Cat. No. 5575
Chemical Name: 11H-Indeno[1,2-b]quinoxalin-11-one oxime sodium salt
Biological ActivityJNK inhibitor (Kd values are 87, 360 and 390 nM for JNK3, JNK2 and JNK1, respectively). Inhibits LPS-induced proinflammatory cytokine and nitric oxide production in vitro. Attenuates collagen-induced arthritis severity and inhibits murine delayed-type hypersensitivity in vivo. Anti-inflammatory and immunosuppressive. Also releases NO upon metabolism by liver microsomes.
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
Certificate of Analysis / Product Datasheet / Safety Datasheet
References are publications that support the products' biological activity.
Atochin et al (2016) A novel dual NO-donating oxime and c-Jun N-terminal kinase inhibitor protects against cerebral ischemia-reperfusion injury in mice. Neurosci.Lett. 618 45. PMID: 26923672.
Schepetkin et al (2015) Anti-Inflammatory effects and joint protection in collagen-induced arthritis after treatment with IQ-1S, a selective c-Jun N-terminal kinase Inhibitor. J.Pharmacol.Exp.Ther. 353 505. PMID: 25784649.
Schepetkin et al (2012) Identification and characterization of a novel class of c-Jun N-terminal kinase inhibitors. Mol.Pharmacol. 81 832. PMID: 22434859.
If you know of a relevant reference for IQ 1S please let us know.
Citations are publications that use Tocris products.
Do you know of a great paper that uses IQ 1S from Tocris? If so please let us know.
View Related Products by Target
View Related Products by Product Action
Keywords: IQ 1S, supplier, IQ1S, JNK, inhibitors, inhibits, anti-inflammatory, immunosuppresents, NO, donor, Tocris Bioscience, JNK/c-Jun Inhibitor products
Find multiple products by catalog number
New Products in this Area
Selective p38α/β inhibitor; orally bioavailable
Follow @Tocris on Twitter
Tocris is now actively tweeting. For regular updates on news, events and special offers, follow @Tocris on Twitter.