产品名称
S1QEL1.1, ≥98% (HPLC)
Quality Segment
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
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).
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
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable