3-deazaneplanocin A (DZNeP) HCl

目录号:S7120 别名: NSC 617989 HCl

3-deazaneplanocin A (DZNeP) HCl Chemical Structure

Molecular Weight(MW): 298.73

3-deazaneplanocin A (DZNeP)HCl,一种腺苷类似物,是竞争性S-adenosylhomocysteine hydrolase抑制剂,无细胞试验中Ki为50 pM。

规格 价格 库存 购买数量  
RMB 1184.96 现货
RMB 4661.96 现货


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  • H3K27me3 inhibitors inducing cell differentiation in the MDS-derived erythroid/myeloid cell line and primary MDS bone marrow cells via reducing H3K27me3 and increasing the expressions of PU.1 and its downstream genes. (a) ChIP experiments show a marked decrease in H3K27me3 at the PU.1 enhancer in the OCI-M2 cells treated with DZNep, compared with that in the cells treated with dimethyl sulfoxide (DMSO). (b) RT-PCRs show a significant increase in the expression of PU.1 mRNA in the OCI-M2 cells treated with DZNep in a dose-dependent manner. (c) Flow cytometric studies show that an increase in the expression of glycophorin A/B, a marker associated with erythroid differentiation, in the OCI-M2 cells treated with 0.25 μM of DZNep for 6 days. Red, isotype control; blue, no drug treatment (DMSO only); green, plus drug. (d) Increased PU.1 mRNA expression in primary MDS bone marrow cells treated with DZNep, compared with that in DMSO control. (e) Increased CD18 mRNA expression in primary MDS bone marrow cells treated with DZNep, compared with that in DMSO control. The primary bone marrow cells were from three cytogenetically normal MDS patients, which had marked trilineage dysplasia with varying numbers of blasts (case-1 with 10% blasts, case-2 with 4.6% blasts and case-3 with 11% blasts). The MDS bone marrow cells were treated with 1 μM DZNep or DMSO (control) for 24 h. The levels of PU.1 and CD18 mRNAs were measured by Q-RT-PCRs, while TBP mRNA was used for the internal normalization

    Leukemia, 2013, 1291-1300. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.

  • Photomicrographs illustrate immunofluorescent staining of NGAL in kidney tissues collected at 48 h after sham and IR injury with or without 3-DZNep administration in C57/black mice.

    Cell Death Dis, 2018, 9(11):1067. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.

  • EZH2 knockdown in pancreatic cancer cells inhibits cell migration and invasion. A, B. The migration and invasion ability of pancreatic cancer cell lines AsPC-1(A), CFPAC-1(B) with EZH2 knockdown. The scales represent 50μm. C, D. we examined the E-cadherin, ZEB1 and Snail expressions after using EZH2 RNAi, DZNeP and EPZ-6438. “*”represent P<0.05 when compared with control group.

    Oncotarget, 2016, 7(10):11194-207. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.

  • HSC‐T6 cells were treated with TGF‐β1 or TGF‐β1 plus DZNep. Real‐time PCR was performed to assess the mRNA expression level of α‐SMA at the three groups. HSC‐T6 cells were treated with TGF‐β1 or TGF‐β1 plus DZNep. Western blotting was carried out to assess the protein levels of EZH2 and α‐SMA at the three groups.

    J Cell Mol Med, 2017, 21(10):2317-2328. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.

  • (A) Representative Western blot images for the analysis of histone H3 repressive methylation marks in Cr(VI)-transformed cells. Cells were treated with vehicle control, a G9a inhibitor BIX01294 (2.5 μM) or an EZH2 inhibitor DZNeP (0.25 μM) for 72 h, and harvested for Western blot analysis. (B) Quantitation of effects of inhibition of G9a or EZH2 on soft agar colony and suspension culture sphere formation by Cr(VI)-transformed cells. Cells were treated with vehicle control, a G9a inhibitor BIX01294 (2.5 μM) or an EZH2 inhibitor DZNeP (0.25 μM) for 72 h, and harvested for soft agar colony and suspension culture sphere formation assay. Results are expressed as relative colony or sphere formation compared to vehicle-treated BEAS-2B-Cr(VI) cells (100%). Data are presented as mean ± SD (n=3). *p< 0.05, compared to vehicle-treated group. Similar results were obtained in two additional experiments.

