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https://irpages2.eqs.com/websites/annovis/English/431010/us-press-release.html?airportNewsID=34982805-7465-4ec1-93e4-46751a70b467
I don’t know how this doesn’t connect to company news?
Thought the snow would melt today so we could play gold tomorrow.
Made tee times
Called my friends
But although it’s 50 degrees
The ground is so cold from arctic blast
That all my plans for tomorrow which seemed reasonable based upon
temperature are for naught.
Didn’t try to lie, didn’t plan on not being able to play..but I will be working upon other aspects of life fulfillment until the snow melts..
The best laid plans of mice and men..
And that happened without people making money if I dont play golf tomorrow..
Thank God no one actively to destroy my financial value..other than democrats
“Every day thousands of patients die from aging-associated non-communicable diseases (AA-NCDs) that might have otherwise been given new treatments that current regulatory systems have no framework to allow them to try. AA-NCDs have been recognized by the United Nations as a “threat
to global development.” and a mandate has been set to improve the consequences of such diseases. Helping patients get access to new drugs is an imperative of the BCM.” Go to the site. Read about it. Sign the petition if you are so inclined. Best Choice Medicine makes sense for patients suffering from aging associated diseases such as AD. By the time a patient is diagnosed, the disease has done irreparable damage, and there is a short window of opportunity to stop the progression of the disease - especially for older patients. Why not allow establish a framework to allow these patients access to new drugs that may help them? Several drugs seem to candidates to help elderly patients with neurological disorders. These patients do not have the time to wait years for a promising drug to be approved according to the current regulatory systems.
https://www.bestchoicemedicine.com/
I did, early this morning, I trade based on momentum and logic, mostly logic and logic tells me, I shouldn't follow the herd, I know ANSV is going to multiple billions early next year.
Just check it out, insiders own over 70% of the float
I am not going anywhere, have been loading this for months now. PXMD can run and do whatever it wants, this one has a legit run in it to triple dollars.
PXMD running like NERV SC-13 filing
Forget AVX*L and SNP*X, best of the best breed here. Nothing like ANV*S. Triple dollars coming here if you are patient.
The best of the best breed out there when it comes to Alzheimers and Parkinson's disease, nothing out there like this biotech. Will be in triple dollars when that data hits the wires.
Awesome sauce
7:36 am ET September 8, 2022
Annovis Bio, Inc. (NYSE:ANVS) ("Annovis" or the "Company"), a late-stage clinical drug platform company addressing neurodegenerative diseases, today released the following letter to stockholders from its Chief Executive Officer Dr. Maria Maccecchini.
Dear Fellow Stockholder,
Over the years we have been talking about the potential of buntanetap to treat more than Alzheimer's disease. In cell models, animal models and human clinical studies, we have seen that buntanetap works in numerous acute and chronic neurodegenerative conditions. I would like to take this opportunity to explain how one drug can be so broadly applicable.
Buntenatap works by inhibiting specific neurotoxic proteins such as amyloid precursor protein (APP), Tau, alpha-synuclein (aSYN), TAR DNA binding protein 43 (TDP-43), huntingtin (HTT) and prion protein. These proteins have normal functions but in their neurotoxic aggregating form, they impair axonal transport, slow synaptic transmission, cause inflammation, and ultimately, kill nerve cells, resulting in the loss of affected function in various neurodegenerative conditions.
The overexpression and aggregation of these proteins is caused by elevated levels of iron in the nerve cell. The mRNAs of neurotoxic aggregating proteins contain an iron response element (IRE) which binds to an iron regulatory protein called IRP1. At normal iron levels, translation occurs at appropriate physiological levels. When iron flows into the cell, the mRNAs are released and translated at higher rates by the ribosome. When massive iron flows in, the mRNAs remain unbound for as long as the iron is high and the proteins for these neurotoxic aggregating proteins are overexpressed. In this high iron situation, buntanetap binds to the atypical IRE-IRP1 complex and prevents the mRNA from being released and, therefore, from being translated and overexpressed.
Buntanetap is able to inhibit the translation of multiple neurotoxic proteins through this mechanism of action, and as a result has the potential to treat numerous acute and chronic neurodegenerative conditions that share this pathway. In mouse or rat models of Alzheimer's, Parkinson's, stroke, frontotemporal dementia, traumatic brain injury, glaucoma, and Down Syndrome, buntanetap has been shown to normalize the levels of these neurotoxic proteins and to restore function.
