方案
99%
表单
powder
mp
188-190 °C (dec.) (lit.)
SMILES字符串
OC(=O)c1cccnc1C(O)=O
InChI
1S/C7H5NO4/c9-6(10)4-2-1-3-8-5(4)7(11)12/h1-3H,(H,9,10)(H,11,12)
InChI key
GJAWHXHKYYXBSV-UHFFFAOYSA-N
基因信息
rat ... Gria1(50592), Grin2a(24409)
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应用
抑制葡萄糖合成。
警示用语：
Warning
危险声明
危险分类
Eye Irrit. 2 - STOT SE 3
靶器官
Respiratory system
储存分类代码
11 - Combustible Solids
WGK
WGK 3
个人防护装备
dust mask type N95 (US), Eyeshields, Gloves
Dorit Cohen-Carmon et al.
Molecular neurobiology, 57(3), 1768-1777 (2019-12-14)
Huntington's disease (HD) is a neurodegenerative late-onset genetic disorder caused by CAG expansions in the coding region of the Huntingtin (HTT) gene, resulting in a poly-glutamine (polyQ) expanded HTT protein. Considerable efforts have been devoted for studying HD and other
L Garcia-Salguero et al.
Archives internationales de physiologie, de biochimie et de biophysique, 99(3), 237-242 (1991-06-01)
The in vitro and in vivo effects of several different inhibitors of carbohydrate metabolism have been studied. The in vitro addition of 5-methoxyindole-2-carboxylic acid (MICA), pent-4-enoic acid, and quinolinic acid to the perfusion medium significantly inhibited liver gluconeogenesis in 48-hour-starved
F Moroni et al.
Journal of neurochemistry, 47(6), 1667-1671 (1986-12-01)
Quinolinic acid (QUIN), an excitotoxic tryptophan metabolite, has been identified and measured in human cerebrospinal fluid (CSF) using a mass-fragmentographic method. Furthermore, its content has been evaluated in frontal cortex obtained at autopsy from the cadavers of patients who died
Katherine R Leaver et al.
ACS chemical neuroscience, 3(2), 114-119 (2012-08-04)
There is evidence that excitotoxicity and prolonged microglial activation are involved in neuronal death in neurodegenerative disorders. Activated microglia express various molecules, including the translocator protein 18 kDa (TSPO; formerly known as the peripheral benzodiazepine receptor) on the outer mitochondrial
Jessica Huyet et al.
Cell chemical biology, 25(6), 666-676 (2018-03-27)
Phosphoribosyltransferases catalyze the displacement of a PRPP α-1'-pyrophosphate to a nitrogen-containing nucleobase. How they control the balance of substrates/products binding and activities is poorly understood. Here, we investigated the human adenine phosphoribosyltransferase (hAPRT) that produces AMP in the purine salvage
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