CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- BM2462
- Product Quantity:
- 0.2 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
- QUIWI (NCT04107727) was a phase II, randomized, double-blind, placebo-controlled trial evaluating quizartinib or placebo added to induction and consolidation chemotherapy and/or allogeneic hematopoietic cell transplantation (allo-HCT), followed by maintenance, in newly diagnosed FLT3-ITD- negative acute myeloid leukemia (AML). This post hoc analysis assessed the impact of allo-HCT, modeled as a time-dependent variable, performed in first composite complete remission (CRc1) on overall survival (OS) and disease-free survival (DFS) according to treatment arm. Among 273 randomized patients, 32.2% in the quizartinib arm and 30.1% in the placebo arm underwent allo-HCT in CRc1. Quizartinib improved OS and DFS compared with placebo regardless of allo-HCT status. In Cox models with allo-HCT as a timedependent covariate, quizartinib remained associated with improved OS (HR 0.59; p=0.008) and DFS (HR 0.67; p=0.03), whereas allo-HCT was not significantly associated with OS (HR 0.91; p=0.62) and showed a numerical DFS benefit (HR 0.73; p=0.08). Multivariable analyses confirmed quizartinib as an independent favorable factor for OS (HR 0.56; p=0.046) and DFS (HR 0.60; p=0.04). No additional safety signals were observed. In patients with newly diagnosed FLT3-ITD-negative AML achieving CRc1, quizartinib improved OS and DFS in the overall population. Notably, the clinical benefit of quizartinib was observed regardless of allo-HCT, and appeared more evident in patients who did not proceed to transplant. - Source: PubMed
Publication date: 2026/05/14
Lloret-Madrid PilarRodríguez-Veiga RebecaBergua Juan MiguelAlgarra Jesús Lorenzo AlgarraBotella CarmenRodríguez-Arbolí EduardoBernal TeresaTormo MarCalbacho MariaSalamero OlgaSerrano JosefinaNoriega VictorLópez-López Juan AntonioVives SusanaLópez-Lorenzo Jose LuisColorado MercedesVidriales Maria-BelénBoyero Raimundo GarcíaOlave Maria TeresaHerrera PilarArce OlgaBarrios ManuelSayas Maria JosePolo MartaGómez-Roncero Maria IsabelBarragán EvaAyala RosaChillón CarmenCalasanz Maria JoséPaiva BrunoBoluda BlancaCasas-Avilés IgnacioSánchez Maria JoséRodríguez-Medina CarlosCuevas LaidaRaposo-Puglia José ÁngelMateos M CarmenOlivares MatxalenMartínez-Chamorro CarmenAlonso NataliaSuárez SandraSánchez-Vadillo IreneRodríguez María SoléGonzález Bernardo JavierMartínez-Francés AntonioCuello RebecaFernández AlfonsoMartínez-Cuadrón DavidLabrador JorgeMontesinos Pau - In this first-in-human open-label study, autologous FLT3 CAR-T cells were delivered to two patients with relapsed and refractory FLT3 AML. Bone marrow examination revealed AML blasts with high but variable surface density of FLT3 expression. Following tumor cytoreduction and lymphodepletion, 1 × 10/kg of FLT3 CAR-T cells were administered, resulting in in vivo CAR-T cell expansion and grade 1 cytokine release syndrome in both patients. Both patients failed to achieve remission after CAR-T cell therapy, but bone marrow examination following therapy revealed the elimination of FLT3 AML blasts, persistence of FLT3 AML blasts, and early post-treatment preservation of normal CD34 hematopoietic stem and progenitor cells (HSPCs) with variable FLT3 expression. Collectively, autologous FLT3 CAR-T cells can be safely administered and can eradicate FLT3⁺ blasts with minimal toxicity, without causing substantial damage to normal CD34⁺ HSPCs; however, they fail to induce leukemic remission due to the heterogeneity of FLT3 expression and the persistence of FLT3⁻ AML blasts. - Source: PubMed
Publication date: 2026/05/14
