ANAVEX NY TRÅD!! FEBRUAR 2022 POSITIV AVATAR FASE 3!
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Anavex. Lane Simonian fra SA tror på 2-73 i Alzheimer.
Som sædvanlig, synes han at kunne underbygge sin tilgang med faglige argumenter - nok bedre og med mere indsigt i mekanismerne end de fleste andre analytiker på området.
" Based on its apparent mechanism of action and previous trial results, Anavex has the potential to set a benchmark which its competitors may not be able to reach.
Phase 2b/3 clinical trial results for blarcamesine for Alzheimer's disease should be available near the end of this year or the beginning of the next. If the results replicate those from small open label trials for blarcamesine, then one can expect at least accelerated approval by the FDA (blarcamesine could then be sold while a confirmatory trial is run)."
Anavex's Blarcamesine: Why It May Treat Alzheimer's Disease
Jun. 02, 2022 7:28 PM ETAnavex Life Sciences Corp. (AVXL)SAVA, ALEC, ANVS, ATHA, IBB, XBI, ARKG, FBT, LABU, BBH, PBE, IDNA, GNOM, SBIO, BIB, LABD, BTEC, IEIH, BBC, BBP, BIS, WDNA, CNCR7 Comments17 Likes
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Lane Simonian
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SummaryDirectly or indirectly, peroxynitrite is responsible for much of the damage done to the brain in Alzheimer's disease.
As a sigma-1 agonist, blarcamesine limits peroxynitrite formation by inhibiting intracellular calcium release.
Blarcamesine likely scavenges peroxynitrite. Its main oxidation product, butyrolactone, converts some of the remaining peroxynitrite into nitrate.
Blarcamesine reverses some of the damage done to the brain by peroxynitrite by acting as an antioxidant and through the de-nitration of critical receptors, transport systems, and enzymes.
Phase 2b/3 trial results for blarcamesine may be available as soon as the end of this year. If the results are positive, the FDA will likely grant the drug accelerated approval.The manner in which Anavex Life Sciences Corp.'s (NASDAQ:AVXL) blarcamesine fits into the following quote and chart helps explain why it should help treat Alzheimer's disease:
The inflammatory mediator peroxynitrite, when generated in excess, may damage cells by oxidizing and nitrating cellular components. Defense against this reactive species may be at the level of prevention of the formation of peroxynitrite, at the level of interception, or at the level of repair of damage caused by peroxynitrite (source of quote).
Primary Pathway to Peroxynitrite (ONOO-) Formation and the Consequences of Peroxynitrite Formation in Alzheimer's Disease (original chart):
G protein-coupled receptor or Receptor Tyrosine Kinase
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Phospholipase C
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Intracellular Calcium Release and Diacylglycerol
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Protein Kinase C
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NMDA Receptor
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Calcium Influx
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Superoxide Anions and Inducible Nitric Oxide
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Peroxynitrite
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Neuronal Cell Death (via caspase-3 activation and Bax translocation)
Mitochondrial Dysfunction
DNA Damage
Neuroinflammation (via toll-like receptors and microglia activation)
Lipid Peroxidation
Tau nitration
Reduced regeneration of neurons, synapses, and axons (via nitration of the pro-survival phosphatidylinositol 3-kinase/Akt pathway).
Decreased levels of neurontransmitters needed for the retrieval of short-term memories, balanced mood, sleep, social recognition, and alertness (multiple studies).
Reduced blood flow in the brain
Damage to the blood-brain barrier
Reduced transport of glucose in the brain
As a sigma-1 receptor agonist, Blarcamesine (Anavex 2-73) inhibits the formation of peroxynitrite by limiting the release of intracellular calcium.
Some of the potential benefits of sigma-1 receptor agonists are as follows:
In an Alzheimer cell line, sigma-1 agonist fabomotizole decreased caspase-3 and Bax levels while limiting microglia activation, thereby reducing inflammation and apoptosis of cultured neurons. With such effects, sigma-1 [receptor] agonists could save neurons and slow disease progression, thereby limiting associated dementia symptoms (source of quote).
However, if a compound only acts as a sigma-1 receptor agonist, it probably only modestly slows down the progression of a variety of neurodegenerative diseases.
Blarcamesine Intercepts Peroxynitrite
Blarcamesine is a tetrahydrofuran derivative. When oxidized by hydrogen peroxide, tetrahydrofuran forms butyrolactones which act as peroxynitrite decomposition catalysts. Put another way, tetrahydrofurans first scavenge/reduce hydrogen peroxide (by donating hydrogen atoms and electrons) and then its oxidation product butyrolactone further detoxifies some of the remaining peroxynitrite. Compounds that scavenge hydrogen peroxide don't always scavenge peroxynitrite, but they often do.
