type
Grade II
assay
≥90% (HPLC)
mp
145-150 °C (lit.)
SMILES string
NC(=S)Nc1ccccc1
InChI
1S/C7H8N2S/c8-7(10)9-6-4-2-1-3-5-6/h1-5H,(H3,8,9,10)
InChI key
FULZLIGZKMKICU-UHFFFAOYSA-N
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signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 1 Oral - Skin Sens. 1
存储类别
6.1B - Non-combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges
法规信息
新产品
此项目有
Xiaolin Ai et al.
Scientific reports, 10(1), 614-614 (2020-01-19)
Toxicity to central nervous system tissues is the common side effects for radiotherapy of brain tumor. The radiation toxicity has been thought to be related to the damage of cerebral endothelium. However, because of lacking a suitable high-resolution vivo model
Xiangguo Shi et al.
Blood, 125(19), 2974-2984 (2015-03-18)
Isocitrate dehydrogenase 1 mutation (IDH1-R132H) was recently identified in acute myeloid leukemia with normal cytogenetics. The mutant enzyme is thought to convert α-ketoglutarate to the pathogenic 2-hydroxyglutarate (2-HG) that affects DNA methylation via inhibition of ten-eleven translocation 2. However, the
Warrick J Brewer et al.
Psychiatry research, 199(1), 8-11 (2012-04-17)
Reports suggesting that schizophrenia participants are more likely to be phenylthiocarbamide (PTC) non-tasters when compared to controls have recently been controversial. If supported, a genetic-based phenotypic variation in PTC taster status is implicated, suggesting a greater illness risk for those
Thomas Grau et al.
Antimicrobial agents and chemotherapy, 56(2), 1142-1145 (2011-11-23)
Ethionamide (ETH) is a second-line drug for the treatment of tuberculosis. As a prodrug, ETH has to be activated by EthA. ethA is controlled by its repressor EthR. 2-Phenylethyl-butyrate (2-PEB) inhibits EthR binding, enhances expression of EthA, and thereby enhances
Marco Venturin et al.
Journal of medical genetics, 51(7), 436-443 (2014-04-09)
Cardiovascular malformations have a higher incidence in patients with NF1 microdeletion syndrome compared to NF1 patients with intragenic mutation, presumably owing to haploinsufficiency of one or more genes included in the deletion interval and involved in heart development. In order
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