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2016 ; 6
(ä): 25509
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A novel small molecule ameliorates ocular neovascularisation and synergises with
anti-VEGF therapy
#MMPMID27148944
Sulaiman RS
; Merrigan S
; Quigley J
; Qi X
; Lee B
; Boulton ME
; Kennedy B
; Seo SY
; Corson TW
Sci Rep
2016[May]; 6
(ä): 25509
PMID27148944
show ga
Ocular neovascularisation underlies blinding eye diseases such as retinopathy of
prematurity, proliferative diabetic retinopathy, and wet age-related macular
degeneration. These diseases cause irreversible vision loss, and provide a
significant health and economic burden. Biologics targeting vascular endothelial
growth factor (VEGF) are the major approach for treatment. However, up to 30% of
patients are non-responsive to these drugs and they are associated with ocular
and systemic side effects. Therefore, there is a need for small molecule ocular
angiogenesis inhibitors to complement existing therapies. We examined the safety
and therapeutic potential of SH-11037, a synthetic derivative of the
antiangiogenic homoisoflavonoid cremastranone, in models of ocular
neovascularisation. SH-11037 dose-dependently suppressed angiogenesis in the
choroidal sprouting assay ex vivo and inhibited ocular developmental angiogenesis
in zebrafish larvae. Additionally, intravitreal SH-11037 (1??M) significantly
reduced choroidal neovascularisation (CNV) lesion volume in the laser-induced CNV
mouse model, comparable to an anti-VEGF antibody. Moreover, SH-11037 synergised
with anti-VEGF treatments in vitro and in vivo. Up to 100??M SH-11037 was not
associated with signs of ocular toxicity and did not interfere with retinal
function or pre-existing retinal vasculature. SH-11037 is thus a safe and
effective treatment for murine ocular neovascularisation, worthy of further
mechanistic and pharmacokinetic evaluation.