Arch Biopartners bags rights to bactericidal drug in wound care

A culture of the Gram-negative bacteria Pseudomonas aeruginosa
Pseudomonas aeruginosa, one of the bacteria targeted by AB569 (By Sun14916 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18864145)

Arch Biopartners has struck a deal with the University of Cincinnati to expand development of the bactericidal drug AB569 into the topical treatment of wounds. The agreement expands on an existing license covering drug-resistant respiratory infections.

AB569 is a combination of acidified nitrite and disodium ethylenediaminetetraacetic acid. Evidence the combination inhibits and kills pathogenic bacteria including the Pseudomonas aeruginosa that infects the lungs of cystic fibrosis and chronic obstructive pulmonary disease spurred interest in the respiratory applications of AB569. 

Earlier this month, researchers published data on the efficacy of AB569 against multidrug resistant Acinetobacter bacteria that the Centers for Disease Control and Prevention regard as an urgent threat. The bacteria cause acquired wound, burn, blast and ventilator-associated pneumonia infections.

Having seen the data, Arch has secured an exclusive license to patent claims covering the use of the combination in the prevention, treatment and healing of wound infections resulting from burns and blasts. The agreement supports further development of AB569 as a topical treatment for wounds. 

“With this new license, Arch now has a commercial path to develop the topical wound gel version of AB569 for clinical use. We look forward to exploring opportunities where Arch can support human trials targeting the prevention and treatment of antibiotic resistant infections in wounds,” Arch Biopartners CEO Richard Muruve said in a statement.

The market opportunity is underpinned by the morbidity and mortality associated with burn and blast injuries, notably in the military, and the limitations of existing products against the multidrug resistant Gram-negative bacteria that can infect such wounds. Such bacteria can mutate to nullify the effects of multiple antibiotic regimens.

There are reasons to think AB569 may fare better. An earlier study found AB569 compromised more than 30 vital pathways in a pathogen that infects wounds. By acting on the biosynthesis of DNA, RNA, protein and ATP, the combination could quickly kill wound pathogens without giving rise to bacteria that are resistant to all of its bactericidal properties.