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BMS-345541

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Chemical Structure| 445430-58-0 同义名 : -
CAS号 : 445430-58-0
货号 : A375644
分子式 : C14H17N5
纯度 : 99%+
分子量 : 255.318
MDL号 : MFCD18089812
存储条件：

粉末 Keep in dark place,Inert atmosphere,2-8°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 9 mg/mL(35.25 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO

H2O: 10 mg/mL(39.17 mM)，配合低频超声，并水浴加热至45℃助溶
动物实验配方：
生物活性
描述 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 p21 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.
细胞研究
细胞系 浓度 检测类型 检测时间 活动说明 数据源
SF9 cells 20 μM Function assay Inhibition of purified recombinant histidine-HA-tagged IKK-beta expressed in SF9 cells at 20 uM 18702457
THP1 cells Function assay Inhibition of LPS-induced TNFalpha secretion in THP1 cells, IC50=4 μM 17197177
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

3.92mL

0.78mL

0.39mL

19.58mL

3.92mL

1.96mL

39.17mL

7.83mL

3.92mL