Most importantly, this has been demonstrated in human clinical trials. In our recent Phase 2 clinical trial in Alzheimer's disease and Parkinson's disease, treatment with buntanetap resulted in reduction of aggregating proteins and statistically significant improvement in motor function in Parkinson's disease patients and cognition in Alzheimer's disease patients.
FUNCTION
TEST
SUBJECT
ANIMALS
Memory, learning
Mazes
AD mice, DS mice, stroke mice, TBI rats
Movement
Colonic motility, grip strength
PD mice, tau mice
Vision
Sight
Glaucoma rats
Infections
Cell death
P. Gingivalis mice, Covid mice
HUMANS
Cognition, memory, learning
ADAScog11
Early AD patients
Attention, thinking speed
WAIS coding
Early AD patients
Movement, coordination
MDS-UPDRS
Early PD patients
Movement speed
WAIS coding
Early PD patients
Table 1: Summary of all animal and human study data.
We look forward to unlocking the full potential of buntanetap and addressing unmet needs across a range of acute and chronic neurological conditions.
Maria L. Maccecchini, Ph.D.,
Founder, President, CEO and Executive Board Member
Data coming hot by end of this year, will send this into to the stratosphere, the only cure for Alzheimers.
Looking for a good day tomorrow $$$$$
Wonder if annovis could give us a company update on Clinicals and new drug developments?
This is good news..
But the hammer is. A phase 1/2 ? in severe ad..of their new drug..
When will THAT news be out?
Congrats Maria!!!!!
But if high was 132 for early to moderate ad..
Wonder what price targe high is for all of
Severe dementia?
Memory care facilities would lose a lot of money!!!
No tears ..only memories
The all time high is 132.. and that was before two additional drugs..
NIH funded trial for severe AD..
Wonder what happens when you bring an AD patient back from the abyss?
Do they remember yesterdays or just tomorrows?
Prayers it’s both
Wonder how long anvs will take to to detangle severe ad? Plenty of patients..
Gosh.. what would happen to the stock
if the NIH trial is a full on success?
Wouldn’t that be crazy
Wonder how that nih trial is going for severe dementia?
???????
Oh my
https://finance.yahoo.com/news/annovis-bio-submits-international-patent-123000706.html
This patent application would have passed as a benign piece of news but for those who have done their scientific research and understood Dr Maccecchini's hypothesis, this is potentially big.
This further confirms the hypothesis that neurons die in similar fashion in most of the neurodegenerative diseases and brain injuries: AD, PD, post-stroke, Niemann-Pick type C, ALS, SMA, Stargadt disease etc
Injured neurons present abnormally large endosomes and axonal transport and synaptic transmissions are impaired... all of which Buntanetap managed to reverse.
Please download my two research slide decks on Annovis's underlying science and how Buntanetap may be the Penicillin of neurodegenerative diseases (warning: scientific DD inside):
Report #1: https://drive.google.com/file/d/1Nt4BJURr0psZ6QkM7UX77TCZI1IJdNSJ/view
Report #2: https://drive.google.com/file/d/1ojb1BbftmDH6VKLRA8GM6gCeB4ulLoLp/view?usp=sharing
Did I mention for severe dementia?
Holy Maccaroni!
Just looked at their website..
They have a new drug already being phase 1 by nih grant?
Missed the presser
Annovis Bio's new entry on ClinicalTrials.gov for Phase 3 Parkinson's Disease: https://clinicaltrials.gov/ct2/show/NCT05357989?term=annovis&draw=2&rank=2
Study start: June 2022
Primary completion: January 2023
Study completion: March 2023
(all estimated dates)
Company is at less than $82M market cap with around $20M in cash and one proven phase 3 asset in PD with promising interim results... This is insanely undervalued!!!
The TIME has come..to OVERWEIGHT your portfolio IN:
ANNOVIS
ANAVEX and
Yes..
CASSAVA
Maybe ACIU..just don’t know it well enough..
STOK..(if memory serves me correctly..)
WHY you ask? Really? Why?
Well half the worlds population has just been injected with
A spike protein that for some(many, all) may cause dementia..
WHY WOULD YOU GIVE THIS CRAP TO A CHILD FOR GOD’s SAKE?
DUE DILIGENCE on Annovis in the document below:
https://drive.google.com/file/u/1/d/1OIWmQENqhj0_ibWuHp7QOJN2lO1RjOW6/view
The Company now has TWO phase 3 assets for AD and PD with an MOA that is potentially best in class (not relying on artificially boosting neurotransmitters or stimulating/antagonizing neuronal receptors of dying neurons). Buntanetap actually HEALS neurons.
