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Merck
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重要文件

SML3008

Sigma-Aldrich

SCIO-469

≥98% (HPLC)

同義詞:

2-(6-Chloro-5-((2R,5S)-4-(4-fluorobenzyl)-2,5-dimethylpiperazine-1-carbonyl)-1-methyl-1H-indol-3-yl)-N,N-dimethyl-2-oxoacetamide, 6-Chloro-5-[[(2R,5S)-4-[(4-fluorophenyl)methyl]-2,5-dimethyl-1-piperazinyl]carbonyl]-N,N,1-trimethyl-a-oxo-1H-indole-3-acetamide, SCIO 469, SCIO469, Scios 469, Scios-469, Scios469, Talmapimod

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About This Item

經驗公式(希爾表示法):
C27H30ClFN4O3
CAS號碼:
分子量::
513.00
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.77

品質等級

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

SMILES 字串

O=C(C(C1=CN(C2=C1C=C(C(Cl)=C2)C(N3[C@@H](CN([C@H](C3)C)CC4=CC=C(C=C4)F)C)=O)C)=O)N(C)C

InChI

1S/C27H30ClFN4O3/c1-16-13-33(17(2)12-32(16)14-18-6-8-19(29)9-7-18)26(35)21-10-20-22(25(34)27(36)30(3)4)15-31(5)24(20)11-23(21)28/h6-11,15-17H,12-14H2,1-5H3/t16-,17+/m0/s1

InChI 密鑰

ZMELOYOKMZBMRB-DLBZAZTESA-N

相關類別

生化/生理作用

Orally active, potent and selective mitogen-activated protein kinase (MAPK) p38alpha (p38α, MAPK14) inhibitor in vitro and in vivo.
SCIO-469 (Talmapimod) is an orally active, potent and selective mitogen-activated protein kinase (MAPK) p38alpha (p38α, MAPK14) inhibitor (IC50 = 9 nM; 10-fold over p38β, >2000-fold over 20 other kinases) with no significant affinity toward a panel of 70 enzymes and receptors. SCIO-469 inhibits multiple myeloma (MM) growth in mice in vivo (150 or 450 mg/kg powder diet; 5T2MM and 5T33MM) and augments proteasome inhibitor in a murine plasmacytoma model of MM (0.2 mg bortezomib/kg i.v. twice weekly with 30 mg SCIO-469/kg b.i.d. p.o.; RPMI8226).

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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Yuan-Feng Lin et al.
Journal of cellular and molecular medicine, 22(4), 2458-2468 (2018-02-03)
Paclitaxel-based chemotherapy is a common strategy to treat patients with triple-negative breast cancer (TNBC). As paclitaxel resistance is still a clinical issue in treating TNBCs, identifying molecular markers for predicting pathologic responses to paclitaxel treatment is thus urgently needed. Here

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