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Merck
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SML2786

Sigma-Aldrich

WRG-28

≥98% (HPLC)

别名:

DDR2 inhibitor WRG-28, N-Ethyl-4-[[(3-oxo-3H-phenoxazin-7-yl)oxy]methyl]-benzenesulfonamide

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About This Item

经验公式（希尔记法）:
C21H18N2O5S
CAS号:
1913291-02-7
分子量:
410.44
MDL號碼:
MFCD32201040
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 very dark orange

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

2-8°C

生化／生理作用

WRG-28 is a potent, selective and extracellularly acting allosteric inhibitor of discoidin domain receptor 2 (DDR2) that potently inhibits invasion and migration in mice model of breast cancer. WRG-28 inhibits metastatic breast tumor cell colonization in the lungs.

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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分析证书(COA)

Lot/Batch Number

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Saumya S Gurbani et al.
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Histone deacetylases regulate a wide variety of cellular functions and have been implicated in redifferentiation of various tumors. Histone deacetylase inhibitors (HDACi) are potential pharmacologic agents to improve outcomes for patients with gliomas. We assessed the therapeutic efficacy of belinostat
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Artificial cells, nanomedicine, and biotechnology, 47(1), 3955-3960 (2019-10-02)
Belinostat is a histone deacetylase inhibitor drug capable of regulating cell growth in diverse cancers. Nonetheless, little information clarified the role of Belinostat in breast cancer. Hence, the functions of Belinostat in breast cancer cells survival was disclosed in this
Li Ren Kong et al.
Nature communications, 11(1), 2086-2086 (2020-05-01)
Gain of function (GOF) DNA binding domain (DBD) mutations of TP53 upregulate chromatin regulatory genes that promote genome-wide histone methylation and acetylation. Here, we therapeutically exploit the oncogenic GOF mechanisms of p53 codon 158 (Arg158) mutation, a DBD mutant found
Wen Chiy Liew et al.
The Journal of allergy and clinical immunology, 146(3), 606-620 (2020-02-24)
Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Skin barrier defects contribute to disease initiation and development; however, underlying mechanisms remain elusive. To understand the underlying cause of barrier defect, we investigated aberrant expression of specific microRNAs (miRNAs)

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