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Potential superbug-killing compound

Date:
March 3, 2020
Source:
Simon Fraser University
Summary:
Researchers are testing a new drug that can kill a wide range of superbugs -- including some bacteria now resistant to all common antibiotics.
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Researchers in Simon Fraser University's Brinkman Laboratory are collaborating with U.S. researchers to test a new drug that can kill a wide range of superbugs -- including some bacteria now resistant to all common antibiotics.

Known as AB569, the drug contains ethylenediaminetetraacetic acid (commonly referred to as EDTA) and acidified nitrite, two inexpensive chemicals that the researchers discovered work together to effectively kill disease-causing bacteria without harming human cells.

"We have a growing crisis with antibiotics becoming less and less effective, and treatments are failing; that's why it's important to test and develop new drugs and approaches to treat disease-causing bacteria that are highly resistant to existing antibiotics," says Geoff Winsor, lead database developer at SFU's Brinkman Lab, which is headed by SFU professor Fiona Brinkman.

SFU researchers characterized, at the molecular level, how the chemicals in the AB569 compound were likely working together to kill the notoriously drug-resistant Pseudomonas aeruginosa, using their Pseudomonas Genome Database hosted at SFU, and computer-based analyses of molecular data.

Pseudomonas aeruginosa is a type of bacteria that can cause infections in the lungs (pneumonia), urinary tract, or blood. It is known as the leading cause of morbidity in patients with cystic fibrosis. People who are in hospital or have compromised immune systems are particularly at risk of developing an infection caused by this bacteria.

Pseudomonas aeruginosa is categorized by the World Health Organization as a "priority pathogen" of concern. These priority pathogens are highlighted as urgently requiring new treatments, and posing the greatest threat to human health.

The top three priority pathogens include highly drug-resistant Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacteriaceae. The AB569 compound has been shown to kill these bacteria, plus a wide variety of others, including the notoriously difficult to treat Methicillin-resistant Staphylococcus aureus or MRSA.

"AB569 will go through additional testing because it shows potential as non-toxic topical drug treatment for a wide range of infections," says Winsor.

The lab tests of AB569 showed promising results in treating priority pathogens, plus additional bacteria that cause foodborne illness such as E. coli and Listeria.

The AB569 compound was developed by a University of Cincinnati scientist and is now in the first phase of human trials. AB569 has been licensed exclusively to Toronto-based biotechnology firm Arch Biopartners.


Story Source:

Materials provided by Simon Fraser University. Note: Content may be edited for style and length.


Journal Reference:

  1. Cameron T. McDaniel, Warunya Panmanee, Geoffrey L. Winsor, Erin Gill, Claire Bertelli, Michael J. Schurr, Prateek Dongare, Andrew T. Paul, Seung-Hyun B. Ko, Gee W. Lau, Nupur Dasgupta, Amy L. Bogue, William E. Miller, Joel E. Mortensen, David B. Haslam, Phillip Dexheimer, Daniel A. Muruve, Bruce J. Aronow, Malcolm D. E. Forbes, Marek Danilczuk, Fiona S. L. Brinkman, Robert E. W. Hancock, Thomas J. Meyer, Daniel J. Hassett. AB569, a nontoxic chemical tandem that kills major human pathogenic bacteria. Proceedings of the National Academy of Sciences, 2020; 117 (9): 4921 DOI: 10.1073/pnas.1911927117

Cite This Page:

Simon Fraser University. "Potential superbug-killing compound." ScienceDaily. ScienceDaily, 3 March 2020. <www.sciencedaily.com/releases/2020/03/200303113327.htm>.
Simon Fraser University. (2020, March 3). Potential superbug-killing compound. ScienceDaily. Retrieved April 30, 2024 from www.sciencedaily.com/releases/2020/03/200303113327.htm
Simon Fraser University. "Potential superbug-killing compound." ScienceDaily. www.sciencedaily.com/releases/2020/03/200303113327.htm (accessed April 30, 2024).

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