USA flag logo/image

An Official Website of the United States Government

MASP-2 MoAB therapeutics for MI/RP injury

Award Information

Agency:
Department of Health and Human Services
Branch:
N/A
Award ID:
75695
Program Year/Program:
2005 / SBIR
Agency Tracking Number:
HL082004
Solicitation Year:
N/A
Solicitation Topic Code:
N/A
Solicitation Number:
N/A
Small Business Information
OMEROS CORPORATION
201 Elliott Avenue West SEATTLE, WA -
View profile »
Woman-Owned: No
Minority-Owned: No
HUBZone-Owned: No
 
Phase 1
Fiscal Year: 2005
Title: MASP-2 MoAB therapeutics for MI/RP injury
Agency: HHS
Contract: 1R43HL082004-01
Award Amount: $127,000.00
 

Abstract:

DESCRIPTION (provided by applicant): The overall goal is to develop monoclonal antibodies capable of blocking human MASP-2 function as potential therapeutic agents for myocardial ischemia/reperfusion injury. MASP-2 is a plasma serine protease uniquely required for complement activation via the lectin pathway and may be an attractive target for the development of novel therapeutics. MASP-2 is also one of the least abundant complement proteins in plasma, and provides a potential rate-limiting target for lectin-mediated complement activation. It is generally accepted that the complement system can be activated through three distinct enzymatic cascades, referred to as the classical, alternative and lectin pathways. The complement system is an important host defense mechanism; however, massive complement activation can trigger an intense inflammatory response that is thought to contribute to the pathogenesis of numerous disease states, including myocardial ischemia/reperfusion injury. To treat myocardial ischemia/reperfusion injury (MIRP) it would be desirable to develop pathway-specific therapeutic agents that inhibit only the complement pathway causing the particular pathology without completely shutting down the host defense capabilities of complement. Recent published studies from the laboratory of one of our collaborators using a rat model implicate the lectin pathway in the pathogenesis of myocardial ischemia/reperfusion injury. A mouse genetically-deficient in the MASP-2 protein has been developed. Since the MASP-2 (-/-) mouse lacks the MASP-2 "self antigen, it is the preferred animal to use in a hybridoma development program to identify inhibitory anti-MASP-2 MAbs and such a program is currently underway. The MASP-2 (-/-) mouse will provide a unique and valuable research tool to establish if the lectin pathway plays a major pathological role in myocardial ischemia/reperfusion injury. In this Phase 1 study our specific objectives are to compare cardio and inflammatory functional outcomes when both MASP-2 (-/-) and matched MASP(+/+) mice are evaluated in a murine model of MIRP.

Principal Investigator:

Clark E. Tedford
2165910034
CTEDFORD@OMEROS.COM

Business Contact:


2066234688
Small Business Information at Submission:

Omeros Corporation
1420 5Th Ave Suite 2600 Seattle, WA 98101

EIN/Tax ID: 911663741
DUNS: N/A
Number of Employees: N/A
Woman-Owned: No
Minority-Owned: No
HUBZone-Owned: No