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Als we zo 7maanden moeten doen ,aiai , spoedig mogelijk met iets afkomen , maar dat betwijfel ik,
Geen zorgen, zeer grote kooporders in de bied tussen 9,6 en 9,8 (totaal van 15K aandelen) Terwijl tot 10,46€ er maar 10K aan aandelen te koop staan ( zeer grote gap na 10,1 -> 10,4)
Ik wil graag instappen in dit aandeel. Vinden jullie dit een goed moment? Of verwachten jullie dat de koers vandaag nog (veel) zal dalen? Ik hoor het graag..
Ik had überhaupt niet verwacht te dalen na de ASH.
trarb schreef op 11 december 2019 11:44 :
Ik wil graag instappen in dit aandeel. Vinden jullie dit een goed moment? Of verwachten jullie dat de koers vandaag nog (veel) zal dalen? Ik hoor het graag..
Mag je zelf beslissen dan ben je beter uit.
trarb schreef op 11 december 2019 11:44 :
Ik wil graag instappen in dit aandeel. Vinden jullie dit een goed moment? Of verwachten jullie dat de koers vandaag nog (veel) zal dalen? Ik hoor het graag..
De daling is nog niet ten einde... volgens mij goed voor vrijdag... maar met Trompet weet men nooit...
@Trarb, het aandeel heeft een grote steun op 9,6-9,7 en op 9,4 , dus ik verwacht een stijging, maar mogelijks zal die stijging zich pas morgen doorzetten, eerst wat paniekzaaiers hun aandelen laten verkopen... De mooie ruimte boven 10€ spreekt boekdelen, vanaf we door de 10€ zijn is de weg weer helemaal open
Als wij dat verwacht hadden Henkie080101 dan waren we wel eerder even uitgestapt om nu weer in te stappen dacht je ook niet?
Dus met andere woorden gaan we 6maanden geen nieuws ontvangen?
Twin schreef op 11 december 2019 12:22 :
Dus met andere woorden gaan we 6maanden geen nieuws ontvangen?
dat zou funest zijn voor de koers
Twin dat is niet te zeggen. Er zou ook een tussentijds update kunnen verschijnen.
Er zitten welgteld 0 verkooporders tussen 10,16 rn 10,4€... Ready to step in guys ;) or we will fly away
Tuurlijk komt er wel nieuws tussendoor. Sowieso komt er nog een kwartaalupdate aan. Verder denk ik dat er nog wel conferenties komen.
Duidelijk grote gap tussen 10,28 en 10,4 :) Let's shuffle it up boys :) -> ZIe bijlage
Moet die wel haast maken.
Leveraging Natural Killer Cells as CAR-T Therapies December 6, 2019 Celyad is developing CAR-T therapies that have the potential to treat both hematological and solid tumors. Differentiated CAR-T Receptor Cancer cells have evolved the capability to elude many antibodies and small molecule drugs. Chimeric antigen receptor (CAR)-T cell therapies take a different approach by leveraging the immune system and its innate biochemical pathways. Successes to date with CD19 targets in lymphoma and leukemia demonstrate the potential for this modality. Celyad is developing CAR-T cell therapies based on research conducted by Charles Sentman and his team at Dartmouth College focused on natural killer (NK) cells. NK cells constitute the first line of defense against external aggression and cancer, holding the line until T cells and other immune cells arrive. Sentman inserted genes into T cells encoding NK-activating receptors (NKG2D) that, rather than bind to a specific antigen, bind to eight different stress ligands found on both hematological and solid tumors. These ligands are naturally expressed by cancer cells in approximately 80% of hematological and solid malignancies. The NKG2D-based T cells also express a co-stimulatory molecule that increases their potency. Manufacturing Advantage We have developed proprietary manufacturing processes that have undergone two amendments (LY to mAb to OptimAb). OptimAb employs a shortened 8-day cell culture and incorporates a selective PI3K inhibitor. The OptimAb process generates a product that is enriched for T cells with a memory-like phenotype while maintaining the high level of manufacturing reliability required to support clinical development. The rapid acceptance of our process amendments by U.S. and European regulatory authorities reflects the expertise Celyad has built around NKG2D CAR-T cell manufacturing. Personalized Therapies CYAD-01 and CYAD-02 Celyad’s lead candidate CYAD-01, a CAR-T cell therapy incorporating the NKG2D receptor, has been shown in preclinical studies to bind to ligands expressed by blood vessels that feed tumors and inhibitory cells that help tumors evade the immune system. CYAD-01 targets and kills the tumor while impacting the micro-environment and potentially inducing an adaptive immune response owing to the creation of long-term cell memory against targeted tumors. CYAD-02 is a next-generation NKG2D-based CAR-T candidate that incorporates short hairpin RNA (shRNA) technology to target the NKG2D ligands MICA and MICB, silencing their gene expression via RNA interference (RNAi) on the CAR-T candidate. With our technology, the single shRNA modulates the expression of both ligands, which translates to increases in in vitro proliferation, in vivo engraftment and antitumor activity in early testing. SMARTvector shRNA technology from Horizon Discovery is deployed to design target shRNA sequences with high specificity, ensuring optimal gene silencing. CYAD-02 also incorporates our OptimAb process to enrich for T cells with memory-like phenotype. Early clinical studies are underway with CYAD-01 in relapsed/refractory acute myeloid leukemia (AML), myelodysplastic syndrome (MDS) and metastatic colorectal cancer (mCRC), and all have provided promising initial results. The focus is now on increasing the potency to potentially deepen the breadth, frequency and duration of clinical responses for next-generation candidates. A phase I dose-escalation trial evaluating the safety and clinical activity of CYAD-02 with the preconditioning chemotherapy cyclophosphamide and fludarabine (CyFlu) for the treatment of relapsed/refractory AML and MDS is scheduled to begin in early 2020. Off-the-Shelf Treatment for Colorectal Cancer In addition to autologous therapies, Celyad is committed to developing effective off-the-shelf NKG2D CAR-T cell therapies for the treatment of solid tumors. Multiple allogeneic technologies are under investigation, including the novel inhibitory peptide TIM (T cell receptor (TCR) inhibitory molecule) and our shRNA platform, which targets the CD3zeta component of the TCR. Both technologies leverage non-gene-edited approaches. Our current lead allogeneic candidate CYAD-101 is a non-gene-edited, healthy donor–derived CAR-T therapy that co-expresses the NKG2D CAR of CYAD-01 and TIM. The expression of TIM reduces signaling of the TCR complex, which is responsible for graft versus host disease (GvHD), a response triggered by the recognition of non-self human leukocyte antigen molecules expressed on recipient cells by the TCRs of donor cells and a key concern with allogeneic cell therapies. Potential for Large Product Pipeline Celyad has established a suite of patents and is strategically positioned for further candidate development. Our approach, based on a differentiated receptor and unique platforms for creating allogeneic treatments for both hematologic and solid tumors, has resonated with investors enabling us to establish Celyad as a leading CAR-T company.www.pharmasalmanac.com/articles/lever...
oud nieuws speedbul…nik interessant zie koers
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