Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Read through the 8/23/19 peer-reviewed Nature publication again, and there were not many companies specifically mentioned, and Anavex was one of the few discussed in a positive & promising light IMO.
Would seem strange for one of their few positive company-specific mentions in this Nature publication to have had incorrect facts listed regarding Anavex FDA granted fast-track status.
One would expect that the authors would’ve obtained that information from a reliable source if accurate?
Original publication submission on 3/28/19 then revised on 7/7/19.
Probably just a coincidence that Anavex filed for the $250 million shelf registration 4 days prior on 7/3/19.
https://www.nature.com/articles/s41392-019-0063-8
credit greenspam3
Excerpts:
"At present, clinical drug treatments are mainly divided into two categories: acetylcholinesterase inhibitors (AChEIs), represented by donepezil, and the antagonist of N-methyl-D-aspartic acid (NMDA) receptor, represented by memantine (Table 1).48 As neurotransmitter regulators, these drugs can only relieve symptoms for a short time but cannot delay the progression of AD. Recent failures and the limited progress of therapeutics in phase III clinical trials suggest that it is time to consider alternative strategies for AD treatment.49”
"Aß-targeting monoclonal antibodies (mAbs) are the major passive immunotherapy treatments for AD. For example, solanezumab (Eli Lilly), which can bind monomeric and soluble Aß, failed to show curative effects in AD patients in phase III, although solanezumab effectively reduced free plasma Aß concentrations by more than 90%.93 Gantenerumab (Roche/Genentech) is a mAb that binds oligomeric and fibrillar Aß and can activate the microglia-mediated phagocytic clearance of plaques. However, it also failed in phase III.94 Crenezumab (Roche/Genentech/AC Immune) is a mAb that can bind to various Aß, including monomers, oligomers, and fibrils. On January 30, 2019, Roche announced the termination of two phase III trials of crenezumab in AD patients. Aducanumab (Biogen Idec) is a mAb that targets aggregated forms of Aß. Although aducanumab can significantly reduce Aß deposition, Biogen and Eisai announced the discontinuation of trials of aducanumab on March 21, 2019. Together, the failure of these trials strongly suggests that it is better to treat Aß deposits as a pathological feature rather than as part of a major mechanistic hypothesis.”
"BACE1 inhibitors aim to reduce Aß and have been tested for years. However, no BACE1 inhibitors have passed clinical trials. Verubecestat (MK-8931, Merck & Co.) reduced Aß levels by up to 90% in the cerebrospinal fluid (CSF) in AD. However, Merck no longer listed verubecestat in its research pipeline since verubecestat did not improve cognitive decline in AD patients and was associated with unfavorable side effects.95 Lanabecestat (AZD3293, AstraZeneca/Eli Lilly) is another BACE1 inhibitor that can lower CSF Aß levels by up to 75%. However, on June 12, 2018, phase II/III trials of lanabecestat were discontinued due to a lack of efficacy. The BACE1 inhibitor atabecestat (JNJ-54861911, Janssen) induced a robust reduction in Aß levels by up to 95% in a phase I trial. However, Janssen announced the discontinuation of this program on May 17, 2018. The latest news regarding the BACE inhibitor umibecestat (Novartis/Amgen) was released on July 11, 2019; it was announced that the evaluation of umibecestat was discontinued in phase II/III trials since an assessment demonstrated a worsening of cognitive function. Elenbecestat (E2609, Eisai) is another BACE1 inhibitor that can reduce CSF Aß levels by up to 80%96,97 and is now in phase III trials (shown in Table 2). Although all BACE1 inhibitors seem to reduce CSF Aß levels, the failure of trials of solanezumab, which can reduce free plasma Aß concentrations by more than 90%,93 may be sufficient to lead us to pessimistic expectations, especially considering that the treatment worsened cognition and induced side effects.”
"Mannose oligosaccharide diacid (GV-971) was developed by researchers at the Shanghai Institute of Medicine, the Chinese Academy of Sciences, the Ocean University of China, and the Shanghai Green Valley Pharmaceutical Co., Ltd. GV-971 is an oceanic oligosaccharide molecule extracted from seaweed. GV-971 may capture multiple fragments of Aß in multiple sites and multiple states, inhibit the formation of Aß filaments, and depolymerize filaments into nontoxic monomers330,331; however, an understanding of the exact mechanism is still lacking. GV-971 has been reported to improve learning and memory in Aß-treated mice.332 In phase II trials, GV-971 improved cognition in AD patients.333 In addition, a phase III clinical trial of GV-971 finished with positive results, and it is on its way to the market in China (Table 2).”
"Perspective
AD, like the aging population, has increasingly become a medical and social concern. There are currently four clinically used drugs (a total of five therapies, the fifth one of which is a combination of two drugs) that have been approved by the FDA, but they only treat the symptoms and have no significant effect on the progression of AD. Based on this retrospective review of AD and the lessons learned, we propose that fluoxetine,402 a selective serotonin reuptake inhibitor (SSRI), may have strong potential for the treatment of AD (Fig. 7).”
"Furthermore, fluoxetine has been reported to bind and inhibit NMDA receptors directly in the CNS,416 and this can reduce the inhibition of a-secretase and thus prevent the production of Aß.203,417 Fluoxetine also inhibits ?-secretase activity and reduces the production of toxic amyloid Aß by activating MEK-ERK signaling.371,372 In addition, fluoxetine can bind to the endoplasmic reticulum protein sigma-1 receptor.418 Sigma-1 receptor ligands can enhance acetylcholine secretion.419,420 The sigma-1 receptor activator Anavex 2–73 has entered a phase III clinical trial after it was granted fast-track status by the FDA because of the promising results in phase II. The sigma-1 receptor is located in the mitochondrion-associated ER membrane so that the activation of the sigma-1 receptor can prolong Ca2+ signaling in mitochondria.421 Consequently, the local and specific elevation of [Ca2+] in the mitochondrial matrix can enhance ATP synthesis,422,423 which ameliorates hypometabolism."
