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Posterior juxtascleral delivery of anecortave acetate for treatment of age-related macular degeneration
Published in A Peyman MD Gholam, A Meffert MD Stephen, D Conway MD FACS Mandi, Chiasson Trisha, Vitreoretinal Surgical Techniques, 2019
Clinical evidence of exudative ARMD places a patient at greatly increased risk for serious vision loss regardless of the location of the CNV1,9–;11 or its angiographic characteristics.11–;13 The two currently approved treatments for this disease – laser photocoagulation and PDT – have shown only limited success in treating this blinding disorder. Anecortave acetate is one diffusible pharmacologic agent currently being evaluated for treatment of this disease. In contrast to VEGF inhibitors, anecortave acetate is unique in that it inhibits the process of vessel growth downstream and is therefore independent of the specific inciting angiogenic stimulus. This angiostatic cortisene is also unique in that it can be administered as a slow-release depot on the outer scleral surface without resorting to intravitreal injection. Completed and ongoing clinical and nonclinical studies have demonstrated that depot administration of anecortave acetate is safe and clinically effective when administered at 6-monthly intervals for at least 2 years.
Age-Related Macular Degeneration Drug Delivery
Published in Glenn J. Jaffe, Paul Ashton, P. Andrew Pearson, Intraocular Drug Delivery, 2006
Kourous A. Rezaei, Sophie J. Bakri, Peter K. Kaiser
Anecortave acetate is a synthetic steroid derivative which is thought to inhibit blood vessel growth by inhibiting the proteases necessary for vascular endothelial cell migration (54,55). It inhibits both urokinase-like plasminogen activator and matrix metalloproteinase-3 (56). Anecortave acetate has been specifically modified to eliminate its in vivo corticoid activity (57). It is administered posterior to the eye as a juxtascleral depot injection onto the outer surface of the sclera near the macula, using a specially designed cannula (see Chapter 5) (57).
Glucocorticoid-induced ocular hypertension: origins and new approaches to minimize
Published in Expert Review of Ophthalmology, 2020
Thomas Yorio, Gaurang C. Patel, Abbot F. Clark
There have been three major experimental approaches to inhibit or block IOP elevation in animal models of GC-OHT (Table 4). The first approach has used concomitant administration of ocular steroid analogs along with the anti-inflammatory GC. Topical ocular administration of the natural cortisol metabolite tetrahydrocortisol reversed DEX-induced ocular hypertension in rabbits [114]. It is interesting to note that this compound also blocked DEX-induced CLAN formation in cultured human TM cells [115], suggesting a potential mechanism by which this metabolite may work. Another cortisol analog, anecortave acetate, was designed as an IOP lowering cortisone. In an open-label clinical trial, subTenon’s injection of an anecortave acetate suspension lowered IOP in GC-induced OHT patients [116]. The average starting IOP was over 31 mmHg, and anecortave acetate provided a sustained (up to 6 months) 30% IOP lowering. It is important to note that these two steroid analogs are not GC receptor antagonists, so they should not interfere with the anti-inflammatory effects of GCs [117].
Scleral Inflammation around Collector Channels in Eyes with Primary Open-Angle Glaucoma
Published in Ocular Immunology and Inflammation, 2021
Maximilian Schultheiss, Bogomil Voykov, Maren Klemm, Ulrich Gross, Heinz-Peter Schultheiss, Martin S. Spitzer, Maria Casagrande
Nevertheless, in POAG-biopsies inflammation exists and this raises several questions. What does the inflammation mean? It is possible that in most patients POAG is a consequence of a subclinical inflammatory process, which does not result in an obvious ocular inflammation observable in slit-lamp examination, but induces an increase in AH outflow resistance. In studies, anecortave acetate, applied as a juxtascleral depot, was found to have a hypotensive effect in steroid-induced elevated intraocular pressure, POAG, and closed-angle glaucoma.26–29 This hypotensive effect was found to be statistically significant over a course of up to 6 months27 with an IOP reduction of about 30% throughout the studies.26–28 Anecortave acetate is an angiostatic cortisone derived from glucocorticoid cortisol acetate, but lacking glucocorticoid activity.30 The mechanism by which anecortave acetate can lower intraocular pressure is not fully understood.27 It is known that it possesses angiostatic activity by inhibiting proteases.27 Elevated TGF-beta can increase the messenger ribonucleic acid (mRNA) and protein expression of plasminogen activator inhibitor-1 (PAI-1) in TM cells.27 In cultured cells, anecortave acetate inhibited this PAI-1 expression.27 The actuality of anecortave acetate having a hypotensive effect and regarding its inhibitory function of proteases, the findings in this study could be an explanation for this effect on IOP in glaucoma patients. Vice versa, the fact that anecortave acetate can have a hypotensive effect by this mechanism can support the relevance of our findings and supports the hypothesis that the immune system influences the AH outflow resistance.