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Merck
CN

P0122

Sigma-Aldrich

Pifithrin-μ

≥97% (HPLC), solid

别名:

2-苯乙炔磺胺, PFTμ

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About This Item

经验公式(希尔记法):
C8H7NO2S
CAS号:
分子量:
181.21
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77

质量水平

方案

≥97% (HPLC)

表单

solid

储存条件

desiccated

溶解性

DMSO: soluble >10 mg/mL, clear
H2O: insoluble

储存温度

2-8°C

SMILES字符串

NS(=O)(=O)C#Cc1ccccc1

InChI

1S/C8H7NO2S/c9-12(10,11)7-6-8-4-2-1-3-5-8/h1-5H,(H2,9,10,11)

InChI key

ZZUZYEMRHCMVTB-UHFFFAOYSA-N

应用

菲丝菌素-μ 已用于:
  • 处理小胶质细胞系以分析其对M1样和M2样表型的神经保护作用
  • 作为热休克蛋白(HSP)-70抑制剂用于处理转染的Marc-145细胞
  • 抑制热休克相关蛋白70(heat shock cognate,Hsc70)以阐明小鼠胚胎干细胞的热休克伴侣蛋白

生化/生理作用

Pifithrin- μ是p53结合和抗凋亡的抑制剂,其可直接抑制p53与线粒体以及Bcl-xL和Bcl-2蛋白的结合。
Pifithrin- μ是p53结合和抗凋亡的抑制剂,其可直接抑制p53与线粒体以及Bcl-xL和Bcl-2蛋白的结合。PFT μ可从致死γ -辐射诱导的细胞死亡中解救细胞。由于pifithrin- μ仅关闭p53-线粒体途径而不影响p53的转录功能,所以它比pifithrin-α 具有更优的性能。
在缺氧缺血(HI)诱发的新生儿脑病的临床前模型中,菲丝菌素μ(PFT-μ)具有防止细胞死亡的神经保护能力。它通过抑制分子伴侣热休克蛋白(HSP)-70与其底物的相互作用来抑制核因子ΙB(NF-ΙB)通路。

象形图

Exclamation mark

警示用语:

Warning

危险声明

危险分类

Acute Tox. 4 Oral

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

dust mask type N95 (US), Eyeshields, Gloves


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

The anti-inflammatory effects of the small molecule pifithrin-mu on BV2 microglia
Fleiss B, et al.
Developmental Neuroscience, 37(4-5), 363-375 (2015)
Tomoya Uchimura et al.
Frontiers in endocrinology, 10, 529-529 (2019-08-21)
Medaka (Oryzias latipes) are teleost fish with a XX/XY sex determination system. Recently, it was reported that high temperature (HT) induced the masculinization of XX medaka by increasing the levels of cortisol, a major glucocorticoid produced by interrenal cells in
Femke M Feringa et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 43(3), 347-358 (2022-12-15)
The presynaptic proteins MUNC18-1, syntaxin-1, and SNAP25 drive SNARE-mediated synaptic vesicle fusion and are also required for neuronal viability. Their absence triggers rapid, cell-autonomous, neuron-specific degeneration, unrelated to synaptic vesicle deficits. The underlying cell death pathways remain poorly understood. Here
Marisa Granato et al.
The international journal of biochemistry & cell biology, 79, 393-400 (2016-09-14)
Burkitt's lymphoma is an aggressive B cell lymphoma whose pathogenesis involves mainly c-Myc translocation and hyperexpression, in addition to antigen-independent BCR signaling and, in some cases, EBV infection. As result of BCR signaling activation, the PI3K/AKT/mTOR pathway results constitutively activated
Christophe Bignon et al.
Biomolecules, 9(1) (2018-12-29)
In this paper we review our recent findings on the different interaction mechanisms of the C-terminal domain of the nucleoprotein (N) of measles virus (MeV) NTAIL, a model viral intrinsically disordered protein (IDP), with two of its known binding partners

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