"The most interesting and challenging phenomena regarding fluoxetine is that fluoxetine is clinically more effective in women than in men440 and that the prevalence of AD and other dementias is higher in women than in men441; meanwhile, women live significantly longer than men.442 These phenomena suggest that there are interplays or trade-offs between AD and longevity. In particular, APOE is the strongest genetic risk factor for AD18,19,20,21 and is the only gene associated with longevity that achieves genome-wide significance (P?<?5?×?10–8).443 APOE4 is associated with a risk of AD that declines after the age of 70; the OR for APOE4 heterozygotes remains above unity at almost all ages; surprisingly, however, the OR for APOE4 homozygotes dips below unity after the age of 89.444 There may be genetic and nongenetic factors that interact with APOE4, lead to shorter survival in more aggressive form of AD, or promote longevity in an age-dependent manner.11 Uncovering the puzzle of APOE4 and the mystery of longevity may provide insights for AD prevention."
Received
28 March 2019
Revised
07 July 2019
Accepted
17 July 2019
Published
23 August 2019
This post from powerwalker appears highly relevant if indeed we’re on the fda fast track.
https://investorshub.advfn.com/boards/read_msg.aspx?message_id=149767660
If we’ve been granted fast track for AD then they must’ve applied in the last 60 days; have regulators been able to unblind our ph2/3 Alzheimer’s trial data? Were results discussed with Anavex to prompt the FT request?
“Fast Track designation must be requested by the drug company. The request can be initiated at any time during the drug development process. FDA will review the request and make a decision within sixty days based on whether the drug fills an unmet medical need in a serious condition.”
https://www.fda.gov/ForPatients/Approvals/Fast/ucm405399.htm
Page Last Updated: 01/04/2018
“Fast track is a process designed to facilitate the development, and expedite the review of drugs to treat serious conditions and fill an unmet medical need. The purpose is to get important new drugs to the patient earlier. Fast Track addresses a broad range of serious conditions.
Determining whether a condition is serious is a matter of judgment, but generally is based on whether the drug will have an impact on such factors as survival, day-to-day functioning, or the likelihood that the condition, if left untreated, will progress from a less severe condition to a more serious one. AIDS, Alzheimer’s, heart failure and cancer are obvious examples of serious conditions. However, diseases such as epilepsy, depression and diabetes are also considered to be serious conditions.
Filling an unmet medical need is defined as providing a therapy where none exists or providing a therapy which may be potentially better than available therapy.
Any drug being developed to treat or prevent a condition with no current therapy obviously is directed at an unmet need. If there are available therapies, a fast track drug must show some advantage over available therapy, such as:
Showing superior effectiveness, effect on serious outcomes or improved effect on serious outcomes
Avoiding serious side effects of an available therapy
Improving the diagnosis of a serious condition where early diagnosis results in an improved outcome
Decreasing a clinical significant toxicity of an available therapy that is common and causes discontinuation of treatment
Ability to address emerging or anticipated public health need
A drug that receives Fast Track designation is eligible for some or all of the following:
More frequent meetings with FDA to discuss the drug's development plan and ensure collection of appropriate data needed to support drug approval
More frequent written communication from FDA about such things as the design of the proposed clinical trials and use of biomarkers
Eligibility for Accelerated Approval and Priority Review, if relevant criteria are met
Rolling Review, which means that a drug company can submit completed sections of its Biologic License Application (BLA) or New Drug Application (NDA) for review by FDA, rather than waiting until every section of the NDA is completed before the entire application can be reviewed. BLA or NDA review usually does not begin until the drug company has submitted the entire application to the FDA
Fast Track designation must be requested by the drug company. The request can be initiated at any time during the drug development process. FDA will review the request and make a decision within sixty days based on whether the drug fills an unmet medical need in a serious condition.
Once a drug receives Fast Track designation, early and frequent communication between the FDA and a drug company is encouraged throughout the entire drug development and review process. The frequency of communication assures that questions and issues are resolved quickly, often leading to earlier drug approval and access by patients.”
Was wondering the same thing. They did just update the pipeline chart and are looking to hire new personnel according to new indeed.com postings yesterday as well. Interesting developments imo
Great find greenspam3, thank you. published yesterday 8/23/19. Granted fast track status?
https://www.nature.com/articles/s41392-019-0063-8
“Sigma-1 receptor ligands can enhance acetylcholine secretion.419,420 The sigma-1 receptor activator Anavex 2–73 has entered a phase III clinical trial after it was granted fast-track status by the FDA because of the promising results in phase II. The sigma-1 receptor is located in the mitochondrion-associated ER membrane so that the activation of the sigma-1 receptor can prolong Ca2+ signaling in mitochondria.421 Consequently, the local and specific elevation of [Ca2+] in the mitochondrial matrix can enhance ATP synthesis,422,423 which ameliorates hypometabolism.”
Market traction may result if more open-minded analysts/ biotech reporters reported publicly on Anavex & the signs and signals and peer reviewed research and publications that are supportive of our MOA & results to date: efficacy as well as SAFETY (compared to current SOC) and reported RWE by patients and caregivers & our own AD trial PI in interviews.
They do realize the need to search for and report on new and upstream approaches to treating these diseases, right?
Emphasis perhaps on promising compounds such as 2-73 that its trial participants/investigators are asking to extend treatment and stay on the drug. Throw in the fact that our reported SAFETY and mild side effects would alone be a big benefit over SOC for disease sufferers.
Michele Sullivan comes to mind; perhaps after the upcoming publication is released that Dr M referred to at the annual meeting, which we think may reference further analysis/data from our AD extension study through 208(?) weeks.
BTW, the below was a note put out on 8/1/19:
"Anavex DSMB review outcome a positive sign, says Janney Montgomery Scott analyst Yun Zhong called it a "positive sign" for ANAVEX 2-73 that the Independent Data Safety Monitoring Board for the company's U.S. Phase 2 Rett syndrome study recommended continuation of the study without modification following a review of the preliminary data. The fact that the company's press release said the board reviewed both efficacy and safety data leads Zhong to believe the study has passed futility analysis, he noted. The analyst, who said he is optimistic that 2-73 could demonstrate efficacy in neurodegenerative and neurodevelopmental disorders, keeps a Buy rating on Avanex shares.”
Read more at:
https://thefly.com/landingPageNews.php?id=2943201
https://thefly.com/landingPageNews.php?id=2943201&headline=AVXL-Anavex-DSMB-review-outcome-a-positive-sign-says-Janney-Montgomery-Scott
Makes sense Attilla, stealth mode likely until results released/regulatory decisions.
IF the situation is quite positive behind the scenes, then stealth would be advisable during this time of suppressed market cap.
