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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
3-Deazaneplanocin is a highly potent inhibitor of S-adenosylhomocysteine hydrolase with Ki value of 0.05 nM [1].
3-Deazaneplanocin was synthesized as an inhibitor of S-adenosylhomocysteine hydrolase. It is an analog of adenosine and inhibits S-adenosylhomocysteine hydrolase through competing with the substrate, adenosine. 3-Deazaneplanocin was not so that potent in cell growth inhibition. 10 μM 3-Deazaneplanocin treatment resulted in moderate cell growth reduction in HL-60 cells. In HCC cell lines Huh1 and Huh7, 3-Deazaneplanocin inhibited growth and non-adherent sphere formation dose-dependently. It decreased the epithelial cell adhesion molecule EpCAMhigh fraction from 49.0% to 12.5% in Huh1 cells and from 44.4% to 11.6% in Huh7 cells. Moreover, in mice implanted with Huh7 cells, administration of 3-Deazaneplanocin suppressed tumor initiation and growth via directly affecting the growth and self-renewal of tumor-initiating cells [1, 2].
References:[1] Glazer R I, Hartman K D, Knode M C, et al. 3-Deazaneplanocin: a new and potent inhibitor of S-adenosylhomocysteine hydrolase and its effects on human promyelocytic leukemia cell line HL-60. Biochemical and biophysical research communications, 1986, 135(2): 688-694.[2] Chiba T, Suzuki E, Negishi M, et al. 3-Deazaneplanocin A is a promising therapeutic agent for the eradication of tumor-initiating hepatocellular carcinoma cells. International Journal of Cancer, 2012, 130(11): 2557-2567.
Cell lines
Human acute myeloid leukemia (AML) cell
Preparation method
The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months.
Reaction Conditions
100-750 nM; 24-72h
Applications
DZNep induced apoptosis in cultured and primary AML cells. DZNep exhausted EZH2 levels, and inhibits trimethylation of lysine 27 on histone H3 in the AML HL-60 and OCI-AML3 cells. DZNep induced the levels of p16, p21, p27, and FBXO32 after cyclin E and HOXA9 levels run out.
Animal models
Sprague-Dawley rats (120–140 g)
Dosage form
5μM DZNep for 24 h pre-treatment before experiment, orally taken with diets
DZNep significantly reduced EZH2 expression and activity, and it increased lipid accumulation, inflammatory molecules and microRNAs in non-alcoholic fatty liver disease (NAFLD) mouse model.
Other notes
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.
References:
1. Fiskus W1, Wang Y, Sreekumar A et al. Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor panobinostat against human AML cells. Blood. 2009 Sep 24;114(13):2733-43.
2. Vella S, Gnani D, Crudele A et al. EZH2 down-regulation exacerbates lipid accumulation and inflammation in vitro and in vivo NAFLD.Int J Mol Sci. 2013 Dec 12;14(12):24154-68.