Anavex og CNS
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Avxl - Hej Steen
Side 17-20 illustrerer måske meget fint, hvilken respons man kan opnå i patienter i høj dosis 2-73 ( men ikke optimal titrering ).
Tænk at kunne bibeholde sin daglige funktionalitet efter 3 år.
Der er ikke taget forbehold for, at 80 % er genetisk mere modtagelig overfor behandling med 2-73.
Envidere har man ikke i nedenstående givet mere end max 50 mg.
Dvs. en evt. forhøjet og tålelig større dosis i patienter med de rette genetiske forudsætninger, ville muligvis kunne give noget der ligner en kurrende behandling.Bare det, at Alzheimer patienter i Australien med den nu tildelte SAS godkendelse nu på 6. år forsætter behandlingen, fortæller rigtig meget.
PS: Biogen havde deres Accumab ( som de skandaløst nu ansøger FDA om godkendelse af ) kørende i 12 sites i Australien - og de fik ikke lov til forlænge behandlingen med en SAS godkendelse.
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Avxl - MJF Partner betaler 50 % af omkostninger af et fremtidige Parkinson forsøg på 48 uger!
Vi har endnu ikke fået resultaterne fra fase 2 PDD, men nu går en sponsor/partner ind og garanterer 50 % af fremtidige omkostninger på et nyt forsøg i Parkinson i Australien. I forvejen betaler AUS, jo 44 % af et sådan forsøg, så det bliver næsten en gratis omgang for Anavex.
Men hvorfor nu dette nye forsøg?
Har de australske myndigheder tænkt sig at tildele en Provisional Approval på baggrund af resultaterne i fase 2 forsøget?
Er dette tilfældet, skal der køres et normalt fase 3 forsøg sideløbene med, at 2-73 under en PA må gå på markedet.
Fase 3 forsøget skal bare være afsluttet inden udløbet af den midlertidige markedstilladelse, der løber i en 3 årig periode.
Husk også, at myndighederne hele tiden har haft adgang til data fra ekstension forsøgene og måske også nu selve fase 2 forsøget!
Tilsvarende kunne det nemt tænkes, at der nu også tildeles PA i Alzheimer - her er fase 2/3 forsøget på ligeledes 48 uger godt i gang. -
Avxl - Parkinson News Today!
Værdifuld sponsor/partner i Parkinson, der har ekspertisen, viljen, økonomi og ikke mindste de rette forbindelser for at fremme processen for 2-73.
Læg mærke til at:
potential disease modifying ( Forbedring )
bliver brugt flere gange!
Hidtil har man i dag kun med lidt held formået at dæmpe symptomerne for Parkinson patienterne.
Her håber/tror man at der er potentiale for en forbedring hos patienterne!Er glad for at andre langt mere kompetente folk/organisationer også tror på casen.
Tror ikke markedet helt har opfanget/forstået betydningen af denne nyhed.
Ligesom TGAs tildeling af SAS for 2-73 i Alzheimer også er sket helt upåagtet af markedet.Shake Up Foundation henviser til de gode prekliniske af 2-73 ( 2-3 år gamle) - men tidspunktet på sponsor aftalen, med forestående resultater fra fase 2 forsøget i Spanien og Australien, virket meget påfaldende - har de fået et smugkig på disse data?
Hvis ikke kunne man ikke have ventet de par uger til disse data var lagt frem - og så vurderer en evt. aftale? -
Avxl - Distribution af 2-73 i Australien!
Anavex ser ud til at være godt igang med at kunne distribuerer 2-73 i AUS.
Iflg. dette er RETT patienter også omfattet af en SAS? - Vi har kun fået pr. på at der var tildelt SAS i Alzheimer! Mangler vi så ikke en vigtig pr. fra Anavex??En SAS i RETT betyder jo, at TGA har set en effekt i RETT og samtidig en god bivirkningsprofil!
Er data fra PD positive, som det nye samarbejde med Shake UP Foundation i Parkinson tyder på, vil Anavex så også her få en SAS eller simpelthen bare få en Provisional Approval for 2-73???
Dvs. reelt gå fuldt ind på det Australske markedet?Tror vi får svar på dette inden for de næste par måneder!!
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Anavex - HL Pharma og distribution af 2-73 kopi.
