S4568
SCH 58261
≥98% (HPLC), adenosine receptor antagonist, solid
别名:
7-(2-苯乙基)-5-氨基-2-(2-呋喃基)-吡唑并-[4,3-e]-1,2,4-三唑并[1,5-c]嘧啶
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关于此项目
经验公式（希尔记法）:
C18H15N7O
化学文摘社编号:
分子量:
345.36
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
产品名称
SCH 58261, ≥98% (HPLC), solid
SMILES string
Nc1nc2n(CCc3ccccc3)ncc2c4nc(nn14)-c5ccco5
InChI key
UTLPKQYUXOEJIL-UHFFFAOYSA-N
InChI
1S/C18H15N7O/c19-18-22-16-13(11-20-24(16)9-8-12-5-2-1-3-6-12)17-21-15(23-25(17)18)14-7-4-10-26-14/h1-7,10-11H,8-9H2,(H2,19,22)
assay
≥98% (HPLC)
form
solid
color
off-white
solubility
DMSO: soluble >10 mg/mL, H2O: insoluble
Quality Level
相关类别
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
Sheikh F Ahmad et al.
Journal of neuroimmunology, 311, 59-67 (2017-08-16)
Autism is a complex heterogeneous neurodevelopmental disorder; previous studies have identified altered immune responses among individuals diagnosed with autism. An imbalance in the production of pro- and anti-inflammatory cytokines and transcription factors plays a role in neurodevelopmental behavioral and autism
Chih W Hsu et al.
Journal of biomedical science, 17, 4-4 (2010-01-16)
Caffeine, a nonselective adenosine A1 and A(2A) receptor antagonist, is the most widely used psychoactive substance in the world. Evidence demonstrates that caffeine and selective adenosine A(2A) antagonists interact with the neuronal systems involved in drug reinforcement, locomotor sensitization, and
Cristiani F Bortolatto et al.
Metabolic brain disease, 32(6), 1919-1927 (2017-08-11)
The aim of the present study was to investigate the effects of SCH58261, a selective adenosine A
Mushtaq A Ansari et al.
Molecular and cellular neurosciences, 82, 76-87 (2017-05-04)
Autism spectrum disorder (ASD) is neurodevelopmental disorders characterized by stereotypical repetitive behavior, impaired social interaction, and deficits in communication. The BTBR T
Irene Paterniti et al.
Journal of neuroinflammation, 8, 31-31 (2011-04-14)
Permanent functional deficits following spinal cord injury (SCI) arise both from mechanical injury and from secondary tissue reactions involving inflammation. Enhanced release of adenosine and glutamate soon after SCI represents a component in the sequelae that may be responsible for
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