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Critical point here:
We are leaps and bounds ahead of them in “proving” our data and should know soon about approval status.
TempePhil...thx...excellent work.
AB-E-NORMAL...for AVXL...
8.20+0.28 (+3.47%)
As of 10:03AM EDT. Market open.
Plexrec.... "well done"...
-"Finally, ANAVEX2-73, a s1 receptor agonist, has been shown to provide significant and sustained improvement in cognitive function in mild-AD patients
"Nuff Said"...The s1 receptor participates in the regulation of intracellular Ca2+ migration and maintains homeostasis and protects cognitive function damage [119,120]. Research on the role of the s1 receptor in mediating mitochondrial function has found that the s1 receptor attenuates hippocampal dendrite formation through scavenging of free radicals, and protects cells from damage by mitochondria-derived reactive oxygen species (ROS) [121,122,123]. The ER stress sensor inositol-requiring enzyme 1 (IRE1) facilitates mitochondrion-ER-nucleus signaling for cellular survival via the s1 receptor chaperone [75,124].[/quote]
https://www.mdpi.com/1422-0067/24/15/12025
Now, we need to hear from the RSD crew...bless the kids and families...helping to support WW sick people and to resolve little kids and their families pain...does not get much better...LETS ALL HAVE A GOOD WEEK FOR ONCE.
Thanks hnbbadger1...Noted no contradictions with AVXL research published to date.
[quote]Increasing evidence has proved that the s1 receptor holds great potential as a biomarker for early AD diagnosis and progression and the monitoring of AD drug efficacy [49]. Hallmarks of human AD include progressive cognitive decline that follows chronic neuroinflammation and the emergence of hyperphosphorylated tau protein aggregates and Aß plaques [46], with all playing critical and perhaps interrelated roles in the progression of AD. In particular, Ca2+ plays a critical role in learning and memory processes [114,115,116,117,118], and Ca2+ dyshomeostasis is a pathological feature of AD and other neurodegenerative diseases [114,115,116,117,118]. The s1 receptor forms a Ca2+-sensitive chaperone complex with the binding immunoglobulin protein/glucose-regulated protein 78 (BiP/GRP78), and prolongs Ca2+-signaling from ER into mitochondria by stabilizing inositol 1,4,5-trisphosphate receptor (IP3R) at the MAM [74]. The s1 receptor participates in the regulation of intracellular Ca2+ migration and maintains homeostasis and protects cognitive function damage [119,120]. Research on the role of the s1 receptor in mediating mitochondrial function has found that the s1 receptor attenuates hippocampal dendrite formation through scavenging of free radicals, and protects cells from damage by mitochondria-derived reactive oxygen species (ROS) [121,122,123]. The ER stress sensor inositol-requiring enzyme 1 (IRE1) facilitates mitochondrion-ER-nucleus signaling for cellular survival via the s1 receptor chaperone [75,124].[/quote]
https://www.mdpi.com/1422-0067/24/15/12025
Anyone else get a sense of comfort (just this side of warm-fuzzy) from last trading session -EOD results?
I like the little bounce we experienced and read it is driven by good news out there waiting. I do also hold out a positive attitude about other credible large Pharma co. having researched AVXL work/results/trials/direction .. .but that is just how I see the way work has been done by Dr.M and team. The AVXL staff-team have been around long enough to recognize the REAL thing when they see it.
My other observations are less positive or certain. I have begun to recognize just how devious/misleading the BP-WS processes are, having previous lab time on my own but never paying attention to just how many types of liars there are around BP/WS. Relying on process results is typically a safe bet for me but that all changed when I tried to get a rational line of thinking in support of FDA Amyloid closed minded status. It looks to me like the entire BP world has wrapped itself around the wrong flag pole and AVXL is not on that path at all. WGT, but it is a tough uphill slough. Anyways, my sense is we will see a breakout soon including AVXL proof by trials of RWD -RSD.
IMO, the other good news I see includes the (certain) avalanche-awakening to the CNS upstream work done by AVXL and the S1R AHAA moments including RSD-PDD-AD trial findings . This black hole cannot last indefinitely...one small lite is all we need...then...BBOOOM.
longtermbeliever:
again i believe they don't show up at AAIC due to partnership deal.
hnbadger1: From MayoMobile’s interview on July 18 at AAIC-
“Dr. Grimmer thinks they're
being approached/in-convo with big pharma for
purchase/partnering which is why we have not
seen data yet.”
Makes sense, if true then some BP name gets in the photo-story when the biggest medical news ever is launched. An old Maine expression comes to mind..."Fish, or CUT BAIT". Doing nothing, is not an option.
tredenwater2...
I have a great feeling we will all sit back and say…..” ahhh, thats why they did things the way the did them.”
Recommended reading: from sokol .... .Nice work....we got this.
[CNS Drugs.](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#) 2023; 37(5): 399--440.
Published online 2023 May 11. doi: [10.1007/s40263-023-01007-6](https://doi.org/10.1007%2Fs40263-023-01007-6)
PMCID: PMC10173947
PMID: [37166702](https://pubmed.ncbi.nlm.nih.gov/37166702)
# Targeting Sigma Receptors for the Treatment of Neurodegenerative and Neurodevelopmental Disorders
.....Drugs such as blarcamesine, dextromethorphan and pridopidine, which have sigma-1 receptor activity as part of their pharmacological profile, are effective in treating multiple aspects of several neurological diseases. ...
### ANAVEX2-73 (Blarcamesine)
Blarcamesine (ANAVEX2-73; Fig. [?Fig.2)2](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/figure/Fig2/)) is a s1R receptor agonist with an affinity of 860 nM (IC50) [[222](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR222)] developed for treating AD. Blarcamesine also has agonist activity at the muscarinic M1 receptor, and the NMDA receptor with affinities of 5 and 8 µM, respectively [[222](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR222)].
#### Alzheimer's Disease
Pre-clinical studies have shown that blarcamesine can reverse scopolamine's long-term amnesic effects in mice [[222](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR222)]. Furthermore, blarcamesine can reverse the effect of learning deficits in mice injected with Aß25--35 [[222](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR222)--[224](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR224)]. Blarcamesine given to mice injected with Aß25--35 restored respiration rates in hippocampal mitochondria and reduced lipid peroxidation levels. Blarcamesine could also prevent tau-hyperphosphorylation and amyloid-ß (1--42) generation in mouse models of AD [[223](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR223)]. Furthermore, indicators of increased toxicity, including Bax/Bcl-2 ratio and cytochrome C release into the cytosol, were reduced [[224](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR224)]. Blarcamesine has protective effects in _Caenorhabditis elegans_ and cell culture models of AD by enhancing autophagic flux and increasing proteostasis [[65](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR65)].
A phase 1 clinical study in healthy male volunteers showed that doses up to 50 mg were well tolerated, with no serious adverse events reported in a poster at the CNS summit in 2014 [[225](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR225)]. At 60 mg, three out of four subjects presented dose-limiting CNS symptoms (dizziness and headache). The study concluded with pharmacokinetic analysis showing extensive biotransformation of blarcamesine to AV19-144 (the bioactive form of the drug) with assumed linear pharmacokinetics after single oral dosing of 1 to 60 mg blarcamesine [[225](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR225)].
A biomarker analysis, phase 2a study ([NCT02244541](https://clinicaltrials.gov/ct2/show/NCT02244541)), that include some exploratory study into the benefits of blarcamesine, where blarcamesine was administered over 57 weeks, showed a significant reduction in cognitive decline [[226](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR226)]. When the study was extended to 265 weeks ([NCT02756858](https://clinicaltrials.gov/ct2/show/NCT02756858)), there was confirmation of this prevention of decline at 148 weeks with analysis of blood concentrations of blarcamesine and its metabolite AV19-144, showing that those with high concentrations of blarcamesine had improved therapeutic responses of 78% and 88% in adjusted MMSE and adjusted AD cooperative study--activities of daily living (ADCS--ADL), respectively, relative to the low/medium concentrations of blarcamesine.
