Patents by Inventor Yashige Kotake

Yashige Kotake has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).

  • Publication number: 20070032453
    Abstract: The present invention involves the use of nitrone free radical trapping agents in the treatment and prevention of gliomas. The agents may be used alone or combined with other traditional chemo- and radiotherapies and surgery, to treat or prevent glioma occurrence, recurrence, spread, growth, metastasis, or vascularization.
    Type: Application
    Filed: July 28, 2006
    Publication date: February 8, 2007
    Inventors: Rheal Towner, Yashige Kotake, Robert Floyd
  • Patent number: 6569902
    Abstract: PBN (&agr;-phenyl-tert-butylnitrone), and its derivatives nitrone-based free radical traps, significantly reduce preneoplastic nodule development as well as inhibit hepatocellular carcinoma (HCC) formation at very low levels. The involvement of reactive oxygen species (ROS) in cancer development has been strongly implicated for many years. The involvement of ROS has been strongly implicated in cancer development is a model system where feeding a choline deficiency (CD) diet to rats leads to hepatocellular carcinoma (HCC) development. Administering PBN in the drinking water inhibits HCC formation. Preneoplastic nodule growth in the liver is significantly suppressed by administering PBN, or some of its natural metabolites, in the diet. The effectiveness of PBN in preventing HCC development in the CD liver model is considered due to its prevention of tumor development after the target cells have already been initiated, i.e. genetically changed into tumor cells.
    Type: Grant
    Filed: March 28, 2001
    Date of Patent: May 27, 2003
    Assignee: Oklahoma Medical Research Foundation
    Inventors: Robert A. Floyd, Yashige Kotake, Kenneth L. Hensley, Dai Nakae
  • Publication number: 20030017148
    Abstract: Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease believed to be caused by an inflammatory process in the pancreas leading to selective destruction of the &bgr; cells. Inducible cyclooxygenase (COX-2) is expressed under inflammatory conditions and its product prostaglandin E2 (PGE2) is an important inflammation mediator. Administration of the selective COX-2 inhibitor such as, e.g., NS-398 prevents the onset of diabetes in mice brought on by multiple low-doses of streptozotocin (STZ). Histological observations indicated that STZ-mediated destruction of &bgr; cells was prevented by NS-398 treatment. Delayed (day 3) administration of NS-398 was also protective in this model. These results demonstrate the critical importance of COX-2 activity in autoimmune destruction of &bgr; cells, and point to the fact that COX-2 inhibition should provide a preventive therapy against IDDM or other autoimmune problems, including allograft rejection.
    Type: Application
    Filed: May 10, 2001
    Publication date: January 23, 2003
    Applicant: Oklahoma Medical Research Foundation
    Inventors: Tahereh Tabatabaie, Yashige Kotake
  • Publication number: 20020004531
    Abstract: PBN (&agr;-phenyl-tert-butylnitrone), and its derivatives nitrone-based free radical traps, significantly reduce preneoplastic nodule development as well as inhibit hepatocellular carcinoma (HCC) formation at very low levels. The involvement of reactive oxygen species (ROS) in cancer development has been strongly implicated for many years. The involvement of ROS has been strongly implicated in cancer development is a model system where feeding a choline deficiency (CD) diet to rats leads to hepatocellular carcinoma (HCC) development. Administering PBN in the drinking water inhibits HCC formation. Preneoplastic nodule growth in the liver is significantly suppressed by administering PBN, or some ofits natural metabolites, in the diet. The effectiveness of PBN in preventing HCC development in the CD liver model is considered due to its prevention of tumor development after the target cells have already been initiated, i.e.genetically changed into tumor cells.
    Type: Application
    Filed: March 28, 2001
    Publication date: January 10, 2002
    Applicant: OKLAHOMA MEDICAL RESEARCH FOUNDATION
    Inventors: Robert A. Floyd, Yashige Kotake, Kenneth L. Hensley, Dai Nakae