质量水平
方案
95%
表单
solid
mp
55.5-57 °C (lit.)
SMILES字符串
S=C=Nc1cccc2ccccc12
InChI
1S/C11H7NS/c13-8-12-11-7-3-5-9-4-1-2-6-10(9)11/h1-7H
InChI key
JBDOSUUXMYMWQH-UHFFFAOYSA-N
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应用
1-萘异硫氰酸酯（NITC）可用作硫脲基团的来源，合成杯[4]芳烃衍生物，作为阴离子受体。也可用于合成萘基取代的1,2,4-三唑和1,3,4-噻二唑。
警示用语：
Danger
危险分类
Acute Tox. 3 Oral - Eye Irrit. 2 - Resp. Sens. 1 - Skin Irrit. 2 - STOT SE 3
靶器官
Respiratory system
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
个人防护装备
Eyeshields, Faceshields, Gloves, type P2 (EN 143) respirator cartridges
法规信息
危险化学品
Synthesis and antimicrobial activity of some pyridyl and naphthyl substituted 1, 2, 4-triazole and 1, 3, 4-thiadiazole derivatives.
Zamani K, et al.
Turkish Journal of Chemistry, 28(1), 95-100 (2004)
Calix [4] arenes containing thiourea and amide moieties: neutral receptors towards ?, ?-dicarboxylate anions.
Liu SY, et al.
Organic & Biomolecular Chemistry, 2(11), 1582-1586 (2004)
Matthew Quinn et al.
American journal of physiology. Gastrointestinal and liver physiology, 302(1), G182-G193 (2011-10-08)
Cholestatic patients often present with clinical features suggestive of adrenal insufficiency. In the bile duct-ligated (BDL) model of cholestasis, the hypothalamic-pituitary-adrenal (HPA) axis is suppressed. The consequences of this suppression on cholangiocyte proliferation are unknown. We evaluated 1) HPA axis
Cen Guo et al.
Toxicology letters, 224(1), 93-100 (2013-10-15)
Alpha-naphthylisothiocyanate (ANIT) induces intra-hepatic cholestasis mixed with hepatocellular injury mainly by bile ductular damage. However, its direct effect on hepatic parenchymal cells (hepatocytes) is unclear. Sandwich-cultured rat hepatocytes (SCRH) were applied to clarify this question. Though cytotoxicity was not observed
James P Luyendyk et al.
Toxicological sciences : an official journal of the Society of Toxicology, 119(1), 233-243 (2010-10-27)
Alpha-naphthylisothiocyanate (ANIT)-induced cholestatic liver injury causes tissue factor (TF)-dependent coagulation in mice, and TF deficiency reduces ANIT-induced liver injury. However, the mechanism whereby TF contributes to hepatotoxicity in this model is not known. Utilizing pharmacological and genetic strategies, we evaluated
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