SML1948
S1QEL1.1
≥98% (HPLC), Mitochondrial complex I inhibitor, powder
Sinónimos:
N1-(3-acetamidophenyl)-N2-(2-(4-methyl-2-(p-tolyl)thiazol-5-yl)ethyl)oxalamide, S1QEL
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Fórmula empírica (notación de Hill):
C23H24N4O3S
Número CAS:
Peso molecular:
436.53
UNSPSC Code:
12352200
NACRES:
NA.77
Servicio técnico
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Permítanos ayudarleNombre del producto
S1QEL1.1, ≥98% (HPLC)
Quality Level
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
shipped in
wet ice
storage temp.
−20°C
SMILES string
CC1=C(CCNC(C(NC2=CC=CC(NC(C)=O)=C2)=O)=O)SC(C3=CC=C(C)C=C3)=N1
InChI
1S/C23H24N4O3S/c1-14-7-9-17(10-8-14)23-25-15(2)20(31-23)11-12-24-21(29)22(30)27-19-6-4-5-18(13-19)26-16(3)28/h4-10,13H,11-12H2,1-3H3,(H,24,29)(H,26,28)(H,27,30)
InChI key
BFNBJUBXXJKBFN-UHFFFAOYSA-N
Application
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
Biochem/physiol Actions
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.
Suppressor of mitochondrial respiratory complex I site IQ electron leak, suppressing superoxide and/or H2O2 production without altering oxidative phosphorylation
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).
Clase de almacenamiento
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_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
Hyewon Kong et al.
Science advances, 6(45) (2020-11-06)
Mitochondria-derived reactive oxygen species (mROS) are required for the survival, proliferation, and metastasis of cancer cells. The mechanism by which mitochondrial metabolism regulates mROS levels to support cancer cells is not fully understood. To address this, we conducted a metabolism-focused
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