I made a slide summarizing everything I learn about Annovis and its drug-candidate. Please share the slide deck so more people know about the comapany.
https://drive.google.com/file/u/1/d/1OIWmQENqhj0_ibWuHp7QOJN2lO1RjOW6/view
Annovis Bio improving information highway of nerve cells to treat AD, PD
Leonard ZehrDecember 14, 2021
Maria Maccecchini, Ph.D., Founder, President, and CEO
Annovis Bio (NYSE:ANVS) is developing a lead drug candidate, ANVS401, to inhibit more than one neurotoxic protein, improving the information highway of nerve cells, known as axonal transport, for the treatment of Alzheimer’s and Parkinson’s diseases, and an orphan indication, AD in Down syndrome (AD-DS).
“When this information flow is impaired, the nerve cell gets sick and dies,” Maria Maccecchini, Ph.D., founder, president, and CEO of Annovis, says in an interview with BioTuesdays.
Last October, Annovis reported that in a Phase 2 trial, ANVS401 improved memory loss in AD/PD patients, as well as motor and motor function in patients with PD. The company also analyzed the biomarkers of the toxic cascade that starts out with high levels of neurotoxic proteins, leading to impairment in axonal transport, inflammation and nerve cell loss and found that neurotoxic protein levels and inflammation are reduced, and axonal and synaptic health is preserved.
“These positive efficacy results combined with the marker results expand on our previous data from AD and PD patients and add clarity to the benefits that ANVS401 may offer patients suffering from these chronic neurodegenerative diseases,” Dr. Maccecchini points out.
Annovis has asked the FDA for end-of-Phase 2 meetings for the development of ANVS401 in AD and in PD and is waiting for further guidance from the agency on how to proceed into Phase 3 trials. Hopefully, the PD Phase 3 pivotal study can start in early 2022 and the AD study a little later.
Dr. Maccecchini suggests that ANVS401 is the only drug in development that targets multiple neurotoxic proteins and inflammation simultaneously to improve axonal transport and protect nerve cells from dying in AD, PD and AD-DS. The multiple ANVS401 targets include amyloid beta, tau and aSynuclein.
“By targeting multiple neurotoxic proteins, ANVS401 resembles a combination therapy approach, with the added convenience of being a single drug with a single drug target,” she adds.
According to Dr. Maccecchini, neurotoxic proteins impair axonal transport and cause a toxic cascade; slow synaptic transmission; cause inflammation; death of nerve cells; and loss of cognitive and motor function.
On the other hand, ANVS401 has the potential to halt and reverse the toxic cascade; lowering levels of neurotoxic proteins to improve axonal transport; increasing synaptic transmission; inhibiting inflammation; maintaining healthy nerve cells; and improving cognitive and motor function.
In preclinical studies, Annovis demonstrated that in four animal models of memory and learning, AD mice, DS mice, stroke mice and traumatic brain injury rats fully recovered after treatment with ANVS401. A similar outcome was achieved in two models of movement disorders with PD and frontotemporal dementia mice.
“So, if ANVS401 worked in the brain and body of mice, we decided to try it in the eye and we induced glaucoma in rats. Left untreated, glaucoma causes pressure in the eye to go up, the retina dies, and the eye goes blind. When we treated our glaucoma-induced rats with ANVS401, the pressure in the eye increased, but the retina did not die and the eye did not go blind,” Dr. Maccecchini says.
Annovis’ Phase 2 trial enrolled 14 early-to-moderate AD patients and 14 PD patients, with an additional 40 PD patients recruited for the second part of the study for a total of 54 subjects. Dr. Maccecchini says AD participants received placebo or 80 mg of ANVS401 once daily, while PD patients received doses of placebo or 5 mg, 10 mg, 20 mg, 40 mg, and 80 mg once daily.
The primary endpoint was reversal of the toxic cascade, with efficacy as an exploratory endpoint. Safety and two psychometric assessments were conducted at day 0 and day 25, comparing ANVS401-dosed PD patients with placebo.
From baseline to 25 days in the ANVS401-treated AD group, Dr. Maccecchini says Alzheimer’s disease assessment scale – cognitive 11-item (ADAS-Cog11) score improved by 4.4 points, a statistically significant improvement of 30%. Compared with placebo at 25 days, the treated group was 3.3 points better than the placebo, an improvement of 22%.
