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Decitabine

Decitabine

产品编号 T1508   CAS 2353-33-5
别名: Dacogen, NSC 127716, 地西他滨, Deoxycytidine, 5-Aza-2'-deoxycytidine

Decitabine (Deoxycytidine) 是脱氧胞苷类似物,一种 DNA 甲基转移酶抑制剂,具有口服活性。Decitabine 具有抗肿瘤活性和抗代谢活性。Decitabine 诱导细胞周期阻滞和凋亡

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Decitabine Chemical Structure
Decitabine, CAS 2353-33-5
规格 价格/CNY 货期 数量
1 mg ¥ 159 现货
5 mg ¥ 335 现货
10 mg ¥ 535 现货
25 mg ¥ 980 现货
50 mg ¥ 1,550 现货
100 mg ¥ 2,490 现货
200 mg ¥ 3,460 现货
500 mg ¥ 4,950 现货
1 g ¥ 6,590 现货
1 mL * 10 mM (in DMSO) ¥ 397 现货
产品目录号及名称: Decitabine (T1508)
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纯度: 99.87%
纯度: 99.17%
纯度: 99.14%
纯度: 99%
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天然产物信息
生物活性
化学信息
存储 & 溶解度
参考文献
产品描述 Decitabine (Deoxycytidine) is a deoxycytidine analog, a DNA methyltransferase inhibitor with oral activity. Decitabine has antitumor activity and antimetabolic activity. Decitabine induces cell cycle arrest and apoptosis.
体外活性 方法:人急性白血病细胞 molt4 用 Decitabine (0.00625-100 μM) 处理 24-96 h,使用 CCK-8 方法检测细胞增殖。
结果:Decitabine 以剂量和时间依赖的方式抑制 molt4 细胞的增殖,处理 72 h 和 96 h 的 IC50 分别为 84.461 μM 和 10.113 μM。[1]
方法:人 BCP-ALL 细胞 SEM 和 RS4;11 用 Decitabine (1000 nM) 处理 72 h,使用 Flow Cytometry 检测细胞周期情况。
结果:Decitabine 引起 SEM 细胞中 G0/G1 停滞。RS4;11 的细胞周期不受 Decitabine 的影响。[2]
体内活性 方法:为检测体内抗肿瘤活性,将 Decitabine (0.4 mg/kg) 腹腔注射给携带 ALL 肿瘤 SEM-ffluc-GFP 或 RS4;11-ffluc-GFP 的 NSG 小鼠,每天一次,持续三十天。
结果:Decitabine 显著延迟了 SEM-ffluc-GFP 和 RS4-ffluc 衍生的异种移植物模型中的白血病细胞增殖。[2]
方法:为检测体内抗肿瘤活性,将 Decitabine (0.8 mg/kg) 腹腔注射给携带人胆管癌肿瘤 TFK-1 的 Balb-c nu/nu 小鼠,每天一次,持续十四天。
结果:在 TFK-1 小鼠异种移植物中,Decitabine 延缓了荷瘤小鼠的肿瘤生长并提高了其存活率。[3]
激酶实验 The rate of DNA synthesis was measured by the incorporation of radioactive thymidine into DNA. HL-60 (5 × 10^3 cells/ml) and KG1a cells (10^4 cells/ml) were suspended in 2 ml RPMI medium containing 10% fetal serum in 6-well (35 mm diameter) dishes and incubated with different concentrations of corresponding drugs for 48 h (drugs were added simultaneously). At 48 h, 0.5 μCi [3H] thymidine (6.7 Ci/mmol) was added to each well and incubated for an additional 24 h. The cells were placed on GF/C glass fiber filters (2.4 cm diameter), washed with cold 0.9% NaCl, 5% cold trichloroacetic acid and ethanol. The filters containing the DNA were then dried, placed in EcoLite scintillation liquid (ICN) and the radioactivity measured using scintillation counter. The IC50 is defined as the concentration of drug that inhibits by 50% the DNA synthesis of the leukemic cell lines from the dose-response curve [1].
细胞实验 For cell cycle analysis, KARPAS-299 cells were incubated for 24 h with 1 μM of 5-aza-CdR in RPMI and grown for 4 days in fresh RPMI only. Then, 105–106 cells were suspended in 500 μl PI-buffer (0.1% Na–citrate dihydrate, 0.1% Triton X-100, 0.1% RNAse (DNAse free) in PBS). Propidium–iodide (ROTH, dissolved in PBS) was added to a concentration of 10 μg/ml and the cells were incubated for 30 min at 37 °C. The analysis was performed on a flow cytometer using the BD FACS Diva Software. Three independent samples of 5-aza-CdR treated and PBS controls were analyzed. Descriptive statistics for analysis are reported as mean ± SEM [4].
动物实验 For xenografts, NOD.CB17-Prkdc?scid/NCrHsd (NOD/SCID, Harlan Laboratories) mice were used. KARPAS-299 human cells were grown as described above, dissolved in sterile PBS to a concentration of 1×107 cells/ml and inoculated subcutaneously (1×10^6 cells/injection) into the right and left flanks of the mice. Tumor range was followed measuring tumor length and tumor width with a calliper. Mice weighed approximately 25 g at the beginning of the therapy. 5-Aza-CdR was dissolved in sterile PBS and was administered intraperitoneally (i.p.). Each mouse received 2.5 mg/kg/mouse per treatment. Control mice were administered 100 μl of sterile PBS. Therapies were adjusted regarding start and duration of the treatment in order to obtain optimal treatment procedures. In schedule A, three mice were treated with 5-aza-CdR 11 days after inoculation, when tumor size was approximately 1 cm2. The control group contained two mice. The mice received 5-aza-CdR or PBS every day for eight days. In schedule B, two mice were treated with 5-aza-CdR three days after inoculation and three mice five days after inoculation when tumors were not or just palpable. 5-Aza-CdR was administered every other day for five times to each mouse. The control group contained two mice [4].
别名 Dacogen, NSC 127716, 地西他滨, Deoxycytidine, 5-Aza-2'-deoxycytidine
化合物与蛋白结合的复合物

