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Beschreibung

A cell-permeable BX795 analog (>Cat. No. 204001) that acts as a potent, ATP-competitive, and reversible dual kinase inhibitor of TBK1/IKKepsilon (IC50 = 19 and 160 nM, respectively) with excellent selectivity over IKKalpha and IKKbeta (IC50 >10 µ,M). Interacts with the TBK1 kinase dimer interface and stabilizes the inactive DFG-out conformation. Also blocks the activity of MARK (microtubule- associated protein (MAP)-microtubule affinity regulating kinase) 1, 2, 3, and 4 (IC50 = 27, 52, 36, and 41 nM, respectively), SIK2 (IC50 = 67 nM) and Aurora B, JAK2, and MLK1,3 (> than 90% inhibition at 1 µ,M) in a 108-kinase panel. Increases TNF-alpha-stimulated NF-kappaB-dependent gene transcription in wild-type macrophages and enhances CREB-dependent gene transcription by promoting dephosphorylation of CREB-regulated transcription coactivator (CRTC3). Shown to aid TLR-stimulated production of anti-Inflammatory cytokines in macrophages while suppressing the secretion of pro-inflammatory cytokines. In response to pro-inflammatory stimuli, pre-treatment of BX795 robustly suppresses the activation of JNK and p38alpha, whereas MRT67307 does not exhibit such off-target effects., A cell-permeable BX795 analog (>Cat. No. 204001) that acts as a potent, ATP-competitive, and reversible dual kinase inhibitor of TBK1/IKKepsilon (IC50 = 19 and 160 nM, respectively) with excellent selectivity over IKKalpha and IKKbeta (IC50 >10 µ,M). Interacts with the TBK1 kinase dimer interface and stabilizes the inactive DFG-out conformation. Also blocks the activity of MARK (microtubule- associated protein (MAP)-microtubule affinity regulating kinase) 1, 2, 3, and 4 (IC50 = 27, 52, 36, and 41 nM, respectively), SIK2 (IC50 = 67 nM) and Aurora B, JAK2, and MLK1,3 (> than 90% inhibition at 1 µ,M) in a 108-kinase panel. Increases TNF-alpha-stimulated NF-kappaB-dependent gene transcription in wild-type macrophages and enhances CREB-dependent gene transcription by promoting dephosphorylation of CREB-regulated transcription coactivator (CRTC3). Shown to aid TLR-stimulated production of anti-Inflammatory cytokines in macrophages while suppressing the secretion of pro-inflammatory cytokines. In response to pro-inflammatory stimuli, pre-treatment of BX795 robustly suppresses the activation of JNK and p38alpha, whereas MRT67307 does not exhibit such off-target effects.Please note that the molecular weight for this compound is batch-specific due to variable water content. Please refer to the vial label or the certificate of analysis for the batch-specific molecular weight. The molecular weight provided represents the baseline molecular weight without water and salt.