NZ716896A - Methods for treating conditions associated with masp-2 dependent complement activation - Google Patents

Methods for treating conditions associated with masp-2 dependent complement activation Download PDF

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Publication number
NZ716896A
NZ716896A NZ716896A NZ71689614A NZ716896A NZ 716896 A NZ716896 A NZ 716896A NZ 716896 A NZ716896 A NZ 716896A NZ 71689614 A NZ71689614 A NZ 71689614A NZ 716896 A NZ716896 A NZ 716896A
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NZ
New Zealand
Prior art keywords
masp
complement activation
complement
dependent
methods
Prior art date
Application number
NZ716896A
Inventor
Thomas Dudler
Gregory Demopulos
Hans-Wilhelm Schwaeble
Original Assignee
Omeros Corp
Univ Leicester
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
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Publication date
Application filed by Omeros Corp, Univ Leicester filed Critical Omeros Corp
Priority to NZ748316A priority Critical patent/NZ748316A/en
Priority claimed from NZ629683A external-priority patent/NZ629683B/en
Publication of NZ716896A publication Critical patent/NZ716896A/en

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  • Medicines Containing Antibodies Or Antigens For Use As Internal Diagnostic Agents (AREA)
  • Peptides Or Proteins (AREA)
  • Pharmaceuticals Containing Other Organic And Inorganic Compounds (AREA)

Abstract

Discloses the use of a MASP-2 inhibitory agent which inhibits MASP-2-dependent complement activation in the manufacture of a medicament for treating or reducing the severity of post stem cell transplant thrombotic microangiopathy (TMA) in a subject receiving an allogeneic hematopoietic stem cell transplant. The MASP-2 inhibitory agent is an anti-MASP-2 monoclonal antibody, or fragment thereof that specifically binds to a portion of SEQ ID NO:6 and selectively inhibits MASP-2-dependent lectin pathway complement activation without substantially inhibiting the C1q-dependent classical complement pathway. Optionally adapted for administration in conjunction with a terminal complement inhibitor that inhibits cleavage of complement protein C5.

Description

PATENTS FORM NO. 5 Our ref: FIP237154NZPR Divisional ation out of NZ 629683 NEW ZEALAND PATENTS ACT 1953 COMPLETE ICATION Methods for treating conditions associated with MASP-2 dependent complement activation We, Omeros Corporation, of 201 Elliott Avenue West, Seattle, 98119, Washington, United States of America; and University of Leicester, of University Road, Leicestershire, LE1 7RH, United Kingdom hereby declare the invention, for which we pray that a patent may be granted to us and the method by which it is to be performed, to be ularly described in and by the following statement: (followed by page 1a) METHODS FOR TREATING CONDITIONS ASSOCIATED WITH MASP-2 DEPENDENT COMPLEMENT ACTIVATION STATEMENT REGARDING SEQUENCE LISTING The sequence listing associated with this application is provided in text format in lieu of a paper copy and is hereby incorporated by reference into the ication. The name of the text file containing the sequence listing is MP_1_0179_US_SequenceListing_20131017; The file is 110 KB, was d on October 17, 2013 and is being submitted via b with the filing of the specification.
BACKGROUND The complement system provides an early acting ism to initiate, amplify and orchestrate the immune response to microbial infection and other acute insults (M.K. Liszewski and J.P. Atkinson, 1993, in Fundamental Immunology, Third Edition, edited by W.E. Paul, Raven Press, Ltd., New York), in humans and other vertebrates. While complement activation provides a valuable first-line defense against potential ens, the activities of complement that e a protective immune response can also represent a potential threat to the host (K.R. Kalli, et al., Springer Semin. Immunopathol. 15 :417-431, 1994; B.P. Morgan, Eur. J. Clinical Investig. 24 :219-228, 1994). For example, C3 and C5 proteolytic products recruit and activate neutrophils. While indispensable for host defense, activated neutrophils are indiscriminate in their release of destructive s and may cause organ damage. In addition, complement activation may cause the deposition of lytic complement components on nearby host cells as well as on microbial targets, resulting in host cell lysis.
The complement system has also been implicated in the enesis of numerous acute and chronic disease states, ing: myocardial infarction, stroke, ARDS, reperfusion injury, septic shock, capillary leakage following l burns, (followed by page 2)
NZ716896A 2013-10-17 2014-09-01 Methods for treating conditions associated with masp-2 dependent complement activation NZ716896A (en)

Priority Applications (1)

Application Number Priority Date Filing Date Title
NZ748316A NZ748316A (en) 2013-10-17 2014-09-01 Methods for treating conditions associated with masp-2 dependent complement activation

Applications Claiming Priority (2)

Application Number Priority Date Filing Date Title
US201361892283P 2013-10-17 2013-10-17
NZ629683A NZ629683B (en) 2013-10-17 2014-09-01 Methods for treating conditions associated with masp-2 dependent complement activation

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NZ716896A true NZ716896A (en) 2022-04-29

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NZ748316A NZ748316A (en) 2013-10-17 2014-09-01 Methods for treating conditions associated with masp-2 dependent complement activation

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Also Published As

Publication number Publication date
NZ748316A (en) 2022-12-23
NZ629683A (en) 2016-03-31

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