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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.
Poster Session Misunderstanding.
It is an error to presume poster presentations at scientific meetings are "relegated" to a reduced status, compared to oral presentations. Let me re-state an earlier posting I made:
Let me point out that at scientific meetings, the posting and presentation of poster data are just as valid and well-received — sometimes even more so — than oral presentations. To presume that a poster presentation of data is less valid or more poorly received than an oral presentation is an error. As a biologist (in a non-medical field) I've done both at national scientific meetings. I've presented graphically-illustrated oral presentations, and also hung detailed posters of my data. Both are equally valid.
In fact, professional readers of well-done posters often take away greater, more significant data. Photocopies of the poster are taken by all interested parties, and detailed discussions with the poster representative are conducted, one on one. In an oral presentation, Q&A time is often limited. In a poster session, where an author of poster data is available at the poster, lengthy, detailed, back-and-forth discussions occur, with the reader taking away far more cogent information than could have been gained in a time-restricted, large-venue oral presentation.
I have no concerns that Anavex's new data will be presented in a poster form. All will be well, with appropriate parties taking away detailed knowedge.
Poster Presentation.
Let me point out that at scientific meetings, the posting and presentation of poster data are just as valid and well-received — sometimes even more so — than oral presentations. To presume that a poster presentation of data is less valid or more poorly received than an oral presentation is an error. As a biologist (in a non-medical field) I’ve done both at national scientific meetings. I’ve presented graphically-illustrated oral presentations, and also hung detailed posters of my data. Both are equally valid.
In fact, professional readers of well-done posters often take away greater, more significant data. Photocopies of the poster are taken by all interested parties, and detailed discussions with the poster representative are conducted, one on one. In an oral presentation, Q&A time is often limited. In a poster session, where an author of poster data is available at the poster, lengthy, detailed, back-and-forth discussions occur, with the reader taking away far more cogent information than could have been gained in a time-restricted, large-venue oral presentation.
I have no concerns that Anavex’s new data will be presented in a poster form. All will be well, with appropriate parties taking away detailed knowedge.
Thank you.
This post is a concise and precise compendium of all of the cogent trials research on Anavex 2-73, first in rodents, then humans.
It appears that those who have elected to take profits by selling AVXL shares in recent days are utterly unaware or unable to understand the profound biological significance of these studies.
As I’ve stated several times before (as a biologist who comprehends the essential and utterly unique biochemistry of 2-73 and its cellular targets, the endoplasmic reticula and mitochondria), the existing studies of 2-73 show conclusively that a) it improves by significant degrees cognition in Alzheimer’s patients, in interestingly short periods (weeks, not months or years), and just as importantly (even more so, to get FDA approval), b) 2-73 simply evokes no side effects of any consequence whatsoever at efficacious dosages.
Now it is clear the majority of recent traders in AVXL are chartists or short-term day traders, playing short-term share price trends for moderate profits (compared to those Anavex will yield in a year or more). I am not a day-trader and have no expertise or interest in this investment approach. I wish those playing those games the best.
My small Anavex position will be held for at least a year. I won’t be selling a single share until Anavex (or its purchaser) attains Big Pharma status, with the literally billions of dollars of annual revenues 2-73 and the other drugs in the pipeline will generate.
Most of those buying and selling today are playing off their knowledge of price trends and charts. More power to them. Personally, I am guided by the profound science of Anavex. It will take longer for me to benefit, but I will be selling AVXL shares valued in three or four digits. The science and sociology (compassionate relief for millions of neurodegenerative disease sufferers) of 2-73 will, in the end, prevail.
Just as antibiotics changed medicine in the ‘40s and ‘50s, Anavex will revolutionize 21st-century medicine in the next decade.
One reputable source claims that there are 5 million people in the US with Alzheimer’s (each year).
Let’s presume (at this stage, only a presumption) that Anavex 2-73 is approved by the FDA and is prescribed and effective for all American Alzheimer’s patients. Let’s presume (perhaps too conservatively) that each patient pays $100 a month for the drug (about $3 a day).
At that rate, Anavex takes in $500 million a month. For a year, the company takes in $6 billion. Expand those revenues proportionately when considering treatments in other countries.
Similar numbers derive from Anavex 2-73 when it is used (eventually) for Parkinson’s disease. Then, add the other geriatric neurodegenerative diseases, such as multiple sclerosis, amyotrophic lateral sclerosis (Lou Gehrig’s disease), and the ever-expanding number of human conditions for which 2-73 might have efficacy.
Ten billion dollars a year in Anavex revenues — or multiples — are certainly reasonable, should 2-73 prove to have the broad-spectrum efficacy that animal and early human clinical data now strongly suggest.
There is abundant evidence that Anavex 2-73 restores and supports normal mitochondrial function, primarily by facilitating normalized junctions of the endoplasmic reticulum with the mitochondrion. Neurons (and other cells) can function normally when the ER connects properly to the mitochondrion. When they become disjointed, a host of neurodegenerative diseases occur (Alzheimer’s, Parkinson’s, Multiple Sclerosis, et. al).
A new report just appeared telling how mitochondrial dysfunction facilitates cancer. Although not directly implicating the sigma-1 molecule, the loss of normal mitochondrial function was determined to be a root factor in many cancers.
