Technologies

Pharmaceuticals & Vitamin D : Ocular

Technologies

Generic Drug to Treat and Prevent Macular Degenerative Diseases

UW–Madison researchers have identified a new treatment option for a number of macular degenerative diseases including AMD, Stargardt’s disease and juvenile macular dystrophy.

The researchers found that a class of compounds called acid sphingomyelinase inhibitors can be used to fight retinal disorders associated with abnormal accumulations of lipofuscin (a cellular waste product), cholesterol or increased inflammation. One such inhibitor, generic name desipramine, is currently sold on the market as an antidepressant. Other acid sphingomyelinase inhibitors also may be suitable.
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Vitamin D Compounds for the Treatment of Ocular Hypertension

UW–Madison researchers have developed a method of treating OHT by administering a vitamin D analog.  The vitamin D compound can be applied topically to one or both of an individual’s eyes to reduce IOP.
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Method of Reducing Neural Cell Death

UW-Madison researchers have developed a method of reducing neuronal cell death. Neuronal cells are exposed to a boron-protected phenylphosphine, such as bis(3-propionic acid methyl ester)phenylphosphine borane complex or (3-propionic acid methyl ester)diphenylphosphine borane complex. These compounds, successfully tested in rats, are highly neuroprotective at nanomolar and picomolar concentrations, respectively.
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Method for Treating or Preventing Steroid-Induced Glaucoma

UW-Madison researchers have developed a method of using integrin antagonists to reduce the incidence of CLAN structures in trabecular meshwork cells, thereby increasing the outflow of fluid. CLAN formation is regulated by signaling mechanisms mediated by integrin receptors. Integrin inhibitors may be administered to a patient undergoing steroid treatment to disrupt those signaling mechanisms. The inhibitors interfere with the binding of a steroid-induced activator to an integrin or with signal transduction to the trabecular meshwork cells, reducing CLAN formation and decreasing the risk of glaucoma.
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Method for Reducing Intraocular Pressure Using Integrin-Linked Kinase Inhibitor

UW-Madison researchers now have developed a method of treating increased intraocular pressure by administering agents that interfere with activities of integrin-linked kinase. Interfering with the ability of ILK to couple integrin signaling to the actin cytoskeleton increases aqueous humor outflow through the trabecular meshwork and decreases intraocular pressure. A PI3K inhibitor can be administered with the ILK inhibitor to further reduce intraocular pressure.
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Method for Treating Glaucoma

UW-Madison researchers have developed a method for reducing intraocular pressure and increasing outflow facility from the eyes to treat glaucoma. The method involves administering caldesmon to the trabecular meshwork of the eye. Alternatively, a genetic construct comprising the nucleic acid for caldesmon linked to a promoter can be delivered to trabecular meshwork cells, so that caldesmon protein is expressed in the eye. 

Caldesmon, a protein found in smooth muscle and non-muscle cells, acts to reduce cellular contractility by interfering with actomyosin interactions, thereby disrupting cell adhesions and the actin cytoskeleton. Caldesmon treats glaucoma by reducing the resistance of the trabecular meshwork to fluid flow and enhancing the outflow from the aqueous humor, thereby reducing intraocular pressure. Experiments have shown that caldesmon increases outflow facility in human and monkey eye anterior segments in organ culture.
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Method for Treating Glaucoma with C3 Transferase

UW-Madison researchers have developed a method for reducing intraocular pressure and increasing outflow facility from the eyes to treat glaucoma. The method involves administering exoenzyme C3 transferase to the trabecular meshwork of the eye. Alternatively, a genetic construct comprising the nucleic acid for C3 linked to a promoter may be delivered to the trabecular meshwork cells so that C3 protein is expressed in the eye.

C3 is an ADP ribosyltransferase that inhibits cellular contractility, leading to changes in cell shape and secondary changes in the actin cytoskeleton and cellular adhesions. To treat glaucoma, C3 reduces intraocular pressure by disrupting actin- and myosin-containing stress fibers and the system of focal adhesions, reducing the resistance of the trabecular meshwork to fluid flow and enhancing outflow from the aqueous humor.
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Method of Reducing Retinal Ganglion Cell Degeneration

A UW-Madison researcher has developed a method for reducing retinal ganglion cell death in glaucoma.  The method involves delivering a therapeutically effective amount of the neuroprotective beta-blocker carvedilol (or related compounds) to the subject’s retinal ganglion cells (RGC) in a sustained release formula.
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