B7263
N-叔丁基-α-苯基硝酮
≥98% (GC), cyclooxygenase-2 inhibitor, powder
别名:
N-苯亚甲基-叔丁胺-N-氧化物, PBN, 苯基·N-叔丁基硝酮
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关于此项目
线性分子式:
C6H5CH=N(O)C(CH3)3
化学文摘社编号:
分子量:
177.24
Beilstein:
2044028
EC 号:
MDL编号:
UNSPSC代码:
12352202
PubChem化学物质编号:
NACRES:
NA.77
产品名称
N-叔丁基-α-苯基硝酮, ≥98% (GC)
方案
≥98% (GC)
表单
powder
颜色
white
mp
73-74 °C (lit.)
溶解性
DMSO: soluble
储存温度
−20°C
SMILES字符串
CC(C)(C)[N+](\[O-])=C\c1ccccc1
InChI
1S/C11H15NO/c1-11(2,3)12(13)9-10-7-5-4-6-8-10/h4-9H,1-3H3/b12-9-
InChI key
IYSYLWYGCWTJSG-XFXZXTDPSA-N
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应用
N-叔丁基-α-苯基硝酮已用于：
- 用作Dneasy Blood&血液组织缓冲液组分，以保留从人类非致瘤性上皮性乳腺癌（MCF10A）细胞中提取的氧化态DNA
- 用作微胶质（MG）细胞系活性氧(ROS)自由基清除试剂
- 衰减不稳定口腔鳞状细胞癌（GU-OSCC）中的成纤维细胞衰老
生化/生理作用
N-叔丁基-α-苯基硝酮（PBN）是一种常用的自由基自旋捕获剂。
N-叔丁基-α-苯基硝酮（PBN）是一种常用的自由基自旋捕获剂。已有研究表明，PBN具有自由基清除活性以及抑制环氧合酶-2活性的能力，因此，它可以减少兔皮质中栓子诱导的脑微梗死的数量并预防肿瘤形成。据报道，PBN可抑制诱导型一氧化氮合酶（iNOS），从而防止一氧化氮（NO）过量产生。 PBN以100 mg/kg腹腔注射，可减少氟替尔诱导大鼠癫痫持续状态中的黑质网状部坏死。它可以预防癫痫动物模型中某些类型的创伤后致癫痫事件。已有研究发现，大鼠的PBN致死剂量约为100 mg/100 g体重（0.564 mmol/100Å g）。
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)
Genome-wide mapping of 8-oxo-7, 8-dihydro-2?-deoxyguanosine reveals accumulation of oxidatively-generated damage at DNA replication origins within transcribed long genes of mammalian cells
Amente S, et al.
Nucleic Acids Research, 47(1), 221-236 (2018)
Progression of genotype-specific oral cancer leads to senescence of cancer-associated fibroblasts and is mediated by oxidative stress and TGF-beta
Hassona Y, et al.
Carcinogenesis, 34(6), 1286-1295 (2013)
microRNA-34a-mediated down-regulation of the microglial-enriched triggering receptor and phagocytosis-sensor TREM2 in age-related macular degeneration
Bhattacharjee S, et al.
Testing, 11(3), e0150211-e0150211 (2016)
Jian-Jun Wen et al.
Journal of the American College of Cardiology, 55(22), 2499-2508 (2010-06-01)
The purpose of this study was to determine the pathological importance of oxidative stress-induced injurious processes in chagasic heart dysfunction. Trypanosoma cruzi-induced inflammatory pathology and a feedback cycle of mitochondrial dysfunction and oxidative stress may contribute to Chagas disease. Sprague-Dawley
June Yowtak et al.
Pain, 152(4), 844-852 (2011-02-08)
Although both a loss of spinal inhibitory neurotransmission and the involvement of oxidative stress have been regarded as important mechanisms in the pathogenesis of pain, the relationship between these 2 mechanisms has not been studied. To determine whether reactive oxygen
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