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Ocular Diseases Small Molecules Library

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—an 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 includes 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

Medicinal and Computational Chemistry Dept., ChemDiv, Inc.
12760 High Bluff Dr, San Diego, CA, 92130
Phone: + 1 916 234 0888
Fax: +1 858 794 4931
Email: ChemDiv@chemdiv.com

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