Also may explain why he wasn’t eager to touch the topics in the cc that I was hoping for: intent/rationale of the shelf offering, and exactly how many in the RS/PDD trials have completed treatment AND how many have asked to extend treatment and do we have access to their trial data yet for analysis?
SIDE POINT: I used to stubbornly view Anavex & its compounds as a binary pass or fail situation in this CNS space; either it works or it doesn’t.
But with such a low bar for SOC currently and with the growing list of S1R therapeutic benefits (ref: peer reviewed pubs and our pipeline and ph2a RWE) for patients’ minds/bodies (purportedly) through:
• restoration of cellular homeostasis
• reduction of inflammation and cellular stress
• tackling mitochondrial dysfunction
• potential sleep improvement
• RWE, mood, agitation relief
• hypertension benefits/normalization
• modulate autophagy
• increase diversity in gut microbiome (adjunct medication opportunities?)
• epileptic seizure and infantile spasm relief
Safety has been established and patients/investigators are asking to extend treatment.
Seems to me and others here that we’ve MANY shots on goal if our SAB/CEO manages this correctly and efficiently.
Yes Mcmagyar, a human drug.
Sign me up for a study so I can take it.
(Disclaimer: I’ve no scientific training and these are ONLY opinions and my current theories. Success is not a certainty of course.)
Quote: “The only question we have to ask is, if they had poor results would they let us know? How? When?”
While awaiting the gold standard results from our double blinded placebo controlled trials:
I recall that after 3.5 years of leading our AD trial in Australia as trial PI, Prof Macfarlane was quoted in an interview in July 2018:
“The cognition of most of the 32 patients who took part in the most recent trial remained stable, when it had been expected to decline.”
https://www.google.com/amp/s/amp.heraldsun.com.au/news/victoria/genetics-key-to-recruiting-alzheimers-patients-for-drug-trial/news-story/5a6fd042d014fc3c5b2f4ac3d4acf588
And that was without precision medicine & biomarker selection and without optimized dosing, right?
To your question, if they were seeing poor results now in 2019, wouldn’t they be advised to make us aware of any material change to Dr Macfarlane’s public assessment?
(I am ASSUMING that Anavex is able to view and analyze data for patients that have completed treatment and/or are on the requested extension treatments.)
IF my assumption is correct and since they’ve not advised us of material changes to Macfarlane’s assessment, is it logical to make positive inferences?
I’ll be appreciative if Dr M could simply share in the CC what the 250mm shelf is all about, AND exactly which peer reviewed publication was he referring to at the annual meeting and will it specifically analyze our ph2a ongoing results in detail?
Just my opinions and observations. GLTY
Quote “All we need now is some evidence that the science is performing as it should. BTW, they could never move this fast if the science was not working well. Risk management would stop the train”
Excellent point. Would seem strange at best if we had moved this fast and far down the tracks on 3 indications and on different continents and numerous trial sites, as well as brought on board a SVP of operations 17 months ago and hired the top international researcher on Rett Syndrome in January “if the science was not working well”.
Wouldn’t make much sense for Drs Toutain or Fadiran or Kaufmann (and other executive/SAB team members) to join us or stick around this long if our compound was not producing desired therapeutic outcomes, or if it was exhibiting serious side effects.
We’ll learn more tomorrow.
Regarding tomorrow:
(a) I’d welcome detail about the purpose/intent for the 250 million shelf offering (which is over twice the current market cap of the Company). Is it primarily for defensive measures, or is it earmarked for anticipated commercialization, or primarily to fund future trials?
(b) it was just 6 months ago that the Company reported: “and non-recurring expenses of approximately $1.0 million associated with large-scale manufacturing of ANAVEX®2-73 in quantities reserved for potential future commercial use.”
Are (a) and (b) connected from a future commercialization standpoint?
If yes, then that speaks volumes to me.
https://www.globenewswire.com/news-release/2019/02/07/1712018/0/en/Anavex-Life-Sciences-Reports-Fiscal-2019-First-Quarter-Financial-Results-And-Provides-Clinical-Study-Updates.html
With the above backdrop, along with Dr Kaufmann (Emory/Cal-Davis/ MIT/Harvard/John Hopkins ties, and founder of RettSearch) reviewing our Company & its molecules and human trial data and earlier preclinical data and agreeing to join Anavex as Chief Medical Officer in 2019:
• it’s difficult for me to view the 250mm shelf as a negative, they’ve 3 years to implement it, if ever; it’s likely designed for a higher market cap environment for the Company, and my hunch is that Dr M would not have taken the step if all known knowns (and Dr Kaufmann’s consultations) behind closed doors were less than positive
• for approx 4-5 years we’ve had human trial data/dosing/concentration info in hand, as well as patients in our current PDD and RS and AD trials request extensions to stay on 2-73
(seems consistent with our positive preclinical results by independent experts)
And our CEO and BOD and SAB appear of very high integrity and scientific experience level.
They must know MUCH about our efficacy behind closed doors, and IF that known info was negative I feel they’d have reported any negative material events by now, OR at least I would not expect them to continue adding countries & trial sites and indications at this stage, or take on a highly-visible Precison Medicine industry leadership role, nor issue new stock option grants to officers recently if this was anything but positive behind the scenes.
Could be wrong of course but logic is telling me that things are looking pretty good to those in the know.
Just my opinions and observations.
https://www.anavex.com/anavex-life-sciences-announces-the-appointment-of-walter-e-kaufmann-md-as-chief-medical-officer/
Completely agree with that assessment jvmho, the Company’s been in stealth mode for at least 2 years, and I’ll trust that Dr M and the BOD have their (competitive) reasons.
And you’re right, there’ve still been multiple signs and signals of confidence in the moa and efficacy to date: expanding the pdd trial to AU; expanding the RS Avatar trial to AU in May; letting us know in a conf call that the Spain pdd participants had requested an extension; purchasing 1 million worth of 2-73 inventory; putting in place a large 250 million shelf (commercialization needs?); new patents such as https://patentscope.wipo.int/search/en/detail.jsf?docId=US236451262&tab=NATIONALBIBLIO&office=&prevFilter=%26fq%3DICF_M%3A%22A61K%22&sortOption=Pub+Date+Desc&queryString=&recNum=213&maxRec=2035248
And,
http://appft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PG01&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.html&r=1&f=G&l=50&s1=%2220180360796%22.PGNR.&OS=DN/20180360796&RS=DN/20180360796
Also telling were the hiring of Dr Walter Kauffman as our CMO this year, and the display of confidence by Dr Missling when explaining Anavex’s moa/efficacy during the March 2019 ROTH conference panel “Alzheimer’s: Beyond the Rise and Fall of Amyloid”.
