BGBIO: FORSKNING OG MEDISINER RELATERT TIL BerGenBio

BGBIO 09.10.2020 kl 15:36 134514

Redigert 21.01.2021 kl 09:40 Du må logge inn for å svare

BioBull

17.01.2021 kl 10:15 7226

Imponerende skaperverk - blir enda bedre med Bemcentinib

https://news.cnrs.fr/videos/the-blob-a-cell-that-learns

Bemcentinib er som skapt for å hjelpe kroppen til å løse sykdom på egen hånd.

Celler tenker og er mye mer løsnings orienterte enn hva mange tror...

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

BioBull

14.01.2021 kl 13:20 7592

Yngling ØH skrev OK. Bra det ikke bare var meg som syntes det var rart. Så det betyr egentlig at de dataene de presen..

Bemcentinib mot Kols ?

KOLS er en infeksjons sykdom som det ikke har vært diskutert så mye om her.
Jeg tror det finnes gode muligheter for at Bemcentinib kan fungere bra mot kols.

Har andre vært inne på samme tanken ?

https://www.naaf.no/fokusomrader/kols/

https://nhi.no/rettigheter-og-helsetjeneste/helsetjenesten/pasientorganisasjoner/landsforeningen-for-hjerte-og-lungesyke-lhl/

https://oslo-universitetssykehus.no/behandlinger/kols

https://indremedisineren.no/2015/01/kronisk-obstruktiv-lungesykdom-kols-forekomst-diagnostikk-og-behandling/

https://www.lhl.no/

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

Yngling ØH

13.01.2021 kl 13:21 7940

Lordstock skrev Enig i din kommentar, men tror ikke data for cALX +ve findes i mono Keytruda. Mange spændende Keytru..

OK. Bra det ikke bare var meg som syntes det var rart. Så det betyr egentlig at de dataene de presenterer er mye, mye bedre, fordi personer som er cAxl positive, men som kun får Keytruda, må forventes å ha mye dårligere prognose enn alle andre gruppene?

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

Lordstock

13.01.2021 kl 12:04 7966

Yngling ØH skrev Siste analyse av BerGenBio fra Edison Group https://www.edisongroup.com/publication/progressing-towa..

Enig i din kommentar, men tror ikke data for cALX +ve findes i mono Keytruda. Mange spændende Keytruda data men husk det er for phase III og fandt ikke en der var 100% sammenlignlig. BGBio har ref på slide 36 til Keytruda mono. https://www.keytrudahcp.com/nsclc/second-line-monotherapy/

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

BioBull

13.01.2021 kl 08:39 8162

~~Slettet bruker~~ skrev Jeg er enig. Likte sammenligningen med Tesla aksjen. Du bør bli med på denne togreisen. Selv den min..

Diversifisering? Hva er det for noe?
Jason DeBolt, en 39 år gammel Amazon- og tidligere Google-ansatt, har helt tydelig aldri hørt om begrepet.
Han begynte å kjøpe Tesla-aksjer da den sto i 7,50 dollar tilbake i mars 2013.
Siden den gang har DeBolt aldri sett seg tilbake, og har fortsatt å laste opp med Tesla-aksjer i årenes løp. Det siste året har aksjen eksplodert på den amerikanske børsen og nå eier DeBolt Tesla-aksjer for 12 millioner dollar, eller 102 millioner kroner.
Og hva gjør en Tesla-millionær i en alder av 39 år? Han pensjonerer seg.
I forrige uke la DeBolt ut følgende Twitter-melding:

Jason DeBolt ⚡️
@jasondebolt
Today I’m retiring from the corporate world at age 39.

Not selling any shares for the foreseeable future. $TSLA

De andre i Tesla-leieren heiet på ham, mens andre krympet seg bare av tanken på å være eksponert ene og alene i én aksje.
En forvalter ved Ritholtz Wealth Management innrømmer overfor Marketwatch at historier som DeBolts gjør at han bli litt sjalu.

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

~~Slettet bruker~~

13.01.2021 kl 08:30 8176

StevenG skrev Helt vilt! Ingen som vil selge og alle vil inn! Ett norsk eventyr på trappen

Jeg er enig.
Likte sammenligningen med Tesla aksjen.
Du bør bli med på denne togreisen.
Selv den minste investering kan bli stor.
Sitt long, selg ikke etter 100%, selv om det blir fristende.

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

StevenG

13.01.2021 kl 08:25 8110

Helt vilt! Ingen som vil selge og alle vil inn! Ett norsk eventyr på trappen

Redigert 21.01.2021 kl 08:49 Du må logge inn for å svare

BioBull

13.01.2021 kl 08:13 8052

Yngling ØH skrev Jeg er sikker på at bemcetninib vil motvirke fibrose, og bemcentinib virker mot fibrose som first li..

Bare å følge med på signings ferden til BerGenBio ! Dette blir bare større og større.

Kanskje også større enn Tesla til slutt...

BERGENBIO TO PRESENT UPDATES FROM ONGOING PHASE II BEMCENTINIB COMBINATION STUDY IN REFRACTORY NSCLC AT WCLC 2020

✨Bemcentinib in combination with pembrolizumab was well-tolerated and showed promising clinical activity in refractory lung cancer (https://www.clinicaltrials.gov/ct2/show/NCT03184571?term=NCT03184571&rank=1)

✨Updated interim data will be presented on second line patients following CPI monotherapy

Bergen, Norway, 13th January 2021 – BerGenBio ASA (OSE:BGBIO), a clinical-stage biopharmaceutical company developing novel, selective AXL kinase inhibitors for severe unmet medical need, will present an update from its Phase II study of bemcentinib in combination with anti-PD-1 therapy pembrolizumab (BGBC008) in refractory non-small cell lung cancer (NSCLC) patients at an oral presentation at the 2020 World Conference on Lung Cancer Singapore (WCLC).

BGBC008 is a Phase II single-arm, two stage study with bemcentinib and pembrolizumab for previously treated Stage IV NSCLC patients, comprising three cohorts; chemotherapy failed patients not treated with immunotherapies (post-chemo), patients progressing on prior checkpoint inhibitor therapy (post-CPI monotherapy) and platinum-doublet chemotherapy in combination with immunotherapy (post-chemo-CPI).

