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IRAK-1-4 Inhibitor I

IRAK-1/4 inhibitor CAS# 509093-47-4

IRAK-1-4 Inhibitor I

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Chemical structure

IRAK-1-4 Inhibitor I

3D structure

Chemical Properties of IRAK-1-4 Inhibitor I

Cas No. 509093-47-4 SDF Download SDF
PubChem ID 11983295 Appearance Powder
Formula C20H21N5O4 M.Wt 395.41
Type of Compound N/A Storage Desiccate at -20°C
Synonyms IRAK-1/4 Inhibitor I
Solubility DMSO : 14.29 mg/mL (36.14 mM; Need ultrasonic)
Chemical Name N-[1-(2-morpholin-4-ylethyl)benzimidazol-2-yl]-3-nitrobenzamide
SMILES C1COCCN1CCN2C3=CC=CC=C3N=C2NC(=O)C4=CC(=CC=C4)[N+](=O)[O-]
Standard InChIKey QTCFYQHZJIIHBS-UHFFFAOYSA-N
Standard InChI InChI=1S/C20H21N5O4/c26-19(15-4-3-5-16(14-15)25(27)28)22-20-21-17-6-1-2-7-18(17)24(20)9-8-23-10-12-29-13-11-23/h1-7,14H,8-13H2,(H,21,22,26)
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.
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.
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.

Biological Activity of IRAK-1-4 Inhibitor I

DescriptionIRAK4 and IRAK1 inhibitor (IC50 values are 0.2 and 0.3 μM, respectively).

IRAK-1-4 Inhibitor I Dilution Calculator

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IRAK-1-4 Inhibitor I Molarity Calculator

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Preparing Stock Solutions of IRAK-1-4 Inhibitor I

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.529 mL 12.6451 mL 25.2902 mL 50.5804 mL 63.2255 mL
5 mM 0.5058 mL 2.529 mL 5.058 mL 10.1161 mL 12.6451 mL
10 mM 0.2529 mL 1.2645 mL 2.529 mL 5.058 mL 6.3226 mL
50 mM 0.0506 mL 0.2529 mL 0.5058 mL 1.0116 mL 1.2645 mL
100 mM 0.0253 mL 0.1265 mL 0.2529 mL 0.5058 mL 0.6323 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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Background on IRAK-1-4 Inhibitor I

IRAK-1-4 Inhibitor I is an inhibitor of both IRAK-1 and IRAK-4 with IC50 values of 0.3μM and 0.2μM , respectively [1].

IL-1 receptor-associated kinases play important roles in signal transduction. There are totally four members of the IRAKs, they are IRAK-1, IRAK-2, IRAK-M and IRAK-4. IRAK-4 can activate NF-κB and MAPK pathways and it is shown that the inhibition of IRAK-4 can be an anti-inflammatory therapy. IRAK-1-4 Inhibitor I is an analog of an Initial IRAK-4 inhibitor hit, which is screened out from a small molecule li brary against IRAK-4. With the less basic N-ethylenemorpholine moiety, IRAK-1-4 Inhibitor I has a higher potency than other analogs. Additionally, it does not show any cytotoxicity in a 72 h proliferation assay in HeLa cells(ED50 >30μM) [1].

References:
[1] Jay P. Powers, Shyun Li, Juan C. Jaen, Jinqian Liu, Nigel P. C. Walker, Zhulun Wang and Holger Wesche. Discovery and initial SAR of inhibitors of interleukin-1 receptor-associated kinase-4. Bioorganic & Medicinal Chemistry Letters. 2006, 16: 2842–2845.

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References on IRAK-1-4 Inhibitor I

A Cascade of Redox Reactions Generates Complexity in the Biosynthesis of the Protein Phosphatase-2 Inhibitor Rubratoxin A.[Pubmed:28370936]

Angew Chem Int Ed Engl. 2017 Apr 18;56(17):4782-4786.

Redox modifications are key complexity-generating steps in the biosynthesis of natural products. The unique structure of rubratoxin A (1), many of which arise through redox modifications, make it a nanomolar inhibitor of protein phosphatase 2A (PP2A). We identified the biosynthetic pathway of 1 and completely mapped the enzymatic sequence of redox reactions starting from the nonadride 5. Six redox enzymes are involved, including four alpha-ketoglutarate- and iron(II)-dependent dioxygenases that hydroxylate four sp(3) carbons; one flavin-dependent dehydrogenase that is involved in formation of the unsaturated lactone; and the ferric-reductase-like enzyme RbtH, which regioselectively reduces one of the maleic anhydride moieties in rubratoxin B to the gamma-hydroxybutenolide that is critical for PP2A inhibition. RbtH is proposed to perform sequential single-electron reductions of the maleic anhydride using electrons derived from NADH and transferred through a ferredoxin and ferredoxin reductase pair.

Phase 2 studies of oral hypoxia-inducible factor prolyl hydroxylase inhibitor FG-4592 for treatment of anemia in China.[Pubmed:28371815]

Nephrol Dial Transplant. 2017 Aug 1;32(8):1373-1386.

