CD135 _ FLT3 pTyr591
- Known as:
- CD135 _ FLT3 pTyr591
- Catalog number:
- AP20941PU-N
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3 pTyr591
Related genes to: CD135 _ FLT3 pTyr591
- 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: CD135 _ FLT3 pTyr591
AC220 AC220 is a uniquely potent and selective FLT3 inhibitor with IC50 of 0.56 +_- 0.3 nM and >10 mM for MC4-11 and A375, respectively. For research use only.anti-Flt3 CD135 (1A11)anti-Flt3 CD135 (1A11) type: Primary antibodies host: Mouseanti-Flt3 CD135 (3H1)anti-Flt3 CD135 (3H1) type: Primary antibodies host: Mouseanti-FLT3 CD135 (BV10A4H2)anti-FLT3 CD135 (BV10A4H2) type: Primary antibodies host: Mouseanti-FLT3 CD135 (Internal)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host Rabbitanti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host RabbitAnti-FLT3 (BV10A4H2), Mouse Monoclonal to FLT3, Isotype IgG1, Host Mouseanti-FLT3 (Phospho-Tyr591) Related articles to: CD135 _ FLT3 pTyr591
- Patients with relapsed or refractory acute myeloid leukaemia (r/r AML) harbouring FMS-like tyrosine kinase 3 (FLT3) mutations generally have poor prognosis and limited treatment options. The second-generation FLT3 inhibitor gilteritinib provides better disease control compared to standard relapse therapies and was approved based on two randomized trials. We analysed its efficacy and safety in a real-world cohort of r/r AML patients undergoing gilteritinib treatment including allogeneic haematopoietic stem cell transplantation (alloHSCT). Data were collected from all consecutive r/r AML patients with FLT3-internal tandem duplication and/or FLT3-tyrosine kinase domain mutations receiving gilteritinib at 25 centres. Response and survival were analysed using descriptive and correlative statistics. A total of 156 patients were analysed, 55.1% with relapse after previous alloHSCT, and 46.2% with prior FLT3 inhibitor exposure. The overall complete remission/incomplete remission (CR/Cri) rate was 45.3%, with a median overall survival (OS) of 10.0 months. Patients receiving gilteritinib only had a 1-year OS of 34%, while those with consolidating alloHSCT had a 1-year OS of 76%-92%, depending on gilteritinib maintenance post-transplant. Resuming gilteritinib post-transplant led to an 85.7% CR/CRi rate. Our real-world data confirm that gilteritinib is an effective single-agent therapy for r/r AML with FLT3 mutations, with best outcomes when used as a bridge to transplant and post-transplant maintenance. - Source: PubMed
Publication date: 2026/08/18
Kunadt DesireeZukunft SvenRöllig ChristophMetzelder StephanBurchert AndreasWagner-Drouet EvaKriege OliverSchliemann ChristophStelljes MatthiasRonnacker JulianBethge WolfgangWeller Jan FredericSteffen BjörnBug GesineKouidri KhouloudBaldus ClaudiaFransecky LarsSala ElisaPlatzbecker UweMetzeler KlausKayser SabineHilgendorf InkenHochhaus AndreasBrümmendorf Tim HJost EdgarDoleschall Anna DorottyaSchroeder ThomasKaivers JenniferKordelas LambrosHoltick UdoUnglaub Julia MSauer TimJäger Paul SebastianKobbe GuidoStauffer ElenaTischer JohannaHerold TobiasSteiner NormannNachbaur DavidKröger NicolausFrietsch Jochen JKraus SabrinaEinsele HermannHänel MathiasSchaffrath JudithKrüger WilliamBrandenburg AnneHolderried Tobias A WReinhardt LauraMaulhardt MarkusThiede ChristianBornhäuser MartinSchetelig JohannesMiddeke Jan MStölzel Friedrich - Nucleoside analogues are traditionally developed as antimetabolites that interfere with nucleic acid synthesis after intracellular phosphorylation. In this study, inspired by the 3',4'-unsaturated sugar scaffold of ddhCTP, we designed and synthesized a series of 3',4'-unsaturated nucleoside analogues to explore their antiproliferative potential and possible non-classical cellular effects. Among the synthesized compounds, 17k, a C-nucleoside bearing both a 3',4'-unsaturated sugar moiety and a chlorinated remdesivir-like base, exhibited potent antiproliferative activity against HepG2 cells, with an IC₅₀ value of 2.27 ± 0.36 μM, lower than that of gemcitabine under the same assay conditions. In the nonmalignant GES-1 epithelial cell line, 17k showed an IC₅₀ value of 34.26 ± 3.45 μM, corresponding to a selectivity index of 15.1 relative to HepG2 cells. Closely related compounds 12 and 17j showed no detectable activity, indicating a narrow structure-activity relationship. Exploratory single-concentration kinase profiling at 20 μM showed strong inhibition of several transcription-associated CDK/cyclin complexes (CDK13/CycK, CDK12/CycK, CDK9/CycT1, CDK19/CycC, and CDK8/CycC) and selected receptor tyrosine kinases (KDR/VEGFR2, RET, EPHA1, and FLT3). Compound 17k also suppressed colony formation and wound closure, induced apoptosis, and caused S-phase accumulation in HepG2 cells. These findings identify 17k as a nucleoside analogue with unanticipated antiproliferative activity and suggest that kinase modulation may contribute to its cellular effects. - Source: PubMed
Publication date: 2026/08/14
Wang SongYang JingYang XinyueHuang HaoZou HaiyangZhang YuZhang XushanLuo CongcongZhao BingLiu Feng-WuHerdewijn Piet - Acute myeloid leukemia (AML) remains the most common cause of death in adults with acute leukemia. Tyrosine kinase inhibitors (TKIs) have shown significant clinical efficacy in defined patient subgroups. Real-world outcomes of AML patients undergoing TKI therapy have not been widely reported. - Source: PubMed
Espinoza-Gutarra Manuel RJarret BrookeWang XiaoliangAfghahi AnoshehBae Sejong - Papillary renal neoplasm with reverse polarity (PRNRP) is a rare renal tumor with distinct histomorphologic features and a strong association with KRAS exon 2 mutations, typically at codon 12. We report two cases that expand the molecular spectrum of this entity. The first tumor, a 3.5 cm mass in a 51-year-old female, harbored the classic KRAS codon 12 mutation (p.G12V), whereas the second, a 2.0 cm mass in a 77-year-old female, exhibited a KRAS p.Q61K mutation, rarely reported in PRNRP. Both tumors showed characteristic histology (tubulopapillary architecture, eosinophilic cytoplasm, apical nuclear polarity) and immunoprofile (GATA3+, CK7+, SDHB-retained, FH-retained). Next-generation sequencing using a 505-gene cancer panel also detected additional alterations in FLT3, POLD1, KMT2C, and WHSC1, the significance of which remains uncertain currently but may emerge with more molecular data from additional PRNRP cases. These findings underscore the value of integrated histopathologic and molecular evaluation, highlight KRAS Q61K as a rare variant, and provide a foundation for future genomic studies in this tumor type. - Source: PubMed
Publication date: 2026/07/15
Zhou GangDong XiuhuaLiu Lina - - Source: PubMed
Publication date: 2026/07/07
Menssen Andrew JAshango Amenech BAlonzo Todd AGerbing Robert BPardo LauraHsu Fan-ChiLott Loren LDai FangyanCooper Todd MPollard Jessica ATarlock KatherineAplenc RichardMeshinchi SoheilBrodersen Lisa EidenschinkWells Denise ALoken Michael RHudson Chad A