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关于此项目
经验公式(希尔记法):
C21H27ClO5
化学文摘社编号:
分子量:
394.89
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
SMILES string
ClCC(O)COc1ccc(cc1)C(C)(C)c2ccc(cc2)OCC(O)CO
InChI
1S/C21H27ClO5/c1-21(2,15-3-7-19(8-4-15)26-13-17(24)11-22)16-5-9-20(10-6-16)27-14-18(25)12-23/h3-10,17-18,23-25H,11-14H2,1-2H3
InChI key
HDTYUHNZRYZEEB-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 15 mg/mL, clear
storage temp.
−20°C
Quality Level
Biochem/physiol Actions
EPI-001 is a specific inhibitor of the AR (androgen receptor) without inhibiting PR or GR transcriptional activities.
EPI-001 is a specific inhibitor of the AR (androgen receptor) without inhibiting PR or GR transcriptional activities. EPI-001 selectively interacts with transactivation unit 5 (Tau-5) of the androgen receptor, which is essential for prostate cells to proliferate in the absence of androgens. EPI-001 is active against castration-resistant prostate cancer (CRPC) in xenografts.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Eva De Mol et al.
ACS chemical biology, 11(9), 2499-2505 (2016-06-30)
Castration-resistant prostate cancer is the lethal condition suffered by prostate cancer patients that become refractory to androgen deprivation therapy. EPI-001 is a recently identified compound active against this condition that modulates the activity of the androgen receptor, a nuclear receptor
Raymond J Andersen et al.
Cancer cell, 17(6), 535-546 (2010-06-15)
Castration-recurrent prostate cancer (CRPC) is suspected to depend on androgen receptor (AR). The AF-1 region in the amino-terminal domain (NTD) of AR contains most, if not all, of the transcriptional activity. Here we identify EPI-001, a small molecule that blocked
Lucas J Brand et al.
Oncotarget, 6(6), 3811-3824 (2015-02-12)
The androgen receptor (AR) is a driver of prostate cancer (PCa) cell growth and disease progression. Therapies for advanced PCa exploit AR dependence by blocking the production or action of androgens, but these interventions inevitably fail via multiple mechanisms including
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