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Novel Valortim(R) Mechanism of Action Data Presented at the Keystone Symposia on Molecular and Cellular Biology
Date:3/31/2009

r. Cross continued, "As is the case with mouse macrophages, our in vitro data suggest that human dendritic cells also kill germinating anthrax bacteria. Importantly, we find that the addition of Valortim(R) (1) enhances the ability of human dendritic cells to kill B. anthracis, (2) increases the upregulation of costimulatory immune molecules on human dendritic cells (CD40 and CD83), and (3) allows for an augmented cytokine response, particularly the pro-inflammatory cytokine IL-23 that is known to stimulate memory T cells and the production of IFN-gamma . Additional work is ongoing to better characterize how Valortim(R) enhances the immune response to B. anthracis infection."

David P. Wright, President and Chief Executive Officer of PharmAthene, commented, "We are delighted to continue our collaboration with Drs. Cross and Basu to better characterize these intriguing results. Valortim(R) has demonstrated efficacy in non-clinical studies as well as favorable safety data collected from our Phase I clinical study. We believe that Valortim(R) may have important competitive advantages, including a novel mechanism of action, which, if demonstrated, would make it a strong choice for procurement consideration in the Strategic National Stockpile."

The work reported by Drs. Cross and Basu is supported by the Maryland Industrial Partnerships Program (MIPS). The MIPS program was developed to accelerate the commercialization of technology in Maryland by jointly funding collaborative R&D projects between companies and University System of Maryland faculty.

About Valortim(R)

Valortim(R) is a fully human monoclonal antibody designed to protect against and treat anthrax infection, including inhalational anthrax, the most lethal form of illness in humans caused by the Bacillus anthracis bacterium. The investigational antibody is designed to target a protein component known as
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SOURCE PharmAthene, Inc.
Copyright©2009 PR Newswire.
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