推荐产品
等级
reagent grade
产品线
Vetec™
方案
≥98%
储存温度
2-8°C
SMILES字符串
NC(=O)NO
InChI
1S/CH4N2O2/c2-1(4)3-5/h5H,(H3,2,3,4)
InChI key
VSNHCAURESNICA-UHFFFAOYSA-N
基因信息
human ... RRM1(6240) , RRM2(6241) , RRM2B(50484)
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生化/生理作用
抗肿瘤剂。通过形成自由基硝基氧灭活核糖核苷还原酶,自由基硝基氧可结合到酶活性位点的酪氨酰自由基。这可阻断脱氧核苷酸的合成,从而抑制 DNA 合成,并且诱导细胞周期同步化或 S-期细胞死亡。
法律信息
Vetec is a trademark of Merck KGaA, Darmstadt, Germany
警示用语:
Danger
危险声明
危险分类
Muta. 1B - Repr. 2
储存分类代码
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Pediatrics, 132(4), 677-683 (2013-09-04)
In the BABY HUG trial, young children with sickle cell anemia randomized to receive hydroxyurea had fewer episodes of pain, hospitalization, and transfusions. With anticipated broader use of hydroxyurea in this population, we sought to estimate medical costs of care
Blood, 122(24), 3892-3898 (2013-09-21)
Recurrent and unpredictable episodes of vaso-occlusion are the hallmark of sickle cell disease. Symptomatic management and prevention of these events using the fetal hemoglobin-reactivating agent hydroxyurea are currently the mainstay of treatment. Discoveries over the past 2 decades have highlighted
British journal of haematology, 161(5), 688-694 (2013-04-12)
Givinostat, a histone-deacetylase inhibitor (HDACi), inhibits proliferation of cells bearing the JAK2 V617F mutation and has shown significant activity with good tolerability in patients with chronic myeloproliferative neoplasms (MPN). In this multicentre, open-label, phase II study, 44 patients with polycythaemia
Neoplasia (New York, N.Y.), 15(3), 263-280 (2013-03-13)
The non-histone chromatin binding protein high mobility group AT-hook 2 (HMGA2) is expressed in stem cells and many cancer cells, including tumor initiating cells, but not translated in normal human somatic cells. The presence of HMGA2 is correlated with advanced
The Journal of investigative dermatology, 135(2), 579-588 (2014-09-04)
The incidence of cutaneous squamous cell carcinoma (cSCC) is rising worldwide. We have examined the role of complement components in the progression of cSCC. Analysis of cSCC cell lines (n=8) and normal human epidermal keratinocytes (n=11) with whole transcriptome profiling
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