Dårlig link - derfor her en udskrift:
Anavex Life Sciences and HL Pharma
HL Pharma is pleased to announce we are working with Anavex Life Sciences Corporation to facilitate the ongoing supply of medication to patients post clinical trial completions for Rett Syndrome and the treatment of Alzheimer's Disease.Supplies are being made under The TGA Special Access Scheme regulations.
https://www.9news.com.au/national/rett-syndrome-alzheimers-drug-medical-testing-underway-on-girls-sydney/c28040fa-31e9-45fd-89d3-d180b3a4ff24
Anavex utilizes precision genetic medicine to treat severe and devastating neurological disorders and is focusing on rare diseases with no available therapy (Rett syndrome) as well as neurodegenerative diseases that are on the rise due to ageing populations (Parkinson's Disease and Alzheimer's Disease)https://hlpharma.com.au/anavex-life-sciences-and-hl-pharma/
Igen - en ekstrem god nyhed, at Anavex allerede har distributionen af 2-73 på plads i Australien!
Man skulle næsten tro, at de også forventer et salg i nær fremtid! -
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Det er en periodemæssig fejl. Vi retter så hurtigt vi kan.
Du skal dog sørge for mellemrum mellem dine smileys. I modsat fald kan der så komme spørgsmålstegn.
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Test af smiley.
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forresten tdt123 har du set nyhed på pti idag
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Anavex - BioPharma Journal den 26. aug. 2020
Bemærk:
Shake It Up Foundation will pay for up to 50% of Anavex's spending on a disease-modifying clinical trial to develop blarcamesine to cure Parkinson's disease. Founder of Shake It Up, Clyde Campbell said the organization is excited to support the development of innovative drugs to cure patients with Parkinson's disease and the like.
To cure bliver anvendt hele to gange!!!
Måske en lidt fri omskrivning af modifying, men lidt vildt at MJF partneren i Australien har så stor tiltro til Anavex og 2-73!
Eksperterne fra MJF Fundation var med inde over designet af fase 2 forsøget og MJF F. understøttede også de prekliniske forsøg i Lund, Sverige økonomisk.
Kan kun komme til den konklusion, at MJF/SIUF har set data fra min. ekstension forsøgene.
Skulle resultaterne fra det ventede fase 2 forsøg fejle, ville det sætte både Anavex og MJF/SIUF i et meget dårligt lys.
Hvorfor dette hastværk og ikke bare afvente data fra fase 2 forsøget???
Anavex Life Sciences Corp (NASDAQ:AVXL) Receives SAS Approval For ANAVEX2-73 To Treat Patients With Alzheimer’s Disease
News Alert: Citius Pharmaceuticals Receives FDA Approval For LYMPHIR™ (Denileukin Diftitox-Cxdl) Immunotherapy For The Treatment Of Adults With Relapsed Or Refractory Cutaneous T-Cell Lymphoma. Click to Read More.The Australian GDH (Government Department of Health) – TGA (Therapeutic Goods Administration) granted SAS (Special Access Scheme) approval Anavex2-73 of Anavex Life Sciences Corp (NASDAQ:AVXL) to treat patients […]
BioPharmaJournal (biopharmajournal.com)
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Anavex - Lidt opdatering.
Missling er på som foredragsholder den 20. okt. på:
Targeting the Undrugged virtual congress.
Understanding Complexities of Underlying Protein Conformation Disorders in CNS
Assess novel protein misfolding therapeutics through clinical development and commonalities in underlying molecular pathologies informing development of new treatment options.Og han er på igen den 27. okt:
Protein Misfolding Drug Discovery Digital Summit.
https://protein-misfolding.com/about/about-event/
Ville virke upassende - ja direkte dumt, når Missling skulle fremstå som ekspert taler på områder med ny innovativ forskning på CNS området, hvis han havde et fejlet forsøg i Parkinson med i baggagen. Mon ikke han havde takket pænt nej til at udstille sig selv og evt. manglende succes på området!
Har en ide om, at hvis Anavex skulle ønske max. eksponering ville Parkinson konferencen den 12.-16. september 2020 være et ideelt sted og tidspunkt at offentliggøre evt. positive Parkinson resultater på.
Dvs. en pr. med overordnet data i løbet af næste uge og så gennemgang på konferencen efterfølgende.
