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Merck
CN
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安全信息

SML2984

Sigma-Aldrich

BIX02188

≥98% (HPLC)

别名:

(3Z)-3-[[[3-[(Dimethylamino)methyl]phenyl]amino]phenylmethylene]-2,3-dihydro-2-oxo-1H-Indole-6-carboxamide

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About This Item

经验公式（希尔记法）:
C25H24N4O2
CAS号:
334949-59-6
分子量:
412.48
MDL编号:
MFCD18157583
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

100

方案

≥98% (HPLC)

表单

powder

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

−20°C

SMILES字符串

N1c2c(ccc(c2)C(=O)N)\C(=C(\Nc4cc(ccc4)CN(C)C)/c3ccccc3)\C1=O

InChI

1S/C25H24N4O2/c1-29(2)15-16-7-6-10-19(13-16)27-23(17-8-4-3-5-9-17)22-20-12-11-18(24(26)30)14-21(20)28-25(22)31/h3-14,27H,15H2,1-2H3,(H2,26,30)(H,28,31)/b23-22-

InChI key

FSZPIAXLCCQFCM-FCQUAONHSA-N

生化/生理作用

BIX02188 is a potent and selective inhibitor of MEK5 with IC50 of 4.3 nM. BIX02188 also inhibits ERK5 catalytic activity with IC50 of 810 nM, and does not inhibit closely related kinases MEK1, MEK2, ERK2, and JNK2.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

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分析证书(COA)

Lot/Batch Number
0000121151
0000121152
0000113075

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Yutaro Obara et al.
Molecular pharmacology, 77(1), 10-16 (2009-10-28)
Extracellular signal-regulated kinases (ERKs) or mitogen-activated protein kinases (MAPKs) are involved in cellular proliferation, differentiation, migration, and gene expression. The MAPK family includes ERK1/2, c-Jun NH(2)-terminal kinases 1, 2, and 3, p38MAPK alpha, beta, gamma, and -delta, and ERK5 as
Revati J Tatake et al.
Biochemical and biophysical research communications, 377(1), 120-125 (2008-10-07)
We have identified two novel MEK5 inhibitors, BIX02188 and BIX02189, which inhibited catalytic function of purified, MEK5 enzyme. The MEK5 inhibitors blocked phosphorylation of ERK5, without affecting phosphorylation of ERK1/2 in sorbitol-stimulated HeLa cells. The compounds also inhibited transcriptional activation
Fang Tai et al.
Nature communications, 11(1), 258-258 (2020-01-16)
BET bromodomain inhibitors (BETi), such as JQ1, have been demonstrated to effectively kill multiple types of cancer cells. However, the underlying mechanisms for BETi resistance remain largely unknown. Our evidences show that JQ1 treatment evicts BRD4 from the FOXD3-localized MIR548D1

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