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Ocular Diseases small molecules library

Ocular Diseases small molecules library

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Ocular Diseases small molecules library.

13,000 compounds, 7 targets, 4 diseases.

 Age-Related Macular Degeneration (AMD) occurs due to an abnormality of the retinal pigment epithelium (RPE) and causes damage to the macula [1, 2]. Age-Related Macular Degeneration is a multifactorial disorder, and there is no predominant etiological element responsible. AMD is considered to be a leading cause of central vision loss in patients aged 65 or over [3]

For the design of the screening library, we use emerging Targets: retinol-binding protein 4 (RBP4), factor D inhibition as alternative complement pathway, and VEGF pathway.

Our library covers several ocular diseases:

Diabetic Macular Edema (DME)

Diabetic macular edema (DME) is caused by a complication of diabetes called diabetic retinopathy. Diabetic retinopathy is the most common diabetic eye disease and the leading cause of irreversible blindness. Vascular adhesion protein-1 (VAP-1) is a homodimeric sialylated glycoprotein. It is believed that inhibition of human VAP-1 enzyme could be a promising approach to the treatment of diabetic macular edema.

 Cataract:

Cataracts are a slowly growing disease condition of the eye in which the lens becomes opaque, leading to cloudiness or a loss of transparency that may affect one or both eyes. Number of discovery programs were conducted to investigate the protective role of Aldose Reductase inhibitors in the prevention of diabetic cataract formation

 Glaucoma:

Glaucoma is irreversible neurodegeneration that involves retinal nerve fiber layer thinning, optic nerve head cupping, and retinal ganglion cell (RGC) death. Ocular hypertension—intraocular pressure is one of the most important risk factors in most glaucomas. The principal proven methods of treatment are (1) IOP reduction based on the use of topical drugs, (2) laser therapy, and surgical intervention. Relevant Protein Targets include Carbonic Anhydrase (CA) inhibitors – IOP reduction by inhibitors decreases the rate of aqueous humor (AH) production. ROCK II inhibitors exert a direct effect on the conventional AH outflow pathway, capacity to increase retinal blood flow and induce neuronal protection against stress

 

Publications

1.        Haddad S, Chen CA, Santangelo SL, Seddon JM. The genetics of age-related macular degeneration: a review of progress to date. Surv Ophthalmol. 2006 Jul-Aug;51(4):316-63. doi: 10.1016/j.survophthal.2006.05.001. PMID: 16818082.

2.        Cheng KJ, Hsieh CM, Nepali K, Liou JP. Ocular Disease Therapeutics: Design and Delivery of Drugs for Diseases of the Eye. J Med Chem. 2020 Oct 8;63(19):10533-10593. doi: 10.1021/acs.jmedchem.9b01033. Epub 2020 Jun 2. PMID: 32482069.

3.        Chou R, Dana T, Bougatsos C, Grusing S, Blazina I. Screening for Impaired Visual Acuity in Older Adults: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2016 Mar 1;315(9):915-33. doi: 10.1001/jama.2016.0783. PMID: 26934261.

Rastoin O, Pagès G, Dufies M. Experimental Models in Neovascular Age Related Macular Degeneration. Int J Mol Sci. 2020 Jun 29;21(13):4627. doi: 10.3390/ijms21134627. PMID: 32610682; PMCID: PMC7370120

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