MLN120BIκB Kinase β Inhibitor CAS# 783348-36-7 |
2D Structure
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Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 783348-36-7 | SDF | Download SDF |
PubChem ID | 9929127 | Appearance | Powder |
Formula | C19H15ClN4O2 | M.Wt | 366.8 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | ML120B | ||
Solubility | DMSO : ≥ 31 mg/mL (84.51 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | N-(6-chloro-7-methoxy-9H-pyrido[3,4-b]indol-8-yl)-2-methylpyridine-3-carboxamide | ||
SMILES | CC1=C(C=CC=N1)C(=O)NC2=C3C(=CC(=C2OC)Cl)C4=C(N3)C=NC=C4 | ||
Standard InChIKey | ZNOLRTPMNMPLHY-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C19H15ClN4O2/c1-10-11(4-3-6-22-10)19(25)24-17-16-13(8-14(20)18(17)26-2)12-5-7-21-9-15(12)23-16/h3-9,23H,1-2H3,(H,24,25) | ||
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 | MLN120B is an inhibitor of IkappaB kinase beta. | |||||
Targets | IkappaB beta |
MLN120B Dilution Calculator
MLN120B Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7263 mL | 13.6314 mL | 27.2628 mL | 54.5256 mL | 68.157 mL |
5 mM | 0.5453 mL | 2.7263 mL | 5.4526 mL | 10.9051 mL | 13.6314 mL |
10 mM | 0.2726 mL | 1.3631 mL | 2.7263 mL | 5.4526 mL | 6.8157 mL |
50 mM | 0.0545 mL | 0.2726 mL | 0.5453 mL | 1.0905 mL | 1.3631 mL |
100 mM | 0.0273 mL | 0.1363 mL | 0.2726 mL | 0.5453 mL | 0.6816 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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MLN120B is a potent and effective inhibitor of IκB kinase beta subunit (IKKβ) with IC50 value of 20 μM [1].
IKK is an enzyme complex which is a part of the upstream of NF-κB signal transduction cascade. It is composed of three subunits, including IKKα, IKKβ and IKKγ. The IKKβ subunit is able to phosphorylate IκBα protein. Normally, IκBα protein inactivate NF-κB transcription factors and keep them sequestering in inactive state in the cytoplasm. However, once IκBα protein is phosphorylated by IKKβ subunit, the IκBα protein will be dissociated from NF-κB transcription factor and thus remove the inactivation effect. Therefore, the transcription of NF-κB will be activated. This signaling pathway is involved in many immune and inflammatory processes.
In multiple myeloma cell line RPMI 8226 and INA 6, treatment of MLN120B resulted in the dose-dependent inhibition of IKKβ-induced IκBα protein phosphorylation and subsequent NF-κB activation. Additionally, it was observed that MLN120B was able to block TNF-α-induced NF-κB activation in MM.1S cell line. These observations suggested the inhibitory action of MLN120B on IKKβ. [1].
In mouse model, polyarthritis was introduced in footpads, where IKKβ-induced NF-κB activation might result in a serial of advert effects. Oral administration of MLN120B (12 mg/kg twice daily) inhibited paw swelling in a dose-dependent manner, and offered protection against arthritis-induced weight loss. Therefore, it could be implied that MLN120B was able to inhibit IKKβ-induced NF-κB activation [2].
References:
[1]. Hideshima T, Neri P, Tassone P. MLN120B, a novel IkappaB kinase beta inhibitor, blocks multiple myeloma cell growth in vitro and in vivo. Clin Cancer Res. 2006, 12(19): 5887-5894.
[2]. Schopf L, Savinainen A, Anderson K. IKKbeta inhibition protects against bone and cartilage destruction in a rat model of rheumatoid arthritis. Arthritis Rheum. 2006, 54(10): 3163-3173.
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MLN120B, a novel IkappaB kinase beta inhibitor, blocks multiple myeloma cell growth in vitro and in vivo.[Pubmed:17020997]
Clin Cancer Res. 2006 Oct 1;12(19):5887-94.
PURPOSE: The purpose of this study is to delineate the biological significance of IkappaB kinase (IKK) beta inhibition in multiple myeloma cells in the context of bone marrow stromal cells (BMSC) using a novel IKKbeta inhibitor MLN120B. EXPERIMENTAL DESIGN: Growth-inhibitory effect of MLN120B in multiple myeloma cells in the presence of cytokines [interleukin-6 (IL-6) and insulin-like growth factor-I (IGF-1)], conventional agents (dexamethasone, melphalan, and doxorubicin), or BMSC was assessed in vitro. In vivo anti-multiple myeloma activity of MLN120B was evaluated in severe combined immunodeficient (SCID)-hu model. RESULTS: MLN120B inhibits both baseline and tumor necrosis factor-alpha-induced nuclear factor-kappaB activation, associated with down-regulation of IkappaBalpha and p65 nuclear factor-kappaB phosphorylation. MLN120B triggers 25% to 90% growth inhibition in a dose-dependent fashion in multiple myeloma cell lines and significantly augments tumor necrosis factor-alpha-induced cytotoxicity in MM.1S cells. MLN120B augments growth inhibition triggered by doxorubicin and melphalan in both RPMI 8226 and IL-6-dependent INA6 cell lines. Neither IL-6 nor IGF-1 overcomes the growth-inhibitory effect of MLN120B. MLN120B inhibits constitutive IL-6 secretion by BMSCs by 70% to 80% without affecting viability. Importantly, MLN120B almost completely blocks stimulation of MM.1S, U266, and INA6 cell growth, as well as IL-6 secretion from BMSCs, induced by multiple myeloma cell adherence to BMSCs. MLN120B overcomes the protective effect of BMSCs against conventional (dexamethasone) therapy. CONCLUSIONS: Our data show that the novel IKKbeta inhibitor MLN120B induces growth inhibition of multiple myeloma cells in SCID-hu mouse model. These studies provide the framework for clinical evaluation of MLN120B, alone and in combined therapies, trials of these novel agents to improve patient outcome in multiple myeloma.
Imaging pulmonary NF-kappaB activation and therapeutic effects of MLN120B and TDZD-8.[Pubmed:21966423]
PLoS One. 2011;6(9):e25093.
NF-kappaB activation is a critical signaling event in the inflammatory response and has been implicated in a number of pathological lung diseases. To enable the assessment of NF-kappaB activity in the lungs, we transfected a luciferase based NF-kappaB reporter into the lungs of mice or into Raw264.7 cells in culture. The transfected mice showed specific luciferase expression in the pulmonary tissues. Using these mouse models, we studied the kinetics of NF-kappaB activation following exposure to lipopolysaccharide (LPS). The Raw264.7 cells expressed a dose-dependent increase in luciferase following exposure to LPS and the NF-kappaB reporter mice expressed luciferase in the lungs following LPS challenge, establishing that bioluminescence imaging provides adequate sensitivity for tracking the NF-kappaB activation pathway. Interventions affecting the NF-kappaB pathway are promising clinical therapeutics, thus we further examined the effect of IKK-2 inhibition by MLN120B and glycogen synthase kinase 3 beta inhibition by TDZD-8 on NF-kappaB activation. Pre-treatment with either MLN120B or TDZD-8 attenuated NF-kappaB activation in the pulmonary tissues, which was accompanied with suppression of pro-inflammatory chemokine MIP-1ss and induction of anti-inflammatory cytokine IL-10. In summary, we have established an imaging based approach for non-invasive and longitudinal assessment of NF-kappaB activation and regulation during acute lung injury. This approach will potentiate further studies on NF-kappaB regulation under various inflammatory conditions.