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SML0273

Sigma-Aldrich

VAS2870

≥97% (HPLC)

Sinónimos:

1,3-Benzoxazol-2-yl-3-benzyl-3H-[1,2,3]triazolo[4,5-d]pyrimidin-7-yl sulfide, 7-(1,3-Benzoxazol-2-ylsulfanyl)-3-benzyl-3H-[1,2,3]triazolo[4,5-d]pyrimidine, 7-(2-Benzoxazolylthio)-3-(phenylmethyl)-3H-1,2,3-triazolo[4,5-d]pyrimidine, VAS 2870, VAS-2870

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About This Item

Fórmula empírica (notación de Hill):
C18H12N6OS
Número de CAS:
722456-31-7
Peso molecular:
360.39
Número MDL:
MFCD03407188
Código UNSPSC:
12352200
ID de la sustancia en PubChem:
329825281
NACRES:
NA.77

Nivel de calidad

100

Ensayo

≥97% (HPLC)

Formulario

powder

color

white to beige

solubilidad

DMSO: ≥5 mg/mL

temp. de almacenamiento

room temp

cadena SMILES

C(c1ccccc1)n2nnc3c(Sc4nc5ccccc5o4)ncnc23

InChI

1S/C18H12N6OS/c1-2-6-12(7-3-1)10-24-16-15(22-23-24)17(20-11-19-16)26-18-21-13-8-4-5-9-14(13)25-18/h1-9,11H,10H2

Clave InChI

HZSOKHVVANONPV-UHFFFAOYSA-N

Aplicación

VAS2870 has been used as a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) inhibitor:
  • to study the importance of NOX-derived reactive oxygen species in cytoskeletal organization, proper localization of E-cadherin and cell motility during zebrafish epiboly
  • to study the function of Nox2 and Nox4 in lipopolysaccharide (LPS)-induced intestinal injury in high-fat diet (HFD) fed mice
  • to reduce the reactive oxygen species level and study its influence on inhibiting the induction of trained innate immunity in monocytes

Acciones bioquímicas o fisiológicas

In addition to NOX4 inhibition, VAS2870 is also known to supress the reactive oxygen species (ROS) production in several cell types. It effectively impairs cell growth and increases apoptosis induced by transforming growth factor β (TGF-β) in liver cancer cells. Thus, inhibition of NOX enzymes by VAS2870 may be considered as a potential therapeutic strategy for liver cancer.
VAS2870 is a cell-permeable and specific NADPH oxidase (NOX) inhibitor that effectively suppresses growth factor-mediated ROS liberation in VSMC.
VAS2870 is a cell-permeable and specific NADPH oxidase (NOX) inhibitor.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
0000289200
0000289200
0000144214
0000130439

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Austin T Robinson et al.
American journal of physiology. Heart and circulatory physiology, 312(5), H896-H906 (2017-02-27)
High blood pressure has been shown to elicit impaired dilation in the vasculature. The purpose of this investigation was to elucidate the mechanisms through which high pressure may elicit vascular dysfunction and determine the mechanisms through which regular aerobic exercise
Patricia Sancho et al.
Biochemical pharmacology, 81(7), 917-924 (2011-02-01)
Liver tumor cells show several molecular alterations which favor pro-survival signaling. Among those, we have proposed the NADPH oxidase NOX1 as a prosurvival signal for liver tumor cells. On the one side, we have described that FaO rat hepatoma cells
Yahya Sohrabi et al.
Frontiers in immunology, 9, 3155-3155 (2019-02-07)
Introduction: Cells of the innate immune system particularly monocytes and macrophages have been recognized as pivotal players both during the initial insult as well as the chronic phase of atherosclerosis. It has recently been shown that oxidized low-density lipoprotein (oxLDL)
Qi-An Sun et al.
Free radical biology & medicine, 52(9), 1897-1902 (2012-03-13)
Specific inhibitors of the production of reactive oxygen species (ROS) by the NADPH oxidases (Nox's) are potentially important therapeutic agents in the wide range of human diseases that are characterized by excessive ROS production. It has been proposed that VAS2870
I-Jung Tsai et al.
International journal of molecular sciences, 20(18) (2019-09-13)
Patients with a relapse of idiopathic nephrotic syndrome have significantly increased levels of serum complement component 5a (C5a), and proteinuria has been noted in mice treated with C5a via changes in permeability of kidney endothelial cells (KECs) in established animal
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