April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Bispecific anti-VEGF/ANG2 antibody exhibits superior efficacy to VEGF monotherapy in a model of spontaneous CNV
Author Affiliations & Notes
  • Peter Lundh von Leithner
    UCL Institute of Ophthalmology, London, United Kingdom
  • Daiju Iwata
    UCL Institute of Ophthalmology, London, United Kingdom
  • Y. Ng
    UCL Institute of Ophthalmology, London, United Kingdom
  • Jorg Regula
    Large Molecule Research, Hoffmann La Roche Ltd, Penzberg, Germany
  • Guido Hartmann
    Pharma Research & Early Development, DTA Cardiovascular & Metabolism, F. Hoffmann-La Roche Ltd, Basel, Switzerland
  • David T Shima
    UCL Institute of Ophthalmology, London, United Kingdom
    NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, United Kingdom
  • Footnotes
    Commercial Relationships Peter Lundh von Leithner, None; Daiju Iwata, None; Y. Ng, None; Jorg Regula, None; Guido Hartmann, None; David Shima, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2356. doi:
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      Peter Lundh von Leithner, Daiju Iwata, Y. Ng, Jorg Regula, Guido Hartmann, David T Shima; Bispecific anti-VEGF/ANG2 antibody exhibits superior efficacy to VEGF monotherapy in a model of spontaneous CNV. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2356.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Purpose
 

Anti-vascular endothelial growth factor-A (anti-VEGF) therapy has revolutionized the treatment of neovascular age-related macular degeneration (nAMD). Next generation treatment goals include achieving a reduced treatment frequency and improving upon the efficacy of existing treatment options. In terms of efficacy, data from pivotal trials of anti-VEGF drugs show that despite the improvement in central vision for many patients, the majority still see 20/50 or worse. To explore improving upon existing treatments, we investigated a combination therapy strategy targeting VEGF-A and angiopoietin 2 (Ang2)

 
Methods
 

A mouse model (JR5558) that develops multi-focal, bi-lateral spontaneous choroidal neovascularization (CNV) was used to assess effects of anti-VEGF, anti-ANG2 or a bispecific antibody combination of the two antagonists. Drugs were administered for a two week period, either during the initiation of angiogenesis (prevention mode), or after CNV vessels were established (intervention mode). Drug efficacy was assessed in vivo using fluorescein (FA) and indocyanine green angiography (ICGA), optical coherence tomography and ERG. Various ex-vivo assessments (isolectin-B4, endomucin, F4/80, GFAP and TUNEL) were used to assess neovessel, macrophage, glial and photoreceptor outcomes.

 
Results
 

Bispecific anti-VEGF/ANG2 treatment consistently outperformed monospecific antibodies alone in both prevention and intervention experiments. Reduction in vascular growth, leakage, edema, and photoreceptor loss was superior in the bi-specific antibody treatment groups. Full field ERG data also suggest the bi-specific may provide better visual function outcomes.

 
Conclusions
 

Targeting Ang2 in addition to VEGF-A may provide a new strategy for the improved management of nAMD

 
 
Anti-VEGF/ANG2 treatment of established CNV significantly improved photopic b-wave amplitude compared with controls (P<0.05).
 
Anti-VEGF/ANG2 treatment of established CNV significantly improved photopic b-wave amplitude compared with controls (P<0.05).
 
 
Representative figure of the same eyes showing a significant reduction of permeability (FA), perfusion (ICGA) and volume (Endomucin-expression) of neoangiogenic vasculature after bispecific anti-VEGF/ANG2 treatment compared with control.
 
Representative figure of the same eyes showing a significant reduction of permeability (FA), perfusion (ICGA) and volume (Endomucin-expression) of neoangiogenic vasculature after bispecific anti-VEGF/ANG2 treatment compared with control.
 
Keywords: 412 age-related macular degeneration • 748 vascular endothelial growth factor • 505 edema  
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