Vi må se - lidt ønske tænkning, men hvis forsøget var fejlet helt, burde de iflg. bestemmelserne fra SEC, efter min mening længe have meldt dette ud.
Der må gå max 5 dage fra man har kendskab til større kurspåvirkende oplysninger, til de skal meldes ud offentligt!
Vi er nu på godt 4 mdr. efter at sidste patient blev færdigbehandlet den 4. maj 2020. -
Anavex - Nu oppe på 45 sites i Alzheimer fase 2/3 forsøget.
Australien, Holland, Canada, England og Skotland.
Anavex har travlt - de manglede at indrulle ca. 40 % af de 450 patienter her i starten af august. Dvs 180 patienter fordelt på 45 sites - 4 pr. site - det burde være muligt at opnå fuld indrulning indenfor de næste par måneder.
Hvis skidtet virker og rygtet kommer ud, vil man så evt. se de første Alzheimer turister rejse til Australien, for at få 2-73 ordineret via. SAS godkendelsen? -
Anavex - En reminder om den hidtil mest omfattende analytiker gennemgang af casen.
"Anavex Is Likely To Report Positive Parkinson's Disease Trial Results For A2-73, Increasing Share Value"
Jul. 7, 2020 2:33 PM ET2 citater fra artiklen:
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The balance of potential effects indicates that A2-73 could have efficacy in Parkinson's and Alzheimer's disease patients. I am predicting an increase in share value with trial results.
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To leverage the bet, I present strong evidence that A2-73 could improve or maintain cognitive ability in PD and AD patients, signaling that imminent trial results could be favorable.
Udskrift af største del af premium artiklen:
Summary
Anavex Life Sciences is developing drugs for the treatment of Alzheimer's disease, Parkinson's disease, frontotemporal dementia, Rett Syndrome, fragile X, Angelman syndrome, and infantile spasms.
Results from the phase 2 Parkinson's disease trial are imminent; results from the phase 2/3 Rett's and Alzheimer's disease trials are expected in June 2021 and late 2021, respectively.
The sigma-1 and M1-muscarinic receptors are well studied, making their activation effects predictable in healthy brains, but less so in neurodegenerations of unknown etiology.
The balance of potential effects indicates that A2-73 could have efficacy in Parkinson's and Alzheimer's disease patients. I am predicting an increase in share value with trial results.
The combined world market for an Alzheimer's disease ("AD") and Parkinson's disease ("PD") drug is estimated to be 21 billion by 2026 and has a compound annual growth rate of 10%. The fortune from investing early in a blockbuster AD and PD drug lures many wishful prospectors. However, trials for dementia treatments have a dismal record and many investors are reluctant to invest in this sector. To leverage the bet, I present strong evidence that A2-73 could improve or maintain cognitive ability in PD and AD patients, signaling that imminent trial results could be favorable.
Anavex Life Sciences Corp. (NASDAQ:AVXL) is running clinical trials to treat Rett's syndrome (RTT), early AD, PD, and frontotemporal dementia ("FTD"). Results from the double-blind placebo controlled 14-week phase 2 trial treating PD patients with ANAVEX2-73 (A2-73) are imminent. A2-73 has been administered to AD patients for several years, so safety is unlikely to be an issue. Rather, the efficacy and future promise of A2-73 for treating dementia will be uncovered. Most drugs fail to pass through the blood brain barrier efficiently. However, A2-73 has a molecular weight of 317.9 g/m and forms only three hydrogen bonds with water (moderate lipid solubility). These properties, plus the ability of A2-73 to displace the sig1R radiotracer [18F]FTC-146 in mouse brain, as visualized by PET, indicate that A2-73 will pass through the blood brain barrier.
Anavex describes A2-73 as a moderate sigma-1 receptor (sig1R) and M1-muscarinic receptor agonist but ascribes most of the therapeutic value to sig1R activation. A2-73 was shown to have only moderate affinity for the sig1R receptor using the vas deferens bioassay. However, this assay was reported to be unreliable for sig1R affinity determination.
Sig1R is involved in a plethora of important cellular functions, including protection from stress, such as hypoxia, excitotoxicity, reactive oxygen species, as well as the regulation of oligodendrocyte differentiation, cholesterol transport, myelin generation, gene transcription, and tau phosphorylation resulting in axon extension and dendrite spine formation.
