2. Cell Cycle/DNA Damage Epigenetics Apoptosis Autophagy Metabolic Enzyme/Protease
  3. Sirtuin Apoptosis Caspase Atg8/LC3 Autophagy Mitochondrial Metabolism
  4. 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.

For research use only. We do not sell to patients.

NCO-90

NCO-90 Chemical Structure

CAS No. : 1382354-18-8

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NCO-90 Related Antibodies

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Description

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[1][2].

IC50 & Target[2]

SIRT2

1.0 μM (IC50)

In Vitro

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.

NCO-90 Related Antibodies

Cell Viability Assay[2]

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)
Concentration: 0.1-100 μM
Incubation Time: 72 h
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.

Apoptosis Analysis[2]

Cell Line: S1T, MT-2, Jurkat, HL60 leukemic cell lines
Concentration: 0.1-100 μM
Incubation Time: 72 h
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.

Cell Autophagy Assay[2]

Cell Line: S1T, MT-2, Jurkat, HL60 leukemic cell lines
Concentration: 25-100 μM (Cyto-ID and western blot assays); 50 μM (autophagic flux analysis)
Incubation Time: 48 h (Cyto-ID and western blot assays); 24 h (autophagic flux analysis)
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.
Molecular Weight

332.40

Formula

C21H20N2O2
CAS No.
SMILES

O=C(C1=C(NC2=CC(OCCC3=CC=CC=C3)=CC=C2)C=CC=C1)N
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Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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NCO-90 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

NCO-901382354-18-8NCO90NCO 90SirtuinApoptosisCaspaseAtg8/LC3AutophagyMitochondrial MetabolismAutophagy-related 8| SIRT2caspaseNAD+mitochondrial superoxideautophagic cell deathSIRT1apoptosisacetyl lysineleukemic cellshuman SIRT2Inhibitorinhibitorinhibit

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