NCO-90
NCO-90 is a selective SIRT2 inhibitor with an IC50 of 1.0 μM. NCO-90 induces Apoptosis via Caspase activation and mitochondrial superoxide anion production, and also induces Autophagic cell death by increasing LC3-II levels and autophagosome accumulation. NCO-90 exhibits anticancer activity against leukemia. NCO-90 can be used in research related to acute lymphoblastic leukemia and acute myeloid leukemia.
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- CAS. Nr.: 1382354-18-8
- Formel: C21H20N2O2
- Molecular Weight:332.40
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
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SIRT2 1.0 μM (IC50) |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| MCF7 | GI |
30 %
Compound: NCO-90
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Growth inhibition of human MCF7 cells at 30 uM measured after 72 hrs by AlamarBlue assay relative to control
Growth inhibition of human MCF7 cells at 30 uM measured after 72 hrs by AlamarBlue assay relative to control
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[PMID: 31144814] |
NCO-90 potently and selectively inhibits purified SIRT2 with an IC50 of 1.74 μM, while exerting no significant inhibitory effect on SIRT1, SIRT3 or SIRT5[1].
NCO-90 is a selective SIRT2 inhibitor with an IC50 of 1.0 μM[2].
NCO-90 (0.1-100 μM; 72 h) inhibits the growth of S1T, MT-2, Jurkat and HL60 leukemia cell lines in a dose-dependent manner, with GI50 values of 38.3 μM, 48.5 μM, 48.2 μM and 40.2 μM, respectively[2].
NCO-90 (0.1-100 μM; 72 h) induces apoptosis in S1T, MT-2, Jurkat and HL60 leukemia cell lines in a dose-dependent manner, with 100 μM NCO-90 increasing the proportion of annexin V-positive specific cells in the above cell lines to 52.5%, 34.7%, 42.3% and 66.5%, respectively[2].
NCO-90 (6 h) induces mitochondrial superoxide anion production in S1T, MT-2, Jurkat and HL60 leukemia cell lines[2].
NCO-90 (50 μM; 72 h) induces both caspase-dependent and caspase-independent cell death in S1T, MT-2, Jurkat and HL60 leukemia cell lines, as Z-VAD-FMK fails to inhibit NCO-90-induced cell death, apoptosis, DNA fragmentation or caspase activation[2].
NCO-90 (72 h) increases the level of acetylated histone H4K16 and promotes the degradation of nuclear p53 in S1T, MT-2, Jurkat and HL60 leukemia cell lines[2].
NCO-90 (25-100 μM; 24-48 h) induces autophagy and autophagosome accumulation in S1T, MT-2, Jurkat and HL60 leukemia cell lines, which is characterized by increased LC3-II levels, enhanced Cyto-ID fluorescence, and inhibited autophagosome degradation[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:S1T (HTLV-1-infected CD4+ T-cell line), MT-2 (HTLV-1-infected T-cell line), Jurkat (T-lineage acute lymphoblastic leukemia cell line), HL60 (acute myeloid leukemia cell line)
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Concentration:0.1-100 μM
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Incubation Time:72 h
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Result:Inhibited the growth of all four leukemic cell lines in a dose-dependent manner.
Achieved GI50 values of 38.3 μM for S1T cells, 48.5 μM for MT-2 cells, 48.2 μM for Jurkat cells, and 40.2 μM for HL60 cells.
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Cell Line:S1T, MT-2, Jurkat, HL60 leukemic cell lines
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Concentration:0.1-100 μM
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Incubation Time:72 h
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Result:Induced a dose-dependent increase in annexin V-positive cells across all four cell lines.
Generated 52.5% specific annexin V-positive cells in S1T cells, 34.7% in MT-2 cells, 42.3% in Jurkat cells, and 66.5% in HL60 cells at 100 μM.
Induced early-phase apoptosis (annexin V+/7-amino-actinomycin D- cells) and DNA fragmentation detected via TUNEL assay.
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Cell Line:S1T, MT-2, Jurkat, HL60 leukemic cell lines
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Concentration:25-100 μM (Cyto-ID and western blot assays); 50 μM (autophagic flux analysis)
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Incubation Time:48 h (Cyto-ID and western blot assays); 24 h (autophagic flux analysis)
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Result:Increased autophagy levels (measured by Cyto-ID fluorescence) and significantly increased LC3-II (lapidated LC3) levels across all four cell lines.
Induced LC3 translocation and inhibited autophagosome degradation shown by autophagic flux analysis.
Chemical Information
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CAS. Nr. 1382354-18-8
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Molecular Weight 332.40
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Formel C21H20N2O2
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SMILES
O=C(C1=C(NC2=CC(OCCC3=CC=CC=C3)=CC=C2)C=CC=C1)N
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Itoh Y. Drug Discovery Researches on Modulators of Lysine-Modifying Enzymes Based on Strategic Chemistry Approaches. Chem Pharm Bull (Tokyo). 2020;68(1):34-45. [Content Brief]
[2]. Kozako T, et al. Novel small molecule SIRT2 inhibitors induce cell death in leukemic cell lines. BMC Cancer. 2018;18(1):791. Published 2018 Aug 6. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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