T1508_1

SAMHD1 HD domain bound to decitabine triphosphate

分子量 228.21
分子式 C8H12N4O4
CAS No. 2353-33-5

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

H2O: 11.4 mg/mL (50 mM)

DMSO: 55 mg/mL (241.01 mM)

溶液配制表

可选溶剂 浓度 体积 质量 1 mg 5 mg 10 mg 25 mg
H2O / DMSO 1 mM 4.3819 mL 21.9096 mL 43.8193 mL 109.5482 mL
5 mM 0.8764 mL 4.3819 mL 8.7639 mL 21.9096 mL
10 mM 0.4382 mL 2.191 mL 4.3819 mL 10.9548 mL
20 mM 0.2191 mL 1.0955 mL 2.191 mL 5.4774 mL
50 mM 0.0876 mL 0.4382 mL 0.8764 mL 2.191 mL
DMSO 100 mM 0.0438 mL 0.2191 mL 0.4382 mL 1.0955 mL

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TargetMol Library Books参考文献

1. Zhang G, et al. Decitabine inhibits the proliferation of human T-cell acute lymphoblastic leukemia molt4 cells and promotes apoptosis partly by regulating the PI3K/AKT/mTOR pathway. Oncol Lett. 2021 May;21(5):340. 2. Roolf C, et al. Decitabine demonstrates antileukemic activity in B cell precursor acute lymphoblastic leukemia with MLL rearrangements. J Hematol Oncol. 2018 May 4;11(1):62. 3. Wang B, et al. Decitabine inhibits the cell growth of cholangiocarcinoma in cultured cell lines and mouse xenografts. Oncol Lett. 2014 Nov;8(5):1919-1924. 4. Hassler MR, et al. Antineoplastic activity of the DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine in anaplastic large cell lymphoma. Biochimie. 2012 Nov;94(11):2297-307. 5. Terse P, et al. Subchronic oral toxicity study of decitabine in combination with tetrahydrouridine in CD-1 mice. Int J Toxicol. 2014 Mar-Apr;33(2):75-85. 6. Yu J, et al. DNA methyltransferase expression in triple-negative breast cancer predicts sensitivity to decitabine. J Clin Invest. 2018 Jun 1;128(6):2376-2388. 7. Thieulent C, Hue E, Sutton G, et al. Identification of antiviral compounds against equid herpesvirus-1 using real-time cell assay screening: efficacy of decitabine and valganciclovir alone or in combination[J]. Antiviral Research. 2020: 104931 8. Chen G, Fan X, Li Y, et al. Promoter aberrant methylation status of ADRA1A is associated with hepatocellular carcinoma[J]. Epigenetics. 2020: 1-18. 9. Fan X, Li Y, Yi X, et al. Epigenome-wide DNA methylation profiling of portal vein tumor thrombosis (PVTT) tissues in hepatocellular carcinoma patients[J]. Neoplasia. 2020, 22(11): 630-643. 10. Zhang M, Wang L, Yue Y, et al. ITPR3 Facilitates Tumor Growth, Metastasis and Stemness by Inducing the NF-ĸB/CD44 Pathway in Urinary Bladder Carcinoma[J]. Journal of Experimental & Clinical Cancer Research. 2021, 40(1): 1-20