The primary endpoint of the study was Overall Response Rate with pre-defined criteria to proceed from the first to second stage in each cohort. Secondary endpoints included Disease Control Rate, Progression Free Survival, Overall Survival and safety.

The interim data shows that bemcentinib in combination with pembrolizumab was well-tolerated and shows promising clinical activity in refractory lung cancer. The presentation will provide updated data from Cohort B of the study, assessing the safety and efficacy of bemcentinib in combination with anti-PD-1 therapy pembrolizumab, in refractory NSCLC patients previously treated with a PD-L1 or PD-1 checkpoint inhibitor (CPI) as a monotherapy.

The full abstract can be found on the WCLC website, and details of the presentation are below.

Title: A phase II study of the oral selective AXL inhibitor bemcentinib with pembrolizumab in refractory patients with advanced NSCLC

Presenting Author: Dr. Matthew G. Krebs PhD.

Session/Abstract ID: Immunotherapy (Phase II/III Trials) / # 3647

Date/Time: Friday 29th January 2021 at 09.50 Singapore Time / 02.50 CET

The presentation will be available on BerGenBio’s website from 29th January 2021

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Ærligtalt

13.01.2021 kl 08:06 8074

Bøggi skrev Har sikkert noen dumme spørsmål så jeg håper å få svar på, for dette har jeg null peiling på. Hvorfo..

Fettere, kusiner, bestikkelser og korrupsjon ispedd vennetjenester...

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Bøggi

13.01.2021 kl 07:55 8149

Har sikkert noen dumme spørsmål så jeg håper å få svar på, for dette har jeg null peiling på. Hvorfor kan det ta 10 - 20 år og kanskje lenger for å lage en medisin som hjelper mot dette, når flere kan lage og få godkjent en vaksine til feks. covid 19 på 10 mnd.?

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

13.01.2021 kl 03:25 8323

Jeg er sikker på at bemcetninib vil motvirke fibrose, og bemcentinib virker mot fibrose som first line treatment. Altså: den medisinen legene vil velge å gi først, og kanskje den eneste medisinen de kommer til å gi mot fibrose.

Om du ikke forstår hvor stort dette kommer til å bli, så vil jeg sammenligne dette med følgende eksempel. Tenk deg at du 29. juni 2010 fikk muligheten til å kjøpe aksjer i Tesla. Om du hadde lest prospektet og satt deg inn i caset, så hadde du kunnet forutsi at Tesla kom til å bli gigantisk, selv om du ikke på det tidspunktet kunne forutse eksakt verdi i dag.
Da kunne du kjøpt aksjer for 17 dollar stykket, og solgt dem i dag for 849 dollar.

Sånn er det med BerGenBio også. Les forskningen, så vil du forstå at det er solid støtte i forskning fra mange ulike hold, som viser at bemcentinib vil virke mot mange typer kreft, og vil bli brukt sammen med mange andre kreftmedisiner. I tillegg vil du forstå at bemcentinib kommer til å virke mot covid. Og bemcentinibs kanskje største fremtidige inntjeningspotensial vil være å behandle fibrosepasienter.
Du kommer ikke til å kunne spå aksjekursen om 10-11 år, men det vil gå opp for deg at dette kommer til å bli sykt stort.
Du vil ikke være den som fikk tilbudet, tok et lite lodd, men fikk ikke med deg potensialet fordi du orket ikke å bruke noen timer på å lese deg opp. Det blir antagelig de best betalte timene du noensinne kommer til å ha i livet ditt.

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

13.01.2021 kl 03:13 8292

DET ER OGSÅ NOEN STUDIER SOM VISER AT BEMCENTINIB MOTVIRKER OG REVERSERER FIBROSE I LEVEREN.
Her er noen få:

"Accordingly; bemcentinib diminished liver inflammation and fibrosis in MCD- and HFD-fed mice."
https://www.researchgate.net/publication/337002385_A_Functional_Role_of_GAS6TAM_in_Nonalcoholic_Steatohepatitis_Progression_Implicates_AXL_as_Therapeutic_Target

"In agreement, sAXL increased in HFD-fed mice before fibrosis establishment, while bemcentinib prevented liver fibrosis/inflammation in early NASH."
https://www.sciencedirect.com/science/article/pii/S2352345X19301468

https://pulmonaryfibrosisnews.com/2018/04/19/bergenbios-therapy-reins-in-pulmonary-fibrosis-tissue-scarring-research-shows/

https://pubmed.ncbi.nlm.nih.gov/25908269/

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

13.01.2021 kl 03:05 8297

After 15 days the ligated bemcentinib-treated kidneys showed less fibrosis compared to the ligated vehicle-treated kidneys in SR analyses and Hyp quantification."
https://researchportal.helsinki.fi/en/publications/axl-targeting-reduces-fibrosis-development-in-experimental-unilat

https://www.researchgate.net/publication/325672474_Targeted_inhibition_of_Axl_receptor_tyrosine_kinase_ameliorates_anti-GBM-induced_lupus-like_nephritis

"ACE2-uttrykk i nyre og testis kan forårsake nyre- og testisskader etter 2019-nCoV-infeksjon"
https://www.medrxiv.org/content/10.1101/2020.02.12.20022418v1

"Furthermore, less F4/80 positive cells, less activity of pathways related to the immune system and lower abundance of MCP1, MCP3, MCP5, and TARC in ligated bemcentinib‐treated kidneys was compatible with reduction in inflammatory infiltrates by bemcentinib treatment. The AXL RTK pathway represents a promising target for pharmacologic therapy of kidney fibrosis.
https://no.linkedin.com/in/tarig-al-hadi-osman-a5a512a3

Denne studien viser at nyretransplantasjon avvisning (rejection) av det nye og fremmede organet, kan reduseres eller hindres med bemcentinib. Om dette også gjelder mennesker, så er det stort håp fremover for personer som har fått, eller kommer til å behøve transplantasjon.
https://insight.jci.org/articles/view/141321

