IRAK inhibitor 1 - CAS 1042224-63-4
Catalog number:
1042224-63-4
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C17H19N5
Molecular Weight:
293.37
COA:
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Targets:
IRAK
Description:
IRAK inhibitor 1 is interleukin-1 receptor associated kinase 4 (IRAK-4) inhibitor.
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Purity:
>98%
MSDS:
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1.Thalidomide represses inflammatory response and reduces radiculopathic pain by inhibiting IRAK-1 and NF-κB/p38/JNK signaling.
Song T1, Ma X2, Gu K2, Yang Y3, Yang L2, Ma P2, Wang W4, Zhao J2, Yan R2, Guan J2, Wang C2, Qi Y2, Ya J2. J Neuroimmunol. 2016 Jan 15;290:1-8. doi: 10.1016/j.jneuroim.2015.11.007. Epub 2015 Nov 14.
Intervertebral disc (IVD) disease, the most common cause of disc failure and low back pain, is characterized by age-related changes in the adult disc. In this study we aimed to analyze the potential of thalidomide for the treatment of IVD disease, through identifying and explaining its anti-inflammatory and anti-catabolic activity in both in vitro IVD cell culture and in vivo animal model. Inflammatory response was induced by IL-1β, then the activity and expression of inflammatory mediators and pathways were assessed in the presence or absence of thalidomide. The p38 inhibitor SB203580 was also used to investigate the involvement of the MAPK pathway in the observed effects. Moreover the analgesic properties of thalidomide were analyzed by the von Frey filament test in Sprague-Dawley rats. Our results indicated that thalidomide significantly inhibited the expression of pro-inflammatory mediators and matrix metalloproteinases in vitro, as well as radiculopathic pain in vivo, most probably by modulation of the activity of IRAK-1 and its downstream effectors p38, JNK and NF-κB.
2.The IRAK-ERK-p67phox-Nox-2 axis mediates TLR4, 2-induced ROS production for IL-1β transcription and processing in monocytes.
Singh A1, Singh V1, Tiwari RL1, Chandra T2, Kumar A3, Dikshit M1, Barthwal MK1. Cell Mol Immunol. 2015 Aug 31. doi: 10.1038/cmi.2015.62. [Epub ahead of print]
In monocytic cells, Toll-like receptor 4 (TLR4)- and TLR2-induced reactive oxygen species (ROS) cause oxidative stress and inflammatory response; however, the mechanism is not well understood. The present study investigated the role of interleukin-1 receptor-associated kinase (IRAK), extracellular signal-regulated kinase (ERK), p67phox and Nox-2 in TLR4- and TLR2-induced ROS generation during interleukin-1 beta (IL-1β) transcription, processing, and secretion. An IRAK1/4 inhibitor, U0126, PD98059, an NADPH oxidase inhibitor (diphenyleneiodonium (DPI)), and a free radical scavenger (N-acetyl cysteine (NAC))-attenuated TLR4 (lipopolysaccharide (LPS))- and TLR2 (Pam3csk4)-induced ROS generation and IL-1β production in THP-1 and primary human monocytes. An IRAK1/4 inhibitor and siRNA-attenuated LPS- and Pam3csk4-induced ERK-IRAK1 association and ERK phosphorylation and activity. LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1β transcription, and IL-1β processing because significant inhibition in AP-1 activity, IL-1β transcription, Pro- and mature IL-β expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.
3.Preconditioning with recombinant high mobility group box 1 induces ischemic tolerance in a rat model of focal cerebral ischemia-reperfusion.
Wang C1,2, Liu XX2, Huang KB2, Yin SB1, Wei JJ1, Hu YF2, Gu Y2, Zheng GQ1. J Neurochem. 2016 Mar 15. doi: 10.1111/jnc.13611. [Epub ahead of print]
Preconditioning with ligands of Toll-like receptors (TLRs) is a powerful neuroprotective approach whereby a low dose of stimulus confers significant protection against subsequent substantial brain damage by reprogramming the ischemia-activated TLRs signaling. Herein, we aim to explore whether preconditioning with recombinant high-mobility group box 1 (rHMGB1), one of the TLRs ligands, decreases cerebral ischemia-reperfusion injury (IRI). Rats were intracerebroventricularly (i.c.v.) pretreated with rHMGB1 1 or 3 days before induction of middle cerebral artery occlusion. Results showed that preconditioning with rHMGB1 1 day, but not 3 days, prior to ischemia dramatically reduced neurological deficits, infarct size, brain swelling, cell apoptosis and blood-brain barrier permeability. Interleukin-1R-associated kinase-M (IRAK-M), a critical negative regulator of TLRs signaling, was robustly increased in response to brain IRI and was further elevated by rHMGB1 pretreatment, indicating its role associated to the rHMGB1 preconditioning-mediated ischemic tolerance.
4.Involvement of interleukin-1 receptor-associated kinase-1 in vascular smooth muscle cell proliferation and neointimal formation after rat carotid injury.
Jain M1, Singh A1, Singh V1, Barthwal MK2. Arterioscler Thromb Vasc Biol. 2015 Jun;35(6):1445-55. doi: 10.1161/ATVBAHA.114.305028. Epub 2015 Apr 23.
OBJECTIVE: Reduced frequency of atherosclerotic plaques is observed in interleukin-1 receptor-associated kinase-1 (IRAK1)-deficient mice; however, the underlying mechanism is not clear. Therefore, this study investigate the role of IRAK1 in vascular smooth muscle cell proliferation and neointimal hyperplasia.
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CAS 1042224-63-4 IRAK inhibitor 1

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