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Utility of a Novel Anthracycline Analog in Psoriasis

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R41AR052955-01
Agency Tracking Number: AR052955
Amount: $149,052.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: N/A
Solicitation Number: PHS2005-2
Timeline
Solicitation Year: 2005
Award Year: 2005
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
941 LAKE FOREST CIRCLE
Birmingham, AL 35244
United States
DUNS: N/A
HUBZone Owned: Unavailable
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 DENISE WINGETT
 (208) 426-2921
 DENISEWINGETT@BOISESTATE.EDU
Business Contact
Phone: (208) 861-1409
Research Institution
N/A
Abstract

DESCRIPTION (provided by applicant): Psoriasis is a common immune-mediated disease that affects approximately 2% of the US and European populations and significantly impacts the quality of life. T cells are recognized as primary mediators of the disease and new generation therapies aimed at eliminating reactive T cells or interfering with the immunologic cascade caused by their activation have been shown to be effective in treating psoriasis. These biologic therapies have the advantage of selectively inhibiting T cell function and are expected to cause fewer systemic side effects than traditional interventions. However, currently available therapies may ultimately be limited by their high cost or if long-term patient follow-up studies yield unsatisfactory results. A current need exists to identify additional drug candidates that effectively inhibit T cell response yet possess limited systemic toxicity. The long-term goal of this research is to identify novel therapeutic agents that are effective in the treatment of psoriasis, safe for long-term use, and well tolerated. The immediate goal is to evaluate the actions of a new anthracycline analog, GPX-150, for use in the treatment of psoriasis. GPX-150 is a recently patented novel doxorubicin analog and preliminary data indicates it has dramatically reduced systemic toxicity compared to doxorubicin yet can effectively inhibit T cell function. Our central hypothesis is that GPX-150 will inhibit T cell activation, proliferation and alter cytokine production in a manner expected to disrupt the inflammatory cascade leading to the initiation and progression of psoriasis. The specific aims for the project are to: I) Determine whether GPX-150 inhibits T cell proliferation and activation. II) Determine whether GPX-150 inhibits the production of psoriasis related cytokines. Ill) Determine whether topical or systemic GPX-150 inhibits inflammation in a murine model of contact hypersensitivity and assess the achievable dermal concentrations of the drug. Proposed studies are expected to help determine the clinical and commercial potential of GPX-150 for treatment of psoriasis.

* Information listed above is at the time of submission. *

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