BERGENBIO SATSER STORT PÅ Å BEHANDLE FIBROSE MED BEMCENTINIB OG ANDRE PRODUKTER SELSKAPET UTVKLER.
"Forsøksdyr: The role of AXL signalling targeted therapy for treatment of kidney fibrosis
Godkjenningsperiode 15.10.2018-15.10.2021

Updated summary: Kidney fibrosis is the pathohistological correlate of chronic kidney disease (CKD), which is common, often unavoidable, irreversible and can eventually lead to end-stage renal disease. Effective therapy for kidney fibrosis is still lacking although it is a common consequence in patients suffering from disorders such as diabetes and/or hypertension. Recently the receptor tyrosine kinase AXL has been shown to play an important role in development of fibrotic diseases of the kidney, liver and lung. Several published papers are supporting the role of AXL in development of fibrosis and targeting the AXL signalling pathway show efficient pre-clinical prevention of fibrosis development.
Recently, a role of sAXL as a predictive biomarker for response to AXL directed therapy has emerged. Understanding the turnover of sAXL in the body is warranted before it can be used as a biomarker in clinical trials.

BerGenBio is developing both small molecule inhibitors and antibodies that target AXL and key AXL signalling pathways. The aim of this project is to explore the effect of AXL signalling inhibitors alone and in combination with standard therapeutic agents being used in the clinic against kidney fibrosis.

We hypothesise that treatment with AXL or AXL signalling inhibitors can prevent and/or reverse the development of kidney fibrosis. This project will help to elucidate further the impact of AXL signalling in kidney fibrosis and investigate the potential anti-AXL therapy for treatment of this disease.

We hereby apply for the use of a total number of 390 mice in this project over the course of 4 years.
Replacement, Reduction and Refinement
-Tissues from the Norwegian Kidney biopsy registry as well as tissue from historic animal experiments have revealed a higher expression levels of AXL and AXL regulated markers in the diseased cohort.
-Previously performed in vivo studies with the AXL targeting agents and multiple ongoing clinical trials in cancer involving bemcentinib have shown effective AXL inhibition. An extensive amount of in vitro and in vivo studies have been performed to establish the rational for targeting AXL in fibrotic diseases. Also the dose range and well tolerability/low toxicity of the AXL inhibitors to be investigated in this project has been thoroughly established.
- Kidney fibrosis is a disease that develops as a consequence of multiple systemic diseases such as hypertension and diabetes. It is not possible to generate a kidney fibrosis model in vitro as several compartments of the kidney are affected and the disease interacts with the systemic impact of e.g. hypertension. Therefore, cell culture studies cannot replace the complexity of a mouse model in response to drug treatment.
- A maximum number of animals per experimental group will be limited to 10. Several experimental groups will be included in one experiment to minimize the number of control animals to be used. Personnel performing these experiments are experienced with the proposed models."
https://www.mattilsynet.no/dyr_og_dyrehold/dyrevelferd/forsoksdyr/forsoksdyrsoknader/the_role_of_axl_signalling_targeted_therapy_for_treatment_of_kidney_fibrosis.32542

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

13.01.2021 kl 03:05 8272

BEMCENTINIB MOT NYREFIBROSE

Jeg anbefaler dere sterkt å lese studien jeg har lenket under.

"
Treatment with bemcentinib reduces fibrosis development in obstructed kidneys
Differences in fibrosis development between ligated kidneys from bemcentinib and vehicle‐treated mice were not detectable after 7 days of obstruction, and renal tissues only displayed a low grade of fibrosis in SR staining as measured by Aperio (6.2 ± 2.9% positive pixels in ligated bemcentinib‐treated and 6.9 ± 4.3% in ligated vehicle‐treated kidneys, P = 0.74) (Fig. 4A). After 15 days, the amount of fibrotic tissue as measured by SR staining remained low in the ligated bemcentinib‐treated kidneys (mean 6.3 ± 3.3%), but was significantly increased in the ligated vehicle‐treated group (14.7 ± 6.1% SD, P < 0.001, one‐way ANOVA) (Figs. 2E, F and 4B). Treatment with ACEI did not result in a significant reduction in fibrosis development in the ligated kidneys compared to the ligated vehicle‐treated controls (11.9 ± 4.4% in ligated ACEI‐treated kidneys). However, bemcentinib treatment resulted in less fibrosis development as measured by SR staining in ligated kidneys as compared to ligated ACEI‐treated kidneys (P = 0.026, one‐way ANOVA). Combined treatment with bemcentinib plus ACEI did not show an additive effect on fibrosis development in ligated kidneys compared to bemcentinib treatment alone (7.9 ± 3.2% in ligated bemcentinib plus ACEI‐treated kidneys) (Fig. 4B)."

"Emerging literature support a role for AXL in fibrosis development and an antifibrotic and anti‐inflammatory role of the AXL inhibitor bemcentinib. A study on liver fibrosis showed that AXL and GAS6 are required to induce fibrogenesis by hepatic stellate cells; Accordingly, exposition to bemcentinib reduced liver fibrosis in mice. In addition, less recruitment of antigen presenting cells, particularly macrophages, were detected as measured by F4/80. Less inflammation was also demonstrated by lower expression of chemokines (Barcena et al. 2015). AXL has also been seen to be up‐regulated in idiopathic lung fibrosis and bemcentinib lead to a reduction in fibrosis development in two mouse lung fibrosis models (Espindola et al. 2018). Recently, a study using murine anti–GBM‐induced renal fibrosis models, showed less inflammation with reduced expression of cytokines and chemokines, and an improved renal function upon bemcentinib treatment. Accordingly, a similar effect was found in AXL knock out mice (Zhen et al. 2018)."

"Results
Analysis of the sequencing data showed that kidney ligation led to a significant dysregulation of mitochondria- and oxidative stress-related genes with significant signs of perturbed mitochondrial dynamics, biogenesis and fatty acid oxidation. Interestingly, two weeks of bemcentinib treatment was found to have a reverse effect (RED ANM: REVERSE EFFECT!! WOW!) and produce an increased expression of most of these mitochondria and oxidative stress related genes, which indicates an improvement of mitochondrial function and reduced oxidative stress in this group as compared to vehicle treatment.

