Below posts copied from IHUB,
Fletch
falconer66a Thursday, 03/21/19 10:02:29 PM
Re: ClosetInvestor post# 186229 0
Post # of 187969
Missling, Like Others, Knows It Won’t Fail
Quote:
...avoid the possibility of 2-73 failing and his shares being worth zero.
To presume there is a considered chance that Anavex 2-73 simply won’t succeed in any one of the three human trials is to (understandably) reveal an ignorance of vertebrate neuron biochemistry, morphology, physiology, and the molecules and organelles in operation within nerves and neurons; and to fail to understand the unique cellular chemistry of this sigma-1 receptor agonist.
Understood: Not wise to make big bets on new, never-used-in-humans drugs targeting difficult diseases. Few diseases are more difficult than the three central nervous system diseases Anavex is being tested against; in real human beings, not diseased lab rats. Why should Anavex 2-73 work, safely, when so few others have? Why is Dr. Missling both wise and diligent in rejecting buyouts or takeovers of any kind? He’s bet the corporate ranch, has he not, on Anavex 2-73 being successful for either Rett syndrome, Parkinson’s, or Alzheimer’s. Fail with all three, and Anavex Life Sciences Corp is but another historic chapter in some new business administration textbook. MBAs, take heed.
Here are some big things that make Anavex 2-73 different from other new, “unproven” neuroactive drugs. Missling knows all of this, and much more.
1. Profound evidence of both efficacies and safety in murine tests against a multitude of nerve (and other) disorders.
Of course, easy (but in this case, inaccurate) to claim that animal studies simply can’t predict assured efficacies or safety in real human with real diseases. In this case, Missling knows that is NOT the case. (So do I.)
2. The cellular and systemic neurology of mammals, whether in lab rats and mice (murines), or real humans, is virtually identical, regarding the maintenance (homeostasis) of normalized nerve function. This is particularly so in transgenic rats, whose disease states arise from human disease genes inserted into their genomes. Anavex 2-73 fixes those conditions, allowing neurons to restore normal biochemical homeostasis — just as it will in humans (and already has, in a few Australians with already poorly-functioning Alzheimer’s nerves).
3. The testing of the drug in humans has failed to reveal any significant, disqualifying adverse events or outcomes (replicating the safety profiles found in treated murines).
Yes, nerve-acting drugs of every sort are particularly associated with adverse events and outcomes. Nothing of the sort in either murines or humans with Anavex 2-73.
4. Most importantly, Anavex 2-73 works altogether differently from any other drug. Too complicated to detail here, trying to explain the precise interactions of mitochondria, endoplasmic reticula, and protein folding; all controlled or moderated by the sigma-1 receptor complexes (when functioning normally). But Missling and his people know with certainty the profound efficacies and viable safety profiles of their molecules. Simply, they are, in every way, different from other, previous neuroactive drugs. They are safe. And they work.
Interestingly, now, no one with any understanding of neuron biology is posting cautions or statements telling that the mechanisms of action of the Anavex molecules are implausible, unknown, or impossible. Recent external papers describe and affirm the data affirming the health-restoring and health-maintaining validity of them.
The reluctance (even antagonism) of many regarding the possibility of great successes in the three human trials of Anavex 2-73 is understood. No offense taken. A few can accurately read the evidence. Most, however, will decide to wait for significant trial results. Everyone must make decisions on what he or she knows and believes — just as Missling has done.
A year from now, public discourse on matters Anavex will be very different. I’m eager to watch, read, and listen (especially to my brokerage statements).
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falconer66a Thursday, 03/21/19 06:31:00 PM
Re: nidan7500 post# 186206 0
Post # of 187969
Why So Many Dollars Failed Against Alzheimer’s
It’s taken most of this century for firms with lots of dollars to come to the harsh realization that trying to treat Alzheimer’s with the moderately variable waste-clearing approaches (chemicals that induce immunological or direct chemical clearing of neurologically-toxic beta-amyloids or tau tangles) simply fail. How (or why) would otherwise intelligent, experienced scientists and their funders (big pharmaceutical firms, etc.) keep throwing so many millions (well, billions) of dollars at the same, failed-so-often process? Two or three times might be understandable. But 146 failures? What did these people learn in med school or schools of business administration that allowed so many, so expensive drug development mistakes?
As I see it (from a science standpoint; with no particular investment expertise), it appears that the prospects of giant payoffs masked reality. An eighth-grade science student could, in an hour’s clicking around the Internet, determine the fantastic corporate incomes that would be generated by any useful treatment of Alzheimer’s. Go for it! Pay so big, let nothing interfere.