Stark contrast between our “rapidly advancing” pipeline compared with the BP giants dropping out of the CNS space and “Biogen on the Brink” (credit Jon Jones & nidan) https://www.bizjournals.com/boston/news/2019/08/02/biogen-on-the-brink-one-of-the-states-largest.html?ana=yahoo&yptr=yahoo
The market forces (BP giants and their entrenched tau/amyloid plaque scientists/media/Hedge funds/FUD agents) are by now aware of Anavex and our consortium/Hampel ties and PM leadership & our expanding/extending CNS trials, and I’m convinced that their game plan has been/is to keep Anavex marginalized for as long as possible.
With compounds that are purported to prompt the body to heal itself and self-correct (as well as modulate autophagy) & thereby potentially treat a WIDE range of various CNS afflictions and diseases (reference our pipeline)
https://www.anavex.com/#!/aboutus
it’s not difficult to understand why our small Company would be quite disruptive and thereby threaten the industry leaders & their treatment centers/billions/side-effect-riddled SOC.
https://www.globenewswire.com/news-release/2019/03/04/1745838/0/en/Anavex-Life-Sciences-Reports-Publication-of-New-Data-that-Show-ANAVEX-2-73-Induces-Cellular-Recycling-Process-Linked-to-the-Prevention-and-Treatment-of-Age-Associated-Diseases.html
Godspeed to the researchers and patients and EU/EMA/AU regulators in our trials.
Will be interesting to see if the BP-beholden Congress/FDA will display leadership & respond quickly and favorably (given our excellent safety record and positive RWE reported by our ph2a patients) if our PDD/Rett trials meet or exceed primary endpoints in the coming 3-4 months.
CNS disease-afflicted patients deserve better treatment options and fewer serious side-effects than the current SOC.
GLTAL
[https://www.google.com/amp/s/finance.yahoo.com/amphtml/news/congress-big-pharma-money-123757664.html
“I’m really much more concerned because Congress is supposed to have oversight for the FDA,” Brown said. “If the FDA isn’t going to hold pharma accountable, and Congress is getting paid to not hold pharma accountable, then it really doesn’t matter who the president is because it’s really about Congress.”]
Those still represent my personal understanding of the facts as it pertains to our phase 2a AD trial. Time will tell how our compound performs in our double blind placebo controlled AD ph2/3, and/or the PDD and RS trials.
Based on various breadcrumbs however, I’m optimistic.
Likely that something is related to the something that caused Dr Walter Kaufmann to join Anavex in January as our Chief Medical Officer.
https://www.anavex.com/anavex-life-sciences-announces-the-appointment-of-walter-e-kaufmann-md-as-chief-medical-officer/
JJ, it appears to me that the BOD has reason to believe that our Company has something very important (and valuable) to protect, they don’t trust BP’s intentions and motives, and that without the blank check preferreds we’re sitting ducks.
GLTY
Plex I’m just adding to my holdings and enjoying the Company’s steady and positive progress. The newly issued patent and Chief Medical Officer position for Dr Kaufmann speak loudly to me.
Good luck to you and to all of the true longs here.
So for today’s update you’re telling us that you are questioning strength and buying momentum, something’s drying up, increased confidence for sellers, slam downs pullbacks, capping, critical, looking low for support.
Noted!
Thank you for this valuable scientific contribution. I hope that it helps Anavex achieve its goals. Great work!
Wait a second, Tom, are you telling me that you’re calling for stepdowns and downwaves and resistance shoulders and intense selling pressure?
Where have I heard that before?
Agreed bourbon, message board attacks have largely shifted to share price bashing and market value suppression; emotional warfare to free up shares and/or derail company progress.
Not surprising. There are billion dollar chips on the table.
Dr M seems indifferent and unconcerned with the current market cap or WS/analysts, instead simply focusing on the 3 active new trials and progressing the science. He assumably plans to simply let the trial results and regulatory bodies’ actions dictate any market value reset.
Can’t say I blame him with trial read outs swiftly approaching in 2019. GLTY
Most longs here are using logic and currently available facts and are paying attention to the gaining momentum and positive presentations and positive efficacy-to-date (in various CNS indications) and positive reported RWE/quality of life benefits for our ph2a patients and the recent trial approvals from EMA and AU and FDA and positive comments in the press from our AU ph2/2a trial principal investigator, coupled with the over 100 scientific peer reviewed papers outlining the positive effects of Sigma-1 receptor agonists (and the corresponding LACK of papers to the contrary).
Contrast the above with our largest competitor in the race for a viable AD treatment which faces the below type of PUBLIC pushback and criticism from analysts and scientific writers of its trial efficacy claims & questionable data presentation:
https://www.google.com/amp/s/www.thestreet.com/amp/investing/stocks/biogen-alzheimer-s-data-leaves-investors-with-more-questions-as-stock-drops-14663952
“Another concern about the data stems from the lack of patients from the treatment group with the highest dose who have a genetic carrier associated with Alzheimer's called ApoE4 compared with the placebo group, which could have influenced what investors saw from an efficacy standpoint, Phipps said.
"You're not doing an apples-to-apples comparison," Suneja said.”
https://endpts.com/eisai-biogen-outline-an-impressive-30-and-47-advantage-for-their-alzheimers-drug-ban2401/
https://www.mdedge.com/clinicalneurologynews/article/171238/alzheimers-cognition/alzheimers-trial-design-problem-throws
https://www.healthnewsreview.org/2018/07/many-questions-linger-about-this-possible-alzheimers-treatment-so-why-the-avalanche-of-news-coverage/
https://www.google.com/amp/s/www.bizjournals.com/boston/news/2018/10/25/biogen-analysts-pounce-on-thin-alzheimers-trial.amp.html
“But analysts weren't convinced, with Geoff Porges of Leerink Partners calling the presentation "thin" and "unconvincing."