Conclusions
Bemcentinib has a beneficial effect on mitochondrial function and oxidative stress in UUO model. Further investigations are needed to decipher the molecular mechanisms involved.
https://physoc.onlinelibrary.wiley.com/doi/full/10.14814/phy2.14091

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Timespa

12.01.2021 kl 15:24 8548

Yngling ØH skrev Nylige videopresentasjoner av BerGenBio: 15. desember: https://dnb-play.screen9.tv/media/E0TATxo3c..

Oppdatert selskapspresentasjon januar 2021: https://www.bergenbio.com/wp-content/uploads/2021/01/BerGenBio_Inv_Jan_2021.pdf

Imponerende pipeline, og vedrørende Covid 19 - sterke skriftlige statements vedrørende forventninger til effekt mot Covid:

- Slide 55 Outlook: "Strong science supporting COVID-19 treatment in 2 randomised phase II trials - Anticipate top line clinical data Q1’21"

- Slide 47: "Bencemtinib control of virus infection LIKELY involves both: reduced viral entry and enhanced interferon responses"

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 14:45 8650

maraud skrev Må si jeg er imponert av det du deler med oss Yngling, takknemlig for alt av granskning og info du d..

Hei,
Det har ikke kommet forskningsrapporter som avklarer problemstillingen sikkert. Jeg har ikke sjekket de databasene grundig siste to dager, men ser heller ikke at noen har rapporter som slike vitenskapelige studier. Pfizer mener vaksinene vil fungere mot B.1.1.7 varianten, men det er andre som har kritisert Pfizer for dette, da de kun hadde testet noen få av de mutasjonene andre mener de burde testet. Kanskje litt uavklart ennå da...
Dette er også "frontline news" som betyr at kvaliteten på nyhetene er lavere. Det kan komme en melding en dag, og kontramelding neste dag.

Jeg tror vi har grunn til å være bekymret for at eksisterende vaksiner ikke er like effektiv mot alle mutasjoner. Det kan derfor komme oppdaterte vaksinevarianter etter hvert.

Det som er mest bekymringsverdig er risikoen for at mutasjonene blir så omfattende-, eller kommer på steder der vaksinene ikke lenger er effektiv og at det ikke er mulig å lage en ny oppdatert vaksine på samme vaksineplatform.
Om den varianten kommer, eller om den allerede er her... det er ikke godt å si ennå. Men risikoen er relativt sett ganske høy for at det kan skje.

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

maraud

12.01.2021 kl 14:05 8775

Må si jeg er imponert av det du deler med oss Yngling, takknemlig for alt av granskning og info du deler. Det gjør det enda mer interessant og ikke minst lettere for meg selv å ta beslutninger, takk :-) . Mener jeg har sett tidligere innlegg fra deg der du nevner at dagens cov 19 vaksine ikke har like stor effekt på mutert cov 19 fra SA/India modeller? Er det noen forskningsrapport på det?

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 03:12 9151

Nylige videopresentasjoner av BerGenBio:

15. desember: https://dnb-play.screen9.tv/media/E0TATxo3cmugURN4iOD2vA/dnb-markets-session-i-bergenbio
3. desember: https://www.bergenbio.com/videos/Panel-discussion-NALS.mp4
30. november: https://soundcloud.com/trouttalks/richard-godfrey-bergenbio-part-of-the-nametag-series-update/s-JCwmaXrymug
9. november: R&D dagen. https://vimeo.com/477021607

For ordentlig innføring i bemcentinib mot covid, se presentasjonen 9. november fra 1:08:00 og utover i presentasjonen.

15. desember 2020 sa CEO Godfrey: "So our clinical trials are now open in the UK, South Africa and India, and I can report that recruitment is STRONG. And that its easy, still eh.. quite high prevalance in these indications. We anticipate being able to report clinical outcomes in the early part of next year".

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 03:03 9134

"Bemcentinib is a selective small molecule inhibitor of Axl kinase, which showed activity to blocks tumor spread and prolongs survival in models of metastatic breast cancer. The receptor tyrosine kinase Axl may play an important role in cancer progression, invasion, metastasis, drug resistance, and patient mortality. R428 inhibits Axl with low nanomolar activity and blocked Axl-dependent events, including Akt phosphorylation, breast cancer cell invasion, and proinflammatory cytokine production. Pharmacologic investigations revealed favorable exposure after oral administration such that R428-treated tumors displayed a dose-dependent reduction in expression of the cytokine granulocyte macrophage colony-stimulating factor and the epithelial-mesenchymal transition transcriptional regulator Snail. In support of an earlier study, R428 inhibited angiogenesis in corneal micropocket and tumor models. R428 administration reduced metastatic burden and extended survival in MDA-MB-231 intracardiac and 4T1 orthotopic (median survival, >80 days compared with 52 days; P < 0.05) mouse models of breast cancer metastasis. Additionally, R428 synergized with cisplatin to enhance suppression of liver micrometastasis. Our results show that Axl signaling regulates breast cancer metastasis at multiple levels in tumor cells and tumor stromal cells and that selective Axl blockade confers therapeutic value in prolonging survival of animals bearing metastatic tumors."
https://www.bocsci.com/bemcentinib-cas-1037624-75-1-item-456603.html

"The Receptor Tyrosine Kinase AXL Is Required at Multiple Steps of the Metastatic Cascade during HER2-Positive Breast Cancer Progression."
https://www.biorxiv.org/content/10.1101/2020.03.15.993147v1.full#ref-75

"R428, a selective small molecule inhibitor of Axl kinase, blocks tumor spread and prolongs survival in models of metastatic breast cancer"
https://pubmed.ncbi.nlm.nih.gov/20145120/

"The study demonstrated a median progression-free survival among cAXL positive patients in Cohort B patients of 4.73 months, compared with 1.87 months among cAXL-negative patients."
https://www.bergenbio.com/bergenbio-presents-phase-ii-bemcentinib-combination-study-in-nsclc-at-annual-sitc-meeting/

https://www.bergenbio.com/worldlung2017/

Det finnes mye mer. Men der er verdt å merke seg at det meste av den publiserte forskningen som viser at hemming av AXL vil hemme en lang rekke krefttyper er uavhengig forskning fra mange ulike grupper og land.