Now, all of the following is speculation, unsupported by any evidence.
There have been isolated references to 2-73 as a possible cancer therapy. If 2-73 can restore normalized mitochondrial function in cancer cells (as well as neurons), an entirely new, expansive mass of therapeutic applications might occur — effective treatment of many forms of cancer.
“...mitochondrial stress induces cancer-related metabolic shifts.”
(Unable to post the URL to this research, at the Univ. of Pennsylvania.)
I much prefer the Anavex biochemistry. Far more broadly applicable; treats a host of neurodegenerative diseases, at low dosages, with virtually no side effects.
I don’t see this as Anavex competition.
Yes, I’ve pondered this, the impossibility of blinding profoundly positive responses to 2-73 in any supposedly double-blind clinical trial.
Now, if 2-73 works slowly and moderately, it might take many months or a year or two before any symptomatic relief might be properly quantified. But there is not a scintilla of evidence that this will be the case; quite the opposite. Restoration of normal behaviors in transgenic dementia in mice has been rapid and rather complete. The two or thee humans who responded so well in the early (and short) Australian trials are examples.
I will not be surprised if the following occurs. When proper double-blind human trials of 2-73 are conducted on a statistically-significant number of humans clearly diagnosed with early-stage Alzheimer’s, it’s going to be very difficult to keep hidden to the patients themselves, their families, and care-givers the remarkable reduction of the symptoms that formerly portended miserable years for both the patients and care-givers. One needn’t be a trained geriatrics nurse to detect the restoration of normal, pre-Alzheimer’s behaviors.
The word will “get out.” Stories will be told how Grandma no longer needs care; she dresses herself, eats normally, converses as she did, and simply has no debilitating dementia since participating in the 2-73 trial.
If this were to occur with only a fraction of those in getting the drug it could be explained away as merely rare incidental outcomes expected on the positive tail of a bell-shaped response curve.
But I don’t think that will be the case. No animal data suggest responses on a depressed bell-shaped curve; rather, they are steeply ascending and rather linear.
The social implications of dozens of people in the trial “getting better” early on will be most interesting. With enough cases, media will jump on this, pointing out that the poor folks who drew the placebo arm of the trial are being screwed. They, too, need to get the drug.
Then, how many citizens will write heartfelt letters to their legislators claiming that FDA hesitancy in rapid approval of 2-73 creates horrible burdens on their Alzheimer’s relatives and care-givers? In the absence of side effects and adverse outcomes, the political pressures for FDA to grant compassionate approval of 2-73 will be great.
Will be engaging to see how all of this plays out. Gonna be tough for the clinics and clinicians to keep results “blinded.”
Honestly, I can’t contribute any useful information on 3-71. I’ve not taken the time to parse out arcane details of the several technical papers on the molecule. My understandings of it are only cursory, derived from a quick read of the text associated with the article links, to whit: it, too, suppresses tau tangles, among other good effects.
I find most interesting the markedly small efficacious doses of this substance: 10 micrograms per kilogram per day. The stuff is apparently very active (although these were daily injections, not the more humanly convenient oral administration — not an obviating factor, as any of us with a treatable neurodegenerative disease would make a daily injection for effective treatment, as with diabetes).
For me (right now, at least, before human applications are revealed), as with 2-73, two controlling factors are known (at least in animals so far): a) low doses are effective, and equally important, b) no detectable side effects or adverse reactions, at experimental doses 50k times efficacy rates.
I challenge anyone to find any approved, “safe” neurologic drug that shows no side effects at 50k times normal dosages.
The drugs of Anavex are unique, unlike any others. They work, and they work in low doses. I’m eager to follow the development and applications of 3-71 and any others that might emerge.
Let me say, parenthetically, that all of this and more is being understood by neurologists and biochemists in a host of Big Pharma firms and academic institutions. I’m just a common biologist, with a modicum of neurological and biochemical expertise, and I can see the Big Picture. The phenomenal traits and potentials of Anavex’s drug candidates are not being neglected or dismissed behind closed doors. Common retail AVXL share purchasers are generally oblivious to the ever more clear future 2-73 and Anavex’s other drugs in development will produce. They tend to regard AVXL as a nice little, obscure equity and might double in a few months, yielding a 100% gain. Those with such perspectives are welcome to them. I wish them the best.
But, quietly, behind closed doors, a lot of pharmaceutical officers and research and development people are talking more openly and accurately about Anavex. The released clinical data are just too gigantic and substantiated to dismiss. Financial editors and writers are pretty much clueless, cautioning readers that most new drugs fail to get approved, or fail to perform. Risky business investing in drug start-ups.
Wish I had some funds to take a larger position. For those with appropriate levels of biochemical and neurological knowledge, it is clear that 2-73 and the others have no parallel and can revolutionize modern geriatric medicine. Gonna be fun watching how all of this develops. The Big Show will start when the curtain opens on the next Anavex act, when applicable human trials results are revealed. Naysayers can easily dismiss lab rat and mice data. Mice are not men. When real human efficacy trials appear, watch out.