"In our view this data is confusing, suggesting only limited value for BAN2401 in the carrier population, while the small number of patients remaining on drug at the 18-month time point and lack of clear dose responses diminish the reliability of this dataset," Porges wrote in a note.”
https://www.google.com/amp/amp.timeinc.net/fortune/2018/07/30/alzheimers-biogen-eisai-ban2401
https://xconomy.com/boston/2018/10/25/fresh-data-add-more-confusion-to-eisai-biogen-alzheimers-drug/
http://www.pmlive.com/pharma_news/big_debate_follows_biogeneisais_alzheimers_study_unveiling_1245863?SQ_DESIGN_NAME=2
https://www.google.com/amp/s/www.cnbc.com/amp/2018/07/26/biogen-eisai-sink-as-much-awaited-alzheimers-results-raise-questions.html
New Anavex AD trial article in Alzheimer’s News Today 10/31/18 https://alzheimersnewstoday.com/2018/10/31/anavex-2-73-slows-cognitive-decline-alzheimers-extension-study/?amp
“Treatment with Anavex‘s investigational therapy Anavex 2-73 significantly reduces cognitive decline in people with Alzheimer’s disease and sustains their ability to perform daily activities, according to interim data from a Phase 2 extension study. Trial results were presented in a late-breaking oral presentation, titled “Longitudinal 148-Week Extension Study for ANAVEX®2-73 Phase 2a Alzheimer’s Disease Demonstrates Maintained Activities.”
New Anavex PDD article in Parkinson’s News Today 11/1/18
https://parkinsonsnewstoday.com/2018/11/01/anavex-recruiting-parkinsons-dementia-patients-spain-anavex-2-73-trial/?amp
“Results from preclinical studies have shown that Anavex 2-73 has the potential to restore function to damaged nerve cells in mouse models of Parkinson’s disease. The compound was also found to target faulty proteins and poorly working mitochondria — the cells’ powerhouses — preventing oxidative stress and inflammation.
As of now, only one medication, Nuplazid (pimavanserin) is approved by the U.S. Food and Drug Administration for the treatment of hallucinations and delusions associated with Parkinson’s disease.”
Thanks for your analysis, inv2014.
At the risk of oversimplification, but in light of the below quotes from Drs Hampel and Afshar at CTAD on Friday, and after reading the Company’s conclusion on slide 21 at CTAD “Excluding the patients with the two identified biomarker variants (approximately 20% of the population), the resulting 80% of the remaining population would lead to further clinically significant improved functional and cognitive scores”:
Couldn’t it be a reasonable ASSUMPTION that the outliers [such as the poor responder participants with high blood concentration on the MMSE test (# 1002 2001 and 2002 at 57 weeks, link below)] are participants that likely have the identified biomarker variants (20% of the population)?
Hence these outliers would be participants (assumably in the 20%) that genetically would not respond as well to a2-73 regardless of high or low blood plasma concentration?
Aren’t the quotes and the company’s stated conclusion supportive of that assumption?
More supportive than not, I would argue.
“These results further confirm the impact of actionable genetic variants that were previously identified through a full, unbiased genomic analysis of ANAVEX®2-73 in Alzheimer’s disease, raising optimism for the future of biomarker-guided precision medicine to effectively combat this devastating disease,” said Professor Harald Hampel, M.D., Ph.D., M.A., M.Sc.
“We are excited to see our initial biomarker hypothesis confirmed at 148 weeks. The biomarkers were selected through a systematic, data-driven analysis of all available genomic and clinical data, which identified a genomic alteration of SIGMAR1, the target of ANAVEX®2-73. The consistency of the DNA and RNA data, as well as multiple endpoints and time-points further strengthen this biomarker hypothesis,” said Mohammad Afshar, M.D., Ph.D., CEO of Ariana Pharma.
https://globenewswire.com/news-release/2018/10/26/1627897/0/en/Anavex-Life-Sciences-Presents-New-Three-Year-Longitudinal-Clinical-Efficacy-Data-for-ANAVEX-2-73-in-Alzheimer-s-Disease-at-the-2018-Clinical-Trials-on-Alzheimer-s-Disease-CTAD-Meet.html
And slides 30 and 31 at May 2018 corporate presentations for patient numbers per blood concentration level at 57 weeks:
https://www.anavex.com/wp-content/uploads/2018/05/Anavex-Presentation-May-2018-1.pdf
Thank you PeterK. And with all that’s been learned and presented over the past 12 months, including Ariana’s positive analysis of a2-73’s dose (blood concentration level) dependent relationship, along with the recent precision medicine 80% treatment-response biomarkers presented by Dr Hampel in July, isn’t the only logical and sensical comparison today between: (a) our 80% inclusive biomarker patients & the >4ng/mL blood concentration participants (THERAPEUTIC LEVEL per Ariana & Anavex) with (b) the historical AD progression charts?
I find it nonsensical and a red herring to include and compare our ph2a trial participants that didn’t receive a therapeutic dose (blood concentration ) of a2-73 (and/or were part of the 20% gene variants of non responders) to historical AD decline.
Should I expect my headache to subside with a less than therapeutic dose of acetaminophen? Does common sense enter the equation here?
IMO the AD results presented today by Anavex are very favorable especially in terms of the Company’s logical graphs on slides 16 & 17 illustrating the high (therapeutic) dose/concentration participants which importantly maintained their adcs-adl scores over 148 weeks and the relatively small 2 point decline in MMSE over the same 148 weeks for those therapeutically-dosed participants.
The afflicted & their caregivers would likely sign up for that result tomorrow if they had the chance (FDA? Advocacy Groups? Journalists? Anybody home?)
GLTAL, and these are my non scientific opinions and observations only.
Yes Nidan and recall too back in December 2017 we discussed that:
• MS was newly discussed in the 2017 10-k (and not in 2016)
• MS was newly mentioned in the p/r on Monday 12/11/17
• Dr M reminded us about the positive & encouraging MS data from WSU testing during the 12/11/17 conf call
• Dr M stated in the December 2017 conference call that they were still moving forward with the MS indication and that updates would be available in 2018 “in the course of the coming year” when they have “better clarity”
• the MS indication was included in the September 2017 CNS Partner Summit abstract
I wonder if their clarity has been bettered by Dr Lisak’s newest conclusions and upcoming 10/10/18 ECTRIMS poster abstract; or by any discussions following the recent 2 year MTA anniversary with Biogen?
IMO Anavex’s SAB will recommend that we pursue this MS indication and a clinical trial in light of the 3rd party experts’ positive preclinical findings at ECTRIMS 2017 and now 2018.
Seems there should be available grants and funding available from the National MS Society or other foundations, right? We are talking about positive preclinical conclusions & a2-73 results from one of the top MS labs and researchers in the US, if not globally.
GLTAL
It is interesting that one of the top Multiple Sclerosis researchers from the WSU MS lab is still spending his valuable time focused on a2-73 and presenting positive conclusions to his peers.
Appears quite encouraging IMO. I doubt that we are the only ones taking notice.
Abstract 10/10/18:
Conclusions: ACTH, DM and Anavex®2-73 are able to inhibit B cell Sup mediated death of OL in vitro. Since there is progression and degeneration in many treated MS patients, development of agonists for MCR and s-1R are potential protective treatments for patients with MS.
http://www.professionalabstracts.com/ectrims2018/iplanner/#/person/2214
Abstract 10/27/17:
Conclusions: ANAVEX2-73 and DM protect OL, OPC and Neu from several toxic molecules involved in pathogenesis of MS. Protection appears to be dependent on signaling through S-1R. Both ANAVEX2-73 and DM increase OPC proliferation. ANAVEX2-73 also accelerates OPC maturation to OL. S-1R agonists could provide both protection and help with repair in MS.
https://www.ectrims-congress.eu/2017.html
http://www.professionalabstracts.com/ectrims2017/iplanner/#/grid
Also from October 2017:
“A unique feature of ANAVEX2-73, compared to another sigma-1 receptor agonist we studied, is that ANAVEX2-73 accelerates the maturation of oligodendrocyte precursor cells (OPC) to oligodendrocytes (OL)” said Dr Robert P. Lisak. “This is an important feature since OPCs can replace lost OLs by maturing into new potential myelin-producing cells. In other words, ANAVEX2-73 might promote remyelination. Further data also demonstrates that ANAVEX2-73 provides protection for OL, OPC’s, as well as central nervous system neurons in addition to helping repair by increasing OPC proliferation and maturation in tissue culture.“
“These findings provide additional evidence for the neuroprotective and neurorestorative effects of ANAVEX2-73, as well as further validating the mechanism of our target,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex.
More about Dr Robert P. Lisak:
http://researchnews.wayne.edu/newsletter/648/category/452/article/10452
https://www.med.wayne.edu/news/2018/04/23/wsu-ms-expert-helps-draft-new-guidelines-that-recommend-patients-begin-drug-therapy-sooner/
https://www.researchgate.net/profile/Robert_Lisak/4
Dr Robert Lisak’s MS abstract for the October 10, 2018 ECTRIMS conference is now available.
http://www.professionalabstracts.com/ectrims2018/iplanner/#/presentation/1121
34th Congress of the European Committee for Treatment and Research in Multiple Sclerosis
P582 - Sigma 1 receptor and melanocortin receptor agonists protect oligodendroglia from death induced by products of B cells from multiple sclerosis patients
R. Lisak1, L. Nedeelkoska1, H. Touil2, A. Bar-Or2, J. Benjamins1 1Neurology, Wayne State University School of Medicine, Detroit, MI, 2Neurology, University of Pennsylvania, Philadlephia, PA, United States
Objective: Determine if melanocortin receptor (MCR) and sigma-1 receptor (s-1R) agonists protect oligodendrocytes (OL) from cytotoxic factors released by B cells from patients with multiple sclerosis (MS).
Background: No disease modifying therapy for relapsing MS has been shown to directly protect OL/myelin. OL express MCRs in vitro that mediate the ability of adrenal cortical stimulating hormone (ACTH 1-39), a melanocortin, to protect OL and OL precursors (OPC) from mechanisms likely important in MS: excitotoxicity, reactive oxygen species, inflammation and apoptosis. Dextromethorphan (DM) and Anavex®2-73, s-1R agonists and weak NMDAR antagonists, protect OL and OPC from these same toxic stimuli. B cells from blood of MS patients, but not normals, release toxic factors/s that kill OL in vitro involving apoptosis. We sought to determine if ACTH, DM and Anavex2®-73 also inhibit OL death induced by products of MS B cells.
Methods: B cells were isolated by positive selection with anti-CD19 MACS beads. B cells were cultured without any in vitro stimulation, supernatants (Sup) harvested and frozen until testing. Glial cell cultures prepared from brains of neonatal rats contained OL, OPC, astrocytes and microglia. ACTH, DM, Anavex®2-73 or additional medium was added to glial cultures prior to adding B cell Sup. OL death was determined by trypan blue uptake.
Results: Sup from MS B cells were toxic to OL, those from normals were not. ACTH, DM and Anavex®2-73 all markedly inhibit OL death induced by MS B cell Sup. Antagonists of MCR or s-1R added prior to Anavex®2-73 reverse the ability to block B cell Sup mediated cytotoxicity.
Conclusions: ACTH, DM and Anavex®2-73 are able to inhibit B cell Sup mediated death of OL in vitro. Since there is progression and degeneration in many treated MS patients, development of agonists for MCR and s-1R are potential protective treatments for patients with MS.
Disclosure: Funding: National Multiple Sclerosis Society (RL, JB, AB-O), Research Foundation of the MS Society of Canada, Parker Webber Chair of Neurology Endowment (DMC Foundation/Wayne State University)., NIH and Melissa and Paul Anderson Chair in Neuroinflammatioin (Univeristy of Pennsylvania) RL has received funding for research from Mallinckrodt, Novartis, Teva, Sanofi-Genzyme, Genentech/Roche, Medimmune and Alexion; has consulted for Alexion, Celegene, Syntimmune, GLG Consulting, Insights Consulting and Alpha Sites Consulting and served as a speaker for non-branded talks for Teva. LN has nothing to declare. HT has nothing to declare. AB-O has participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from: Atara Biotherapeutics, Biogen Idec, Celgene,/Receptos, Genentech/Roche, GlaxoSmith Kline, MAPI, Medimmune, Merck/EMD Serono, Novartis, Sanofi-Genzyme. JB has nothing to declare.
Appears to be a new video up at
http://www.anavexaustralia.com/
Insomnia is specifically mentioned at the 35 second mark. Would seem strange if it was not a secondary endpoint.
“Our molecule, Anavex 2-73, has shown positive results in clinical studies. We have seen improvement in patients suffering from Alzheimer’s Disease; specifically in Working Memory, Insomnia, Processing Speed and Attention.”
Improvement in an Alzheimer’s Disease trial. That has been pharma’s goal for the last 30 years, right? At least the Australians are paying attention.
Thank you for your fact based and logical response. You make it easy to separate the wheat from the chaff around here.
