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SML2984

Sigma-Aldrich

BIX02188

≥98% (HPLC)

同義詞:

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

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About This Item

經驗公式（希爾表示法）:
C25H24N4O2
CAS號碼:
334949-59-6
分子量：:
412.48
MDL號碼:
MFCD18157583
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

100

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

−20°C

SMILES 字串

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 密鑰

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.
Selective MEK5 Inhibitor; inhibitor of MEK5/ERK5 signaling.

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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分析證明 (COA)

Lot/Batch Number

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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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