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  • ||||||||||  Promacta (eltrombopag) / Novartis
    ELTROMBOPAG INHIBITS THE PROLIFERATION OF CD8 T CELLS THROUGH AN IRON CHELATION MANNER () -  May 15, 2024 - Abstract #EHA2024EHA_2950;    
    Weproposed that eltrombopag may have a dual mechanism of action: inhibiting the proliferation of CD8+ TEMRAcells and inducing G1 cell cycle arrest. This iron chelation-dependent effect suggests a novelimmunomodulatory role for eltrombopag.
  • ||||||||||  Nplate (romiplostim) / Amgen, Kyowa Kirin, Promacta (eltrombopag) / Novartis, Rituxan (rituximab) / Roche
    THE PLATELET VARIABILITY INDEX (PVI) SCORE AS A MEASURE OF THE EFFECT OF TREATMENTS FOR IMMUNE THROMBOCYTOPENIA (ITP) () -  May 15, 2024 - Abstract #EHA2024EHA_2943;    
    Splenectomy was associated with the greatest reduction in PVI scores, and TPO receptor agonists wereassociated with the smallest reduction in PVI scores. Along with an increase in platelet count levels, a reductionin PVI scores may be an indicator of the quality of the response to ITP treatments.
  • ||||||||||  Tavalisse (fostamatinib) / Rigel
    ITALIAN REAL-WORLD EXPERIENCE WITH FOSTAMATINIB IN ADULT PATIENTS WITH CHRONIC IMMUNE THROMBOCYTOPENIA (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_2907;    
    Fosta was used in most cases as fourth or further line of therapy, after failure of TPO-RAs. Our findings indicate that a significant proportion of patients (nearly 40% of the overall population)benefit from fosta after 6 months, suggesting that this treatment may be considered as a manageable andeffective therapeutic option in the real-world practice.
  • ||||||||||  EFFECT OF NOVEL AGENTS ON THE MECHANISM OF FIBROCYTE-MEDIATED INDUCTION OF MYELOFIBROSIS (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_2712;    
    In vitro experiments demonstrated that the novel agents examined in this studyeffectively inhibited monocyte differentiation into fibrocytes and reduced certain profibrotic cytokinelevels in the culture supernatant. Further investigation into these mechanisms is anticipated to provideinsights into the antifibrotic mechanisms underlying the action of these novel agents.
  • ||||||||||  Prolia (denosumab) / Amgen
    CHARACTERIZATION OF BONE MARROW NICHE AND IMMUNOPHENOTYPING IN A MULTIPLE MYELOMA MOUSE MODEL DRIVEN BY COMBINED EXPRESSION OF ACTIVE RANK AND TCL1 (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_2375;    
    It offers a detailed understanding of the bone marrow niche dynamics,immunosurveillance mechanisms, and genomic alterations, establishing a significant advancement in MMresearch. Our findings not only closely mirror human myeloma, but also unveil potential novel targets fortherapeutic intervention, such as the microenvironment-modulating protein CD39, and allow furtherexploration of the autophagy-linked protein p62, shedding light on its role in drug resistance to proteasomalinhibition.
  • ||||||||||  Undisclosed CDK4/6 inhibitor / CS Group, narazaciclib (HX301) / Traws Pharma
    THE MULTIKINASE CDK4/6 INHIBITOR NARAZACICLIB OVERCOMES BTK-I RESISTANCE IN MANTLE CELL LYMPHOMA BY TARGETING USP24-P53 SIGNALING AXIS (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_2120;    
    Our findings demonstrate that narazaciclib is safe and effective as a single agent in preclinical models of MCL,including BTKi-resistant cases. Its combination with ibrutinib achieved a synergistic tumoricidal effect in vitroand in vivo, accelerating cell cycle blockade and, specifically in the BTK-resistant cases, promoting thephosphorylation of USP24, followed by the activation of P53 and the modulation of DNA repair pathway.
  • ||||||||||  Ibrance (palbociclib) / Pfizer, Verzenio (abemaciclib) / Eli Lilly
    INHIBITION OF CDK4/6 AUGMENTS ATRA-INDUCED DIFFERENTIATION ACROSS ACUTE MYELOID LEUKAEMIA SUBTYPES () -  May 15, 2024 - Abstract #EHA2024EHA_1065;    
    Additionally, we observed that ATRA-induced differentiation isenhanced when in combination with CDK4/6 inhibitors across a wide range of AML subtypes. Although theseresults should be validated in additional AML models, they show that a primary mechanism of action ofCDK4/6 inhibitors is cell cycle arrest accompanied by the induction of differentiation, and that, in combinationwith ATRA, this effect can be augmented.
  • ||||||||||  Ibrance (palbociclib) / Pfizer
    DUAL TARGETING OF FLT3-ITD AND CLK BY SCREENED DONATED CHEMICAL PROBES IN ACUTE MYELOID LEUKEMIA (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_1039;    
    The unexpected discovery of potent FLT3 signalinginhibition specifically in FLT3-ITD mutated AML cases introduces a dual-targeting approach that couldsignificantly improve AML treatment. This finding not only highlights the utility of DCPs in therapeutic discoverybut also paves the way for innovative, more effective AML treatment protocols.
  • ||||||||||  Blincyto (blinatumomab) / Astellas, Amgen, Nailike (olverembatinib) / Ascentage Pharma, Takeda
    COMBINATION OF THIRD GENERATION TKI OLVEREMBATINIB AND CHEMOTHERAPY OR BLINATUMOMAB FOR NEW DIAGNOSED ADULT PH+ ALL PATIENTS (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_873;    
    Among the 31 patients enrolled, a notable rate of 1-years survival and CMR was observed, whichholds promise for improved long-term survival. Both the TKI+chemotherapy and TKI+BITE groups showedgood clinical outcomes, although the TKI+BITE group had the potency of better survival thanTKI+chemotherapy group.
  • ||||||||||  Blincyto (blinatumomab) / Astellas, Amgen, Besponsa (inotuzumab ozogamicin) / Pfizer, UCB
    TARGETED- AND IMMUNO-BASED THERAPIES FOR ADULTS WITH TP53-MUTATED ACUTE LYMPHOBLASTIC LEUKEMIA (Poster Area (Hall 7)) -  May 15, 2024 - Abstract #EHA2024EHA_871;    
    Our results show that novel therapies are effective in ALL withTP53 mutations, leading to high remission rates and MRD- responses. Previous exposure to novel therapies didnot seem to impact response to subsequent novel therapies.