IRAK inhibitor 3CAS# 1012343-93-9 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 1012343-93-9 | SDF | Download SDF |
| PubChem ID | 25103689 | Appearance | Powder |
| Formula | C21H21N5O4S | M.Wt | 439.49 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 13 mg/mL (29.58 mM; Need ultrasonic and warming) | ||
| Chemical Name | 4-[[[3-(3,4-dimethoxyphenyl)imidazo[1,2-b]pyridazin-6-yl]amino]methyl]benzenesulfonamide | ||
| SMILES | COC1=C(C=C(C=C1)C2=CN=C3N2N=C(C=C3)NCC4=CC=C(C=C4)S(=O)(=O)N)OC | ||
| Standard InChIKey | UPFVAHVWLNBVSG-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C21H21N5O4S/c1-29-18-8-5-15(11-19(18)30-2)17-13-24-21-10-9-20(25-26(17)21)23-12-14-3-6-16(7-4-14)31(22,27)28/h3-11,13H,12H2,1-2H3,(H,23,25)(H2,22,27,28) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | IRAK inhibitor 3 is an interleukin-1 (IL-I) receptor-associated kinase (IRAK) kinase modulator extracted from patent WO2008030579 A2.In Vitro:IRAK inhibitor 3 is an IRAK modulator, which can be used for treating an inflammatory condition, cell proliferative disorder, immune disorder[1]. References: | |||||
IRAK inhibitor 3 Dilution Calculator
IRAK inhibitor 3 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.2754 mL | 11.3768 mL | 22.7536 mL | 45.5073 mL | 56.8841 mL |
| 5 mM | 0.4551 mL | 2.2754 mL | 4.5507 mL | 9.1015 mL | 11.3768 mL |
| 10 mM | 0.2275 mL | 1.1377 mL | 2.2754 mL | 4.5507 mL | 5.6884 mL |
| 50 mM | 0.0455 mL | 0.2275 mL | 0.4551 mL | 0.9101 mL | 1.1377 mL |
| 100 mM | 0.0228 mL | 0.1138 mL | 0.2275 mL | 0.4551 mL | 0.5688 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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IRAK inhibitor 3 is interleukin-1 receptor associated kinase inhibitor.
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Immunomodulatory Molecule IRAK-M Balances Macrophage Polarization and Determines Macrophage Responses during Renal Fibrosis.[Pubmed:28701510]
J Immunol. 2017 Aug 15;199(4):1440-1452.
Activation of various innate immune receptors results in IL-1 receptor-associated kinase (IRAK)-1/IRAK-4-mediated signaling and secretion of proinflammatory cytokines such as IL-12, IL-6, or TNF-alpha, all of which are implicated in tissue injury and elevated during tissue remodeling processes. IRAK-M, also known as IRAK-3, is an inhibitor of proinflammatory cytokine and chemokine expression in intrarenal macrophages. Innate immune activation contributes to both acute kidney injury and tissue remodeling that is associated with chronic kidney disease (CKD). Our study assessed the contribution of macrophages in CKD and the role of IRAK-M in modulating disease progression. To evaluate the effect of IRAK-M in chronic renal injury in vivo, a mouse model of unilateral ureteral obstruction (UUO) was employed. The expression of IRAK-M increased within 2 d after UUO in obstructed compared with unobstructed kidneys. Mice deficient in IRAK-M were protected from fibrosis and displayed a diminished number of alternatively activated macrophages. Compared to wild-type mice, IRAK-M-deficient mice showed reduced tubular injury, leukocyte infiltration, and inflammation following renal injury as determined by light microscopy, immunohistochemistry, and intrarenal mRNA expression of proinflammatory and profibrotic mediators. Taken together, these results strongly support a role for IRAK-M in renal injury and identify IRAK-M as a possible modulator in driving an alternatively activated profibrotic macrophage phenotype in UUO-induced CKD.
Lactobacillus paracasei modulates LPS-induced inflammatory cytokine release by monocyte-macrophages via the up-regulation of negative regulators of NF-kappaB signaling in a TLR2-dependent manner.[Pubmed:28088611]
Cytokine. 2017 Apr;92:1-11.
The application of the probiotic lactobacillus is suggested in the treatment of some inflammatory diseases of intestines due to its potential ability to attenuate inflammation. However, the mechanism is not completely understood. In PBMCs, Lactobacillus paracasei (L. Paracasei) down-regulated the LPS-induced production of TNF-alpha and IL-6. Using a macrophage-like differentiated THP-1 cell line induced by PMA, we investigated the effect of L. paracasei on the production of pro-inflammatory cytokines by monocyte-macrophages. Treatment of the differentiated THP-1 cells with L. paracasei either concurrently with or before LPS challenge attenuated the LPS-induced secretion of TNF-alpha and IL-1beta. This effect was due to a decrease in IkappaB phosphorylation and NF-kappaB nuclear translocation. Furthermore, treatment of the differentiated THP-1 cells with L. paracasei induced the expression of negative regulators of the NF-kappaB signaling pathway, including the deubiquitinating enzyme A20, suppressor of cytokine signaling (SOCS) 1, SOCS3, and IL-1 receptor-associated kinase (IRAK) 3. Pretreatment with an IRAK4 inhibitor suppressed the L. paracasei-induced expression of these negative regulators and further increased the LPS-mediated expressions of TNF-alpha and IL-1beta. Moreover, treatment with an antibody against Toll-like receptor (TLR) 2 reversed the effect of L. paracasei on inducing negative regulators and inhibiting TNF-alpha and IL-1beta productions. Our findings suggest that L. paracasei inhibits the production of pro-inflammatory cytokines by monocyte-macrophages via the induction of negative regulators of the NF-kappaB signaling pathway in a TLR2-IRAK4-dependent manner.