The diverse roles for sig1R are defined by its numerous protein interactions, which are modified by ligands, both synthetic and natural. Synthetic sig1R agonists bind different sites on sig1R with different affinities. Since A2-73's binding site and affinity are unknown, extrapolating other synthetic sig1R agonists effects to A2-73 could be misleading. Thankfully, several researchers have tested A2-73 and found promising effects on neuroprotection and autophagy.
Lisak et. al. recently reported that A2-73 significantly inhibited oligodendrocyte (OL), oligodendrocyte precursor cell (OPC), and neuron cell death after exposure to cytotoxic agents (quinolinic acid, glutamate, H2O2, and staurosporine--for apoptosis induction). OPC are depleted in AD brain compared to healthy controls, and A2-73 treatment increased OPC proliferation by 3-fold. The authors did not address whether reduced OPC cell death is related to increased OPC proliferation (cell death reported as percent trypan blue). Lisak reported no increase in oligodendrocyte differentiation with A2-73 treatment. However, this is contrary to Hayashi's work establishing that sig1R activation increases OL differentiation. OL generates axon-insulating myelin, and AD, but not PD, is associated with reduced myelin in the brain. Apparently, Dr. Lisak started receiving funding from Anavex shortly after submission (reported here, search for Anavex). Hold on, it gets better...
Christ et. al. reported that A2-73 stimulates autophagy in cultured human cells and C. elegans. Autophagy is the way cells remove garbage and recycle. AD and PD are both associated with impaired autophagy, so stimulating autophagy flux is desirable. A2-73 activates autophagy by somehow increasing phosphorylation of the protein ULK1 at a serine amino acid located at position 555 (pS555). This is exciting because S555 phosphorylation of ULK1 can block age-related enhanced mTORC1-mediated ULK1 phosphorylation at S757 and subsequent autophagy downregulation. (Remember AD and PD are age-related). However, autophagy impairment in both AD and PD appears to be downstream from ULK1, with increased accumulation of autophagosomes and defective lysosomal fusion and digestion. Interestingly, mTORC1 is hyperactive in AD an PD, and hyperactive mTORC1 decreases transcription factor TEFB activity to downregulate autophagy and lysosomal gene expression. And here is the clincher... Cocaine, a sig1R agonist, decreases mTORC1 activity and increases autophagy.
I think it is safe to extrapolate that A2-73 will have the same effect as cocaine since it explains how ULK1 was phosphorylated by A2-73 treatment. In absence of sig1R, autophagosome clearance is impaired, which is exactly what happens in AD and PD. Thus, A2-73 should increase autophagy in AD and PD and this is huge! I am not too worried about the sig1R-agonist inducing cell death for two reasons. First, cocaine certainly has a much higher affinity for sig1R than A2-73. Second, cell death was mediated by continuous incubation in 1 mM cocaine in cells that did not have hyper-mTORC1 activation.
Hypoxia may contribute to AD and PD neurodegeneration. Hypoxia is caused by constricted and degenerating capillaries, and sleep apnea. Treatment of stroke patients with the sig1R agonist cutamesine in a phase 2 trial improved motor scores. In AD, amyloid-ß in blood vessels (cerebral amyloid angiopathy) activates the enzyme NOX2 to release reactive oxygen species ("ROS"), which damage cells. ROS induces capillary constriction (via pericytes), reducing blood flow. Increased hypoxia further increases amyloid-ß disposition to occlude blood flow; thus, creating a vicious cycle ending in capillary collapse. Unfortunately, sigR1 agonists are known to increase reactive oxidative species. However, Goguadze et. al. 2019 reported that A2-73, and other sig1R agonists, reduced amyloid-ß induced increase in ROS. A2-73 also increased mitochondrial complex I activity, which is dysfunctional in PD neurons.
Anavex reports that A2-73 treatment normalizes brain derived neurotrophic factor (BDNF) protein expression in the hippocampus of the Fmr1 knock-out mouse (fragile-X mouse model). However, Louhivuori and colleagues report that BDNF protein expression in the Fmr1 knock-out mouse is increased in the hippocampus but decreased in the cortex compared to wild-type. Thus, it is not clear whether A2-73 really increases BDNF in the mouse Fmr1 knock-out hippocampus. Anavex contracted with PsychoGenics to test A2-73 on Rett mouse models.