I am a retired advanced placement biology teacher. I taught the details of molecular and genetic biochemistry to dozens of students who went on to become physicians, biology researchers, etc. I conducted an extensive high school science research program, where my talented students conducted science research in industrial, institutional, and commercial laboratory environments. For their work, they won numerous state science competitions and attained undergraduate science scholarships.
In “retirement,” I professionally design and manage natural landscapes, primarily native tallgrass prairies and oak savannas. I am a contractor employee of NASA at their 6400-acre Plum Brook Station, where I oversee the eventual restoration of 3000 acres of native tallgrass prairies.
I maintain professional memberships in AAAS and other scientific societies, and closely follow a number of research directions, particularly those related to neurodegenerative conditions (one of which, hereditary spastic paraplegia, in mild form, I have myself — hence my intense interest in Anavex).
And yes (very off-topic), I maintain a holding in FSNR, Freestone Resources, continuing to believe the new management and production of their unique Petrozene product will facilitate crude oil storage and transport without the sludge buildup and corrosion raw crude oil induces.
As a biologist, I scrutinized this presentation. Once again, the presented data are incontrovertible, at this early research stage in murine (mouse) subjects. 2-73 clearly treats the cellular symptoms of Alzheimer’s (Tau tangles, A-beta accumulations), resulting in restored and normalized behavioral functions.
Importantly, the Alzheimer’s disease conditions were chemically and genetically induced in the mice, to thereafter discern 2-73's efficacy. This murine model of Alzheimer’s is exactly parallel to the conditions in human Alzheimer’s cells ---- where I fully expect equivalent efficacy.
2-73 was administered in the drinking water of the mice, not by injection. This oral administration was effective, without any noted side effects or adverse outcomes. This indicates that 2-73 is able to be effectively absorbed without digestion or premature ejection, and even more importantly, it is able to independantly cross the blood/brain barrier and be sufficiently absorbed by neurons. This favorable constellation of traits is exceptionally rare, and without the detailed lab work on the mice described in the presentation, would not be anticipated. Seemingly too good to be true. But the lab work authenticates the absorption observations. (The blood/brain barriers and cellular membranes of mice are essentially identical to human ones. There is no reason whatsoever to think these results will not occur in humans with Alzheimer’s.)
As I’ve posted before, Anavex 2-73 is not just “some other” new Alzheimer’s (and general neurodegenerative) treatment guess or gamble. Biochemically, it is in a class of its own. It works differently from conventional drugs, and it fixes the root cause of the majority of neurodegenerative diseases, the disconnection or malfunction of the mitochondrion-endoplasmic reticulum junction.
There continues to be an overwhelming belief that either amyloid-beta (A-beta) deposits or tau protein tangles are the cause of Alzheimer’s. Yes, those neuron abnormalities can be easily detected with microscopic examination of affected brain tissue. They are universal in those with Alzheimer’s.
But there is increasing evidence that A-beta deposits or tau tangles are merely a result of the root cause(s) of the disease, not the causes themselves.
The real question is this: What neuron abnormality allows A-beta deposits or tau tangles to occur?
In fact, elimination of either of these may simply fail to stop the progression of the disease. And getting the immune system or other cellular mechanism to selectively degrade and clear A-beta and tau proteins will be a daunting task; one likely to incur any number of unknown severe side effects. The clearing agent, somehow, must cross the blood/brain barrier and then ensconce itself inside affected neurons — without changing or affecting other normal neuron chemistries. Personally, I doubt this approach can or will work.
Instead, the root cause of Alzheimer’s neuron dysfunction must be addressed — and that’s exactly what 2-73 does. It restores normalized mitochondrial interactions and connections with the endoplasmic reticula, allowing the neuron to function normally. In virtually every neurological disease, mitochondria and endoplasmic reticula fail to properly connect, causing dysfunction in both organelles. In neurons, the results are always bad. Anavex 2-73
simply (without side effects of note, at low concentrations) uniquely reconnects mitochondria with the adjacent endoplasmic reticula.
Problem solved.
Yes, a lengthy, protracted clinical safety and efficacy period might be expected for the new Flex spasticity drug --- if it were conventional.
But, crucially, the active ingredient derives from some existing GRAS (generally accepted as safe) food component; merely placed by Flex in an oral pill form that is most-easily absorbed in oral, esophogeal, and stomach tissues.
Flex's claim of clinical availability of their drug to treat motor neuron hyperexitabiilty in 2017 is reasonable.
Yes, I’m increasingly hopeful that 2-73 can bring for me a more natural gait, etc.
The question of off-label usage hasn’t, to my knowledge, been much addressed or considered. Understandably, the primary therapeutic focus is on Alzheimer’s. Should 2-73 be therapeutic only for that disease, it (and Anavex) will be exceedingly successful. With a moderate but solid bit of emerging evidence, I’m hoping for that, at least.
What, however, might be the implications of FDA approval for, let’s say, Alzheimer’s at the beginning? Inasmuch as the molecule has failed in both murine (animal, mouse) and human trials to elicit objectionable side effects or adverse outcomes, I can see little reason practicing physicians might not eventually start off-label treatments for any number of diseases and conditions. “Take this. Let’s see what happens.”
