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S-adenosylhomocysteine and EZH2 inhibitor

Catalog No.A1905
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Sample solution is provided at 25 µL, 10mM.

Product Citations

1. Hardik Rameshchandra Mody. "Investigation of Micro-RNA-based Approaches to Overcome Epithelial-Mesenchymal Transition in Pancreatic Cancer" Ohio State University.2017.
2. Shi X, Tasdogan A, et al. "The abundance of metabolites related to protein methylation correlates with the metastatic capacity of human melanoma xenografts." Sci Adv. 2017 Nov 1;3(11):eaao5268. PMID:29109980
3. Lin B, Coleman JH, et al."Injury Induces Endogenous Reprogramming and Dedifferentiation of Neuronal Progenitors to Multipotency." Cell Stem Cell. 2017 Nov 20. pii: S1934-5909(17)30375-2. PMID:29174332
4. Bassem M. Shoucri, Eric S. Martinez, et al. "Retinoid X receptor activation alters the chromatin landscape to commit mesenchymal stem cells to the adipose lineage." Endocrinology. 2017 Jul.

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Chemical structure


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Biological Activity

Description 3-deazaneplanocin A (DZNeP), an analog of adenosine, is a competitive inhibitor of S-adenosylhomocysteine hydrolase with Ki of 50 pM.
Targets S-adenosylhomocysteine hydrolase          
IC50 50 pM (Ki)          


Cell experiment:[1]

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


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 experiment:[2]

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.


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.

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Chemical Properties

Cas No. 102052-95-9 SDF Download SDF
Synonyms DZNep, 3-Deazaneplanocin A,NSC 617989,NSC617989
Chemical Name (1S,2R,5R)-5-(4-aminoimidazo[4,5-c]pyridin-1-yl)-3-(hydroxymethyl)cyclopent-3-ene-1,2-diol
Canonical SMILES C1=CN=C(C2=C1N(C=N2)C3C=C(C(C3O)O)CO)N
Formula C12H24N4O3 M.Wt 262.26
Solubility Soluble in Water Storage Store at -20°C
Physical Appearance A crystalline solid Shipping Condition Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request
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.

Research Update

1. Cell-based proteome profiling using an affinity-based probe (AfBP) derived from 3-deazaneplanocin A (DzNep). Chem Asian J. 2013 Aug;8(8):1818-28. doi: 10.1002/asia.201300303. Epub 2013 Jun 7.
A novel probe derived from DzNep, an inhibitor of histone methylation, was used to identify potential cellular targets of DzNep in living mammalian cells.
2. 3-Deazaneplanocin A (DZNep), an inhibitor of S-adenosyl-methionine-dependent methyltransferase, promotes erythroid differentiation. J Biol Chem. 2014 Feb 3. [Epub ahead of print]
DZNep significantly induced erythroid differentiation in K562 cells and human primary erythroblasts derived from cord blood CD34-positive cells and reduced levels of ETO2 protein in K562 cells, which indicates DZNep induced erythroid differentiation may be partially attributed to its inhibition of ETO2 rather than EZH2 inhibition.
3. PRIMA-1, a Mutant p53 Reactivator, Restores the Sensitivity of TP53 Mutant-type Thyroid Cancer Cells to the Histone Methylation Inhibitor 3-Deazaneplanocin A (DZNep). J Clin Endocrinol Metab. 2014 Feb 10:jc20133147. [Epub ahead of print]
DZNep inhibited the growth of TP53 wild-type cells by promoting p53 protein accumulation and activating p53 pathways and failed to inhibit the growth of TP53 mutant-type cells, even though DZNep induced EZH2 depletion and H3K27me3 histone mark reduction were observed in both thyroid cancer cells. However, the combination of DZNep/PRIMA-1 restored the sensitivity of TP53 mutant-type cells to DZNep by reactivating p53.
5. Epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A inhibits the growth of cholangiocarcinoma cells. Oncol Rep. 2014 Feb;31(2):983-8. doi: 10.3892/or.2013.2922. Epub 2013 Dec 13.
DZNep depleted EZH2, inhibited histone lysine 27 trimethylation and suppressed proliferation partially through upregulation of p16INK4a and p17KIP1 in cholangiocarcinoma cell lines RBE and TFK-1 resulting in induced G1 arrest and apoptosis.


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].

[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.