Ja, det er jo det store spørsmålet
Abstrakt release denne uke
MAY 22, 2025, at 5PM ET
Majority of abstracts are released on asco.org/abstracts at 5:00 PM ET (Late-breaking Abstracts will be released at 7:00 AM CT on their day of presentation at the meeting)
MAY 30 - JUNE 3
Da har Arrowstreet kjøpt inn litt, men de hadde bare 0,51 % short så ikke nødvendigvis mange aksjene de har dekket inn.
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0.01% av aksjene tilsvarer under 33 000 aksjer, så det er ikke veldig mye som skal til for å flytte seg under terskelen.
De var short 1 689 661 aksjer på 0.51%, og 19. mai var totalvolumet under 600 000. Sett i forhold til volumet så kan de nok ha fått kjøpt opp mot 100 k aksjer som da vil gjøre det mulig å komme ned rett under 0.5%.
Når vi først er inne på denne type tall så er det interessant at da Connor økte shorten med 328 k (fra 0.60 til 0.70) var totalvolumet 785 k. Det var en uvanlig stor andel av totalvolumet. Dette store shortsalgspresset fra Connor passer med det relativt store kursfallet på over 4% denne dagen.
Det nye støttenivået på 2.6 ble respektert, og så har det fortsatt å sige sakte men sikkert oppover igjen.
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Kan vi få asco forventningsrally I morgen?
Kl 23 i kveld kommer abstractene. Ser ikke ut som noen har dette på sin radar, hverken her, XI eller andre forum. Mener dette er meldepliktig, men ikke før abstractene er ute. Inntil da kan de bare melde tittel og det var ikke verdt en børsmelding. Men når data er ute i abstract skal det meldes.
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Mistenker en big fat nothing burger, men vi får se 
Skal ikke se bort i fra at short har økt i dag, så enten vet de mer enn oss andre eller så tar de risken.
Induction of neoantigen-specific immune responses by VB10.NEO in combination with atezolizumab in heavily pretreated patients with advanced solid tumors: Final analysis of the phase 1b VB N-02 trial.
Background: VB10.NEO, a personalized DNA-based neoantigen vaccine, was evaluated with atezolizumab in a Phase 1b trial to assess safety, clinical activity, and immune responses in heavily pretreated patients with advanced solid tumors. The NeoSELECT platform enriches for clonal neoantigens by analyzing RNA and circulating tumor DNA, incorporating frameshift antigens and single nucleotide variants.
Methods: This open-label, dose-escalation trial investigated VB10.NEO across three dose levels (3, 6 and 9 mg) combined with atezolizumab (1200 mg Q3W). Eligible patients had advanced or metastatic solid tumors, sufficient tumor material for vaccine manufacturing, at least 10 identified tumor neoantigens, and measurable disease. Immune responses were assessed using ELISpot assays (in vitro stimulation and ex vivo), T cell receptor sequencing, and flow cytometry. Endpoints included safety, immune response, and antitumor activity per RECIST v1.1.
Results: At study completion (October 2024), 26 patients (median age 61 years, range 28–72; 62% female) received at least one dose of VB10.NEO. Median prior therapy lines for advanced disease were three (range 1–6), and 54% had prior immunotherapy, including checkpoint inhibitors. Tumor types included head and neck squamous cell carcinoma (15%), triple-negative breast cancer (15%), and others (31%; most were tumors with low tumor mutational burden). The majority (69%) of evaluable patients had low or negative PD-L1 expression. Injection site reactions (15%) and fatigue (12%), mainly Grades 1–2, were the most common adverse events. A dose-limiting Grade 3 transient blood pressure increase occurred in the 9 mg cohort. No treatment-related serious events or deaths occurred. Across all dose levels, VB10.NEO induced robust and durable neoantigen-specific immune responses. In vitro stimulated ELISpot assays detected vaccine-induced T cell responses in 85% (11/13) of evaluable patients and in 58% of evaluated neoantigens, while ex vivo ELISpot demonstrated responses in 22% (4/18) of patients and 5% of evaluated neoantigens. T cell receptor sequencing showed persistent T cell clone expansion in 9/11 patients, indicating durable immune responses. Putative neoantigen-specific clones were detected in 6/7 analyzed patients, with persistent expansion in 4. All patients achieving stable disease (34.8%, 8/23) exhibited neoantigen-specific immune responses.
Conclusions: VB10.NEO combined with atezolizumab demonstrated a favorable safety profile while eliciting robust, durable immune responses across all dose levels, even in heavily pretreated patients with advanced solid tumors. The potential correlation between immunogenicity and clinical benefit supports further exploration in earlier treatment settings.