Of course, when a physician does this he or see opens themselves up to monstrous tort actions. Medical tort lawyers will park the good doctor on the witness stand and force him or her to admit that standard medical practice simply does not yet support off-label usage of 2-73, and the adverse outcomes experienced by the lawyer’s client were a direct consequence of the physician’s inattention to safety and FDA recommendations, etc. The jury will find in favor of the aggrieved patient, of course.
So, before off-label usage begins, those receiving chronic 2-73 therapy must demonstrate safety, with few or no side effects.
Should that be the case — and I believe it will be — safe off-label use would then begin, against any number of diseases. As I posted, 2-73 already has demonstrated or projected favorable therapeutic outcomes for a wide spectrum of human diseases, including some unrelated to neurology.
As with everything related to this remarkable molecule and company, this is going to be fun to watch; and, perhaps, wonderfully rewarding to both patients and shareholders.
The Cognitive Deficit reversal data shown are important. All of this in five weeks.
But no one has (or is treated) for Alzheimer’s for just five weeks.
What, perchance, might these data be after five months, or five years of therapy? Human clinical trials will plot these data. Will the plot be linear, continuing to yield increasing good results as therapy progresses (I think that’s most likely), or, will symptomatic suppression be merely sigmoid (S-shaped), where symptoms decline a bit at the start of therapy, and for a period they are significantly less, but finally, at the top of the S, symptoms no longer improve.
Actually, that’s the plot of Alzheimer’s symptoms when treated by the common acetylcholinesterase drugs. For a short time, nothing good is noticed; then, for a short period of time (weeks or months), patients have more normalized cognitive function. But, finally, cognitive decline resumes, in ever greater degrees. Ultimately, the patient returns to profound cognitive decline, as though the therapy had not been used.
In summary, I’m eager to see long-term 2-73 therapies. I’m projecting that such therapies will continue to yield efficacy linearly — longer continues to be better, perhaps to complete, normalized function.
Hey, might that be a “cure?” Nope. 2-73 won’t change root genetic perturbations at the base of most applicable diseases. Not a cure any more than injected insulin can be considered a cure for diabetes. Diseases suppressed by 2-73 most likely will require life-long dosing (what a revenue stream that will be for the final owner of 2-73 rights).
The potential of Anavex 2-73 as a therapy for a host of diverse diseases and conditions is yet little understood or perceived. Nonetheless, a wide diversity of diseases have been shown, at least in animal models, to be effective.
Unfortunately, as I’ve perused the postings and literature on 2-73 I’ve failed to document all of these potential applications. Presently, the lay public (day trading types, etc.) focus rather solely on 2-73 as a treatment for Alzheimer’s disease, perhaps Parkinson’s, and now, Rett’s syndrome. But, there are many others. And many of these are not neurological dysfunctions. A recent posting notes potential therapy for retinal deterioration in a particular disease or treatment scenario.
Yes, I have a small position in AVXL, and follow daily share price fluctuations. But I peruse the information on Anavex primarily as a biologist, not an investor. From that perspective I am extremely encouraged by two emerging stories about 2-73.
Most importantly — drug testing and approvals never occur otherwise — 2-73 simply does not produce side effect or adverse outcomes in any of the animal and human tests that have been conducted (and released). The molecule appears to work in rather low dosages, and appears not to adversely affect non-target organelles, organs, or organ systems. Every indication is that the stuff is safe.
Moreover, there is now indication that the molecule is authentically effective; therapeutic, at least for Alzheimer’s. No, full-scale human trials must yet be conducted to ascertain 2-73's efficacy in clinical applications in real human populations with Alzheimer’s, etc. Those, I’m certain, will occur (no, don’t know when or where). But if 2-73 can merely slow the progression or reduce the symptomatic severity of Alzheimer’s for any period of time, it will be approved. Current Alzheimer’s treatments primarily use acetylcholinesterase inhibitors, which yield merely a mild suppression of cognitive deficits, for only a short period of time. Approved, competing Alzheimer’s drugs have a very low clinical barrier over which 2-73 must jump. I have every assurance expanded human trials will reveal logarithmic suppression of AD symptoms, even reversal and/or prophylaxis (prevention).
Now, in full revelation, I have a mild form of hereditary spastic paraplegia, where certain motor neurons in my spinal cord are hyperactive, causing the adductors of my legs to be in constant tension. This apparently is a dysfunction of the mitochondria and endoplasmic reticula of my spinal motor neurons. I have good reason to believe that 2-73 will suppress or reverse the hyperexcitability of my affected motor neurons, restoring proper, normalized neuron physiology.
Again, 2-73 has never shown adverse results or side effects of any consequence, and its efficacy against an expanding list of human diseases continues to grow. The molecule is unique in each of these respects. It has the potential of revolutionizing medicine to the degree, or greater than, the appearance of antibiotics in the 40s and 50s.
I’m having fun watching all of this. (And thank the many who post clinical perspectives for our consideration.)
Day- and momentum-traders of AVXL should not pay any attention to this posting. It has little validity for the data sets and perspectives of those who are invested in Anavex for near- or mid-term price increases; holders of the stock whose primary purpose is to make a quick or mid-term buck.
