CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- NBP1-19979
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3
Related genes to: CD135 _ FLT3
- 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
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
- Quizartinib is a FMS-like tyrosine kinase 3 (FLT3) inhibitor indicated for FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukemia (AML). We aimed to evaluate quizartinib resistance mechanisms, in addition to efficacy and safety outcomes, in patients with relapsed or refractory FLT3-ITD-positive AML. This multicenter, single-arm study in Japan (jRCTs071200015) enrolled 18 patients between May 2020 and December 2022. Of these, 15 patients received oral quizartinib (up to 53 mg once daily) for up to 12 cycles of 28 days each, then were followed for 12 months. The primary endpoint was to evaluate the type and rate of quizartinib resistance mutations; secondary endpoints included composite complete remission (CRc) rate, overall response rate (ORR), hematopoietic stem cell transplantation (HSCT) rate, relapse-free survival (RFS), overall survival (OS), and adverse events (AEs). Among seven evaluable patients, acquired mutations were detected in four patients (NF1 [R2616X], CSF3R [Q754X], NRAS [G13R], and FLT3 [D835Y] in one patient each), while loss of FLT3-ITD was observed in two patients. In efficacy analyses (n = 15), CRc rate was 66.7% (95% confidence interval [CI], 38.4-88.2), ORR was 73.3% (44.9-92.2), and median OS was 13.6 months (5.4-not evaluable). Three patients (20.0%) received HSCT directly after quizartinib; in these patients, median RFS was 8.5 months (95% CI, 6.2-not evaluable). Grade ≥ 3 non-hematologic AEs and grade 1 QT prolongation were each reported in three patients (20.0%). These data offer additional information on potential resistance mechanisms in patients with relapsed or refractory FLT3-ITD-positive AML. Trial Registration: Japan Registry of Clinical Trials (jRCTs071200015). - Source: PubMed
Publication date: 2026/08/12
Semba YuichiroMiyamoto ToshihiroKasahara SenjiKikushige YoshikaneMaeda TakahiroYoshimoto GoichiOta ShuichiSaito AkioNajima YuhoHosoi HirokiNiiya DaigoKato KojiNagafuji KojiAkasaka TakashiKamimura TomohikoTakita AtsushiNarahara MaikoToki TadashiIwanaga KoichiYonemoto KojiHarada MineAkashi Koichi - - Source: PubMed
Strohbehn Garth WTu S SeanWang XiaodongRatain Mark J - Orally administered small-molecule programmed death ligand 1 (PD-L1) inhibitors may have the potential to improve patient outcomes in the treatment of a range of cancers compared with their antibody-based counterparts. A small molecule might achieve better tumor tissue penetration, and oral administration could significantly improve convenience and access for patients. - Source: PubMed
Publication date: 2026/08/11
Prenen HansRottey SylviePinato David JLesimple ThierryVan Cutsem EricRobert MarieGalot RachelPiha-Paul Sarina ATomasini PascaleKotecki NuriaKristeleit RebeccaLe Tourneau ChristophePlummer RuthBanerji UdaiMeniawy TarekHowe JasonDaniel JeanniePulini JenniferSpitz SusanGong XiaohuaHalloran MollyItaliano Antoine - Although FMS-like tyrosine kinase-3 (FLT3) inhibitors initially induce a favorable response in AML patients, their long-term efficacy is often limited by the development of resistance. Bone marrow stromal cells (BMSCs), a key component of AML bone marrow niche, support leukemia cell survival and drive drug resistance through multiple approaches like direct contact, cytokine secretion, and exosome release. BMSC-mediated AML resistance involves complex and heterogeneous mechanisms that vary depending on the drug type and the characteristics of the leukemic cells. Therefore, this study seeks to elucidate how BMSCs interact with FLT3-ITD-mutated AML cells to confer FLT3 inhibitor resistance, aiming to identifying potential therapeutic targets to overcome such resistance. We discovered that BMSCs co-cultured with leukemia cells exhibited elevated expression of COX-2 and its product PGE2. BMSC-derived PGE2 suppressed ferroptosis in AML cells by modulating fatty acid metabolism and enhancing the glutathione antioxidant system. Additionally, PGE2 activated the GSK3β/β-catenin signaling pathway, facilitating the nuclear translocation of β-catenin, which influenced the apoptotic rates of AML cells. Proinflammatory cytokines such as TNF-α and IL-1β secreted by FLT3-ITD-mutated AML cells suppressed NR2F2 expression in BMSCs, leading to de-repression of COX-2 and subsequent PGE2 secretion, further amplifying this regulatory loop. Taken together, our findings reveal a novel mechanism whereby the NR2F2/COX-2/PGE2 axis modulates the sensitivity of AML cells to FLT3 inhibitors, and targeting this circuit may serve as an adjuvant therapy to improve FLT3 inhibitor efficacy. - Source: PubMed
Publication date: 2026/08/11
Wang JingmingTang LuJiang HuiwenYin HaifengLi YingyingChen ZhaozhaoXie QinyingWu ZhongZhang WanyingShu JinhuiWang MoranMei HengHu Yu - Ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation, has emerged as a potential therapeutic strategy for therapy-resistant cancers. Glutathione peroxidase 4 and the selenoprotein biosynthesis pathway essential for its translation are key regulators of ferroptosis but lack effective therapeutic targeting. In a drug screening using a selenoprotein translation reporter, here we identify FMS-like tyrosine kinase 3 (FLT3) inhibitors as suppressors of selenoprotein translation that induce ferroptosis in FLT3-mutant acute myeloid leukaemia. Mechanistically, FLT3 inhibition disrupts selenocysteine recoding, in which a UGA stop codon is recoded as selenocysteine via the SECIS element and associated binding proteins. Notably, the antileukemic efficacy of the FLT3 inhibitor gilteritinib was markedly reduced by dietary vitamin E, which attenuated ferroptosis. This study highlights ferroptosis as a vulnerability in FLT3-mutant acute myeloid leukaemia and suggests that high vitamin E intake may compromise tyrosine kinase inhibitor efficacy partly by suppressing ferroptosis. - Source: PubMed
Publication date: 2026/08/07
Li MinhuaZhu YudanKageyama YukiFurudate KenKitano AyumiTan TaotaoFeng MengdieZhou JingWang TaoTaylor Robert JStevens Alexandra MSamee Md Abul HassanMagee Jeffrey ATakahashi KoichiNakada Daisuke