People with the dollars (pharmaceutical executives) were certain that if they just hired the best-educated researchers, those deep-science types would find and develop real Alzheimer’s treatments. Like all other financial problems, they only needed money.
Only two Alzheimer’s treatment approaches were offered by the neurology science people.
One, inhibit acetylcholinesterase. With that, ample, useful concentrations of acetylcholine will be maintained in nerves, allowing their normalized, healthful function. That worked, actually, but only for short periods of time; whereupon the lethal progression Alzheimer’s progressed.
Or, much bigger and much better, somehow induce the immune system of the body to react with and dispose of waste beta-amyloids and/or tau tangles. They inhibit nerve function; cause Alzheimer’s symptoms.
But that never worked, in any of the concept’s iterations. Too many debilitating adverse events (side effects), or simply poor clearance of the toxic waste proteins.
The drug companies, for several decades, have followed the Thomas Edison method of new-concept product development. Keep throwing things at Alzheimer’s neurons and eventually, something will stick and work. For light bulb filaments, that worked. Edison tested hundreds of materials before finding a form of bamboo from Japan that worked.
Neurons with Alzheimer’s (well, and those without) are extremely complicated, with a multitude of chemical reaction pathways. The pharmaceuticals and their scientists tried to fix Alzheimer’s as though they merely needed to fix a burned out light bulb. Burned out neurons were the target.
But the approach was to restore neuron function by working at downstream disease stages. The toxins, mechanistically, were “downstream,” at the end of the pathogenic process. Like trying to re-attach already-broken light bulb filaments.
Anavex, instead, restores normalized neuron chemistries (proper protein folding, etc.) “upstream,” so that toxic waste proteins never accumulate. Instead of fixing burned-out neurons, Anavex molecules maintain neuron functions. With that (as the many preclinical and murine studies show), success.
I will be watching closely, to see how the media explain the positive clinical results later this year. How will they explain to the public how the Anavex sigma-1 receptor agonists actually work. Their biochemical functions are very complex; difficult to understand (or convey) without a rather deep understanding of neuron physiology and morphology. A wonderful problem to be presented with.
“Dr. Missling, our viewers here at CBS want to know the magic of your new drug. The new clinical results are astounding. Tell us how it works. Until now, nothing else has. What’s your secret?”
Private Reply | Keep | Public Reply | View Replies (3) | Mark as Last Read
Fletch
falconer66a Thursday, 03/21/19 10:02:29 PM
Re: ClosetInvestor post# 186229 0
Post # of 187969
Missling, Like Others, Knows It Won’t Fail
Quote:
...avoid the possibility of 2-73 failing and his shares being worth zero.
To presume there is a considered chance that Anavex 2-73 simply won’t succeed in any one of the three human trials is to (understandably) reveal an ignorance of vertebrate neuron biochemistry, morphology, physiology, and the molecules and organelles in operation within nerves and neurons; and to fail to understand the unique cellular chemistry of this sigma-1 receptor agonist.
Understood: Not wise to make big bets on new, never-used-in-humans drugs targeting difficult diseases. Few diseases are more difficult than the three central nervous system diseases Anavex is being tested against; in real human beings, not diseased lab rats. Why should Anavex 2-73 work, safely, when so few others have? Why is Dr. Missling both wise and diligent in rejecting buyouts or takeovers of any kind? He’s bet the corporate ranch, has he not, on Anavex 2-73 being successful for either Rett syndrome, Parkinson’s, or Alzheimer’s. Fail with all three, and Anavex Life Sciences Corp is but another historic chapter in some new business administration textbook. MBAs, take heed.
Here are some big things that make Anavex 2-73 different from other new, “unproven” neuroactive drugs. Missling knows all of this, and much more.
1. Profound evidence of both efficacies and safety in murine tests against a multitude of nerve (and other) disorders.
Of course, easy (but in this case, inaccurate) to claim that animal studies simply can’t predict assured efficacies or safety in real human with real diseases. In this case, Missling knows that is NOT the case. (So do I.)
2. The cellular and systemic neurology of mammals, whether in lab rats and mice (murines), or real humans, is virtually identical, regarding the maintenance (homeostasis) of normalized nerve function. This is particularly so in transgenic rats, whose disease states arise from human disease genes inserted into their genomes. Anavex 2-73 fixes those conditions, allowing neurons to restore normal biochemical homeostasis — just as it will in humans (and already has, in a few Australians with already poorly-functioning Alzheimer’s nerves).
3. The testing of the drug in humans has failed to reveal any significant, disqualifying adverse events or outcomes (replicating the safety profiles found in treated murines).
Yes, nerve-acting drugs of every sort are particularly associated with adverse events and outcomes. Nothing of the sort in either murines or humans with Anavex 2-73.
