Præsentation på AD/PD konference i Wien den 5. april 2025.
https://www.anavex.com/post/anavex-life-sciences-announces-positive-up-to-4-years-oral-blarcamesine-results-from-phase-iib-iii-o
Slides:
https://www.anavex.com/_files/ugd/79bcf7_4e15217c129541228327838b534afe4d.pdf
Webcast mandag den 7. april 2025:
https://finance.yahoo.com/news/anavex-life-sciences-present-24th-113000852.html
Relevante Links:
Accept af ansøgning til EMA.
https://www.anavex.com/post/blarcamesine-receives-ema-filing-acceptance-for-treatment-of-alzheimer-s-disease
Peer Review.
https://www.sciencedirect.com/science/article/pii/S2274580724006083?ref=pdf_download&fr=RR-7&rr=8fb42ede99289298
https://www.anavex.com/post/anavex-life-sciences-announces-positive-up-to-4-years-oral-blarcamesine-results-from-phase-iib-iii-o
Slides:
https://www.anavex.com/_files/ugd/79bcf7_4e15217c129541228327838b534afe4d.pdf
Webcast mandag den 7. april 2025:
https://finance.yahoo.com/news/anavex-life-sciences-present-24th-113000852.html
Relevante Links:
Accept af ansøgning til EMA.
https://www.anavex.com/post/blarcamesine-receives-ema-filing-acceptance-for-treatment-of-alzheimer-s-disease
Peer Review.
https://www.sciencedirect.com/science/article/pii/S2274580724006083?ref=pdf_download&fr=RR-7&rr=8fb42ede99289298
Hvis EMA ikke godkender Anavex 2-73, med disse OLE data oven i hatten,så fatter jeg nada. Hvad skulle diskvalificere en godkendelse, inden for denne forfærdelige og meget komplekse invaliderende sygdom?
Mayomobile med en update på OLE resultaterne https://www.sotcanalytics.com/update-compendium-2025#h.ftkrccicu22h
Han fastholder, at det stadig er en mulighed, at tidlig og uafbrudt behandling med Blarcamesine kan stoppe det kognitive forfald man ser i Alzheimers. Men forsøget beviser ikke dette.
Pga OLE forsøgets design med en 10 ugers titration under indkøring i OLE mister pts effekten og falder til et lavere kognitivt niveau i denne periode (96 mdrs målingen). Var pts der havde været på Blarcamesine i hovedforsøget fortsat med fulddosis kunne noget tyde på, at de kunne have fået pænt bedre resultat på de 4 år.
Muligt at Missling kan forklare lidt om det på dagens konference.
Men Anavex har stadig de bedste resultater på alzheimers behandling set til dato.
Han fastholder, at det stadig er en mulighed, at tidlig og uafbrudt behandling med Blarcamesine kan stoppe det kognitive forfald man ser i Alzheimers. Men forsøget beviser ikke dette.
Pga OLE forsøgets design med en 10 ugers titration under indkøring i OLE mister pts effekten og falder til et lavere kognitivt niveau i denne periode (96 mdrs målingen). Var pts der havde været på Blarcamesine i hovedforsøget fortsat med fulddosis kunne noget tyde på, at de kunne have fået pænt bedre resultat på de 4 år.
Muligt at Missling kan forklare lidt om det på dagens konference.
Men Anavex har stadig de bedste resultater på alzheimers behandling set til dato.
Anavex Lidt omtale - husk webcast 21.45 i aften!
https://www.alzheimer-europe.org/news/anavex-presents-results-phase-2b/3-open-label-extension-trial-early-ad
https://www.clinicaltrialsarena.com/analyst-comment/ad-pd-2025-anavex-blarcamesine-early-alzheimers/?cf-view
“ A significant opportunity exists for blarcamesine, with its convenient oral dosing and favourable safety profile. This is particularly apparent in Europe where both Eisai/Biogen’s Leqembi (lecanemab) and Eli Lilly’s Kisunla (donanemab) are yet to be approved by the European Medicines Agency (EMA), with concerns around safety a key challenge for both applications. Anavex’s marketing authorisation application for blarcamesine was accepted by the EMA in December 2024. Blarcamesine therefore has the potential to establish itself in the European market as a first-choice disease-modifying therapy for Alzheimer’s.”
Webcast kl. 21.45 DK-tid:
https://wsw.com/webcast/needham146/register.aspx?conf=needham146&page=avxl&url=https://wsw.com/webcast/needham146/avxl/2275487
Alt er "lidt" kaotisk lige nu - men dette slutter som alle andre finaniselle kriser på et tidspunkt og så vil en ufarlig pille, der potentiel kan bremse tabet af hjernevæv og bremse Alzheimer og andre CNS sygdomme få en fair værdisætning.
Alle data er overbevisende og EMA og andre sundhedsmyndigheder vil anerkende værdien og højst sandsynlig godkende Blarcamesine i sidste ende.
Tingene skal bare gå sin gang - uanset en tosset U.S. president eller ej.
https://www.alzheimer-europe.org/news/anavex-presents-results-phase-2b/3-open-label-extension-trial-early-ad
https://www.clinicaltrialsarena.com/analyst-comment/ad-pd-2025-anavex-blarcamesine-early-alzheimers/?cf-view
“ A significant opportunity exists for blarcamesine, with its convenient oral dosing and favourable safety profile. This is particularly apparent in Europe where both Eisai/Biogen’s Leqembi (lecanemab) and Eli Lilly’s Kisunla (donanemab) are yet to be approved by the European Medicines Agency (EMA), with concerns around safety a key challenge for both applications. Anavex’s marketing authorisation application for blarcamesine was accepted by the EMA in December 2024. Blarcamesine therefore has the potential to establish itself in the European market as a first-choice disease-modifying therapy for Alzheimer’s.”
Webcast kl. 21.45 DK-tid:
https://wsw.com/webcast/needham146/register.aspx?conf=needham146&page=avxl&url=https://wsw.com/webcast/needham146/avxl/2275487
Alt er "lidt" kaotisk lige nu - men dette slutter som alle andre finaniselle kriser på et tidspunkt og så vil en ufarlig pille, der potentiel kan bremse tabet af hjernevæv og bremse Alzheimer og andre CNS sygdomme få en fair værdisætning.
Alle data er overbevisende og EMA og andre sundhedsmyndigheder vil anerkende værdien og højst sandsynlig godkende Blarcamesine i sidste ende.
Tingene skal bare gå sin gang - uanset en tosset U.S. president eller ej.
Hvordan er det nu, Anavex har en "poison pill" i tilfælde af fjendtlig ønske om overtagelse?
Omtale i Streetwise med bla. et 12 mdr. kursmål på 42 $
Den 7. april gentog HC Wainwright sin Køb-rating på Anavex Life Sciences og fastholdt et 12-måneders kursmål på US$42 pr. aktie. Firmaet fremhævede de nyligt rapporterede fire-årige open-label udvidelsesdata fra ATTENTION-AD-studiet, og anførte, at blarcamesine-behandling viste en "fortsat klinisk og meningsfuld fordel for patienter med tidlig Alzheimers sygdom."
https://www.streetwisereports.com/article/2025/04/07/biotech-company-finds-high-impact-alzheimers-therapy-in-europe.html?fbclid=IwY2xjawJhBZlleHRuA2FlbQIxMQABHp4hgnUvuTEVIJmuZqWTQmqK26D61ca3caXEN7VFHZHNN_wQenviAzjB-vzJ_aem_sfanofT7v-VBFyUpZJuhhg
Den 7. april gentog HC Wainwright sin Køb-rating på Anavex Life Sciences og fastholdt et 12-måneders kursmål på US$42 pr. aktie. Firmaet fremhævede de nyligt rapporterede fire-årige open-label udvidelsesdata fra ATTENTION-AD-studiet, og anførte, at blarcamesine-behandling viste en "fortsat klinisk og meningsfuld fordel for patienter med tidlig Alzheimers sygdom."
https://www.streetwisereports.com/article/2025/04/07/biotech-company-finds-high-impact-alzheimers-therapy-in-europe.html?fbclid=IwY2xjawJhBZlleHRuA2FlbQIxMQABHp4hgnUvuTEVIJmuZqWTQmqK26D61ca3caXEN7VFHZHNN_wQenviAzjB-vzJ_aem_sfanofT7v-VBFyUpZJuhhg
Bestemt ikke en positiv artikel, der spåes ikke mange chancer for en godkendelse.
Det der taler for (godkendelse) for er at der ikke er nogle alternativer til Alzheimers.
Har fulgt debatten længe, spændt på at høre flere eksperter om de nylige OLE data.
Søren
Det der taler for (godkendelse) for er at der ikke er nogle alternativer til Alzheimers.
Har fulgt debatten længe, spændt på at høre flere eksperter om de nylige OLE data.
Søren
Ja, puha. Som Søren skriver, så mener forfatteren i artiklen på seekingalpha, at chancen for godkendelse hos EMA er "unlikely".
Jeg er bestemt ikke nogen ekspert i de videnskabelige udlægninger. Hvad mener Tasso om artiklen?
Jeg er bestemt ikke nogen ekspert i de videnskabelige udlægninger. Hvad mener Tasso om artiklen?
Anavex CC Abbot har konsekvent været negativ på Blarcamesine og har indrømmet, at have shortpositioner i Anavex.
Konklusionen fra 58 eksperter i Peer Reviewet mener dog noget andet.
Her mener man at Blarcamesine er overlegne de allerede godkendte fedtfjernelses stoffer på både effekt og bivirkningsprofil!
https://www.sciencedirect.com/science/article/pii/S2274580724006083?ref=pdf_download&fr=RR-7&rr=8fb42ede99289298
" Blarcamesine, a small molecule administered orally once daily, has numerically superior clinical efficacy to approved therapies while also slowing neurodegeneration in early AD patients. Blarcamesine has a demonstrated safety profile and does not require routine MRI monitoring, and given its differentiated mechanism of action, could represent a novel treatment that is complementary or an alternative to the anti-beta amyloid drugs."
Bare det at Anavex er sluppet gennem nåleøjet og har fået en opfordret ansøgning accepteret af EMA, siger en hel del, når man antager sandsynligheden for en endelig godkendelse historisk set vil ligger over 90 %.
EMAs relative nyindførte 80 dages evaulering er enten ikke færdig eller ikke offentliggjort - der er delte meninger om, at denne er mere intern og går forud for den normale 120 dages evaulering.
120 dages evaulering, som går forud for 1. Stop Clock, hvor EMA både evaluerer og stiller naturlige uddybende spørgsmål til Anavex ses ofte offentliggjort og dele heraf vil fremgå af EMAs oversigt fra deres månedlige 3-dags møder.
Denne evaulering vil være en afgørende milepæl for at se EMAs indstilling til Blarcamesine.
En blåstempling og evt. veloverstået 1. Stop Clock vil øge chancerne for en endelig godkendelse i sidste ende - dette vil et normalt fungerende aktiemarkedet også anerkende.
120 dage efter den 27. december 2024 er omkring den 26. april 2025.
Intet er dog sikkert i biotek, men der er så mange penge og modstridende interesser i både positive og negative udfald, at det kan være svært at have tillid til forskellige artikler og skribenter.
Det eneste der i sidste ende er afgørende er hvordan EMA (myndighederne) ser på Blarcamesine!
Anavex har iflg egne udsagn fuld fart på allerede nu at udbrede kendskabet til Blarcamesine hos de forskellige aktører, så de står klar til at leverer ved en evt. markedsgodkendelse.
De har også allerede produceret en tilstrækkelig mængde Blarcamesine til en lancering i EU i Alzheimer.
Man må også stille sig det spørgsmål - ville man selv eller lade pårørende bruge Blarcamesine frem for næsten ikke eksisterende og farlige alternativer?
På baggrund af de data vi nu har set ville jeg ikke tøve et sekund med at anvende Blarcamesine eller anbefale det til pårørende.
Er overbevist om, at EMA vil komme til samme konklusion!
Konklusionen fra 58 eksperter i Peer Reviewet mener dog noget andet.
Her mener man at Blarcamesine er overlegne de allerede godkendte fedtfjernelses stoffer på både effekt og bivirkningsprofil!
https://www.sciencedirect.com/science/article/pii/S2274580724006083?ref=pdf_download&fr=RR-7&rr=8fb42ede99289298
" Blarcamesine, a small molecule administered orally once daily, has numerically superior clinical efficacy to approved therapies while also slowing neurodegeneration in early AD patients. Blarcamesine has a demonstrated safety profile and does not require routine MRI monitoring, and given its differentiated mechanism of action, could represent a novel treatment that is complementary or an alternative to the anti-beta amyloid drugs."
Bare det at Anavex er sluppet gennem nåleøjet og har fået en opfordret ansøgning accepteret af EMA, siger en hel del, når man antager sandsynligheden for en endelig godkendelse historisk set vil ligger over 90 %.
EMAs relative nyindførte 80 dages evaulering er enten ikke færdig eller ikke offentliggjort - der er delte meninger om, at denne er mere intern og går forud for den normale 120 dages evaulering.
120 dages evaulering, som går forud for 1. Stop Clock, hvor EMA både evaluerer og stiller naturlige uddybende spørgsmål til Anavex ses ofte offentliggjort og dele heraf vil fremgå af EMAs oversigt fra deres månedlige 3-dags møder.
Denne evaulering vil være en afgørende milepæl for at se EMAs indstilling til Blarcamesine.
En blåstempling og evt. veloverstået 1. Stop Clock vil øge chancerne for en endelig godkendelse i sidste ende - dette vil et normalt fungerende aktiemarkedet også anerkende.
120 dage efter den 27. december 2024 er omkring den 26. april 2025.
Intet er dog sikkert i biotek, men der er så mange penge og modstridende interesser i både positive og negative udfald, at det kan være svært at have tillid til forskellige artikler og skribenter.
Det eneste der i sidste ende er afgørende er hvordan EMA (myndighederne) ser på Blarcamesine!
Anavex har iflg egne udsagn fuld fart på allerede nu at udbrede kendskabet til Blarcamesine hos de forskellige aktører, så de står klar til at leverer ved en evt. markedsgodkendelse.
De har også allerede produceret en tilstrækkelig mængde Blarcamesine til en lancering i EU i Alzheimer.
Man må også stille sig det spørgsmål - ville man selv eller lade pårørende bruge Blarcamesine frem for næsten ikke eksisterende og farlige alternativer?
På baggrund af de data vi nu har set ville jeg ikke tøve et sekund med at anvende Blarcamesine eller anbefale det til pårørende.
Er overbevist om, at EMA vil komme til samme konklusion!
8/4 2025 09:59 kontorchefen 3
125681 Kære Tasso: Tak for endnu et kompetent opslag, som i hvert fald giver mig ro i maven, men ja: "Der er så mange penge og modstridende interesser i både positive og negative udfald"
CC Abbot er i bund og grund nok en af shorternes lajkajer !
CC Abbot er i bund og grund nok en af shorternes lajkajer !
Har du bemærkninger til Seeking alpha artiklen, hvor forfatteren hælder OLE ned af brædtet?
Vestasfan
Det er netop det Tasso beskriver !
Tak Tasso for store arbejde.
Jeg tænkte det samme da jeg læste artiklen at det er sjovt at Blarcamesine er blåstemplet i et stort Peer Review at det så pludselug skulle være useless. Han er en scammer og intet andet !
Det er netop det Tasso beskriver !
Tak Tasso for store arbejde.
Jeg tænkte det samme da jeg læste artiklen at det er sjovt at Blarcamesine er blåstemplet i et stort Peer Review at det så pludselug skulle være useless. Han er en scammer og intet andet !
hmm jeg læser det ikke sådan. Placebo kontra 2-73 giver jo ingen mening, hvis begge kontrolgrupper, ved de bliver behandlet med Blarcamesine!
Anavex Her en stik modsat rettet analyse af SA!
https://www.stocktitan.net/news/AVXL/anavex-life-sciences-announces-positive-up-to-4-years-oral-sbdu01wsmp1b.html
Igen er det de helt samme data man kigger på og kommer her til en meget positiv konklusion!
"Positive
Significant cognitive improvement demonstrated over 4 years (-3.83 points in ADAS-Cog13)
Meaningful functional benefits shown (ADCS-ADL +4.30 points)
Strong safety profile with no treatment-related deaths or severe adverse events
Reduced side effect profile (dizziness decreased from 25.2% to 9.6%)
Long-term treatment viability proven with some patients on medication for 9+ years
Negative
Initial titration phase requires careful management of side effects
Treatment interruption may reduce therapeutic benefits
Early treatment initiation required for optimal results"
Ovenstående passer fint med den opfattelse jeg får fra resultaterne.
Øvrig omtale positiv:
https://www.streetwisereports.com/article/2025/04/07/biotech-company-finds-high-impact-alzheimers-therapy-in-europe.html
https://www.stocktitan.net/news/AVXL/anavex-life-sciences-announces-positive-up-to-4-years-oral-sbdu01wsmp1b.html
Igen er det de helt samme data man kigger på og kommer her til en meget positiv konklusion!
"Positive
Significant cognitive improvement demonstrated over 4 years (-3.83 points in ADAS-Cog13)
Meaningful functional benefits shown (ADCS-ADL +4.30 points)
Strong safety profile with no treatment-related deaths or severe adverse events
Reduced side effect profile (dizziness decreased from 25.2% to 9.6%)
Long-term treatment viability proven with some patients on medication for 9+ years
Negative
Initial titration phase requires careful management of side effects
Treatment interruption may reduce therapeutic benefits
Early treatment initiation required for optimal results"
Ovenstående passer fint med den opfattelse jeg får fra resultaterne.
Øvrig omtale positiv:
https://www.streetwisereports.com/article/2025/04/07/biotech-company-finds-high-impact-alzheimers-therapy-in-europe.html
Fint Tasso1
Jeg håber at dine informationer er rigtige og valide, da det ser ud som der skrives i forhold til hvilke interesse man har i forhold til Anavex -- læs Short eller Investeret
Limer sidste nyt ind fra US om detektering af Alzheimers, vil jo passe glimrende i forhold til Anavex.
Limer hele teksten ind da jeg ikke kan lime Link ind uden at der kommer alt muligt skrammel med -- håber det går.
For en god ordens skyld har jeg investeret -- Kurs ca 9,2 :-(
Artikel:
Amazing' reduction in Alzheimer's risk verified by blood markers, study says
Sandee LaMotte, CNN
Tue, April 8, 2025, 2:00 AM GMT+2
9 min read
49
A combined blood test for cognitive decline has a 90% accuracy rate in determining whether memory loss is due to Alzheimer's disease. Dr. Sanjay Gupta explains.
- Clipped From Video
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Editor's note: CNN Chief Medical Correspondent Dr. Sanjay Gupta and writerSandee LaMotte are part of the study covered in this story and have written about their experiences.
When Penny Ashford's father was diagnosed with early-stage Alzheimer's disease at age 62, she knew the devastating brain disorder might one day steal her memory. In her late 50s, her free-floating anxiety turned to outright panic when she began struggling to find words.
"I couldn't tell a story. I couldn't get my words out," said Ashford, now 61. "I remember sitting at a dinner party one time, and I couldn't finish my thoughts. It was the most unbelievable moment.
"I came home and sobbed and told my husband, 'Something is wrong with me. I can't talk,'" she said. "I was petrified."
Penny Ashford's father Barry Murphy, 75, blows out his candles while granddaughters look on. - Courtesy Penny Ashford
Today, after a complete revamp of her lifestyle and overall health, Ashford's struggles with retrieving words have eased, while measures of amyloid and tau proteins and neuroinflammation - all hallmark signs of Alzheimer's - have fallen.
Ashford knows about these improvements because she's part of a unique study tracking her progress via key blood biomarkers now being used to help diagnose early dementia. Instead of relying on painful spinal taps and expensive brain scans, these blood tests are heralded as a new, less invasive and time-consuming way to determine risk and aid in an earlier diagnosis of Alzheimer's.
The preliminary data, presented Monday at the American Academy of Neurology annual meeting in San Diego, analyzed biomarkers on 54 participants in an ongoing preventive neurology study called the Biorepository Study for Neurodegenerative Diseases, or BioRAND.
"The field is primarily using various biomarkers to determine if you have dementia or not," said lead study author Dr. Kellyann Niotis, a preventive neurologist who researches risk reduction for Alzheimer's and Parkinson's diseases at the Institute for Neurodegenerative Diseases in Boca Raton, Florida.
"No one is really looking at the changes in these biomarkers as outcome measures, as a way of tracking progress in a person's journey to improve their brain," Niotis said. "We believe these biomarkers may show how the disease progression is being modified biologically by a person's actions."
Less invasive test for Alzheimer's risk
Alzheimer's blood tests are the key to widespread prevention of dementia, experts say. If people can be diagnosed in their doctor's office, they can more immediately move into preventive care and implement lifestyle changes designed to slow the progression of their disease.
The problem, said senior study author Dr. Richard Isaacson, is the variability in how well these new blood biomarker tests work to predict or track disease progression.
"There is a dirty little secret in the Alzheimer's blood testing community where so many testing platforms, biotech companies, and a flurry of new blood tests are released," Isaacson said, "but it's unclear which of these tests are most accurate to track progression and evaluate response to therapies to slow progression toward dementia."
More in Health
Men's Fitness
To address this gap, Isaacson's research team and collaborators at five sites across the United States and Canada set forth to evaluate and eventually cross-compare the clinical use of what the neurologist said he believes will one day become "the cholesterol test for the brain."
