Drug for Pulmonary Infections in Cystic Fibrosis Is Focus of Collaboration with Arch Biopartners, University of Cincinnati

Drug for Pulmonary Infections in Cystic Fibrosis Is Focus of Collaboration with Arch Biopartners, University of Cincinnati

Arch Biopartners is collaborating with the University of Cincinnati (UC) for a new drug candidate, AB569, for treating Pseudomonas aeruginosa pulmonary infections in patients with cystic fibrosis.

Last year, the U.S. FDA granted orphan drug status to Arch Biopartners’ AB569. The company also applied for orphan drug designation from the European Medicines Agency (EMA). That request is currently under consideration.

AB569 is a drug that targets P. aeruginosa pulmonary infections that are resistant to traditional antibiotics. AB569 combines two active ingredients: sodium nitrite and ethylenediaminetetraacetic acid. The drug is administered to patients as a nebulized (inhaled) solution.

Clinical development for AB569 to test the drug’s safety and efficacy in cystic fibrosis patients who have P. aeruginosa pulmonary infection began last year, with Arch Biopartners working closely with the inventor of AB569, Dr. Daniel Hassett from the UC College of Medicine. The results demonstrated AB569’s efficacy in the treatment of pulmonary infections.

“Given these positive developments of the AB569 program and our plans to do the first human trial involving CF patients with P. aeruginosa respiratory infections, management of Arch decided it was time to exercise its option to exclusively license the commercial rights to AB569 from UC,” said Richard Muruve, CEO of Arch Biopartners, in a press release.

UC will received an initial payment from Arch Biopartners as part of the license agreement. Future payments will be based on milestones from clinical trials and revenues.

P. aeruginosa is one of the most common bacterial infections in patients with respiratory diseases, including cystic fibrosis, pneumonia, and chronic obstructive pulmonary disease (COPD).

Cystic fibrosis is a recessive genetic disease caused by the loss or dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) channel activity as a result of mutations in the CFTR gene.

CFTR is a major regulator of sweat, digestive fluids, and mucus production. Its loss or malfunction leads to abnormal mucus production in the lungs and airways of patients, and as a result, patients with cystic fibrosis have an increased risk for infections, such as those with P. aeruginosa. The infection is associated with a rapid decline in lung function, leading to a poor prognosis.

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