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1 General aspects (0)   1.1 Epidemiology (13)   1.2 Population genetics (0)   1.3 Pathogenesis (6)   1.4 Quality of life (7)   1.5 Glaucomas as cause of blindness (5)   1.6 Prevention and screening (6) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (6)   2.2 Cornea (17)   2.3 Sclera (14)   2.4 Anterior chamber angle (6)   2.5 Meshwork (0)     2.5.1 Trabecular meshwork (16)     2.5.2 Schlemms canal (4)     2.5.3 Scleral outlet channels (2)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (0)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (1)   2.7 Episcleral veins and venous pressure (0)   2.8 Iris (6)   2.9 Ciliary body (1)   2.10 Lens (1)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (18)   2.13 Retina and retinal nerve fibre layer (33)   2.14 Optic disc (34)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (4)   2.17 Stem cells (5)   2.20 Other (0) 3 Laboratory methods (0)   3.1 Microscopy (5)   3.2 Electron microscopy (0)   3.3 Immunohistochemistry (4)   3.4 Molecular genetics (0)     3.4.1 Linkage studies (2)     3.4.2 Gene studies (29)   3.5 Molecular biology incl. 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associated with intraocular tumors (3)     9.4.9 Glaucomas associated with elevated episcleral venous pressure (2)       9.4.10 Glaucomas associated with hemorrhage (1)     9.4.11 Glaucomas following intraocular surgery (0)       9.4.11.1 Ciliary block (malignant) glaucoma (1)       9.4.11.2 Glaucomas in aphakia and pseudophakia (7)       9.4.11.3 Epithelial, fibrous, and endothelial proliferation (0)       9.4.11.4 Glaucomas associated with corneal surgery (3)       9.4.11.5 Glaucomas associated with vitreoretinal surgery (3)     9.4.15 Glaucoma in relation to systemic disease (42)     9.4.20 Other (2) 10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy (4) 11 Medical treatment (0)   11.1 General management, indication (6)   11.2 Cholinergic drugs (0)   11.3 Adrenergic drugs (0)     11.3.1 Epinephrine (0)     11.3.2 Thymoxamine, dapiprazole (0)     11.3.3 Apraclonidine, brimonidine (5)     11.3.4 Betablocker (4)     11.3.5 Other (0)   11.4 Prostaglandins 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    12.8.1 Without tube implant (13)     12.8.2 With tube implant or other drainage devices (29)     12.8.3 Non-perforating (2)     12.8.4 Using laser (0)     12.8.5 Other (2)     12.8.10 Woundhealing antifibrosis (13)     12.8.11 Complications, endophthalmitis (10)   12.9 Trabeculotomy, goniotomy (10)   12.10 Cyclodestruction (3)   12.11 Cyclodialysis (1)   12.12 Cataract extraction (1)     12.12.1 Intracapsular (0)     12.12.2 Extracapsular (0)     12.12.3 Phacoemulsification (4)   12.14 Combined cataract extraction and glaucoma surgery (0)     12.14.1 Intracapsular (0)     12.14.2 Extracapsular (0)     12.14.3 Phacoemulsification (7)   12.15 Capsulotomy (0)   12.16 Vitrectomy (2)   12.17 Anesthesia (5)   12.20 Other (1) 13 Therapeutic prognosis and outcome (0)   13.1 Prognostic factors (2)   13.2 Outcome (0)     13.2.1 IOP (2)     13.2.2 Visual field (0)       13.2.2.1 Progression (0)       13.2.2.2 Improvement (0)     13.2.3 Other (0) 14 Costing studies; pharmacoeconomics (4) 15 Miscellaneous (23)

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Abstract #69485 Published in IGR 18-1

Biocompatibility and Pharmacokinetic Analysis of an Intracameral Polycaprolactone Drug Delivery Implant for Glaucoma

Kim J; Kudisch M; Mudumba S; Asada H; Aya-Shibuya E; Bhisitkul RB; Desai TA
Investigative Ophthalmology and Visual Science 2016; 57: 4341-4346

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PURPOSE: We developed polycaprolactone (PCL) implants that achieve zero-order release of a proprietary ocular hypotensive agent (DE-117) over 6 months. METHODS: The release rates of DE-117-loaded PCL devices were tuned based on an established predictive model and confirmed by in vitro release studies. Devices containing DE-117 and empty devices were implanted intracamerally in normotensive rabbits for up to 8 weeks' duration. Devices were retrieved after rabbits were euthanized and evaluated for tissue adherence. The drug remaining in each device was analyzed by high performance liquid chromatography. Drug distribution in ocular tissues was measured by liquid chromatography coupled with a tandem mass spectrometry (LC/MS/MS). RESULTS: In vitro release of DE-117 showed zero-order release with a release rate of 0.5 μg/day over 6 months. Implantation in rabbit eyes demonstrated that the devices were well tolerated in the intracameral space. Quantification of DE-117 and hDE-117 (the hydrolyzed active form of DE-117) in ocular tissues (cornea, iris-ciliary body, aqueous humor, and vitreous humor) indicated sustained release of DE-117 and its conversion to hDE-117 when released from the device. Analysis of drug remaining in the device found that concentration of hDE-117 was below the limit of detection, indicating the encapsulated drug was protected from hydrolysis in the device. CONCLUSIONS: Proof-of-concept PCL drug delivery devices containing DE-117 show promise as a long-term glaucoma treatment based on their zero-order drug release profile in vitro, biocompatibility in vivo, and effective distribution of released drug in relevant ocular tissues.

UCB-UCSF Graduate Program in Bioengineering, San Francisco, California, United States.

Full article

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Classification:

11.16 Vehicles, delivery systems, pharmacokinetics, formulation (Part of: 11 Medical treatment)
5.3 Other (Part of: 5 Experimental glaucoma; animal models)

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