Abstract: The present disclosure is directed to isolated or recombinant proteins, such as antibodies, which bind to, and inhibit or reduce the function of, midkine (MK) and their use as therapeutic and/or diagnostic agents for midkine-related disorders. The present disclosure is also related to nucleic acid sequences which encode said proteins and their expression in recombinant host cells. In particular, the present disclosure is directed towards humanized antibodies derived from murine antibody IP14 which specifically bind to human MK.
Type:
Grant
Filed:
October 14, 2015
Date of Patent:
March 17, 2020
Assignee:
CELLMID LIMITED
Inventors:
Maria Halasz, Darren Jones, Nico Mertens, Phillip Cunnah
Abstract: The present disclosure relates to isolated or recombinant proteins, such as antibodies, which inhibit or reduce the function of midkine (hereinafter, referred to as “MK”) for use in the treatment or prevention of midkine-related disorders.
Type:
Grant
Filed:
March 13, 2012
Date of Patent:
April 18, 2017
Assignee:
Cellmid Limited
Inventors:
Sadatosi Sakuma, Maria Halasz, Darren Jones
Abstract: A method to treat the chronic stage of heart injury after ischemia or reperfusion by administering Midkine to a subject in need of such treatment is described.
Abstract: The present disclosure relates to isolated or recombinant proteins, such as antibodies, which inhibit or reduce the function of midkine (hereinafter, referred to as “MK”) for use in the treatment or prevention of midkine-related disorders.
Type:
Application
Filed:
March 13, 2012
Publication date:
June 19, 2014
Applicant:
Cellmid Limited
Inventors:
Sadatosi Sakuma, Maria Halasz, Darren Jones
Abstract: The present inventors discovered that oligonucleotides which suppress midkine expression and antibodies which suppress midkine activity can be used to prevent post-surgical intraperitoneal adhesions.
Abstract: The inventors examined the role of MK in experimental autoimmune encephalomyelitis, which is a human model for multiple sclerosis. As a result, they discovered that MK has the effect of inhibiting regulatory T cells, and that the autoimmune mechanism induced by type 1 helper T cells can be suppressed by inhibiting MK expression or its activity, thereby increasing the number of regulatory T cells. Furthermore, it was found that diseases associated with the functional disorder of regulatory T cells can be treated with the administration of an inhibitor that inhibits MK expression or activity.