    Toxicol Appl Pharmacol, 2018, 342:22-30. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.

  • Tumor samples from three distinct groups underwent immunohistochemistry for STAT3, p-STAT3 (Tyr705), EZH2, H3K27me3, MMP2, MMP6, E-cadherin, N-cadherin and Vimentin expression (scale bar, 100 μm; magnification, ×200).

    Int J Oncol, 2018, 52(4):1149-1164. 3-deazaneplanocin A (DZNeP) HCl purchased from Selleck.


Histone Methyltransferase抑制剂选择性比较


产品描述 3-deazaneplanocin A (DZNeP)HCl,一种腺苷类似物,是竞争性S-adenosylhomocysteine hydrolase抑制剂,无细胞试验中Ki为50 pM。
特性 Carbocyclic analog of adenosine, and acts as anti-tumor and anti-virus inhibitor of EZH2.
S-adenosylhomocysteine hydrolase [1]
50 pM(Ki)

3-Deazaneplanocin A (1.0 μM) 作用于人类急性髓细胞白血病OCI-AML3细胞,导致G0/G1期(58.5%)细胞积累显著增加,从而导致S期(35.2%)和G2/M期(6.3%)细胞数量减少。3-Deazaneplanocin A (1.0 μM) 作用于OCI-AML3 (~50%) 和 HL-60细胞(~50%),诱导细胞凋亡处理48小时,细胞剂量生长降低90%以上。3-Deazaneplanocin A作用于HL-60和OCI-AML3细胞及原代AML细胞,降低EZH2水平,抑制组蛋白H3在赖氨酸27位点的三甲基化。3-Deazaneplanocin A处理,诱导p16, p21, p27,和FBXO32,而降低cyclin E和HOXA9水平。500 nM 3-Deazaneplanocin A处理48小时,诱导HL-60细胞分化为CD11b+细胞近3倍。[2]3-Deazaneplanocin A作用于几种病毒类型,具有极好的活性。3-Deazaneplanocin A有效作用于L929细胞的水疱性口炎病毒,H.Ep-2的副流感病毒,vero细胞的牛痘和黄热病病毒,IC50分别为0.2, 3.6, 2.1 和 2.9 μg/mL。[3] 3-Deazaneplanocin A作用于美国 Leishmania (L mexicanaand L brasiliensis)株,具有强的抗什曼原病的疗效,平均ID50 为 96 ng/mL, 而即使浓度高达10 μg/mL,也不抑制一些 T. cruzi 和 T. rangeli 菌株。3-Deazaneplanocin A 按200 ng/mL剂量处理,4天后,通过前鞭毛体抑制 S-腺苷-L-3H-甲基蛋氨酸和3-胸苷渗透。3-Deazaneplanocin A按100 ng/mL剂量处理,消除约56%感染人巨噬细胞的L mexicana 和L brasiliensis 。[4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human HCT116 cells MWHDfZRwfG:6aXRCpIF{e2G7 Mlm2O|IhcA>? NVTafm5yS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUEOWMUG2JINmdGy|IHHzd4V{e2WmIHHzJIlvcGmkaYTpc44hd2ZiY3XscEBxem:uaX\ldoF1cW:wIHHmeIVzKDd{IHjyd{BjgSC|dXzmc5Jpd2SjbXnu[UBDKGG|c3H5MEBKSzVyPUCuNlYh|ryPLh?= MnH1NlYxOTB3OEW=
human MDA-MB-231 cells M{fqZ2N6fG:2b4jpZ:Kh[XO|YYm= MUm3NkBp NYOybYUxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUSDLV3CMVI{OSClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJINmdGxicILvcIln\XKjdHnvckBi\nSncjC3NkBpenNiYomgd5Vt\m:{aH;kZY1qdmViQjDhd5Nige,:jDDJR|UxRTBwMzFOwG0v M{n1VlI3ODFyNUi1
human SKHEP1 cells Ml\IR5l1d3SxeHnjxsBie3OjeR?= NGHnSpg4OiCq NEnUPHFEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUU0iHUEGgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iClZXzsJJBzd2yrZnXyZZRqd25iYX\0[ZIhPzJiaILzJIJ6KHO3bH\vdohw\GGvaX7lJGIh[XO|YYmsJGlEPTB;MD63NkDPxE1w NWCwNFBvOjZyMUC1PFU>
human SNU638 cells NWfPZlhbS3m2b4TvfIlkyqCjc4PhfS=> NX3NOGpKPzJiaB?= NY[1XHlxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW06XNkO4JINmdGy|IHHzd4V{e2WmIHHzJIlvcGmkaYTpc44hd2ZiY3XscEBxem:uaX\ldoF1cW:wIHHmeIVzKDd{IHjyd{BjgSC|dXzmc5Jpd2SjbXnu[UBDKGG|c3H5MEBKSzVyPUCuPVEh|ryPLh?= MnznNlYxOTB3OEW=
human A549 cells MV7DfZRwfG:6aXRCpIF{e2G7 MoXWO|IhcA>? NXPMeZBvS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSTV2OTDj[YxteyCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKGOnbHygdJJwdGmoZYLheIlwdiCjZoTldkA4OiCqcoOgZpkhe3WuZn;ybI9l[W2rbnWgRkBie3OjeTygTWM2OD1zLkSg{txONg>? NVq1ZXpwOjZyMUC1PFU>
human PC3 cells MWjDfZRwfG:6aXRCpIF{e2G7 NGjwZYc4OiCq MYjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDQR|Mh[2WubIOgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDj[YxtKHC{b3zp[oVz[XSrb36gZYZ1\XJiN{KgbJJ{KGK7IIP1cIZwemixZHHtbY5mKEJiYYPzZZktKEmFNUC9PU4{QSEQvF2u NHrabJozPjBzMEW4OS=>

