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质量水平
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
其他客户在看
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
Gilles J Guillemin et al.
Neuro-degenerative diseases, 2(3-4), 166-176 (2006-08-16)
The kynurenine pathway (KP) is a major route of L-tryptophan catabolism leading to production of several neurobiologically active molecules. Among them is the excitotoxin quinolinic acid (QUIN) that is known to be involved in the pathogenesis of several major inflammatory
Valéry Combes et al.
Trends in parasitology, 28(8), 311-319 (2012-06-26)
Homeostasis implies constant operational defence mechanisms, against both external and internal threats. Infectious agents are prominent among such threats. During infection, the host elicits the release of a vast array of molecules and numerous cell-cell interactions are triggered. These pleiomorphic
Gilles J Guillemin
The FEBS journal, 279(8), 1356-1365 (2012-01-18)
Over the last two decades, evidence for the involvement of quinolinic acid (QUIN) in neuroinflammatory diseases has been exponentially increasing. Within the brain, QUIN is produced and released by infiltrating macrophages and activated microglia, the very cells that are prominent
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