9 Results for "

primary AML

" in MedChemExpress (MCE) Product Catalog:
Products (9)

9 Results for "primary AML" in MCE Product Catalog:

2
2 Cited Publications
Cat. No.: HY-13680
CAS No.: 97207-47-1
Purity:  99.91%
Synonyms: Dian III; N-Methylisoindigotin; Natura-α
Meisoindigo (Dian III), a derivative of Indirubin (HY-N0117), halts the cell cycle at the G0/G1 phase and induces apoptosis in primary acute myeloid leukemia (AML) cells. Meisoindigo exhibits high antitumor activity .
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Cat. No.: HY-P9983
CAS No.: 166089-32-3
Synonyms: SGN-33; HuM-195; GLK-33 Antibody
Lintuzumab (HUM-195) is an anti-CD33 humanized monoclonal antibody. Lintuzumab reduces the production of TNFα-induced pro-inflammatory cytokines and chemokines by AML cells. Lintuzumab promotes tumor cell killing through antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP) activities against MDR and MDR+ AML cell lines and primary AML patient samples. Lintuzumab enhances survival and reduces tumor burden in mice .
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Cat. No.: HY-163707
CAS No.: 866127-80-2
Target:  

Apoptosis

Research Areas:  

Cancer

UR778Br targets the GTPase-activating protein-related domain (GRD domain) of IQGAP1 proteins. UR778Br inhibits the proliferation of human acute myeloid leukemia (AML), arrests the cell cycle at the G2/M phase, and induces apoptosis. UR778Br inhibits colony formation of primary and AML cells, without significant impacts on normal bone marrow cells .
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Cat. No.: HY-162265A
Target:  

Apoptosis

Research Areas:  

Cancer

UCM-13369 (Compound 4b) is a NPM1 inhibitor. UCM-13369 downregulates the pathway associated with mutant NPM1 C+, and specifically recognizes the C-end DNA-binding domain of NPM1 C+. UCM-13369 induces apoptosis in AML cell lines and primary cells. UCM-13369 can be used for leukemia research .
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Cat. No.: HY-162265
CAS No.: 2921944-77-4
Target:  

Apoptosis

Research Areas:  

Cancer

UCM-13369 (Compound 4b) is a NPM1 inhibitor. UCM-13369 downregulates the pathway associated with mutant NPM1 C+, and specifically recognizes the C-end DNA-binding domain of NPM1 C+. UCM-13369 induces apoptosis in AML cell lines and primary cells, that can be used for the research of AML .
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Cat. No.: HY-149359
CAS No.: 3049485-80-2
Research Areas:  

Cancer

IHMT-IDH1-053 (compound 16) is a highly selectivity and irreversible IDH1-mutant inhibitor with an IC50 of 4.7 nM for IDH1 R132H. IHMT-IDH1-053 displays high selectivity against IDH1 mutants over IDH1 wt and IDH2 wt/mutants. IHMT-IDH1-053 inhibits 2-hydroxyglutarate (2-HG) production in IDH1 R132H mutant transfected 293T cells (IC50=28 nM). IHMT-IDH1-053 binds to the IDH1 R132H protein in the allosteric pocket adjacent to the NAPDH binding pocket through a covalent bond with residue Cys269. IHMT-IDH1-053 inhibits the proliferation of HT1080 cell line and primary AML cells which both bear IDH1 R132 mutants .
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Cat. No.: HY-13680R
CAS No.: 97207-47-1
Synonyms: Dian III (Standard); N-Methylisoindigotin (Standard); Natura-α (Standard)
Meisoindigo (Standard) is the analytical standard of Meisoindigo. This product is intended for research and analytical applications. Meisoindigo (Dian III), a derivative of Indirubin (HY-N0117), halts the cell cycle at the G0/G1 phase and induces apoptosis in primary acute myeloid leukemia (AML) cells. Meisoindigo exhibits high antitumor activity .
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Cat. No.: HY-158160
CAS No.: 2918263-09-7
Target:  

Sodium Channel

Research Areas:  

Metabolic Disease

LBA-3 is a selective, orally active inhibitor for sodium-coupled citrate transporter SLC13A5, with an IC50 of 67 nM. LBA-3 decreases levels of triglyceride and total cholesterol in oleic and palmitic acid (OPA)-stimulated AML12 cells, PCN-stimulated primary mouse hepatocytes and in mouse models, without detectable toxicity. LBA-3 is blood-brain barrier permeable .
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Cat. No.: HY-108417
CAS No.: 1332329-27-7
Target:  

STAT JAK Bcr-Abl

Research Areas:  

Cancer

Debio 0617B, a multi-kinase inhibitor, reduces maintenance and self-renewal of primary human AML CD34 + stem/progenitor cells. Debio 0617B has a unique profile targeting key kinases upstream of STAT3/STAT5 signaling such as JAK, SRC, ABL, and class III/V receptor tyrosine kinases (TKs). Debio 0617B has documented efficacy in STAT3-driven solid tumors .
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