4(2'- aminoethyl)amino- 1,8- dimethylimidazo(1,2- a)quinoxaline

01/01/2015 - "In vivo and in vitro treatment with BMS-345541 was ineffective at altering these variables when administered at concentrations that were highly effective in models of acute inflammation. "
01/01/2020 - "BMS-345541 reversed the inflammation-induced atrophy program as indicated by a reduced expression of the atrogenes Trim63/MuRF1, Fbxo32/Atrogin1, and Fbxo30/MuSA1. "
01/01/2020 - "Analysis of the fiber type specific myocyte cross-sectional area showed that BMS-345541 reduced inflammation-induced atrophy of slow/type I and fast/type II myofibers compared with vehicle-treated septic mice. "
01/01/2020 - "Morphological and molecular analyses were used to investigate the phenotype of inflammation-induced muscle atrophy and the effects of BMS-345541 treatment. "
01/01/2020 - "BMS-345541 diminished inflammation-induced atrophy as shown by a reduced weight loss of the gastrocnemius/plantaris (vehicle: -21.2% and BMS-345541: -10.4%; P < 0.05), tibialis anterior (vehicle: -22.7% and BMS-345541: -17.1%; P < 0.05) and soleus (vehicle: -21.1% and BMS-345541: -11.3%; P < 0.05) in septic mice. "

12/01/2003 - "Against dextran sulfate sodium-induced colitis in mice, BMS-345541 administered orally at doses of 30 and 100 mg/kg was effective in blocking both clinical and histological endpoints of inflammation and injury. "
12/01/2003 - "An inhibitor of IkappaB kinase, BMS-345541, blocks endothelial cell adhesion molecule expression and reduces the severity of dextran sulfate sodium-induced colitis in mice."

10/15/2007 - "Since deregulation of the cell cycle is one of the hallmarks of tumor formation and progression, the newly discovered level of BMS-345541 function could be useful for cell cycle control studies and may provide valuable clues for the design of future therapeutics."
06/06/2017 - "Breast tumor-bearing mice treated with BMS-345541 showed a statistically significant decrease in tumor volume and exhibited prolonged survival compared to control mice, with a median survival of 78 d for the BMS-345541-treated group vs. 58 d for the controls. "
12/01/2013 - "In contrast to other cancer cell lines, viral titer is not recovered by BMS-345541 when myeloma cells are pretreated with interferon β. "
11/01/2018 - "Previous studies have shown that BMS-345541 (BMS, a specific IκB kinase β inhibitor) sensitized various tumor cells including MCF-7 breast cancer cells to ionizing radiation (IR). "
02/01/2006 - "BMS-345541 down-regulation of IKK activity results in mitochondria-mediated apoptosis of tumor cells because the programmed cell death machinery in melanoma cells is highly regulated by NF-kappaB signaling. "

06/06/2017 - "Thus, the suppression of NFκB signaling by BMS-345541 is a potentially important advance in controlling breast cancer growth and metastases."
06/06/2017 - "Breast tumor-bearing mice treated with BMS-345541 showed a statistically significant decrease in tumor volume and exhibited prolonged survival compared to control mice, with a median survival of 78 d for the BMS-345541-treated group vs. 58 d for the controls. "
02/01/2013 - "BMS-345541 sensitizes MCF-7 breast cancer cells to ionizing radiation by selective inhibition of homologous recombinational repair of DNA double-strand breaks."
11/01/2018 - "Previous studies have shown that BMS-345541 (BMS, a specific IκB kinase β inhibitor) sensitized various tumor cells including MCF-7 breast cancer cells to ionizing radiation (IR). "
02/01/2013 - "Our study was to elucidate the mechanisms whereby BMS-345541 (BMS, a specific IκB kinase β inhibitor) inhibits the repair of DNA double-strand breaks (DSBs) and evaluate whether BMS can sensitize MCF-7 breast cancer cells (MCF-7 cells) to ionizing radiation (IR) in an apoptosis-independent manner. "

03/05/2012 - "BMS-345541 inhibited activation of caspase-3, and attenuated apoptotic cell death in spinal cord by modulating Bcl-2 and Bax expression following SCI. Our study indicates that BMS-345541 may play an important role on the anti-inflammatory and anti-apoptotic effects with experimental SCI. Our results imply the IKK inhibitors may be useful in the therapy of spinal cord injury."