Aricept (donepezil) and Cassava Sciences' (SAVA) simufilam contain ketone groups that can also act as peroxynitrite decomposition catalysts (by changing peroxynitrite to nitrate: ONOO- to NO3-), but there is no evidence that either are peroxynitrite scavengers (ketones are not easily oxidized). Moreover, Aricept is and simufilam may be sigma-1 receptor agonists. They thus fulfill two of the three conditions set out in the opening quote to treat peroxynitrite-mediated neurodegenerative diseases. That is probably one of the reasons why each leads to some minor improvements in cognition at one year (simufilam better than Aricept). However, only blarcamesine appears to fit the third requirement.
Blarcamesine Repairs Part of the Damage Caused by Peroxynitrite
Blarcamesine acts as an antioxidant by donating hydrogen atoms and electrons. As a probable peroxynitrite scavenger, it produces water which helps de-nitrate critical enzymes, transport systems, and receptors in the brain. Blarcamesine produces greater improvements in cognition over longer periods of time than other Alzheimer's drug candidates and produces improvements that are on a par with panax ginseng at a year and a half (a natural product that also matches the criteria set forth in the opening quote) (previous article). As such, it provides a unique opportunity for investors and a major source of hope for Alzheimer's patients and their caregivers.
Financial Considerations
Despite a recent substantial drop in stock value (which has affected almost all drug companies working in the Alzheimer's space), Anavex has more than sufficient resources to complete its current trials: approximately $150 million in cash and cash equivalents (fiscal report). It is ahead of many of its competitors such as Cassava Sciences, Alector (ALEC), Athira (ATHA), and Annovis (ANVS) in terms of completion of a large-scale clinical trial for Alzheimer's disease. Based on its apparent mechanism of action and previous trial results, Anavex has the potential to set a benchmark which its competitors may not be able to reach.
Phase 2b/3 clinical trial results for blarcamesine for Alzheimer's disease should be available near the end of this year or the beginning of the next. If the results replicate those from small open label trials for blarcamesine, then one can expect at least accelerated approval by the FDA (blarcamesine could then be sold while a confirmatory trial is run).
Lane Simonian:
History instructor. Alzheimer's disease researcher for the past decade.My goal is to give investors solid advice based on the mechanisms of action of Alz
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Anavex. Hvis han køber nogen dobler jeg min position. Men ja, meget flot arbejde han laver
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Anavex ...TDT123 ikke fordi jeg vil diskutere, men køberen af Anavex aktien har tabsrisiko på aktien, idet han får aktien tilbage, når shorteren har lukket positionen.
At han får den tilbage fra shorteren, hvis kursen stiger over et vist niveau kan næppe betegnes for en risiko for ejeren af aktien
Men lad os ikke diskutere det
God dag til alle.
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Hej Solsen...
Præcis ejerne har ikke risikoen, han tjener renter på udlån..
Men ja, der er da altid en risiko ved at være aktionærer, ens beholdning kan tabe værdi...Men vi lukker den der, for som skrevet er jeg ikke expert, og det svært at finde information, der kommer med en forklaring som kan tolkes 100%
Rigtig god weekend
Også til alle andre
Mvh
Torben
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Anavex her en artikel hapset fra FB gruppen. Den styrker troen på vores tilgang. https://neurosciencenews.com/autophagy-amyloid-alzheimers-20726/
God pinse
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Og må jeg indskyde: Hvis det er den samme mus som Missing brugte i 2014 , ja så er vi sgu godt på vej.
God pinse derude, også i Thailand
MM -
Anavex .... En af de rigtigt gode skribenter på IHub har fundet denne
https://onlinelibrary.wiley.com/doi/10.1002/ajmg.a.62853Blacamesine in FragileX works
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Anavex Konferencer i juni.
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juni R & D
Anavex har lovet nyheder/opdateringer før.
22.-23. juni:Rare & Genetic & Neurodegenerative:
https://rare-genetic-neurodegenerative-development.com/whats-on/speakers/
MM - fin artikel!
Bekræfter kun igen det vi nok vidste, at fedtdannelser i hjernen kun er symptomer på at noget er galt i hjernen og ikke årsagen.
Anavex går efter behandlingen af årsagen og ikke symptombehandling!Solsen - Det kan igen undre mig, at Anavex ikke lige smider en lille PR på dette?
Brain cell signaling abnormalities are detected in blood in a murine model of Fragile X syndrome and corrected by Sigma-1 receptor agonist Blarcamesine
Anavex ville jo komme med et eller andet mere, som skulle vise, hvorfor de mente, at 2-73 ville have en god effekt i Fagile X og dermed opstart af et fase 3 forsøg - er denne afhandling mon ikke en del af dette?
Ellers er ingen nyheder ensbetydende med, at vi pr. autohandel blot følger XBI-indekset.
Ser i første omgang frem til de lovede nyheder op til R & D dagen.
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Anavex Nasdaq er lukket på R&D den 20. juni.
Opdagede lige, at US markedet er lukket mandag den 20. juni!
Dvs. at Anavex i princippet kun har denne og næste uge til de lovede nyheder.