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 03:01 9090

"AXL is a key factor for cell plasticity and promotes metastasis in pancreatic cancer"
https://www.biorxiv.org/content/10.1101/2020.07.06.190363v1.abstract

https://www.nature.com/articles/s41598-019-55702-w
https://cancerres.aacrjournals.org/content/70/4/1544
https://www.google.com/url?sa=t&source=web&rct=j&url=https://helse-bergen.no/seksjon/Fotnoten/Documents/Gry%2520Haaland%2520thesis.pdf&ved=2ahUKEwiNx6ux_I7uAhUEmYsKHfVCCIYQFjAGegQICBAB&usg=AOvVaw2flzyGxwXogN3GgZQxMvSQ
https://mct.aacrjournals.org/content/10/10/1763
https://www.google.com/url?sa=t&source=web&rct=j&url=https://

bora.uib.no/bitstream/1956/21558/4/Accepted%252Bmanuscript_SurOnc.pdf&ved=2ahUKEwiNx6ux_I7uAhUEmYsKHfVCCIYQFjAIegQICRAB&usg=AOvVaw3EVM6Qyh6wySLn2aZKXOj8
https://link.springer.com/referenceworkentry/10.1007%2F978-1-4419-0717-2_114
https://medcraveonline.com/JCPCR/angiogenesis-inhibitors-in-the-treatment-of-breast-cancer-exploring-avenues-of-new-therapeutic-targets.html

Hudkreft
November 2019:
"Cabozantinib (XL184) and R428 (BGB324) Inhibit the Growth of Esophageal Squamous Cell Carcinoma (ESCC)"
"R428 alone significantly inhibited ESCC tumor growth compared to the vehicle; however, no synergistic effect with cisplatin was observed. Notably, the dramatic efficacy of cabozantinib alone was observed in the mouse xenograft model. Collectively, our study demonstrated that both cabozantinib and R428 inhibit ESCC growth in cell and xenograft models."
https://www.frontiersin.org/articles/10.3389/fonc.2019.01138/full

Brystkreft
"AXL as a Target in Breast Cancer Therapy"
"In cancer, AXL has been shown to promote epithelial to mesenchymal transition (EMT), metastasis formation, drug resistance, and a role for AXL in modulation of the tumor microenvironment and immune response has been identified. In light of these activities multiple AXL inhibitors have been developed, and several of these have entered clinical trials in the U.S. In breast cancer, high levels of AXL expression have been observed."
"
14.1.1. BGB324/Bemcentinib/R428
BGB324 is a small molecule AXL inhibitor that has entered clinical trials (Table 1). In preclinical models, BGB324 reduces the invasion of MDA-MB-231 and murine 4T1 cells, both of which are highly migratory and invasive cell lines [98]. In orthotopic models with 4T1 cells and intracardiac injection of MDA-MB-231 cells, BGB324 reduced the amount of metastases observed [98]. BGB324 alone or in combination with nivolumab, an anti-PD-1 antibody, prolonged the survival of mice with mesenchymal glioblastoma tumors [9]. Not just mesenchymal tumors have shown effects with BGB324 treatment. Long-term systemic treatment with BGB324 decreased circulating tumor cells and lung metastases in a mouse model of HER2+ breast cancer but had no effect on primary tumor growth [4].

AXL-targeted therapies currently in clinical trials in the U.S.
Results of phase II trials with BGB324 have recently been reported. 26 patients with AML received BGB324 in combination with cytarabine or decitabine, and 20 were evaluated for response. Four out of nine patients receiving BGB324 plus cytarabine achieved a complete response with an incomplete hematologic recovery, and two others achieved stable disease. Of the 11 patients receiving decitabine plus BGB324, four achieved a complete response with an incomplete hematologic recovery, and one progressed to stable disease [99]. Another clinical trial evaluated BGB324 in combination with an anti-PD1 immunotherapy in patients with advanced NSCLC. Out of 29 patients, seven partial responses were reported, and 40% of patients with AXL-positive biopsies achieved objective responses. The median progression-free survival for patients expressing AXL was 5.9 months, compared to 4.0 months for AXL negative patients [100]. Clinical trials for BGB324 in TNBC and other cancers are ongoing [101]."
https://www.hindawi.com/journals/jo/2020/5291952/

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 03:01 9064

"Leveraging AXL

More recently, there has been growing interest in selectively targeting AXL. The first AXL-specific TKI to enter clinical testing was bemcentinib.2 AXL inhibition has been shown to block the constitutive activation of FLT3 caused by internal tandem duplication, the most common type of FLT3 mutation in AML.22,26 Bemcentinib was explored in AML and myelodysplastic syndrome and demonstrated encouraging activity as monotherapy.27

The results of a phase II, open-label study of bemcentinib (at the recommended phase II dose of 200 mg/day) in combination with low-dose cytarabine (n = 11) or decitabine (n = 15) in patients unfit for chemotherapy (median age, 77 years; range, 50-83 years) were presented at the 2019 American Society of Clinical Oncology Annual Meeting (2019 ASCO). Four of the 9 evaluable patients in the low-dose cytarabine group achieved rapid complete remission with incomplete hematologic recovery, and 2 achieved durable stable disease (SD). In the decitabine group, 4 of the 11 evaluable patients achieved incomplete hematologic recovery, and 1 achieved durable SD.27 Bemcentinib has received fast track designation from the FDA for the treatment of elderly patients with relapsed AML.6

Bemcentinib is also being evaluated in other cancer types, including NSCLC. A recent report showed that it had significant activity in combination with the ICI pembrolizumab (Keytruda) in patients with chemotherapy-refractory, immunotherapynaïve disease. Among 38 evaluable patients at the time of a presentation at the 2019 European Society of Molecular Oncology Congress (2019 ESMO), the overall response rate was 26% and the median overall survival was 12.2 months. A subset of 19 patients with AXL-expressing tumors also had a median overall survival of 12.2 months, and their overall response rate was 38%."

