CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- NB110-39048
- Product Quantity:
- 0.05 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
- FLT3 is a critical therapeutic target for acute myeloid leukemia (AML), and its inhibition remains a key strategy in AML management. In this study, we optimized the known compound CHEMBL4444839 to design a novel analogue, CHEMBL4444839-Analogue, showing improved pharmacological and structural characteristics. Pharmacokinetic profiling evaluation revealed that the analogue had enhanced drug-likeness, metabolic stability, and intestinal permeability, along with reduced predicted toxicity. Molecular docking revealed that CHEMBL4444839-Analogue exhibited a binding energy of -10.4 kcal/mol versus -8.7 kcal/mol for the parent compound, forming additional hydrogen bonds and hydrophobic contacts with GLU661, CYS694, LEU818, and PHE830 in the ATP binding pocket. Molecular dynamics simulation over 100 ns demonstrated lower average RMSD (1.78 Å vs 2.34 Å) and reduced RMSF fluctuations at the activation loop and DFG-out region, indicating enhanced conformational stability. Free energy calculations confirmed higher thermodynamic stability of the analogue versus CHEMBL4444839. The analogue also restricted domain motion and improved residue correlation, indicating better stabilization of FLT3 in its inactive conformation. Incorporation of a fluorocyclobutane moiety significantly contributed to enhanced rigidity and optimized interaction geometry, collectively establishing CHEMBL4444839-Analogue as a more promising and selective FLT3 inhibitor for AML therapy. - Source: PubMed
Publication date: 2026/05/18
Das UddalakRegati DheemanthSowdhamini RKumar Jitendra - Acute myeloid leukemia (AML) is a fatal blood cancer with cytotoxic chemotherapy offering at best 25% 5-year survival. While targeted BCL2 and FLT3 inhibitors venetoclax and gilteritinib are used upfront in the treatment of a subset of adult patients with AML and help to extend the survival of some patients, a curative treatment combination with minimal side effects has yet to be discovered. We find that use of the dual histone acetyltransferase p300/CBP bromodomain inhibitor CCS1477 (inobrodib), together with venetoclax and gilteritinib, virtually eliminates leukemia stem cells in an aggressive preclinical model of -mutant AML by impairing pro-oncogenic survival and proliferation factors to effectively block leukemogenesis. This work identifies potential clinical utility of a targeted, triplet combination therapy for treatment of AML. - Source: PubMed
Publication date: 2026/05/15
Goetz Melanie LRomer-Seibert Jennifer SVersace Amanda MKogan ScottJeurkar ChetanBowman Robert LBrooks NigelFrese KrisMeyer Sara E - Anthracyclines are key components of induction therapy for acute myelogenous leukemia with well-understood cardiotoxicity. Quizartinib inhibits FLT3 and has been shown to potentiate apoptosis and promote maladaptive remodeling after myocardial infarction in mice; however, the impact of FLT3 inhibition on a heart already exposed to anthracyclines is poorly understood. - Source: PubMed
Publication date: 2026/05/14
Spahr Zachary RVasquez Moises ATangella AdarshvardhanHusain Mohammad SaadTaylor Allen J - Despite advances, over half of AML patients relapse or become refractory to chemotherapy. TREM1 (CD354), a regulator of tumor inflammation and immune evasion in solid cancers, remains poorly characterized in AML, especially in underrepresented populations like Egyptians. We aimed to evaluate TREM1 expression in de novo AML, its association with high-risk features (FLT3-ITD, CD123), and its prognostic impact on treatment response and survival. - Source: PubMed
Publication date: 2026/05/14
Mansor Shima GafarElgamal RashaSaleh Mostafa F MohammedOthman Amira A ANawar Sarah M - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by PML::RARA fusion, typical morphology, and a characteristic flow cytometric immunophenotype that enables rapid diagnosis. However, immunophenotypic aberrancies may occur and can mimic mixed phenotype acute leukemia (MPAL), leading to diagnostic and therapeutic dilemmas. We report two adult male patients with APL confirmed by fluorescence in situ hybridization (FISH) demonstrating PML::RARA fusion. Both cases exhibited unusual immunophenotype. In the first case, peripheral blood flow cytometry revealed blasts with bright cMPO, CD34, dim HLA-DR, along with aberrant expression of CD19 (moderate), cCD79a (dim), cCD3 (heterogeneous), and CD7, raising a suspicion for MPAL. However, lineage defining criteria for T- and B-lineages were not fulfilled. Marrow showed abnormal promyelocytes with bundles of Auer rods, and molecular studies confirmed APL. In the second case, morphology suggested microgranular variant APL. Flow cytometry demonstrated aberrant expression of lymphoid and monocytic markers, including CD19 (dim), sCD3 (moderate), CD7, and CD14 (moderate), in addition to cMPO. Cytogenetics and molecular studies confirmed t(15;17)/PML::RARA in both cases, along with FLT3-ITD mutations. One patient developed differentiation syndrome and responded to all-trans-retinoic acid, while the follow-up of the second patient is unavailable. APL may exhibit immunophenotypic aberrancies mimicking MPAL. Molecular confirmation of PML::RARA and an integrated diagnostic approach are essential to avoid misclassification and ensure timely therapy. - Source: PubMed
Publication date: 2026/05/14
Prattipati Lumen AgarkarKar RakheeGupta Arvind KumarRonanki KavyaThangavel Prem Venkatt