I marvel at the plethora of postings where the most minute (even inconsequential) deliberations on anticipated 2-73 clinical results are cogitated on. Those who engage in all of this are certainly welcome to post their astute findings and projections. I, for one, will pay little attention.
I have a small position in AVXL, anticipating that in three to five years it will be very rewarding. Whether the share price appreciates in the coming weeks or months is of no concern to me, because of my belief, based upon my moderate understanding of mitochondrial and endoplasmic reticulum physiology that 2-73 is a remarkable sigma-1 chaperone and is able to restore normal neuron function. This belief derives from the remarkable French work done with 2-73 in genetically-modified rodents who have neuron complications chemically equivalent to Alzheimer’s disease in humans. Simply, in summary, 2-73 fixes neuron anomalies, without untoward or adverse outcomes — at remarkably low concentrations. (I’m a retired biology teacher, who taught these rather arcane subjects).
Yes, before the FDA approves 2-73 for medical use, any number of more complicated and well-controlled human trials will have to be conducted, with demonstrated efficacy and safety. Presently I’m not going to lose any sleep in anxious anticipation of tardy or negative clinical results. The principals of Anavex are very capable researchers and know more about this than anyone who posts here. So much of what’s being posted is pure speculation. The real data exist in Anavex clinical databases, which have been artfully analyzed to guide future clinical trials. Those who work with the clinical 2-73 databases, even just those from rodent subjects, by now know full well the efficacy and safety of 2-73.
All of that, especially human clinical data, will be revealed in good time. Until then, perhaps some time next year, day-trader types will continue to squish incomplete data sets or corporate announcements to guide their trading. My best wishes to all of you who do this. Hope you are rewarded.
Personally, I’ll quietly monitor the postings, and will especially scrutinize any new clinical data that are released. I have every reason to believe they will affirm my efficacy and safety contentions. I’m here for the long-haul. Day to day share price fluctuations are, for me, of no concern or indication.
My best wishes to all — especially to those with the diseases 2-73 should so effectively treat.
The primary value of pre-clinical murine studies is not to assess potential human outcomes; rather, they are to detect potential adverse outcomes.
An innumerable number of pre-clinical murine trials have been conducted on hundreds of candidate treatment molecules for virtually every disease. And probably the majority of these have revealed adverse outcomes, thereby terminating further investigations with the potential drug.
That's the sole value and purpose of murine studies: detect rather certain side effects, inefficiencies, improper dosages and/or durations, or other unexpected adverse outcomes, before conducting human trials. Saves a lot of time, money, and troubles.
But trying to plot murine trials data onto some sort of potential human outcomes equation is utterly futile. We are dealing multi-factoral and extremely complex cellular and systems biochemistries — all of which are still hazy and murky. If they weren’t, molecular biologists would merely plug known molecular chemistries into known cellular biochemical pathways and every result would be revealed. That can work in non-cellular chemistry, physical systems, and perhaps in some financial economic models. Not so in real cells and organisms. Gotta do the real tests, first in mice, then people. Impossible to predict final efficacies and safety without those.
Even if one could know the percentage of successful drugs approved after successful murine trials, that datum would be useless for anything other than a considered bet. I won’t be making any of my equity purchases based on such hazy conjectures. I want to see human results first. Positive murine results suggest (but don’t guarantee) positive human outcomes. I want to see the hard human data, not hazy projections from lab mice.
Positively, no adverse outcomes were revealed in the Fragile X murine outcomes. The door to human trials remains open for 2-73 for this most unfortunate condition.
I was delighted to read the announcement of Anavex’s positive results in treating Fragile X syndrome, in a murine (mouse) form. (http://ih.advfn.com/p.php?pid=nmona&article=71659522 )
For those unfamiliar with modern medical research, in every case possible initial treatment and safety work is conducted on genetically-modified or genetically-selected lab mice that have genomic (DNA) errors identical to those in humans with the diseases and conditions being tested.
The advantages, of course, are several. Untoward results in the mice can indicate possible, even probable similar undesired outcomes in human trials — without the legal, ethical, and medical problems those would entail in real patients.
Ample numbers of mice can be used, at a fraction of the cost of testings in humans. And, because of short murine life spans, results come quicker. A lot easier to assess a population of treated mice in a lab than a statistically significant larger population of real people affected by the disease or condition of concern.
The concern, of course, is whether or not the murine form of the disease or conditions is exactly parallel or equivalent to the human condition. Mice are not men, at least in some respects.
Of course, that’s why initial outcomes of safety and efficacy in lab mice must than be affirmed in real humans, in proper clinical trials.
No, mice are not men. But the cellular genetics and physiology of murine and human neurons are virtually identical. Because of that, and this Anavex Fragile X news, I am further convinced that 2-73 will have a wide diversity of treatment option for a host of neuron-based (and other) human diseases.
It continues to be interesting to follow the initial clinical developments of 2-73, even if still in only murine forms. Fragile X now. What next?
Very intelligent question — what sort of dividends might Anavex be able to throw off when 2-73 is FDA-approved and used worldwide for Alzheimer’s and any number of other neurological or physiological conditions?
Frankly, that’s not a question anyone could answer right now. Some self-proclaimed (even demonstrated) financial analysts might lay out any range of numbers on this. But, presently, it is impossible for these numbers to be usefully accurate. At best, any of them would be well-worded (seemingly expert) quesses.
