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品質等級
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
SMILES 字串
[S](=O)(=O)(NCC)c1ccc(cc1)COc2cc3[o]c4c(nc3cc2)cc[c](c4)=O
InChI 密鑰
AARVTLIQNGAELZ-UHFFFAOYSA-N
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.
potent, selective and extracellularly acting allosteric inhibitor of DDR2 that potently inhibits invasion and migration tumor cells
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
Saumya S Gurbani et al.
Tomography (Ann Arbor, Mich.), 5(1), 53-60 (2019-03-12)
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
Pengwei Lu et al.
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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