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Merck

SML1414

Sigma-Aldrich

利普司他丁-1

>98% (HPLC), powder, ferroptosis inhibitor

别名:

N-[(3-氯苯基)甲基] 螺-[4H-喹喔啉-3,4′-哌啶 ]-2-胺, N-[(3-氯苯基)甲基]-螺 [哌啶-4,2′ (1′H)-喹喔啉]-3′-胺

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About This Item

经验公式(希尔记法):
C19H21ClN4
分子量:
340.85
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

产品名称

利普司他丁-1, >98% (HPLC)

品質等級

化驗

>98% (HPLC)

形狀

powder

顏色

white to light brown

溶解度

DMSO: 10 mg/mL, clear

儲存溫度

−20°C

SMILES 字串

ClC1=CC(CNC2=NC3=CC=CC=C3NC24CCNCC4)=CC=C1

InChI

1S/C19H21ClN4/c20-15-5-3-4-14(12-15)13-22-18-19(8-10-21-11-9-19)24-17-7-2-1-6-16(17)23-18/h1-7,12,21,24H,8-11,13H2,(H,22,23)

InChI 密鑰

YAFQFNOUYXZVPZ-UHFFFAOYSA-N

應用

Liproxstatin-1 在细胞活力试验和脂质过氧化测定中用作细胞死亡抑制剂。

生化/生理作用

Liproxstatin-1 是铁死亡的强效抑制剂。
Liproxstatin-1 是铁死亡的强效抑制剂,铁死亡是一种非凋亡形式的细胞死亡,以铁依赖性致死脂质活性氧簇 (ROS) 蓄积为特征。Liproxstatin-1 在人类细胞和缺血/再灌注诱导的小鼠组织损伤模型中抑制了铁死亡。谷胱甘肽过氧化物酶 4 (Gpx4) 的基因敲除已被证明可引起细胞死亡的铁死亡。Liproxstatin-1 能够抑制 Gpx4 基因敲除小鼠的铁死亡。

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Selenium utilization by GPX4 is required to prevent hydroperoxide-induced ferroptosis.
Ingold I, et al.
Cell, 172(3), 409-422 (2018)
Yilei Zhang et al.
Nature cell biology, 20(10), 1181-1192 (2018-09-12)
The roles and regulatory mechanisms of ferroptosis (a non-apoptotic form of cell death) in cancer remain unclear. The tumour suppressor BRCA1-associated protein 1 (BAP1) encodes a nuclear deubiquitinating enzyme to reduce histone 2A ubiquitination (H2Aub) on chromatin. Here, integrated transcriptomic
Tae-Jun Park et al.
Cell death & disease, 10(11), 835-835 (2019-11-07)
Ischaemic heart disease (IHD) is the leading cause of death worldwide. Although myocardial cell death plays a significant role in myocardial infarction (MI), its underlying mechanism remains to be elucidated. To understand the progression of MI and identify potential therapeutic
Masahiro Yoshida et al.
Nature communications, 10(1), 3145-3145 (2019-07-19)
Ferroptosis is a necrotic form of regulated cell death (RCD) mediated by phospholipid peroxidation in association with free iron-mediated Fenton reactions. Disrupted iron homeostasis resulting in excessive oxidative stress has been implicated in the pathogenesis of chronic obstructive pulmonary disease
Alejandra M Martinez et al.
FEBS open bio, 9(4), 582-593 (2019-04-16)
Ferroptosis is a form of regulated cell death that is driven by lethal accumulation of lipid peroxides upon inhibition of glutathione peroxidase 4 (GPx4). Deletion of the Gpx4 gene in mice revealed that neurons are sensitive to ferroptosis in vivo. However

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