ABSTRACT
Degenerative eye conditions such as age-related macular degeneration (AMD), diabetic retinopathy, and retinal vein occlusion are major contributors to significant vision loss in developed nations. The primary therapeutic approach for managing complications linked to these diseases involves the intravitreal delivery of anti-vascular endothelial growth factor (VEGF) treatments. Faricimab is a novel, humanised, bispecific antibody that simultaneously binds all VEGF-A isoforms and Angiopoietin-2, which has been approved by regulatory agencies, such as the US Food and Drug Administration (FDA), the UK Medicines and Healthcare products Regulatory Agency (MHRA) and the European Medicines Agency (EMA), for the treatment of neovascular AMD and diabetic macular oedema (DMO). Intravitreal faricimab holds the promise of reducing the treatment burden for patients with these conditions by achieving comparable or superior therapeutic outcomes with fewer clinic visits. The scope of faricimab's application includes addressing complex macular conditions such as DMO. This review intends to elucidate the distinctive pharmacological characteristics of faricimab and provide an overview of the key clinical trials and real-world studies that assess its effectiveness and safety in treating degenerative macular diseases.
Subject(s)
Diabetic Retinopathy , Macular Edema , Wet Macular Degeneration , Humans , Vascular Endothelial Growth Factor A , Ranibizumab/therapeutic use , Angiogenesis Inhibitors/therapeutic use , Bevacizumab/therapeutic use , Receptors, Vascular Endothelial Growth Factor/therapeutic use , Visual Acuity , Wet Macular Degeneration/drug therapy , Macular Edema/drug therapy , Diabetic Retinopathy/drug therapy , Intravitreal InjectionsSubject(s)
Retinoschisis/diagnosis , Female , Fluorescein Angiography , Fovea Centralis , Humans , Tomography, Optical CoherenceABSTRACT
Diabetic macular oedema (DMO) is a common complication of diabetic retinopathy and may lead to severe visual loss. In this review, we describe the pathophysiology of DMO and review current therapeutic options such as macular laser photocoagulation, anti-vascular endothelial growth factor agents, and steroid implants with a focus on the new fluocinolone acetonide implant, ILUVIEN®. The results of the Fluocinolone Acetonide in Diabetic Macular Edema (FAME) studies are also presented together with the results of real-world studies to support the clinical use of ILUVIEN® in achieving efficient resolution of DMO and improving vision and macular anatomy in this challenging group of patients.
Subject(s)
Angiogenesis Inhibitors/pharmacology , Anti-Inflammatory Agents/pharmacology , Diabetic Retinopathy/therapy , Drug Implants/chemistry , Fluocinolone Acetonide/pharmacology , Macular Edema/therapy , Angiogenesis Inhibitors/pharmacokinetics , Anti-Inflammatory Agents/pharmacokinetics , Diabetic Retinopathy/complications , Diabetic Retinopathy/metabolism , Diabetic Retinopathy/physiopathology , Fluocinolone Acetonide/pharmacokinetics , Humans , Intravitreal Injections , Light Coagulation/methods , Low-Level Light Therapy/methods , Macular Edema/etiology , Macular Edema/metabolism , Macular Edema/physiopathology , Patient Safety , Treatment Outcome , Vascular Endothelial Growth Factor A/antagonists & inhibitors , Vascular Endothelial Growth Factor A/metabolismABSTRACT
BACKGROUND: Prolonged exposure to infrared (IR) radiation is associated with different types of damage to cornea and lens. The aim of our study was to investigate the effect of acute and chronic exposure to IR radiation on the activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 and on the expression of glycosaminoglycans (GAG) in the rabbit cornea and crystalline lens. METHODS: New Zealand rabbits were subjected to IR radiation for 4 months (chronic exposure to IR) or to normal light (control group). In experiments regarding acute exposure, animals were subjected to IR radiation or normal light for 12 h, in the presence of 0.1% diclofenac sodium (eye drops instilled in the right eye of animals) or saline (instilled in the left eye of animals). The cornea and lens were dissected away and homogenized. The activity of MMP-2 and MMP-9 was assayed by gelatine zymography. Total GAG were isolated from tissue specimens after lipid extraction and extensive digestion with pronase and DNase and characterized by treatment with GAG-degrading enzymes, followed by electrophoresis on cellulose acetate membranes. RESULTS: Acute or chronic exposure to IR radiation induced the activity of MMP-2 in cornea and lens, whereas only acute IR radiation increased the content of heparan sulphate in crystalline lens. Local administration of diclofenac sodium did not prevent the above effects of acute IR radiation. CONCLUSIONS: The detrimental effects of excessive or prolonged exposure of the eyes to IR radiation are associated with induced activity of MMP-2 in cornea and lens and alterations in the content of heparan sulphate in lens. Thus, MMP and GAG may offer alternative targets for pharmacological intervention to confront ocular damages associated with IR radiation.