TargetMol Library Books文献引用

1. Chen Y, Li K, Gong D I, et al. ACLY: A biomarker of recurrence in breast cancer. Pathology-Research and Practice. 2020, 216(9): 153076 2. Zhang M, Wang L, Yue Y, et al. ITPR3 Facilitates Tumor Growth, Metastasis and Stemness by Inducing the NF-ĸB/CD44 Pathway in Urinary Bladder Carcinoma. Journal of Experimental & Clinical Cancer Research. 2021, 40(1): 1-20 3. Fan X, Li Y, Yi X, et al Epigenome-wide DNA methylation profiling of portal vein tumor thrombosis (PVTT) tissues in hepatocellular carcinoma patients. Neoplasia. 2020, 22(11): 630-643 4. Thieulent C, Hue E, Sutton G, et al. Identification of antiviral compounds against equid herpesvirus-1 using real-time cell assay screening: efficacy of decitabine and valganciclovir alone or in combination. Antiviral Research. 2020: 104931 5. Zhou H, Ning Y, Zeng G, et al. Curcumin promotes cell cycle arrest and apoptosis of acute myeloid leukemia cells by inactivating AKT. Oncology Reports. 2021, 45(4): 1-1. 6. Fan X, Guo H, Dai B, et al. The association between methylation patterns of DNAH17 and clinicopathological factors in hepatocellular carcinoma. Cancer Medicine. 2019 Jan;8(1):337-350 7. Łagosz-Ćwik K, Melnykova M, Nieboga E, et al.Mapping of DNA methylationsensitive cellular processes in gingival and periodontal ligament fibroblasts in the context of periodontal tissue homeostasis.Frontiers in Immunology.2023, 14. 8. He S, Li Y, Shi X, et al.DNA methylation landscape reveals LIN7A as a decitabine-responsive marker in patients with t (8; 21) acute myeloid leukemia.Clinical Epigenetics.2023, 15(1): 1-13. 9. He S, Li Y, Wang L, et al.DNA methylation landscape reveals GNAS as a decitabine-responsive marker in patients with acute myeloid leukemia.Neoplasia.2024, 49: 100965. 10. Hoang N M, Liu Y, Bates P D, et al.Targeting DNMT3A-mediated oxidative phosphorylation to overcome ibrutinib resistance in mantle cell lymphoma.Cell Reports Medicine.2024
Karanjin PG-11047 2HCl SF5 Bendamustine VAS 3947 ONC212 PHT-427 Mitoguazone

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该产品包含在如下化合物库中:
抗癌活性化合物库 抗癌临床化合物库 药物功能重定位化合物库 抗癌药物库 EMA 上市药物库 抗癌上市药物库 抑制剂库 天然产物库 肝脏毒性化合物库 干细胞分化化合物库

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母液配置方法:2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL), 如您需要配置的浓度超过该产品的溶解度,请先与我们联系。

体内配方的制备方法:取 50 μL DMSO 主液,加入 300 μL PEG300, 混匀澄清,再加 50 μL Tween 80,混匀澄清,再加 600 μL ddH2O, 混匀澄清。

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Keywords

Decitabine 2353-33-5 Apoptosis Cell Cycle/Checkpoint Chromatin/Epigenetic DNA Damage/DNA Repair Nucleoside Antimetabolite/Analog DNA Methyltransferase DNMTs NSC-127716 Dacogen inhibit NSC 127716 地西他滨 DNA MTases NSC127716 Deoxycytidine 5-Aza-2'-deoxycytidine Inhibitor inhibitor

 

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