"In the not so far future, people in their 30s, 40s, 50s, 60s and beyond will get a baseline test to evaluate risk and help track progress over time - similar to how traditional cholesterol tests are used today," said Isaacson, founder of one of the first Alzheimer's prevention clinics in the United States.
"Our eventual goal is to offer a blood panel at cost to help democratize access and broaden the ability for people to receive care," he added.
What Alzheimer's blood tests currently measure
Measuring levels of both amyloid and tau is key to understanding and diagnosing Alzheimer's and other forms of dementia.
This illustration depicts cells in an Alzheimer's affected brain. The brown areas depict beta-amyloid protein plaques. The blue areas represent tau proteins that accumulate and form tangles. - NIH/AP
Amyloid plaques play a key role in the development of Alzheimer's when small clusters gather at synapses in the brain and interfere with the nerve cells' ability to communicate. Such plaques are thought to trigger changes in tau proteins,which form into tangles in parts of the brain controlling memory.
Tau tangles are also implicated in other neurological diseases such as frontal lobe dementia, or FTD, and Lewy body dementia in which abnormal clumps of a protein called alpha-synuclein accumulate in the brain's neurons.
The biomarker plasma phosphorylated tau 217, or p-tau217 for short, is a top contender in the diagnosis of mild cognitive impairment and early-stage Alzheimer's disease. Its cousin, p-tau 181, is also a helpful indicator.
P-tau 217 is a "beautiful marker for Alzheimer's," Dr. Maria Carrillo, chief science officer of the Alzheimer's Association, told CNN in an earlier interview.
"You're not really measuring amyloid, but the test is telling you it's there, and that's been backed up with objective PET (positron emission tomography) scans that can see amyloid in the brain," Carrillo said. "... If you have elevated tau in your brain, however, then we know that's a sign of another type of dementia."
Another biomarker test is the amyloid 42/40 ratio scan, which measures two types of amyloid proteins, another key biomarker of Alzheimer's disease. At times, such tests work best when used together. In an earlier study, a combination of both amyloid and p-tau 217 tests, called the amyloid probability score, showed a 90% accuracy rate in determining whether memory loss is due to Alzheimer's disease.
Glial fibrillary acidic protein, or GFAP, and neurofilament light chain, or NfL, which indicate brain inflammation and degenerative decay, are also helpful in tracking the progression of Alzheimer's disease. Dozens more biomarkers are being tested in labs around the world.
Isaacson's team at the Institute for Neurodegenerative Diseases is studying more than 125 individual markers from a variety of commercial and research-based tests, some of which may soon be available in a clinical setting.
Why investigate so many? Because personalized medicine may demand it, Niotis said.
"Neurodegenerative diseases present so differently in different people," she said. "It may be we will need a very nuanced, individualized approach in clinical practice to monitor the effectiveness of what we're doing for a given patient."
Hard work pays off in reduced risk
The ongoing preventive neurology study called BioRAND reported on 71 participants, with biomarkers being analyzed on 54 people. The other 17 people served as the control group.
The group of 54 received a series of personalized lifestyle recommendations designed to improve their brain. Such interventions have been shown in past research to improve memory and thinking skills by five points on a cognitive test for people with mild cognitive impairment.
The recommendations include a focus on blood pressure control, diet, exercise, stress reduction, sleep hygiene and weight control as well as addressing metabolic, hormonal and nutrient imbalances. Medications, vitamins and supplements are tailored to each person's unique needs.
Similar to a 2019 study led by Isaacson and Niotis, people who fulfilled at least 60% of the lifestyle recommendations were considered high compliance, while those who implemented less than 60% were low compliance. Periodic blood tests tracked progress in various brain biomarkers.
The outcome? The more work people put into change, the better their brains. Just look at Penny Ashford.
"My blood work was terrible; my eating habits were terrible. I didn't exercise, so my muscle tone was really bad - I had no muscles in my bottom or on my thighs," Ashford said.
"I got the lecture of a lifetime," she said. "They told me, 'Your window is closing, your markers are so bad. Either you've got to do this, or you're done.'"
'A 10 out of 10' on diet and exercise
A lifelong sugar addict, Ashford stopped eating sweets.
"I used to think I had a chemical imbalance because I was such a crazy freak about sugar - I could polish off a whole bag of Oreos, no problem, and I love ice cream," Ashford said.
"I haven't had a dessert. I haven't had ice cream. I haven't had anything except fruit since a year ago March."
By working hard to improve her lifestyle, Penny Ashford has greatly improved blood biomarkers that track brain health. - Ted Ashford
She began an intense exercise program of cardio and resistance training, along with yoga for stress reduction, and moved to a plant-based Mediterranean style of eating. Under a doctor's supervision, she added supplements and vitamins to boost energy and lower stress.
"She was a 10 out of 10 with her diet and exercise," Niotis said. "She lost around 30 pounds and gained lean muscle mass. It was amazing."
A year later, Ashford's blood biomarkers told a completely different story about her brain health. Her p-tau 217 dropped by 43% and her p-tau 181 by 75%.
"We also looked at GFAP and neurofilament light, the markers of neuroinflammation and neurodegeneration," Niotis said. "Penny's GFAP went down by 66% and her NfL went down by 84%.
"These are really impressive changes in these markers of neuronal health," she said. "And the best part about it is it really did track with her clinical symptoms. Her word retrieval problems improved, and she felt so much better."
'I'm so proud of myself'
Ashford wasn't the only top performer in the study. Blood biomarkers also significantly improved across the entire group given risk reduction advice, Isaacson said, even those who were not as committed as Ashford.
"I've lost count on how many people have shown blood markers of brain disease trend in the right direction, but every time it amazes me," he said. "For over 20 years, I was told that what is happening right in front of my eyes was impossible, but the patients' stories, clinical improvements and test results speak for themselves."
Much more work remains before blood testing for Alzheimer's becomes a routine part of clinical practice, Isaacson said.
"Our group has a saying, 'Promise not to overpromise.' By this we mean it's critical to be transparent about the current limitations of these tests, and the variability across different platforms," he said.
While science works out the kinks, Ashford counts herself lucky to be able to track changes in her biomarker numbers - a key motivator in her journey toward better brain health.
"It's huge, huge," she said. "I'm so proud of myself. And each success that I have empowers me to do more, keep going and not let up.
"I look back at my dad. He didn't have any of these options. I watched my dad deteriorate, and I thank God, I am so lucky. We are so lucky."
I må selv oversætte !!!
Søren
Jeg håber at dine informationer er rigtige og valide, da det ser ud som der skrives i forhold til hvilke interesse man har i forhold til Anavex -- læs Short eller Investeret
Limer sidste nyt ind fra US om detektering af Alzheimers, vil jo passe glimrende i forhold til Anavex.
Limer hele teksten ind da jeg ikke kan lime Link ind uden at der kommer alt muligt skrammel med -- håber det går.
For en god ordens skyld har jeg investeret -- Kurs ca 9,2 :-(
Artikel:
Amazing' reduction in Alzheimer's risk verified by blood markers, study says
Sandee LaMotte, CNN
Tue, April 8, 2025, 2:00 AM GMT+2
9 min read
49
A combined blood test for cognitive decline has a 90% accuracy rate in determining whether memory loss is due to Alzheimer's disease. Dr. Sanjay Gupta explains.
- Clipped From Video
More
Editor's note: CNN Chief Medical Correspondent Dr. Sanjay Gupta and writerSandee LaMotte are part of the study covered in this story and have written about their experiences.
When Penny Ashford's father was diagnosed with early-stage Alzheimer's disease at age 62, she knew the devastating brain disorder might one day steal her memory. In her late 50s, her free-floating anxiety turned to outright panic when she began struggling to find words.
"I couldn't tell a story. I couldn't get my words out," said Ashford, now 61. "I remember sitting at a dinner party one time, and I couldn't finish my thoughts. It was the most unbelievable moment.
"I came home and sobbed and told my husband, 'Something is wrong with me. I can't talk,'" she said. "I was petrified."
Penny Ashford's father Barry Murphy, 75, blows out his candles while granddaughters look on. - Courtesy Penny Ashford
Today, after a complete revamp of her lifestyle and overall health, Ashford's struggles with retrieving words have eased, while measures of amyloid and tau proteins and neuroinflammation - all hallmark signs of Alzheimer's - have fallen.
Ashford knows about these improvements because she's part of a unique study tracking her progress via key blood biomarkers now being used to help diagnose early dementia. Instead of relying on painful spinal taps and expensive brain scans, these blood tests are heralded as a new, less invasive and time-consuming way to determine risk and aid in an earlier diagnosis of Alzheimer's.
The preliminary data, presented Monday at the American Academy of Neurology annual meeting in San Diego, analyzed biomarkers on 54 participants in an ongoing preventive neurology study called the Biorepository Study for Neurodegenerative Diseases, or BioRAND.
"The field is primarily using various biomarkers to determine if you have dementia or not," said lead study author Dr. Kellyann Niotis, a preventive neurologist who researches risk reduction for Alzheimer's and Parkinson's diseases at the Institute for Neurodegenerative Diseases in Boca Raton, Florida.
"No one is really looking at the changes in these biomarkers as outcome measures, as a way of tracking progress in a person's journey to improve their brain," Niotis said. "We believe these biomarkers may show how the disease progression is being modified biologically by a person's actions."
Less invasive test for Alzheimer's risk
Alzheimer's blood tests are the key to widespread prevention of dementia, experts say. If people can be diagnosed in their doctor's office, they can more immediately move into preventive care and implement lifestyle changes designed to slow the progression of their disease.
The problem, said senior study author Dr. Richard Isaacson, is the variability in how well these new blood biomarker tests work to predict or track disease progression.
"There is a dirty little secret in the Alzheimer's blood testing community where so many testing platforms, biotech companies, and a flurry of new blood tests are released," Isaacson said, "but it's unclear which of these tests are most accurate to track progression and evaluate response to therapies to slow progression toward dementia."
More in Health
Men's Fitness
To address this gap, Isaacson's research team and collaborators at five sites across the United States and Canada set forth to evaluate and eventually cross-compare the clinical use of what the neurologist said he believes will one day become "the cholesterol test for the brain."
"In the not so far future, people in their 30s, 40s, 50s, 60s and beyond will get a baseline test to evaluate risk and help track progress over time - similar to how traditional cholesterol tests are used today," said Isaacson, founder of one of the first Alzheimer's prevention clinics in the United States.
"Our eventual goal is to offer a blood panel at cost to help democratize access and broaden the ability for people to receive care," he added.
What Alzheimer's blood tests currently measure
Measuring levels of both amyloid and tau is key to understanding and diagnosing Alzheimer's and other forms of dementia.
This illustration depicts cells in an Alzheimer's affected brain. The brown areas depict beta-amyloid protein plaques. The blue areas represent tau proteins that accumulate and form tangles. - NIH/AP
Amyloid plaques play a key role in the development of Alzheimer's when small clusters gather at synapses in the brain and interfere with the nerve cells' ability to communicate. Such plaques are thought to trigger changes in tau proteins,which form into tangles in parts of the brain controlling memory.
Tau tangles are also implicated in other neurological diseases such as frontal lobe dementia, or FTD, and Lewy body dementia in which abnormal clumps of a protein called alpha-synuclein accumulate in the brain's neurons.
The biomarker plasma phosphorylated tau 217, or p-tau217 for short, is a top contender in the diagnosis of mild cognitive impairment and early-stage Alzheimer's disease. Its cousin, p-tau 181, is also a helpful indicator.
P-tau 217 is a "beautiful marker for Alzheimer's," Dr. Maria Carrillo, chief science officer of the Alzheimer's Association, told CNN in an earlier interview.
"You're not really measuring amyloid, but the test is telling you it's there, and that's been backed up with objective PET (positron emission tomography) scans that can see amyloid in the brain," Carrillo said. "... If you have elevated tau in your brain, however, then we know that's a sign of another type of dementia."
Another biomarker test is the amyloid 42/40 ratio scan, which measures two types of amyloid proteins, another key biomarker of Alzheimer's disease. At times, such tests work best when used together. In an earlier study, a combination of both amyloid and p-tau 217 tests, called the amyloid probability score, showed a 90% accuracy rate in determining whether memory loss is due to Alzheimer's disease.
Glial fibrillary acidic protein, or GFAP, and neurofilament light chain, or NfL, which indicate brain inflammation and degenerative decay, are also helpful in tracking the progression of Alzheimer's disease. Dozens more biomarkers are being tested in labs around the world.
Isaacson's team at the Institute for Neurodegenerative Diseases is studying more than 125 individual markers from a variety of commercial and research-based tests, some of which may soon be available in a clinical setting.
Why investigate so many? Because personalized medicine may demand it, Niotis said.
"Neurodegenerative diseases present so differently in different people," she said. "It may be we will need a very nuanced, individualized approach in clinical practice to monitor the effectiveness of what we're doing for a given patient."
Hard work pays off in reduced risk
The ongoing preventive neurology study called BioRAND reported on 71 participants, with biomarkers being analyzed on 54 people. The other 17 people served as the control group.
The group of 54 received a series of personalized lifestyle recommendations designed to improve their brain. Such interventions have been shown in past research to improve memory and thinking skills by five points on a cognitive test for people with mild cognitive impairment.
The recommendations include a focus on blood pressure control, diet, exercise, stress reduction, sleep hygiene and weight control as well as addressing metabolic, hormonal and nutrient imbalances. Medications, vitamins and supplements are tailored to each person's unique needs.
Similar to a 2019 study led by Isaacson and Niotis, people who fulfilled at least 60% of the lifestyle recommendations were considered high compliance, while those who implemented less than 60% were low compliance. Periodic blood tests tracked progress in various brain biomarkers.
The outcome? The more work people put into change, the better their brains. Just look at Penny Ashford.
"My blood work was terrible; my eating habits were terrible. I didn't exercise, so my muscle tone was really bad - I had no muscles in my bottom or on my thighs," Ashford said.
"I got the lecture of a lifetime," she said. "They told me, 'Your window is closing, your markers are so bad. Either you've got to do this, or you're done.'"
'A 10 out of 10' on diet and exercise
A lifelong sugar addict, Ashford stopped eating sweets.
"I used to think I had a chemical imbalance because I was such a crazy freak about sugar - I could polish off a whole bag of Oreos, no problem, and I love ice cream," Ashford said.
"I haven't had a dessert. I haven't had ice cream. I haven't had anything except fruit since a year ago March."
By working hard to improve her lifestyle, Penny Ashford has greatly improved blood biomarkers that track brain health. - Ted Ashford
She began an intense exercise program of cardio and resistance training, along with yoga for stress reduction, and moved to a plant-based Mediterranean style of eating. Under a doctor's supervision, she added supplements and vitamins to boost energy and lower stress.
"She was a 10 out of 10 with her diet and exercise," Niotis said. "She lost around 30 pounds and gained lean muscle mass. It was amazing."
A year later, Ashford's blood biomarkers told a completely different story about her brain health. Her p-tau 217 dropped by 43% and her p-tau 181 by 75%.
"We also looked at GFAP and neurofilament light, the markers of neuroinflammation and neurodegeneration," Niotis said. "Penny's GFAP went down by 66% and her NfL went down by 84%.
"These are really impressive changes in these markers of neuronal health," she said. "And the best part about it is it really did track with her clinical symptoms. Her word retrieval problems improved, and she felt so much better."
'I'm so proud of myself'
Ashford wasn't the only top performer in the study. Blood biomarkers also significantly improved across the entire group given risk reduction advice, Isaacson said, even those who were not as committed as Ashford.
"I've lost count on how many people have shown blood markers of brain disease trend in the right direction, but every time it amazes me," he said. "For over 20 years, I was told that what is happening right in front of my eyes was impossible, but the patients' stories, clinical improvements and test results speak for themselves."
Much more work remains before blood testing for Alzheimer's becomes a routine part of clinical practice, Isaacson said.
"Our group has a saying, 'Promise not to overpromise.' By this we mean it's critical to be transparent about the current limitations of these tests, and the variability across different platforms," he said.
While science works out the kinks, Ashford counts herself lucky to be able to track changes in her biomarker numbers - a key motivator in her journey toward better brain health.
"It's huge, huge," she said. "I'm so proud of myself. And each success that I have empowers me to do more, keep going and not let up.
"I look back at my dad. He didn't have any of these options. I watched my dad deteriorate, and I thank God, I am so lucky. We are so lucky."
I må selv oversætte !!!
Søren
Lidt fra CNN
Noget om biomarker målinger.
https://edition.cnn.com/2025/04/07/health/alzheimer-risk-blood-biomarkers-wellness/index.html
Noget om biomarker målinger.
https://edition.cnn.com/2025/04/07/health/alzheimer-risk-blood-biomarkers-wellness/index.html
Slidene viser at Anavex selv er forsigtige i deres konklusion så seekingalpha artiklen bibringer ikke noget nyt; men "glemmer" en meget vigtig pointe som er de meget små bivirkninger over den meget lange periode.
Anavex skriver:
-There were no deaths related to the study drug
-No adverse effects on liver enzymes, vital signs, ECGs, or physical/neurological examination findings
Det er et meget vigtigt resultat ikke mindst i forhold til de meget alvorlig bivirkninger ved mapperne (Lecanemab og donanemab).
Hvis dataene kunne bære det ville Anavex skrive "The data/trial SHOWS"; men i stedet skriver de "suggest (antyder)" i deres konklusion i slidene: "Suggests earlier oral blarcamesine treatment initiation may have continued long-term beneficial therapeutic effect".
Dvs. for nye studier skal der fokuseres på pts med milde/tidlige symptomer på Alzheimer.
En anden vigtig funktion af OLE er at det ville være uetisk at afbryde behandlingen, fordi hovedstudiet vist jo at behandlingen havde en effekt.
Anavex skriver:
-There were no deaths related to the study drug
-No adverse effects on liver enzymes, vital signs, ECGs, or physical/neurological examination findings
Det er et meget vigtigt resultat ikke mindst i forhold til de meget alvorlig bivirkninger ved mapperne (Lecanemab og donanemab).
Hvis dataene kunne bære det ville Anavex skrive "The data/trial SHOWS"; men i stedet skriver de "suggest (antyder)" i deres konklusion i slidene: "Suggests earlier oral blarcamesine treatment initiation may have continued long-term beneficial therapeutic effect".
Dvs. for nye studier skal der fokuseres på pts med milde/tidlige symptomer på Alzheimer.
En anden vigtig funktion af OLE er at det ville være uetisk at afbryde behandlingen, fordi hovedstudiet vist jo at behandlingen havde en effekt.
Anavex - Godkendte ansøgninger af EMA i 2024.
I 2024 gennemgik EMA 127 lægemiddelansøgninger og anbefalede 114 af dem til godkendelse. (5 blev ikke anbefalet, og 8 trak deres ansøgning tilbage). Det er en godkendelsesprocent på 90 %.
Anavex kom officiel på ansøgningslisten den 27. december 2024.
Som tidligere nævnt udfærdiger de 2 rapportører, der har fulgt Anavex siden omkring marts 2024, en evalueringsrapport til CHMP/EMA og Anavex efter ca. 120 dage. (80 dags rapporten blev først indført 2022/2023 og synes at være uofficiel og til internt brug?)
Denne første vigtige officelle evalueringsrapport vil være en indikation på hvordan CHMP/EMA ser på en mulig markedsgodkendelse i sidste ende!
120 dage svarer til ca. den 26. april 2025.
Side 20:
https://www.ema.europa.eu/da/documents/other/laboratory-patient-journey-centrally-authorised-medicine_da.pdf
https://clinicaldata.ema.europa.eu/web/cdp/home
Aktiemarkedet og den normale prissætning af selskabers værdi, er pt blevet kortsluttet af U.S. administrationen.
Vi ved dog også, at normalen vil vende tilbage på et eller andet tidspunkt, som efter alle øvrige div. kriser.
For Anavex betyder alene hvordan myndighederne (EMA) ser på casen - og Anavex ville aldrig være kommet så langt i processen, hvis ikke EMA - også i kraft af mentorordningen med de 2 rapportører, havde en positiv tilgang ved accept af ansøgningen.
Vedr. ansøgningen til EMA, så har Anavex bekræftet, at de seneste OLE data også var inkluderet i ansøgning, som blev indsendt den 26. november 2024.
Alt andet er bare støj lige nu!
Kalu - tror helt sikkert at Anavex formulering som “suggest” bare er et udtryk for ydmyghed ift. at man pt. er i en evauleringsfase af EMA.
I 2024 gennemgik EMA 127 lægemiddelansøgninger og anbefalede 114 af dem til godkendelse. (5 blev ikke anbefalet, og 8 trak deres ansøgning tilbage). Det er en godkendelsesprocent på 90 %.
Anavex kom officiel på ansøgningslisten den 27. december 2024.
Som tidligere nævnt udfærdiger de 2 rapportører, der har fulgt Anavex siden omkring marts 2024, en evalueringsrapport til CHMP/EMA og Anavex efter ca. 120 dage. (80 dags rapporten blev først indført 2022/2023 og synes at være uofficiel og til internt brug?)
Denne første vigtige officelle evalueringsrapport vil være en indikation på hvordan CHMP/EMA ser på en mulig markedsgodkendelse i sidste ende!
120 dage svarer til ca. den 26. april 2025.
