855286
5-氨基尿嘧啶
98%
别名:
5-氨基-2,4-二羟基嘧啶, 5-氨基-2,4-嘧啶二醇
质量水平
方案
98%
表单
powder
mp
>300 °C (lit.)
SMILES字符串
NC1=CNC(=O)NC1=O
InChI
1S/C4H5N3O2/c5-2-1-6-4(9)7-3(2)8/h1H,5H2,(H2,6,7,8,9)
InChI key
BISHACNKZIBDFM-UHFFFAOYSA-N
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International journal of molecular sciences, 21(17) (2020-09-05)
Hypoxia-a hallmark of solid tumors-dramatically impairs radiotherapy, one of the most common anticancer modalities. The adverse effect of the low-oxygen state can be eliminated by the concomitant use of a hypoxic cell radiosensitizer. In the present paper, we show that
Asmaa M Fahim et al.
Current computer-aided drug design, 16(4), 486-499 (2019-07-11)
In this investigation, 2-cyano-N-(2,4-dioxo-1,2,3,4-tetrahydropyrimidin-5-yl) acetamide (3) reacts with dimethylformamide dimethyl acetal (DMF-DMA) to afford the corresponding (E)- 2-cyano-3-(dimethylamino)-N-(2,4-dioxo-1,2,3,4-tetrahydropyrimidin-5-yl)acrylam-ide (4) utilizing microwave irradiation. The condensation reactions of acrylamide derivative 4 with hydrazine derivatives obtain pyrazole derivatives 6a and 6b; respectively. The
F Cortés et al.
Experimental cell research, 148(2), 503-507 (1983-10-15)
Meristematic cells of Allium cepa were treated with 5-amino-uracil (5-AU) while incorporating 5-bromodeoxyuridine (BrdU) into DNA until complete inhibition of mitosis was obtained. The pattern of BrdU substitution in interphase nuclei detected by FPG technique in the cells so treated
D Suciu
The International journal of biochemistry, 23(11), 1245-1249 (1991-01-01)
1. The results of this study have contributed to the definition of three categories of chemical inhibitors of DNA replication in mammalian cells. 2. Inhibitors of replicon cluster initiation [4-nitroquinoline-N-oxide (4-NQO), etoposide (VP-16), teniposide (VM-26), amsacrine (m-AMSA), N-methyl-N'-nitro-N-nitrozoguanidine (MNNG), cis-Pt(II)diammine
A González-Fernández et al.
Mutation research, 149(2), 275-281 (1985-04-01)
Proliferating plant cells treated during the late S period with 5-aminouracil (AU), give the typical response that DNA-damaging agents induce, characterized by: an important mitotic delay, and a potentiation of the chromosome damage by caffeine post-treatment. The study of labelled
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