Patents by Inventor Natalia Bogatcheva

Natalia Bogatcheva 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).

  • Patent number: 10899829
    Abstract: EMAPII is a monocyte- and endothelial cell-activating protein with prominent pro-apoptotic activity on endothelial and epithelial cells. Provided herein are compositions and methods for treating or preventing endothelial and epithelial apoptosis induced by EMAPII. More particularly, provided herein are compositions and methods for treating or preventing Influenza A virus (IAV)-induced weight loss, impairment of blood oxygenation, lung edema, and endothelial/epithelial apoptosis associated with IAV infections. In addition, anti-EMAPII therapy provides a novel complementary treatment strategy to existing anti-viral and anti-inflammatory approaches.
    Type: Grant
    Filed: February 23, 2017
    Date of Patent: January 26, 2021
    Assignees: INDIANA UNIVERSITY RESEARCH AND TECHNOLOGY CORPORATION, THE UNITED STATES GOVERNMENT AS REPRESENTED BY THE DEPARTMENT OF VETERANS AFFAIRS
    Inventors: Natalia Bogatcheva, Matthias Alexander Clauss, Keith L. March
  • Publication number: 20190153087
    Abstract: EMAPII is a monocyte- and endothelial cell-activating protein with prominent pro-apoptotic activity on endothelial and epithelial cells. Provided herein are compositions and methods for treating or preventing endothelial and epithelial apoptosis induced by EMAPII. More particularly, provided herein are compositions and methods for treating or preventing Influenza A virus (IAV)-induced weight loss, impairment of blood oxygenation, lung edema, and endothelial/epithelial apoptosis associated with IAV infections.
    Type: Application
    Filed: February 23, 2017
    Publication date: May 23, 2019
    Inventors: Natalia Bogatcheva, Matthias Alexander Clauss, Keith L. March
  • Publication number: 20190117702
    Abstract: Disclosed herein is that the systemic administration of ASC conditioned media diminished LPS-induced lung injury by inhibiting epithelial permeability, neutrophil inflammatory response, and secretion of pro-inflammatory TNF?. It is also shown that ARDS lung is able to retain IV-delivered ASC for a substantial amount of time, with no evidence of the significant cell distribution to other organs at this time point. These findings provide optimization of cell-based and cell-free therapy for the treatment of ARDS, including occurrences of ARDS caused by upper respiratory tract infections such as SARS and MERS.
    Type: Application
    Filed: October 31, 2018
    Publication date: April 25, 2019
    Applicants: Indiana University Research and Technology Corporation, The United States of America as represented by the Department of Veterans Affairs
    Inventors: Keith March, Natalia Bogatcheva
  • Patent number: 10143709
    Abstract: Disclosed herein is that the systemic administration of ASC conditioned media diminished LPS-induced lung injury by inhibiting epithelial permeability, neutrophil inflammatory response, and secretion of pro-inflammatory TNF?. It is also shown that ARDS lung is able to retain IV-delivered ASC for a substantial amount of time, with no evidence of the significant cell distribution to other organs at this time point. These findings provide optimization of cell-based and cell-free therapy for the treatment of ARDS, including occurrences of ARDS caused by upper respiratory tract infections such as SARS and MERS.
    Type: Grant
    Filed: May 6, 2015
    Date of Patent: December 4, 2018
    Assignees: Indiana University Research and Technology Corporation, The United States of America Department of Veteran Affairs As Represented By The Technology Transfer Program
    Inventors: Keith March, Natalia Bogatcheva
  • Publication number: 20150320801
    Abstract: Disclosed herein is that the systemic administration of ASC conditioned media diminished LPS-induced lung injury by inhibiting epithelial permeability, neutrophil inflammatory response, and secretion of pro-inflammatory TNF?. It is also shown that ARDS lung is able to retain IV-delivered ASC for a substantial amount of time, with no evidence of the significant cell distribution to other organs at this time point. These findings provide optimization of cell-based and cell-free therapy for the treatment of ARDS, including occurrences of ARDS caused by upper respiratory tract infections such as SARS and MERS.
    Type: Application
    Filed: May 6, 2015
    Publication date: November 12, 2015
    Inventors: Keith March, Natalia Bogatcheva