NCH 51Histone deacetylase (HDAC) inhibitor CAS# 848354-66-5 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 848354-66-5 | SDF | Download SDF |
PubChem ID | 11395181 | Appearance | Powder |
Formula | C20H26N2O2S2 | M.Wt | 390.56 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | PTACH | ||
Solubility | DMSO : ≥ 100 mg/mL (256.04 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | S-[7-oxo-7-[(4-phenyl-1,3-thiazol-2-yl)amino]heptyl] 2-methylpropanethioate | ||
SMILES | CC(C)C(=O)SCCCCCCC(=O)NC1=NC(=CS1)C2=CC=CC=C2 | ||
Standard InChIKey | MDYDGUOQFUQOGE-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C20H26N2O2S2/c1-15(2)19(24)25-13-9-4-3-8-12-18(23)22-20-21-17(14-26-20)16-10-6-5-7-11-16/h5-7,10-11,14-15H,3-4,8-9,12-13H2,1-2H3,(H,21,22,23) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Histone deacetylase (HDAC) inhibitor. Inhibits growth of various cancer cells in vitro (EC50 = 1.1 - 9.1 μM). |
NCH 51 Dilution Calculator
NCH 51 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.5604 mL | 12.8021 mL | 25.6043 mL | 51.2085 mL | 64.0107 mL |
5 mM | 0.5121 mL | 2.5604 mL | 5.1209 mL | 10.2417 mL | 12.8021 mL |
10 mM | 0.256 mL | 1.2802 mL | 2.5604 mL | 5.1209 mL | 6.4011 mL |
50 mM | 0.0512 mL | 0.256 mL | 0.5121 mL | 1.0242 mL | 1.2802 mL |
100 mM | 0.0256 mL | 0.128 mL | 0.256 mL | 0.5121 mL | 0.6401 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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NCH 51 is a potent and novel inhibitor of histone deacetylase [1].
Histone deacetylases (HADC) are a series of enzymes that remove acetyl groups from an ε-N-acetyl lysine amino acid on a histone and make the histones to wrap the DNA more tightly, which prevent transcription.
NCH-51 inhibited cells growth with EC50 values of 2.1 and 4.4 μM in NCI-H460 cells and MDA-MB-231 cells, respectively. Also, it inhibited proliferation of various cancer cell lines with EC50 values of 1.1 - 9.5 μM [1][2]. In HCT 116 cells, NCH-51 increased levels of acetylated histone H4 and p21WAF1/CIP1 in dose-dependent way [2]. In a series of lymphoid malignant cell lines, NCH-51 induced apoptosis. In U266 cells, NCH-51 activated caspase-3, -8 and -9. Also, NCH-51 increased expression of p21 and reduced expression of anti-apoptotic molecules, such as survivin, bcl-w and c-FLIP. At the protein level, NCH-51 increased the levels of peroxiredoxin 1 and 2, glutathione S-transferase and reactive oxygen species (ROS) [3]. In HIV-1 latently infected-cells, NCH 51 increased histone hyperacetylation, reduced HDAC1 occupancy and recruited positive transcription factors at the HIV-1 promoter, which increased the expression of HIV-1 [4].
References:
[1]. Suzuki T, Hisakawa S, Itoh Y, et al. Identification of a potent and stable antiproliferative agent by the prodrug formation of a thiolate histone deacetylase inhibitor. Bioorg Med Chem Lett, 2007, 17(6): 1558-1561.
[2]. Suzuki T, Nagano Y, Kouketsu A, et al. Novel inhibitors of human histone deacetylases: design, synthesis, enzyme inhibition, and cancer cell growth inhibition of SAHA-based non-hydroxamates. J Med Chem, 2005, 48(4): 1019-1032.
[3]. Sanda T, Okamoto T, Uchida Y, et al. Proteome analyses of the growth inhibitory effects of NCH-51, a novel histone deacetylase inhibitor, on lymphoid malignant cells. Leukemia, 2007, 21(11): 2344-2353.
