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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
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
Reece G Kenny et al.
Journal of inorganic biochemistry, 206, 110981-110981 (2020-02-24)
Vorinostat (suberoylanilide hydroxamic acid; SAHA) and Belinostat are two hydroxamate-based histone deacetylase inhibitors that are used clinically as potent anti-cancer agents. Their metabolic breakdown into inactive metabolites such as carboxylic acid and glucuronic derivatives results in them having short half-lives
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
Frank C Passero et al.
British journal of haematology, 188(2), 295-308 (2019-08-28)
Ixazomib activity and transcriptomic analyses previously established in T cell (TCL) and Hodgkin (HL) lymphoma models predicted synergistic activity for histone deacetylase (HDAC) inhibitory combination. In this present study, we determined the mechanistic basis for ixazomib combination with the HDAC
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