CD160-targeted murine CL1-R2 monoclonal antibody, alone or in combotherapy with Avastin®, inhibits early and late formed corneal neovascularization in rabbit model

Poster Details

First Author: T.Menguy FRANCE

Co Author(s):    A. Briaux   V. Soler   J. Giustiniani   A. Bensussan   I. Raymond   P. Le Bouteiller              

Abstract Details


Murine CL1-R2 monoclonal antibody (mAb) targeted against human CD160 receptor was previously described as a novel anti-angiogenic therapy in rodent models (Chabot et al., 2011). Efficacy of CL1-R2 mAb after early and late subconjunctival injections was addressed using the rabbit corneal neovascularization (CNV) model, to assess its effects as a standalone or in combination therapy with Avastin®.


Impact of early and late subconjonctival administrations of murine anti-CD160 CL1-R2 mAb alone or in combination with Avastin® in a rabbit CNV model.


Corneal NV was induced by a FGF2- or VEGF-containing lens inserted in rabbit corneas. Two subconjunctival injections (100 µg) of CL1-R2 monoclonal antibody (mAb) in the upper side of the limbus were performed at days 1 and 3 (early treatment group) or at days 6 and 8 (late treatment group) after induction of corneal NV. Comparison with a murine IgG1 control mAb, bevacizumab (Avastin®) and aflibercept (Eylea®) was made using a similar protocol. In the combotherapy setting, Avastin® (25µg) was co-injected at day 1 and 3 with different doses (25, 50 and 100 µg) of anti-CD160 mAb. Neovascularisation measurements were first evaluated by a four-grade scale based on the length of the neovessel formed from the limbus to the VEGF- or FGF2-containing lens. Second, photographs of corneal NV at days 6, 8 and 10-12 after lens implantation were analyzed by image processing, using or by image processing using MorphoExpert Explora Nova software (La Rochelle, France) that allows quantification of corneal NV density as well as individual NV length. Immunohistochemical study was performed on paraformaldehyde-fixed corneal tissue sections using different NV markers.


Early subconjunctival administration of CL1-R2 inhibited both FGF2- and VEGF-induced CNV in a similar manner. No significant difference of the level of CNV inhibition was observed between CL1-R2 and bevacizumab late treatments. Late treatment of CL1-R2 and Eylea® induced a significant decrease of both CNV area and neovessels length. CL1-R2 administration showed however a less rapid inhibiting effect than Eylea®. Immunohistochemical studies indicated that CL1-R2 treatment induced a significant regression of neovessels expressing CD31, Sma and KI-67. An additive effect of CL1-R2 with Avastin® was obtained in the rabbit CNV model at all doses of anti-CD160 mAb.


Early and late subconjunctival injections of murine anti-CD160 CL1-R2 mAb significantly inhibited CNV. Furthermore, the additive effect observed when the anti-CD160 mAb is given with Avastin®, suggests that both CD160 and VEGF pathways are contributing to the observed efficacy and that the two mAbs are possibly acting via different pathways. This could open new therapeutic ways for co-targeted or combination therapies on top of the anti-VEGFs.

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