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Merck
CN
所有图片(1)

主要文件

N8534

Sigma-Aldrich

Nilutamide

solid

别名:

5,5-Dimethyl-3-[4-nitro-3-(trifluoromethyl)phenyl]-2,4-imidazolidinedione, Anandron, RU-23908

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About This Item

经验公式(希尔记法):
C12H10F3N3O4
CAS号:
分子量:
317.22
MDL编号:
UNSPSC代码:
51111800
PubChem化学物质编号:
NACRES:
NA.77

表单

solid

质量水平

创始人

Sanofi Aventis

SMILES字符串

CC1(C)NC(=O)N(c2ccc(c(c2)C(F)(F)F)[N+]([O-])=O)C1=O

InChI

1S/C12H10F3N3O4/c1-11(2)9(19)17(10(20)16-11)6-3-4-8(18(21)22)7(5-6)12(13,14)15/h3-5H,1-2H3,(H,16,20)

InChI key

XWXYUMMDTVBTOU-UHFFFAOYSA-N

基因信息

human ... AR(367)

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应用

Nilutamide has been used:
  • as a nuclear androgen receptor (nAR) inhibitor to study its effects on oocyte maturation in zebrafish
  • to determine its effects on bioluminescent Saccharomyces cerevisiae bioreporters in BLYAS assay
  • as a substrate in hydrogenation reaction

生化/生理作用

Nilutamide is a nuclear androgen receptor inhibitor. It is a nonsteroidal antiandrogen that competitively inhibits the binding of dihydrotestosterone to the androgen receptor. Nilutamide shows a therapeutic effect against prostate cancer.

特点和优势

This compound is featured on the Nuclear Receptors (Steroids) page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
This compound was developed by Sanofi Aventis. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

象形图

Skull and crossbonesHealth hazard

警示用语:

Danger

危险声明

预防措施声明

危险分类

Acute Tox. 3 Oral - Repr. 1B

储存分类代码

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Faceshields, Gloves, type P3 (EN 143) respirator cartridges


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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A Desai et al.
Urology, 58(6), 1016-1020 (2001-12-18)
To study the ability of nilutamide to induce prostate-specific antigen (PSA) responses in patients with hormone-resistant prostate cancer who had been exposed to prior antiandrogen therapy, because resistance to antiandrogens may be mediated by altered binding to a mutated or
Ravi A Madan et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 14(14), 4526-4531 (2008-07-17)
We reported previously the first randomized study of any kind in patients with nonmetastatic, castrate-resistant prostate cancer. The study employed vaccine, the hormone nilutamide, and the combined therapy (crossover for each arm) with an endpoint of time to progression. We
Richard Choo et al.
International journal of radiation oncology, biology, physics, 75(4), 983-989 (2009-05-05)
To determine the efficacy of a combined approach of radiotherapy (RT) plus 2-year androgen suppression (AS) as salvage treatment for prostate-specific antigen (PSA) relapse after radical prostatectomy (RP). Seventy-five patients with PSA relapse after RP were treated with salvage RT
Jing Yu et al.
Endocrinology, 151(4), 1822-1828 (2010-03-03)
The mechanisms of testosterone-induced vasodilatation are not fully understood. This study investigated the effect of testosterone on nitric oxide (NO) synthesis and its molecular mechanism using human aortic endothelial cells (HAEC). Testosterone at physiological concentrations (1-100 nm) induced a rapid
Masayasu Urushibara et al.
The Prostate, 67(8), 799-807 (2007-03-22)
Molecular basis for secondary antiandrogen therapy in prostate cancer with mutant androgen receptors (ARs) is not fully elucidated. Effects of steroidal and non-steroidal antiandrogens on transcriptional activities of wild-type and mutant (W741C, T877A, and W741C+T877A) ARs were measured. Crystal structure

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