Side 20:
https://www.ema.europa.eu/da/documents/other/laboratory-patient-journey-centrally-authorised-medicine_da.pdf
https://clinicaldata.ema.europa.eu/web/cdp/home
Aktiemarkedet og den normale prissætning af selskabers værdi, er pt blevet kortsluttet af U.S. administrationen.
Vi ved dog også, at normalen vil vende tilbage på et eller andet tidspunkt, som efter alle øvrige div. kriser.
For Anavex betyder alene hvordan myndighederne (EMA) ser på casen - og Anavex ville aldrig være kommet så langt i processen, hvis ikke EMA - også i kraft af mentorordningen med de 2 rapportører, havde en positiv tilgang ved accept af ansøgningen.
Vedr. ansøgningen til EMA, så har Anavex bekræftet, at de seneste OLE data også var inkluderet i ansøgning, som blev indsendt den 26. november 2024.
Alt andet er bare støj lige nu!
Kalu - tror helt sikkert at Anavex formulering som “suggest” bare er et udtryk for ydmyghed ift. at man pt. er i en evauleringsfase af EMA.
Suggest/indicate bruges næsten altid til at beskrive hypoteser i videnskabelige artikler. Studiet var jo ikke designet til at påvise den indikation. Selv meeeget lang anavex og har skrevet en del videnskabelige artikler så mit svar et ikke rette mod at tale negativt om anavex
Anavex Super med dit arbejde og input kalu :)
Opfattede på ingen måde din udlægning som negativ kritik, men som en konstruktiv anskuelse af det du ser.
Synes bare Anavex tidligere har brugt ydmyge udtalelser for ikke at foregribe, hvordan EMA måtte opfatte data.
Synes dog at både forskellen i point og p-værdierne taler deres eget sprog.
Synes i øvrigt godt, at Anavex kunne have lagt en kurve ind fra den database, som viser forventet udvikling i Alzheimer patienter - mener Mayo eller Pior har sat denne kurve ind på OLE-kurverne, hvor man ser en meget stor positiv forskel på de grupper, der fik Blarcamesine og kurven fra Alzheimerdatabasen.
Opfattede på ingen måde din udlægning som negativ kritik, men som en konstruktiv anskuelse af det du ser.
Synes bare Anavex tidligere har brugt ydmyge udtalelser for ikke at foregribe, hvordan EMA måtte opfatte data.
Synes dog at både forskellen i point og p-værdierne taler deres eget sprog.
Synes i øvrigt godt, at Anavex kunne have lagt en kurve ind fra den database, som viser forventet udvikling i Alzheimer patienter - mener Mayo eller Pior har sat denne kurve ind på OLE-kurverne, hvor man ser en meget stor positiv forskel på de grupper, der fik Blarcamesine og kurven fra Alzheimerdatabasen.
.. ("mener Mayo eller Pior har sat denne kurve ind på OLE-kurverne, hvor man ser en meget stor positiv forskel på de grupper, der fik Blarcamesine og kurven fra Alzheimerdatabasen...")
Men er det brugbart, hvis begge grupper fik Blarcamesine? (Boersboe evt??)
Men er det brugbart, hvis begge grupper fik Blarcamesine? (Boersboe evt??)
Armen fra alzheimersbasen vil ikke kunne bruges. Men det giver nok en god indikation.
OLE forsøget er dog informativt nok uden placebo-arm (ubehandlet). Forsøget viser, at det er en signifikant fordel at komme i tidlig behandling og at forblive i behandling.
OLE forsøget var dobbelt blinded, hvor hverken patienter eller behandler ved hvilken arm pts er i. Forsøget opfylder dermed et væsentligt fagligt kriterium for validitet.
Fra Needham konferencen lyder det som om, at partneren måske er fundet. Det gætter Mayomobile også på.
Næste skridt er ansøgning om godkendelse på flere markeder - måske Australien. FDA er næppe på plads endnu med deres nye vejledning on ansøgning om godkendelse af stoffer i tidlige alzheimers patienter.
En evt meddelelse om partner vil smadre shorterne - som sikkert får lukket lidt ned i dag.
Mayomobile gætter på, at vi ikke hører om partner før en godkendelse hos EMA.
Tror selv på, at vi hører om en partner tidligere. Det ville i min optik være dumt ikke at tage imod en mindre upfront fra en heldig partner inden evt. godkendelse.
PS
NBI stod i 4900 for et år siden. I dag 3600. Et fald der nærmer sig 30% !
OLE forsøget er dog informativt nok uden placebo-arm (ubehandlet). Forsøget viser, at det er en signifikant fordel at komme i tidlig behandling og at forblive i behandling.
OLE forsøget var dobbelt blinded, hvor hverken patienter eller behandler ved hvilken arm pts er i. Forsøget opfylder dermed et væsentligt fagligt kriterium for validitet.
Fra Needham konferencen lyder det som om, at partneren måske er fundet. Det gætter Mayomobile også på.
Næste skridt er ansøgning om godkendelse på flere markeder - måske Australien. FDA er næppe på plads endnu med deres nye vejledning on ansøgning om godkendelse af stoffer i tidlige alzheimers patienter.
En evt meddelelse om partner vil smadre shorterne - som sikkert får lukket lidt ned i dag.
Mayomobile gætter på, at vi ikke hører om partner før en godkendelse hos EMA.
Tror selv på, at vi hører om en partner tidligere. Det ville i min optik være dumt ikke at tage imod en mindre upfront fra en heldig partner inden evt. godkendelse.
PS
NBI stod i 4900 for et år siden. I dag 3600. Et fald der nærmer sig 30% !
9/4 2025 18:57 ProInvestorNEWS 4125737 Se her her Kontorchef.Linket finder du altid oppe i vores værktøjslinje under marked.
https://indexes.nasdaqomx.com/Index/Overview/NBI
https://indexes.nasdaqomx.com/Index/Overview/NBI
Hmm forfatteren har en anden opfattelse;
"As for the open-label [vs. DB, randomized, placebo-controlled] trial, those who chose to remain in the ATTENTION-AD trial knew that everyone would receive blarcamesine, as there's no longer a placebo group. (See below)."
https://seekingalpha.com/article/4773574-anavex-understanding-their-alzheimers-open-label-extension-data-skeptically
"As for the open-label [vs. DB, randomized, placebo-controlled] trial, those who chose to remain in the ATTENTION-AD trial knew that everyone would receive blarcamesine, as there's no longer a placebo group. (See below)."
https://seekingalpha.com/article/4773574-anavex-understanding-their-alzheimers-open-label-extension-data-skeptically
9/4 2025 19:02 ProInvestorNEWS 2125739 Se Boersboe´s seneste kommentarer og efterfølgende snak med Solsen i den anledning:
https://proinvestor.com/boards/123186/
https://proinvestor.com/boards/123186/
vestasfan - jeg tror OLE forsøget mest skal ses som bekræftelse på bivirkningsprofilen på Blarcamesine.
Forsøget indgår næppe med andet end bivirkningsregistreringer til EMA.
Forsøget indgår næppe med andet end bivirkningsregistreringer til EMA.
Shorts øget pr 28/3 https://stocktwits.com/J60611/message/611131326
Missling skulle have udtalt, at man vil gå til fda og søge om accelerated approval https://stocktwits.com/Blarcamesine/message/611103795
https://www.streetwisereports.com/article/2025/04/07/new-drug-for-early-ad-shown-to-be-efficacious-safe.html
Cirkus Trump kapitulerede. Svækker tilliden til deres evner.
Shorterne sveder i dag.
Missling skulle have udtalt, at man vil gå til fda og søge om accelerated approval https://stocktwits.com/Blarcamesine/message/611103795
https://www.streetwisereports.com/article/2025/04/07/new-drug-for-early-ad-shown-to-be-efficacious-safe.html
Cirkus Trump kapitulerede. Svækker tilliden til deres evner.
Shorterne sveder i dag.
Nogle gange kan man godt miste tilliden til aktiemarkedet. Toldsatserne har ingen betydning for Anavex, alligevel bevæger kursen sig voldsomt ned og nu op.
Anavex Første gang vi har hørt, at Anavex muligvis påtænker at forsøge acc. proces i U.S.
H.C. Wainwright nævner også at dialog med FDA allerede pågår.
Tænker Missling burde have nævnt dette ved sidste præsentation, hvis det er tilfældet
Ellers ser analytikeren meget positiv på udviklingen i casen. - igen modsat SA artiklen!
Raghuram Selvaraju, Ph.D er en af de 2-3 faste analytiker, der følger Anavex - fra tidligere ved vi også, at han også før har talt direkte med Missling udover ved selve præsentationerne.
https://www.streetwisereports.com/article/2025/04/09/four-year-data-on-new-drug-for-early-ad-positive.html
"European Approval First
Selvaraju reported that Anavex is looking to get blarcamesine approved for early Alzheimer's disease in Europe, first. A decision on the Marketing Authorization Application could be made before year-end, purported the analyst. If approved, the drug could be launched commercially late in 2026 in multiple countries there. Nearly 8 million people have Alzheimer's disease in Europe, and according to the European Brain Council, this number is expected to double by 2030.
"From our vantage point, therefore, the European market opportunity could be highly lucrative," Selvaraju commented.
Once and if blarcamesine is greenlighted in Europe, Anavex may pursue approval in the United Kingdom, Canada and Australia as well. The biopharma is having ongoing discussions about the same in the U.S., with the Food and Drug Administration.
"A favorable European regulatory decision could have meaningful impact upon the willingness of regulators in other territories to approve the drug," added the analyst."
H.C. Wainwright nævner også at dialog med FDA allerede pågår.
Tænker Missling burde have nævnt dette ved sidste præsentation, hvis det er tilfældet
Ellers ser analytikeren meget positiv på udviklingen i casen. - igen modsat SA artiklen!
Raghuram Selvaraju, Ph.D er en af de 2-3 faste analytiker, der følger Anavex - fra tidligere ved vi også, at han også før har talt direkte med Missling udover ved selve præsentationerne.
https://www.streetwisereports.com/article/2025/04/09/four-year-data-on-new-drug-for-early-ad-positive.html
"European Approval First
Selvaraju reported that Anavex is looking to get blarcamesine approved for early Alzheimer's disease in Europe, first. A decision on the Marketing Authorization Application could be made before year-end, purported the analyst. If approved, the drug could be launched commercially late in 2026 in multiple countries there. Nearly 8 million people have Alzheimer's disease in Europe, and according to the European Brain Council, this number is expected to double by 2030.
"From our vantage point, therefore, the European market opportunity could be highly lucrative," Selvaraju commented.
Once and if blarcamesine is greenlighted in Europe, Anavex may pursue approval in the United Kingdom, Canada and Australia as well. The biopharma is having ongoing discussions about the same in the U.S., with the Food and Drug Administration.
"A favorable European regulatory decision could have meaningful impact upon the willingness of regulators in other territories to approve the drug," added the analyst."
Anavex Mayos opdatering på OLE forsøget.
https://www.sotcanalytics.com/update-compendium-2025
" Conclusion
Patients in Anavex's Phase 2b/3 study began treatment at an approximate age of 74. According to a Johns Hopkins report from last year, average U.S. life expectancy is 75.9 years for men and 81.3 for women, with European averages slightly higher. Based on this data, if real-world outcomes mirror our projections, it is highly likely that patients who begin Blarcamesine treatment in very early-stage Alzheimer's or MCI may never progress to late-stage Alzheimer's. Instead, they could spend the remainder of their lives in early-stage Alzheimer's or an uncharacteristically slowly progressing moderate-stage. Given Blarcamesine's mechanism of action in targeting very early pathology, we believe that combining the drug with lifestyle interventions during preclinical stages could halt cognitive decline entirely.
To finalize, our previous analysis was a good peer-to-peer comparison, but this analysis opens the window to what Blarcamesine therapy could look like in the real world with full spectrum, real world conditions. Our placebo arm at week-192 is in line with academic generalizations of 8-12 point annual ADAS-COG13 declines."
Her sammenligner og fremskriver han placebo patienter fra i alt 6 andre tilsvarende forsøg - i alt 2885 pts, herunder fra LLYs U.S. godkendte Donemab på en ADAS Cog13 skala.
Her ser man bl.a at selv for den mindst acc. sammenlignelige gruppe og de OLE pts der fik Blarcamesine fra starten, en bedre score på 14,875 og hele 21,211 point ift. gennemsnittet af alle 2885 pts.
Som Mayo skriver skal talene tages med forbehold, da der sker en fremskrivning til de 192 uger.
Forskellen er dog stadig så markant, iflg. Mayo, på både forskellen og sandsynligheden for at en tidligere medicinering med Blarcamesine, ville kunne bremse eller måske endda stoppe udviklingen af Alzheimer!
Så selvom Anavex ikke selv havde en sammenlignelig placebo gruppe i deres forsøg, er det næstbedste en sammenligning med en placebo gruppe fra tilsvarende forsøg.
Tror også bl.a EMA muligvis ville skelne til sådanne markante resultater - især når bivirkningsprofilen på Blarcamesine er så positiv .
https://www.sotcanalytics.com/update-compendium-2025
" Conclusion
Patients in Anavex's Phase 2b/3 study began treatment at an approximate age of 74. According to a Johns Hopkins report from last year, average U.S. life expectancy is 75.9 years for men and 81.3 for women, with European averages slightly higher. Based on this data, if real-world outcomes mirror our projections, it is highly likely that patients who begin Blarcamesine treatment in very early-stage Alzheimer's or MCI may never progress to late-stage Alzheimer's. Instead, they could spend the remainder of their lives in early-stage Alzheimer's or an uncharacteristically slowly progressing moderate-stage. Given Blarcamesine's mechanism of action in targeting very early pathology, we believe that combining the drug with lifestyle interventions during preclinical stages could halt cognitive decline entirely.
To finalize, our previous analysis was a good peer-to-peer comparison, but this analysis opens the window to what Blarcamesine therapy could look like in the real world with full spectrum, real world conditions. Our placebo arm at week-192 is in line with academic generalizations of 8-12 point annual ADAS-COG13 declines."
Her sammenligner og fremskriver han placebo patienter fra i alt 6 andre tilsvarende forsøg - i alt 2885 pts, herunder fra LLYs U.S. godkendte Donemab på en ADAS Cog13 skala.
Her ser man bl.a at selv for den mindst acc. sammenlignelige gruppe og de OLE pts der fik Blarcamesine fra starten, en bedre score på 14,875 og hele 21,211 point ift. gennemsnittet af alle 2885 pts.
Som Mayo skriver skal talene tages med forbehold, da der sker en fremskrivning til de 192 uger.
Forskellen er dog stadig så markant, iflg. Mayo, på både forskellen og sandsynligheden for at en tidligere medicinering med Blarcamesine, ville kunne bremse eller måske endda stoppe udviklingen af Alzheimer!
Så selvom Anavex ikke selv havde en sammenlignelig placebo gruppe i deres forsøg, er det næstbedste en sammenligning med en placebo gruppe fra tilsvarende forsøg.
Tror også bl.a EMA muligvis ville skelne til sådanne markante resultater - især når bivirkningsprofilen på Blarcamesine er så positiv .
Anavex Marwan Sabbagh skyder med skarpt mod forsøg på manipulation!
Jesse Brodkin, en kendt shortlakaj, sendte en mail til JPAD i forsøg på at underminerer og skabe usikkerhed omkring Peer Reviewet for Blarcamesine og resultaterne fra AD fase 2/3 forsøget.
Marwan Sabbagh, formand for Anavexs adviser board og nok en af de aller største kapacitetet indenfor Alzheimer, der samtidig også var en af hovedforfatterne af Peer Reviewet, giver Jesse Brodkin hårdt igen.
Alle resultater i Peer Reviewet er korrekte og veldokumenteret!
Til sidste beskylder Marwan Sabbagh mere eller mindre Jesse Brodkin for at foretage ulovlig og strafbar manipulation!
Jesse Brodkin har tilmed forsøgt dette gentagende gange!
Endnu engang ser vi eksempler på, hvordan shortlakajer forsøger at skabe usikkerhed omkring valide resultater - kun med det ene formål genere profit!
Dejligt at Anavex, via Marwan Sabbagh tager til genmæle!
Har stor tiltro til at EMA har mere tillid til kapaciteter som Marwan Sabbagh og hans validering af resultaterne, end disse grådige og falske short/hedgefond banditter!
https://www.sciencedirect.com/science/article/pii/S2274580725000809?dgcid=raven_sd_aip_email&fbclid=IwY2xjawJnQstleHRuA2FlbQIxMQABHssW5lOyp3hYHLJt15Wrh7_KT3t0wDOluNjlJ_gm_mIJ7fO_JiT7Z7RxxUmq_aem_0v4gKy_2jJcU1xbckr6ayA
" In summary, all questions have been answered and have no scientific merit. Again, this Letter to the Editor follows the same pattern as the previous email inquiries sent by Jesse Brodkin to disparage the Sponsor and JPAD. Specifically, hedge funds target companies to disparage them and their scientific work within respected papers in order to gain financially by shorting them, which is illegal and criminal.
Sincerely,
Marwan Noel Sabbagh"
Jesse Brodkin, en kendt shortlakaj, sendte en mail til JPAD i forsøg på at underminerer og skabe usikkerhed omkring Peer Reviewet for Blarcamesine og resultaterne fra AD fase 2/3 forsøget.
Marwan Sabbagh, formand for Anavexs adviser board og nok en af de aller største kapacitetet indenfor Alzheimer, der samtidig også var en af hovedforfatterne af Peer Reviewet, giver Jesse Brodkin hårdt igen.
Alle resultater i Peer Reviewet er korrekte og veldokumenteret!
Til sidste beskylder Marwan Sabbagh mere eller mindre Jesse Brodkin for at foretage ulovlig og strafbar manipulation!
Jesse Brodkin har tilmed forsøgt dette gentagende gange!
Endnu engang ser vi eksempler på, hvordan shortlakajer forsøger at skabe usikkerhed omkring valide resultater - kun med det ene formål genere profit!
Dejligt at Anavex, via Marwan Sabbagh tager til genmæle!
Har stor tiltro til at EMA har mere tillid til kapaciteter som Marwan Sabbagh og hans validering af resultaterne, end disse grådige og falske short/hedgefond banditter!
https://www.sciencedirect.com/science/article/pii/S2274580725000809?dgcid=raven_sd_aip_email&fbclid=IwY2xjawJnQstleHRuA2FlbQIxMQABHssW5lOyp3hYHLJt15Wrh7_KT3t0wDOluNjlJ_gm_mIJ7fO_JiT7Z7RxxUmq_aem_0v4gKy_2jJcU1xbckr6ayA
" In summary, all questions have been answered and have no scientific merit. Again, this Letter to the Editor follows the same pattern as the previous email inquiries sent by Jesse Brodkin to disparage the Sponsor and JPAD. Specifically, hedge funds target companies to disparage them and their scientific work within respected papers in order to gain financially by shorting them, which is illegal and criminal.
Sincerely,
Marwan Noel Sabbagh"
Tror desværre at vi kan forvente tiltagende grove forsøg på misinformation og at skabe tvivl. Der er ekstrem mange penge på spil og tilsyneladende tages der større og større risiko.
Turbolens forude!
Turbolens forude!
Det er helt hen i vejret, at man kan slippe afsted med at lyve - manipulere marked i sådan en grad pga. grådighed. Dejligt at der bliver svaret igen med hård hånd...
Anavex Næste CHMP møde 22.-25. april.
Næste møde i CHMP regi afholdes 22.-25. april.
Den 25. april er tilfældigvis 120-dages evalueringstidspunktet - måske ser vi Anavex og Blarcamesine blive diskuteret på et af punkterne.
https://www.ema.europa.eu/en/events/committee-medicinal-products-human-use-chmp-22-25-april-2025
Missling taler i Kina:
https://www.gala-tech.cn/bioexpo2025en/default.asp
Næste møde i CHMP regi afholdes 22.-25. april.
Den 25. april er tilfældigvis 120-dages evalueringstidspunktet - måske ser vi Anavex og Blarcamesine blive diskuteret på et af punkterne.
https://www.ema.europa.eu/en/events/committee-medicinal-products-human-use-chmp-22-25-april-2025
Missling taler i Kina:
https://www.gala-tech.cn/bioexpo2025en/default.asp
Lacanemab godkendt i Europa med begrænsninger
https://www.alzheimer-europe.org/news/european-commission-authorises-lecanemab-treatment-early-alzheimers-disease?language_content_entity=en
https://www.alzheimer-europe.org/news/european-commission-authorises-lecanemab-treatment-early-alzheimers-disease?language_content_entity=en
Anavex Tegner godt for Blarcamesine, som er bedre på alle parameter og endda også har et langtidsstudie i form af OLE forsøget, til at underbygge effekt og den gode bivirkningsprofil.
Har svært ved at se, hvordan EMA ikke skulle godkende Blarcamesine nu?
Pga. af begrænsningerne reagerer Biogenaktien heller ikke positiv på udmeldingen - ligger i ca. -1 % pt.
Har svært ved at se, hvordan EMA ikke skulle godkende Blarcamesine nu?
Pga. af begrænsningerne reagerer Biogenaktien heller ikke positiv på udmeldingen - ligger i ca. -1 % pt.
Ja vi skal ikke tage godkendelsen op negativt, når vi ser på Blarcamesine muligheder.
