-selected clinical populations in the study, will positive outcomes become so predominant and evident to family members that a profusion of anecdotal accounts of efficacy proliferate?
Personally, knowing the arcane biology of the molecule and the dysfunctional cellular organelles it rehabilitates, I think positive results will emerge before the formal end of the study — perhaps within a few months. Let’s watch.
Mitochondria, Endoplasmic Reticula Don’t Follow The Tape
Fact is, mitochondrial and endoplasmic reticular functions are not in any way disrupted nor enhanced by the AVXL share price. They are affected, however, very positively by Anavex sigma-1 receptor agonists.
The Anavex science stands. It’s perception by most shareholders will remain hazy until FDA-acceptable clinical results appear. Most shareholders are not scientists; didn’t take an Avavex holding for scientific reasons. They wanted to make some $$, and that derived from the hope for an increasing share price.
So, until trial results appear, the AVXL share price is going to wander up, down, and sideways, to the consternation or joy of those playing the swing-trade, day-trade, or quick-profit games.
Those of us holding positions we never had any intent of ever selling are looking for profitable dividend disbursements many years (not months) down the road. With some humor, we will continue to follow the postings here. We know what we have, and where it will end up for us. Holding tight. Holding long, no matter. The science will prevail. Someday, several years from now, dividend checks will be coming our way.
Best wishes to all, regardless.
Not All Investors Unable to Understand the Science
I would argue that the "dynamic complexities" of CNS diseases should cause investors to be highly skeptical of the simplistic notion that "restoring cellular homeostasis" by A273 will cure CNS diseases, cancer, pain, high cholesterol, insomnia, high blood pressure, etc.
Yes, but he retired at age 48. Sarcopenia got to him, too. The fate of us all, in time... UNLESS....
Might Anavex Prevent Sarcopenia?
Sarcopenia is the withering of muscles experienced with age. No 55-year old plays in the NFL.
The referenced article attributes mitochondrial dysfunction as a cause. “Decreased mitochondrial function is suspected to impede energy demanding processes such as skeletal muscle protein turnover, which is critical for maintaining protein quality and thus skeletal muscle health with advancing age.”
Anavex 2-73 and other Anavex sigma-1 receptor agonists restore normalized mitochondria-endoplasmic reticula connections, thereby restoring normalized protein (enzyme) production in the endoplasmic reticula. Might, then, an Anavex sigma-1 receptor agonist also restore specific mitochondrial function, thereby preventing sarcopenia?
From one perspective, not likely. Decline of mitochondrial function related to the onset of sarcopenia may be caused by the internal loss of mitochondrial function. The Anavex molecules re-connect mitochondria with external endoplasmic reticula. That may not effectively fix aging mitochondria, by themselves. Sarcopenia my involve only aging mitochondria, without regard to adjacent endoplasmic reticula failing to produce well-formed enzymes.
Or, the enzymes properly formed in attached endoplasmic reticula might also then get transferred and function well inside the mitochondria. With that, mitochondrial function is restored, and sarcopenia prevented.
All of this needs to be examined with aging rats or mice. Shouldn’t be hard to assess. Sarcopenic muscles are revealed in both anatomical and microscopic examinations.
But yet another potential Anavex application. Test it, someone. Good project for a master’s thesis, perhaps even a doctoral thesis.
An Anavex Veterinary Role Not Yet Considered
Yes, consider, if you will, a reversed development of Anavex 2-73. Humans to animals.
Virtually all drugs being proposed for human use are first tested on animals, usually lab rats and mice, testing for both safety and efficacy. Without such animal testing, without positive animal outcomes, no subsequent human testing is allowed or performed. Understood — because the biological mechanisms and chemical pathways of lab animals very much parallel those of humans.
Because of that, the paralleled animal/human similarities, what prohibits the use of new drugs targeted at humans back into animals? What is the chance that Anavex 2-73 (or other Anavex pipeline drug) might have a useful application for veterinary uses in farm animals?
Might it be discovered that Anavex 2-73 fed to feedlot cattle reduces anxieties, increases sleep quality, or inhibits various pathologies of close confinement; any of which thereby increases growth?
As I implied in my earlier posting on this, lab techs dosing and caring for lab murines dosed with Anavex 2-73 must accurately and precisely monitor and record all behaviors. Should Anavex 2-73 have induced any incidental, albeit peripheral good health benefits to any of those lab rats or mice, it would be noted and further investigated.
What if Anavex 2-73, incidentally, slowed aging and maintained reproductive abilities for longer periods of time. What if those dosed lab rats had better metabolism of their food? If any of this were so, then next start dosing feeder cattle in confined feedlots, or chickens in hatcheries and poult-production facilities. If production increases in any way, with no residual molecules or metabolites in derived market eggs or meat, Anavex Life Sciences Corp has a many billions of dollars new market segment.
In a few years, could Anavex Life Sciences Corp, or a spin-off, be a major veterinary drug supplier?
Schwab and BarChart both report merely 1760 shares traded today.
Strong Buy Recommendation
For what it's worth, BarChart now has AVXL as a "Strong Buy."
The Barchart Technical Opinion rating is a 88% Buy with a Strongest short term outlook on maintaining the current direction.
Longer term, the trend strength is Maximum. Long term indicators mostly agree with the trend.
How Many Might Anavex Treat?
