Sign In to View Organizational & Contract Pricing
Select a Size
About This Item
Empirical Formula (Hill Notation):
C9H8N2OS2
CAS Number:
Molecular Weight:
224.30
UNSPSC Code:
12352200
NACRES:
NA.77
Quality Level
Assay
≥97% (HPLC)
form
powder
color
white to light brown
solubility
DMSO: 10 mg/mL, clear
storage temp.
2-8°C
SMILES string
[s]1c(cc(c1C(=O)N)N)c2c[s]cc2
InChI
1S/C9H8N2OS2/c10-6-3-7(5-1-2-13-4-5)14-8(6)9(11)12/h1-4H,10H2,(H2,11,12)
InChI key
BMUACLADCKCNKZ-UHFFFAOYSA-N
Related Categories
Application
SC-514 has been used to study its effect on lipopolysaccharide (LPS)-induced phosphorylation of NF-κB (nuclear factor-κB) p65 and p38 MAPK (mitogen-activated protein kinase).
Biochem/physiol Actions
SC-514 is a cell-permeable, potent and selective ATP competitive inhibitor of nuclear factor kappa-B kinase-2 (IKK-2) that specifically blocks NF-?B-dependent gene expression. SC-514 exhibits anti-inflammatory properties.
SC-514 is a cell-permeable, potent and selective ATP competitive inhibitor of nuclear factor kappa-B kinase-2 (IKK-2).
SC-514 is an amino-acetamide compound. It is selective for IKKβ with an IC50 value of 3−12 μM. SC-514 also inhibits cytokines such as interleukin-6 (IL-6) and IL-8, mediated by IKKβ. IKKβ is responsible for osteoclast survival, hence its inhibition affects osteogenesis.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
新产品
This item has
Choose from one of the most recent versions:
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
SC-514, a selective inhibitor of IKKbeta attenuates RANKL-induced osteoclastogenesis and NF-kappaB activation
Liu Q, et al.
Biochemical Pharmacology, 86(12), 1775-1783 (2013)
Lipopolysaccharide-binding protein downregulates fractalkine through activation of p38 MAPK and NF-kappaB
Huang X, et al.
Mediators of Inflammation, 2017 (2017)
Wei You et al.
Aging, 11(11), 3574-3584 (2019-05-31)
Formation of aortic aneurysms as a consequence of augmented transforming growth factor β (TGF-β) signaling and vascular smooth muscle cell (VSMC) dysfunction is a potentially lethal complication of Marfan syndrome (MFS). Here, we examined VSMC senescence in patients with MFS
Nur77 attenuates endothelin-1 expression via downregulation of NF-kappaB and p38 MAPK in A549 cells and in an ARDS rat model
Jiang Y, et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology, L1023-L1035 (2016)
Yujie Jiang et al.
American journal of physiology. Lung cellular and molecular physiology, 311(6), L1023-L1035 (2016-10-22)
Acute respiratory distress syndrome (ARDS) is characterized by inflammatory injury to the alveolar and capillary barriers that results in impaired gas exchange and severe acute respiratory failure. Nuclear orphan receptor Nur77 has emerged as a regulator of gene expression in
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service