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Documenti fondamentali

SML0557

Sigma-Aldrich

SC-514

≥97% (HPLC)

Sinonimo/i:

4-Amino-[2,3"]bithiophenyl-5-carboxylic acid amide

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5 MG
CHF 84.60
25 MG
CHF 260.00

CHF 84.60


Spedizione prevista il13 aprile 2025


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5 MG
CHF 84.60
25 MG
CHF 260.00

About This Item

Formula empirica (notazione di Hill):
C9H8N2OS2
Numero CAS:
Peso molecolare:
224.30
Codice UNSPSC:
12352200
NACRES:
NA.77

CHF 84.60


Spedizione prevista il13 aprile 2025


Richiedi un ordine bulk

Livello qualitativo

Saggio

≥97% (HPLC)

Stato

powder

Colore

white to light brown

Solubilità

DMSO: 10 mg/mL, clear

Temperatura di conservazione

2-8°C

Stringa SMILE

[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)
BMUACLADCKCNKZ-UHFFFAOYSA-N

Applicazioni

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).[1][2]

Azioni biochim/fisiol

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.[3]

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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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

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