And, as a biologist, I’m least qualified to offer any useful prognostications on future Anavex earnings or dividends. Nonetheless, anyone can discern the high numbers of moderns who are and will be afflicted with Alzheimer’s. One needn’t be a financial analyst specializing in health care issues to understand the magnitude (if not the exact size) of the Alzheimer’s treatment/prevention market in coming years and decades.
In 1990, who could have predicted the size, earnings, and dividends of a small western company claiming rights to lines of binary code (Microsoft)? Might Anavex be a 21st-century health-care Microsoft? I just read that presently typical annual medication costs for Alzheimer’s patients is in the range of $35,000. What are the financial implications for all parties, patients, physicians, healthcare facilities, insurance companies, and Anavex shareholders if 2-73 might significantly reduce AD medication costs, even prevent or suppress the disease? One can see that Anavex won’t be charging $10 per week dosage costs. 2-73 won’t be an Alzheimer’s aspirin, at least price-wise.
So, might there be future Anavex dividends? Unless Phase 3 clinical trials reveal poor efficacy and/or adverse outcomes, the market for 2-73 will be gigantic, perhaps in the range of some of Microsoft’s code lines.
Why would one ask the question, “How big might Anavex dividends be?” It’s an unknowable datum. The only cogent fact (for me, at least), is that with 2-73 approval Anavex will become exceedingly profitable (or be bought out at a price reflecting future market returns).
Prudently, I’m not mortgaging a new condo against anticipated Anavex values or dividends. Those will appear in their own good time. If someone wants to plug in a future dividend number, just make up that number in your head and plug it into your financial spreadsheet. Until dividends are forthcoming, that made-up number will have as much validity as any, including any I might conjure up.
In short. I have no idea the size of future Anavex dividends. I do have the idea, however, that they will large and continuing (all people grow old, and a large fraction become vulnerable to Alzheimer’s and other geriatric degenerative diseases).
Since I’m a long-term investor, I won’t spend any time trying to work out dividend projections. Waste of time at this juncture. I will be contented merely to learn of the company’s regulatory approval and eventual sales progress for 2-73. I won’t be checking AVXL share prices through the day. Probably once or twice every week. I’m more interested in clinical trials results, so I’ll watch those corporate announcements. I don’t have a day-trader’s perspective on any of this.
As I see it (not always so well), there are essentially three categories of AVXL shareholders.
Day and Momentum Traders. These people have no real interest in the future of 2-73 or the company, per se. These types buy stocks on the thought that the equities they so intelligently purchase are likely to be heading higher in the near term. Buy low, sell higher, in short to moderate time frames. These people are not long-term holders or “investors” in the company. They just want to mark up some fractional buy/sell trading gains. If you can do that time and again through the year, 1 to 5% trading gains can add up.
Near-term Investors. These people are convinced that the share price will appreciate nicely in several months to a year or so, from, say, 10% to 100%. As with day-traders, these people will have tried to buy low and intend to sell high. But because they are holding for months or a year or more, and because they see the future market for 2-73 as being very large, they are aiming for those nice, much higher percentage gains.
Long-term Investors. These people are not buy-now-sell-later shareholders. They purchase shares for one or two goals. The first would be for long-term, many-years appreciation; say, 3 to 10 years out. Then, perhaps in retirement, the shares can be sold for substantial gains. Secondly, in this scenario, corporate dividends are envisioned, where not only does the share price appreciate over the years, but annual dividends are likewise accumulated.
I delight in musing on the many postings here, where I conveniently categorize them into one of the three groupings just mentioned. The postings of the day-trading types simply do not affect my perceptions of Anavex or 2-73.
Presently, I have a small position in Anavex, and assign myself to the third category, a long-term investor, anticipating both share price appreciations and eventual annual dividends. When funds become available, weighed against positive up-coming clinical trials results, I hope to take a much larger position.
As a retired biologist who taught the elements of biochemistry and cellular biology, I can more clearly discern the very technical details of 2-73's function in endoplasmic reticula, etc. But, in honesty, I haven’t spent the requisite time parsing out the molecule’s exact chemistry in neurons. It’s very arcane stuff. But it does favorable things in neurons (and perhaps other cells) that no other existing class of substances can. I’m not a day- or momentum-trader, hoping to profit from the biochemical ignorances of an overly-hopeful investing public. The existing evidence of safety and efficacy is strong — needing only to be clinically verified for regulatory approval. I have every expectation 2-73 will yield strong clinical results and eventually be FDA-approved for sale (who knows when).
I’m a long-term investor. I can wait. In the nonce, I’ll mentally thresh the many postings on this board.
My best to all.
Well, I'm not really on the sidelines; perhaps way up in the cheap seats.
Don't have available funds. Own just a small position in AVXL. Hope to expand that when a) new funds are available, and b)new clinical trials data affirm my conjectures.
Yes, just the questions I ponder.
Whether 2-73 will have therapeutic efficacy for conditions beyond AD and similar CNS disease remains to be determined. But the receptors are almost surely active in all neurons, and perhaps in other tissues, too.
