Project/Area Number |
23390388
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Obstetrics and gynecology
|
Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
KANAYAMA Naohiro 浜松医科大学, 医学部, 教授 (70204550)
ITOH Hiroaki 浜松医科大学, 医学部附属病院, 准教授 (70263085)
TAMURA Naoaki 浜松医科大学, 医学部附属病院, 助教 (90402370)
|
Project Period (FY) |
2011-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2013: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2011: ¥8,970,000 (Direct Cost: ¥6,900,000、Indirect Cost: ¥2,070,000)
|
Keywords | 創薬 / 産婦人科学 / 子宮内膜症 / DDS型分子標的治療薬 |
Research Abstract |
Endometriosis is a common gynecological disease associated with pelvic pain and infertility. Current treatments include oral contraceptives combined with NSAIDs or surgery to remove lesions, all of which provide a temporary but not complete cure. As most endometriosis occurs on organ surfaces facing the peritoneum, we subtracted a phage display library with female mouse peritoneum tissue and selected phage clones by binding to human endometrial epithelial cells. We identify an endometriosis-targeting peptide internalized by cells, designated z13. Proteomics analysis revealed the z13 receptor as the CNGB3. We then linked z13 with an apoptosis inducing peptide and with an endosome-escaping peptide. When these peptides were coadministered into the peritoneum of baboons with endometriosis, cells in lesions selectively underwent apoptosis with no effect on neighboring organs. This study reports a potential therapeutic capable of eliminating endometriosis from the human peritoneum.
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