Arch Biopartners, Inc., recently announced that it has entered an exclusive license agreement with the University of Cincinnati (UC) for commercial rights to UC’s AB569, a drug candidate for the treatment of pulmonary infections with Pseudomonas aeruginosa in patients with cystic fibrosis (CF).
AB569 was invented at UC in the laboratory of Dr. Daniel Hassett, and the drug combines two active ingredients, sodium nitrite and ethylenediaminetetraacetic acid, both approved as safe for use in people. The use of AB569 has shown a dramatic effect at killing P. aeruginosa both in vitro and in vivo, including antibiotic-resistant strains.
In the past year, Arch and Dr. Hassett collaborated in building a patent portfolio for the drug, and in developing clinical trials to test AB569’s safety and efficacy in CF patients, which are expected to begin later this year or in 2017. AB569 was designated an Organ Drug by the U.S. Food and Drug Administration (FDA) in November 2015, and Arch recently applied to the European Medicines Agency for a similar designation. That application is under review.
“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,” Richard Muruve, CEO of Arch Biopartners, said in a press release. Under the agreement’s terms, the company will pay UC a one-time licensing fee. Future payments will be based on clinical trial and revenue milestones.
CF, a life-threatening condition, is characterized by the buildup of mucus in the lungs and the obstruction of airways. Patients are vulnerable to infections, likely due to the loss of airway clearance ability, malfunction of antibacterial peptides, and overall loss of defense mechanisms. P. aeruginosa is the pathogen with highest prevalence in CF patients’ lungs, often leading to chronic infection. Its prevalence in lung infections is 40 percent in CF patients ages 6 to 10, a frequency that increases to 60 percent of patients by age 17, and reaches some 75 percent between the ages of 25 and 34. Antibiotic resistance to these infections further complicates treatment, resulting in a progressive decline of lung function.