Furthermore, genomic analysis also indicated the significant effects of biomarkers on clinical outcomes of blarcamesine. Two patients showed an exceptional therapeutic response at 148 weeks. Both subjects had s1R wild type and a high mean concentration of blarcamesine in plasma, with a baseline MMSE > 20 [[226](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR226)].
The study of biomarkers that predict the potential therapeutic outcome of a drug is especially useful in a disease with such heterogeneity as AD [[226](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR226)]. The ApoE e4 genotype alone lacks predictive power since only approximately 25% of people carry this genotype. The study discussed above identified that patients with a baseline MMSE greater than 20 who had the s1R wild type with a high mean blarcamesine serum concentration and _ApoE3_ alleles had significantly better outcomes in the ADCS--ADL. The _SIGMAR1_ Q2P variant, having a baseline MMSE score lower than 20 and a low mean serum concentration of blarcamesine were predictive of poor outcomes in the ADCS--ADL [[226](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR226)].
Blarcamesine is undergoing further phase 2b/3 clinical trials (ongoing: [NCT04314934](https://clinicaltrials.gov/ct2/show/NCT04314934); completed with data yet to be published: [NCT03790709](https://clinicaltrials.gov/ct2/show/NCT03790709)). The results of these clinical trials will be interesting, given the promise blarcamesine has shown in the pre-clinical studies.
#### Multiple Sclerosis
Blarcamesine increased the proliferation of oligodendrocyte progenitor cells to myelin sheath-producing oligodendrocytes in a s1R-dependent manner and protected them from excitotoxic insults [[227](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR227)]. There are no currently listed clinical trials for blarcamesine in MS on [www.clinicaltrials.gov](http://www.clinicaltrials.gov/).
#### Rett Syndrome
Long-term administration of blarcamesine to mice deficient in MeCP2 restores physiological and neurological abnormalities that mimic the human Rett syndrome, including ameliorating motor and acoustic startle deficits and reversing expiratory apnoea [[228](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR228)]. Several s1R-related mechanisms could benefit the neurological and motor symptoms seen in this and other models of Rett syndrome. Enhancement of calcium homeostasis via s1R shuttling of calcium to the mitochondria leads to improved mitochondrial function and the activation of autophagy via s1R activation, resulting in a reduction of misfolded proteins and fewer damaged organelles or the restoring/upregulation of BDNF [[65](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR65), [228](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR228), [229](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR229)]. This leads to potential improvements in synaptic function in multiple brain regions.
Blarcamesine is currently in phase 2/3 clinical trials ([NCT03758924](https://clinicaltrials.gov/ct2/show/NCT03758924), [NCT03941444](https://clinicaltrials.gov/ct2/show/NCT03941444) and [NCT04304482](https://clinicaltrials.gov/ct2/show/NCT04304482)). Blarcamesine has shown positive results in a phase 2 clinical trial ([NCT03758924](https://clinicaltrials.gov/ct2/show/NCT03758924)) in female patients diagnosed with Rett syndrome (positive _MeCP2_ gene mutation), meeting both primary and secondary endpoints with no reported serious adverse events (press release) [[230](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR230)]. In another phase 3 ([NCT03941444](https://clinicaltrials.gov/ct2/show/NCT03941444)) clinical trial the primary and secondary endpoints were met with significant improvements versus placebo in the clinical global-impression of improvement scale (CGI-I); the anxiety, depression and mood scale (ADAMS); and drug exposure-dependent response of the Rett Syndrome Behaviour Questionnaire (RSBQ), all with a low incidence of adverse events (press release) [[230](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR230)]. It is important to note that the data available from these studies has not been peer reviewed and formally published. There are further ongoing phase 3 studies organized by Anavex Life Sciences ([NCT04304482](https://clinicaltrials.gov/ct2/show/NCT04304482)). However, while the data look promising, it will be important to see some independent studies with peer-reviewed results to fully assess the efficacy and safety of blarcamesine for Rett syndrome treatment.
