SML0177
AUDA
≥98% (HPLC)
别名:
12-[[(tricyclo[3.3.1.13,7]dec-1-ylamino)carbonyl]amino]-dodecanoic acid
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关于此项目
经验公式（希尔记法）:
C23H40N2O3
化学文摘社编号:
分子量:
392.58
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
产品名称
AUDA, ≥98% (HPLC)
InChI
1S/C23H40N2O3/c26-21(27)10-8-6-4-2-1-3-5-7-9-11-24-22(28)25-23-15-18-12-19(16-23)14-20(13-18)17-23/h18-20H,1-17H2,(H,26,27)(H2,24,25,28)/t18-,19+,20-,23-
SMILES string
OC(=O)CCCCCCCCCCCNC(=O)NC12C[C@@H]3C[C@@H](C[C@@H](C3)C1)C2
InChI key
XLGSEOAVLVTJDH-UKBVAGSOSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: ≥10 mg/mL at warmed to 60 °C
storage temp.
−20°C
Quality Level
相关类别
Application
AUDA has been used in the inhibition of epoxide hydrolase in human macrophages and in inhibition of tumor necrosis factor α (TNF-α)- induced phosphorylation in human aortic smooth muscle cells.
AUDA may be used in soluble epoxide hydrolase-mediated cell signaling studies.
Biochem/physiol Actions
AUDA is a potent inhibitor of soluble epoxide hydrolase
Inhibition of soluble epoxide hydrolase by AUDA inhibits the metabolism of epoxyeicosatrienoic acids (EETs) and protects end-organs against the damaging effects of salt-sensitive hypertension. AUDA also renders protection against myocardial ischemia-reperfusion injury and cerebral ischemia.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Alexis N Simpkins et al.
The American journal of pathology, 174(6), 2086-2095 (2009-05-14)
Inhibition of soluble epoxide hydrolase (SEH), the enzyme responsible for degradation of vasoactive epoxides, protects against cerebral ischemia in rats. However, the molecular and biological mechanisms that confer protection in normotension and hypertension remain unclear. Here we show that 6
PD n-3 DPA Pathway Regulates Human Monocyte Differentiation and Macrophage Function
Pistorius K, et al.
Cell Chemical Biology, 25(6), 749-760 (2018)
Chun-Hu Wu et al.
Journal of neuroinflammation, 14(1), 230-230 (2017-11-28)
Inflammatory responses significantly contribute to neuronal damage and poor functional outcomes following intracerebral hemorrhage (ICH). Soluble epoxide hydrolase (sEH) is known to induce neuroinflammatory responses via degradation of anti-inflammatory epoxyeicosatrienoic acids (EET), and sEH is upregulated in response to brain
You-Yang Qu et al.
Neurochemical research, 40(1), 1-14 (2014-11-05)
Epoxyeicosatrienoic acids (EETs), the cytochrome P450 epoxygenase metabolite of arachidonic acid, have been demonstrated to have neuroprotective effect. Phosphatidylinositol 3-kinase (PI3K)/Akt and ATP-sensitive potassium (KATP) channels are thought to be important factors that mediate neuroprotection. However, little is known about
Soluble epoxide hydrolase activity determines the severity of ischemia-reperfusion injury in kidney.
Jung Pyo Lee et al.
PloS one, 7(5), e37075-e37075 (2012-05-17)
Soluble epoxide hydrolase (sEH) in endothelial cells determines the plasma concentrations of epoxyeicosatrienoic acids (EETs), which may act as vasoactive agents to control vascular tone. We hypothesized that the regulation of sEH activity may have a therapeutic value in preventing
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