Helpful posts PeterKarol and Falconer regarding inflammation. Allow me to piggyback:
There have been National Institutes of Health & Harvard researchers & Dr Perry with published articles and studies linking sleep/restoring cellular homeostasis/reduction of oxidative stress & inflammation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921176/#!po=1.60550
https://medium.com/thrive-global/the-fascinating-link-between-inflammation-and-sleep-9d57c2eca013
https://therivardreport.com/utsa-pursues-progress-against-alzheimers-cancer-and-biological-warfare/
Regarding Multiple Sclerosis:
Could reducing chronic inflammation be part of the reason that Dr Lisak believes a2-73 may promote remyelination in MS?
By reducing chronic inflammation (upstream approach), could this thereby reduce the persistent opening in the blood brain barrier, which then would help to stop the entry of blood-borne coagulation factors, etc? (See below how & why I’m asking)
First the company says about a2-73:
“The drug candidate has the potential to restore the molecular balance of cells by targeting misfolded proteins and mitochondria dysfunction. This ultimately prevents oxidative stress, inflammation, and cellular stress, processes that are shared by many neurological disorders and known to contribute for nerve cell degeneration.”
The below Multiple Sclerosis article and link from Nature.com regarding possibly inhibiting fibrinogen from entering the brain which may then allow for cells to repair myelin sheaths: https://www.nature.com/articles/d41586-017-08232-2?WT.mc_id=TWT_newsandviews
The article made a key contention:
“Demyelinated areas that arise in MS can also be considered as local ‘brain injuries’. Although there is no bleeding and subsequent blood clotting involving coagulation factors in MS, chronic inflammation causes a persistent opening of the blood–brain barrier (BBB), across which these factors might pass in large amounts. Could the permanent entry of blood-borne coagulation factors prevent OPC differentiation and myelin repair?”
The Nature article indicates that “chronic inflammation” is a root problem to solve in MS.
Perhaps a2-73 is (hopefully) proven effective in promoting remyelination in MS because of its ability to prevent brain inflammation?
Thereby reducing the persistent opening in the blood brain barrier, which helps to stop the entry of blood-borne coagulation factors?
Regarding Alzheimer’s Disease & Inflammation:
monarch6500 had also posted this back in December:
https://cosmosmagazine.com/biology/brain-inflammation-sows-the-seeds-of-alzheimer-s
And again Anavex says about a2-73:
“The drug candidate has the potential to restore the molecular balance of cells by targeting misfolded proteins and mitochondria dysfunction. This ultimately prevents oxidative stress, inflammation, and cellular stress, processes that are shared by many neurological disorders and known to contribute for nerve cell degeneration.”
Regarding Parkinson’s Disease & Inflammation:
https://parkinsonsnewstoday.com/2017/10/31/anavex-2-73-investigational-therapy-restored-nerve-cell-function-in-mice-with-parkinsons-disease-in-lab-study/
“Researchers at Lund University, in collaboration with Anavex, had already shown that Anavex 2-73 significantly improved motor function in micewith Parkinson’s-like disease. In particular, the treatment was found to restore the structure of brain nerve fibers while reducing the activity of brain immune cells.”
“More recent data provided further insight: Anavex 2-73 activates a series of brain restructuring processes that ultimately restore nerve fibers in the substantia nigra of the Parkinson’s mice. This was further confirmed with a maker of cell growth – the growth associated protein 43 (GAP43) – which was only present in the brains of treated mice, and not on untreated animals.”
It is arguably quite positive that our upstream MOA and processes appear similar across multiple (historically difficult-to-treat) neurological indications.
Disclaimer: I have no scientific training whatsoever. DYODD
Ofp, it’ll be interesting to see if the French decision is adopted in other EU countries as well. The common side effects and damage of Donepezil (when contrasted with the benefit of the drug) seem to have been the main factor, according to steadyt’s post earlier.
https://www.rxlist.com/aricept-side-effects-drug-center.htm#overview
“Common side effects of Aricept include
feeling unwell (malaise),
appetite loss,
weight loss,
sleep problems (insomnia),
muscle cramps,
tiredness,
drowsiness,
dizziness,
weakness,
shakiness (tremor),
itchy skin,
nausea,
vomiting, or
diarrhea.”
Posted by steadyt:
“Paris – In France, from August, the cost of Alzheimer’s drugs will no longer be reimbursed. The damage of the drugs is rated higher than the benefit, health minister Agnès Buzyn said the announcement today.
Four Alzheimer drugs costing the health service €90million a year will no longer be reimbursed as the ministry moves to stop them being prescribed due to harmful side effects, which include falls and broken bones.”
A lot has happened since this Dr M interview, and yes it’s over 3 years old, but at the 40 second mark he speaks about DPZ with 2-73.
Longer term results may have differed since then however.
It appeared to me that you believe the Company’s timing and decisions over the last 12-18 months have been motivated largely by ambiguous delay tactics primarily to raise money.
While raising funds is necessary, I think rather that any delays or radio silence these last 12-18 months related to precision medicine data gathering and proprietary analysis steps through & with world class data firms and leading CNS precision medicine biomarker experts such as Dr Hampel.
All coinciding nicely with the 21st CCA passage and ensuing FDA industry guidances.
I’m curious when would you have advised the Company to start utilizing the Ariana/KEM/Illumina/RNA/DNA/genomic technological harvesting of big data from our smaller number of ph2a patients.
a) In late 2016 after the 57 weeks as they did?
b) Wait 2 or 3 more years to implement after a large and costlier phase 3 and miss out on the Ariana and Illumina trial design tools currently available?
c) Perhaps skip the big data tools altogether and go with a BP styled conventional & expensive ph3?
Yes despite the fact that as outsiders we have only a fraction of the info to work with, let’s attribute Anavex’s timing and decisions to mostly questionable & foot dragging & purposefully-ambiguous methods.
That makes alot of sense Flash; rather than acknowledging the timing of the passage of the 21st Century Cures Act in December 2016 which provided for new technological precision medicine aspects in drug development, that COINCIDED CLOSELY with the hiring of Ariana and later Illumina et al to LOGICALLY HARVEST BIG DATA from our SMALLER POOL of study participants.
I’m curious when exactly you would have advised the Company to start utilizing the Ariana/KEM/Illumina/RNA/DNA/genomic technological harvesting of big data from our smaller number of ph2a patients?
