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SML0264

Sigma-Aldrich

AEG 3482

≥98% (HPLC)

别名:

6-Phenyl-imidazo[2,1-b]-1,3,4-thiadiazole-2-sulfonamide

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About This Item

经验公式（希尔记法）:
C10H8N4O2S2
CAS号:
63735-71-7
分子量:
280.33
MDL號碼:
MFCD02064987
分類程式碼代碼:
12352200
PubChem物質ID:
329825272
NACRES:
NA.77

品質等級

100

化驗

≥98% (HPLC)

形狀

powder

顏色

faintly yellow to dark yellow

溶解度

DMSO: ≥15 mg/mL

儲存溫度

2-8°C

SMILES 字串

NS(=O)(=O)c1nn2cc(nc2s1)-c3ccccc3

InChI

1S/C10H8N4O2S2/c11-18(15,16)10-13-14-6-8(12-9(14)17-10)7-4-2-1-3-5-7/h1-6H,(H2,11,15,16)

InChI 密鑰

MQUYTXDAVCOCMX-UHFFFAOYSA-N

生化／生理作用

AEG 3482 is an imidazothiadiazole sulfonamide of 281 D with an anti-apoptotic property.
AEG3284 is a compound that binds to heat shock protein 90 (HSP90), leading to heat shock factor 1 (HSF1) dependent expression of HSP70, an endogenous inhibitor of c-Jun N-terminal kinase (JNK) activity. Treatment of PC12 cells with AEF3284 blocks JNK dependent apoptosis.

特點和優勢

This compound is featured on the MAPKs page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

象形圖

Exclamation mark
GHS07

訊號詞

Warning

危險聲明

H302

危險分類

Acute Tox. 4 Oral

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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Amir H Salehi et al.
Chemistry & biology, 13(2), 213-223 (2006-02-24)
We describe a group of small-molecule inhibitors of Jun kinase (JNK)-dependent apoptosis. AEG3482, the parental compound, was identified in a screening effort designed to detect compounds that reduce apoptosis of neonatal sympathetic neurons after NGF withdrawal. We show that AEG3482
Karthiga Santhana Kumar et al.
SpringerPlus, 4, 19-19 (2015-01-28)
Medulloblastoma (MB) comprises four molecularly and genetically distinct subgroups of embryonal brain tumors that develop in the cerebellum. MB mostly affects infants and children and is difficult to treat because of frequent dissemination of tumor cells within the leptomeningeal space.
Zhen Ning Wee et al.
Nature communications, 6, 8746-8746 (2015-10-28)
Metastatic tumour recurrence due to failed treatments remains a major challenge of breast cancer clinical management. Here we report that interleukin-1 receptor-associated kinase 1 (IRAK1) is overexpressed in a subset of breast cancers, in particular triple-negative breast cancer (TNBC), where

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