Asthma is a leading cause of respiratory disease worldwide, with an estimated 300 million people affected and up to 250,000 deaths per year. Even in developed countries, asthma continues to be a burden for nearly 10% of the population with substantial time lost from work and school and considerable health care expenditures. The principal cause of asthma exacerbations is viral respiratory infections, estimated to be responsible for more than 70%. Pulmotect's Solution: Pulmotect has identified and is developing a novel technology to prevent respiratory infections. The lead drug (PUL-042) is a combination of two TLR ligands that stimulates the lung's own innate defense mechanisms to create a hostile environment for pathogens and prevent or attenuate respiratory infections. Both in vitro and in vivo experiments have been completed to validate this technology and the drug is progressing through the regulatory process for a treatment to benefit cancer patients during periods of immunocompromise. The focus of this proposal is to accomplish key milestones that will further transition this technology for commercialization for the asthma market by showing the direct benefit of PUL-042 in mouse asthma models. The project is organized into three measurable Specific Aims that include evaluating the safety and efficacy of PUL-042 in a mouse models of asthma.
Pulmotect, Inc is developing novel therapeutics that stimulate the innate immune system to protect against infectious diseases, even in cases of severely compromised immunity. Proof-of-concept data has shown that this technology effectively protects against a broad range of inhaled pathogens. This project will provide significant data to help transition this technology from the lab to the clinic for asthmatics. This work will leverage ongoing activities in developing the technology for cancer patients.
Drake, Matthew G; Evans, Scott E; Dickey, Burton F et al. (2013) Toll-like receptor-2/6 and Toll-like receptor-9 agonists suppress viral replication but not airway hyperreactivity in guinea pigs. Am J Respir Cell Mol Biol 48:790-6 |