rHuman FLt3 Active
- Known as:
- rHuman FLt3 Active
- Catalog number:
- rf00394041-10
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Agrenvec
- Gene target:
- rHuman FLt3 Active
Related genes to: rHuman FLt3 Active
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: rHuman FLt3 Active
Related articles to: rHuman FLt3 Active
- The combination of azacitidine and venetoclax (Aza/Ven) is an effective treatment for acute myeloid leukemia (AML); however, biological factors underlying heterogeneous treatment responses across diverse genetic backgrounds remain incompletely defined. We analyzed 97 AML patients treated with Aza/Ven in the prospective HM-SCREEN-Japan 02 study using targeted next-generation sequencing (NGS) of 53 genes, cytogenetic analyses, and clinical variables. Somatic mutations were categorized into type 1 (FLT3, PTPN11, WT1, IDH1/2, NPM1, NRAS) and type 2 (GATA2, KRAS, TP53, RUNX1, STAG2, ASXL1, ZRSR2, TET2) groups based on a previously proposed framework describing clonal characteristics. Complete remission (CR) or CR with incomplete hematologic recovery (CRi) was achieved in 53.8%, 52.1%, and 50.0% of patients treated in the first-, second-, and ≥third-line settings, respectively. Among 53 first-line patients with pre-treatment NGS data, type 1-only mutations were more frequently observed in responders (CR/CRi 72%), whereas type 2-only mutations were enriched in non-responders (CR/CRi 33%). In the first-line setting, achievement of CR/CRi following Aza/Ven was associated with improved overall survival. In addition, an exploratory mathematical model integrating baseline clinical variables demonstrated strong discriminatory performance for treatment response, including in cases without established prognostic mutations. In conclusion, Aza/Ven demonstrated consistent clinical activity across treatment lines in this real-world cohort. Mutational patterns classified by a type 1/type 2 framework were associated with differential response patterns in the first-line setting. Integrative modeling approaches may support the interpretation of response heterogeneity, particularly in genetically uninformative AML. - Source: PubMed
Publication date: 2026/10/01
Ueda TomoakiFukushima KentaroChi SunggiHaeno HiroshiYoshimoto GoichiArai HironoriIkeda DaisukeIchikawa MotoshiTakahashi NaotoHosono NaokoYamauchi TakahiroKondo TakeshiKusumoto ShigeruKuroda JunyaMinami Yosuke - Recent advancements in our understanding of the molecular underpinnings of acute myeloid leukemia (AML) disease biology have translated into breakthroughs in clinical management. In this review, we summarize the latest data incorporating precision approaches to treatment of FLT3-mutated AML with a focus on augmenting the curative role allogeneic hematopoietic cell transplantation (alloHCT) plays in the current treatment paradigm. - Source: PubMed
Publication date: 2026/10/01
Mort Joseph FAmbinder Alex J - CAR-T cell therapy (Chimeric Antigen Receptor T cells) is a promising approach for immune-mediated inflammatory diseases (IMIDs). Plasmacytoid dendritic cells (pDCs), which infiltrate tissues and secrete type I interferons (IFN-I), play a central early role in IMIDs and represent an attractive therapeutic target. - Source: PubMed
Publication date: 2026/09/30
Caël BlandineBôle-Richard ElodieBelakri ImaneZuffo Ludivine DalMazars JérémyHumbert SebastienSônego FabianeCreusat FlorentThiam KaderGalaine JeanneAubin FrançoisGarnache-Ottou Francine - Acute myeloid leukemia (AML) exemplifies how malignant transformation can be driven by both epigenetic deregulation and genetic mutation. Aberrant DNA methylation, histone modifications, and chromatin remodelling cooperate to block myeloid differentiation, sustain leukemic self-renewal, and promote immune evasion. This review examines the molecular mechanisms underlying epigenetic dysregulation in AML and highlights recent advances in epigenetic and immune-based therapeutic strategies. - Source: PubMed
Publication date: 2026/09/29
Ghosh DevangiAyoub MohdKarmakar SurajitRoy Choudhury Subhasree - Acute myeloid leukaemia (AML) remains associated with poor outcomes in relapsed or refractory disease and in molecularly defined high-risk subgroups. AML with KMT2A rearrangements (KMT2Ar) or NPM1 mutations (NPM1m) shares a dependence on the menin-KMT2A interaction, which sustains HOXA/MEIS1-driven transcription required for leukaemic maintenance. This dependence has provided the rationale for developing menin inhibitors as a targeted approach in selected AML subsets. This review summarises the mechanistic basis, clinical pharmacology, and current clinical role of menin inhibitors in AML. Revumenib, ziftomenib, bleximenib, and enzomenib are orally administered small molecules that disrupt menin-dependent transcription, induce myeloid differentiation, and have shown clinical activity in KMT2Ar and NPM1m AML. Monotherapy has produced clinically relevant remission rates in relapsed or refractory disease, and early-phase combinations with venetoclax-based therapy, hypomethylating agents, intensive chemotherapy, or FLT3 inhibitors have shown higher response rates in selected settings. Despite sharing a common target, these agents differ in dosing schedule, pharmacokinetic profile, CYP3A4-mediated drug-drug interaction potential, sensitivity to food or gastric pH, and safety profile. Differentiation syndrome and QTc prolongation are the principal toxicities requiring monitoring, although QT liability appears to vary across compounds. Acquired resistance-mediated by MEN1 binding-pocket mutations, co-occurring genomic alterations, and adaptive transcriptional or epigenetic programmes-remains a clinical limitation. Current evidence supports menin inhibition as a targeted strategy for molecularly selected AML. Ongoing studies will be important for defining optimal sequencing, combination regimens, approaches to resistance, and the role of pharmacologically informed dose optimisation in routine practice. - Source: PubMed
Publication date: 2026/09/28
Ma ChenchenWang XinWang Jingyi