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
- Phlegmonous gastritis (PG) is a rare disorder in which a bacterial infection arises in the gastric wall. We report a patient in his 60s with FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD)-mutated acute myeloid leukemia (AML) who developed PG during the consolidation therapy with high-dose cytarabine and the FLT3 inhibitor quizartinib. The patient developed fever, abdominal pain, hematemesis, and hypovolemic shock during neutropenia on day 17. Contrast-enhanced computed tomography (CT) showed edematous thickening of the gastric wall with perigastric fat stranding. Upper gastrointestinal endoscopy revealed diffuse edematous mucosa with erosions, and a gastric biopsy culture yielded . Intravenous piperacillin/tazobactam, followed by ampicillin/sulbactam after clinical improvement, achieved complete clinical and radiologic resolution without surgical intervention. This case highlights the importance of early suspicion, prompt contrast-enhanced CT, and endoscopic biopsy with concurrent microbiological evaluation, followed by timely broad-spectrum antimicrobial therapy in immunocompromised patients with chemotherapy-induced neutropenia in the setting of hematological malignancy. - Source: PubMed
Publication date: 2026/07/29
Itamura HidekazuMihashi TatsuyaHirano YusukeKimura Shinya - Patients with relapsed or refractory (R/R) acute myeloid leukemia (AML) are characterized by a disastrous prognosis. For most patients with R/R AML, allogeneic hematopoietic stem cell transplantation (HSCT) is the only curative option. It is important to conduct mutational analysis again when the disease relapses to identify any new genetic abnormalities that can be targeted with novel treatments. As part of a conditioning regimen or post-transplant maintenance therapy, new targeted agents support HSCT in patients with R/R AML in various forms, including combination chemotherapy to improve complete remission (CR) prior to HSCT. For R/R AML patients with mutated FMS-related tyrosine kinase 3 (FLT3), sorafenib and quizartinib have shown encouraging therapeutic effects either in combination with chemotherapy for bridging to transplantation or as maintenance therapy after HSCT. Ivosidenib and enasidenib, which are inhibitors that target mutated isocitrate dehydrogenase (IDH) 1 and 2, respectively, have been approved by the US Food and Drug Administration (FDA) for the treatment of IDH1/IDH2-mutated R/R AML. Venetoclax, an inhibitor of B-cell lymphoma-2 (BCL2), is widely used in the salvage treatment of R/R AML and has better therapeutic effects and controllable drug toxicity than traditional chemotherapy. In addition, chimeric antigen receptor (CAR) T-cell immunotherapy (targeting CD33, CD123, and CLL1) has achieved encouraging clinical response rates in phase I and phase II clinical trials for R/R-AML, and subsequent bridging HSCT has significantly improved patient survival. - Source: PubMed
Publication date: 2026/08/28
Cao LiqinHu DaihongCui LijuanZhang Xiaohui - - Source: PubMed
Publication date: 2026/08/28
Xu Zhaodong - In order to investigate the synergistic antibacterial effects of the novel FLT3 inhibitor G-749 in combination with colistin against Escherichia coli (E. coli). - Source: PubMed
Pan TianleLiu LianHuang RuyueWang MiFei ChenzhongLiu Yingchun - To date, the treatment of acute myeloid leukaemia (AML) remains a major challenge in hematologic malignancies, particularly among elderly patients who are unfit for intensive chemotherapy. Venetoclax, a BCL-2 inhibitor, in combination with azacitidine, has significantly improved the prognosis and survival of this patient population. However, approximately 30% of patients do not respond to venetoclax-based combination regimens, and most initial responders eventually experience relapse. Therefore, resistance to venetoclax has become a critical bottleneck limiting its long-term clinical benefits. A thorough understanding of the underlying resistance mechanisms and the development of novel strategies to overcome resistance are central to improving survival outcomes in elderly AML patients. The resistance mechanisms of venetoclax are complex and multifaceted, including genetic drivers such as TP53 mutations, FLT3-ITD, and NRAS/KRAS mutations, as well as the upregulation of anti-apoptotic proteins (e.g., MCL-1, BCL-xL), metabolic reprogramming, and altered cellular differentiation states. In response to these factors, emerging therapeutic strategies are rapidly evolving toward precision-based and combination approaches, including combinations with targeted agents (e.g., IDH2 inhibitors, FLT3 inhibitors), MCL-1 inhibitors, optimization of current dosing regimens (e.g., DEC3-VEN), and the development of novel modalities (e.g., antibody-drug conjugates, CAR-T cell therapy). Focusing on the disease characteristics of elderly AML, this narrative review summarizes the clinical efficacy of venetoclax, critically examines the multifaceted mechanisms of venetoclax resistance, and discusses current and emerging therapeutic strategies to overcome this resistance. The goal is to inform clinical practice and guide future translational research. KEY POINTS: This review elucidates the current mechanism of action, therapeutic effects, and limitations of venetoclax, focusing on its use and combination regimens in the specific patient population of elderly individuals with AML who are not suitable for intensive therapy, as well as strategies to overcome resistance, and provides future perspectives for addressing venetoclax resistance. - Source: PubMed
Zhang JinlinLiu JileZhao MohanZhang XiaoyuLiu LinlinLi MengnanCao ChangzeZhang RuiZhao Mingfeng