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Breakthrough Molecule 'Lariocidin' Offers Fresh Hope Against Superbugs Amid Rising Global AMR Threat

McMaster University scientists uncover a potential game-changer in antibiotic development after three-decade drought

• By Pooja Chaturvedi Sah
• New Delhi
• Jun 10, 2025

News

In what could be a watershed moment for antimicrobial research, scientists at McMaster University in Canada have discovered a new antibiotic molecule, lariocidin, that demonstrates potent activity against some of the most drug-resistant bacterial strains known to modern medicine. This comes at a time when the world is grappling with an alarming surge in antimicrobial resistance (AMR), which already contributes to over 4.5 million deaths globally every year.

The discovery, led by Professor Gerry Wright and his team at the Michael G. DeGroote Institute for Infectious Disease Research, marks the emergence of a new class of antibiotics—something not seen in nearly 30 years. The findings were published in Nature on March 26, 2025.

A Novel Lasso Peptide with a Distinct Target

The newly identified molecule, lariocidin, belongs to a class of naturally occurring compounds known as lasso peptides. Unlike conventional antibiotics that target cell walls or DNA replication, lariocidin binds directly to the protein synthesis machinery of bacteria, attacking the ribosome in a completely new way. This novel mode of action makes it especially effective against strains that have become resistant to most existing therapies.

“This is a new molecule with a new mechanism,” said Wright. “It’s a big leap forward for us in the fight against antibiotic-resistant infections.”

From Backyard Soil to Laboratory Discovery

Interestingly, the molecule was derived from Paenibacillus, a bacterium found in a simple backyard soil sample from Hamilton, Ontario. The research team allowed the bacteria to grow for nearly a year in lab conditions, helping isolate slow-growing species that might otherwise be overlooked. One of them was found to produce a compound with unusually high antimicrobial activity.

Postdoctoral fellow Dr. Manoj Jangra, part of Wright’s team, called it a “breakthrough moment” when the team understood how the molecule was killing off other bacteria.

Initial tests have been promising—lariocidin has shown effectiveness in animal models, is non-toxic to human cells, and appears resistant to known antibiotic resistance mechanisms. The researchers are now focused on modifying the compound for large-scale production and clinical trials.

However, Wright warned that bringing a new antibiotic to market is a long road. “Bacteria don’t make drugs for us—they make them for themselves. So we now need to engineer this compound to become a viable clinical candidate,” he said.

Ciprofloxacin Study Reveals Why Antibiotics May Be Fueling Resistance—Not Just Fighting It

Rutgers scientists show how energy stress in bacteria makes them stronger and more likely to mutate

In a parallel revelation that could have implications for how antibiotics are prescribed and developed, researchers at Rutgers New Jersey Medical School have found that ciprofloxacin—a commonly used antibiotic for urinary tract infections—may inadvertently be aiding bacterial survival and accelerating resistance.

Published in Nature Communications, the study reveals how ciprofloxacin throws E. coli into a bioenergetic crisis by depleting its ATP (adenosine triphosphate) reserves. This stress response paradoxically helps some bacteria survive and evolve into more drug-resistant strains.

Stress Response Sparks Persister Cells and Faster Mutations

Using genetically engineered E. coli strains with drained ATP and NADH (cellular energy molecules), researchers Barry Li and Jason Yang discovered that stressed bacteria didn’t slow down—they revved up. This metabolic overdrive caused oxidative damage, triggering a stress alarm system called the stringent response, which made bacteria more tolerant to the antibiotic and more likely to mutate.

In time-kill studies, these stressed cells produced up to 10 times more persisters—dormant bacteria that evade antibiotic action and re-emerge after treatment ends.

Even more concerning, the team found that these energy-stressed bacteria reached full resistance to ciprofloxacin in four fewer rounds of drug exposure compared to normal cells.

“The bacteria are turning our attack into a training camp,” said Yang. “We need to cut the power to that camp.”

Broader Implications for Antibiotic Development

The findings raise serious concerns about high-dose antibiotic regimens and support the idea that metabolic consequences of treatment should be factored into drug development. Gentamicin and ampicillin—other widely used antibiotics—also appear to cause ATP depletion, suggesting this stress-induced resistance mechanism could span several drug classes.

Future strategies may include combining antibiotics with stress-buffering agents to prevent this unintended bacterial hardening, as well as designing new drug candidates that avoid triggering such energy crises in pathogens.

What This Means for India’s Pharma and AMR Policy Landscape

As a global leader in generic drugs and antibiotics manufacturing, India stands to play a pivotal role in turning both these discoveries into actionable solutions. While lariocidin could emerge as a valuable licensing opportunity or R&D collaboration for Indian drugmakers, the ciprofloxacin findings reinforce the urgent need for India’s clinical community to rethink antibiotic stewardship and dosing strategies.

With AMR already causing over 58,000 neonatal deaths annually in India and rising resistance in hospital-acquired infections, these studies provide both hope and warning: new drug classes are possible—but they must be handled with scientific foresight, not just market enthusiasm.