ADAS-Cog11 is designed to assess the level of cognitive dysfunction in AD and is considered the gold standard for measuring efficacy of antidementia treatments.
In addition, treated AD patients in the Phase 2 trial showed a statistically significant 23% improvement from baseline in the Wechsler Adult Intelligence Scale (WAIS) and PD patients a statistically significant 30.5% improvement, compared with placebo.
The WAIS coding subtest measures visual-motor dexterity, associative nonverbal learning, and nonverbal short-term memory. It also measures fine-motor dexterity, speed, accuracy, and ability to manipulate a pencil and perceptual organization.
Dr. Maccecchini says data from 54 PD patients showed the most improved function at doses of 10 mg and 20 mg of ANVS401 once daily. And across dose response patients, the WAIS coding test showed statistically significant improvements in speed of movement and coordination.
“Because our Phase 2 was a small study, we would have been happy to see any trends in cognition and motor function. The fact we achieved statistically significant results is very exciting. And the fact that the efficacious dose of 10 mg to 20 mg in humans was the same as in animals is a huge confirmation of what we were thinking,” she adds.
Annovis has filed four new families of patents that expire between 2031 and 2042.
Dr. Maccecchini says patent estate is multi-layered with method of use protection of the mechanism of action for the prevention and treatment of acute and chronic disease; treatment of viral and bacterial infections of the brain; acute brain and nerve injuries like stroke and traumatic brain injury; and neurodegenerative diseases like PD and AD.
At the end of June 2021, Annovis had $49-million of cash, making the company fully funded through two anticipated Phase 3 trial and two years of operations.
“Ours is a novel approach to stop AD and PD, and our Phase 2 program demonstrated improvements in cognition in AD patients, and motor and brain function in PD patients,” she says.
• • • • •
To connect with Annovis Bio or any of the other companies featured on BioTuesdays, send us an email at editor@biotuesdays.com.
I remember annovis anticipating data from NIH by year end.. maybe I got totmeline wrong.. but maybe I didn’t
Also needs specific and solid bio marker data to be published
Murocman
No fund flow into the stock recently.
Market is waiting for additional data or confirmation of well-known players about Posiphen because on its own, it only understands p-values.
ANVS is really struggling here. Despite insiders buying.
May I Just say it is a beautiful and rare occurrence in this day and age
when a successful CEO of any company
buys stock in their enterprise outright!
No options exercised. no insider gimme..
Just I believe in my company and want more of it.
Maria knows a good thing when she sees it..
Fun
I just checked the still on-goind AD trial:
NCT02925650
24 patients
60mg/120mg/180mg/placebo
I got a reply from Maria about what she thinks of the dosage response in terms of efficacy.
She pointed out this is what was seen in animal models for AD and PD.
For PD mouse model: positive response was seen at 3mg/kg, optimal dose was 10mg and the mice did worse at 25mg/kg.
For AD mouse model: positive response was seen at 10mg/kg, optimal dose was 25mg/kg and mice did worse at 50mg/kg.
On the biomarker and dosage, she said some of them was down to 50% at almost toxic dose of Posiphen (based on previous human trials, I assume the dosage is around 180mg/kg). So far, we are seeing 5% to 20% in optimal doses (Maria mentioned she is considering 10mg to 30mg for future trials), we are actually no that far off in terms of dose dependent response for biomarkers. Maria said that for PD, a 5% decrease in alpha-synucleins is "absolutely adequate". When you think about Posiphen's MOA, it is sensible as you don't want to inhibit APP 100% since this protein precursor is still needed.
My take on all the data we have so far:
- It is not incommon for drugs to demonstrate a non-linear relationship and that's why you have phase 2 trials.
- All the results on humans are consistent with animal models so far.
- Given the short duration of the trial, we have seen consistent improvement in anything related to short-term and working memory, which is what deteriorates first at the onset of the disease (We have seen improvement in WAIS coding test, ADAS-cog3, 6 &11).
- The design of the trial just did what Maria intended to do: determining the optimal dosage to demonstrate efficacy.
Really I think this sets up NIH trial as a win..
Don’t remember specific dosages of NIH
But this certainly increases odds nih trial a success
No, phase2b 40 PD patient trial.
I missed call..was this NIH study?
I’m guessing the price reacted negatively because they didn’t publish any bio marker data.
They did this last time as well. The top line was great but didn’t look as good when the bio marker details got published, which is why the price tanked.
You would think management might have learned from that experience but it appears not.
GLTA,
Murocman
Imagine shorts suppressing good data
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