Collection: Collection of Blood Research On April 23, 2020

THE BIVV001 is used for haemophilia ahttps://doi.org/10.1182/blood.2019001292https://doi.org/10.1182/blood.2019001292FVIII substitutes to provide comprehensive protection for haemophilia A patientsThe goal of treatment for severe haemophilia type A is expanding beyond reducing the annualized haemorrhage rate, but also includes long-term prognosis associated with persistent high Levels of FVIIIalthough endogenous VWF can stabilize FVIII from degradation and removal, it can only keep the half-life of FVIII at a maximum of 15-19 hoursFurther increase in the half-life of recombinant FVIII (rFVIII) depends on endogenous VWF and rFVIII decouplingresearchers have developed a new alternative to FVIII, rFVIIIFC-VWF-XTEN (BIVV001), which, under physiological conditions, can be decoupled with endogenous VWF and has enhanced pharmacokinetic properties compared to all previous FVIII productsBIVV001 is a unique fusion protein consisting of the fusion of the VWF-D D3 domain through the immune globulin rFVIII G1 Fc domain and two XTEN peptides and rFVIII fusionAfter THE ADMINISTRATION OF BIVV001, the plasma FVIII half-life of mice and monkeys was 25-31 hours and 33-34 hours, respectively, suggesting that the half-life of FVIII was extended by 3-4 timesflT3 suppression causes HDAC8 to raise the p53 inactivatedhttps://doi.org/10.1182/blood.2019003538FMS-like receptor tyrosine kinase-3 (FLT3) internal series repeat (ITD) mutations are found in up to 25 to 30% of patients with acute myeloid leukemia (AML), associated with poor prognosisAlthough FLT3 tyrosine kinase inhibitors (TKIs) have shown clinical effects, these inhibitors do not eliminate primitive FLT3-ITD-AML cells, which are potential sources of recurrenceTherefore, it is essential to clarify the mechanisms for the maintenance and resistance of FLT3-ITD-AML and to develop new and effective treatment strategies in this study, the researchers found that in FLT3-itd-AML cells, FLT3 inhibition induced histone deacetylase 8 (HDAC8) upward through the anti-activation action mediated by FOXO1 and FOXO3 HDAC8 uplift edified p53 deacetylinization inactivation, leading to TKI treatment after leukemia maintenance and drug resistance Genetic or drug inhibition HDAC8 can reactivate p53, abolish leukemia maintenance, and significantly enhance TKI-mediated FLT3-ITD-AML cell elimination Importantly, flT3 TKI (AC220) was used in conjunction with HDAC8 inhibitors (22d) in the hetero-transplant model of FLT3-ITD-AML patient serorance, significantly inhibiting leukemia progression and effectively reducing the original FLT3-ITD-AML cells : Brincidofovir is used for the of human herpes virus infection type 6B after allogeneic HCT
https://doi.org/10.1182/blood.2019004315 human herpes virus type 6B (HHV-6B) is often reactivated after allogeneic hematopoietic cell transplantation (HCT) In vitro, brincidofovir has high activity against HHV-6B and other DNA viruses, but in vivo activity of HHV-6B has not been confirmed researchers conducted an after-the-fact analysis of a randomized controlled trial to effect on HHV-6B reactivation In the study, subjects were given the allogeneic HCT twice a week orally to prevent cytomegalovirus infection A total of 153 patients were included, 92 were given brincidofovir and 61 were given placebos The cumulative incidence of HHV-6B plasma detection in patients receiving propadownia was significantly lower than in the placebo group (14.2% vs 32.4%) 42 days after HCT In the corrected Cox model, brincidofovir exposure was still associated with a low risk (risk ratio 0.40) in HHV-6B plasma detection prognostic markers of non-recurrent death after transplantation of allogeneic hematopoietic stem cells in https://doi.org/10.1182/blood.2019002334 there is still a lack of assessment of prognostic biomarkers for non-recurrent death (NRM) after the pediatric age age variant hematopoietic stem cell transplant (HCT) To meet this need, the researchers conducted a prospective cohort study (NCT02194439) evaluated 4 plasma biomarkers (stimulation factor-2 (ST2), interlestin-6, regenerative islet driver 3 alpha (REG3) and tumor necrosis factor receptor 1 (TNFR1) on the 7th, 14th and 21st days of HCT, respectively Post-HCT biomarker analysis showed that ST2 (?26 ng/mL), TNFR1 (-3441 pg/mL) and REG3 alpha (?25 ng/mL) were all associated with NRM in children up to 10 years of age and children/adults over 10 years of age When pre-HCT biomarkers are included in the analysis, only ST2 remains significant in both queues After adjustment, ST2 is associated with NRM only in recipients of 10 years of age In the first 3 weeks after HCT, THE ST2, TNFR1, and REG3 alpha trials were predictive for NRM in children and adult patients ST2 before HCT is a prognostic biomarker for NRM in children with 10 years of age, which promotes further stratification Source: MedSci Original