NS-398_DataSheet_MedChemExpress

Inhibitors, Agonists, Screening Libraries

https://www.sodocs.net/doc/2c11647026.html, Data Sheet

BIOLOGICAL ACTIVITY:

NS–398 is a COX–2 inhibitor. The COX–1 activity is completely unaffected by 100 μM NS–398, whereas the COX–2 activity was concentration–dependently inhibited, the IC50 value being 3.8 μM.

IC50 value: 3.8 μM [3]

Target: COX–2

in vitro: NS–398 suppresses DOX–Induced Cytotoxicity and p53 Accumulation in U2OS and MCF–7 Cell Lines. NS–398 pre–treatment significantly reduces DOX–induced cytotoxicity in both cell lines. NS–398 reduces doxorubicin (DOX)–induced p53 accumulation and cytotoxicity. [1]

in vivo: NS–398 attenuates subretinal fibrosis, in an experimental model of subretinal scarring observed in neovascular AMD, by down–regulation of TGF–β2 in the retinal pigment epithelium–choroid complex. NS–398 can attenuate CNV and subretinal fibrosis lesions by suppressing macrophage infiltration and downregulating VEGF and TGF–β2, respectively. [2]

PROTOCOL (Extracted from published papers and Only for reference)

Cell assay (Trypan Blue Viability Assay) [1]

Cells were seeded in 6–well plates (1.25×105 cells/well) and 48 h later, treated with the NS–398 and/or DOX in DMSO. At the end of the treatment, both the adherent and detached cells were collected and stained with trypan blue dye for 5 min at room temperature.Cell viability was measured by using the TC10 automated cell counter, following manufacturer's instructions. The cells stained with trypan blue were considered as dead cells.

Animal administration [2]

C57BL/6 mice that were 7–10 weeks old were used. The mice were intraperitoneally treated with a COX–2–selective antagonist

(NS–398) (30mg/kg) or PBS or MF1 (25mg/kg) + DC101 (25mg/kg) 1 h before photocoagulation, and treatments were continued daily until the end of the study. MF1 and DC101 are neutralizing antibodies specific for mouse VEGFR1 (MF1) and VEGFR2 (DC101) as a positive control. Mouse RPE cultures were washed with serum–free media (SFM), incubated in SFM for 12 h, washed again with SFM,and further incubated for 12 h in six–well plates. NS–398 (0 ng/mL, 25 ng/mL, 50 ng/mL, and 100 ng/mL) was added to the cultures.After 1 h, TNF–α (10 ng/mL) was added to these plates.

References:

[1]. Kim J, et al. COX–2 inhibitor NS–398 suppresses doxorubicin–induced p53 accumulation through inhibition of ROS–mediated Jnk activation. Mol Carcinog. 2016 Jan 12. doi: 10.1002/mc.22458.

[2]. Zhang R, et al. The COX–2–Selective Antagonist (NS–398) Inhibits Choroidal Neovascularization and Subretinal Fibrosis. PLoS One. 2016 Jan 13;

Product Name:

NS–398Cat. No.:

HY-13913CAS No.:

123653-11-2Molecular Formula:

C 13H 18N 2O 5S Molecular Weight:

314.36Target:

COX Pathway:

Immunology/Inflammation Solubility:

DMSO: 9 mg/mL

11(1):e0146808.

[3]. Futaki N, et al. NS–398, a new anti–inflammatory agent, selectively inhibits prostaglandin G/H synthase/cyclooxygenase (COX–2) activity in vitro. Prostaglandins. 1994 Jan;47(1):55–59.

Caution: Product has not been fully validated for medical applications. For research use only.

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