Clinical Use of Home OCT Data to Manage Neovascular Age-Related Macular Degeneration.

To investigate how home optical coherence tomography (OCT) influences the clinical decision-making of retina specialists for the management of neovascular age-related macular degeneration (nAMD). In this retrospective imaging review, 15 retina specialists each evaluated 10 home OCT data segments from 29 eyes being treated for nAMD. Based on OCT data, indications were identified for when eyes should be treated, which antivascular endothelial growth factor should be used, and the specific retinal fluid and time thresholds for notification.

A Small-Molecule Pan-Id Antagonist Inhibits Pathologic Ocular Neovascularization.

Id helix-loop-helix (HLH) proteins (Id1-4) bind E protein bHLH transcription factors, preventing them from forming active transcription complexes that drive changes in cell states. Id proteins are primarily expressed during development to inhibit differentiation, but they become re-expressed in adult tissues in diseases of the vasculature and cancer. We show that the genetic loss of Id1/Id3 reduces ocular neovascularization in mouse models of wet age-related macular degeneration (AMD) and retinopathy of prematurity (ROP).

Patterns of Early and Delayed Visual Response to Ranibizumab Treatment for Neovascular Age-Related Macular Degeneration.

Importance: Understanding the range of temporal responses to ranibizumab is critical for the assessment of individualized treatment regimens for neovascular age-related macular degeneration.

Objective: To examine patterns of visual and anatomical response to ranibizumab treatment.

Design, Setting, And Participants: This study is a retrospective subanalysis of HARBOR (a phase 3, double-masked, multicenter, randomized, active treatment-controlled study of the efficacy and safety of 0.

Future Perspectives: Agents on the Horizon.

As demonstrated in the previous chapters of this textbook, retinal pharmacotherapeutics is a rapidly developing area. The enormous burden of disease in an aging population will hopefully be met by significant improvements in our understanding and treatment of disease processes such as age-related macular degeneration (AMD) and diabetic retinopathy. This chapter will provide perspectives on select anti-angiogenic drugs currently in development, as well as therapies directed against the complement cascade for the treatment of AMD, and an anti-inflammatory monoclonal antibody for the treatment of diabetic macular edema, among others, that have not been discussed elsewhere in this book.

Prevention of ocular scarring after glaucoma filtering surgery using the monoclonal antibody LT1009 (Sonepcizumab) in a rabbit model.

Purpose: Excessive scarring leading to failure of the filtering bleb continues to be a major problem after glaucoma filtration surgery. This study examines the antifibrotic effects of the anti-S1P monoclonal antibody LT1009 (Sonepcizumab) in prolonging bleb survival in a rabbit model of glaucoma filtering surgery.

Methods: The frequency of LT1009 dosage was determined initially using an enzyme-linked immunosorbent assay assay measuring LT1009 eye tissue retention in 6 New Zealand White rabbits.

Anatomical benefit from ranibizumab treatment of predominantly classic neovascular age-related macular degeneration in the 2-year anchor study.

Purpose: To compare lesion anatomical responses to ranibizumab versus verteporfin photodynamic therapy (PDT) in the ANCHOR (Anti-VEGF Antibody for the Treatment of Predominantly Classic Choroidal Neovascularization [CNV] in Age-Related Macular Degeneration) study.

Methods: In this 2-year, Phase III, randomized, multicenter, double-masked trial, 423 patients received ranibizumab (0.3 or 0.

Vitreous nonsteroidal antiinflammatory drug concentrations and prostaglandin E2 levels in vitrectomy patients treated with ketorolac 0.4%, bromfenac 0.09%, and nepafenac 0.1%.

Purpose: To assess vitreous concentrations of nonsteroidal antiinflammatory drugs (NSAIDs) and prostaglandin E(2) in patients treated with NSAIDs before vitrectomy.

Methods: This was an investigator-masked, randomized, multicenter study. Patients received ketorolac 0.

Blockade of sphingosine-1-phosphate reduces macrophage influx and retinal and choroidal neovascularization.

Sphingosine-1-phosphate (S1P) is a bioactive lipid molecule that stimulates endothelial cell migration, proliferation, and survival in vitro, and tumor angiogenesis in vivo. In this study, we used a humanized monoclonal antibody (sonepcizumab) that selectively binds S1P to investigate its role in retinal and choroidal neovascularization (NV). Intraocular injection of sonepcizumab significantly reduced macrophage influx into ischemic retina and strongly suppressed retinal NV in mice with oxygen-induced ischemic retinopathy.

Anti-sphingosine-1-phosphate monoclonal antibodies inhibit angiogenesis and sub-retinal fibrosis in a murine model of laser-induced choroidal neovascularization.

The efficacy of novel monoclonal antibodies that neutralize the pro-angiogenic mediator, sphingosine-1-phosphate (S1P), were tested using in vitro and in vivo angiogenesis models, including choroidal neovascularization (CNV) induced by laser disruption of Bruch's membrane. S1P receptor levels in human brain choroid plexus endothelial cells (CPEC), human lung microvascular endothelial cells, human retinal vascular endothelial cells, and circulating endothelial progenitor cells were examined by semi-quantitative PCR. The ability of murine or humanized anti-S1P monoclonal antibodies (mAbs) to inhibit S1P-mediated microvessel tube formation by CPEC on Matrigel was evaluated and capillary density in subcutaneous growth factor-loaded Matrigel plugs was determined following anti-S1P treatment.

Sphingosine-1-phosphate (S1P) is a novel fibrotic mediator in the eye.

Sphingosine-1-phosphate (S1P) is a pleiotropic lysolipid that has recently been implicated in the regulation of tissue fibrosis. However, the fibrogenic potential of S1P in the eye has not previously been investigated. In the current study, we evaluated cells from the anterior and posterior segments of the eye for the presence of S1P and their potential ability to produce and respond to S1P.