Molecular Weight(MW): 356.42
QNZ (EVP4593) shows potent inhibitory activity toward both NF-κB activation and TNF-α production with IC50 of 11 nM and 7 nM in Jurkat T cells, respectively.
Cited by 21 Publications
6 Customer Reviews
TE7 cells (2 × 105) were pretreated with PD98059 (20 μM), QNZ (EVP4593; 20 μM), AZD5363 (20 μM), S1155 (20 μM) and Tra (40 ng/ml) for 1 h and stimulated with IL6 (40 ng/ml) for 48 h.
Oncogene, 2018, 37(7):873-883. QNZ (EVP4593) purchased from Selleck.
H1650/shRNF25 or H1650/shControl cells were pretreated with an NF-κB inhibitor (QNZ, 600 nM) for 2 h, and then treated with 5 μM gefitinib. Cell proliferation was measured by cell counting. Values are mean ± SD of three independent experiments.
Cell Death Dis, 2018, 9(6):587. QNZ (EVP4593) purchased from Selleck.
Activation of p38, ERK1/2 and NF-κB pathways was required for HBcAg-induced IL-6 production. L-02 cells, Huh7 cells and SMMC-7721 cells were transfected with HBcAg-GFP or GFP plasmids for 12 hours, the supernatant were replaced, and the cells were washed three times and treated with 20μM SB203580, 15μM U0126 and 10μM QNZ individually or mixedly for another 12 hours, then the secreted IL-6 protein was detected by ELISA. The differences among groups were analyzed by one-way ANOVA (LSD). The different letters above the bars indicates significant difference (p<0.05) among treatments.
Cell Physiol Biochem, 2017, 41(1):91-100. QNZ (EVP4593) purchased from Selleck.
NF-κB partly mediated resveratrol (Res) inhibition on PKD inflammation. (A) Expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB in QNZ-treated OX161 cells. (B) OX161 cells were pretreated with QNZ for 2 h and followed by the treatment of resveratrol for 46 h. The expression of p-p65, p65, p105, p50, TNF-α, MCP-1 and CFB were evaluated by western blot. (C) MCP-1 or CFB of QNZ-and/or resveratroltreated OX161 cell supernatants were measured by ELISA. One representative of three independent experiments is shown.
Nephrol Dial Transplant, 2016: 1–9.. QNZ (EVP4593) purchased from Selleck.
(B-E) THP-1 cells were treated with or without NF-κB inhibitor QNZ and JNK inhibitor SP600125. (B-C) THP-1 cells treated with NF-κB inhibitor QNZ;
Toxicol Appl Pharmacol, 2015, 289(2):133-41.. QNZ (EVP4593) purchased from Selleck.
Purity & Quality Control
Choose Selective NF-κB Inhibitors
|Description||QNZ (EVP4593) shows potent inhibitory activity toward both NF-κB activation and TNF-α production with IC50 of 11 nM and 7 nM in Jurkat T cells, respectively.|
EVP4593 inhibits TNF-a production from murine splenocytes stimulated with LPS with IC50 of 7 nM.  EVP4593 (300 nM) entails a significant decrease of amplitude of store-operated currents (approximately by 60%), induced by application of 1 μM thapsigargin in Htt138Q cells, thus prevents abnormal store-operated calcium entry. EVP4593 is able to inhibit the activity of channels containing TRPC1 as one of the subunits, but has no effect on homooligomer channels composed exclusively of TRPC1.  QNZ (40 nM) completely abolishes the enhancement of neurite number and length evoked by laminin treatment of the schwann cells. QNZ reduces the neurite length by 61.36% of the schwann cells. QNZ significantly inhibits laminin-induced neurite outgrowth. QNZ also greatly diminishes the neurite elongation after 72 hours culture implying that both initial sprouting and longer term growth and extension seen in response to schwann cells seeded on laminin is mediated by NF-κB.  QNZ (10 nM) abolishes LPS-induced up-regulation of CSE expression in rat neutrophil.  QNZ (100 nM) blocks the induction effects of GRO/KC on K currents in IB4-negative neurons. 
|In vivo||EVP4593 (1 mg/kg, i.p.) dose-dependently inhibits carrageenin-induced paw edema in rats. |
|In vitro||DMSO||5 mg/mL warmed (14.02 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
0.5% hydroxyethyl cellulose
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
Instructions to calculate molar mass (molecular weight) of a chemical compound:
To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.