Perhaps never? Or wait 2 or 3 more years after a large and costlier phase 3 and miss out on the larger trial design tools currently available from Ariana and Illumina?
Or perhaps skip our pioneering and comprehensive data analysis steps altogether? Stick instead to conventional old-school tried-and-true CNS trial methods that have been inordinately expensive and largely unsuccessful for decades?
GLTAL
https://www.google.com/amp/s/healthitanalytics.com/news/amp/21st-century-cures-act-for-precision-medicine-set-for-house-vote
"It is time to vote on 21st Century Cures, mental health legislation, and help fund the fight against opioid abuse. It will advance President Obama’s personalized medicine initiative, Vice-President Biden’s cancer moonshot, Alzheimer’s research and move many treatments and cures more rapidly and safely through the regulatory process and into doctors’ offices," said House Energy and Commerce Committee Chairman Fred Upton (R-MI) and Senate HELP Chairman Lamar Alexander (R-TN).
“What we have in the 21st Century Cures Act is an innovation game-changer, a transformational bill to bring our health infrastructure light years ahead to best match the incredible breakthroughs that are happening by the day. And it is critical to remember that passing 21st Century Cures is the best way to ensure some of this funding occurs immediately in Fiscal 2017.””
https://blogs.fda.gov/fdavoice/index.php/2017/07/two-recent-scientific-advances-underscore-an-encouraging-future-for-precision-medicine-at-fda/
https://www.google.com/amp/s/healthitanalytics.com/news/amp/fda-to-streamline-regulations-in-light-of-21st-century-cures-act
I’m convinced the founder of our new investment newsletter has a background in either P/R or motivational speaking. It’s going to do very well.
Hard hitting analysis as usual. I’m now intrigued by your theories and wish to subscribe to your newsletter.
dramnesia1, it seems you’re spending some time this evening (again) questioning and invalidating our efficacy signals and results to date. I’m not sure it takes a medical degree though to figure out if the Company is referencing positive response and efficacy in strong correlation with dose/concentration in its ph2a a2-73 participants.
I’m no doctor, but when Ariana and Anavex presented and concluded the below, what the #%@* type of response are they referring to? (if not various cognitive/function/biomarker measures as it relates to efficacy endpoints for AD patients)
I’ve provided the Ariana CEO’s conclusions and presentations below for your convenience.
If you’re short on time, skip to slide 25 in particular.
The below language is seemingly quite positive on its face, most would agree. I’m assuming then it’s just your personal decision to not believe Ariana and Anavex, correct?
[Below are quotes/cites from the October 2017 PK/PD presentation outlining Ariana’s & Anavex’s representations regarding dose/concentration relationships (from our 57 week ph2a AD participants):
http://www.anavex.com/my_uploads/ANAVEX2-73-PKPD-Phase-2a-2017.pdf
· Slide 3: in depth analysis using Ariana technology demonstrates “relationship between Anavex2-73 measured exposure and dose (PK) are consistent across study periods”
· Slide 3: in depth analysis using Ariana technology demonstrates “strong drug concentration / response relationship revealed for key Alzheimer’s disease trial endpoints cognition and function, MMSE and ADCS-ADL (PK/PD). This relationship is consistent across multiple time periods”
· Slide 3: “same applies for the brain activity biomarker ERP (PK/PD)”
· Slide 6: across the 5 weeks and the 52 weeks their slides say that the achieved (check mark) “dose-effect relationship”
· Slide 12: Ariana indicates “confirmed reliable inter-individual variability (dispersion) for the Anavex2-73 phase 2a study with 32 patient cohort” and that “this is confirmation that the sample of 32 patients of the Phase 2a provides reliable information regarding dispersion and as such allows for meaningful predictions for larger populations”
· Slide 13: Ariana indicates “relation between Anavex2-73 exposure and dose (PK) are consistent across administrations”
· Slide 14: “High Dose of Anavex2-73 correlates with exposure”
· Slide 19: “ERP Biomarker Shows Significant Drug Response: P3a Amplitude Increases with Anavex2-73”
· Slide 24: through Ariana’s KEM Systematic Analysis, they found 83 rules (possible relations across variables, endpoints, PK parameters and time) and “97% of them showing coherent dose-response relation”
· Slide 25: entitled “Robust Dose (Concentration) / Response Effect of Anavex2-73” and their KEM analysis provided “consistency for 6 main exploratory endpoints cognition, function and biomarker (MMSE, ADCS-ADL & EEG/ERPs) demonstrated through systemic exploration of the full data matrix”
· Slide 25: “97% consistency: MMSE, ADCS-ADL and EEG/ERPs: Identified relations show that high dose (concentration) is linked to improved response and low dose (concentration) to poor response”
· Slide 26: chart shows that for our participants that achieved >4ng/mL blood concentration level (9 total) during the 57 week study, that 4 improved on the MMSE tests and 1 remained at baseline (5 out of 9 is a majority)
· Slide 28: “an increase of MMSE is a rare event.” And “a patient receiving a higher concentration of Anavex2-73 has a +110% (2.1 fold) chance of improving its MMSE during 57 weeks”
· Slide 29: “KEM identifies strong non linear relations linking concentration with response for both MMSE and ADCS-ADL”
· Slide 30: High Anavex2-73 concentration linked to improved response consistently across all analytes and periods” and “both Anavex2-73 and metabolite show a consistent response across the 3 different time frames”
· Slide 32: “KEM analysis has identified exclusion / inclusion criteria. Each criteria has the potential to improve MMSE / ADAS-Cog for mild to moderate Alzheimer’s patients treated with Anavex2-73” and “these criteria will be incorporated into the upcoming Anavex2-73 phase 2/3 trial”]
Darn right, and there’s a lot to celebrate about this Company lately, irrespective of what 4 or 5 anonymous posters type here.
The writing is on the wall, at least for those that believe in our leadership team and SAB. GLTY
Great post Nidan, I appreciate your logical and fact based contributions here. I thought the conference call was excellent yesterday by the way.
Enjoyed the fact-based analysis and charts provided in Lane’s article this afternoon. He seems to continually favor Anavex’s 2-73 approach and promising results to date over SOC and Biogen’s controversial ban2401.
I speculate it’s because of our favorable safety profile and quality of life benefits and method of administration and lack of brain swelling and Australian trial extensions at the request of patients/caregivers/physicians and our cognitive improvements from baseline (that our Company has reported).
Excellent postings today biostockclub, as usual.