### ANAVEX3-71
ANAVEX3-71 (AF710B) (Fig. [?(Fig.2)2](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/figure/Fig2/)) is an agonist at the muscarinic M1 receptor and s1R, and the second drug developed by for AD treatment. ANAVEX3-71 has an affinity for the s1R of 1.3 nM and an affinity for the s2R of 10 µM [[62](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR62)]. The affinity for the M1 receptor is approximately 0.05 nM. ANAVEX3-71 also has affinities for the µ opioid receptor and serotonin receptor (approximately 10 µM for each) [[62](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR62)].
#### Alzheimer's Disease
Given the complex pathology of AD, it is of interest that a drug such as AF710B may interact with multiple target sites to have a beneficial effect in AD [[52](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR52)].
Pre-clinical studies have shown ANAVEX3-71 to be worthy of further study. AF710B has been shown to modify the disease-defining hallmarks of AD in transgenic (3×Tg-AD) mice, such as cognitive deficits, amyloid and tau pathologies, and beneficial effects on mitochondrial dysfunction and neuroinflammation [[62](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR62), [231](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR231)].
Phase 1 clinical trials ([NCT04442945](https://clinicaltrials.gov/ct2/show/NCT04442945)) in healthy individuals have been reported on Anavex Life Sciences' website, suggesting that in healthy volunteers, 5--200 mg daily had no serious adverse events. The pharmacokinetics of ANAVEX3-71 (serum concentration of AF710B) was also proportional to the dose for doses up to 160 mg. Furthermore, there were no clinically significant electrocardiogram (ECG) parameters throughout the study (press release) [[232](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/#CR232)].
There are no further registered ([www.clinicaltrials.gov](http://www.clinicaltrials.gov/)) ongoing clinical trials with ANAVEX3-71. However, Anavex states on its website that they plan further phase 2 clinical trials. More independent studies are required. However, pre-clinical data on ANAVEX3-71 suggest it could be useful in treating dementia and AD.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10173947/
You have not replied to my recent post regarding titration.
Sokol,
Many thanks for this excellent compilation of AVXL trial data. Obviously the tools required to keep track of and analyze the findings for the CNS clinical world to deal with are badly needed.
All of this will make more sense some day, hopefully in our lifetimes.
If only the trials could get better synchronized then we could make better use of resources WW.
Danke.
nidan,
What is it that you question, exactly?
bas2020
I anticipate the XBI breaking to the upside
Broke support. 6 coming
hnbadger1: Thank you for posting this well done AD paper. In fact it emphasizes what some of us have been saying here for a long time. That is, the FDA has done a poor job of being clear about Aymloid Plaque role as a cause for AD.
But ß-amyloid rides on. Funders fund amyloid. Many PhD students study the effects of amyloid, their findings lead to prestigious post-doctoral positions, then senior positions and the circle remains unbroken. If you hear words like “breakthrough” about these drugs, or claims that we’re in a new era of hope for Alzheimer’s disease, it’s because of this self-perpetuating feedback loop inside the field that drives it all forward.
So this is where we’re at, folks. A patient organization running amok, a field that is riven by controversy on basic questions of disease pathogenesis, companies looking to make a killing on drugs with little or no proven clinically meaningful benefit and real harms to patients, and an FDA willing to do their bidding. This is a race to the bottom, incentivizing the worst behavior of everyone involved. Those who have succumbed to neurodegenerative conditions such as Alzheimer’s, like my father, and those now living with the disease all deserve better than this.
georgejjl...Any proof, PR, news from AVXL, other about this claim??Have not seen such claim posted ...
There is a lot of talk here because after or due to inappropriate titration some trial participants ask to down titrate from 50 mg/day to 30 moper day of oral dosing due to dizziness
Thanks for the information.
IGNORE ...suggestion to all longs
plexrec
" positive AD P2b/3 that met all endpoints, "
it appears many have now caught on.
Unfortunately due to FUD this message board has become virtually useless.
