9 Results for "

anti-AML activity

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

9 Results for "anti-AML activity" in MCE Product Catalog:

3
3 Cited Publications
Cat. No.: HY-B1336
CAS No.: 67-45-8
Furazolidone is a monoamine oxidase (MAO) inhibitor with antiproliferative, apoptosis-inducing and differentiation-promoting activities. Furazolidone may inhibit leukemia fusion protein-mediated bone marrow transformation by upregulating the stability of the tumor suppressor protein p53. Furazolidone exhibits anti-leukemic activity in acute myeloid leukemia (AML) cell lines and can be used for anti-AML research [2].
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Cat. No.: HY-142696A
CAS No.: 2677026-15-0
Purity:  99.38%
Target:  

CDK Pim Apoptosis

Research Areas:  

Cancer

CDK6/PIM1-IN-1 (Compound 51) hydrochloride is an orally active and potent dual CDK6/PIM1 inhibitor with IC50 values of 39 and 88 nM, respectively. CDK6/PIM1-IN-1 hydrochloride inhibits CDK4 (IC50=3.6 nM). CDK6/PIM1-IN-1 hydrochloride significantly inhibits acute myeloid leukemia (AML) cell proliferation, arrest cell cycle at the G1 phase, and promote cell apoptosis. CDK6/PIM1-IN-1 exhibits potent anti-AML activity .
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Cat. No.: HY-173444
CAS No.: 2989934-63-4
Research Areas:  

Cancer

HDAC11-IN-3 (Compound A9) is a selective HDAC11 inhibitor (IC50: 4.1 nM). HDAC11-IN-3 has inhibitory effects on U937 and OCI-AML2 acute myeloid leukemia (AML) cell lines (IC50: 10 μM). HDAC11-IN-3 has significant anti-AML activity, inducing apoptosis, cell cycle arrest, and differentiation. HDAC11-IN-3 upregulates the iron transporters transferrin (TF) and transferrin receptor (TFRC), and activates the p62-Keap1-Nrf2-HMOX1 pathway, which together lead to increased intracellular iron levels and induce ferroptosis in AML cells. HDAC11-IN-3 can be used alone or in combination with Cytarabine (HY-13605) for AML research .
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Cat. No.: HY-142696
CAS No.: 2677026-14-9
Target:  

CDK Pim Apoptosis

Research Areas:  

Cancer

CDK6/PIM1-IN-1 is a potent and balanced dual CDK6/PIM1 inhibitor with IC50 values of 39 and 88 nM, respectively. CDK6/PIM1-IN-1 inhibits CDK4 (IC50=3.6 nM). CDK6/PIM1-IN-1 significantly inhibits acute myeloid leukemia (AML) cell proliferation, arrest cell cycle at the G1 phase, and promote cell apoptosis. CDK6/PIM1-IN-1 exhibits potent anti-AML activity .
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Cat. No.: HY-P11076
Target:  

Complement System

Research Areas:  

Cancer

CP-EPS8-NLS is a peptide with anti-AML property. CP-EPS8-NLS interferes with EPS8-associated signaling and exerts anti-AML activity in various AML cell types. CP-EPS8-NLS has potent antitumor activity in xenograft tumor models. CP-EPS8-NLS downregulates EPS8 expression and its downstream pathway .
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Cat. No.: HY-143895
CAS No.: 2499966-67-3
Target:  

FLT3

Research Areas:  

Cancer

FLT3-IN-12 is a potent, selective and orally active FLT3 kinase inhibitor with IC50s of 1.48 nM and 2.87 nM for FLT3-WT and FLT3-D835Y, respectively. FLT3-IN-12 possesses high selectivity over c-KIT (>1000-fold). FLT3-IN-12 has an excellent anti-AML (acute myeloid leukemia) activity (MV4-11, IC50 of 0.75 nM) .
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Cat. No.: HY-162293
CAS No.: 2924193-12-2
Target:  

CDK

Research Areas:  

Cancer

CDK8-IN-14 (compound 12) inhibits CDK8 with an IC50 value of 39.2 nM and has anti-AML cell proliferation activity (molm-13 GC50 = 0.02±0.01μM, MV4-11 GC50 = 0.03±0.01μM) .
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Cat. No.: HY-155594
CAS No.: 2143089-35-2
Target:  

FLT3

Research Areas:  

Cancer

LT-540-717 (compound 32) is a potent FLT3 inhibitor (IC50=0.62 nM) with antiproliferative activity. LT-540-717 also inhibits several acquired FLT3 mutations, FLT3 (ITD, D835V), FLT3 (ITD, F691L), FLT3 (D835Y) and FLT3 (D835V). LT-540-717 has potential to be an anti-AML agent .
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Cat. No.: HY-122670
CAS No.: 1627962-21-3
Research Areas:  

Cancer

VS-II-173 is a pan-Pim kinase inhibitor with IC50 values ​​of 0.07 μM and 0.02 μM for Pim1 and Pim3, respectively, and a residual activity of 46% for Pim2 at 1 μM. VS-II-173 also inhibits kinases such as HIPK2, PRK2, RSK1, DYRK1a and AMPKα1, selectively inhibiting acute myeloid leukemia (AML) cells with significantly lower toxicity to non-malignant cells (EC50 > 30 μM). VS-II-173 weakens the phosphorylation of substrates such as Stat5 (Y694), MDM2 (S166), Bad (S112), and 4E-BP1 (T37/46) by inhibiting Pim kinase-mediated signaling pathways, blocking pro-survival signals in AML cells and inducing apoptosis. VS-II-173 synergistically enhances anti-AML activity when combined with Daunorubicin (HY-13062A). VS-II-173 can be used in AML research, especially for AML with FLT3-ITD mutations and NPM1 mutations .
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