In a development that could reshape the fight against drug-resistant infections, researchers at the Indian Institute of Technology (IIT), Bombay have unveiled a novel way to make existing antibiotics work again.
Instead of trying to invent entirely new drugs, the team has focused on protecting the ones already in use. Their approach uses tiny, lab-made DNA fragments to block the tricks bacteria use to evade treatment.
Early results suggest that this method can restore the power of commonly used antibiotics against resistant microbes.
At its core, the idea is surprisingly simple. Many antibiotics fail not because they are weak, but because bacteria have learnt how to disable them. The IIT Bombay team designed short DNA strands, called aptamers, that act like molecular “shields.”
These aptamers latch onto bacterial enzymes responsible for resistance and stop them from working. When those enzymes are blocked, the antibiotic can once again attach to its target inside the bacteria and kill it. In lab experiments, resistant bacteria that once survived treatment became vulnerable again.
“Given the long, expensive path from drug discovery to clinic, improving existing drugs may be a more practical route. We know its safety and effects over the years and can use existing resources,” said Ruchi Anand from the department of chemistry at IIT, Bombay, who co-led the study.
The crisis related to antimicrobial resistance (AMR) – when commonly used antibiotics no longer work against common pathogens – is a worldwide problem but particularly acute in India, where, according to a report by The Lancet, around 10.7 lakh people were infected with deadly, drug-resistant bacteria in 2021.
BLOCKING BACTERIAL DEFENCES
The science behind the discovery builds on how certain antibiotics function. Drugs like erythromycin kill bacteria by attaching to their ribosome, the cell’s protein-making machinery. Once attached, the ribosome stops working, and the bacteria die.
However, some bacteria produce special enzymes that subtly alter the ribosome. This small chemical change prevents the antibiotic from binding, allowing the bacteria to survive and multiply.
The researchers targeted one such enzyme using aptamers. They screened millions of DNA sequences to find ones that could tightly bind to the enzyme and shut it down. After refining these sequences, they identified aptamers that not only attached to the enzyme but also blocked its activity.
This prevented the chemical modification that causes resistance, effectively reopening the door for antibiotics to do their job.
Getting these DNA molecules inside bacteria posed another challenge. DNA on its own is fragile and struggles to cross bacterial barriers. To solve this, the team packaged the aptamers inside liposomes – tiny fat-based bubbles similar to cell membranes.
These act as delivery vehicles, protecting the DNA and helping it enter bacterial cells efficiently. In experiments, more than 90 percent of bacteria took up the packaged DNA, compared to almost none when the DNA was used alone.
The result was a sharp increase in bacterial death when antibiotics were used alongside the aptamers.
RISING RESISTANCE CRISIS
The need for such innovation is urgent. Antibiotics are the backbone of modern medicine, used not just to treat infections but also to prevent complications during surgeries, organ transplants, and cancer treatments.
Yet their effectiveness is steadily eroding. Overuse and misuse have accelerated the rise of antimicrobial resistance, turning once-manageable infections into serious health threats.
Recent global data highlight the scale of the problem. In 2023, one in six clinical laboratories worldwide reported bacterial infections that no longer responded to standard antibiotics.
This trend is particularly worrying because the pipeline of new antibiotics is running dry. Between 2017 and 2022, only a few new antibiotics reached the market, and most were variations of existing drugs, according to the World Health Organisation (WHO). This means bacteria often already have the tools to resist them.
FEW NEW DRUGS
Even when new antibiotics are introduced, resistance can develop quickly. Bacteria evolve rapidly, adapting to new threats with remarkable speed.
This constant arms race has forced scientists to rethink their strategy. Instead of focusing only on killing bacteria, attention is shifting toward disabling their defence mechanisms. By doing so, existing drugs can remain effective for longer, buying valuable time in the fight against resistance.
The IIT Bombay approach fits squarely into this new thinking. By targeting resistance enzymes directly, it sidesteps the need for entirely new antibiotics.
This could make it faster and more cost-effective to bring treatments to patients, since the safety profiles of existing antibiotics are already well understood.
HOPE WITH CAUTION
While the findings are promising, researchers caution that several hurdles remain before the approach can be used in clinics. The aptamers must be carefully tested to ensure they do not interact with unintended targets in the human body.
According to Pradeepkumar, another senior researcher involved in the project, several factors would need careful evaluation.
For example,“the selected aptamers would need to avoid unintended interactions with proteins in the body, and the liposome would have to be safe for human cells,” he said.
Therefore, further studies, including animal testing and detailed analysis of how the treatment behaves in the body, will be essential.
If successfully developed, this strategy could be used alongside existing antibiotics as a combination therapy. By neutralising bacterial resistance mechanisms, the aptamers would allow older, widely available drugs to regain their effectiveness.
– Ends
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