Background: FG-4592 (roxadustat) is an oral hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor (HIF-PHI) promoting coordinated erythropoiesis through the transcription factor HIF. Two Phase 2 studies were conducted in China to explore the safety and efficacy of FG-4592 (USAN name: roxadustat, CDAN name: ), a HIF-PHI, in patients with anemia of chronic kidney disease (CKD), both patients who were dialysis-dependent (DD) and patients who were not dialysis-dependent (NDD). Methods: In the NDD study, 91 participants were randomized to low (1.1-1.75 mg/kg) or high (1.50-2.25 mg/kg) FG-4592 starting doses or to placebo. In the DD study, 87 were enrolled to low (1.1-1.8 mg/kg), medium (1.5-2.3 mg/kg) and high (1.7-2.3 mg/kg) starting FG-4592 doses or to continuation of epoetin alfa. In both studies, only oral iron supplementation was allowed. Results: In the NDD study, hemoglobin (Hb) increase >/=1 g/dL from baseline was achieved in 80.0% of subjects in the low-dose cohort and 87.1% in the high-dose cohort, versus 23.3% in the placebo arm (P < 0.0001, both). In the DD study, 59.1%, 88.9% (P = 0.008) and 100% (P = 0.0003) of the low-, medium- and high-dose subjects maintained their Hb levels after 5- and 6-weeks versus 50% of the epoetin alfa-treated subjects. In both studies, significant reductions in cholesterol were noted in FG-4592-treated subjects, with stability or increases in serum iron, total iron-binding capacity (TIBC) and transferrin (without intravenous iron administration). In the NDD study, hepcidin levels were significantly reduced across all FG-4592-treated arms as compared with no change in the placebo arm. In the DD study, hepcidin levels were also reduced in a statistically significant dose-dependent manner in the highest dose group as compared with the epoetin alfa-treated group. Adverse events were similar for FG-4592-treated and control subjects. Conclusions: FG-4592 may prove an effective alternative for managing anemia of CKD. It is currently being investigated in a pivotal global Phase 3 program.

Bosutinib, an SRC inhibitor, induces caspase-independent cell death associated with permeabilization of lysosomal membranes in melanoma cells.[Pubmed:28371355]

Vet Comp Oncol. 2018 Mar;16(1):69-76.

BACKGROUND: SRC kinase (SRC proto-oncogene, non-receptor tyrosine kinase) is a promising target for the treatment of solid cancers including human melanoma. Bosutinib (Bosu), a SRC inhibitor, has already been applied to the treatment of human chronic myelogenous leukemia and also has been assessed its safety in dogs. AIM: The aim of this study was to clarify a novel anti-tumour mechanism of Bosu in canine and human melanoma cells. MATERIALS AND METHODS: The canine and human melanoma cells were treated with Bosu and its effects were evaluated by the cell viability, the protein expression levels such as caspase-3 and LC3, Annexin V/Propidium iodide staining, and confocal immunostaining. RESULTS: Bosu induced the massive caspase-independent cell death, and blocked autophagy flux, which resulted from lysosomal dysfunction. Lysosomal dysfunction caused by Bosu was due to lysosomal membrane permeabilization (LMP), which resulted in the release of lysosomal hydrolases including cathepsin B. CONCLUSION: Our data suggest that Bosu induces the cell death through induction of LMP in melanoma cells and is a promising therapeutic agent for treatment of melanoma in both dogs and humans.

Development of a Hypoxic Radiosensitizer-Prodrug Liposome Delivery DNA Repair Inhibitor Dbait Combination with Radiotherapy for Glioma Therapy.[Pubmed:28371526]

Adv Healthc Mater. 2017 Jun;6(12).

Gliomas are highly radioresistant tumors, mainly due to hypoxia in the core region of the gliomas and efficient DNA double-strand break repair. However, the design of a radiosensitizer incorporating the two above mechanisms is difficult and has rarely been reported. Thus, this study develops a hypoxic radiosensitizer-prodrug liposome (MLP) to deliver the DNA repair inhibitor Dbait (MLP/Dbait) to achieve the simultaneous entry of radiosensitizers with two different mechanisms into the glioma. MLP/Dbait effectively sensitizes glioma cells to X-ray radiotherapy (RT). Histological and microscopic examinations of dissected brain tissue confirm that MLP effectively delivers Dbait into the glioma. Furthermore, the combination of MLP/Dbait with RT significantly inhibits growth of the glioma, as assessed by in vivo bioluminescence imaging. These findings suggest that MLP is a promising candidate as a Dbait delivery system to enhance the effect of RT on glioma, owing to the synergistic effects of the two different radiosensitizers.

Discovery and initial SAR of inhibitors of interleukin-1 receptor-associated kinase-4.[Pubmed:16563752]

Bioorg Med Chem Lett. 2006 Jun 1;16(11):2842-5.

High-throughput screening of a small-molecule compound library resulted in the identification of a novel series of N-acyl 2-aminobenzimidazoles that are potent inhibitors of interleukin-1 receptor-associated kinase-4.

Description

IRAK-1-4 Inhibitor I is an inhibitor of interleukin-1 receptor-associated kinase 1/4 (IRAK 1/4) with IC50s of 0.2 μM and 0.3 μM, respectively.

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