4. Most importantly, Anavex 2-73 works altogether differently from any other drug. Too complicated to detail here, trying to explain the precise interactions of mitochondria, endoplasmic reticula, and protein folding; all controlled or moderated by the sigma-1 receptor complexes (when functioning normally). But Missling and his people know with certainty the profound efficacies and viable safety profiles of their molecules. Simply, they are, in every way, different from other, previous neuroactive drugs. They are safe. And they work.
Interestingly, now, no one with any understanding of neuron biology is posting cautions or statements telling that the mechanisms of action of the Anavex molecules are implausible, unknown, or impossible. Recent external papers describe and affirm the data affirming the health-restoring and health-maintaining validity of them.
The reluctance (even antagonism) of many regarding the possibility of great successes in the three human trials of Anavex 2-73 is understood. No offense taken. A few can accurately read the evidence. Most, however, will decide to wait for significant trial results. Everyone must make decisions on what he or she knows and believes — just as Missling has done.
A year from now, public discourse on matters Anavex will be very different. I’m eager to watch, read, and listen (especially to my brokerage statements).
Private Reply | Keep | Public Reply | View Replies (1) | Mark as Last Read
falconer66a Thursday, 03/21/19 06:31:00 PM
Re: nidan7500 post# 186206 0
Post # of 187969
Why So Many Dollars Failed Against Alzheimer’s
It’s taken most of this century for firms with lots of dollars to come to the harsh realization that trying to treat Alzheimer’s with the moderately variable waste-clearing approaches (chemicals that induce immunological or direct chemical clearing of neurologically-toxic beta-amyloids or tau tangles) simply fail. How (or why) would otherwise intelligent, experienced scientists and their funders (big pharmaceutical firms, etc.) keep throwing so many millions (well, billions) of dollars at the same, failed-so-often process? Two or three times might be understandable. But 146 failures? What did these people learn in med school or schools of business administration that allowed so many, so expensive drug development mistakes?
As I see it (from a science standpoint; with no particular investment expertise), it appears that the prospects of giant payoffs masked reality. An eighth-grade science student could, in an hour’s clicking around the Internet, determine the fantastic corporate incomes that would be generated by any useful treatment of Alzheimer’s. Go for it! Pay so big, let nothing interfere.
People with the dollars (pharmaceutical executives) were certain that if they just hired the best-educated researchers, those deep-science types would find and develop real Alzheimer’s treatments. Like all other financial problems, they only needed money.
Only two Alzheimer’s treatment approaches were offered by the neurology science people.
One, inhibit acetylcholinesterase. With that, ample, useful concentrations of acetylcholine will be maintained in nerves, allowing their normalized, healthful function. That worked, actually, but only for short periods of time; whereupon the lethal progression Alzheimer’s progressed.
Or, much bigger and much better, somehow induce the immune system of the body to react with and dispose of waste beta-amyloids and/or tau tangles. They inhibit nerve function; cause Alzheimer’s symptoms.
But that never worked, in any of the concept’s iterations. Too many debilitating adverse events (side effects), or simply poor clearance of the toxic waste proteins.
The drug companies, for several decades, have followed the Thomas Edison method of new-concept product development. Keep throwing things at Alzheimer’s neurons and eventually, something will stick and work. For light bulb filaments, that worked. Edison tested hundreds of materials before finding a form of bamboo from Japan that worked.
Neurons with Alzheimer’s (well, and those without) are extremely complicated, with a multitude of chemical reaction pathways. The pharmaceuticals and their scientists tried to fix Alzheimer’s as though they merely needed to fix a burned out light bulb. Burned out neurons were the target.
But the approach was to restore neuron function by working at downstream disease stages. The toxins, mechanistically, were “downstream,” at the end of the pathogenic process. Like trying to re-attach already-broken light bulb filaments.
Anavex, instead, restores normalized neuron chemistries (proper protein folding, etc.) “upstream,” so that toxic waste proteins never accumulate. Instead of fixing burned-out neurons, Anavex molecules maintain neuron functions. With that (as the many preclinical and murine studies show), success.
I will be watching closely, to see how the media explain the positive clinical results later this year. How will they explain to the public how the Anavex sigma-1 receptor agonists actually work. Their biochemical functions are very complex; difficult to understand (or convey) without a rather deep understanding of neuron physiology and morphology. A wonderful problem to be presented with.
“Dr. Missling, our viewers here at CBS want to know the magic of your new drug. The new clinical results are astounding. Tell us how it works. Until now, nothing else has. What’s your secret?”
Private Reply | Keep | Public Reply | View Replies (3) | Mark as Last Read
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