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Merck
CN

N2255

Sigma-Aldrich

S-(4-硝基苄基)-6-硫肌苷

≥98%, Adenosine uptake inhibitor, solid

别名:

6-[(4-硝基苄基)硫代]-9-β-D-呋喃核糖基嘌呤, NBMPR, NBTI

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关于此项目

经验公式(希尔记法):
C17H17N5O6S
化学文摘社编号:
分子量:
419.41
EC 号:
MDL编号:
UNSPSC代码:
12352202
PubChem化学物质编号:
NACRES:
NA.77
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产品名称

S-(4-硝基苄基)-6-硫肌苷, ≥98%, solid

方案

≥98%

表单

solid

颜色

white

mp

187-190 °C (lit.)

溶解性

0.1 M HCl: slightly soluble
0.1 M NaOH: slightly soluble
DMSO: soluble
H2O: insoluble

储存温度

2-8°C

SMILES字符串

OC[C@H]1O[C@H]([C@H](O)[C@@H]1O)n2cnc3c(SCc4ccc(cc4)[N+]([O-])=O)ncnc23

InChI

1S/C17H17N5O6S/c23-5-11-13(24)14(25)17(28-11)21-8-20-12-15(21)18-7-19-16(12)29-6-9-1-3-10(4-2-9)22(26)27/h1-4,7-8,11,13-14,17,23-25H,5-6H2/t11-,13-,14-,17-/m1/s1

InChI key

DYCJFJRCWPVDHY-LSCFUAHRSA-N

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一般描述

S-(4-硝基苄基)-6-硫代肌苷(NBTI)属于S6取代的6-硫代嘌呤核苷家族,可调节动物体内的核苷转运机制。它能作为腺苷转运蛋白的一种配体。NBTI的结合位点位于脑毛细血管上。它可作为共价光亲和探针用于核苷转运。

生化/生理作用

中枢神经系统和血管平滑肌中平衡核苷转运蛋白(ENT),尤其是腺苷转运蛋白的抑制剂。
有效的腺苷摄取抑制剂

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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A Tandon et al.
Journal of neurochemistry, 60(6), 2124-2133 (1993-06-01)
The present study was initiated to examine the effects of ATP on acetylcholine (ACh) synthesis. The exposure of superior cervical ganglia to ATP increased ACh stores by 25%, but this effect was also evident with ADP, AMP, and adenosine, but
Methods Used in Adenosine Research, 268(1), 14-18 (2013)
Sebastián Alarcón et al.
Cells, 9(8) (2020-08-23)
Glioblastoma multiforme is one of the most malignant types of cancer. This is mainly due to a cell subpopulation with an extremely aggressive potential, called glioblastoma stem-like cells (GSCs). These cells produce high levels of extracellular adenosine which has been
Thomas Pleli et al.
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 45(6), 2516-2528 (2018-03-28)
Signaling of Gs protein-coupled receptors (GsPCRs) is accomplished by stimulation of adenylyl cyclase, causing an increase of the intracellular cAMP concentration, activation of the intracellular cAMP effectors protein kinase A (PKA) and Epac, and an efflux of cAMP, the function
Blood-brain barrier transport and brain metabolism of adenosine and adenosine analogs.
Pardridge WM, et al.
Journal of Pharmacology and Experimental Therapeutics, 268(1), 14-18 (1994)

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