PZ0135
PHA-543613
≥98% (HPLC)
别名:
N- [(3R)-1-氮杂双环 [2.2.2] 辛-3-基] 呋喃 [2,3-c] 吡啶-5-甲酰胺
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关于此项目
经验公式（希尔记法）:
C15H17N3O2
化学文摘社编号:
分子量:
271.31
UNSPSC Code:
51111800
PubChem Substance ID:
NACRES:
NA.77
产品名称
PHA-543613, ≥98% (HPLC)
SMILES string
O=C(N[C@H]1CN2CC[C@H]1CC2)c3cc4ccoc4cn3
InChI
1S/C15H17N3O2/c19-15(12-7-11-3-6-20-14(11)8-16-12)17-13-9-18-4-1-10(13)2-5-18/h3,6-8,10,13H,1-2,4-5,9H2,(H,17,19)/t13-/m0/s1
InChI key
IPKZCLGGYKRDES-ZDUSSCGKSA-N
assay
≥98% (HPLC)
form
powder
color
white to off-white
solubility
DMSO: ≥20 mg/mL
storage temp.
room temp
Quality Level
Gene Information
human ... CHRNA7(1139)
Application
PHA-543613已被用于研究其在接受β-淀粉样蛋白（Aβ）25-35-治疗小鼠中识别记忆和神经血管偶联（NVC）反应中的作用。它还被用于研究其对小鼠中Aβ25-35诱导的受体改变和认知障碍的影响。
Biochem/physiol Actions
PHA-543613 是一种强效选择性 α⑦nAChR 激动剂。烟碱型乙酰胆碱受体是由烟碱激活的配体门控离子通道，在多组织中表达，在脑内有较高的功能表达。同源亚型 α7 是精神分裂症和阿尔茨海默病认知缺陷的潜在治疗靶点。PHA-543613 在 体外 （结合、钙通量、膜片钳）和 体内 （听觉门控、新物体识别）试验中均具有活性。
PHA-543613 是一种强效选择性 a7 nAChR 激动剂。
PHA-543613具有快速的脑部渗透特性。
Features and Benefits
该化合物在《受体分类和信号转导》手册的 乙酰胆碱受体（烟碱） 页面上有详细描述。想要浏览手册的其他页面， 请单击此处。
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Mark R Albertini et al.
Environmental and molecular mutagenesis, 49(9), 676-687 (2008-08-21)
The identification of specific lymphocyte populations that mediate tumor immune responses is required for elucidating the mechanisms underlying these responses and facilitating therapeutic interventions in humans with cancer. To this end, mutant hypoxanthine-guanine phosphoribosyltransferase (HPRT) deficient (HPRT-) T-cells were used
Effect of alpha-7 nicotinic acetylcholine receptor activation on beta-amyloid induced recognition memory impairment. Possible role of neurovascular function
Sadigh-Eteghad S, et al.
Acta Cirurgica Brasileira / Sociedade Brasileira Para Desenvolvimento Pesquisa em Cirurgia, 30(11), 736-742 (2015)
Stefan M Gold et al.
Journal of neuroinflammation, 5, 32-32 (2008-08-02)
Multiple sclerosis is a chronic inflammatory disease of the central nervous system with a pronounced neurodegenerative component. It has been suggested that novel treatment options are needed that target both aspects of the disease. Evidence from basic and clinical studies
Selective activation of $\alpha$7 nicotinic acetylcholine receptor by PHA-543613 improves A$\beta$25--35-mediated cognitive deficits in mice
Sadigh-Eteghad S, et al.
Neuroscience, 298(11), 81-93 (2015)
Cleber A Trujillo et al.
EMBO molecular medicine, 13(1), e12523-e12523 (2021-01-28)
Duplication or deficiency of the X-linked MECP2 gene reliably produces profound neurodevelopmental impairment. MECP2 mutations are almost universally responsible for Rett syndrome (RTT), and particular mutations and cellular mosaicism of MECP2 may underlie the spectrum of RTT symptomatic severity. No
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