Natural Products
- ChemFaces is a professional high-purity natural products manufacturer.
- Product Intended Use
- 1. Reference standards
- 2. Pharmacological research
- 3. Inhibitors
| Size /Price /Stock | 10 mM * 1 mL in DMSO / $58.6 / In-stock | Other Packaging | *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap |
| Size /Price /Stock | 10 mM * 100 uL in DMSO / Inquiry / In-stock 10 mM * 1 mL in DMSO / Inquiry / In-stock | Related Libraries |
| Description: | 1. Decitabine (5-Aza-2'-deoxycytidine) is a DNA methyltransferase inhibitor and an archetypal epigenetic drug for the therapy of myeloid leukemias. 2. Aza-2'-deoxycitidine exerts its anti-tumor effects in hepatocellular carcinoma(HCC) cells by inhibiting the telomerase activity. |
| Targets: | Telomerase | DNA Methyltransferase | p21 |
| Source: | |
| Solvent: | DMSO, Pyridine, Methanol, Ethanol, etc. |
| Storage: | Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C). Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour. Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com |
| After receiving: | The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling. |
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 4.3819 mL | 21.9096 mL | 43.8193 mL | 87.6386 mL | 109.5482 mL |
| 5 mM | 0.8764 mL | 4.3819 mL | 8.7639 mL | 17.5277 mL | 21.9096 mL |
| 10 mM | 0.4382 mL | 2.191 mL | 4.3819 mL | 8.7639 mL | 10.9548 mL |
| 50 mM | 0.0876 mL | 0.4382 mL | 0.8764 mL | 1.7528 mL | 2.191 mL |
| 100 mM | 0.0438 mL | 0.2191 mL | 0.4382 mL | 0.8764 mL | 1.0955 mL |
| Citation [1] Br J Haematol. 2014 Nov;167(3):356-65. | Safety and clinical activity of 5-aza-2'-deoxycytidine (decitabine) with or without Hyper-CVAD in relapsed/refractory acute lymphocytic leukaemia.[Pubmed: 25066676] |
| To test the safety and activity of 5-Aza-2'-deoxycytidine (decitabine) in patients with relapsed/refractory acute lymphocytic leukaemia (ALL), we conducted a phase 1 study with two parts: administering 5-Aza-2'-deoxycytidine alone or in combination with Hyper-CVAD (fractionated cyclophosphamide, vincristine, doxorubicin and dexamethasone alternating with high-dose methotrexate and cytarabine). Patients participated in either part of the study or in both parts sequentially. In the initial part, 5-Aza-2'-deoxycytidine was administered intravenously at doses of 10-120 mg/m(2) per d for 5 d every other week in cycles of 28 d. In the combination part, patients were treated on the first 5 d of Hyper-CVAD with intravenous 5-Aza-2'-deoxycytidine at 5-60 mg/m(2) per d. A total of 39 patients received treatment in the study: 14 in the first part only, 16 sequentially in both parts and 9 in the second part only. 5-Aza-2'-deoxycytidine was tolerated at all doses administered, and grade 3 or 4 toxic effects included non-life-threatening hepatotoxicity and hyperglycaemia. Induction of DNA hypomethylation was observed at doses of 5-Aza-2'-deoxycytidine up to 80 mg/m(2) . Some patients who had previously progressed on Hyper-CVAD alone achieved a complete response when 5-Aza-2'-deoxycytidine was added. Decitabine alone or given with Hyper-CVAD is safe and has clinical activity in patients with advanced ALL. | |
| Citation [2] J Biol Chem. 2015 Jun 17. | The DNA Methyltransferase DNMT1 and Tyrosine-Protein Kinase KIT Cooperatively Promote Resistance to 5-aza-2'-deoxycytidine (Decitabine) and Midostaurin (PKC412) in Lung Cancer Cell.[Pubmed: 26085088] |
| Lung cancer cells are sensitive to 5-Aza-2'-deoxycytidine (decitabine) or midostaurin (PKC412), since decitabine restores the expression of methylation-silenced tumor suppressor genes (TSGs), while PKC412 inhibits hyperactive kinase signaling, which are essential for cancer cell growth. Here, we demonstrated that resistance to 5-Aza-2'-deoxycytidine (decitabineR) or PKC412 (PKC412R) eventually results from simultaneously re-methylated DNA and re-activated kinase cascades. Indeed, both 5-Aza-2'-deoxycytidine and PKC412R displayed the upregulation of DNA methyltransferase DNMT1 and tyrosine-protein kinase KIT, the enhanced phosphorylation of KIT and its downstream effectors and the increased global and gene-specific DNA methylation