Wu XiaojinLu GaoTian LeiChen SuningCaligiuri Michael AYu Jianhua - We report a large cohort of 95 adult patients with acute myeloid leukemia (AML) harboring NUP98 rearrangements (NUP98r). Patient characteristics included a young age (median 50 years [IQR 38-64]), 20% of therapy-related AML, a high WBC count (median 52×10/L), normal karyotype in 32%, FLT3-ITD in 48% and WT1 mutations in 34%. NUP98::NSD1 fusion was the most common (54%), and these patients were significantly younger (41 y vs. 61 y), had more de novo AML (94% vs. 64%), higher rates of normal karyotypes (56% vs. 4.5%), FLT3-ITD (76% vs. 18%) and WT1 mutations (50% vs. 16%) than other NUP98r AML. The median overall survival (OS) for the entire cohort was 15.2 months (95% CI, 11.9-20.8) and event-free survival was 5.8 months (2-7.5). Among patients treated intensively (n = 73), age (HR = 2.7), FLT3 inhibitor therapy (HR = 0.45) and hematopoietic stem cell transplant (HR = 0.5) influenced OS in univariate analysis. Compared with NUP98 wild-type (WT) AML, NUP98r patients had a prognosis more similar to that of NUP98 WT ELN adverse patients whether initially classified as intermediate (20.3 months [11.7-30.2]) or adverse (15.7 months [13.5-42.9]). However, treatment with FLT3 inhibitors improved prognosis, with median OS not reached and 5-year OS of 53.3%, approaching that of intermediate-risk patients. - Source: PubMed
Publication date: 2026/05/12
Ducourneau BenoitPages ArnaudStruski StéphanieDecamp MatthieuRaffoux EmmanuelBerthon CélineFenwarth LaurèneMarmouset VincentPautas CécileCluzeau ThomasLebon DelphineUzunov MadalinaPereyra PatricioHeiblig MaëlMalfuson Jean-ValèreFarnault LaureDumas Pierre-YvesHieulle JuliaBertoli SarahChantepie SylvainAuger NathalieBidet AudreyMozziconacci Marie-JoelleBoudry AugustinLuquet IsabelleChat LaureenLoyaux RomainEl-Mur LinaClappier EmmanuelleGardin ClaudeHunault MathildeDe Botton StéphanePigneux ArnaudPenther DominiqueDelabesse EricItzykson RaphaelPreudhomme ClaudeDombret HervéRecher ChristianDuployez NicolasMicol Jean-Baptiste - To determine midostaurin and posaconazole plasma concentrations and investigate adverse events (AEs) resembling drug-drug interactions (DDI) when both drugs were administered concomitantly during induction chemotherapy for acute myeloid leukemia (AML). Patients with FLT3-mutated AML who received midostaurin and posaconazole concomitantly between May 2019 and December 2022 were included and followed up to March 2023. Twice-weekly trough levels for midostaurin and posaconazole were measured with validated liquid chromatography-tandem mass spectrometry methods. Potential DDIs were independently reviewed by two physicians and attributed using the Drug Interaction Probability Scale (DIPS). Population pharmacokinetics analysis was done via nonlinear mixed-effect modeling. In 29 patients, concentrations ranged from 0.6 to 24.5 mg/L for midostaurin and from <30 to 2,572 µg/L for posaconazole. A total of 375 AEs in 66 midostaurin cycles, with 280 AEs classified as grade ≥3, were recorded. Probable DDI with a DIPS score of ≥5 was attributed in 14/375 AEs; no highly probable AEs were registered. Eight AEs led to dose modification or discontinuation of midostaurin in seven patients. Clearance for midostaurin during co-administration with posaconazole was 0.52 L/h (95% CI, 0.42-0.62 L/h). A breakthrough fungal infection was recorded in eight patients (27.5%). DDI of midostaurin and posaconazole is clinically meaningful but infrequent. High inter- and intra-individual variabilities of midostaurin and posaconazole plasma exposure were observed. Midostaurin clearance was delayed during co-administration. Midostaurin therapeutic drug monitoring may serve for decision-making when DDI with CYP3A4 inhibitors is suspected. - Source: PubMed
Publication date: 2026/05/12
Joisten Carolin SMellinghoff Sibylle CSeidel DanilaMüller CarstenMüller-Ohrem CharlotteKreuzer Karl-AntonFrenzel Lukas PSimon FlorianHallek MichaelKoehler PhilippCornely Oliver AStemler Jannik - Chimeric antigen receptor T cell (CAR-T cell) therapy is an immunotherapy for acute leukemias utilizing recombinant receptors specific to antigens involved in T-cell function to direct tumor cell recognition and elimination. However, major limitations include relapse due to antigen escape and tumor heterogeneity, as well as on-target off-tumor effects. Bispecific CAR-T cells are developed to overcome these issues. - Source: PubMed
Publication date: 2026/04/23
Husodho Gabriela Valencia PutriKumalasari Anatalya Diah AyuFaiza Agyta HanifaLimijadi Edward Kurnia SetiawanHendrianingtyas Meita