High affinity VEGF binder could be CNV treatment of the future

February 6, 2008

A single intravitreal injection of the fusion protein KH902 can effectively inhibit leakage and growth of choroidal neovascularization in rhesus monkeys.

A single intravitreal injection of the fusion protein KH902 can effectively inhibit leakage and growth of choroidal neovascularization (CNV) in rhesus monkeys, according to a study published online by Molecular Vision.

Ming Zhang from Sichuan University and fellow researchers from Chengdu Kanghong Biotechnology, Sichuan Province, China measured the binding affinity of KH902 with vascular endothelial growth factor (VEGF) by using the human VEGF ELISA kit. The biological activity effect of KH902 was assayed by an in vitro inhibition experiment on human umbilical vein endothelial cell proliferation that was induced by VEGF. The experimental CNV was induced by causing perimacular laser injury in the eyes of rhesus monkeys and confirmed by fluorescence fundus angiography (FFA), optical coherence tomography (OCT) and multifocal electroretinograms (mf-ERG) 20 days following the infliction of the laser injury.

KH902 was delivered to the animals through intravitreal injection at various doses and the monkeys were observed four-weeks following the injection by ophthalmic injection, FFA, OCT, mf-ERG, histopathology and immunohistochemistry analysis.

Overall, the team found that KH902 binds VEGF with high affinity and hence can completely block VEGF-induced cell proliferation and cell growth.

The reduction of experimental CNV was greater in eyes treated with 300 and 500 µg than in eyes treated with 0.1 mg KH902. In eyes treated with 100 µg, there was fibre-vasculosa membrane proliferation, but not in the 300 and 500 µg groups. The results of mf-ERG demonstrated that there was a greater improvement in the 300 and 500 µg groups than in the 100 µg group.

The researchers believe that, since KH902 can effectively inhibit leakage and growth of CNV, it may have uses in the future as an anti-angiogenic treatment for age-related macular degeneration.