2014 Fiscal Year Final Research Report
Role of VEGF165b in neovascular vitreoretinal diseases and development of treatments for it
Project/Area Number |
24592668
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Ophthalmology
|
Research Institution | Shiga University of Medical Science |
Principal Investigator |
OHJI Masahito 滋賀医科大学, 医学部, 教授 (90252650)
|
Co-Investigator(Kenkyū-buntansha) |
KAKINOKI Masashi 滋賀医科大学, 医学部, 助教 (80531516)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Keywords | VEGF / VEGF165b / 抗VEGF薬 / 眼内薬物動態 |
Outline of Final Research Achievements |
VEGF concentration increased after intravitreal injection of pegaptanib sodium into macaque eyes and there was no difference in the increase among the isoforms. Pegaptanib increased VEGF165 production by cultured ARPE65 cells while it did not increase VEGF165b production. In monkey experiments, the half-lives of intravitreally injected ranibizumab (IVR) and aflibercept (IVA) in the aqueous humor were similar and they were shorter in vitrectomized eyes. IVA suppressed VEGF level in the injected eyes for longer period compared with IVR. IVA also, but not IVR suppressed VEGF level in untreated fellow eye for a short period. The pharmacokinetics of anti-VEGF drugs and its effect may be different among drugs. It is also different between in vitrectomized eyes and non-vitrectomized eyes. In AMD patients, IVA completely suppress aqueous VEGF for 2 months while IVR partially suppress VEGF at 2 month after injection. IVA suppressed serum and plasma VEGF while IVR did not.
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Free Research Field |
眼科
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