"Undoubtedly, AXL presents a promising therapeutic target, and it has been on the radar for investigators and drug companies for many years. Until recently, however, AXL had only been an inadvertent target of multitargeted kinase inhibitors that were predominantly designed to block other kinases.2,3,14-17

Meanwhile, BerGenBio’s bemcentinib (BGB324), a selective AXL inhibitor, and Aravive’s AVB-S6-500, an Fc-fusion protein that blocks activation of AXL pathway signaling, have received Fast Track designations from the FDA for relapsed acute myeloid leukemia (AML) and platinum-resistant ovarian cancer, respectively, suggesting that first-in-class drug approvals may be on the horizon.6,7 A variety of other novel agents also are in development"
https://www.onclive.com/view/axl-kinase-becomes-a-therapeutic-target-in-its-own-right

"AXL receptor tyrosine kinase as a promising anti-cancer approach: functions, molecular mechanisms and clinical applications" (Review)
"BGB324 (Bemcentinib, R428; Rigel Pharmaceuticals/BerGenBio)
R428, a specific and highly selective AXL inhibitor, acts on AXL at nanomolar concentrations (IC50 = 14 nM) with 100-fold higher affinity for AXL over ABL in cellular assays [46, 154]. R428 blocks the catalytic activities of AXL and reduces AXL and p-AXL expression [46, 58, 155]. When used alone or in combination with cytotoxic agents to treat AML cells, R428 inhibits the AKT and MAPK pathways through the upregulation of Puma and subsequently suppresses BCL-2 [156]. R428 has been shown to recover drug sensitivity in many models of acquired resistance; for example, R428 inhibits erlotinib-resistant head and neck cancer cell growth and migration [114, 116]. In 2014, R428 was the first AXL-specific TKI to enter clinical trials, and this drug is now in phase I/II clinical trials for AML, myelodysplastic syndromes (MDS), triple-negative breast cancer (TNBC), metastatic melanoma, pancreatic cancer, and NSCLC either alone or in combination with other chemotherapy regimens (NCT02424617, NCT02922777, NCT03184558, NCT02488408, NCT03184571, NCT03649321, NCT03824080, and NCT02872259)."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827209/

"Axl inhibitor R428 induces apoptosis of cancer cells by blocking lysosomal acidification and recycling independent of Axl inhibition"
https://pubmed.ncbi.nlm.nih.gov/30210917/

"Axl and Growth Arrest–Specific Gene 6 Are Frequently Overexpressed in Human Gliomas and Predict Poor Prognosis in Patients with Glioblastoma Multiforme"
"At present, targeted therapies inhibiting receptor tyrosine kinases critically involved in oncogenesis and tumor angiogenesis seem to be one of the most promising therapeutic approaches for a variety of neoplastic diseases, including malignant gliomas (42). Therefore, the Axl/Gas6 signaling pathway represents a novel target for glioma treatment directed against tumor cell migration and survival as well as tumor neoangiogenesis. This could become clinically applicable by designing either small molecular inhibitors or gene expression interference approaches ."
https://clincancerres.aacrjournals.org/content/14/1/130?ijkey=15e7143867b41959700cb393221c0cf1fcd2e31d&keytype2=tf_ipsecsha

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 03:00 9061

"LUNG CANCER—NON-SMALL CELL METASTATIC
May 26, 2019
A phase II study of bemcentinib (BGB324), a first-in-class highly selective AXL inhibitor, with pembrolizumab in pts with advanced NSCLC: OS for stage I and preliminary stage II efficacy."
"Conclusions: Overall, bemcentinib in combination with pembrolizumab was well tolerated and promising clinical activity was seen, particularly in pts with AXL positive disease."
https://ascopubs.org/doi/abs/10.1200/JCO.2019.37.15_suppl.9098

10/23/2017
BerGenBio annonserer samarbeid med Prof Straume ved UiB vedrørende utprøving av bemcentinib, dabrafenib, trametinib og pembrolizumab (Keytruda).
https://ascopost.com/News/58176?utm_source=TrendMD&utm_medium=cpc&utm_campaign=Skin_Cancer_TrendMD_0

Se denne videoen om du ikke allerede har sett den. Den vil gjøre det enklere for deg å forstå alt det andre som diskuteres på forumet, og forstå informasjon som senere kommer til å blir publisert av BerGenBio:
BerGenBio Virtual R&D Day https://vimeo.com/477021607

"Axl inhibitor R428 induces apoptosis of cancer cells by blocking lysosomal acidification and recycling independent of Axl inhibition"
"R428 (BGB324) is an anti-cancer drug candidate under clinical investigation. It inhibits the receptor tyrosine kinase Axl and induces apoptosis of many types of cancer cells, but the relationship between the two has not been well established. We investigated the molecular mechanisms of the R428-induced apoptosis and found that R428 induced extensive cytoplasmic vacuolization and caspase activation, independent of its inhibitory effects on Axl. Further analyses revealed that R428 blocked lysosomal acidification and recycling, accumulated autophagosomes and lysosomes, and induced cell apoptosis. Inhibition of autophagy by autophagy inhibitors or autophagic gene-knockout alleviated the R428-induced vacuoles formation and cell apoptosis. Our study uncovered a novel function and mechanism of R428 in addition to its ability to inhibit Axl. These data will help to better direct the application of R428 as an anti-cancer reagent. It also adds new knowledge to understand the regulation of autophagy and apoptosis."
https://www.researchgate.net/publication/327653193_Axl_inhibitor_R428_induces_apoptosis_of_cancer_cells_by_blocking_lysosomal_acidification_and_recycling_independent_of_Axl_inhibition

