C0496
CRT0044876
≥98% (HPLC)
别名:
7-硝基-1H-吲哚-2-羧酸, 7-硝基吲哚-2-羧酸, NSC 69877
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关于此项目
经验公式（希尔记法）:
C9H6N2O4
化学文摘社编号:
分子量:
206.15
NACRES:
NA.25
PubChem Substance ID:
UNSPSC Code:
12352200
EC Number:
230-154-6
MDL number:
产品名称
CRT0044876, ≥98% (HPLC)
Quality Level
InChI key
BIUCOFQROHIAEO-UHFFFAOYSA-N
InChI
1S/C9H6N2O4/c12-9(13)6-4-5-2-1-3-7(11(14)15)8(5)10-6/h1-4,10H,(H,12,13)
SMILES string
OC(=O)c1cc2cccc([N+]([O-])=O)c2[nH]1
assay
≥98% (HPLC)
form
powder
solubility
DMSO: >20 mg/mL
storage temp.
room temp
Biochem/physiol Actions
APE1 的作用靶点是脱嘌呤核酸内切酶 (APE1)，抑制其 3′-磷酸二酯酶和 3′-磷酸酶活性——切除修复的基本步骤——即使在浓度高达 100 μg 时，对核酸内切酶 IV、BamH1 限制性内切酶或拓扑异构酶 I 的影响极小在非细胞毒性浓度下，CRT0044876 可增强几种 DNA 碱基靶向化合物的细胞毒性，使脱嘌呤位点蓄积。
CRT0044876 靶向 APE1 活性站点，抑制 3′-磷酸二酯酶和 3′-磷酸酶活性。
signalword
Danger
hcodes
Hazard Classifications
Eye Irrit. 2 - Resp. Sens. 1
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Faceshields, Gloves
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Junqiu Zhai et al.
Nucleic acids research, 45(6), e45-e45 (2016-12-08)
Human apurinic/apyrimidinic endonuclease/redox effector factor 1 (APE1) is an essential DNA repair protein. Herein, we demonstrate that avidin-oriented abasic site-containing DNA strands (AP-DNA) on the surface of silica coated magnetic nanoparticles (SiMNP) can selectively respond to APE1 while resist the
Jeroen E J Guikema et al.
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Antibody class switch recombination (CSR) occurs by an intrachromosomal deletion requiring generation of double-stranded breaks (DSBs) in switch-region DNA. The initial steps in DSB formation have been elucidated, involving cytosine deamination by activation-induced cytidine deaminase and generation of abasic sites
Base excision repair-inspired DNA motor powered by intracellular apurinic/apyrimidinic endonuclease.
Lidan Li et al.
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The transition of DNA nanomachines from test tubes to living cells would realize the ultimate goal of smart therapeutic dynamic DNA nanotechnology. The operation of DNA nanomachines in living cells remains challenging because it is difficult to utilize an endogenous
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Dihydroxy-1-selenolane (DHS) previously reported to exhibit radioprotective activity was investigated to understand its mechanism of action in CHO cells of epithelial origin. DHS pre-treatment at 25 μM for 16 h significantly protected CHO cells from radiation (4-11 Gy)-induced delayed mitotic cell death. Further
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