Good article on untrustworthy clinical trials.
https://www.nature.com/articles/d41586-023-02299-w
Alberto J Espay @Alberto... 4d
We are treating Alzheimer's as if it
were cancer. It isn't. The brain still
shrinks at any level of amyloid
detection, as @Kariem_Ezzat
reminds us. Amyloid is a normal
reaction to pathogens of various
kinds. By shooting the messenger,
we only create the illusion of
success.
Excellent material here. New tool suite will/may actually add to CNS diseases overall scope/knowledge and complexity. BP is going to hate this. One Size does/may not fit all. AND, the social shoe horns in use must be shat-canned. IMO. Intelligence is a beautiful thing, even if it is artificial . We are all just @ the tip of beginning,, IMO.
HUH...https://alz-journals.onlinelibrary.wiley.com/toc/15525279/2023/19/S8
Retail AVXL holders need to rethink what ever (BUY/HOLD/SELL) price-time clocks you have running, IMO.
Anyone w/ some experience using/AI systems and the impact they may/might have on decisions would suggest the decision horizons can move as new reasoning-time lines become factors...(WAIT_SELL-BUY_ OTHER).
Expect that the new tools will likely introduce new variables and paths b/c their fields of data and decision factors . Some new variable paths may cause you to rethink what might have previously been/seemed obvious. One reaction may be that you will have new-more (what if ???) process questions to reason over than you typically do now.
It's all good, just stand back and rethink unintended possible consequences. This will be particularly true as the tool becomes more populated w/facts which you consider important but which you would have previously not even considered.
IMO, Dr.M. and staff may be spending a lot of time right now going through AI models-data being available and accuracy of data being used to reason over. Things/factors that previously (seemed) not have been in the decision pot may now show up w/various timelines attached. So, a quick obvious choice from the past may now take a lot longer, depending on data sources and the speed of the new AI system to respond to variables/questions.
bas2020
I'm fully expecting to see a journal that incorporates a wealth of information, covering several indications, raising the expectations of a generally effective drug for most all CNS disorders.
https://www.nytimes.com/2023/07/19/us/stanford-president-resigns-tessier-lavigne.html
Interesting Stanford U. findings. A key professor and AD academic leader has been determined to have been "at least" very sloppy in his area of responsibility ref AD reporting . Corruption and lies in academia are disappointing (to say the least). IMO, the AVXL WW team are much more insightful and valuable than we suspect they might be. We recognize that 50+ years is a long time to remain clueless as to AD cause. IMO, once we get the REAL-STORY (answer) many, many stories like this one will -may percolate to the surface, IMO. This should just NOT BE HAPPENING.
Any of us who have a sense that 50+ years of research in AD and still no solid published -proven proof of " root cause" ...HUH?? Dr. M is a low key guy, as he chooses . IMO< there is lot more of the same kind of academic outings in the future, once absolute proof of CNS diseases causes are proven. It may be that AVXL and AI methods and affiliations will be key to these future moments of truth.
Everyone...Keep the faith .
Nice Catch...
The role of sigma 1 receptor (S1R)
This guidance is what AVXL will/are providing. Anyone who has ever lead during systemic changes knows it is hard -time consuming painful work. Maybe that is why people avoid doing it. FDA process controls and disciplines are critical and required. The regulatory headset and making changes that work is tough to do, ask anyone who has ever had to do that.
IMO, that is what Dr.M. and his AVXL team are leading ...it's all about CHANGE ,it takes time. Sad to say.
Senge, P. (1990/2006). The fifth discipline: The art and practice of the learning organization. Doubleday.
