Novel Treatments and Technologies for Retinal Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmaceutical Technology".

Deadline for manuscript submissions: 25 July 2024 | Viewed by 969

Special Issue Editor


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Guest Editor
1. Department of Ophthalmology, University of Central Florida College of Medicine, Orlando, FL 32827, USA
2. Department of Ophthalmology, Orlando College of Osteopathic Medicine, Orlando, FL 34787, USA
3. Aviceda Therapeutics, Cambridge, MA 02142, USA
Interests: age related macular degeneration; diabetic retinopathy; retinal degeneration; innate immune modulation; glyobiology; glyco-mimetic therapeutics; nanoparticles; non-viral/viral gene therapy; RNA interference; artificial intelligence; imaging biomarker; neuroprotection; clinical trials; ocular drug delivery; regenerative medicine; complement; macrophage; microglia; anti-VEGF

Special Issue Information

Dear Colleagues,

Recent advances in the pathophysiologic understanding, imaging biomarkers, artificial intelligence and clinical trial design of retinal diseases combined with technological advancements in aptamer antagonists, non-viral/viral gene-therapy, RNA interference, high affinity antibodies, receptor traps, and nanoparticle glyco-mimetics have led to several FDA-approved therapies for formerly unmet medical needs. These FDA approvals combined with the prevalence of these retinal diseases have led to an increase in the research interest in retinal diseases. The purpose of this Special Issue is to provide a snapshot of all aspects of these advancements from basic science to the identification of pathogenic molecular targets, the development of novel classes of therapeutics, the development of clinically relevant pre-clinical models, the use of artificial intelligence to determine when and how we use these novel therapeutics, and the validation of new FDA-approved endpoints. We aim for a focused yet comprehensive Special Issue.

Dr. Michael John Tolentino
Guest Editor

Manuscript Submission Information

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Keywords

  • age-related macular degeneration
  • diabetic retinopathy
  • retinal degeneration
  • novel therapeutics
  • imaging biomarkers
  • artificial intelligence
  • clinical trials

Published Papers (1 paper)

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19 pages, 2710 KiB  
Article
PolySialic Acid Nanoparticles Actuate Complement-Factor-H-Mediated Inhibition of the Alternative Complement Pathway: A Safer Potential Therapy for Age-Related Macular Degeneration
by Sheri L. Peterson, Anitha Krishnan, Diyan Patel, Ali Khanehzar, Amit Lad, Jutamas Shaughnessy, Sanjay Ram, David Callanan, Derek Kunimoto, Mohamed A. Genead and Michael J. Tolentino
Pharmaceuticals 2024, 17(4), 517; https://doi.org/10.3390/ph17040517 - 17 Apr 2024
Viewed by 808
Abstract
The alternative pathway of the complement system is implicated in the etiology of age-related macular degeneration (AMD). Complement depletion with pegcetacoplan and avacincaptad pegol are FDA-approved treatments for geographic atrophy in AMD that, while effective, have clinically observed risks of choroidal neovascular (CNV) [...] Read more.
The alternative pathway of the complement system is implicated in the etiology of age-related macular degeneration (AMD). Complement depletion with pegcetacoplan and avacincaptad pegol are FDA-approved treatments for geographic atrophy in AMD that, while effective, have clinically observed risks of choroidal neovascular (CNV) conversion, optic neuritis, and retinal vasculitis, leaving room for other equally efficacious but safer therapeutics, including Poly Sialic acid (PSA) nanoparticle (PolySia-NP)-actuated complement factor H (CFH) alternative pathway inhibition. Our previous paper demonstrated that PolySia-NP inhibits pro-inflammatory polarization and cytokine release. Here, we extend these findings by investigating the therapeutic potential of PolySia-NP to attenuate the alternative complement pathway. First, we show that PolySia-NP binds CFH and enhances affinity to C3b. Next, we demonstrate that PolySia-NP treatment of human serum suppresses alternative pathway hemolytic activity and C3b deposition. Further, we show that treating human macrophages with PolySia-NP is non-toxic and reduces markers of complement activity. Finally, we describe PolySia-NP-treatment-induced decreases in neovascularization and inflammatory response in a laser-induced CNV mouse model of neovascular AMD. In conclusion, PolySia-NP suppresses alternative pathway complement activity in human serum, human macrophage, and mouse CNV without increasing neovascularization. Full article
(This article belongs to the Special Issue Novel Treatments and Technologies for Retinal Diseases)
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