| Project/Area Number |
17K16780
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Urology
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| Research Institution | Chiba University |
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Principal Investigator |
Imamura Yusuke 千葉大学, 大学院医学研究院, 助教 (10568629)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 前立腺癌 / 去勢抵抗性前立腺癌 / 新規薬剤の治療効果比較 / 癌 |
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| Outline of Final Research Achievements |
As a mechanism of castration-resistant prostate cancer, increased expression of Splice Variants lacking the ligand binding domain (LBD) of the androgen receptor (AR) has attracted attention. In recent years, a new drug was developed (EPI-506) which can inhibit all ARs including splice Variants, and clinical trials were conducted in North America. In this study, the therapeutic effect of a similar compound (I-EPI) which is expected to have an inhibitory effect equivalent to or higher than EPI by using immunodeficient mice in animal experiments. Compared with EPI, a certain tumor-reducing effect was observed but not equivalent to EPI.
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| Academic Significance and Societal Importance of the Research Achievements |
進行癌である去勢抵抗性前立腺癌のメカニズムとして、アンドロゲン受容体（Androgen Receptor; AR）のリガンド結合部位（Ligand-binding domain;LBD）が欠失したSplice Variantsの発現増加が注目され、近年、ARのN末端に直接結合し、このSplice Variants含めあらゆるARを阻害可能な新規薬剤が開発され（EPI-506）、北米で臨床試験が行われていた。本研究では、主にこのEPIと同等あるいはそれ以上の阻害効果が期待できる類似化合物（I-EPI）の治療効果を、動物実験をもとに比較・解析し、今後の臨床応用が可能かどうか模索した。
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