Retinoid replacements and opsin agonists and methods for the use thereof

Abstract

Compositions of and methods for using synthetic retinoids as retinoid replacements and opsin agonists are provided.

Description

CROSS-REFERENCES TO RELATED APPLICATIONS [0001] This application claims the benefit of U.S. Provisional Patent Application No. 60 / 455,182, filed Mar. 14, 2003, the disclosure of which is incorporated by reference herein.STATEMENT AS TO RIGHTS TO INVENTIONS MADE UNDER FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT [0002] This research was supported by United States Public Health Service Grants EY01730, EY02048, EY08061, EY09339, EY11850, EY13385 and EY66388 from the NEI, National Institutes of Health grants. The Government has certain rights in the invention.BACKGROUND OF THE INVENTION [0003] A diminished visual acuity or total loss of vision may result from a number of eye diseases or disorders caused by dysfunction of tissues or structures in the anterior region of the eye and / or posterior region of the eye. The eye is divided anatomically into an anterior and posterior segment. The anterior segment includes the cornea, anterior chamber, iris and ciliary body (anterior choroid), poste...

AI Technical Summary

Benefits of technology

[0031] In another aspect, a method is provided of treating or preventing loss of night vision or contrast sensitivity in an aging vertebrate subject. The method generally includes administering to the subject an effective amount of a synthetic retinoid in a pharmaceutically acceptable vehicle. The synthetic retinoid can bind to opsin in the vertebrate eye and form an opsin / synthetic retinoid complex. For example, the synthetic retinoid can bind to free opsin in the eye.

Problems solved by technology

AMD results in damage to the macula, a small circular area in the center of the retina.

Because the macula is the area which enables one to discern small details and to read or drive, its deterioration may bring about diminished visual acuity and even and to read or drive, its deterioration may bring about diminished visual acuity and even blindness.

However, the wet form is a more serious disease than the dry form and is responsible for about 90% of the instances of profound visual loss resulting from the disease.

In most patients, this leads to scarring and severe central vision loss, including distortion, blind spots, and functional blindness.

Patients who have wet AMD in one eye are at increased risk of developing CNVs in the other eye.

Reactions that go on in the RPE lead to oxidative products that in turn lead to cell death and neovascularization.

They all have a final common pathway of night blindness and peripheral vision loss that can lead to narrowing of the visual field and eventual loss of all vision in many patients.

This abnormal opsin protein forms a protein aggregate that eventually leads to cell death.

Both result in a person's inability to make 11-cis-retinal in adequate quantities.

Aging also leads to the decrease in night vision and loss of contrast sensitivity due to a shorting of 11-cis-retinal.

This can create noise in the system, and thus more light and more contrast is necessary to see well.

Some forms of CSNB are due to a delay in the recycling of 11-cis-retinal.

Currently, there are few treatments for retinoid deficiency.

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