[4]. Victoriano AF, Imai K, Togami H, et al. Novel histone deacetylase inhibitor NCH-51 activates latent HIV-1 gene expression. FEBS Lett, 2011, 585(7): 1103-1111.
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Novel histone deacetylase inhibitor NCH-51 activates latent HIV-1 gene expression.[Pubmed:21402072]
FEBS Lett. 2011 Apr 6;585(7):1103-11.
Pharmacological manipulations to purge human immunodeficiency virus (HIV) from latent reservoirs have been considered as an adjuvant therapeutic approach to highly-active antiretroviral therapy for the eradication of HIV. Our novel histone deacetylase inhibitor NCH-51 induced expression of latent HIV-1 with minimal cytotoxicity. Using chromatin immunoprecipitation assays, we observed a reduction of HDAC1 occupancy, histone hyperacetylation and the recruitment of positive transcription factors at the HIV-1 promoter in latently infected-cells under the treatment with NCH-51. Mutation studies of the long terminal repeat (LTR) revealed NCH-51 mediated gene expression through the Sp1 sites. When Sp1 expression was knocked-down by small interfering RNA, the NCH-51-mediated activation of a stably integrated HIV-1 LTR was attenuated. Moreover, the Sp1 inhibitor mithramycin A abolished the effects of NCH-51.
Proteome analyses of the growth inhibitory effects of NCH-51, a novel histone deacetylase inhibitor, on lymphoid malignant cells.[Pubmed:17690692]
Leukemia. 2007 Nov;21(11):2344-53.
Recent reports showing successful inhibition of cancer and leukemia cell growth using histone deacetylase inhibitor (HDACi) compounds have highlighted the potential use of HDACi as anti-cancer agents. However, high incidence of toxicity and low stability in vivo were observed with hydroxamic acid-based HDACi such as suberoylanilide hydroxamic acid (SAHA), thus limiting its clinical applicability. In this study, we found that a novel non-hydroxamate HDACi NCH-51 could inhibit the cell growth of a variety of lymphoid malignant cells through apoptosis induction, more effectively than SAHA. Activation of caspase-3, -8 and -9, but not -7 was detected after the treatment with NCH-51. Gene expression profiles showed that NCH-51 and SAHA similarly upregulated p21 and downregulated anti-apoptotic molecules including survivin, bcl-w and c-FLIP. Proteome analysis using two-dimensional electrophoresis revealed that NCH-51 upregulated anti-oxidant molecules including peroxiredoxin 1 and 2 and glutathione S-transferase at the protein level. Interestingly, NCH-51 induced reactive oxygen species (ROS) after 8 h whereas SAHA continuously declined ROS. Pretreatment with an antioxidant, N-acetyl-L-cysteine, abolished the cytotoxicity of NCH-51. These findings suggest that NCH-51 exhibits cytotoxicity by sustaining ROS at the higher level greater than SAHA. This study indicates the therapeutic efficacy of NCH-51 and novel insights for anti-HDAC therapy.
Novel inhibitors of human histone deacetylases: design, synthesis, enzyme inhibition, and cancer cell growth inhibition of SAHA-based non-hydroxamates.[Pubmed:15715470]
J Med Chem. 2005 Feb 24;48(4):1019-32.
To find novel non-hydroxamate histone deacetylase (HDAC) inhibitors, a series of compounds modeled after suberoylanilide hydroxamic acid (SAHA) was designed and synthesized. In this series, compound 7, in which the hydroxamic acid of SAHA is replaced by a thiol, was found to be as potent as SAHA, and optimization of this series led to the identification of HDAC inhibitors more potent than SAHA. In cancer cell growth inhibition assay, S-isobutyryl derivative 51 showed strong activity, and its potency was comparable to that of SAHA. The cancer cell growth inhibitory activity was verified to be the result of histone hyperacetylation and subsequent induction of p21(WAF1/CIP1) by Western blot analysis. Kinetical enzyme assay and molecular modeling suggest the thiol formed by enzymatic hydrolysis within the cell interacts with the zinc ion in the active site of HDACs.