Desember 2020:
Denne studien er svært interessant, og åpner for nye muligheter relatert til kreftbehandling for bemcentinib.
"Abstract
AXL, a TAM (TYRO3, AXL, and MERTK) family receptor tyrosine kinase, is increasingly being recognized as a key determinant of resistance to targeted therapies, as well as chemotherapy and radiation in non–small cell lung cancer (NSCLC) and other cancers. We further show here that high levels of AXL and epithelial-to-mesenchymal transition were frequently expressed in subsets of both treatment-naïve and treatment-relapsed NSCLC. Previously, we and others have demonstrated a role for AXL in mediating DNA damage response (DDR), as well as resistance to inhibition of WEE1, a replication stress response kinase. Here, we show that BGB324 (bemcentinib), a selective small-molecule AXL inhibitor, caused DNA damage and induced replication stress, indicated by ATR/CHK1 phosphorylation, more significantly in TP53-deficient NSCLC cell lines. Similar effects were also observed in large-cell neuroendocrine carcinoma (LCNEC) cell lines. High AXL protein levels were also associated with resistance to ATR inhibition. Combined inhibition of AXL and ATR significantly decreased cell proliferation of NSCLC and LCNEC cell lines. Mechanistically, combined inhibition of AXL and ATR significantly increased RPA32 hyperphosphorylation and DNA double-strand breaks and induced markers of mitotic catastrophe. Notably, NSCLC cell lines with low levels of SLFN11, a known predictive biomarker for platinum and PARP inhibitor sensitivity, were more sensitive to AXL/ATR cotargeting. These findings demonstrate a novel and unexpected role for AXL in replication stress tolerance, with potential therapeutic implications."
https://mcr.aacrjournals.org/content/early/2020/12/18/1541-7786.MCR-20-0414

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

12.01.2021 kl 02:58 9020

Siste analyse av BerGenBio fra Edison Group
https://www.edisongroup.com/publication/progressing-towards-key-inflection-points/28511

BEMCENTINIB MOT KREFT
(Bemcentinib = R428 = BGB324)
I studier på kreftpasienter er det allerede presentert overbevisende data som viser at bemcentinib virker langsomt men effektivt. BGBIO fant at pasienter som klarte å holde ut noen måneder på bemcentinib hadde svært lav (til null) dødelighet deretter.

Lunger

Dec 2020:
Combining bemcentinib with Keytruda (pembrolizumab) is effective and delays disease progression in people with previously treated advanced non-small cell lung cancer (NSCLC), particularly in those with AXL-positive tumors.
Those updated results from a Phase 2 clinical trial show, to researchers’ surprise, that benefits also were seen in people with low levels of PD-L1 protein in tumor cells. Usually, when cancer cells have a high PD-L1 levels, the patient may benefit more from immune checkpoint inhibitors, such as Keytruda.
“I am impressed by these results that clearly demonstrate the durable clinical benefits in this difficult to treat low PD-L1 patient population,” Hani Gabra, MD, PhD, said in a press release. Gabra is chief medical officer at BerGenBio, developer of bemcentinib.
Results were presented recently in an oral presentation, “A phase II study of bemcentinib (BGB324), a first-in-class selective AXL inhibitor, in combination with pembrolizumab in patients with advanced NSCLC: Updated analysis,” (abstract O26) at the Society for Immunotherapy of Cancer 34th Annual Meeting, held in Maryland.
BerGenBio’s investigational therapy and Keytruda — an immune checkpoint inhibitor marketed by Merck (known as MSD outside the U.S. and Canada) — are designed to boost the body’s anti-tumor response. They target proteins involved in mechanisms used by cancer cells to evade anti-tumor immune responses.
Bemcentinib targets the AXL receptor on cancer cells, which is also involved in tumor’s migration and invasion of other organs. Keytruda targets the PD-1 protein on T-cells (immune cells involved in the fight against cancer), suppressing its interaction with PD-L1 in cancer cells.
Previous studies have suggested that AXL is implicated in resistance to anti-PD-1 therapy, and that bemcentinib may boost the effects of immune checkpoint inhibitors, such as Keytruda.
.… artikkelen fortsetter...
https://immuno-oncologynews.com/2019/12/13/bemcentinib-keytruda-combo-effective-in-some-advanced-nsclc-patients-with-poor-prognosis/

Bemcentinib + Keytruda ved NSCLC (lungekreft)
4-fold improvement in PFS in cAXL +ve vs. cAXL -ve patients.
• 12 mo OS in cAXL positive patients 79% vs 60% in cAXL negative patients
• Clinical benefit reflected in mOS of cAXL +ve patients vs. cAXL -ve
• cAXL -ve patient survival data is comparable to historic controls

For kontekst til siste avsnitt over; se side 36 i presentasjonen jeg har lenket under:
https://www.bergenbio.com/wp-content/uploads/2021/01/BerGenBio_Inv_Jan_2021.pdf

Kommentar: Det ser ut til at BGBIO sammenligner overlevelse i gruppen cAXL positive som fikk bemcentinib med overlevelse i cAXL negative og cAXL negative som fikk bemcentinib. Burde ikke gruppen cAXL positive som fikk bemcentinib blitt sammenlignet med en kontrollgrupper med cAXL postive som kun fikk Keytruda? Har jeg lest dette feil? Noen som har noe å tillegge her?

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 23:23 9217

Londonmannen skrev Det eneste vi kan slå fast er at kursen går godt i dag. Hvorvidt det er artikkelen eller dagens meld..

Jeg tipper mange sitter med fingeren på avtrekkeren og lurer på når det er rett med inngang.
Triggerne står i kø fremover. Overgang til fase 3 studier for AML og NSCLC må garantert medføre oppjustering av kursmål fra meglerhusene. Om de endrer fra15-20% sannsynlighet for suksesd, til 25-30% sannsynlighet, så skal laveste kursmål, eks covid oppjusteres til 73 kroner. Ved samtidig covid suksess kan du plusse på 50-80 kroner. Ved gode fibrose resultat, kan du legge på ytterligere en hundrelapp eller 2. Minst.

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Londonmannen

11.01.2021 kl 14:24 9458

focuss skrev Mikrofly Ser du mener at aksjen skal gå bra i morgen grunnet den artikkelen og jeg er heldig om jeg ..

Det eneste vi kan slå fast er at kursen går godt i dag. Hvorvidt det er artikkelen eller dagens melding kan diskuteres. Men enkelte har jo hevdet at dagens melding ikke innholder Moe ny eller betydningsfull info. Basert på det er det ikke dagens melding som er årsak til den pene oppturen. Men interessen rundt BGBIO er betydelig større i dag enn den har vært på lenge. Hmmm...

