Molecular Weight(MW): 255.32
BMS-345541 is a highly selective inhibitor of the catalytic subunits of IKK-2 and IKK-1 with IC50 of 0.3 μM and 4 μM in cell-free assays, respectively.
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(E) After transfection with control or catalase siRNAs for 24 h, A375 and G361 cells were treated with vehicle or 2.5 µM BMS-345541, 20 µM PS-1145 and/or 50 µM of fotemustine for an additional 48 h. Cell viability was then assessed. *, p<0.05. (F) A375 and G361 cells were treated with vehicle or 2.5 µM BMS-345541, 20 µM PS-1145 and/or 50 µM of fotemustine, in the presence or absence of catalase inhibitor 3-Amino-1,2,4-triazole (ATZ, 50 µM) for 48 h. Cell viability was then assessed. *, p<0.05.
Redox Biol, 2017, 11:562-576. BMS-345541 purchased from Selleck.
Sub-cellular fractionation of cellular lysates from a representative cell line (KMJR138) was probed for the indicated proteins. Cells were treated with DMSO (control), IFN-γ (IFN, +), I-BET151 (IBET), BMS-345541 (BMS) for 48 hours and separated into cytosolic (C) or nuclear (N) fractions. One representative blot out of two independent experiments is shown.
PLoS One, 2015, 10(4): e0123410 . BMS-345541 purchased from Selleck.
NF-κB-specific inhibitor BMS‐345541 (2 µM) dissolved in DMSO was added together with bleomycin (2 µg/ml) in the culture medium and treated A549 and AEC2 for 5 days; NF-κB activation and P21WAF1 expression was detected by western blot.
Immunol Res, 2017, 65(5):1065-1073. BMS-345541 purchased from Selleck.
LPS/IFNγ-induced Gas7 expression inM1 alveolar macrophages was dependent on the NF-κB pathway. Gene expressions of Tnf, Il1b, and Gas7 in primary alveolar macrophage from C57BL/6 were analyzed by RT-qPCR. Cells were pretreated with DMSO or BMS (4 μM) for 2 h; afterwards, LPS/IFNγ was added for another 6 and 24 h. Untreated cells (M0) served as controls. Relative expression was normalized to Actb and then converted to the fold change overM0 (M0 omitted because = 1.0 by definition). Results are the mean of three independent experiments. Twotailed Student’s t test (all M1 vs. M1 + BMS column), *p < 0.05, **p < 0.01, ***p < 0.001)
Immunol Res, 2017, 65(5):1065-1073. BMS-345541 purchased from Selleck.
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Choose Selective IκB/IKK Inhibitors
|Description||BMS-345541 is a highly selective inhibitor of the catalytic subunits of IKK-2 and IKK-1 with IC50 of 0.3 μM and 4 μM in cell-free assays, respectively.|
|Features||Allosteric IKK inhibitor with anti-inflammatory activity.|
BMS-345541 dose-dependently inhibits the TNF-α-stimulated phosphorylation of IκBα in THP-1 monocytic cells with an IC50 of ~4 μM. BMS-345541 inhibits lipopolysaccharide-stimulated tumor necrosis factorα, interleukin-1β, interleukin-8, and interleukin-6 in THP-1 cells with IC50 values in the 1- to 5 μM range. BMS-345541 binds in a mutually exclusive manner with respect to a peptide inhibitor corresponding to amino acids 26 - 42 of IκBα with Ser-32 and Ser-36 changed to aspartates and in a non-mutually exclusive manner with respect to ADP. BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, which then affects the active sites of the subunits differently.  BMS-345541 affects several mitotic cell cycle transitions, including mitotic entry, prometaphase to anaphase progression and cytokinesis. Adding BMS-345541 to the cells released form arrest in G-phase blocks the activation of Aurora A, B, and C, Cdk1 activation and histone H3 phosphorylation. Treatment of the mitotic cells with BMS-345541 results in precocious cyclin B1 and securin degradation, defective chromosome separation and improper cytokinesis. BMS-345541 is also found to override the spindle checkpoint in nocodazole-arrested cells. These effects are not primarily due to a direct inhibitory effect of BMS-345541 on mitotic kinases such as Cdk1, Aurora A or B, Plk1 or NEK2.  