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Merck
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文件

SML1948

Sigma-Aldrich

S1QEL1.1

≥98% (HPLC)

别名:

N1-(3-acetamidophenyl)-N2-(2-(4-methyl-2-(p-tolyl)thiazol-5-yl)ethyl)oxalamide, S1QEL

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About This Item

经验公式（希尔记法）:
C23H24N4O3S
CAS号:
897613-29-5
分子量:
436.53
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

100

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

運輸包裝

wet ice

儲存溫度

−20°C

SMILES 字串

CC1=C(CCNC(C(NC2=CC=CC(NC(C)=O)=C2)=O)=O)SC(C3=CC=C(C)C=C3)=N1

應用

S1QEL1.1 has been used as a reverse electron transport (RET)-induced mitochondrial (mito) reactive oxygen species (ROS) suppressor:
  • to investigate the role of mitochondrial-derived superoxide in triggering ferroptosis
  • to study the mechanism involved in the regulation of anti-fungal responses of macrophages against Aspergillus infection
  • in combination with mito-antioxidant to study their influence on mitochondria-derived H2O2 in cancer cells
  • to determine the effect of oxidative stress depletion on myoblast differentiation

生化／生理作用

S1QEL1.1 is a suppressor of mitochondrial respiratory complex I site IQ electron leak, suppressing superoxide and/or H2O2 production without altering oxidative phosphorylation. S1QEL1.1 had an IC50 values of 70 nM against superoxide-H2O2 production from site IQ. It decreased caspase activation in a in a cardiomyocyte cell model of ER stress and decreased ischemia-reperfusion injury in the Langendorff-perfused mouse heart model.
Suppressors of the site IQ electron leak (S1QEL)1.1 reduces cytokine secretion and fungicidal activity of macrophages infected with swollen A. fumigatus conidia by suppressing reverse electron transport (RET)-induced mitochondrial reactive oxygen species (ROS).

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

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Martin D Brand et al.
Cell metabolism, 24(4), 582-592 (2016-09-27)
Using high-throughput screening we identified small molecules that suppress superoxide and/or H
Takujiro Homma et al.
Archives of biochemistry and biophysics, 700, 108775-108775 (2021-01-26)
Ferroptosis is a type of iron-dependent, non-apoptotic cell death, which is typically induced by cysteine starvation or by the inhibition of glutathione peroxidase 4 (GPX4) activity with the accompanying elevation in lipid peroxidation product levels. Despite the central role of
Remi Hatinguais et al.
Frontiers in immunology, 12, 641495-641495 (2021-04-13)
Reactive Oxygen Species (ROS) are highly reactive molecules that can induce oxidative stress. For instance, the oxidative burst of immune cells is well known for its ability to inhibit the growth of invading pathogens. However, ROS also mediate redox signalling

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