Redigert 21.01.2021 kl 08:47 Du må logge inn for å svare

Timespa

11.01.2021 kl 10:44 4626

focuss skrev Meldingen ville jo gitt noe info av verdi om de hadde informert om antall behandlede pasienter så la..

Synes dette var en edruelig og positiv melding - at studiene fortsetter er jo det 3 beste alternativet etter noe ala: (1) "medisinen virker og rulles ut umiddelbart" (2) "Studiene har vist positiv effekt."

At studier øker i omfang og fortsettes over tid, er utelukkende positivt. At studiene gjennomføres i SA og India gjør også at rekrutteringen vil være sikret fremover. Det ble vel signalisert 3 måneder for første del av studien, deretter 3 nye måneder med neste del. Dette tar tid, men sålangt går det rett vei - hvis ikke hadde meldingen vært: "Studiene avsluttes"

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Nanoq

11.01.2021 kl 10:19 4731

Yngling ØH skrev Har du link til FA artikkel? Finner den ikke

https://finansavisen.no/nyheter/helse/2021/01/11/7606245/ekspertkomite-anbefaler-fortsettelse-av-bergenbio-studie

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Talent

11.01.2021 kl 10:15 4756

Yngling ØH skrev Har du link til FA artikkel? Finner den ikke

Får ikke delt link nå men den søk opp Bergenbio i søkefeltet.

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 10:11 4792

Amerikanerne lurer også på om de enorme covid tallene de har kan skyldes en eller flere andre covid varianter

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 10:06 4810

Siste ord er ikke sagt når det gjelder vaksinenes effektivitet mot nye mutasjoner av sars-cov-2.
https://www.thailandmedical.news/news/vaccine-news-pfizer-s-study-on-vaccine-effectiveness-against-new-variants-and-claims-are-misleading,-numerous--professional-experts-aghast-

Enda en ny, farlig variant begynner å få fotfeste:
https://www.thailandmedical.news/news/covid-19-mutations-university-of-hawaii-scientists-warns-p681h-mutation-emerging-on-sequencings-of-many-globally-prevalent-sars-cov-2-strains

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 09:57 4854

Talent skrev Kan ikke se noen Artikkel på E24 i dag men FA har en artikkel. Er ikke det litt spesielt?

Har du link til FA artikkel? Finner den ikke

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Talent

11.01.2021 kl 09:34 4957

Yngling ØH skrev Det er ikke noen meglerhus som har endret kursmålet siste 4-5 måneder, selv om både AML og NSCLC stu..

Kan ikke se noen Artikkel på E24 i dag men FA har en artikkel. Er ikke det litt spesielt?

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 09:29 4974

Det er ikke noen meglerhus som har endret kursmålet siste 4-5 måneder, selv om både AML og NSCLC studiene har innfridd.
Det har også blitt publisert forskning som ytterligere styrker caset, pluss att det er et solid rasjonale i dag for å behandle fibrose med bemcentinib.
Det tvinger seg frem snart at meglerhusene må oppgradere kursmålene sine.

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Yngling ØH

11.01.2021 kl 09:21 5001

Single Malt skrev Slår dette til er vel kanskje aksjen doblingskandidat

De fleste meglerhus mener aksjen allerede i dag omsettes under halvparten av nåverdi. Med positive resultat i covidstudiene, så bør bare covid-delen prises til 40-50 kroner eller mer. Da regner jeg ikke inn potensialet i kreft og fibrose.
Billigere aksje enn denne finner du ikke

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Single Malt

11.01.2021 kl 09:04 5074

klaesp skrev Selvfølgelig har de tilgang til progresjon og midlertidige resultater fra sin egen betalte studie. ..

Slår dette til er vel kanskje aksjen doblingskandidat

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

~~Slettet bruker~~

11.01.2021 kl 08:52 5031

focuss skrev BGBio har neppe tilgang til om de har gode resultater. Hadde de hatt det måtte de børsmeldt det.

Dette kan du umulig mene seriøst.

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

StevenG

11.01.2021 kl 08:32 5113

Dette kommer til å bli en spennende reise 😎👌

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

klaesp

11.01.2021 kl 08:27 5123

focuss skrev BGBio har neppe tilgang til om de har gode resultater. Hadde de hatt det måtte de børsmeldt det.

Selvfølgelig har de tilgang til progresjon og midlertidige resultater fra sin egen betalte studie.

https://finansavisen.no/nyheter/helse/2021/01/11/7606245/ekspertkomite-anbefaler-fortsettelse-av-bergenbio-studie

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

focuss

11.01.2021 kl 08:06 5252

klaesp skrev Det vil selvsagt komme flere oppdateringer(husk det er enorm med data som skal kartlegges)) , med s..

BGBio har neppe tilgang til om de har gode resultater. Hadde de hatt det måtte de børsmeldt det.

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

klaesp

11.01.2021 kl 07:54 5233

Hayen skrev Tja.....dette er selskapets eget studie. De har nok uansett tenkt å gjennomføre det. Ordlyden i mel..

Det vil selvsagt komme flere oppdateringer(husk det er enorm med data som skal kartlegges)) , med stor sannsynlighet er resultater meget gode. Hvem vil kaste penger til en studie uten gode underliggende resultater:)

Redigert 21.01.2021 kl 08:08 Du må logge inn for å svare

Du må logge inn for å svare Til toppen

Du må logge inn for å søke i innlegg

Alle fora

Debattforum

Debatt

Teknisk analyse

Kryptovaluta

Krypto

Makrokalender

Makro

Farma

Opprett ny tråd

BGBIO: FORSKNING OG MEDISINER RELATERT TIL BerGenBio

Logg inn

Del innlegg

Glemt passord

Debattforum

Debatt

Teknisk analyse

Kryptovaluta

Krypto

Makrokalender

Makro

Spør om tilgang

Farma

Opprett ny tråd

BGBIO: FORSKNING OG MEDISINER RELATERT TIL BerGenBio