Synspira, a privately held company developing a new class of inhaled glycopolymer-based therapeutics for the treatment of pulmonary disease, announced that it has received up to a $3 million award from the Cystic Fibrosis (CF) Foundation to advance clinical development of its lead candidate, SNSP113, for use in pulmonary complications of cystic fibrosis (CF). SNSP113 is a novel glycopolymer representing a new class of molecules developed to treat infection, inflammation and congestion in the lungs associated with CF. Bacteria colonize and eventually form biofilms in the inflamed and mucus obstructed airways of persons with CF. Biofilms diminish the susceptibility of bacteria to antibiotics. SNSP113 breaks up bacterial biofilms and weakens bacteria, allowing for the potentiation of antibiotics. In addition, it diminishes mucus viscosity, reducing inflammation and promoting clearance of the lungs. “This award will support the clinical development of SNSP113, which successfully completed a Phase 1a first-in-human trial to assess the safety and tolerability of single ascending doses in healthy individuals and will advance into stable CF patients in 2018,” said Shenda Baker, Ph.D., Chief Executive Officer of Synspira. “We have been working closely with the CF Foundation and are honored by their support and encouragement as we continue to develop therapies that are designed to improve quality of life for CF patients.” About SNSP113 SNSP113 is a glycopolymer-based therapeutic being developed as an inhaled treatment to improve lung function in patients with cystic fibrosis. As a modified polysaccharide molecule, SNSP113 interacts with structural polymers in protective bacterial biofilms, breaking them apart, and with native glycoproteins in mucus, reducing mucus viscosity and adhesion. SNSP113 also interacts with the cell walls of invading bacteria increasing their permeability, thereby reducing their inherent viability and potentiating the efficacy of antibiotics. SNSP113 is designed to reduce infection and inflammation, the key drivers of pulmonary exacerbations and pulmonary decline in cystic fibrosis patients.