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
EZH2 / H3K27me3; 

PubMed: 27223261     

DZNep decreased the expression of EZH2 and H3K27me3 in osteosarcoma cells in a dose-dependent manner.

Suz12 / H3K4me3 / H3K36me2; 

PubMed: 23001792     

A marked decrease in H3K27me3 levels in DZNep treated HT29 and SW480 cells compared to untreated controls. While the effect of DZNep was relatively specific for H3K27me3 inhibition in HT29 cells, DZNep also reduced H3K4me3 and H3K36me2 marks in SW480 cells. As reported by others, DZNep treatment caused a decrease in Suz12 protein levels in SW480 cells, whereas Suz12 protein level was unaffected in HT29 cells

TGFBR1 / TGFBR2 / Smad3; 

PubMed: 28373289     

DZNep decreased TGFBR1 and TGFBR2 but not Smad3 protein levels in a dose-dependent fashion in pancreatic cancer. 

EED / p21 / p-RB / p27 / p-CDC2; 

PubMed: 26579445     

Relative protein expression levels affected by DZNep in HCT116 cells. The cells were treated with 5 μmol/L DZNep for 72 h before being subjected to immunoblot assay.

HOXA6 / HOXB3 / HOXC4 / HOXD13; 

PubMed: 26812882     

Western blot analysis showed that both DZNep and EPZ005687 reduced EZH2 expression and H3K27me3 levels. 

p-JNK / JNK / p-p38 / p38 / p-ERK / ERK / p-IκB-α / IκB-α; 

PubMed: 28744016     

DZNep reduced MAPK pathway activation by IL-1β. Primary chondrocytes were treated or not with DZNep (1 µM) in the presence of IL-1β (1ng/mL) for 0min, 5min or 10min. Afer treatment, proteins were extracted, and levels of P-JNK and JNK, P-p38 and p38, P-ERK and ERK, P-IκB-α and IκB-α were determined in cells by western blotting.

27223261 23001792 28373289 26579445 26812882 28744016

PubMed: 27226494     

Representative confocal microscopy images of oocytes with DZNep or GSK343 treatment. The oocytes presented with a typical barrel-shaped spindle and well-aligned chromosomes on the metaphase plate not only in DZNep or GSK343 treated group but also in the control group. Spindle was recognized by α-tubulin (green) and DNA was recognized by PI (Propidium iodide, red). Scale bar = 4 μm.

F-actin / Paxillin; 

PubMed: 23826380     

DZNep treatment impaired actin cytoskeleton and caused cell shrinkage in MHCC97L cells. Stress fiber was stained with FITC-conjugated phalloidin and focal adhesions were stained with anti-paxillin antibody. Nuclei were counterstained with DAPI. Mock-treated cells showed organized bundles of stress fibers and well attached paxillin. DZNep-treated cells shrank and lost proper actin cytoskeleton network.