BMS-345541 (10 μM) inhibits growth of Normal human epidermal melanocytes, and metastatic melanoma cells (SK-MEL-5, A375, and Hs 294T) by 96% and 99% at 72h, respectively. Application of 100 μM of BMS-345541 to SK-MEL-5 cell culture results in 87% apoptotic cells at 24 h through caspase-independent and AIF-dependent mitochondria-mediated manner. BMS-345541 treatment (10 μM) results in 76% and 95% reduction in IKK activities and NF-kB activity, as well as CXCL1 production.  BMS-345541 inhibits the growth of T-cell acute lymphoblastic leukemia (T-ALL) cells line BE-13, RPMI-8402 and DND-41, all three harboring a Notch1 mutation, and T-ALL primary cells from pediatric patients, with IC50 of 2-6 μM. 5 μM BMS-345541 induces an arrest in the G2/M phase of the cell cycle in BE-13 and DND-41 cells, and sub-G1 peak increase in RPMI-8402 cells. 5 μM BMS-345541 treated for 16 h leads to an increase in apoptotic cells in all these cell, accompanied by a time-dependent cleavage of procaspase-8, procaspase-3 and poly (ADP-ribose) polymerase (PARP). BMS-34554 (5 μM) induces a time dependent dephosphorylation of IκBα and p65. T-ALL cells treated with BMS-345541 displays nuclear translocation of FOXO3a and restoration of its functions, including control of p21Cip1 expression levels.  BMS-345541 inhibits the TNFα-induced expression of both ICAM-1 and VCAM-1 in human umbilical vein endothelial cells with IC50 of 5 μM. 
BMS-345541 effectively inhibits melanoma tumor growth in a dose-dependent manner. Tumor-bearing mice treated with 75 mg/kg of BMS-345541 shows effective inhibition of growth of SK-MEL-5, A375, and Hs 294T tumors by 86 %, 69% and 67%, respectively, when compared with control animals treated with vehicle alone.  BMS-345541 administered orally at doses of 100 mg/kg, reduces the severity of dextran sulfate sodium-induced colitis in mice with weight ratio, clinical scoring of colons, mean injury score and mean inflammation score of 0.86 (vs 0.77 of vehicle group), 1.0 (vs 2.5 of vehicle group), 5.66 (vs 8.52 of vehicle group), 6.82 (vs 12.33 of vehicle group), respectively.  BMS-345541 (100 mg/kg), when administered by oral gavage in water once daily beginning at the time of the first collagen immunization, inhibits clinical signs of disease in the murine CIA model (0 vs ~8 of vehicle group), accompanied by reduced paw swelling. BMS-345541 (100 mg/kg) reduces cumulative arthritis injury score from 4.4 to 0, accompanied by lower degrade of tibiotarsal joints and severity of inflammation, synovial hyperplasia, bone resorption, and cartilage erosion. No discernible injury is observed in the joints of animals, which is histologically indistinguishable from those from age-matched, disease-free control animals. BMS-345541 dose-dependently inhibits IL-1β message, with animals in the 100 mg/kg dose group showing levels comparable with those of disease-free control animals. 
Enzyme Assays:Assays measuring the enzyme-catalyzed phosphorylation of GST-IκBα are performed by adding enzyme (a final concentration of 0.5 μg/mL) at 30 ℃ to solutions of 100 μg/mL GST- IκBα and 5 μM [33P]ATP in 40 mM Tris HCl, pH 7.5, containing 4 mM MgCl2, 34mM sodium phosphate, 3 mM NaCl, 0.6 mM potassium phosphate, 1 mM KCl, 1 mM dithiothreitol, 3% (w/v) glycerol, and 250 μg/mL bovine serum albumin. The specific activity of [33P]ATP used in the assay is 100 Ci/mmol. After 5 min, the kinase reactions are stopped by the addition of 2× Laemmli sample buffer and heat-treated at 90 ℃ for 1 min. The samples are then loaded on to NuPAGE 10% BisTris gels. After completion of SDS-PAGE, gels are dried on a slab gel dryer. The bands are then detected using a 445Si PhosphorImager, and the radioactivity is quantified using ImageQuant software. Under these conditions, the degree of phosphorylation of GST-IκBα is linear with time and concentration of enzyme.
-  Burke JR, et al. J Biol Chem, 2003, 278(3), 1450-1456.
-  Blazkova H, et al. Cell Cycle, 2007, 6(20), 2531-2540.
-  Yang J, et al. Clin Cancer Res, 2006, 12(3 Pt 1), 950-960.
|In vitro||DMSO||9 mg/mL (35.24 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
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