T27006
2-噻吩甲酰三氟丙酮
99%
别名:
4,4,4-三氟-1-(2-噻吩基)-1,3-丁二酮, TTA（萃取剂）, TTB, TTFA
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关于此项目
经验公式（希尔记法）:
C8H5F3O2S
化学文摘社编号:
分子量:
222.18
UNSPSC Code:
12352100
NACRES:
NA.22
PubChem Substance ID:
EC Number:
206-316-7
Beilstein/REAXYS Number:
168645
MDL number:
产品名称
2-噻吩甲酰三氟丙酮, 99%
InChI key
TXBBUSUXYMIVOS-UHFFFAOYSA-N
InChI
1S/C8H5F3O2S/c9-8(10,11)7(13)4-5(12)6-2-1-3-14-6/h1-3H,4H2
SMILES string
FC(F)(F)C(=O)CC(=O)c1cccs1
assay
99%
bp
96-98 °C/8 mmHg (lit.)
mp
40-44 °C (lit.)
storage temp.
2-8°C
Quality Level
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Application
用于锕系元素和镧系元素的测定。
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
233.6 °F - closed cup
flash_point_c
112 °C - closed cup
ppe
dust mask type N95 (US), Eyeshields, Gloves
Vladimir A Kokorekin et al.
Molecules (Basel, Switzerland), 25(18) (2020-09-17)
In this article, we demonstrate how an original effective "metal-free" and "chromatography-free" route for the synthesis of 3-thiocyanatopyrazolo[1,5-a]pyrimidines has been developed. It is based on electrooxidative (anodic) C-H thiocyanation of 5-aminopyrazoles by thiocyanate ion leading to 4-thiocyanato-5-aminopyrazoles (stage 1, yields
Jeffery, G.H. et al.
Vogel's Textbook of Quantitative Chemical Analysis, 170-170 (1989)
David González-Aragón et al.
Biochemical pharmacology, 73(3), 427-439 (2006-11-25)
Dicoumarol, a competitive inhibitor of NAD(P)H:quinone oxidoreductase 1 (NQO1), increases intracellular superoxide and affects cell growth of tumor cells. This work was set to establish a mechanistic link between dicoumarol, superoxide and cell cycle alterations in HL-60 cells. Using ES936
Tao Huang et al.
Journal of cellular biochemistry, 107(5), 973-983 (2009-06-06)
Gap junctional intercellular communication (GJIC) plays a critical role in the control of multiple cell behavior as well as in the maintenance of tissue and organ homeostasis. However, mechanisms involved in the regulation of gap junctions (GJs) have not been
Sashi Nadanaciva et al.
Toxicology in vitro : an international journal published in association with BIBRA, 21(5), 902-911 (2007-03-10)
Mitochondrial dysfunction has been shown to be a pharmacotoxicological response to a variety of currently-marketed drugs. In order to reduce attrition due to mitochondrial toxicity, high throughput-applicable screens are needed for early stage drug discovery. We describe, here, a set
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