Faricimab: an investigational agent targeting the Tie-2/angiopoietin pathway and VEGF-A for the treatment of retinal diseases

@article{Nicol2021FaricimabAI,
  title={Faricimab: an investigational agent targeting the Tie-2/angiopoietin pathway and VEGF-A for the treatment of retinal diseases},
  author={Massimo Nicol{\`o} and Lorenzo Ferro Desideri and Aldo Vagge and Carlo E Traverso},
  journal={Expert Opinion on Investigational Drugs},
  year={2021},
  volume={30},
  pages={193 - 200}
}
ABSTRACT Introduction Intravitreal antivascular endothelial growth factor (VEGF) drugs represent the first-line treatment option for wet age-related macular degeneration (w-AMD) and diabetic macular edema (DME); however, the frequent injection intervals have illuminated to the necessity for new molecules allowing a more prolonged treatment regimen. Faricimab is a promising bispecific drug targeting VEGF-A and the Ang-Tie/pathway. Phase II STAIRWAY and AVENUE Trials showed its clinical efficacy… 
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The emerging role of the Angiopoietin-Tie pathway as therapeutic target for treating retinal diseases
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Among the investigational drugs targeting the Ang/Tie pathway, faricimab has shown promising results in phase II/III trials and in the near future may represent a viable treatment option for the management of exudative macular diseases.
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A systematic review of the current literature available in the MEDLINE library, focusing on current intravitreal molecules and on new emerging therapies, describes the molecular features of classic retinal drugs, highlighting the main therapeutic targets, and provides an overview of new emerging molecules.
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Observations provide a strong experimental basis and scientific rationale for the progression of a therapeutic anti-LRG1 monoclonal antibody into clinical trials with patients with nvAMD.
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Findings showed that eyes undergoing anti-VEGF therapy for nAMD with more stable OCT CST variability during the follow-up period were associated with better visual outcomes, and clinicians should consider adopting treatment strategies to reduce CST variability During the treatment course for n AMD.
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