What can be inferred if we assume that A2-73 has similar effects as other sig1R agonists?
Choline is Sig1R's natural ligand. Treating AD and PD patients with choline improves cognitive and motor performance, respectively. Choline is deficient in AD brains and PD brains (male), and supplementation could translate into increased acetylcholine and phosphatidylcholine production, lipid transport, methyl donation, and sig1R activation. A2-73 treatment will mitigate one aspect of choline deficiency by activating sig1R.
Activation of sig1R upregulates IL-10 cytokine expression. Increased IL-10 blocks innate immunity, increases amyloid-B accumulation, and reduces synaptic integrity. However, IL-10 levels and signaling are already significantly upregulated in AD and PD. It is unknown whether further IL-10 upregulation will increase AD-like pathology.
A2-73 could improve cognition by acting as a muscarinic agonist. Early trials of the M1/M4-selective muscarinic agonist (xanomeline) produced a modest effect in AD patients, but intolerable gastrointestinal side effects. Xanomeline efficacy could have failed because it actually reduced acetylcholine release by activating presynaptic muscarinic receptors to enhance feedback inhibition. A more recent trial of the selective M1 muscarinic allosteric agonist (MK-7622) failed to improve cognitive function in AD patients.
Unfortunately, muscarinic receptor G-protein signal transduction (coupling) is defective in AD (I'm first author). However, PD patients have normal M1 to G-protein coupling. Interestingly, muscarinic G-protein coupling is sensitive to magnesium deficiency in the aged rat hippocampus tissue (I'm second author); and serum magnesium levels are lower in AD patients. However, allosteric sig1R agonists increase acetylcholine release in rat frontal cortex and thus, A2-73 may increase acetylcholine release independently of muscarinic receptors.
Regardless of the mechanism, A2-73-mediated muscarinic receptor activation may not benefit PD patients. Agonists of the central muscarinic receptors activate acetylcholine release from the vagal nerve innervating the mucosal wall of the intestines. Acetylcholine binds and downregulates immune cells, in what is called the cholinergic anti-inflammatory pathway (CAP). Patients with vagal nerve transections have significantly reduced PD risk.
PD is characterized by abnormal dopamine signaling due to the loss of dopamine producing neurons. Dopamine receptors 1 and 2 (D1R and D2R) form a heteroreceptor complex with Sig1R. When cocaine, a Sig1R agonist, binds Sig1R it reduces D2R internalization, increasing dopamine binding capacity (Bmax) and signaling. Similarly, cocaine and another Sig1R agonist PRE084, altered the configuration of the Sig1R-D1R-D1R heteroreceptor complex resulting in enhanced D1R signal transduction. This enhancement could result from cocaine acting on Sig1R to bias D2R signaling to G-protein (Gai/o) signaling rather than the arrestin pathway with subsequent receptor internalization and D2R desensitization. Thus, cocaine, and perhaps A2-73 too, enhance D1R and D2R signaling.
Cocaine can also increase dopamine in the extracellular space by binding and blocking the dopamine transporter (DAT) in the outward conformation. PD patients have sworn that cocaine relieves their dyskinesia during "off" episodes. Too much dopamine can be harmful though; toxic dopamine levels increase a-synuclein expression in chronic cocaine users and this increases PD risk.
Sig1R agonists increase Sig1R monomer binding to DAT, stabilizing DAT, and increasing extracellular dopamine. In several different mouse models of PD, treatment with the SigR1 agonist PRE084 significantly attenuated motor impairment. Increased dopamine signaling relieves PD motor symptoms, but there is also evidence that patients with higher Levodopa dosages (dopamine) maintain their cognitive ability.
Interestingly, a sig1R sequence polymorphism (G241T/-C240T) is associated with AD risk in Japanese and Hungarian cohorts. However, the protective allele reduced Sig1R expression in a gene reporter assay. This result however, could be cell-type specific, since sig1R expression is significantly decreased in only some brain regions with age and in AD.