] The fifth discipline: The art and practice of the learning organization
PM Senge
2006•books.google.com
Completely Updated and Revised This revised edition of Peter Senge’s bestselling classic, The Fifth Discipline, is based on fifteen years of experience in putting the book’s ideas into practice. As Senge makes clear, in the long run the only sustainable competitive advantage is your organization’s ability to learn faster than the competition. The leadership stories in the book demonstrate the many ways that the core ideas in The Fifth Discipline, many of which seemed radical when first published in 1990, have become deeply integrated into people’s ways of seeing the world and their managerial practices. In The Fifth Discipline, Senge describes how companies can rid themselves of the learning “disabilities” that threaten their productivity and success by adopting the strategies of learning organizations—ones in which new and expansive patterns of thinking are nurtured, collective aspiration is set free, and people are continually learning how to create results they truly desire. The updated and revised Currency edition of this business classic contains over one hundred pages of new material based on interviews with dozens of practitioners at companies like BP, Unilever, Intel, Ford, HP, Saudi Aramco, and organizations like Roca, Oxfam, and The World Bank. It features a new Foreword about the success Peter Senge has achieved with learning organizations since the book’s inception, as well as new chapters on Impetus (getting started), Strategies, Leaders’ New Work, Systems Citizens, and Frontiers for the Future. Mastering the disciplines Senge outlines in the book will:• Reignite the spark of genuine learning driven by people focused on what truly matters to them• Bridge teamwork into macro-creativity• Free you of confining assumptions and mindsets• Teach you to see the forest and the trees• End the struggle between work and personal time
Leading is hard work,, particularly when the people/industry/structure you are dealing with are entrenched (up to their eyeballs) in a wrongheaded thesis (CNS Amyloid system) . Change is tough-impossible, particularly when the issues we want to resolve involve regulatory bodies and (virtually) the entire BIO-MED-academic-practicing CNS universe believe something else. AVXL are working on WW systemic change models.
https://link.springer.com/referenceworkentry/10.1007/978-3-319-49820-1_100-2
The reality is AVXL are not only leading a new field of medical reasoning but we are simultaneously asking others to abandon much of what they currently believe. This is going to be complicated before we are done, but someone has to do it.
bas2020. Thanks for a well written and realistic assessment of AVXL strategy and implementation plans.
[ don't be concerned by the silence. Missling is playing this out appropriately given the cesspool "market" that he's operating in. He'll wait until everything is in place before making announcements and revealing the stellar data... as well as securing the voucher./quote]
I am curious myself on why we are seeing this quiet period. It is quiet for other CNS-Pharma as well.
tsch...
240K volume as of 11:00...seems higher than usual for this point in time...
bourban...
Well we could make it perfectly clear by getting an NDA filed for Rett in the 3rd quarter.
Anyone still wondering why Dr. M. just hired a bunch (most) of FDA tech senior leadership while he simultaneously partnered w/THE AI frat bros @Ariana. We might be looking for a new road map-skill set (not ole schoolers in WS) to start giving signals on the future of the W/S-BP-NIH-FDA compass.
Hey, it's what leaders do, they can't NOT LEAD. NICE, IMO. ...BTW, looking like the FDA crew were fully on board w/the plan. NICE.
Anavex Life Sciences and Ariana Pharma Collaborate to Accelerate Timelines and Improve Efficiency
October 5, 2016
[You see, one of the first things Dr. Missling did was to follow the FDA's lead in AI technology...so now both the FDA and Anavex are using Ariana's KEM technology to analyze data. (Not bad for a German, aye?)]
https://www.anavex.com/post/anavex-life-sciences-and-ariana-pharma-collaborate-to-accelerate-timelines-and-improve-efficiency
abew4me
Anavex Life Sciences and Ariana Pharma Collaborate to Accelerate Timelines and Improve Efficiency
October 5, 2016
[You see, one of the first things Dr. Missling did was to follow the FDA's lead in AI technology...so now both the FDA and Anavex are using Ariana's KEM technology to analyze data. (Not bad for a German, aye?)]
https://www.anavex.com/post/anavex-life-sciences-and-ariana-pharma-collaborate-to-accelerate-timelines-and-improve-efficiency
tredenwater2
“When you see what we did you will know why we did things the way we did”
Some need answers and adas cog scores now to justify their belief. I hope they dont get it until the end. I hope Dr. Missling keeps on his plan and gives them nothing. What “they” dont understand is that the market is just as much in the dark and has a hard time calculating Anavex’s moves. This doesntmatter because its all about me isms is t it?
You might consider the ignore option..