with the downregulation of TSG epithelial cadherin CDH1. Interestingly, decitabineR and PKC412R had higher capability of colony-formation and wound-healing than parental cells in vitro, which were attributed to the hyperactive DNMT1 or KIT, since inactivation of KIT or DNMT1 reciprocally blocked 5-Aza-2'-deoxycytidine or PKC412R cell proliferation. Further, DNMT1 knockdown sensitized PKC412R cells to PKC412; conversely, KIT depletion synergized with 5-Aza-2'-deoxycytidine in eliminating decitabineR. Importantly, when engrafted into nude mice, decitabineR and PKC412R had faster proliferation with stronger tumorigenicity that was caused by the reactivated KIT kinase signaling and the further CDH1 silencing. These findings identify a functional crosstalk between KIT and DNMT1 in the development of drug resistance, implying the reciprocal-targeting of protein kinases and DNA methyltransferases as an essential strategy for durable responses in lung cancer. | |
| Citation [3] World J Gastroenterol. 2012 May 21; 18(19): 2334–2343. | Anti-tumor effect of 5-aza-2'-deoxycytidine by inhibiting telomerase activity in hepatocellular carcinoma cells[Pubmed: 22654424 ] |
| To investigate the effect of the demethylating reagent 5-Aza-2'-deoxycytidine(DAC) on telomerase activity in hepatocellular carcinoma(HCC) cell lines,SMMC-7721 and HepG2.METHODS:The related gene expression in cell lines was examined by real-time reverse transcription-polymerase chain reaction and Western blotting analysis.The telomerase activity was examined by telomeric repeat amplification protocol-enzyme-linked immunosorbent assay and DNA methylation was determined by methylation-specific polymerase chain reaction.RESULTS:The telomerase activity was significantly reduced in both cell lines treated with DAC,accompanied by downregulation of telomerase reverse transcriptase(hTERT).We also observed the effect of DAC on the methylation status of hTERT promoter and the expression of regulatory genes,such as c-myc,p15,p16,p21,E2F1,and WT1.The methylation status of hTERT promoter could be reversed in SMMC-7721 by DAC,but not in HepG2 cells.However,p16 expression could be reactivated by demethylation of its promoter,and c-Myc expression was repressed in both cell lines.Moreover,DAC could enhance the sensitivity to the chemotherapeutic agents,such as cisplatin,by induction of apoptosis of HCC cells.CONCLUSION:The DAC exerts its anti-tumor effects in HCC cells by inhibiting the telomerase activity. | |
| Citation [4] Nucleic Acids Res. 2014 Oct 29;42(19):e152. | Quantitative determination of decitabine incorporation into DNA and its effect on mutation rates in human cancer cells.[Pubmed: 25159616] |
| Decitabine (5-Aza-2'-deoxycytidine) is a DNA methyltransferase inhibitor and an archetypal epigenetic drug for the therapy of myeloid leukemias. The mode of action of 5-Aza-2'-deoxycytidine strictly depends on the incorporation of the drug into DNA. However, DNA incorporation and ensuing genotoxic effects of 5-Aza-2'-deoxycytidine have not yet been investigated in human cancer cell lines or in models related to the approved indication of the drug. Here we 5-Aza-2'-deoxycytidine a robust assay for the quantitative determination of 5-Aza-2'-deoxycytidine incorporation rates into DNA from human cancer cells. Using a panel of human myeloid leukemia cell lines we show appreciable amounts of 5-Aza-2'-deoxycytidine incorporation that closely correlated with cellular drug uptake. 5-Aza-2'-deoxycytidine incorporation was also detectable in primary cells from myeloid leukemia patients, indicating that the assay is suitable for biomarker analyses to predict drug responses in patients. Finally, we also used next-generation sequencing to comprehensively analyze the effects of 5-Aza-2'-deoxycytidine incorporation on the DNA sequence level. Interestingly, this approach failed to reveal significant changes in the rates of point mutations and genome rearrangements in myeloid leukemia cell lines. These results indicate that standard rates of 5-Aza-2'-deoxycytidine incorporation are not genotoxic in myeloid leukemia cells. |
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)