Anavex is currently running three phase 2 trials for treating RTT; two are treating adult RTT (NCT03758924 and NCT03941444), and one trial is treating pediatric patients (NCT04304482). RTT is a rare X-linked neurodevelopmental disordered characterized by abnormal cognitive and motor development. Most RTT patients carry a mutation in the gene MECP2. MECP2 is involved in regulating gene expression in the brain. There is currently no treatment beyond managing symptoms for Rett syndrome. In a preliminary open-label pharmacokinetics study, treating 6 RTT patients for 7 weeks with A2-73, all measured endpoints significantly improved. For instance, treatment significantly reduced glutamate, which is increased in the cerebrospinal fluid of RTT patients. Interestingly, a sigR1 agonist can also reduce glutamate release in rat cerebral nerve endings. After reviewing the promising preliminary data, the FDA granted Anavex fast track designation to facilitate A2-73 development and review. On June 16, 2020, Anavex reported that enrollment in the US trail exceeded the target by 50%.
Rett syndrome shares some biochemical and pathological features with AD and PD disease. For instance, common clinical features include autonomic dysfunction, immune dysfunction, chronic hypoxia, oxidative stress, mitochondrial abnormality, synapse pathology, abnormal excitability, and white matter damage, disturbed sleep, and adult parkinsonian movement disorder. However, Rett is a developmental disease driven by faulty cell differentiation, while AD and PD are complex diseases involving genetic susceptibility, multiple environmental risk factors, and unknown drivers.
Reports of AD patient's effects in the A2-73 trial are encouraging. The high dose cohort had a significantly lower MMSE decline (-1.1) compared to a matched control cohort (-4.4) at week 104 (p < 0.01).
(There is more to the excellently researched article, this is just the
first section, including two videos of long term recovering AD patients in the link at the bottom) -
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Anavex - CC både den 14. og 17. september!
Man skulle næsten tro at de er ivrige efter at fortælle hvordan det går, når de er på hele 2 gange i træk! ( Har ikke set dem gøre det tidligere )
Mon ikke vi får resultater fra Parkinson inden da - Anavex ved udmærket, at det er det aktionærene venter på.Kun 4 handelsdage inden den 14. september!!!
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Tasso. Ja, vi mangler i den grad nyt fra dem, og selvfølgelig helst godt nyt. Der er lidt tale (bange teorier) om datoen den 30/9 på yahoo, men det har du sikkert læst. Jeg er enig i at det ville virke underligt at fremlægge dårlige resultater 2 gange i streg. Jeg vil dog også sige at det på ingen måde er usædvanligt at deltage i flere konferencer tæt på hinanden i denne genre. Jeg får VILDT mange IR meddelelser af den slags (40% af mine penge står i biotek).
Pøj pøj til os
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Anavex - 3 mulige senarier for de 2CCer.
Intet nyt.
Anavex koger suppe på gl. nyheder i 2 omgange for at få kursen højere op for salg af nye aktier.- De par aktier flere de ville kunne sælge til en højere kurs, ville ikke kunne redde noget som helst ved efterfølgende dårlig nyt fra Parkinson og svigt af investorernes tillid.
Dårligt nyt.
Anavex har så dårlige nyheder fra Parkinson, at de har brug for hele 2 CCer, for at redde stumperne.- Hvis Anavex havde dårlige resultater fra Parkinson, ville de nok holde en CC efter markedet er lukket en fredag aften og ikke udstille sin manglende succes hele 2 gange mens markedet er åben.
Gode nyheder.
Anavex offentliggøre data fra Parkinson i denne uge eller senest i premarkedet mandag den 14. september.
De starter med en CC, som primært henvender sig til investorer midt i åbningstiden for markedet på første dag i ugen, med de overordnede resultater fra Parkinson.
Dette er nok til at skabe opmærksomhed og for at få nye investor til at gå ind i aktien og starte et momentum.
Senere - når markedet har absorberet resultaterne går de den 17. september på en mere videnskabelig CC, hvor man får mulighed at gå mere ned i detaljerne og nørde data for fagfolk, der også forstår mekanismerne.
Endvidere har man samtidig mulighed for at bevare et vist momentum en tid frem.- Vælg selv, men nægter simpelthen at tro på, at Anavex vil bruge 2 CCer på at udstille sig selv, uden at have noget positivt med. Dette ville i den grad være et kæmpe selvmål over for dem selv, men også overfor deres nye Shake It Up MJFF. partner, som vil betale 50 % af næste fase 3 forsøg i PD.
Og hvorfor er ca. 100 % af disse Parkinson patienter forsat i ekstension forsøget, hvis der ikke var nogen effekt med 2-73?
Snart får vi svaret!!!
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