Der kommer sikkert en del restriktioner og krav til Lecanemab.
Der kommer sikkert en del restriktioner og krav til Lecanemab.
Man kan normalt ikke regne med kurserne i de mindre aktier i formarkedet.
Jeg gætter på, at du, hr. kontorchef, er kunde hos Nordnet, som fra i dag pludselig angiver din porteføljeværdi efter kurser i formarkedet. Fuldstændig håbløst når man ligger tungt i en lille aktie som Anavex.
Ifølge Yahoo er sidste handel til kurs 8,10, men hvis du ser på Investorshub er der senere en handel til kurs 9,00, og det samlede volumen i formarkedet angives til 300 aktier, dvs. helt ubetydeligt.100 aktier til kurs 8,10 og 200 aktier til kurs 9,00. Ligesom vi i Danmark har en tossetime, kan man betragte formarkedet i usa som tossenatten, især når der tale om en meget lille aktie.
Ifølge Yahoo er sidste handel til kurs 8,10, men hvis du ser på Investorshub er der senere en handel til kurs 9,00, og det samlede volumen i formarkedet angives til 300 aktier, dvs. helt ubetydeligt.100 aktier til kurs 8,10 og 200 aktier til kurs 9,00. Ligesom vi i Danmark har en tossetime, kan man betragte formarkedet i usa som tossenatten, især når der tale om en meget lille aktie.
Anavex Blarcamesine ift. Donepezil
Dygtige Piotr henviser til en anden skribent, der sammenligner ADAS cog data fra Blarcamesine og det i dag mest anvendte medicin mod Alzheimer, Donepezil.
Sammenligningen sker som svar på en SA-artikel, hvor ellers positive Lane Simonien mener, at Blarcamesine måske ikke er meget mere effektiv end Donepezil.
(Donepezil er i øvrigt, som Blarcamesine, også baseret på en Sigma-1 virkemåde)•
Konklusionen er i denne sammenligning, at Blarcamesine er 46 % mere effektiv efter 192 uger (varigheden af OLE forsøget)
Resultaterne skal dog tages med forbehold, som alle indlæg i øvrigt!
" DISCLAIMER: THIS IS NOT INVESTMENT ADVICE. I AM NOT A FINANCIAL ADVISOR. THIS IS FOR EDUCATIONAL PURPOSES ONLY. DO NOT USE THIS INFORMATION FOR INVESTMENTS --MAX HITEK"
http://maxhitek.com/anavex/DonepezilCompare.html
Har selv et nært familiemedlem med fremskreden Alzheimer, som nok som alle andre Alzheimer patienter også bliver medicineret med Donepezil, der blev godkendt for ca. 20 år siden.
Synes her at have registreret en vis form for effekt, uden dog at have et sammenlignings forhold, hvilket lover godt for hele Sigma-1 tilgangen.
Donepezil har fra tidligere studier vist den største effekt i de første 3-5 mdr., hvorefter kroppen "mættes" og effekten aftager.
Blarcamesine synes derimod at bibeholde en effekt over tid.
Dygtige Piotr henviser til en anden skribent, der sammenligner ADAS cog data fra Blarcamesine og det i dag mest anvendte medicin mod Alzheimer, Donepezil.
Sammenligningen sker som svar på en SA-artikel, hvor ellers positive Lane Simonien mener, at Blarcamesine måske ikke er meget mere effektiv end Donepezil.
(Donepezil er i øvrigt, som Blarcamesine, også baseret på en Sigma-1 virkemåde)•
Konklusionen er i denne sammenligning, at Blarcamesine er 46 % mere effektiv efter 192 uger (varigheden af OLE forsøget)
Resultaterne skal dog tages med forbehold, som alle indlæg i øvrigt!
" DISCLAIMER: THIS IS NOT INVESTMENT ADVICE. I AM NOT A FINANCIAL ADVISOR. THIS IS FOR EDUCATIONAL PURPOSES ONLY. DO NOT USE THIS INFORMATION FOR INVESTMENTS --MAX HITEK"
http://maxhitek.com/anavex/DonepezilCompare.html
Har selv et nært familiemedlem med fremskreden Alzheimer, som nok som alle andre Alzheimer patienter også bliver medicineret med Donepezil, der blev godkendt for ca. 20 år siden.
Synes her at have registreret en vis form for effekt, uden dog at have et sammenlignings forhold, hvilket lover godt for hele Sigma-1 tilgangen.
Donepezil har fra tidligere studier vist den største effekt i de første 3-5 mdr., hvorefter kroppen "mættes" og effekten aftager.
Blarcamesine synes derimod at bibeholde en effekt over tid.
Meget interessant. Det ser endda ud til at Donepezil blev godkendt af FDA helt tilbage i 1996, så det er i den grad på tide med noget nyere med bedre virkning.
Grok gav mig dette svar på hvad Donepezil er ift. Blarcamesine.
"Donepezil er et lægemiddel, der anvendes til behandling af Alzheimers sygdom (AD), primært i mild til moderat stadie, og i nogle lande også i svær AD. Det er en acetylcholinesterasehæmmer, hvilket betyder, at det hæmmer enzymet acetylcholinesterase, som nedbryder neurotransmitteren acetylcholin i hjernen. Ved at øge niveauet af acetylcholin forbedrer Donepezil kommunikationen mellem neuroner, hvilket kan lindre kognitive symptomer som hukommelsestab, forvirring og problemer med tænkning.
Interessant i forhold til Blarcamesine: I modsætning til Blarcamesine, der har en potentiel sygdomsmodificerende effekt gennem sigma-1-receptoraktivering og autofagi, er Donepezils virkning rent symptomatisk og påvirker ikke de underliggende patologier som amyloid-beta eller tau. Dette gør Donepezil til en kortsigtet lindring, mens Blarcamesine sigter mod at ændre sygdomsforløbet."
Grok gav mig dette svar på hvad Donepezil er ift. Blarcamesine.
"Donepezil er et lægemiddel, der anvendes til behandling af Alzheimers sygdom (AD), primært i mild til moderat stadie, og i nogle lande også i svær AD. Det er en acetylcholinesterasehæmmer, hvilket betyder, at det hæmmer enzymet acetylcholinesterase, som nedbryder neurotransmitteren acetylcholin i hjernen. Ved at øge niveauet af acetylcholin forbedrer Donepezil kommunikationen mellem neuroner, hvilket kan lindre kognitive symptomer som hukommelsestab, forvirring og problemer med tænkning.
Interessant i forhold til Blarcamesine: I modsætning til Blarcamesine, der har en potentiel sygdomsmodificerende effekt gennem sigma-1-receptoraktivering og autofagi, er Donepezils virkning rent symptomatisk og påvirker ikke de underliggende patologier som amyloid-beta eller tau. Dette gør Donepezil til en kortsigtet lindring, mens Blarcamesine sigter mod at ændre sygdomsforløbet."
Anavex Marwan Sabbagh taler den 20. april i Abu Dhab.
Bemærk at Marwan Sabbagh også sidder i komiten for konferencen!
Måske han kan få nogle rige oliesheiker til at købe et par aktier:)
9th International Conference on Alzheimer's Disease
and Related Disorders in the Middle East
https://mco.ae/icadme/agenda/
Dr.Sabbagh to speak Sunday April 20
08:30 AM - 09:00 AM
Oral Blarcamesine Novel Mechanism for Alzheimer Disease: Autophagy Restoration through Upstream SIGMAR1 Activation Clinical Efficacy Phase IIb/III Trial
Prof. Marwan Sabbagh
Bemærk at Marwan Sabbagh også sidder i komiten for konferencen!
Måske han kan få nogle rige oliesheiker til at købe et par aktier:)
9th International Conference on Alzheimer's Disease
and Related Disorders in the Middle East
https://mco.ae/icadme/agenda/
Dr.Sabbagh to speak Sunday April 20
08:30 AM - 09:00 AM
Oral Blarcamesine Novel Mechanism for Alzheimer Disease: Autophagy Restoration through Upstream SIGMAR1 Activation Clinical Efficacy Phase IIb/III Trial
Prof. Marwan Sabbagh
Anavex/Blarcamesine figurerer under punkt 3.3.2 på EMA dagsorden.
CHMP møde den 22.-25. april 2025.
Blarcamesine skal diskuteres vedr. 120. Dages spørgsmål.
Dette er den naturlige liste af uddybende spørgsmål Anavex får stillet i forbindelse med den vigtige "1. Stop Clock".
Listen udspringer fra 120 dages evalueringen, som de to rapportører fra CHMP har udformet.
Ordlyden og typen af spørgsmål i denne rapport afspejler, hvordan CHMP ser muligheden for et evt. positivt udfald i ansøgningen for "Alzheimer og Demens."
Anavex får så typisk 1-3 mdr., alt efter omfanget og typen af spørgsmål, til at svare og dokumenterer.
Er svarende fyldestgørende vil Anavex/Blarcamesine kunne forsætte evalueringen - dette ville i så fald betyde et meget stort skridt hen mod en endelig godkendelse!
120 dages rapporten eller dele af den foreløbige evaulering, bliver ofte tilgængelig på EMAs hjemmeside.
https://www.ema.europa.eu/en/documents/agenda/agenda-chmp-meeting-22-25-april-2025_en.pdf?fbclid=IwY2xjawJ0mApleHRuA2FlbQIxMAABHqF9o_MreR0RIYSOJQgvbKaENEL6cNAiwQT-9l3IZLPlPOwJ6G0dOt-h4Tg0_aem_8RGyMKPsJlkLsEMyvPRphQ
CHMP møde den 22.-25. april 2025.
Blarcamesine skal diskuteres vedr. 120. Dages spørgsmål.
Dette er den naturlige liste af uddybende spørgsmål Anavex får stillet i forbindelse med den vigtige "1. Stop Clock".
Listen udspringer fra 120 dages evalueringen, som de to rapportører fra CHMP har udformet.
Ordlyden og typen af spørgsmål i denne rapport afspejler, hvordan CHMP ser muligheden for et evt. positivt udfald i ansøgningen for "Alzheimer og Demens."
Anavex får så typisk 1-3 mdr., alt efter omfanget og typen af spørgsmål, til at svare og dokumenterer.
Er svarende fyldestgørende vil Anavex/Blarcamesine kunne forsætte evalueringen - dette ville i så fald betyde et meget stort skridt hen mod en endelig godkendelse!
120 dages rapporten eller dele af den foreløbige evaulering, bliver ofte tilgængelig på EMAs hjemmeside.
https://www.ema.europa.eu/en/documents/agenda/agenda-chmp-meeting-22-25-april-2025_en.pdf?fbclid=IwY2xjawJ0mApleHRuA2FlbQIxMAABHqF9o_MreR0RIYSOJQgvbKaENEL6cNAiwQT-9l3IZLPlPOwJ6G0dOt-h4Tg0_aem_8RGyMKPsJlkLsEMyvPRphQ
Fra facebookgruppen er delt et link til nyt patent.
https://ppubs.uspto.gov/api/pdf/downloadPdf/12280034?requestToken=eyJzdWIiOiI3Y2QwZTU1Ny1hODZlLTQ2ODAtYjQ3NC1kOGM2Mjc0Yjk3NjAiLCJ2ZXIiOiI2YjU5MTYzNi04ZTFhLTQwODItODlhNC02MjQ3NzE2NGI5MzMiLCJleHAiOjB9&fbclid=IwY2xjawJ03wZleHRuA2FlbQIxMAABHo4HzXo-TzlwHqMvs98iYIWRjh80c-FROyYzNcK91bkXlNSeXMxnVPB8WHHC_aem_3-IG1WJMCxuz7b9V3U3nQQ
https://ppubs.uspto.gov/api/pdf/downloadPdf/12280034?requestToken=eyJzdWIiOiI3Y2QwZTU1Ny1hODZlLTQ2ODAtYjQ3NC1kOGM2Mjc0Yjk3NjAiLCJ2ZXIiOiI2YjU5MTYzNi04ZTFhLTQwODItODlhNC02MjQ3NzE2NGI5MzMiLCJleHAiOjB9&fbclid=IwY2xjawJ03wZleHRuA2FlbQIxMAABHo4HzXo-TzlwHqMvs98iYIWRjh80c-FROyYzNcK91bkXlNSeXMxnVPB8WHHC_aem_3-IG1WJMCxuz7b9V3U3nQQ
Bristol Myers misser et fase 3 med Cobenfy i Skizofreni https://www.investors.com/news/technology/bristol-myers-squibb-cobenfy-adjunctive-treatment-schizophrenia/
Bristol købte Karuna og stoffet for $12 bn for godt et års tid siden. Men stoffet er godkendt på et tidligere forsøg. Bristol købte dog Karuna inden godkendelsen - altså på samme tidspunkt, som Anavex står i i dag med Blarcamesine i alzheimers.
Viser ar Skizofreni er en svær sygdom at behandle og at der er mange penge i Anavex 3-71, hvis det viser sig effektiv. Hvilket vi mangler beviset på.
Medio 2025 skulle vi få resultater fra Anavex 3-71 fase 2 i skizofreni.
Bristol købte Karuna og stoffet for $12 bn for godt et års tid siden. Men stoffet er godkendt på et tidligere forsøg. Bristol købte dog Karuna inden godkendelsen - altså på samme tidspunkt, som Anavex står i i dag med Blarcamesine i alzheimers.
Viser ar Skizofreni er en svær sygdom at behandle og at der er mange penge i Anavex 3-71, hvis det viser sig effektiv. Hvilket vi mangler beviset på.
Medio 2025 skulle vi få resultater fra Anavex 3-71 fase 2 i skizofreni.
Anavex tilføjer Professor Dr. Audrey Gabelle, MD, PhD til deres Scientific advisory board https://finance.yahoo.com/news/anavex-life-sciences-announces-appointment-113000662.html
En meget anerkendt og erfaren videnskabskvinde med mange peer review artikler på cv'et - giver tiltro til Anavex !
En meget anerkendt og erfaren videnskabskvinde med mange peer review artikler på cv'et - giver tiltro til Anavex !
Anavex Sammenfaldet med 120 dags rapporten er spændende.
Anavex må være bekendt med hovedpunkterne eller har måske allerede fået 120 dags rapporten fra EMA.
Uanset må Anavex have en rigtig god ide om, hvor de står med Blarcamesine, ift. CHMP/EMA på nuværende tidspunkt.
I forbindelsen med ansættelsen af Professor Dr. Audrey Gabelle, må hun have fået et vist indblik i situationen/stadet med ansøgningen.
Tror næppe hun ville have takket ja til Anavex, hvis der ikke var en meget positiv indikation/dialog med rapportørerne/CHMP.
Kan kun gætte, men hun har helt sikkert fået adgang til meget mere viden, end os alm. investorer - selvfølge under en tavshedsklausul!
Hun var faktisk også den, som fik lov til først at præsenterer de resultater fra Alzheimer forsøget for et par mdr. siden!
Anavex forsætter billedet med at håndplukke store kapaciteter på Alzheimer området - Marwan Sabbagh, Timo Grimmer mfl.
Vedr. uddybning af 120 dages spørgsmål fra CHMP, så burde Anavex med tidligere FDA ansatte og de øvrige eksperter på området, relativt nemt kunne argumenterer/dokumenterer tilfredsstillende i casen.
Samtidig ser vi shorterne øge deres andel?
Nu hele 24.590.000 shortede aktier eller 29,89 % af udestående aktier - det hidtil højeste til dato!
Synes de lever livet farligt, men intet er som tidligere nævnt 100 % sikkert i biotek - tror dog selv mest på, at tilgangen af eksperter taler for en meget positiv resultat funderet vinkel på casen!
Anavex må være bekendt med hovedpunkterne eller har måske allerede fået 120 dags rapporten fra EMA.
Uanset må Anavex have en rigtig god ide om, hvor de står med Blarcamesine, ift. CHMP/EMA på nuværende tidspunkt.
I forbindelsen med ansættelsen af Professor Dr. Audrey Gabelle, må hun have fået et vist indblik i situationen/stadet med ansøgningen.
Tror næppe hun ville have takket ja til Anavex, hvis der ikke var en meget positiv indikation/dialog med rapportørerne/CHMP.
Kan kun gætte, men hun har helt sikkert fået adgang til meget mere viden, end os alm. investorer - selvfølge under en tavshedsklausul!
Hun var faktisk også den, som fik lov til først at præsenterer de resultater fra Alzheimer forsøget for et par mdr. siden!
Anavex forsætter billedet med at håndplukke store kapaciteter på Alzheimer området - Marwan Sabbagh, Timo Grimmer mfl.
Vedr. uddybning af 120 dages spørgsmål fra CHMP, så burde Anavex med tidligere FDA ansatte og de øvrige eksperter på området, relativt nemt kunne argumenterer/dokumenterer tilfredsstillende i casen.
Samtidig ser vi shorterne øge deres andel?
Nu hele 24.590.000 shortede aktier eller 29,89 % af udestående aktier - det hidtil højeste til dato!
Synes de lever livet farligt, men intet er som tidligere nævnt 100 % sikkert i biotek - tror dog selv mest på, at tilgangen af eksperter taler for en meget positiv resultat funderet vinkel på casen!
Kan vi forvente, at der kommer en udtalelse/opdatering fra Anavex idag i forhold til de 120 dage?
vi hører nok kun fra dem hvis det er en nyhed som rykker på SP.
Hvor anavex er i processen, vil intet nyt er godt nyt.
Hvor anavex er i processen, vil intet nyt er godt nyt.
Det er lykkedes shorterne at lukke ca 500k i første halvdel af april https://www.nasdaq.com/market-activity/stocks/avxl/short-interest
Markedet krakkede i den periode og var en oplagt mulighed for dem, idet mange sikkert solgte på den usikkerhed der var i markedet. Nogle sikkert tvunget til at sælge.
Det bliver ikke nemt at lukke de resterenden 24 mio aktier i et forhåbentligt mere roligt marked.
Markedet krakkede i den periode og var en oplagt mulighed for dem, idet mange sikkert solgte på den usikkerhed der var i markedet. Nogle sikkert tvunget til at sælge.
Det bliver ikke nemt at lukke de resterenden 24 mio aktier i et forhåbentligt mere roligt marked.
26/4 2025 17:56 oneofakind 1126072 Jeg shorter ikke i denne aktie, men køber nær bunde.. Forventer at 10,2 bliver toppen, hvis der ikke bliver afgørende nyt. Dette korrigeres naturligvis mht. den svækkede dollar!
Anavex Audrey Gabelle kommenterer på OLE resultaterne på sociale medier.
Hun ser virkelig et stort lys og håb i Blarcamesine!
Tror det, at hun nu er en del af rejsen med Anavex, vil især i Europa skabe positiv opmærksomhed omkring Blarcamesine og hele den nye og innovative tilgang Anavex repræsenterer.
På et meget vigtigt tidpunkt i EMA processen (120 dage og 1. Stop Clock), at endnu en højt profileret professor (endda en europæisk), kan se noget særdeles lovende i Blarcamesine - må et eller andet sted også vægte, når EMA evaluerer på resultaterne.
Vil holde øje med, om der skulle komme et referat fra CHMP mødet den 25. april, hvor Blarcamesine var på som et af punkterne.
Kan se at der er kommet CHMP kommentarer fra nogle af de andre stoffer, som også er under evaluering.
1. Stop Clock er normalt den største og vigtigste hurdle, da dette typisk omhandler effekten og bivikningsprofilen.
2. Stop Clock få mdr. før afgørelsen fra EMA, går typisk på kvalitet af produktionen og andre praktiske elementer.
https://media.stocktwits-cdn.com/api/3/media/3509988/default.png
Hun ser virkelig et stort lys og håb i Blarcamesine!
Tror det, at hun nu er en del af rejsen med Anavex, vil især i Europa skabe positiv opmærksomhed omkring Blarcamesine og hele den nye og innovative tilgang Anavex repræsenterer.
På et meget vigtigt tidpunkt i EMA processen (120 dage og 1. Stop Clock), at endnu en højt profileret professor (endda en europæisk), kan se noget særdeles lovende i Blarcamesine - må et eller andet sted også vægte, når EMA evaluerer på resultaterne.
Vil holde øje med, om der skulle komme et referat fra CHMP mødet den 25. april, hvor Blarcamesine var på som et af punkterne.
Kan se at der er kommet CHMP kommentarer fra nogle af de andre stoffer, som også er under evaluering.
1. Stop Clock er normalt den største og vigtigste hurdle, da dette typisk omhandler effekten og bivikningsprofilen.
2. Stop Clock få mdr. før afgørelsen fra EMA, går typisk på kvalitet af produktionen og andre praktiske elementer.
https://media.stocktwits-cdn.com/api/3/media/3509988/default.png
Anavex EMA link for nyheder.
https://www.ema.europa.eu/en/news-events
Indholdet bliver løbende opdateret og de sidste kommentarer fra CHMP mødet 22.-25. april kommer i løbet af de næste par uger.
For 2025 fremgår det bl.a, at der hidtil er blevet godkendt 33 ny medicin, 1 afvist og 8 der har trukket ansøgningen tilbage af ansøger.
Blarcamesine er her efter 120 dage ikke klar til godkendelse endnu, men vi kan dog se, at ansøgningen for Blarcamesine heller ikke er trukket tilbage - og derfor forsætter i forløbet.
https://www.ema.europa.eu/en/news/meeting-highlights-committee-medicinal-products-human-use-chmp-22-25-april-2025
Næste CHMP møde er sat til den 19.-22. maj.