Selective IRAK4 Inhibition Attenuates Disease in Murine Lupus Models and Demonstrates Steroid Sparing Activity.[Pubmed:28003376]
J Immunol. 2017 Feb 1;198(3):1308-1319.
The serine/threonine kinase IL-1R-associated kinase (IRAK)4 is a critical regulator of innate immunity. We have identified BMS-986126, a potent, highly selective inhibitor of IRAK4 kinase activity that demonstrates equipotent activity against multiple MyD88-dependent responses both in vitro and in vivo. BMS-986126 failed to inhibit assays downstream of MyD88-independent receptors, including the TNF receptor and TLR3. Very little activity was seen downstream of TLR4, which can also activate an MyD88-independent pathway. In mice, the compound inhibited cytokine production induced by injection of several different TLR agonists, including those for TLR2, TLR7, and TLR9. The compound also significantly suppressed skin inflammation induced by topical administration of the TLR7 agonist imiquimod. BMS-986126 demonstrated robust activity in the MRL/lpr and NZB/NZW models of lupus, inhibiting multiple pathogenic responses. In the MRL/lpr model, robust activity was observed with the combination of suboptimal doses of BMS-986126 and prednisolone, suggesting the potential for steroid sparing activity. BMS-986126 also demonstrated synergy with prednisolone in assays of TLR7- and TLR9-induced IFN target gene expression using human PBMCs. Lastly, BMS-986126 inhibited TLR7- and TLR9-dependent responses using cells derived from lupus patients, suggesting that inhibition of IRAK4 has the potential for therapeutic benefit in treating lupus.
Dual Inhibition of Rip2 and IRAK1/4 Regulates IL-1beta and IL-6 in Sarcoidosis Alveolar Macrophages and Peripheral Blood Mononuclear Cells.[Pubmed:27402699]
J Immunol. 2016 Aug 15;197(4):1368-78.
Sarcoidosis is a multisystem granulomatous disease of unknown etiology that primarily affects the lungs. Our previous work indicates that activation of p38 plays a pivotal role in sarcoidosis inflammatory response. Therefore, we investigated the upstream kinase responsible for activation of p38 in sarcoidosis alveolar macrophages (AMs) and PBMCs. We identified that sustained p38 phosphorylation in sarcoidosis AMs and PBMCs is associated with active MAPK kinase 4 but not with MAPK kinase 3/6. Additionally, we found that sarcoidosis AMs exhibit a higher expression of IRAK1, IRAK-M, and receptor interacting protein 2 (Rip2). Surprisingly, ex vivo treatment of sarcoidosis AMs or PBMCs with IRAK1/4 inhibitor led to a significant increase in IL-1beta mRNA expression both spontaneously and in response to TLR2 ligand. However, a combination of Rip2 and IRAK-1/4 inhibitors significantly decreased both IL-1beta and IL-6 production in sarcoidosis PBMCs and moderately in AMs. Importantly, a combination of Rip2 and IRAK-1/4 inhibitors led to decreased IFN-gamma and IL-6 and decreased percentage of activated CD4(+)CD25(+) cells in PBMCs. These data suggest that in sarcoidosis, both pathways, namely IRAK and Rip2, are deregulated. Targeted modulation of Rip2 and IRAK pathways may prove to be a novel treatment for sarcoidosis.
LPS enhances TLR4 expression and IFNgamma production via the TLR4/IRAK/NFkappaB signaling pathway in rat pulmonary arterial smooth muscle cells.[Pubmed:28714001]
Mol Med Rep. 2017 Sep;16(3):3111-3116.
The aim of the present study was to investigate the role of the Tolllike receptor (TLR)4 signaling pathway in cellular response to lipopolysaccharide (LPS) in rat pulmonary artery smooth muscle cells (PASMCs). Chronic obstructive pulmonary disease (COPD) rats were established with passive inhaling cigarette smoke plus injection of LPS. The TLR4 protein in lung tissues was determined with immunohistochemical staining and protein levels of the components of the TLR4 pathway in PASMCs were analyzed with western blotting. The production of interferon (IFN)gamma upon LPS stimulation in PASMCs was measured with ELISA. TLR4 expression in lung tissue from COPD rats was increased obviously compared with that in normal group. LPS enhances TLR4 expression in rat PASMCs and induced production of IFNgamma dramatically. LPS treatment resulted in increased phosphorinterleukin1 receptorassociated kinase (IRAK), IkappaB and IkappaB kinase, as well as the total protein of nuclear factor (NF)kappaB p65. TLR4 inhibitor TAK242, IRAK1/4 inhibitor and NFkappaB inhibitor Bay 117082 were capable of suppressing the effects of LPS. TLR4 signaling pathway is functional in PASMCs, and may be involved in the inflammatory response during the pathogenesis of COPD.
