Flt3 Ligand Blocking Peptide
- Known as:
- Flt3 Ligand Blocking Peptide
- Catalog number:
- 33r-9360
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Flt3 Ligand Blocking Peptide
Related genes to: Flt3 Ligand Blocking Peptide
- 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: Flt3 Ligand Blocking Peptide
α - Calcitonin Gene Related Peptide, α - CGRP, rat&_945;2&_946;1 Integrin Ligand Peptide&_946;_catenin peptide(1R,2R)_(+)_1,2_Diaminocyclohexane_N, min. 94%rost ligand (na(1S,2S)_(+)_1,2_Cyclohexanediamino_N, (S,S)_Jacobsen ligand(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N min. 94% rost ligand (n(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N Rost ligand(Ala92)-Peptide 6 98% C93H155N31O26 CAS:(Arg)9 Peptide (Arg8)-Vasopressin Biotin peptide This is (Arg8)-Vasopressin Biotin peptide. For research use only.(Asn5)-Delta-Sleep Inducing Peptide
(Asn5)-Delta-Sleep Inducing Peptide (rabbit), (Asn5)-DSIP (rabbit) 98% C35H49N11O14 CAS: 80064-67-1(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Asn5)_Delta_Sleep Inducing Peptide Salt _ Binding _ Synonym (Asn5)_Delta_Sleep Inducing Peptide (rabbit), (Asn5)_DSIP (rabbit) SumFormula C35H49N11O14(Biotin Conjugates) Dopamine D2 Receptor Immunogen: peptide Host: Rabbit(Biotin Conjugates) Glucose Transporter 1 Immunogen: peptide Host: Rabbit Related articles to: Flt3 Ligand Blocking Peptide
- The prognostic relevance of IDH1 mutations remains unclear in acute myeloid leukemia (AML). This study, representing the first Turkish AML cohort characterized for IDH1 mutations, aimed to determine the frequency of IDH1, FLT3 and NPM1 mutations and to describe the associated clinical characteristics. We retrospectively analyzed clinical, cytogenetic, and molecular data for 57 AML patients. Bone marrow aspirates were evaluated cytogenetically using G-banding, and molecular mutations were assessed by PCR or NGS (MiSeq-Illumina). IDH1 mutations were detected in 7% of patients; FLT3 and NPM1 mutations were detected in 38.6% and 19.3% of patients, respectively. A significant positive correlation existed between IDH1 and NPM1 mutations (r = 0.388, = 0.003). Overall mortality was 56.1% and remission was achieved in 43.9%. Older age ( = 0.029) and comorbidities ( = 0.009) were significantly linked to mortality. Mortality was 100% in the four IDH1-mutant patients and significantly higher in NPM1-mutant patients. Overall survival was shorter in IDH1-mutants, although the difference did not reach statistical significance (log-rank = 0.057). Relapse occurred in 26.3%, rising to 50% in the IDH1-mutated subgroup. In this limited cohort, IDH1-mutant cases were associated with shorter overall survival and higher mortality; however, the small number of IDH1-mutant patients ( = 4) precludes definitive prognostic conclusions. Outcomes in NPM1-mutated patients were also less favorable than typically expected, possibly related to co-occurring IDH1 mutations. These descriptive findings characterize the molecular landscape of AML in an underrepresented Turkish population and may provide a foundation for larger, multicenter studies rather than confirming a prognostic role for these mutations. - Source: PubMed
Publication date: 2026/07/24
Catma YunusErdem SimgeAday AynurBayrak Tokac AysegulGuzel Mastanzade MetbanOzbalak MuratYonal Hindilerden IpekYenerel Mustafa NuriNalcaci MelihaOzturk SukruKalayoglu Besisik Sevgi - Indolo[2,3-]quinoxalines, along with their -substituted derivatives, exhibit pronounced anticancer activity, although the mechanisms of their biological action may vary. Herein, a panel of sixty-five 6-(2-aminoethyl)-6-indolo[2,3-]quinoxaline derivatives comprising eight series with distinct amine moieties connected to the tetracyclic indoloquinoxaline core via a dimethylene linker was evaluated as drug-like candidates for kinase binding and cytotoxic activity. The ADME (Absorption, Distribution, Metabolism, and Excretion) properties of the compounds included in this set were preliminarily determined using the SwissADME tool. Analysis revealed that the library of quinoxaline derivatives largely complies with the drug-likeness rule for kinase-targeted compounds. As part of the biological screening, the compounds were initially tested on two cell lines MonoMac-6 and THP-1 (both derived from patients with acute monocytic leukemia) using sunitinib, a known antitumor agent acting as a multi-target receptor tyrosine kinase inhibitor, as a reference compound. Compound , which demonstrated the highest activity in the cytotoxicity analysis (IC = 1.9 and 3.5 μM for the MonoMac-6 and THP-1 cell lines, respectively), was screened using the Eurofins DiscoverX scanEDGE panel, comprising 97 distinct kinases representing all known kinase families. Subsequently, the compound was tested using the Eurofins DiscoverX scanTK™ panel, covering 135 distinct receptor and non-receptor tyrosine kinases. Based on initial screening results, compound exhibits relatively high binding activity against fourteen tyrosine kinases, including TYK2, ZAP70, eight mutant forms of ABL1, two mutant forms of FLT3, and one mutant form of ALK, and demonstrates relatively high binding selectivity with respect to non-mutant tyrosine kinases (S-score: 0.024). Secondary screening of nine selected analogs of compound led to the identification of compound , which demonstrates relatively high binding affinity for FLT3 (D835V) (K = 0.41 μM). Molecular modeling suggested modes of binding interaction of the compounds and in the FLT3 (D835V) catalytic site. Our results demonstrate that 6-(2-aminoethyl)-6-indolo[2,3-]quinoxaline derivatives could be potential candidates for developing anticancer drugs. - Source: PubMed
