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Fenretinide
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Fenretinide图片
CAS NO:65646-68-6
规格:98%
分子量:391.55
包装与价格:
包装价格(元)
10mg电议
50mg电议

产品介绍
Synthetic retinoid agonist
CAS:65646-68-6
分子式:C26H33NO2
分子量:391.55
纯度:98%
存储:Store at -20°C

Background:

Fenretinide(4HPR) is an inhibitor of Focal adhesion kinase (FAK) [1].


Fenretinideis a vitamin A analogue, it has been shown toinhibit the growth of many tumor cells, including small-cell lung cancer, malignant hemopoietic cells, and breast cancer cells. Fenretinide may also protectwomen against the development of ovarian cancer. The effect of Fenretinide on several gynecologic cancer cell lines shows the IC50 values of Fenretinide are only 0.3 and 0.4μM in two ovarian cancer cell lines(222and UCI 101) and are from 1 to 10μM in other ovarian cancer cell lines and cervical, endometrial cancer cell lines [2].


Fenretinide has also been shown to induce apoptosis inhuman prostate carcinoma cells (HPC).The IC50s of Fenretinide in LNCaP, DU145, and PC-3 are 0.9±0.16μM, 4.4±0.45μM and 3.0±1.0μM,respectively.Fenretinide induces this apoptosis through increasingROS and increasing enzymatic labeling of DNA breaks and formation of a DNA ladder. It is also reported that Fenretinide can impair prostate cancer cell migration and invasion by interfering with FAK/AKT/GSK3β pathway and β-catenin stability [1, 3].


参考文献:
[1] Roberto Benelli, Stefano Monteghirfo, Roberta Venè, Francesca Tosettiand Nicoletta Ferrari.The chemopreventive retinoid 4HPR impairs prostate cancer cell migration and invasion by interfering with FAK/AKT/GSK3β pathway andβ-catenin stability. Molecular Cancer.2010, 9:142-154.
[2] Anita L. Sabichi, Denver T. Hendricks, Mary A. Bober, Michael J. Birrer. Retinoic acid receptorβexpression and growthinhibition of gynecologic cancer cells by thesynthetic retinoidn-(4-hydroxyphenyl) retinamide. Journal of the National Cancer Institute. 1998, 90(8): 597-605.
[3] Shi-Yong Sun, Ping Yue, and Reuben Lotan. Induction of apoptosis by n-(4-hydroxyphenyl)retinamide andits association with reactive oxygen species, nuclearretinoic acid receptors, and apoptosis-related genes in human prostate carcinoma cells.Molecular Pharmacology. 1999, 55:403–410.