Targeting NCCA-ATP channel for organ protection following ischemic episode
US-9511075-B2 · Dec 6, 2016 · US
US8980952B2 · US · B2
| Field | Value |
|---|---|
| Publication number | US-8980952-B2 |
| Application number | US-35994606-A |
| Country | US |
| Kind code | B2 |
| Filing date | Feb 22, 2006 |
| Priority date | Mar 20, 2002 |
| Publication date | Mar 17, 2015 |
| Grant date | Mar 17, 2015 |
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The present invention is directed to therapeutic compounds, treatment methods, and kits affecting the NC Ca-ATP channel of neural tissue, including neurons, glia and blood vessels within the nervous system, and methods of using same. The NC Ca-ATP channel is newly expressed in neural tissue following injury such as ischemia, and is regulated by the sulfonylurea receptor SUR1, being inhibited by sulfonylurea compounds, e.g., glibenclamide and tolbutamide, and opened by diazoxide. Antagonists of the NC Ca-ATP channel, including SUR1 antagonists, are useful in the prevention, diminution, and treatment of injured or diseased neural tissue, including astrocytes, neurons and capillary endothelial cells, that is due to ischemia, tissue trauma, brain swelling and increased tissue pressure, or other forms of brain or spinal cord disease or injury. Agonists of the NC Ca-ATP channel may be are useful in the treatment neural tissue where damage or destruction of the tissue, such as a gliotic capsule, is desired.
Opening claim text (preview).
What is claimed is: 1. A method of ameliorating the effect of a reduction in blood flow in peri-infarct brain tissue in ischemic disease or injury in a subject comprising administering to a subject having a reduction in blood flow in peri-infarct brain tissue in ischemic disease or injury an amount of a compound that is effective to inhibit the activity of a NC Ca-ATP channel in a neuronal cell, a neuroglia cell, or a neural endothelial cell and that is effective to ameliorate the…
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