I 2024 blev kvartalsrapporten afholdt den 9. maj.
Der er også indkaldte til til den årlige generalforsamling (kun virtuelt) den 10. juni 2025.
Mon ikke vi får nyt her op til de næste par møder?
Vi kan kun afvente, men intet nyt er også godt nyt - dette indikere sandsynligvis at tingene kører sin gang.
Afventer især 120 dages rapporten fra CHMP, samt hvor langt Anavex er kommet med ansøgninger til FDA og øvrige dele af verden.
Vi nærmer os også vinduet, hvor de vigtig data fra 3-71 fra fase 2b forsøget i Skizofreni er stillet i udsigt.
Vil selv bare afvente og nyde det sommerlige vejr.
Har helt ro i maven!
https://www.ema.europa.eu/en/news-events
Indholdet bliver løbende opdateret og de sidste kommentarer fra CHMP mødet 22.-25. april kommer i løbet af de næste par uger.
For 2025 fremgår det bl.a, at der hidtil er blevet godkendt 33 ny medicin, 1 afvist og 8 der har trukket ansøgningen tilbage af ansøger.
Blarcamesine er her efter 120 dage ikke klar til godkendelse endnu, men vi kan dog se, at ansøgningen for Blarcamesine heller ikke er trukket tilbage - og derfor forsætter i forløbet.
https://www.ema.europa.eu/en/news/meeting-highlights-committee-medicinal-products-human-use-chmp-22-25-april-2025
Næste CHMP møde er sat til den 19.-22. maj.
I 2024 blev kvartalsrapporten afholdt den 9. maj.
Der er også indkaldte til til den årlige generalforsamling (kun virtuelt) den 10. juni 2025.
Mon ikke vi får nyt her op til de næste par møder?
Vi kan kun afvente, men intet nyt er også godt nyt - dette indikere sandsynligvis at tingene kører sin gang.
Afventer især 120 dages rapporten fra CHMP, samt hvor langt Anavex er kommet med ansøgninger til FDA og øvrige dele af verden.
Vi nærmer os også vinduet, hvor de vigtig data fra 3-71 fra fase 2b forsøget i Skizofreni er stillet i udsigt.
Vil selv bare afvente og nyde det sommerlige vejr.
Har helt ro i maven!
Anavex Nyt patent - bedre søvn og beroligende effekt.
Som det fremgår af denne officielle liste, har Anavex godt gang i patenterne for deres pipeline.
Der bliver lagt en stort arbejde i at beskytte mod fremtidig kopiering!
Anavex annoncerer kun sjældent vedr. patenter, men den store aktivitet indikere stor tiltro til værdien af deres pipeline.
Skriv Anavex i søger feltet under “ Basic search”.
https://ppubs.uspto.gov/pubwebapp/static/pages/ppubsbasic.html
Fin illustration af et forsøg på at vise omverden og nok især de kommende potentielle sundheds instanser og køber/bruger mekanismen for Blarcamesine.
En del af den annoncerede oplysningskampagne, som Anavex har sat i gang forud for en evt. markedsgodkendelse.
https://3dforscience.com/projects/case-study-anavex/
Som det fremgår af denne officielle liste, har Anavex godt gang i patenterne for deres pipeline.
Der bliver lagt en stort arbejde i at beskytte mod fremtidig kopiering!
Anavex annoncerer kun sjældent vedr. patenter, men den store aktivitet indikere stor tiltro til værdien af deres pipeline.
Skriv Anavex i søger feltet under “ Basic search”.
https://ppubs.uspto.gov/pubwebapp/static/pages/ppubsbasic.html
Fin illustration af et forsøg på at vise omverden og nok især de kommende potentielle sundheds instanser og køber/bruger mekanismen for Blarcamesine.
En del af den annoncerede oplysningskampagne, som Anavex har sat i gang forud for en evt. markedsgodkendelse.
https://3dforscience.com/projects/case-study-anavex/
Vil det betyde en melding om partnerskabet på den anden side af 1. Clock stop!
Anavex Alene i dag har shorterne lånt 800.000 aktier!
https://media.stocktwits-cdn.com/api/3/media/3575390/medium.png
Med en omsætning, der nok ikke kommer meget over 500.000 aktier, er det ikke så sært at kursen presses ned, når der bare smides aktier til salg i den størrelsesorden.
Typisk forsøger shorterne at sælge dem umiddelbart, når de bliver lånt.
Synes godt nok de lever livet farligt for dels at beskytte deres nuværende shortpositioner eller oprette nye - på et tidspunkt hvor Blarcamesine er 1/3 henne i EMA processen og uden der har været nogle negative udmeldinger.
Anavex har endnu en præsentation den 7. maj:
https://finance.yahoo.com/news/anavex-life-sciences-participate-citizens-113000660.html
Dog tilsyneladende ikke som webcast.
Vi må dog også blive afholdt en CC for 2. kvartal rapporten i løbet af næste uge - normalt skal denne afholdes senest 45 dage efter endt kvartal - dvs. senest den 15. maj.
Blev som nævnt afholdt den 9. maj i 2024 for tilsvarende kvartal.
https://media.stocktwits-cdn.com/api/3/media/3575390/medium.png
Med en omsætning, der nok ikke kommer meget over 500.000 aktier, er det ikke så sært at kursen presses ned, når der bare smides aktier til salg i den størrelsesorden.
Typisk forsøger shorterne at sælge dem umiddelbart, når de bliver lånt.
Synes godt nok de lever livet farligt for dels at beskytte deres nuværende shortpositioner eller oprette nye - på et tidspunkt hvor Blarcamesine er 1/3 henne i EMA processen og uden der har været nogle negative udmeldinger.
Anavex har endnu en præsentation den 7. maj:
https://finance.yahoo.com/news/anavex-life-sciences-participate-citizens-113000660.html
Dog tilsyneladende ikke som webcast.
Vi må dog også blive afholdt en CC for 2. kvartal rapporten i løbet af næste uge - normalt skal denne afholdes senest 45 dage efter endt kvartal - dvs. senest den 15. maj.
Blev som nævnt afholdt den 9. maj i 2024 for tilsvarende kvartal.
Anavex annoncerer fuld tilmelding af fase 2-studie af ANAVEX ®3-71 - med i alt 71 deltagere
Forventede toplinjedata i andet halvår af 2025
https://www.anavex.com/post/anavex-life-sciences-announces-full-enrollment-of-phase-2-study-of-anavex-3-71-for-the-treatment-of?fbclid=IwY2xjawKAP8NleHRuA2FlbQIxMAABHoXHwucDQ44J8reXolnwU8HpJOgAuf1WXJUJbSpr8DVxC1VphUV7L9yziMKN_aem_nALXNlEP7rdRXveiliuDwA
Forventede toplinjedata i andet halvår af 2025
https://www.anavex.com/post/anavex-life-sciences-announces-full-enrollment-of-phase-2-study-of-anavex-3-71-for-the-treatment-of?fbclid=IwY2xjawKAP8NleHRuA2FlbQIxMAABHoXHwucDQ44J8reXolnwU8HpJOgAuf1WXJUJbSpr8DVxC1VphUV7L9yziMKN_aem_nALXNlEP7rdRXveiliuDwA
1/5 2025 17:58 oneofakind 1126143 Damn. lagde salgsordre i dag.. Men rigtigt godt for Anavex! Køber den igen, hvis traderne giver mig lov.
Nyhederne har en artikel om Lecanemab. Kunne være spændende hvis man kunne rette journalistens interesse for Anavex
Tror jeg dropper et link til hende om deres hjemmeside. (har gjort det nu)
https://nyheder.tv2.dk/2025-05-01-ny-medicin-giver-haab-for-alzheimerpatienter
Tror jeg dropper et link til hende om deres hjemmeside. (har gjort det nu)
https://nyheder.tv2.dk/2025-05-01-ny-medicin-giver-haab-for-alzheimerpatienter
Vær opmærksom på at Frederiksen har forbindlese til Eisai AD!
Selv om han ikke personlig har gevinst ud af det bliver hans institut støttet. Dette burde have fremgået af artiklen.
Dermed ikke sagt at han ikke er uvildig. Han har tidligere betvivlet at Lecanemab kunne blive godkendt i EU.
Dog må han anses som en kapacitet i DK/EU/Verden på området, ville være interesant at høre hans syn på Anavex.
Jeg vil dog ikke rette henvendelse.
Edited - navn
.
Selv om han ikke personlig har gevinst ud af det bliver hans institut støttet. Dette burde have fremgået af artiklen.
Dermed ikke sagt at han ikke er uvildig. Han har tidligere betvivlet at Lecanemab kunne blive godkendt i EU.
Dog må han anses som en kapacitet i DK/EU/Verden på området, ville være interesant at høre hans syn på Anavex.
Jeg vil dog ikke rette henvendelse.
Edited - navn
.
Alzheimerforeningen har lagt følgende på Linkedin i dag: https://www.linkedin.com/posts/alzheimerforeningen_ny-medicin-giver-h%C3%A5b-for-alzheimerpatienter-activity-7324354690236760064-cWvh?utm_source=share&utm_medium=member_ios&rcm=ACoAABFxhtUByRdrPQ37Cc571sC-QTGGur0ugcw
De skriver: "Medicinen er det største håb på demensområdet i årevis ✨ - men hvis den skal gøre reel forskel, kræver det hurtigere udredning ⏱️, bedre adgang og styrket kapacitet i systemet ⚙️. Og ikke mindst vedvarende støtte og forståelse for de mange, der lever med sygdommen - også dem, der ikke kan få behandlingen"
Samtidig, fra passage i tilknyttet TV2 artikel: "Kun udvalgte alzheimerpatienter vil få mulighed for at få medicinen, fordi der er risiko for alvorlige bivirkninger med blødninger og hævelser i hjernen.
Overlæge Kristian Steen Frederiksen vurderer, at det vil være mellem 5 og 15 procent af patienterne, som er kandidater til behandlingen."
Kender Alzheimerforeningen vitterligt ikke til Blarcamesine, eller er det ikke nævneværdigt så længe der ikke foreligger en godkendelse?
De skriver: "Medicinen er det største håb på demensområdet i årevis ✨ - men hvis den skal gøre reel forskel, kræver det hurtigere udredning ⏱️, bedre adgang og styrket kapacitet i systemet ⚙️. Og ikke mindst vedvarende støtte og forståelse for de mange, der lever med sygdommen - også dem, der ikke kan få behandlingen"
Samtidig, fra passage i tilknyttet TV2 artikel: "Kun udvalgte alzheimerpatienter vil få mulighed for at få medicinen, fordi der er risiko for alvorlige bivirkninger med blødninger og hævelser i hjernen.
Overlæge Kristian Steen Frederiksen vurderer, at det vil være mellem 5 og 15 procent af patienterne, som er kandidater til behandlingen."
Kender Alzheimerforeningen vitterligt ikke til Blarcamesine, eller er det ikke nævneværdigt så længe der ikke foreligger en godkendelse?
Det er skræmmende at de vender ryggen til på trods af at de gentagende gange er blevet kontaktet mht. at fortælle dem om Blarcamesine. Det er svært at tage dem seriøst. Selv ved en evt. EMA godkendelse forventer jeg at de forholder sig tavse i den første tid.
Det kan da ikke nytte noget at anbefale medicin som ikke er på market så ville det jo blive det vilde vesten med falske forhåbninger til medicin man ikke kan få.
Blarcamesine skal nok får sin formentlige store plads når det er godkendt. Der er jo ingen i sundhedsvæsenet som vil foretrække en så ressourcetung behandling som Lecanemab hvis det kan undgåes
Blarcamesine skal nok får sin formentlige store plads når det er godkendt. Der er jo ingen i sundhedsvæsenet som vil foretrække en så ressourcetung behandling som Lecanemab hvis det kan undgåes
Kalu, hvad med dette fra 2023 hos Alzheimerforeningen? De refererer til en yderligere artikel fra januar 2023.
https://www.alzheimer.dk/nyheder/2023/endnu-en-ny-medicin-spirer-haabet-for-personer-med-alzheimers-sygdom/
https://www.alzheimer.dk/nyheder/2023/endnu-en-ny-medicin-spirer-haabet-for-personer-med-alzheimers-sygdom/
Man kan også se mod UK, hvor der også ses på (forhåbentlig) kommende muligheder.
https://www.alzheimers.org.uk/about-dementia/treatments/researching-new-drugs-alzheimers-disease
https://www.alzheimers.org.uk/about-dementia/treatments/researching-new-drugs-alzheimers-disease
Anavex Institutionals øger forsat - nu 42,11 % andel.
https://fintel.io/so/us/avxl
Mens kursen på aktien stadig ikke får lov at udvikle sig positiv, trods bl.a. en positiv EMA proces, så øger Institutionals til det hidtil højeste andel på 42,11 % af udestående aktier i Anavex.
Virker lidt som om, at de større investor stiliieog roligt formår at lokke flere og flere aktier ud af småinvestorerne?
Anavex havde en præsentation i aften, uden webcast, så nok ikke noget vi ikke vidste i forvejen - blot en udbredning af casen.
Den 13. maj kl. 14.30 DK-tid får vi dog en kvartalsrapport inkl. webcast.
https://finance.yahoo.com/news/anavex-life-sciences-announce-fiscal-113000910.html
Så gerne at vi fik noget informativt omkring EMA processen eller øvrig dialog med andre lande/sundhedsmyndigheder.
Indtil da er kursudviklingen bare koblet på især resten af bioteksektoren - uden nogen form for afspejling fra den meget positive udvikling Anavex gennemgår.
Så længe vi har den "knallert" siddende i U.S. administrationen, så bliver kursutvikling også derefter - indtil vi får en eller form for EMA eller partner udvikling.
https://fintel.io/so/us/avxl
Mens kursen på aktien stadig ikke får lov at udvikle sig positiv, trods bl.a. en positiv EMA proces, så øger Institutionals til det hidtil højeste andel på 42,11 % af udestående aktier i Anavex.
Virker lidt som om, at de større investor stiliieog roligt formår at lokke flere og flere aktier ud af småinvestorerne?
Anavex havde en præsentation i aften, uden webcast, så nok ikke noget vi ikke vidste i forvejen - blot en udbredning af casen.
Den 13. maj kl. 14.30 DK-tid får vi dog en kvartalsrapport inkl. webcast.
https://finance.yahoo.com/news/anavex-life-sciences-announce-fiscal-113000910.html
Så gerne at vi fik noget informativt omkring EMA processen eller øvrig dialog med andre lande/sundhedsmyndigheder.
Indtil da er kursudviklingen bare koblet på især resten af bioteksektoren - uden nogen form for afspejling fra den meget positive udvikling Anavex gennemgår.
Så længe vi har den "knallert" siddende i U.S. administrationen, så bliver kursutvikling også derefter - indtil vi får en eller form for EMA eller partner udvikling.
Spændende update. Tak Tasso1.
Short interest er også steget til 29.2%.
Jeg gad virkeligt godt se deres reaktion ved EMA positiv update eller Partner udmelding.
Det er selvfølgeligt stadig en risiko, at vi ikke får en EMA godkendelse, men synes selv at Anavex har en rigtig god case og stærke data.
Antal af patienter i deres 2b/3 trial er nok min eneste rigtig bekymring.
Short interest er også steget til 29.2%.
Jeg gad virkeligt godt se deres reaktion ved EMA positiv update eller Partner udmelding.
Det er selvfølgeligt stadig en risiko, at vi ikke får en EMA godkendelse, men synes selv at Anavex har en rigtig god case og stærke data.
Antal af patienter i deres 2b/3 trial er nok min eneste rigtig bekymring.
Wolfgang Liedtke er tilsyneladende ny head of neurology hos Anavex.
Se TTTav66 indlæg på Stockwits https://stocktwits.com/TTTav66/message/614173403
Mere om Wolfgang: https://scholar.google.com/citations?user=jTiCDhYAAAAJ&hl=en
Ansat indtil december 2024 i Regeneron.
https://www.linkedin.com/in/wolfgangliedtke/
Mon ikke det er endnu en styrkelse og anerkendelse af Avavex !
Se TTTav66 indlæg på Stockwits https://stocktwits.com/TTTav66/message/614173403
Mere om Wolfgang: https://scholar.google.com/citations?user=jTiCDhYAAAAJ&hl=en
Ansat indtil december 2024 i Regeneron.
https://www.linkedin.com/in/wolfgangliedtke/
Mon ikke det er endnu en styrkelse og anerkendelse af Avavex !
13/5 2025 17:40 klemmensen 14126350 Opsummering Q&A-spørgsmål på Anavex Q2 2025 webcast (AI genereret)
1. Tidslinje og status for EMA-godkendelse
• Spørgsmål: Hvornår forventer Anavex at modtage feedback fra EMA på blarcamesine, og er der modtaget kommentarer undervejs?
• Svar: Forventet feedback i slutningen af 2025 eller starten af næste kvartal. Løbende opdateringer gives ikke under vurderingsprocessen.
2. Kliniske milepæle og pipeline
• Spørgsmål: Hvilke vigtige kliniske milepæle forventes i 2025, især for ANAVEX®3-71 i skizofreni?
• Svar: Top-line data fra fase 2-studiet i skizofreni forventes i 2. halvår 2025. Fokus på sikkerhed og biomarkør-effekt, især hos patienter med negative symptomer.
3. Detaljer om skizofreni-studiet
• Spørgsmål: Hvilke patientkarakteristika indgår, og hvad er succeskriterierne?
• Svar: Svært behandlelige patienter indgår. Succeskriterier er biomarkør-effekt og sikkerhed over tid, med EEG ERP som biomarkør.
4. Finansiel robusthed og runway
• Spørgsmål: Hvordan ser den finansielle runway ud, og er der planer om kapitalrejsning?
• Svar: $115,8 mio. i kassen, svarende til ca. 4 års runway. Ingen aktuelle planer om kapitalrejsning, men markedet overvåges løbende.
5. Langtidsdata for blarcamesine
• Spørgsmål: Hvilke resultater viser de nyeste data fra OLE-studiet?
• Svar: Data viser fortsat klinisk fordel efter 3 års behandling, hvilket styrker blarcamesines profil.
6. Udvidelse af videnskabeligt råd
• Spørgsmål: Hvilken betydning har tilføjelsen af Dr. Audrey Gabelle?
• Svar: Dr. Gabelle tilfører stærk neurologisk ekspertise og styrker klinisk udvikling, især i Europa.
7. Strategiske prioriteter for 2025
• Spørgsmål: Hvad er de overordnede strategiske prioriteter?
• Svar: Fokus på pipelineudvikling, regulatoriske fremskridt og forberedelse til markedsintroduktion.
8. Samarbejdspartnerskab og kommercialisering
• Spørgsmål: Hvordan forbereder Anavex sig på markedsintroduktion i Europa? Planlægges partnerskaber eller egen salgsstyrke?
• Svar: Selskabet har igangsat dialoger med potentielle partnere for distribution og markedsadgang i Europa. Samtidig overvejes muligheden for at opbygge egen salgsstyrke. Beslutningen vil blive baseret på, hvad der bedst maksimerer aktionærværdi. Begge muligheder arbejdes der aktivt med for at sikre hurtig og effektiv markedsadgang ved godkendelse
1. Tidslinje og status for EMA-godkendelse
• Spørgsmål: Hvornår forventer Anavex at modtage feedback fra EMA på blarcamesine, og er der modtaget kommentarer undervejs?
• Svar: Forventet feedback i slutningen af 2025 eller starten af næste kvartal. Løbende opdateringer gives ikke under vurderingsprocessen.
2. Kliniske milepæle og pipeline
• Spørgsmål: Hvilke vigtige kliniske milepæle forventes i 2025, især for ANAVEX®3-71 i skizofreni?
• Svar: Top-line data fra fase 2-studiet i skizofreni forventes i 2. halvår 2025. Fokus på sikkerhed og biomarkør-effekt, især hos patienter med negative symptomer.
3. Detaljer om skizofreni-studiet
• Spørgsmål: Hvilke patientkarakteristika indgår, og hvad er succeskriterierne?
• Svar: Svært behandlelige patienter indgår. Succeskriterier er biomarkør-effekt og sikkerhed over tid, med EEG ERP som biomarkør.
4. Finansiel robusthed og runway
• Spørgsmål: Hvordan ser den finansielle runway ud, og er der planer om kapitalrejsning?
• Svar: $115,8 mio. i kassen, svarende til ca. 4 års runway. Ingen aktuelle planer om kapitalrejsning, men markedet overvåges løbende.
5. Langtidsdata for blarcamesine
• Spørgsmål: Hvilke resultater viser de nyeste data fra OLE-studiet?
• Svar: Data viser fortsat klinisk fordel efter 3 års behandling, hvilket styrker blarcamesines profil.
6. Udvidelse af videnskabeligt råd
• Spørgsmål: Hvilken betydning har tilføjelsen af Dr. Audrey Gabelle?
• Svar: Dr. Gabelle tilfører stærk neurologisk ekspertise og styrker klinisk udvikling, især i Europa.
7. Strategiske prioriteter for 2025
• Spørgsmål: Hvad er de overordnede strategiske prioriteter?
• Svar: Fokus på pipelineudvikling, regulatoriske fremskridt og forberedelse til markedsintroduktion.
8. Samarbejdspartnerskab og kommercialisering
• Spørgsmål: Hvordan forbereder Anavex sig på markedsintroduktion i Europa? Planlægges partnerskaber eller egen salgsstyrke?
• Svar: Selskabet har igangsat dialoger med potentielle partnere for distribution og markedsadgang i Europa. Samtidig overvejes muligheden for at opbygge egen salgsstyrke. Beslutningen vil blive baseret på, hvad der bedst maksimerer aktionærværdi. Begge muligheder arbejdes der aktivt med for at sikre hurtig og effektiv markedsadgang ved godkendelse
Anavex Fint referat af Q-10 - Anavex er et rigtig godt sted lige nu!
Tror mange BP/biotek selskaber ville give meget for at kunne være i samme position som Anavex lige nu!
Indtil nu, har de bare ikke villet betale det, som Anavex mener er en fair pris!
Og billetprisen for at kunne komme med på rejsen/casen vil kun stige, når vi nærmer os en EMA afgørelse.
Blarcamesine er 5 mdr. henne i en normal 12 mdr. godkendelsesproces for en EMA godkendelse.
Anavex gav udtryk for, at man ikke vil informerer om den igangværende proces - tænker man ikke vil foregribe eller forstyrre EMA`s ellers relative åbne behandling af ansøgningen.
Vi kan dog godt få en indikation via. tidligere vedhæftede link til EMA, hvor der løbende opdateres fra stadiet af de forskellige kandidater - evt. i referat fra de månedlige 3-4 dages møder i CHMP regi.
Fredag udløber optionsspillet, hvor alle spil på en aktiekurs over 8 $, højst sandsynlig bliver ugyldige/tabt, når MM sikkert vil forsøge at få presset kursen ned under de 8 $.
Næste større nyhed kan være kommende 3-71 data i skizofreni, hvor behandlingen af de 72 pts burde være afslutte i løbet af juni - herefter følger så udredningen af data - så august/sep med evt. TLD.
Måske afhængig af hvor godt processen med EMA løber - evt. positive 120-dages feedback og forsættelse efter 1. Stop Clock, kan vi få nyheder om den annoncerede dialog Anavex vil tage med andre lande/verdensdele.
Partneraftaler kan også komme som et lyn fra en klar himmel, hvilket ville katapulterer selskabet op i en helt anden liga.
Vi kan kun afvente og de sidste 7 mdr. til den ultimative EMA-afgørelse er trods alt en håndfast og overskuelig tidshorisont - og typisk begynder markedet nogle mdr. før at bekende kulør og satse på forventningerne til et evt. positivt udfald.
Har forsat 100 % tro på casen!
Tror mange BP/biotek selskaber ville give meget for at kunne være i samme position som Anavex lige nu!
Indtil nu, har de bare ikke villet betale det, som Anavex mener er en fair pris!
Og billetprisen for at kunne komme med på rejsen/casen vil kun stige, når vi nærmer os en EMA afgørelse.
Blarcamesine er 5 mdr. henne i en normal 12 mdr. godkendelsesproces for en EMA godkendelse.
Anavex gav udtryk for, at man ikke vil informerer om den igangværende proces - tænker man ikke vil foregribe eller forstyrre EMA`s ellers relative åbne behandling af ansøgningen.
Vi kan dog godt få en indikation via. tidligere vedhæftede link til EMA, hvor der løbende opdateres fra stadiet af de forskellige kandidater - evt. i referat fra de månedlige 3-4 dages møder i CHMP regi.
Fredag udløber optionsspillet, hvor alle spil på en aktiekurs over 8 $, højst sandsynlig bliver ugyldige/tabt, når MM sikkert vil forsøge at få presset kursen ned under de 8 $.
Næste større nyhed kan være kommende 3-71 data i skizofreni, hvor behandlingen af de 72 pts burde være afslutte i løbet af juni - herefter følger så udredningen af data - så august/sep med evt. TLD.
Måske afhængig af hvor godt processen med EMA løber - evt. positive 120-dages feedback og forsættelse efter 1. Stop Clock, kan vi få nyheder om den annoncerede dialog Anavex vil tage med andre lande/verdensdele.
Partneraftaler kan også komme som et lyn fra en klar himmel, hvilket ville katapulterer selskabet op i en helt anden liga.
Vi kan kun afvente og de sidste 7 mdr. til den ultimative EMA-afgørelse er trods alt en håndfast og overskuelig tidshorisont - og typisk begynder markedet nogle mdr. før at bekende kulør og satse på forventningerne til et evt. positivt udfald.
Har forsat 100 % tro på casen!
Anavex Positiv omtale i "Walter Town Research"
Kender ikke analyseselskabet, men det er vel altid godt med lidt tilsyneladende kvaliteter omtale.
Blarcamesines bedre data sammenlignes og illustrer fint med godkendte stoffer.
"Udover de allerede godkendte stoffer mod Alzheimer er det mest udviklede og lovende medicin Blarcamsine"
https://media.stocktwits-cdn.com/api/3/media/3902141/default.png
Kender ikke analyseselskabet, men det er vel altid godt med lidt tilsyneladende kvaliteter omtale.
Blarcamesines bedre data sammenlignes og illustrer fint med godkendte stoffer.
"Udover de allerede godkendte stoffer mod Alzheimer er det mest udviklede og lovende medicin Blarcamsine"
https://media.stocktwits-cdn.com/api/3/media/3902141/default.png
Anavex Udmærket og positiv SA-artikel.
(Vedr. sidste indlæg, så er navnet "Water Town Research" - stavekontrolfejl)
Valgte at indsætte en kopi, så man slipper for at oprette en gratis adgang til SA - lidt lang.
Beskriver især resultaterne fra AD fase 2/3 og OLE og hvilken betydning dette ville have for patienterne.
Noget vi allerede har diskuteret herinde, men synes denne beskrivelse er meget fin og forståelig.
Synes også det illustrerer, at EMA vil have svært ved at argumenterer for, hvorfor Blarcamesine ikke skulle få en godkendelse - især når man ser på alternativerne eller mangel på samme!
https://seekingalpha.com/article/4787391-does-anavex-life-sciences-alzheimers-drug-actually-confer-benefit#scroll_comments
Does Anavex's Alzheimer's Drug Actually Confer Benefit?
May 15, 2025 8:49 PM ETAnavex Life Sciences Corp. (AVXL) StockBIIB, LLY, AVXL8 Comments
The Political Economist
668 Followers
Play
(37min)
Summary
Anavex Life Sciences' OLE study demonstrates that its Alzheimer's drug works for years beyond the clinical study. The OLE expands efficacy to include patients' behavioral abilities.
The Anavex drug may offer years of extra mental lucidity and greater self-sufficiency among Alzheimer's patients.
The EU's approval of Blarcamesine could increase Anavex's market value from $800 million to $8 billion.
Mental health, jigsaw pieces, puzzle in brain shape on black background
akinbostanci/iStock via Getty Images
Last year, top researchers in Alzheimer's Disease treatments published a scientific journal article describing how a new drug can slow the cognitive decline of Alzheimer's patients by 36%, and by nearly 50% for people with a particular genotype. About 70% of humans have that particular genotype, so an enormous portion of the population would likely gain years of mental lucidity if they used this new drug.
The new drug is called Blarcamesine, and it was invented by Anavex Life Sciences (NASDAQ:AVXL). The European Medicines Agency has accepted Anavex's application to market Blarcamesine as a daily pill for Alzheimer's treatment. By the end of the year, Alzheimer's patients around the world will know if the EU has ushered in a new hope for them.
The Phase 2b/3 clinical trial demonstrated that taking Blarcamesine over the course of 48 weeks slows cognitive-behavioral decline by 27% as measured by the CDR-SB. This performance equals that of the leading FDA-approved drug: Biogen's Lecanemab.
Plus, Blarcamesine does not cause brain-bleeding, while Lecanemab does. And Blarcamesine took about thirty weeks less than Lecanemab to produce the impressive results.
And yet, for many whose family members suffer from Alzheimer's Disease, a lingering question remains. Would Blarcamesine work beyond the first 48 weeks of treatment? A prolonged effect could mean the difference between months of extra mental lucidity and years of extra mental lucidity.
An Open-Label Extension (OLE) study of Blarcamesine attempted to answer that question.
The OLE Study
The Open Label Extension Study for Anavex's Blarcamesine drug went on for 144 weeks. It started after the original 48-week, double-blind Phase 2b/3 clinical trial ended.
In an early April presentation at the AD/PDTM 2025 Conference in Vienna, Austria, Dr. Timo Grimmer presented the results in a paper entitled, "Phase IIb/III ATTENTION-AD Study: Over Three Years of Continuous Treatment with Oral Blarcamesine Continues to Significantly Benefit Early Alzheimer's Disease Patients."
I agree that the OLE provided crucial evidence that Blarcamesine confers clinical benefits for three years or possibly close to four years.
Let me describe the OLE. Both the treatment group and the placebo group patients of the clinical trial were offered an opportunity to take Blarcamesine as a daily pill as part of the extension study.
The OLE patients were not unblinded, meaning, they were not told which group they belonged to in the original study -- the placebo group or the treatment group. This means that the patients could not draw any definitive conclusions about whether the drug had an effect on them in the original drug trial. In this way, a proper comparison could be made between the two groups in the OLE study.
The OLE compared two groups: the early starters (the group who had taken the drug during the clinical trial) and the late starters (the former placebo group, who started taking the drug only at the start of the OLE).
How will the rate of cognitive decline of the early starters compare to that of the late starters after 144 weeks? Will the late starters "catch up" to the early starters in their cognitive abilities?
And can any conclusions be drawn about the performance of the drug in slowing cognitive decline in general?
Better to Start Taking Blarcamesine Earlier than Later
All participants of the original clinical trial were composed of people diagnosed with Alzheimer's Disease. They were in the earlier stages of disease progression -- some suffered from Mild Cognitive Impairment (MCI) and some from Mild Dementia due to Alzheimer's. Among the trial participants there were a disproportionate number of people who carry the APOE4 gene, a gene variant that causes earlier and more severe Alzheimer's symptoms.
Anavex reported that the early starters declined cognitively at a slower pace than the late starters. The benefit of starting just 48 weeks earlier on Blarcamesine was rather great.
All of the findings were statistically significant at 192 weeks (the end of the study). The original study found that use of Blarcamesine slowed cognitive decline as measured by the ADAS-Cog13 by 36% over the course of 48 weeks. Of course, slowing decline by such a degree was extremely encouraging. The fact that the originally medicated patients widened its cognitive "lead" over the original placebo group over the course of an additional 144 weeks is meaningful.
Exactly how meaningful?
In the original clinical trial, the treatment group scored over 2 points "better" (a lower score) than the placebo on the ADAS-Cog13. That was after 48 weeks of treatment for the treatment group and 48 weeks of a placebo for the placebo group.
Then, during the OLE, both groups were treated daily with Blarcamesine. After an additional 144 weeks, the early starters extended their "lead" from 2.0 points to 3.83 points over the late starters. Even though the late starters had been treated for 144 weeks, the early starters nearly doubled their original "lead" over the late starters. The late starters not only did not catch up to the early starters, but they actually fell behind much further.
Anavex described the results in this manner:
The delayed-start analysis for ADAS-Cog13 showed a significant difference between early start and late start treatment groups up to Week 192 (LS mean difference -3.83, P = 0.0165), favoring the early start group. Together these results suggest that participants who initiated treatment with blarcamesine earlier in their disease progression showed greater stability of cognitive function compared to those who did not initiate blarcamesine until ~1 year later.
To put it another way, the group of patients who took Blarcamesine for 192 weeks scored a good deal better on the ADAS-Cog13 than the group of patients who took Blarcamesine for only 144 weeks. This way of looking at it makes it sound like taking Blarcamesine for just 48 weeks longer makes a huge difference. And that may very well be true.
It may also be true that taking Blarcamesine 48 weeks earlier in one's disease progression is of vast importance. That is the conclusion that Anavex drew from the OLE study, except without the "vast" descriptor.
What is very interesting is that the graph in Anavex's presentation shows that the late starters did indeed "catch up" to the early starters at "Week 96" on the graph (Week 48 of the OLE). So, after just 48 weeks of treatment during the OLE, the late-starters were approximately equal to the early-starters in their ADAS-Cog13 scores, despite the late starters having taken the drug for 48 weeks fewer than the early starters. What does this mean? It might mean that the first 48 weeks of treatment are quite powerful and that the second 48 weeks of treatment are not as powerful.
Over the next 96 weeks (Week 96 to Week 192 on the graph), the early starters pulled ahead by a great deal, speeding nearly 4 points "ahead" of the late-starters on the ADAS-Cog13 scores.
Interestingly, there was a subset of patients who had a much smaller delay between the original trial study and the OLE, specifically less than 19 days. This group, which enjoyed almost continuous access to Blarcamesine, actually sped ahead to a 4.2 point lead over the late-starters. So, those who had little or no interruption in their treatment opened up a 4.2 point lead over the late-starters, versus a 3.8 point lead for the entire group of early-starters. This indicates that uninterrupted intake of Blarcamesine has benefits over interrupting one's intake of the drug. To characterize the degree of the "lead," those who took Blarcamesine with little or no interruption more than doubled their already-large lead over the late starters.
All of the above-mentioned findings further demonstrate the efficacy of Blarcamesine to slow cognitive decline.
ADCS-ADL Results
The participants in the original trial took the ADCS-ADL test to measure their behavioral habits -- how well were they taking care of themselves and doing daily activities. The ADCS is based on caretaker interviews.
In the placebo-controlled original trial, the treatment group slowed their behavioral deterioration by 0.775 points compared to the placebo group. This 10% slowing of behavioral decline was not statistically significant. However, during the OLE, this 0.775 point "lead" that the treatment group held over the placebo group ballooned to 4.3 points. This was statistically significant, and represents a 5.5X multiplication of the original "gap" of .775 points.
For those who suffered little or no interruption in treatment, the multiple was 7.4X! The gap or "lead" was 5.75 points. To give some context, the original placebo group deteriorated by over 7.5 points during the 48-week clinical trial, and the treatment group deteriorated by over 6.7 points during that period. So, the gap that opened up between the two groups over 196 weeks (5.75 points) represents a major slowdown in behavioral decline for the early starters. It represents something like a 9-month delay in behavioral decline for the late-starters.
For further context, a typical Alzheimer's patient loses about 4 points per year on the ADCS-ADL, according to one journal article.
The weak spot of the original clinical study was the ADCS-ADL. Blarcamesine performed extremely well in slowing cognitive decline as measured by the ADAS-Cog13 and performed very well in slowing cognitive-behavioral decline as measured by the CDR-SB. But, like I said above, the drug did not show a statistically significant effect on a purely behavioral scale as measured by the ADCS-ADL.
The OLE shows with excellent statistical significance that the drug, taken earlier, produces a substantial effect in slowing behavioral deterioration, when compared to those who take the drug later. A not-unblinded OLE is not as good as the gold-standard placebo-controlled study, but the OLE results have strong statistical significance. And one of the top Alzheimer's researchers, Dr. Timo Grimmer, asserts that this demonstrates that taking Blarcamesine at the MCI/Early Alzheimer's stage slows behavioral deterioration.
On a practical level, taking Blarcamesine for four years may buy Alzheimer's patients an extra year of being able to cook, dress, or take a walk by themselves. And, based on the ADAS-Cog13, it looks like Blarcamesine taken early and over 196 weeks might enable a patient to remember their family members, friends, and homes for an extra year or two. These are estimations on my part.
Normal Rate of Decline Vs. OLE Patients' Rate of Decline
To give you an example as to how quickly AD patients' cognitive decline can accelerate, examine Graph D of this important study regarding the cognitive decline of Alzheimer's patients as measured by the ADAS-Cog13. The researchers followed two groups of patients: one "preclinical" group and another, worse-off group suffering from MCI. For our purposes, we are interested in patients who had an ADAS-Cog13 score of between 25 and 35, which would represent the patient population of the original Blarcamesine clinical trial.
It can easily take 18 years for a patient to advance from "preclinical" Alzheimer's Disease to Mild Cognitive Impairment (MCI) due to Alzheimer's and a score of 30 on the ADAS-Cog13; see Graph C. But once reaching an ADAS-Cog13 score of 30, a typical group of Alzheimer's patients tends to suffer a tremendous acceleration in their cognitive decline.
NOTE: the worse one's cognition, the higher one scores on the ADAS-Cog13, and the scale ranges from 0 to 85.
On Graph D, in Year 10 on the X-axis, we see that the 14 worst-performing patients on the ADAS-Cog13 were suffering from MCI and all 14 of them scored between 25 and 35 on the ADAS-Cog13; these 14 patients can serve as a stand-in for the patients in the Blarcamesine study. The patients in the Blarcamesine trial had an average ADAS-Cog13 score of about 30. In Year 13, just three years later, the 8 worst-off patients scored between 50 and 70 on the ADAS-Cog13; the next 6 worst-off patients score between 30 and 40. So you can see that cognitive decline can accelerate severely when patients reach the 25 to 35 range on the ADAS-Cog13. My point? We should see significant acceleration of cognitive decline for a group of patients scoring around 30 on the ADAS-Cog13.
The question, then, is, did the placebo patients in the clinical trial accelerate their cognitive decline over the course of the 144-week OLE study, as one might expect if Blarcamesine was ineffective?
Blarcamesine Slows Cognitive Decline For Three Years
Seeking Alpha scientist-writer Dr. C.C. Abbott proposed that though there was no placebo group for the OLE, we could use the original placebo group's clinical trial performance as a stand-in for a placebo group's would-be performance. In the original clinical trial, the placebo group worsened by over 5.58 points on the ADAS-Cog13 while the treatment group only worsened by 3.555 points; hence, the 2.0 point gap cited to prove efficacy for Blarcamesine.
Now let's examine the performance of the placebo group, now known as the late-starters, from Week 48 to Week 196 of the OLE. At Week 48 of the original study the placebo group had slid 5.582 points on the ADAS-Cog13. At Week 196, these late-starters had taken Blarcamesine for 144 Weeks, and their ADAS-Cog13 scores were about 20 points lower than baseline, or about 14.4 points worse than at the end of the clinical trial.
That means that over the course of 144 weeks of the OLE, they deteriorated at an average rate of 4.806 points every 48 weeks. Compare this rate -- 4.806 -- to the rate of decline during the clinical trial -- 5.582. The rate of cognitive decline had slowed by 13.890% after taking Blarcamesine, compared to the first 48 weeks. Imagine an Alzheimer's patient slowing their cognitive decline by nearly 14% each year for three years. The accumulated preservation of brainpower would be tremendous.
So, this is evidence, according to C.C. Abbott's methods, that Blarcamesine is indeed effective over the course of three years!
Now, there is a problem with C.C. Abbott's method. The first 48 weeks cannot serve as a proper stand-in for a placebo group for the late-starters because these patients, who started at about a 30 on the ADAS-Cog13 and then declined to a score of about 35 at the end of the clinical trial, should be accelerating their decline at this point in the disease progression. Meaning, these patients should be declining at a rate significantly greater than 5.582 points per 48 weeks.
So, let's say, without medication or placebo, they would have declined by 7 points per 48 weeks. Then what we see is that Blarcamesine is blowing open an enormous gap between the late-starters and our "would-be" stand-in placebo group. Declining 4.8 points as opposed to 7.0 points per 48 weeks means that Blarcamesine is slowing cognitive decline by 2.2 points per 48 weeks, similar to the findings of the clinical trial. These results from a safe, daily pill, if true, would be simply revolutionary.
IMPORTANT NOTE: The 20 point deterioration over 196 weeks I mentioned above was not a precise number supplied by Anavex. I had to blow up Graph 1 on page 19 of their presentation and use a virtual ruler to see where exactly the late-starters scored on the ADAS-Cog13 at Week 196. And that turned out be 20.0. It may be 19.9 or it may be 20.1. Neither of those levels would change my ultimate conclusions.
The Original Treatment Group
And how did the original treatment group perform over the course of the OLE? Again, by blowing up the image of Graph 1 on Page 19 of the presentation, I estimated that the treatment group had deteriorated by a total of approximately 16.1 points to 16.2 points. If you assume they deteriorated by 16.2 points, it would mean that the original treatment group deteriorated by a total of 12.645 points over the course of the 144 weeks of the OLE. That averages out to 4.215 points per 48-week period. This indicates that the original treatment group accelerated their rate of decline during the 144 weeks of treatment following the 48 weeks of the original trial. They accelerated their decline by 18.565%, which is unfortunate.
But if we compare that 4.215 point deterioration against the 5.582 point deterioration of the placebo group during the original trial, then this early-starter group is maintaining a major advantage. They are declining, even in these later stages of disease, at a 24.489% slower pace. Even as their decline accelerates, the early starters enjoy a nearly 25% slower rate of decline compared to a "would-be" placebo pace.
The fact that the treatment group, while continuing treatment, accelerated in their decline is not surprising, even if assuming that Blarcamesine works. After all, their disease stage and ADAS-Cog13 score indicate that their decline was due to accelerate. But because their rate of decline at about 4.2 points per 48 weeks was extremely slow relative to an expected rate of 5.5 or even 7 points per 48 weeks, it seems Blarcamesine continues to confer benefit up to nearly 4 years of treatment. All of this occurred even as some patients in this group likely descended into moderate Alzheimer's, a terrible stage of the disease where patients "fall off a cliff" in their cognitive abilities.