Now, the following conjecture should not be regarded as anything to guide any future investments in AVXL. It's merely that, a conjecture, based upon the possibility that functional 2-73 receptors exist in many cell types, not just neurons. The conjecture is this: 2-73 may facilitate a diversity of normal cell functions, treating any number of geriatric conditions, where normal cell physiology no longer can work.
What might those conditions be, and what sorts of positive outcomes might occur? Utterly unknown. 2-73 has had (at least publicly) only the most limited clinical demonstration. Perhaps those who have worked with the substance in the lab, perhaps in animal models, have some experience and evidence for widespread treatment applications. Of course, none of us have heard a word of any of this. SEC rules prohibit such disclosure (as appropriate).
But, from my perspective, the crucial fulcrum point with 2-73 is this: it works like no other drug. There is nothing whatsoever to compare it to, to assess potential applications and treatments. The normalized cellular physiology that it facilitates in aged neurons (those with Alzheimer's dysfunctions) may well be therapeutic for any number of other diseases and conditions, not only in neurons but in other tissues (and diseases) as well.
I will follow the clinical development of this drug with great interest. It's unique, and may eventually have greatly expanded therapeutic applications.
But all of that is far in the future. Presently, we must be content with final clinical trials for AD, whenever they are announced.
And to be further impressive (and grammatically correct), the plural of endoplasmic reticulum is endoplasmic reticula.
Clearly, endoplasmic reticula are deeply involved in the biochemistry of this new drug (which, I can state as a biologist, has great potential of playing a major therapeutic role in the symptomatic suppression treatment of AD and probably several other neurodegenerative diseases).
I will continue stand on the sidelines, watching all that develops. The efficacy of this new drug continues to be proven strong.
This announcement of Petrozene sales confirms everything a number of us who have scrutinized Freestone have assumed:
a) Petrozene is the real deal, it actually does effectively, efficiently, and economically remove crude oil sludge from tank cars, pipelines, and storage tanks;
b) Freestone’s Ennis TX facility now produces Petrozene in commercial quantities, and
c) once crude oil storage and transport firms use and learn of these useful properties, significant orders will follow.
All of these three factors are now in place. It’s going to be rewarding to watch the growth of this game-changing, innovative company. Those who know the applicability of Petrozene and the world-class management of Freestone (with a manager, Michael McGhan, who has previously built two one-billion dollar firms) have already taken substantial equity positions. It will take a while for common retail stock investors to learn of Freestone’s future. I don’t expect any near-term share price expansions. But when the first actual expanding sales numbers are announced later in the year, things will get interesting.
Presently, Freestone is an unknown start-up, with an un-developed story. The house lights have dimmed, and the curtain is about to open. A bare stage will be seen. Then, the drama begins, with new sales, revenues, and future plans and announcements of new production facilities. Just the first act will be exciting. Who knows who the actors appearing after intermission might be? Big Oil buy-out?
Let’s watch. I’ve got a front-row seat.
A personal perspective on Freestone Resources, Inc.
I very seldom post here, and have no intention of many (or any) new messages beyond this one.
I have accumulated a substantial number of FSNR shares in the last several years, with a cost basis now of $0.10. I’ve essentially doubled my investment value; because of several factors.
I’ve done extensive corporate diligence. Unlike many who post here, I’ve actually spoken with company officials, to discern their competencies and thorough understandings of both the company’s proprietary technologies and the many obstacles of bringing those to a profitable outcome (yet in the future).
I have an extensive scientific background. I understand much of the arcane chemistry operating in the company’s technologies. I understand the profound positive outcomes for both Freestone customers and Freestone shareholders once Freestone chemical processes begin commercial operation.
I also speak with and have researched other oil industry officials and sources cognizant with the potential applications of Petrozene.
Lastly, I’ve also researched the potential markets for Petrozene synthesis side-products, particularly the massive quantities of elemental carbon — for which there is the very high prospect of converting to high-value activated carbon. Many, here, are utterly unaware of (or suppressing) any understanding of the remarkable revenue stream this product category offers to Freestone. My analysis is that it will equal or exceed that of Petrozene.
The sale of recovered steel tire components will be moderate.
I could go on at length on these topics; but my perusal of the postings on this board by all of the usuals, pro and con, are unlikely to turn anyone’s perspective on Freestone. A good number are convinced that the company is worthless, with no prospects of ever generating a penny from the commercial sales of any product or service. Others, think (for their own reasons, not necessarily the ones I’ve expressed) that Freestone will eventually become very profitable.
I rationally examine the basis — as have been best determined — all of the pros and cons posted here. They, particularly for the cons, are a marvelous insight into investment thought perspectives. Investment theater, as it were.
No, no one in Freestone has divulged inside information. But my very brief but cogent conversations with them have proven their corporate vision and competencies. Freestone is real, not imagined or imaginary.
A final thought. I have every reason to believe that Mr. Johnston, like myself, has done his diligence, and has discovered as I have the company’s great future — one that he endorsed with a personal position of over 12 million shares. No one of Mr. Johnston’s corporate accomplishments and stature makes such an investment unless he is sure of its future outcome.
Welcome aboard, Mr. Johnston. Freestone shareholders will prosper, as your even-more intensive diligence has persuaded.
