rHuman FLt3 Active
- Known as:
- rHuman FLt3 Active
- Catalog number:
- RF00394041-500
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Agren
- 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
- Quizartinib is an oral, potent, selective FMS-like tyrosine kinase 3 (FLT3) inhibitor, approved for the treatment of FLT3-internal tandem duplication (ITD)-positive acute myeloid leukemia (AML) and under investigation in patients with newly diagnosed FLT3-ITD-negative AML. Quizartinib is metabolized by cytochrome P450 3A (CYP3A) in vitro, primarily into the active metabolite AC886, a CYP3A substrate. These phase 1, open-label, randomized, parallel-group trials assessed the effect of efavirenz, a moderate CYP3A inducer, and rufinamide, a weak CYP3A inducer, on the pharmacokinetics of quizartinib and AC886, and the safety and tolerability of quizartinib in healthy participants. Each study enrolled 32 participants; 16 received 60 mg quizartinib alone and 16 received 60 mg quizartinib plus either 600 mg efavirenz or 400 mg rufinamide. Coadministration with efavirenz decreased the maximum plasma concentration (C) and area under the plasma concentration-time curve extrapolated to infinity (AUC) of quizartinib by ~45% and ~90%, respectively, versus quizartinib alone; AC886 C and AUC also decreased by ~68% and ~96%, respectively. Coadministration with rufinamide had modest impact on quizartinib exposure (C and AUC decreased by ~19% and ~34%, respectively, vs. quizartinib alone). Coadministration of rufinamide and quizartinib decreased AC886 C and AUC by ~47% and ~53%, respectively, versus quizartinib alone. Quizartinib was well tolerated and no new safety signals were observed. These results suggest that concomitant use of quizartinib and moderate CYP3A inducers should be avoided. Concomitant use of weak CYP3A inducers does not warrant dose adjustment, since the impact on quizartinib exposure is clinically nonrelevant. - Source: PubMed
Yoo YoungJunZahir HamimInaba ShinichiKoo KyoinGarimella TusharAbutarif MalazZheng MingKamiyama EmiXu Yuan - Wild-type (WT) gastrointestinal stromal tumors (GISTs) are a rare and molecularly heterogeneous subset of GISTs lacking and mutations. These tumors pose significant diagnostic and therapeutic challenges due to resistance to standard tyrosine kinase inhibitors and a wide spectrum of genetic drivers. - Source: PubMed
Publication date: 2026/06/05
Xue ShuangLi ChunxiaoLi MeiFu FangfangZhang GuangtanLu ChangLiu Qiuyu - Invasive fungal sinusitis (IFS) profoundly impacts individuals with hematological malignancies, with rapid progression and high mortality rates. In an evolving therapeutic landscape, outcomes for patients with hematological malignancies who develop IFS warrant further evaluation. - Source: PubMed
Publication date: 2026/05/15
Athni Tejas SStrauch Carolyn BKovac VictorArbona-Haddad EstherVilla Inia PerezGupta SimranAleissa Muneerah MLiakos Alexis DTong AlexandraVedula Rahul SMaxfield Alice ZBergmark Regan WSherman Amy C - FLT3-ITD measurable residual disease (MRD) testing for patients in remission from acute myeloid leukemia (AML) is now recommended by the recently updated clinical standard of care guidelines. This companion technical note provides important laboratory and clinical recommendations regarding such testing. - Source: PubMed
Publication date: 2026/06/03
Hourigan Christopher SBeugelink LisanneOthman JadGui GegeIvey AdamDillon Richard JamesThiede ChristianLevis Mark JDillon Laura WWei Andrew HTiong Ing SooLoo SunDöhner KonstanzeArnhardt IsabellKowalik ArturPotter NicolaKim Dennis Dong HwanPreudhomme ClaudeDuployez NicolasHeuser MichaelValk Peter Jm - Acute myeloid leukemia (AML) is a diverse and complex haematological cancer that cannot be fully characterized, even with the combination of morphology and cytogenetics. As a result, molecular biomarkers have become the focus of diagnosis, risk stratification, therapeutic planning and monitoring of disease. Of these, FLT3 mutations have been identified as being clinically relevant, clinically important, and easily detected during various phases of AML care. This review examines the diagnostic, prognostic, predictive and monitoring role of FLT3 mutations in AML, with a focus on the clinical applications in the laboratory. We review the evidence for FLT3 internal tandem duplication (FLT3-ITD) and FLT3 tyrosine kinase domain (FLT3-TKD) mutations, their association with relapse risk, remission duration, survival, response to FLT3 inhibitors and measurable residual disease testing. The impact of allelic burden, variant allele frequency, insertion site, structural characteristics, co-mutational background, interpretation of FLT3 results in ELN 2022, and treatment exposure help clarify the clinical significance of FLT3 results. A particular focus is placed on laboratory assay implementation, including PCR-based assays, fragment analysis, next-generation sequencing and droplet digital PCR, as well as assay sensitivity, mutation quantification, structural annotation, and inter-platform standardization. FLT3 should be used as an integrated clinical laboratory biomarker and not a simple mutation-positive or mutation-negative result. Its mutation subtype, molecular context, treatment setting, assay performance and standardized reporting determine its diagnostic, prognostic, predictive and MRD-related value. This review offers a clinical laboratory perspective on how to interpret FLT3 mutations as actionable biomarkers in AML. - Source: PubMed
Publication date: 2026/06/02
Thapa RiyaFuloria Neeraj KumarBhat Asif AhmadPorwal OmjiAnsari Mohammed TahirNarain KamalBiswas AnupamBiswas SangitaBhatia SumitaFuloria Shivkanya