Three Years of Behavioral Benefits from Blarcamesine
The ADCS-ADL test measures the behavioral performance of Alzheimer's patients. The lower the score, the worse the patient is performing.
The placebo/late-starter group declined by 7.560 points in their behavior as measured by the ADCS-ADL in the 48 weeks of the original clinical trial. Over the course of the entire 196 weeks, this group declined by about 27.7 points on the ADCS-ADL. On average, over the course of the latter 144 weeks, constituting the OLE, the late-starters declined 6.71 points per 48-week period. So, it could be said that the late starters slowed their behavioral decline by over 11%, using the first 48 weeks as a would-be placebo.
The early start group saw a decline in their behavior of 6.785 points on the ADCS-ADL scale in the 48 weeks of the original trial. Over the following 144 weeks, the early starters saw a total decline of approximately 15.2 points. Again, I am using an online ruler to estimate this. The average loss of behavioral skills was about 5.066 points per 48-week period during the OLE. I conclude that the rate of decline during the latter 144 weeks was significantly slower than in the original 48 weeks, as measured by points on the ADCS-ADL. In fact, behavioral decline was 25.335% slower during the 144 weeks of the OLE than in the 48 weeks of the clinical trial. This is extremely encouraging!
Why did Blarcamesine seem to work better in Year 2, Year 3, and Year 4? It may be because by Year 2, the titration period had long ended, and patients no longer suffered the side effect of dizziness. After 48 weeks of taking the medication, their bodies may have adapted to Blarcamesine's side effects, and they may have learned to better deal with them mentally too.
Another theory is this. Blarcamesine effected a major deceleration in cognitive decline. This slower cognitive decline eventually slowed their decline in behavior too. However, this follow-on effect took time to be realized. After the initial year of medication, the behavioral benefits began to shine.
When the performance of the early starters during the OLE is compared to the rate of decline in the original placebo group during the clinical trial, we see a 33.000% slowing of behavioral decline. This, of course, is astounding, if it is true.
For those who experienced at most a short interruption in treatment (19 days or less), the average behavioral decline per 48-week period was only 4.5833 points. This represents a 32.450% slower decline in behavior than the rate of the treatment group in the initial 48-week study. And it represents a 39.374% slower decline in behavior from the placebo arm's decline rate in the first 48 weeks.
The slowing of behavioral decline and the slowing of cognitive decline are both quite amazing if they are indeed true and real.
The EU should organize another study of Blarcamesine's long-term efficacy, but it should allow ten million Alzheimer's patients to participate.
Market value of Blarcamesine
Of course, our family would have liked to have had access to Blarcamesine 192 weeks ago or even 48 weeks ago.
Families struggling with Alzheimer's Disease are ready to buy any pharmaceutical that has proven to work and has no serious side effects.
What are people willing to pay? Caring for someone with Alzheimer's Disease can cost in the $10,000s. For every year that that person can take care of themselves, the family may save that sum, plus maintain their own employment.
So, $10,000 a year would be a pretty low price tag for both the family and for the government. The EU spends about $30 billion on Alzheimer's patients a year.
The EU is home to 7 or 8 million AD patients. If the EU were willing to spend $10,000 each for 3 million AD patients annually, that amounts to a $30 billion price tag, translating to $30 billion or so in revenues for Anavex Life Sciences.
Is there price elasticity for an AD drug? Let's say the price tag is only $5000, and it's purchased for 8 million AD patients. That produces a $40 billion annual revenue stream.
The company is currently valued at about $800 million. Without product price information, I would expect the value of the company to increase immediately to between $8 billion and $16 billion, if and when the EU approves Blarcamesine for the treatment of people with MCI or early-stage dementia as a result of Alzheimer's Disease.
If the EU approves Blarcamesine for only a specific, smaller population as it has for Lecanemab, then, of course, the total annual revenue shrinks, but the global market would still be enormous.
If the EU rejects Blarcamesine outright, then the company may look for other avenues for drug approval, such as in the United States, Australia, or East Asian nations. But in that case, I foresee an immediate steep drop in stock value. I don't know where it would drop to; it would likely depend on what the EU stated exactly in its rejection. For instance, the EU rejected Lecanemab based on its brain-bleeding dangers to Alzheimer's patients. Biogen appealed the initial EU rejection and was able to win approval for Lecanemab for a smaller patient population.
If only one nation approves the drug, say, for instance, China, then it would likely attract millions of Alzheimer's families to buy the drug either in China, or through mail-order. In fact, China has made medical tourism, especially on the island of Hainan, a highly profitable industry in that nation.
If the drug were approved by Mexico, expect a lower price point and millions of people flocking to Mexico for Blarcamesine.
If the drug is rejected worldwide, the company could still carry on with some drug studies for its two candidates, but the stock price would plummet, and the company would be on the clock with its four-year cash-burn runway.
In that case, a larger company may buy Anavex out to see what they can do with Blarcamesine. Dr. Christopher Missling, the CEO of Blarcamesine, has mentioned on several occasions that Blarcamesine could be taken in tandem with infusions of Lecanemab.
Blarcamesine would fit neatly among Biogen's array of neurological treatments for dementia and MS. Dr. Missling hinted that the two drugs may produce a combined effect on slowing cognitive decline among those suffering from MCI or early Alzheimer's. Each drug slowed cognitive-behavioral decline by 27% as measured by the CDR-SB; Blarcamesine did it much faster and more safely.
Dr. Missling also seemed to hint that using the drugs together might produce a synergistic effect, as each drug works on a different facet of the disease.
Eli Lilly boasts a market cap of nearly $700 billion. Like Biogen, it has an antibody-based Alzheimer's drug called Kisunla, which slowed cognitive-behavioral decline by 29% on the CDR-SB over the course of 76 weeks (similar time frame as Lecanemab). Eli Lilly could buy out Anavex with no strain to its budget.
Lecanemab and Kisunla together killed about five patients during their drug trials due to the aforementioned brain bleeding side effects, as they both function in the same manner, draining amyloid plaques from the brain. (The patient liaison I spoke with could not or would not tell me exactly how many people died while taking Lecanemab during its drug trials)
Perhaps a combination therapy with Blarcamesine could allow for lower doses of these brain-bleeding drugs and mitigate the brain bleeding. This is pure speculation, but based on the fact that Blarcamesine manipulates autophagy, the brain's own chemical self-regulatory system. If Blarcamesine can help the brain produce fewer amyloid plaques and tau tangles, then there will be less need for amyloid-clearing drugs.
Sadly, families suffering from Alzheimer's have few options and if, say, a Chinese company stole or licensed the Blarcamesine formula and synthesized it at scale, it could probably make a fortune selling pills without any government marketing approval. The results of the Phase 2, Phase 2b/3, and multiple OLEs are so impressive, I would buy unapproved Blarcamesine for my mother who is at the moderate Alzheimer's stage now. And I would buy some for myself.
This type of fantasizing may not be necessary, as the EU approves the vast majority of drugs for which it accepts applications.
RISKS to owning AVXL stock
Anavex has only one drug that has ever been considered for approval by a regulatory agency. With each quarter, that Blarcamesine has not yet begun to generate revenues, the company loses millions of dollars. In the recently reported Q1 results, the company reported a loss of over $12 million and held nearly $121 million in cash and cash equivalents. The company spent over $10 million in R&D.
The press release stated that "As of quarter end, the Company anticipates, at current cash utilization rates and ranges, a runway of approximately 4 years."
If Anavex's Blarcamesine application is rejected by the EU, the stock price will plummet; this may happen later this year. It's not clear where it would drop to -- it would depend on if any progress was being made in applying to other regulatory bodies like the FDA or the Australian drug agency.
In the recent earnings call, the CEO Christopher Missling would not clue listeners in on exactly the progress they have made in their discussions with the FDA and other drug regulators.
An outside risk would involve a patient overdosing on Blarcamesine, or a patient becoming confused and suffering an accident and this being blamed on Blarcamesine. Sarepta's (SRPT) stock value was chopped nearly in half this year by one patient's death.
Other Drug Applications and Near-Term Catalysts
Anavex is working with J.P. Morgan to partner with a larger company in Europe to market Blarcamesine, as discussed in the recent earnings call. If an announcement is made that a large pharma company has partnered with Anavex, the stock price will spike. This could happen in weeks or months.
Blarcamesine has a great deal of potential as a treatment for Parkinson's Disease, as demonstrated by a Phase 2 double-blind, placebo-controlled trial. In fact, the results of the study were so stunning that Blarcamesine may prove even more effective at treating Parkinson's than Alzheimer's. Those in the Parkinson's Phase 2 study also participated in an OLE study. And much like the participants in the Alzheimer's OLE, those who suffered through a delay in treatment saw their Parkinson's symptoms worsen; when the drug was re-administered, the patients recovered gains they had lost during the interruption (due to Covid).
When the Parkinson's Phase 3 trial is completed, in 2026 at the earliest, it may provide an enormous catalyst for the stock price.
The company has one other molecule that is being tested in a tiny, early trial for people suffering from Schizophrenia. Results will be reported in H2. However, if the second drug candidate proves promising, it may put a stronger floor under the stock price in case Blarcamesine is rejected by the EU.
Conclusion
This is a classic binary situation with massive implications on the stock price and the fate of Anavex Life Sciences. If the EU approves Blarcamesine as a treatment for Alzheimer's Disease, the value of the stock will multiply by some whole-number factor.
If the EU rejects the drug, then the stock will be cut down.
The current valuation of the company leans heavily toward the "failure" end of the see-saw.
One may try to divine the drug's fate by carefully studying the Phase 2b/3 trial and the OLE study of Blarcamesine. But ultimately, the EU will make the decision, based on their own biases and ethical standards.
My bet is on approval, based on the results of the trials and based on the extreme need for a safe, effective brake on the brain-consuming machine called Alzheimer's Disease.
Addendum 1: More Evidence for the Acceleration of Symptoms from Preclinical to MCI to Early AD to Moderate AD
Those patients who participated in the original Blarcamesine clinical study were all originally in two categories: MCI and mild dementia due to AD. Some of those who started out in MCI likely descended into mild dementia during the study and some larger portion likely descended from mild dementia into moderate dementia due to AD.
One would expect many or most of these patients to accelerate their cognitive decline during a 192-week period, a period of almost four years.
This study published in Nature documents that the slope of change on the ADAS-Cog13 steepens between the time one is diagnosed with MCI and when one has entered mild dementia due to Alzheimer's Disease. That is to say, the worsening of symptoms accelerates from Preclinical to MCI to Mild Dementia (Early AD).
Furthermore, according to another study, disease progression (worsening of cognition and behavior) accelerates when a patient degenerates from MCI or mild dementia due to Alzheimer's into moderate dementia due to Alzheimer's Disease.
"Participants with MCI or mild dementia due to AD, compared to participants with moderate dementia due to AD, had numerically higher baseline iADRS scores and slower progression on the iADRS, the ADAS-Cog13, and ADCS-iADL."
This study actually used test scores attained from the placebo branches of several Alzheimer's drug trials.
Addendum 2: ADCS-ADL vs. ADCS-ADL MCI
Anavex's Blarcamesine and Biogen's Lecanemab cannot really be compared directly based on their ADCS-ADL score results. Biogen specifically aimed their drug trial at patients who were less debilitated. The Biogen Lecanemab patients at baseline scored 22% better on the CDR-SB scale of cognitive-behavioral function than the Blarcamesine trial patients.
The patients in the Anavex study were suffering worse symptoms and were further along in disease progression.
In fact, I even question whether some of the patients in the Biogen Lecanemab study had Alzheimer's Disease, specifically the patients with extremely low levels of tau tangles in their brain. Biogen and Eli Lilly both brag about how well their drugs work on people with low levels of tau. That's not surprising since these patients started their studies with far fewer of the chemicals that cause Alzheimer's Disease.
Because Biogen's Lecanemab patients suffered from less cognitive impairment, they took the ADCS-ADL MCI test rather than the ADCS-ADL test. The MCI stands for Mild Cognitive Impairment. This means that it was meant for people with MCI rather than for people who had progressed to early Alzheimer's Disease. This is appropriate, as the MCI test is likely far more sensitive as a measure, for people who are entirely in the MCI stage. The Blarcamesine patients were in both the MCI and the Early Dementia due to Alzheimer's stages.
Addendum 3: Regarding Dr. Timo Grimmer
Dr. Timo Grimmer was the primary author and presenter of the Blarcamesine OLE research. He is highly respected worldwide for his research into Alzheimer's Disease. The presentation included this disclaimer:
Dr. Grimmer received [or is] receiving consulting fees from Acumen, Advantage Ther., Alector, Anavex, Biogen, BMS; Cogthera, Eisai, Eli Lilly, Functional Neuromod., Grifols, Janssen, Neurimmune, Noselab, Novo Nordisk, Roche Diagnostics, and Roche Pharma; lecture fees from Cogthera, Eisai, Eli Lilly, FEO, Grifols, Pfizer, Roche Pharma, Schwabe, and Synlab; and has received grants to his institution from Biogen and Eisai.
This list helps us understand just how well-respected and powerful Dr. Grimmer is in the field of biopharmaceutical treatments for Alzheimer's. He has conducted research for major Alzheimer's treatment competitors such as Biogen, Eisai, and Eli Lilly. Most of these companies are many times larger than Anavex, and yet, Dr. Grimmer is deeply involved in an Alzheimer's drug invented by a tiny pharmaceutical company.
(Vedr. sidste indlæg, så er navnet "Water Town Research" - stavekontrolfejl)
Valgte at indsætte en kopi, så man slipper for at oprette en gratis adgang til SA - lidt lang.
Beskriver især resultaterne fra AD fase 2/3 og OLE og hvilken betydning dette ville have for patienterne.
Noget vi allerede har diskuteret herinde, men synes denne beskrivelse er meget fin og forståelig.
Synes også det illustrerer, at EMA vil have svært ved at argumenterer for, hvorfor Blarcamesine ikke skulle få en godkendelse - især når man ser på alternativerne eller mangel på samme!
https://seekingalpha.com/article/4787391-does-anavex-life-sciences-alzheimers-drug-actually-confer-benefit#scroll_comments
Does Anavex's Alzheimer's Drug Actually Confer Benefit?
May 15, 2025 8:49 PM ETAnavex Life Sciences Corp. (AVXL) StockBIIB, LLY, AVXL8 Comments
The Political Economist
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Summary
Anavex Life Sciences' OLE study demonstrates that its Alzheimer's drug works for years beyond the clinical study. The OLE expands efficacy to include patients' behavioral abilities.
The Anavex drug may offer years of extra mental lucidity and greater self-sufficiency among Alzheimer's patients.
The EU's approval of Blarcamesine could increase Anavex's market value from $800 million to $8 billion.
Mental health, jigsaw pieces, puzzle in brain shape on black background
akinbostanci/iStock via Getty Images
Last year, top researchers in Alzheimer's Disease treatments published a scientific journal article describing how a new drug can slow the cognitive decline of Alzheimer's patients by 36%, and by nearly 50% for people with a particular genotype. About 70% of humans have that particular genotype, so an enormous portion of the population would likely gain years of mental lucidity if they used this new drug.
The new drug is called Blarcamesine, and it was invented by Anavex Life Sciences (NASDAQ:AVXL). The European Medicines Agency has accepted Anavex's application to market Blarcamesine as a daily pill for Alzheimer's treatment. By the end of the year, Alzheimer's patients around the world will know if the EU has ushered in a new hope for them.
The Phase 2b/3 clinical trial demonstrated that taking Blarcamesine over the course of 48 weeks slows cognitive-behavioral decline by 27% as measured by the CDR-SB. This performance equals that of the leading FDA-approved drug: Biogen's Lecanemab.
Plus, Blarcamesine does not cause brain-bleeding, while Lecanemab does. And Blarcamesine took about thirty weeks less than Lecanemab to produce the impressive results.
And yet, for many whose family members suffer from Alzheimer's Disease, a lingering question remains. Would Blarcamesine work beyond the first 48 weeks of treatment? A prolonged effect could mean the difference between months of extra mental lucidity and years of extra mental lucidity.
An Open-Label Extension (OLE) study of Blarcamesine attempted to answer that question.
The OLE Study
The Open Label Extension Study for Anavex's Blarcamesine drug went on for 144 weeks. It started after the original 48-week, double-blind Phase 2b/3 clinical trial ended.
In an early April presentation at the AD/PDTM 2025 Conference in Vienna, Austria, Dr. Timo Grimmer presented the results in a paper entitled, "Phase IIb/III ATTENTION-AD Study: Over Three Years of Continuous Treatment with Oral Blarcamesine Continues to Significantly Benefit Early Alzheimer's Disease Patients."
I agree that the OLE provided crucial evidence that Blarcamesine confers clinical benefits for three years or possibly close to four years.
Let me describe the OLE. Both the treatment group and the placebo group patients of the clinical trial were offered an opportunity to take Blarcamesine as a daily pill as part of the extension study.
The OLE patients were not unblinded, meaning, they were not told which group they belonged to in the original study -- the placebo group or the treatment group. This means that the patients could not draw any definitive conclusions about whether the drug had an effect on them in the original drug trial. In this way, a proper comparison could be made between the two groups in the OLE study.
The OLE compared two groups: the early starters (the group who had taken the drug during the clinical trial) and the late starters (the former placebo group, who started taking the drug only at the start of the OLE).
How will the rate of cognitive decline of the early starters compare to that of the late starters after 144 weeks? Will the late starters "catch up" to the early starters in their cognitive abilities?
And can any conclusions be drawn about the performance of the drug in slowing cognitive decline in general?
Better to Start Taking Blarcamesine Earlier than Later
All participants of the original clinical trial were composed of people diagnosed with Alzheimer's Disease. They were in the earlier stages of disease progression -- some suffered from Mild Cognitive Impairment (MCI) and some from Mild Dementia due to Alzheimer's. Among the trial participants there were a disproportionate number of people who carry the APOE4 gene, a gene variant that causes earlier and more severe Alzheimer's symptoms.
Anavex reported that the early starters declined cognitively at a slower pace than the late starters. The benefit of starting just 48 weeks earlier on Blarcamesine was rather great.
All of the findings were statistically significant at 192 weeks (the end of the study). The original study found that use of Blarcamesine slowed cognitive decline as measured by the ADAS-Cog13 by 36% over the course of 48 weeks. Of course, slowing decline by such a degree was extremely encouraging. The fact that the originally medicated patients widened its cognitive "lead" over the original placebo group over the course of an additional 144 weeks is meaningful.
Exactly how meaningful?
In the original clinical trial, the treatment group scored over 2 points "better" (a lower score) than the placebo on the ADAS-Cog13. That was after 48 weeks of treatment for the treatment group and 48 weeks of a placebo for the placebo group.
Then, during the OLE, both groups were treated daily with Blarcamesine. After an additional 144 weeks, the early starters extended their "lead" from 2.0 points to 3.83 points over the late starters. Even though the late starters had been treated for 144 weeks, the early starters nearly doubled their original "lead" over the late starters. The late starters not only did not catch up to the early starters, but they actually fell behind much further.
Anavex described the results in this manner:
The delayed-start analysis for ADAS-Cog13 showed a significant difference between early start and late start treatment groups up to Week 192 (LS mean difference -3.83, P = 0.0165), favoring the early start group. Together these results suggest that participants who initiated treatment with blarcamesine earlier in their disease progression showed greater stability of cognitive function compared to those who did not initiate blarcamesine until ~1 year later.
To put it another way, the group of patients who took Blarcamesine for 192 weeks scored a good deal better on the ADAS-Cog13 than the group of patients who took Blarcamesine for only 144 weeks. This way of looking at it makes it sound like taking Blarcamesine for just 48 weeks longer makes a huge difference. And that may very well be true.
It may also be true that taking Blarcamesine 48 weeks earlier in one's disease progression is of vast importance. That is the conclusion that Anavex drew from the OLE study, except without the "vast" descriptor.
What is very interesting is that the graph in Anavex's presentation shows that the late starters did indeed "catch up" to the early starters at "Week 96" on the graph (Week 48 of the OLE). So, after just 48 weeks of treatment during the OLE, the late-starters were approximately equal to the early-starters in their ADAS-Cog13 scores, despite the late starters having taken the drug for 48 weeks fewer than the early starters. What does this mean? It might mean that the first 48 weeks of treatment are quite powerful and that the second 48 weeks of treatment are not as powerful.
Over the next 96 weeks (Week 96 to Week 192 on the graph), the early starters pulled ahead by a great deal, speeding nearly 4 points "ahead" of the late-starters on the ADAS-Cog13 scores.
Interestingly, there was a subset of patients who had a much smaller delay between the original trial study and the OLE, specifically less than 19 days. This group, which enjoyed almost continuous access to Blarcamesine, actually sped ahead to a 4.2 point lead over the late-starters. So, those who had little or no interruption in their treatment opened up a 4.2 point lead over the late-starters, versus a 3.8 point lead for the entire group of early-starters. This indicates that uninterrupted intake of Blarcamesine has benefits over interrupting one's intake of the drug. To characterize the degree of the "lead," those who took Blarcamesine with little or no interruption more than doubled their already-large lead over the late starters.
All of the above-mentioned findings further demonstrate the efficacy of Blarcamesine to slow cognitive decline.
ADCS-ADL Results
The participants in the original trial took the ADCS-ADL test to measure their behavioral habits -- how well were they taking care of themselves and doing daily activities. The ADCS is based on caretaker interviews.