Nano Lab’s new arthropod-killing coatings technology has profound applications.
I’m a biologist with some knowledge of how this technology might work, and whether or not if it uses the following mineral to kill bugs, widespread use of the technology will be both hygienically and financially rewarding, for all parties.
It is known, for example, that borax (which includes all of the several sodium borates), causes perforations in the chitinous exoskeletons of arthropods (insects, spiders, etc), causing them to desiccate, to dry out and die. The bugs can generate no resistance to this class of minerals. Get them touching the “skin,” and the bugs slowly die.
The very recent Nano Lab announcement that they now make coatings (paints) with arthropod-killing nano-tech surfaces with “minerals” perhaps implies the incorporation of sodium borates, which eat microscopic holes in the chitin covering of all arthropods that step or rest on such paints.
What, then, are the implications for Nano Labs per se, and NL investors?
I see two gigantic applications and outcomes (there are others).
First, imagine the applications of paints that use no toxic or short-term insecticides that are universally lethal to any cockroaches that step or crawl upon them. The announcement already states that the new coatings have acceptable, conventional paint traits, but with the additional lethality against “bugs,” arthropods.
Should such commercial coatings come into production, I can see that they will be applied on every paintable surface in restaurants, hotels, schools, hospitals, food-processing facilities—anywhere where cockroaches are current problems. Imagine the sales volume of such paints in the next few years.
But consider the other, even more difficult to control pestiferous arthropod of modern times: the bed bug.
Currently, expanding large fractions of urban bed bug populations are becoming resistant to all available and applicable insecticides. Control of bed bug populations is very expensive, involving durations of high heat (120+F), or mechanical removal of embedded populations in walls and furniture.
As most now know, it’s wise to keep your belongings in bug-proof plastic baggage when staying overnight in commercial hotels, even five-star ones. Bed bugs are proliferating, and nothing—except Nano Lab’s new paint components—offers any useful relief.
Nano Labs need to get some of their paints to some entomologists, who will demonstrate that beg bugs that try to crawl along, over, or rest on Nano Lab Bug-Zapping paints soon dry out and die—without the application or release of a single toxic molecule. And such lethality persists in the painted surface. It doesn’t evaporate away or degrade. Paint the wall or the furniture, and bed bugs are repelled or killed in perpetuity. No other such bed bug solution exists.
Soon, hotels, motels, theaters, and other public places can claim to be bed bug-free. “We use Nano Labs Bug-Zapping Paints.”
If your house becomes infested, instead of hiring an exterminator to spray toxic insecticides, you’ll hire a painter, who will use Nano Lab’s licensed Bug-Zapping paints.
I’m delighted to own a moderate position in Nano Labs. If only Nano Lab’s Bug-Zapping coatings come to commercial success, I will be handsomely rewarded. (But I’m convinced of the commercial applicability of the other techs, too.)
–Falconer66a
It is crucial to note the blog’s statement on Petrozene:
“We field tested Petrozene extensively before marketing and selling the first shipments in order to ensure that we had the best possible formulation.”
Pretty clearly, this isn’t last-century Petrozene. It’s a new “formulation,” with demonstrated efficacy, from the account of the posted user.
Those unfamiliar with the oil industry will not perceive the importance of new Petrozene’s ability to quickly, inexpensively, and effectively deal with the BS&W (bottom sediment and water) problem. As alluded to in the blog, this contamination is frequent and profuse. New Petrozene’s ability to clean up BS&W from the thousands upon thousands of oil storage tanks around the world is profound.
–Falconer66a
New Water Rules for Texas Oil Wells
Of course, the real issue in the exploitation of any of the existing or new tight oil plays in Texas is the a) the availability of frackwater, and b) its disposal or reuse after reprocessing for recycling.
The Texas Railroad Commission, the state agency charged with oil production regulation, continues to examine, define, and usefully regulate oil production water use in the state. Up here in Ohio, in my state, the availability of frackwater is not an issue, with almost 40 inches of precipitation across the state each year. We’ve got ample amounts of water, but Ohio (in the Utica and Marcellus plays) faces the same frackwater disposal or recycling problems Texas does.
Dry Texas has the problem both ways, getting enough new frackwater in that otherwise very arid state (except for the few easternmost counties); and also in disposing and recycling of the produced or extracted frackwater.
The following new article touches upon new regulations on the matter in Texas, showing that regulatory prompts and requirements for recycling are and will become more stringent.
Again, Freestone and it’s JV, Aqueous Solutions, are in the right place, at the right time, and soon, with the right (recycling) technologies, resources, location, and services — all of which are or will become essential for oil and gas extraction in the new Texas tight oil plays mentioned prevously.
The Dallas article is here:
http://www.bizjournals.com/dallas/news/2013/03/27/company-that-recycles-fracking-water.html
–Falconer66a
And the Texas Cline Will Be Bigger
As giant as the Eagle Ford will become, the massive Cline Shale formation in west Texas, under the existing Permian Basin plays, will change the game even more. It's bigger than the Eagle Ford.
Info here (and elsewhere):
http://theexaminer.com/stories/news/cline-shale-play
--Falconer66a