Good question. What percent of those with Alzheimer’s might Anavex 2-73 effectively and efficiently treat? Presently, unknown, of course.
For a start, presently, the question is, what percent of the Alzheimer’s people in the upcoming clinical trial will be effectively treated? How many will benefit? With the ability to carefully select for the trail only those with Anavex-favorable Alzheimer’s genetics, efficacy rates in the trial should be very high, if not just downright remarkable. With trial results approaching any of that, FDA approval of the drug should be coming forthwith.
Will that mean, then, that Anavex 2-73 will work on only a small fraction of Alzheimer’s patients? If it’s for only 10% with the disease, Anavex Life Sciences Corp will be a success (and our AVXL share prices will be rewarding).
But there is good reason that the drug will help with the successful treatment of a diversity of CNS diseases — including, at least to a degree, Alzheimer’s cases lacking a strong genetic component. Why? Because in all cases the mitochondrial dysfunction I described in a previous post causes the problems. At least to a degree, if not altogether markedly, our drug restores cellular function (“homeostasis”).
Now, for people with advanced cases, where nerve function is significantly disrupted, after several years of debility, the drug may not be able to put things back together. At some point, Alzheimer’s may have incurred permanent, irreparable nerve damage.
But what hasn’t been yet tested or known is the prophylactic abilities of Anavex 2-73, the ability of the administered drug to prevent or reverse the onset of Alzheimer’s and other degenerative CNS diseases. Because of the drug’s unique and powerful mechanism of action, there is every reason to believe it will have profound prophylactic capabilities. Aunt Matilda might be prescribed the drug at the very first sign of memory deficiency. “Doc, I’m forgetting where I left my keys in the house.” “Well then, here, get this prescription filled. Your insurance company will be relieved. In a few weeks, you’ll be remembering all sorts of things. This new Anavex drug is really remarkable.”
Good chance that the biggest, most effective use of Anavex 2-73 will be to prevent or treat the early onset of CNS diseases. Giant global market for such.
Good Question --- Age and/or Genetics
What causes, then, the mitochondria to no longer function properly? What causes them to no longer connect effectively with endoplasmic reticula? Two probable reasons (and there may be more).
The first is simple age. No one can contest that by middle age, organs and tissues no longer function as well as in the first half of life. Mechanisms weaken. Likewise, in neurons. The structural chemistry holding things, literally, together, weakens. Anavex 2-73 re-connects and supports the otherwise weakened sub-cellular structure in the neuron.
In other cases, particularly with early-onset Alzheimer's, defective genetics prevents full structural architecture and function.
And, as the genomic analyses performed in the Australian trial have apparently discovered, there are specific genetic patterns that correlate very positively with Anavex 2-73 efficacy. The neuron aging process has genetic controlling components, which Anavex Life Sciences Corp has now discovered. With these predictive genomic data, the company will be able to select for the upcoming clinical trial of Anavex 2-73 only participants who have those specific Alzheimer's-prone, Anavex 2-73-favorable genes.
The trial process is now stacked in Anavex's favor. Only those who have Alzheimer's genes open to Anavex 2-73 efficacy will be allowed to participate in the trial. Precise stuff. "Precision medicine."
Ponder, then, who will benefit.
Mitochondrial Dysfunction Is the Root Cause of Alzheimer’s
According to the unique Anavex 2-73 mechanism of action, the root, basal cause of at least some Alzheimer’s cases (perhaps most or all), is the incomplete or error-prone folding of essential proteins (enzymes) that modulate and control proper, healthful neuron chemistry. These folding errors occur because the rough endoplasmic reticula, adjacent to and normally touching mitochondria, normally fold proteins into functioning enzymes.
This requires ample concentrations of energy-supplying adenosine triphosphate (ATP), which is synthesized in the mitochondria. In the case of Alzheimer’s, the endoplasmic reticula no longer functionally connect to the mitochondria, restricting normal transport of ATPs into the rough ER. With this deficit, there is insufficient energy to power protein folding. Hence, proteins are made, but they are improperly shaped and can no longer facilitate normal chemical reactions in the neuron. Consequently, toxic molecules are made and no longer removed or destroyed. Beta-amyloids and tau tangles accumulate, disrupting and slowing normal neuron and nerve function. Alzheimer’s symptoms present.
In review (briefly, incompletely), Anavex 2-73 re-connects the rough endoplasmic reticula with adjacent mitochondria, and restores normalized molecular and ion (Ca++) exchanges, allowing proper, normalized protein folding. Consequently, neurons and nerves function normally again.
As a large number of papers on the disease will attest, Alzheimer’s (and most other CNS diseases) is a disease of mitochondrial dysfunction. Anavex 2-73 restores effective ATP synthesis and transport from mitochondria into the rough ER. After that, things work normally.
Up A Dime in After-hours Trading
Just saw this: 3.88 +0.10 (+2.65%) 16:45 ET
AVXL trading at $3.88, up a dime 45 minutes after the market close.
How come? What could possibly prompt such after-hours trades, at an increased price? Why not wait for the opening tomorrow and see what happens?
Is a trend developing?
An “Expert” Responded.
Wrote me a private posting, telling that he recommended some time ago that I should have gotten out around $8 or so.
So, presently my understanding of Anavex science, at today’s close, is worth only $3.78. If it touches $4 tomorrow, should I liquidate? (Ha.)
Might the trend be my friend? What if real news breaks?