EZH2 / Mst1; 

PubMed: 24499724     

Co-IF staining of EZH2 and MST1 protein in C4–2 cells treated with DMSO or 5 µM DZNep for 72h in serum-fed growth conditions. Alexa Fluor 488 stained MST1 (green), Alexa Fluor 568 stained EZH2 (red), and DAPI stained cell nuclei (blue). Magnification is 20x. Micrographs are representative of multiple images from two independent experiments.

27226494 23826380 24499724
Growth inhibition assay
Cell viability; 

PubMed: 27223261     

DZNep inhibited osteosarcoma cell proliferation. Cells were treated with DZNep at the indicated concentrations. The relative sensitivity of each line to DZNep was determined by the MTT assay.

体内研究 3-Deazaneplanocin A在体内具有抗白血病活性。3-Deazaneplanocin A(1 mg/kg)处理移植AML细胞的小鼠,显著延长小鼠的生存期,与对照组(36天)相比,中位生存期为43天,与10 mg/kg pan-HDAC抑制剂(HDI)Panobinostat(中位生存期52天)联用可进一步提高治疗。[2]3-Deazaneplanocin A按8 mg/kg剂量处理牛痘病毒,在体内显示抗病毒活性。[3] 3-Deazaneplanocin A每天按0.5 到1.5 mg/kg剂量处理接种L. b. guyanensis的近交BALB/c小鼠,显著降低皮肤利什曼病的的感染。[4] 3-Deazaneplanocin A处理感染Ebola病毒的小鼠,显著诱导干扰-α 的产量增加。3-Deazaneplanocin A(感染后按2 mg/kg 剂量皮下注射)处理感染1000 pfu (30 000 LD50) 小鼠适应性EBO-Z 的小鼠,防止死亡。3-Deazaneplanocin A处理第1天降低平均血清病毒滴度,与安慰剂对照组相比,第2天降低100倍,第3天降低100000倍,产生的平均血清IFN-α水平在第2天为1420 pg/mL,第3天为1830 pg/mL。[5]




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AdoHcyase检测的反应混合物有0.5 mL, 50 mM 磷酸钾 (pH 7.6), 5 mM 二硫苏糖醇, 1 mM EDTA, 10%甘油,和酶。L-[8-14C]AdoHcy用作底物,包括5个单位小牛肠腺苷脱氨酶。加入100 μL 5 M甲酸终止反应,然后反应混合物加到SP-Sephadex C-25柱(0.8×2.5 cm)中,在 0.1 M 甲酸中平衡。每个试管使用0.5 mL 0.1 M甲酸进行漂洗。3.5 mL 0.1 M甲酸加到闪烁瓶中,从从柱中洗脱形成[14C]肌苷。加入10mL闪烁液后测定放射性。使用的酶量约为105 pU, 或75 ng纯化的酶。在37°C下,1分钟内形成1 pmol产物需要的酶量为一个单位。


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  • Cell lines: 人类急性髓细胞白血病HL-60细胞
  • Concentrations: ~1 μM
  • Incubation Time: 2 天
  • Method:

    使用指定浓度的3-Deazaneplanocin A 处理细胞48小时。 处理后,收集细胞,并用PBS洗涤两次, 约500个细胞接种到完全Methocult中,在37°C下含5% CO2的环境中培养7到10天。使用结晶紫进行细胞染色,通过溶解结晶紫染料在10%乙酸中,然后测量450nm处的吸光度,而测定相对细胞集落密度。

    (Only for Reference)


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  • Animal Models: 人类急性髓细胞白血病移植瘤HL-60
  • Formulation: --
  • Dosages: 1 mg/kg
  • Administration: 实验第7天开始,每周腹腔处理两次(周二-周四),持续2周
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 52 mg/mL (174.07 mM)
Water 52 mg/mL (174.07 mM)
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。


分子量 298.73


CAS号 120964-45-6
储存条件 powder
in solvent
别名 NSC 617989 HCl





质量 (mg) = 浓度 (mM) x 体积 (mL) x 分子量 (g/mol)


  • 质量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。




开始浓度 x 开始体积 = 最终浓度 x 最终体积


稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.


  • 连续稀释

  • 计算结果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):




注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2


质量 浓度 体积 分子量





  • * 必填项

Histone Methyltransferase Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID