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Biological Activity for NS 398
NS 398 is a selective cyclooxygenase-2 inhibitor (IC50 values are 3.8 and > 100 μM for COX-2 and COX-1 respectively). Induces apoptosis in colorectal tumor cells and elevates COX-2 protein expression in vitro. Orally active and non-ulcerogenic analgesic and anti-inflammatory in vivo.
Compound Libraries for NS 398
Technical Data for NS 398
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for NS 398
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for NS 398
The following data is based on the product molecular weight 314.36. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.18 mL||15.91 mL||31.81 mL|
|5 mM||0.64 mL||3.18 mL||6.36 mL|
|10 mM||0.32 mL||1.59 mL||3.18 mL|
|50 mM||0.06 mL||0.32 mL||0.64 mL|
References for NS 398
References are publications that support the biological activity of the product.
Elder et al (2002) The MEK/ERK pathway mediates COX-2-selective NSAID-induced apoptosis and induced COX-2 protein expression in colorectal carcinoma cells. Int.J.Cancer 99 323 PMID: 11992399
Futaki et al (1993) NS-398, a novel non-steroidal anti-inflammatory drug with potent analgesic and antipyretic effects, which causes minimal stomach lesions. Gen.Pharmacol. 24 105 PMID: 8482483
Futaki et al (1994) NS-398, a new anti-inflammatory agent, selectively inhibits prostaglandin G/H synthase/cyclooxygenase (COX-2) activity in vitro. Prostaglandins 47 55 PMID: 8140262
If you know of a relevant reference for NS 398, please let us know.
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Keywords: NS 398, NS 398 supplier, Cyclooxygenase, COX-2, inhibitors, inhibits, COX, Oxygenases, Oxidases, NS398, 0942, Tocris Bioscience
14 Citations for NS 398
Citations are publications that use Tocris products. Selected citations for NS 398 include:
Ho et al (2015) Peripheral inflammation increases seizure susceptibility via the induction of neuroinflammation and oxidative stress in the hippocampus. J Virol 22 46 PMID: 26100815
Sunters et al (2010) Mechano-transduction in osteoblastic cells involves strain-regulated estrogen receptor alpha-mediated control of Ins-like growth factor (IGF) I receptor sensitivity to Ambient IGF, leading to phosphatidylinositol 3-kinase/AKT-dependent Wnt/LRP5 receptor-i J Biol Chem 285 8743 PMID: 20042609
Wei et al (2015) Proinflammatory cytokines upregulate sympathoexcitatory mechanisms in the subfornical organ of the rat. Hypertension 65 1126 PMID: 25776070
Ray et al (2004) Cyclooxygenase-1 and -2 are required for production of infectious pseudorabies virus. PLoS One 78 12964 PMID: 15542648
Messerschmidt et al (2019) Osmotic induction of cyclooxygenase-2 in RPE cells: Stimulation of inflammasome activation. Mol Vis 25 329 PMID: 31341381
Font-Nieves et al (2012) Induction of COX-2 enzyme and down-regulation of COX-1 expression by lipopolysaccharide (LPS) control prostaglandin E2 production in astrocytes. J Biol Chem 287 6454 PMID: 22219191
Sugiyama et al (2013) The cyclooxygenase-2 selective inhibitor NS-398 does not influence trabecular or cortical bone gain resulting from repeated mechanical loading in female mice. Osteoporos Int 24 383 PMID: 22349912
Wong et al (2009) Cyclooxygenase-2-derived prostaglandin F2alpha mediates endothelium-dependent contractions in the aortae of hamsters with increased impact during aging. Circ Res 104 228 PMID: 19096033
Bourquin et al (2011) Systemic cancer therapy with a small molecule agonist of toll-like receptor 7 can be improved by circumventing TLR tolerance. Cancer Res 71 5123 PMID: 21697281
Chia et al (2011) Protection of protease-activated receptor 2 mediated vasodilatation against angiotensin II-induced vascular dysfunction in mice. BMC Pharmacol 11 10 PMID: 21955547
Bonfill-Teixidor et al (2017) Differential expression of E-type prostanoid receptors 2 and 4 in microglia stimulated with lipopolysaccharide. J Neuroinflammation 14 3 PMID: 28086956
Liu et al (2014) Uncoupling protein-2 mediates DPP-4 inhibitor-induced restoration of endothelial function in hypertension through reducing oxidative stress. Antioxid Redox Signal 21 1571 PMID: 24328731
Tunaru et al (2016) Arachidonic acid metabolite 19(S)-HETE induces vasorelaxation and platelet inhibition by activating prostacyclin(IP) receptor. PLoS One 11 e0163633 PMID: 27662627
Buenestado et al (2012) Roflumilast inhibits the release of chemokines and TNF-α from human lung macrophages stimulated with lipopolysaccharide. Br J Pharmacol 165 1877 PMID: 21913898
Do you know of a great paper that uses NS 398 from Tocris? Please let us know.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.