Ved ikke hvor normalt det ellers er at komme med nyheder/udmeldinger på en lukkedag?Ville være rart med lidt positive nyheder med en efterfølgende større omsætning i aktierne - nuværende handel er jo næsten gået i stå og fortæller reelt ikke noget om hvilket kursniveau Anavex burde befinde sig i efter min mening - ingen køber og ingen sælger for alvor!
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Anavex Helt korrekt Solsen med den 21. juni!
I princippet ændre det måske ikke det store angående forventninger til nyheder i denne eller næste uge - ellers skal Anavex vente helt hen til kl. 13.00 den 21. juni - og sådan opfattede jeg ikke hans udmelding.
Han gav efter min mening udtryk for, at man fik oplysninger/nyheder lidt/noget før selve mødet - at give disse umiddelbart før mødet giver ikke den store mening i min optik, hvis man ønsker at tiltrække sig opmærksomhed til denne særlig og hidtil ikke tidligere afholdte mødeform.- Vi kan ikke andet end afvente!
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Anavex ... Det er jeg enig i
Håber dælme, at de kommer med en forløsning af den viden de sidder inde med. Ikke mindst de mange data vi mangler og forklaring på deres SIGMAR1 platform.
De kan heller ikke blive ved med at udskyde igangsætning af de mange udmeldte forsøg.
FragileX håber jeg snart starter. Denne indikation sammen med rett er i sig selv mangedobling af kursen værd, hvis data holder til en godkendelse.
Jeg er bekymret for, at de ikke formår, at analysere data fra alzheimers i år henset til det tempo de tidligere har udvist omkring lignede arbejdsopgaver.
Den akkumulering af aktier hos profferne ser godt ud.
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Det er mig lidt en gåde, hvorfor de ikke går sammen med en partner og for forløst potentialet. Det er som om de er mere drevet af forskningen (nusse med data) end at få produkterne ud af døren. Det efterlader alt for meget rum for fortolkning. De har tidligere indikeret, at de ville gå sammen med en partner når Alzheimers skulle realiseres. Vi får snart syn for sagen.
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Anavex Authophagy - fjernelse af affaldsstoffer fra cellerne er sandsynligvis en del af løsningen.
Ny forskning understøtter igen det Anavex længe har postuleret: - At fedtet i hjernen først dannes, når skaden er sket.
Samtidig understøttes også Anavex`s MOA, at Authopagy - fjernelse af affaldsstoffer i hjernecellerne vil kunne modvirke at mekanismerne opretholdes/forbedres og dermed kan modvirke bl.a. udviklingen af Alzheimer og en række af andre CNS indikationer (platform).
Samtidig har 2-73 også den egenskab, at det modvirker fejlbehæftet MRNA (softwareprogrammet til dannelse af nye celler), at få lov til at indgå i cellemekanismen.Anavex`s 2-73 understøtter/fremmer bevisligt Authopagy!
Når en gang dette, sammen med de andre egenskaber 2-73 har, siver ind hos de større aktører i markedet/sektoren og understøttes af snarlige håndgribelige resultater - så vil Anavex få et helt andet niveau af anerkendelse!!!Det er måske bl.a. dette Anavex igen vil forsøge at underbygge og skære ud i pap på R & D dagen den 21. juni?
"This new evidence changes our fundamental understanding of how Alzheimer's disease progresses," said study senior investigator Ralph Nixon, M.D., Ph.D. "[I]t also explains why so many experimental therapies designed to remove amyloid plaques have failed to stop disease progression, because the brain cells are already crippled before the plaques fully form outside the cell."
"The new findings add to a growing body of evidence supporting issues with the cellular waste management process as a key sign of Alzheimer's." - AUTHOPAGY!!!
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Anavex Iflg. CEOen har der også været interesse/dialog fra div. aktører, men at det ville være "premature", at lave en aftale på nuværende tidspunkt, umiddelbar før de ventede gode data ville kunne give Anavex et meget bedre udgangs for at lave en mere attraktiv aftale.
Missling har gentagene gange meldt ud, at planen er et partnerskab i Alzheimer i erkendelse af, at markedet og omfanget overgår Anavexs kapacitet.Med den eller de rigtig partner, ville Anavex kunne opnå en større markedsandel meget hurtigere - så gør det ikke noget, at man skal dele lidt i porten med nogen der har hele det kommercielle setup på plads i forvejen.
En pæn upfront betaling fra en evt. AD partner ville også kunne speede Anavexs udvikling af resten af pipelinen op. -
Anavex. Peer-reviewed Fragile X udgivelse!
Peer-reviewed publication in American Journal of Medical Genetics
Anavexs Publication Supports Clinical Biomarker for ANAVEXÂ
2-73 in Fragile X SyndromeFlash Alert
Real-time alerts about equities, ETFs, cryptocurrencies and more sent to any device
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Nu må der langt om længe være grønt lys for fase 3 forsøget i Fragile X!!!
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