Publication date: 2026/08/12
Schepetkin Igor AUvarov Alexander VEvriinov Egor AKhlebnikov Andrei I - Pediatric acute myeloid leukemia (AML) is a highly heterogeneous malignancy, with cytogenetic and molecular abnormalities playing a critical role in determining prognosis and guiding treatment decisions. Despite therapeutic advances, patients with high-risk genetic mutations and translocations continue to experience suboptimal outcomes. As new targeted therapies emerge, the treatment of pediatric AML could undergo a paradigm shift, where "one-size-fits-all" chemotherapy is no longer the only frontline approach. Identifying genetic markers inform risk stratification and have greater impact on shaping the therapeutic approach, including the integration of targeted therapies such as FLT3 and menin inhibitors into frontline therapy. Furthermore, pediatric AML treatment options are being driven by recent discoveries in adult AML, broadening their clinical trials to include pediatric patients, in part due to the RACE for Children Act that went into effect in August 2020. This review identifies the most prevalent high-risk cytogenetic lesions in pediatric AML, emphasizing their incidence, prognostic significance, and implications for clinical management. By synthesizing current research on these key genetic abnormalities and their associated therapies, we aim to provide an updated perspective on the evolving landscape of high-risk pediatric AML management that can then lead to the establishment of an agile framework to rapidly evaluate, approve, and deploy novel agents. - Source: PubMed
Publication date: 2026/08/19
Ayerbe CamilaFan Aaron EScanlan RyanRaj ReejaCatueno SamantaRay AnweshaAguirre HuberMcCall DavidRoth MichaelGarcia Miriam BNunez CesarSheikh Irtiza NGarcia-Manero GuillermoCuglievan BrankoGibson Amber - internal tandem duplication (-ITD) mutations occur in approximately 20-25% of patients with acute myeloid leukemia (AML) and are associated with increased relapse risk and inferior survival outcomes. Although measurable residual disease (MRD) has become a key prognostic tool for guiding post-remission treatment decisions, -ITD was historically considered a suboptimal MRD marker because of its subclonal nature, structural heterogeneity and dynamic behavior during disease evolution. In addition, -ITD has not yet been fully integrated into routine MRD monitoring due to methodological limitations and a lack of standardized workflows. The latest European LeukemiaNet (ELN)-DAVID 2025 recommendations stressed the use of ultra-high sensitivity (UHS) next-generation sequencing (NGS) technologies to detect -ITD MRD with improved precision, enabling reliable longitudinal tracking of patient-specific clones at very low variant allele frequencies (VAF). Indeed, despite prospective evidence supporting this approach remaining limited, -ITD-based MRD monitoring is emerging as a clinically relevant prognostic indicator, contributing to the identification of patients at increased risk of relapse and refining risk stratification, while also informing therapeutic decision-making, particularly in the peri-transplant setting. The present review summarizes the biological underpinnings of -ITD mutated (-ITD) AML, discusses the methodological challenges of MRD detection, and critically evaluates the evolving role of MRD in refining relapse prediction, supporting post-remission therapy tailoring, and contributing to a harmonized framework for -ITD AML management. - Source: PubMed
Publication date: 2026/08/11
Silvestrini GiorgiaTravaglini SerenaGuarnera LucaLelli NicoleDivona MariadomenicaCasciani ElisaCeccolini SaraFalconi GiuliaOttone TizianaVoso Maria Teresa - Acute myeloid leukemia (AML) is a molecularly heterogeneous malignancy where next-generation sequencing (NGS) has revolutionized risk stratification and treatment paradigms. However, the interplay between mutation cooperativity, clinical phenotypes, and biochemical markers of organ dysfunction remains poorly characterized. This study investigates how co-mutational patterns influence hematological/biochemical parameters and survival outcomes in AML. - Source: PubMed
Publication date: 2026/08/12
Xu ZhengrongZheng YingZheng YiYao YanyanGeng HailiLi XiaofanWang Shao-YuanPan Lili