In the placebo-controlled original trial, the treatment group slowed their behavioral deterioration by 0.775 points compared to the placebo group. This 10% slowing of behavioral decline was not statistically significant. However, during the OLE, this 0.775 point "lead" that the treatment group held over the placebo group ballooned to 4.3 points. This was statistically significant, and represents a 5.5X multiplication of the original "gap" of .775 points.
For those who suffered little or no interruption in treatment, the multiple was 7.4X! The gap or "lead" was 5.75 points. To give some context, the original placebo group deteriorated by over 7.5 points during the 48-week clinical trial, and the treatment group deteriorated by over 6.7 points during that period. So, the gap that opened up between the two groups over 196 weeks (5.75 points) represents a major slowdown in behavioral decline for the early starters. It represents something like a 9-month delay in behavioral decline for the late-starters.
For further context, a typical Alzheimer's patient loses about 4 points per year on the ADCS-ADL, according to one journal article.
The weak spot of the original clinical study was the ADCS-ADL. Blarcamesine performed extremely well in slowing cognitive decline as measured by the ADAS-Cog13 and performed very well in slowing cognitive-behavioral decline as measured by the CDR-SB. But, like I said above, the drug did not show a statistically significant effect on a purely behavioral scale as measured by the ADCS-ADL.
The OLE shows with excellent statistical significance that the drug, taken earlier, produces a substantial effect in slowing behavioral deterioration, when compared to those who take the drug later. A not-unblinded OLE is not as good as the gold-standard placebo-controlled study, but the OLE results have strong statistical significance. And one of the top Alzheimer's researchers, Dr. Timo Grimmer, asserts that this demonstrates that taking Blarcamesine at the MCI/Early Alzheimer's stage slows behavioral deterioration.
On a practical level, taking Blarcamesine for four years may buy Alzheimer's patients an extra year of being able to cook, dress, or take a walk by themselves. And, based on the ADAS-Cog13, it looks like Blarcamesine taken early and over 196 weeks might enable a patient to remember their family members, friends, and homes for an extra year or two. These are estimations on my part.
Normal Rate of Decline Vs. OLE Patients' Rate of Decline
To give you an example as to how quickly AD patients' cognitive decline can accelerate, examine Graph D of this important study regarding the cognitive decline of Alzheimer's patients as measured by the ADAS-Cog13. The researchers followed two groups of patients: one "preclinical" group and another, worse-off group suffering from MCI. For our purposes, we are interested in patients who had an ADAS-Cog13 score of between 25 and 35, which would represent the patient population of the original Blarcamesine clinical trial.
It can easily take 18 years for a patient to advance from "preclinical" Alzheimer's Disease to Mild Cognitive Impairment (MCI) due to Alzheimer's and a score of 30 on the ADAS-Cog13; see Graph C. But once reaching an ADAS-Cog13 score of 30, a typical group of Alzheimer's patients tends to suffer a tremendous acceleration in their cognitive decline.
NOTE: the worse one's cognition, the higher one scores on the ADAS-Cog13, and the scale ranges from 0 to 85.
On Graph D, in Year 10 on the X-axis, we see that the 14 worst-performing patients on the ADAS-Cog13 were suffering from MCI and all 14 of them scored between 25 and 35 on the ADAS-Cog13; these 14 patients can serve as a stand-in for the patients in the Blarcamesine study. The patients in the Blarcamesine trial had an average ADAS-Cog13 score of about 30. In Year 13, just three years later, the 8 worst-off patients scored between 50 and 70 on the ADAS-Cog13; the next 6 worst-off patients score between 30 and 40. So you can see that cognitive decline can accelerate severely when patients reach the 25 to 35 range on the ADAS-Cog13. My point? We should see significant acceleration of cognitive decline for a group of patients scoring around 30 on the ADAS-Cog13.
The question, then, is, did the placebo patients in the clinical trial accelerate their cognitive decline over the course of the 144-week OLE study, as one might expect if Blarcamesine was ineffective?
Blarcamesine Slows Cognitive Decline For Three Years
Seeking Alpha scientist-writer Dr. C.C. Abbott proposed that though there was no placebo group for the OLE, we could use the original placebo group's clinical trial performance as a stand-in for a placebo group's would-be performance. In the original clinical trial, the placebo group worsened by over 5.58 points on the ADAS-Cog13 while the treatment group only worsened by 3.555 points; hence, the 2.0 point gap cited to prove efficacy for Blarcamesine.
Now let's examine the performance of the placebo group, now known as the late-starters, from Week 48 to Week 196 of the OLE. At Week 48 of the original study the placebo group had slid 5.582 points on the ADAS-Cog13. At Week 196, these late-starters had taken Blarcamesine for 144 Weeks, and their ADAS-Cog13 scores were about 20 points lower than baseline, or about 14.4 points worse than at the end of the clinical trial.
That means that over the course of 144 weeks of the OLE, they deteriorated at an average rate of 4.806 points every 48 weeks. Compare this rate -- 4.806 -- to the rate of decline during the clinical trial -- 5.582. The rate of cognitive decline had slowed by 13.890% after taking Blarcamesine, compared to the first 48 weeks. Imagine an Alzheimer's patient slowing their cognitive decline by nearly 14% each year for three years. The accumulated preservation of brainpower would be tremendous.
So, this is evidence, according to C.C. Abbott's methods, that Blarcamesine is indeed effective over the course of three years!
Now, there is a problem with C.C. Abbott's method. The first 48 weeks cannot serve as a proper stand-in for a placebo group for the late-starters because these patients, who started at about a 30 on the ADAS-Cog13 and then declined to a score of about 35 at the end of the clinical trial, should be accelerating their decline at this point in the disease progression. Meaning, these patients should be declining at a rate significantly greater than 5.582 points per 48 weeks.
So, let's say, without medication or placebo, they would have declined by 7 points per 48 weeks. Then what we see is that Blarcamesine is blowing open an enormous gap between the late-starters and our "would-be" stand-in placebo group. Declining 4.8 points as opposed to 7.0 points per 48 weeks means that Blarcamesine is slowing cognitive decline by 2.2 points per 48 weeks, similar to the findings of the clinical trial. These results from a safe, daily pill, if true, would be simply revolutionary.
IMPORTANT NOTE: The 20 point deterioration over 196 weeks I mentioned above was not a precise number supplied by Anavex. I had to blow up Graph 1 on page 19 of their presentation and use a virtual ruler to see where exactly the late-starters scored on the ADAS-Cog13 at Week 196. And that turned out be 20.0. It may be 19.9 or it may be 20.1. Neither of those levels would change my ultimate conclusions.
The Original Treatment Group
And how did the original treatment group perform over the course of the OLE? Again, by blowing up the image of Graph 1 on Page 19 of the presentation, I estimated that the treatment group had deteriorated by a total of approximately 16.1 points to 16.2 points. If you assume they deteriorated by 16.2 points, it would mean that the original treatment group deteriorated by a total of 12.645 points over the course of the 144 weeks of the OLE. That averages out to 4.215 points per 48-week period. This indicates that the original treatment group accelerated their rate of decline during the 144 weeks of treatment following the 48 weeks of the original trial. They accelerated their decline by 18.565%, which is unfortunate.
But if we compare that 4.215 point deterioration against the 5.582 point deterioration of the placebo group during the original trial, then this early-starter group is maintaining a major advantage. They are declining, even in these later stages of disease, at a 24.489% slower pace. Even as their decline accelerates, the early starters enjoy a nearly 25% slower rate of decline compared to a "would-be" placebo pace.
The fact that the treatment group, while continuing treatment, accelerated in their decline is not surprising, even if assuming that Blarcamesine works. After all, their disease stage and ADAS-Cog13 score indicate that their decline was due to accelerate. But because their rate of decline at about 4.2 points per 48 weeks was extremely slow relative to an expected rate of 5.5 or even 7 points per 48 weeks, it seems Blarcamesine continues to confer benefit up to nearly 4 years of treatment. All of this occurred even as some patients in this group likely descended into moderate Alzheimer's, a terrible stage of the disease where patients "fall off a cliff" in their cognitive abilities.
Three Years of Behavioral Benefits from Blarcamesine
The ADCS-ADL test measures the behavioral performance of Alzheimer's patients. The lower the score, the worse the patient is performing.
The placebo/late-starter group declined by 7.560 points in their behavior as measured by the ADCS-ADL in the 48 weeks of the original clinical trial. Over the course of the entire 196 weeks, this group declined by about 27.7 points on the ADCS-ADL. On average, over the course of the latter 144 weeks, constituting the OLE, the late-starters declined 6.71 points per 48-week period. So, it could be said that the late starters slowed their behavioral decline by over 11%, using the first 48 weeks as a would-be placebo.
The early start group saw a decline in their behavior of 6.785 points on the ADCS-ADL scale in the 48 weeks of the original trial. Over the following 144 weeks, the early starters saw a total decline of approximately 15.2 points. Again, I am using an online ruler to estimate this. The average loss of behavioral skills was about 5.066 points per 48-week period during the OLE. I conclude that the rate of decline during the latter 144 weeks was significantly slower than in the original 48 weeks, as measured by points on the ADCS-ADL. In fact, behavioral decline was 25.335% slower during the 144 weeks of the OLE than in the 48 weeks of the clinical trial. This is extremely encouraging!
Why did Blarcamesine seem to work better in Year 2, Year 3, and Year 4? It may be because by Year 2, the titration period had long ended, and patients no longer suffered the side effect of dizziness. After 48 weeks of taking the medication, their bodies may have adapted to Blarcamesine's side effects, and they may have learned to better deal with them mentally too.
Another theory is this. Blarcamesine effected a major deceleration in cognitive decline. This slower cognitive decline eventually slowed their decline in behavior too. However, this follow-on effect took time to be realized. After the initial year of medication, the behavioral benefits began to shine.
When the performance of the early starters during the OLE is compared to the rate of decline in the original placebo group during the clinical trial, we see a 33.000% slowing of behavioral decline. This, of course, is astounding, if it is true.
For those who experienced at most a short interruption in treatment (19 days or less), the average behavioral decline per 48-week period was only 4.5833 points. This represents a 32.450% slower decline in behavior than the rate of the treatment group in the initial 48-week study. And it represents a 39.374% slower decline in behavior from the placebo arm's decline rate in the first 48 weeks.
The slowing of behavioral decline and the slowing of cognitive decline are both quite amazing if they are indeed true and real.
The EU should organize another study of Blarcamesine's long-term efficacy, but it should allow ten million Alzheimer's patients to participate.
Market value of Blarcamesine
Of course, our family would have liked to have had access to Blarcamesine 192 weeks ago or even 48 weeks ago.
Families struggling with Alzheimer's Disease are ready to buy any pharmaceutical that has proven to work and has no serious side effects.
What are people willing to pay? Caring for someone with Alzheimer's Disease can cost in the $10,000s. For every year that that person can take care of themselves, the family may save that sum, plus maintain their own employment.
So, $10,000 a year would be a pretty low price tag for both the family and for the government. The EU spends about $30 billion on Alzheimer's patients a year.
The EU is home to 7 or 8 million AD patients. If the EU were willing to spend $10,000 each for 3 million AD patients annually, that amounts to a $30 billion price tag, translating to $30 billion or so in revenues for Anavex Life Sciences.
Is there price elasticity for an AD drug? Let's say the price tag is only $5000, and it's purchased for 8 million AD patients. That produces a $40 billion annual revenue stream.
The company is currently valued at about $800 million. Without product price information, I would expect the value of the company to increase immediately to between $8 billion and $16 billion, if and when the EU approves Blarcamesine for the treatment of people with MCI or early-stage dementia as a result of Alzheimer's Disease.
If the EU approves Blarcamesine for only a specific, smaller population as it has for Lecanemab, then, of course, the total annual revenue shrinks, but the global market would still be enormous.
If the EU rejects Blarcamesine outright, then the company may look for other avenues for drug approval, such as in the United States, Australia, or East Asian nations. But in that case, I foresee an immediate steep drop in stock value. I don't know where it would drop to; it would likely depend on what the EU stated exactly in its rejection. For instance, the EU rejected Lecanemab based on its brain-bleeding dangers to Alzheimer's patients. Biogen appealed the initial EU rejection and was able to win approval for Lecanemab for a smaller patient population.
If only one nation approves the drug, say, for instance, China, then it would likely attract millions of Alzheimer's families to buy the drug either in China, or through mail-order. In fact, China has made medical tourism, especially on the island of Hainan, a highly profitable industry in that nation.
If the drug were approved by Mexico, expect a lower price point and millions of people flocking to Mexico for Blarcamesine.
If the drug is rejected worldwide, the company could still carry on with some drug studies for its two candidates, but the stock price would plummet, and the company would be on the clock with its four-year cash-burn runway.
In that case, a larger company may buy Anavex out to see what they can do with Blarcamesine. Dr. Christopher Missling, the CEO of Blarcamesine, has mentioned on several occasions that Blarcamesine could be taken in tandem with infusions of Lecanemab.
Blarcamesine would fit neatly among Biogen's array of neurological treatments for dementia and MS. Dr. Missling hinted that the two drugs may produce a combined effect on slowing cognitive decline among those suffering from MCI or early Alzheimer's. Each drug slowed cognitive-behavioral decline by 27% as measured by the CDR-SB; Blarcamesine did it much faster and more safely.
Dr. Missling also seemed to hint that using the drugs together might produce a synergistic effect, as each drug works on a different facet of the disease.
Eli Lilly boasts a market cap of nearly $700 billion. Like Biogen, it has an antibody-based Alzheimer's drug called Kisunla, which slowed cognitive-behavioral decline by 29% on the CDR-SB over the course of 76 weeks (similar time frame as Lecanemab). Eli Lilly could buy out Anavex with no strain to its budget.
Lecanemab and Kisunla together killed about five patients during their drug trials due to the aforementioned brain bleeding side effects, as they both function in the same manner, draining amyloid plaques from the brain. (The patient liaison I spoke with could not or would not tell me exactly how many people died while taking Lecanemab during its drug trials)
Perhaps a combination therapy with Blarcamesine could allow for lower doses of these brain-bleeding drugs and mitigate the brain bleeding. This is pure speculation, but based on the fact that Blarcamesine manipulates autophagy, the brain's own chemical self-regulatory system. If Blarcamesine can help the brain produce fewer amyloid plaques and tau tangles, then there will be less need for amyloid-clearing drugs.
Sadly, families suffering from Alzheimer's have few options and if, say, a Chinese company stole or licensed the Blarcamesine formula and synthesized it at scale, it could probably make a fortune selling pills without any government marketing approval. The results of the Phase 2, Phase 2b/3, and multiple OLEs are so impressive, I would buy unapproved Blarcamesine for my mother who is at the moderate Alzheimer's stage now. And I would buy some for myself.
This type of fantasizing may not be necessary, as the EU approves the vast majority of drugs for which it accepts applications.
RISKS to owning AVXL stock
Anavex has only one drug that has ever been considered for approval by a regulatory agency. With each quarter, that Blarcamesine has not yet begun to generate revenues, the company loses millions of dollars. In the recently reported Q1 results, the company reported a loss of over $12 million and held nearly $121 million in cash and cash equivalents. The company spent over $10 million in R&D.
The press release stated that "As of quarter end, the Company anticipates, at current cash utilization rates and ranges, a runway of approximately 4 years."
If Anavex's Blarcamesine application is rejected by the EU, the stock price will plummet; this may happen later this year. It's not clear where it would drop to -- it would depend on if any progress was being made in applying to other regulatory bodies like the FDA or the Australian drug agency.
In the recent earnings call, the CEO Christopher Missling would not clue listeners in on exactly the progress they have made in their discussions with the FDA and other drug regulators.
An outside risk would involve a patient overdosing on Blarcamesine, or a patient becoming confused and suffering an accident and this being blamed on Blarcamesine. Sarepta's (SRPT) stock value was chopped nearly in half this year by one patient's death.
Other Drug Applications and Near-Term Catalysts
Anavex is working with J.P. Morgan to partner with a larger company in Europe to market Blarcamesine, as discussed in the recent earnings call. If an announcement is made that a large pharma company has partnered with Anavex, the stock price will spike. This could happen in weeks or months.
Blarcamesine has a great deal of potential as a treatment for Parkinson's Disease, as demonstrated by a Phase 2 double-blind, placebo-controlled trial. In fact, the results of the study were so stunning that Blarcamesine may prove even more effective at treating Parkinson's than Alzheimer's. Those in the Parkinson's Phase 2 study also participated in an OLE study. And much like the participants in the Alzheimer's OLE, those who suffered through a delay in treatment saw their Parkinson's symptoms worsen; when the drug was re-administered, the patients recovered gains they had lost during the interruption (due to Covid).
When the Parkinson's Phase 3 trial is completed, in 2026 at the earliest, it may provide an enormous catalyst for the stock price.
The company has one other molecule that is being tested in a tiny, early trial for people suffering from Schizophrenia. Results will be reported in H2. However, if the second drug candidate proves promising, it may put a stronger floor under the stock price in case Blarcamesine is rejected by the EU.
Conclusion
This is a classic binary situation with massive implications on the stock price and the fate of Anavex Life Sciences. If the EU approves Blarcamesine as a treatment for Alzheimer's Disease, the value of the stock will multiply by some whole-number factor.
If the EU rejects the drug, then the stock will be cut down.
The current valuation of the company leans heavily toward the "failure" end of the see-saw.
One may try to divine the drug's fate by carefully studying the Phase 2b/3 trial and the OLE study of Blarcamesine. But ultimately, the EU will make the decision, based on their own biases and ethical standards.
My bet is on approval, based on the results of the trials and based on the extreme need for a safe, effective brake on the brain-consuming machine called Alzheimer's Disease.
Addendum 1: More Evidence for the Acceleration of Symptoms from Preclinical to MCI to Early AD to Moderate AD
Those patients who participated in the original Blarcamesine clinical study were all originally in two categories: MCI and mild dementia due to AD. Some of those who started out in MCI likely descended into mild dementia during the study and some larger portion likely descended from mild dementia into moderate dementia due to AD.
One would expect many or most of these patients to accelerate their cognitive decline during a 192-week period, a period of almost four years.
This study published in Nature documents that the slope of change on the ADAS-Cog13 steepens between the time one is diagnosed with MCI and when one has entered mild dementia due to Alzheimer's Disease. That is to say, the worsening of symptoms accelerates from Preclinical to MCI to Mild Dementia (Early AD).
Furthermore, according to another study, disease progression (worsening of cognition and behavior) accelerates when a patient degenerates from MCI or mild dementia due to Alzheimer's into moderate dementia due to Alzheimer's Disease.
"Participants with MCI or mild dementia due to AD, compared to participants with moderate dementia due to AD, had numerically higher baseline iADRS scores and slower progression on the iADRS, the ADAS-Cog13, and ADCS-iADL."
This study actually used test scores attained from the placebo branches of several Alzheimer's drug trials.
Addendum 2: ADCS-ADL vs. ADCS-ADL MCI
Anavex's Blarcamesine and Biogen's Lecanemab cannot really be compared directly based on their ADCS-ADL score results. Biogen specifically aimed their drug trial at patients who were less debilitated. The Biogen Lecanemab patients at baseline scored 22% better on the CDR-SB scale of cognitive-behavioral function than the Blarcamesine trial patients.
The patients in the Anavex study were suffering worse symptoms and were further along in disease progression.
In fact, I even question whether some of the patients in the Biogen Lecanemab study had Alzheimer's Disease, specifically the patients with extremely low levels of tau tangles in their brain. Biogen and Eli Lilly both brag about how well their drugs work on people with low levels of tau. That's not surprising since these patients started their studies with far fewer of the chemicals that cause Alzheimer's Disease.
Because Biogen's Lecanemab patients suffered from less cognitive impairment, they took the ADCS-ADL MCI test rather than the ADCS-ADL test. The MCI stands for Mild Cognitive Impairment. This means that it was meant for people with MCI rather than for people who had progressed to early Alzheimer's Disease. This is appropriate, as the MCI test is likely far more sensitive as a measure, for people who are entirely in the MCI stage. The Blarcamesine patients were in both the MCI and the Early Dementia due to Alzheimer's stages.
Addendum 3: Regarding Dr. Timo Grimmer
Dr. Timo Grimmer was the primary author and presenter of the Blarcamesine OLE research. He is highly respected worldwide for his research into Alzheimer's Disease. The presentation included this disclaimer:
Dr. Grimmer received [or is] receiving consulting fees from Acumen, Advantage Ther., Alector, Anavex, Biogen, BMS; Cogthera, Eisai, Eli Lilly, Functional Neuromod., Grifols, Janssen, Neurimmune, Noselab, Novo Nordisk, Roche Diagnostics, and Roche Pharma; lecture fees from Cogthera, Eisai, Eli Lilly, FEO, Grifols, Pfizer, Roche Pharma, Schwabe, and Synlab; and has received grants to his institution from Biogen and Eisai.
This list helps us understand just how well-respected and powerful Dr. Grimmer is in the field of biopharmaceutical treatments for Alzheimer's. He has conducted research for major Alzheimer's treatment competitors such as Biogen, Eisai, and Eli Lilly. Most of these companies are many times larger than Anavex, and yet, Dr. Grimmer is deeply involved in an Alzheimer's drug invented by a tiny pharmaceutical company.