Her er rosinen i pølsa “All patients achieving stable disease (34.8%, 8/23) exhibited neoantigen-specific immune responses”, men når 85% av samtlige uansett gjorde det, så blir ikke dette MYE mer enn nok et bevis på at VB10.NEO induserer en immunrespons (og ikke nødvendigvis meningsfull klinisk nytte)
Edit: 46% sannsynlig er det at disse fire SD-pasientene testet positivt for immunrespons når 11/13 uansett gjorde det
Integrative analysis of VB10.16 and atezolizumab in advanced HPV16-positive cervical cancer: Linking biomarker insights to clinical outcomes.
Background: Therapeutic cancer vaccines combined with immune checkpoint inhibitors offer a promising strategy to enhance anti-tumor responses. We recently demonstrated the safety and clinical efficacy of VB10.16, a DNA-based therapeutic cancer vaccine encoding HPV16 E6/E7 oncoproteins fused to CCL3L1 for antigen-presenting cell targeting, in HPV16-positive persistent, recurrent or metastatic cervical cancer1. This analysis explores the association between HPV16-specific T cell responses, tumor microenvironment (TME) characteristics, and clinical outcomes in the phase 2a trial. Methods: In this multicenter, open-label trial, 52 patients with advanced HPV16-positive cervical cancer received VB10.16 (3 mg intramuscularly) combined with atezolizumab (1200 mg intravenously) for up to 48 weeks. Primary endpoints were safety and objective response rate per RECIST v1.1. Secondary endpoints included overall survival (OS) and HPV16-specific T cell responses via IFN-γ ELISpot (n=36). Predefined exploratory endpoints included systemic immunosuppression and TME inflammatory status in baseline tumors, assessed via myeloid cell counts (baseline to ~week 9, n=47), flow cytometry (T cell/myeloid-derived suppressor cells [MDSC] ratio, n=21), and gene expression analyses (n=29). Results: Patients with reduced on-treatment systemic immunosuppression demonstrated stronger HPV16-specific T cell responses than patients without (myeloid cell counts decreased in 17/47 patients; T cell/MDSC ratio increased in 12/21 patients). On-treatment reduction in systemic immunosuppression was associated with a higher clinical benefit rate (complete response [CR]/partial response [PR]/stable disease [SD] in 17/28 vs 4/19 patients by myeloid counts and 10/12 vs 2/9 by T cell/MDSC ratio), suggesting associations between T cell response, systemic immunosuppression and effect of immunotherapies. Among the 9 responders in the efficacy population (n=47; 3 CR; 6.4% and 6 PR; 12.8%), 5 patients had available gene expression data from baseline tumors. Patients with pro-inflammatory/proliferative TME signatures demonstrated higher CR/PR rates (4/14 vs. 1/15) and longer OS compared to patients with stromal/immunosuppressive signaling (mOS not reached vs 8.3 months). Clinical benefit was also observed in stromal/immunosuppressive TMEs (1/15 CR, 6/15 SD), highlighting VB10.16’s potential to overcome local immunosuppression. Conclusions: VB10.16 combined with atezolizumab induces durable responses, mitigates local and systemic immunosuppression, and demonstrates synergy between biomarkers and clinical outcomes. High CR/PR rates with favorable immune and TME characteristics highlight the promise of this combination therapy, warranting further exploration. 1Hillemanns P et al , 2025 doi:10.1136/jitc-2024-010827.
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Hur ska vi tolka de? Bra dåligt?
Det er et visst signal om at VB10.NEO funker, og det er et ganske sterkt signal om at VB10.16 gjør “kalde” tumorer “varme” (og dermed funker). Er min tolkning
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Anybodies guess, vanskelig å trekke noen konklusjoner.
Kanondata på VB10-16. Vil støtte en pivotal studie sånn jeg ser det. NEO-data var sa ikke så veldig mye, men dette var en særdeles syk populasjon som har prøvd opptil 6 tidligere linjer behandling. De oppnådde stabilisering hos en god del pasienter.
Det vil jo du tydeligvis fortsette å skrive helt til man har de randomiserte dataene da 
Hæ?! Har de penger til å generere randomiserte data? 
Ja!
.
Er dette data fra C-04 studien som ble stoppet pga. endring av SOC og problemer med rekruttering??
Da får vi vente på fasiten da ja. Blir spennende å se hva de får til av randomiserte data på kreft, data på toleranse og la oss ikke glemme autoimmunitet.
Hvor mye cash har de igjen egentlig? Trodde de hadde 300mill igjen etter utbytte og ca 100 ansatte igjen.