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    Available Technologies / Life Sciences / LifeScienceTech - #6335
     
    Inhibitors of Prostasin
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    Background
    Prostasin is a prostate-abundant serine protease originally discovered in human seminal fluid. Prostasin mRNA is found in normal prostate epithelial cells, but is not expressed in invasive prostate cancer lines. Expression of prostasin in invasive cancer lines reduces the invasiveness of cells in vitro.  Prostasin is also known to be an activator of the epithelium sodium channel, in vitro, and is present in tissues that absorb Na+ such as kidneys, colon, lung, and salivary glands.  The proper regulation of the epithelial sodium channels is crucial to maintaining sodium balance, extracellular fluid volume, and blood pressure. Serine proteases are inhibited by a group of inhibitors called serpins.  Serpins work by mimicking the 3-D structure of a normal substrate of the protease.  These inhibitors can then be instrumental in such diseases as cystic fibrosis and chronic obstructive pulmonary disease (COPD).

    Application
    This invention relates to inhibitors of prostasin and their use in the treatment of diseases or dysfunctions which result from disorders of prostasin function or regulation.

    Invention
    A novel serine protease inhibitor designated PN-1, which has been shown to inhibit prostasin.

    Advantages
    •    PN-1 is an irreversible inhibitor of prostasin.
    •    PN-1 could be used to treat such disease as cystic fibrosis and chronic obstructive pulmonary disease, which are known to have sodium channel disregulation.

    Lead Inventor
    Karl Chai, Ph.D.

    Selected References
    Chen LM, Zhang X, Chai KX. Regulation of prostasin expression and function in the prostate. Prostate. 2004; 59(1): 1-12.

    Chen LM, Skinner ML, Kauffman SW, et al. Prostasin is a glycosylphosphatidylinositol-anchored active serine protease. J Biol Chem 2001; 276: 21434-42.

    Chen LM, Chai KX. Prostasin serine protease inhibits breast cancer invasiveness and is transcriptionally regulated by promoter DNA methylation. J Biol Chem 2001; 276: 21434-42.

    Contact
    Attn: Svetlana Shtrom, Ph.D., MBA
    University of Central Florida
    Office of Research and Commercialization
    12201 Research Parkway, Suite 501
    Orlando, Fl 32826-3246
    Phone: 407.823.5150
    Fax: 407.823.3299
    sshtrom@mail.ucf.edu


    UCF ID# 6335

     
     
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