Arch Biopartners, a biotechnology company that develops new products and technologies for pharmaceutical and industrial companies, has entered into a one year option agreement to license the commercial rights of a University of Cincinnati-developed technology for treating bacterial respiratory infections associated with diseases such as cystic fibrosis and COPD. The novel treatment utilizes acidified nitrite, a non-antibiotic method developed by Dr. Daniel Hasset, a UC Professor in the Department of Molecular Genetics, Biochemistry and Microbiology.
During the one year option, the company will be working with Dr. Hassett and his team to assess the potential and logistics of conducting a Phase II clinical trial. The goal is to test how effective the UC technology can be when bacteria is resistant to antibiotics.
Gram-negative bacterium Pseudomonas aeruginosa (PA) represents a major concern in this area. Highly resistant to antibiotics and phagocyte-mediated killing, it is the primary cause of pulmonary exacerbations that leads cystic fibrosis and COPD patients to frequent hospitalizations. These two diseases, characterized by airway bacterial infections, are both deadly and chronic, and affect approximately 40,000 and 14.2 million individuals, respectively, in the United States.
When patients come in contact with the mucoid form of PA, their overall lung function declines, which is why it is so urgent to develop novel treatments in this field. In the first phase II human trial, Arch and Dr. Hassett’s team are will test the technology on cystic fibrosis patients presenting with mucoid PA. If the technology proves to be successful, testing will be expanded to include COPD patients.
Phase I Clinical Trial Results
The Phase I results revealed that the new drug is safe at or below the maximal tolerated dose. The previous trial involved over 80 healthy volunteers with single dose and multiple ascending dose studies for up to one week.
Although some adverse events were observed, such as dizziness, methemoglobinemia (methemoglobin was less than 5% of hemoglobin), and a drop in systemic blood pressure, the drug had no adverse effect on human epithelial cells at concentrations up to 300 millimolar, 20 times higher than the dose needed to kill mucoid PA. The 14 patients with pulmonary arterial hypertension (PAH) had no significant adverse events.