Study Discovers Molecule of Gut Bacteria That Boosts Immunotherapy Response

Scientists have identified a compound produced by gut bacteria that sharply improves how tumors respond to immunotherapy, offering a potential breakthrough for patients who currently see little benefit from these treatments. The discovery centers on a small molecule called Bac429, which enhanced lung cancer treatment outcomes in mice and is now being developed into a drug suitable for human trials. 

The research was led by a team at the UF Health Cancer Institute and focuses on immune checkpoint inhibitors, a class of cancer drugs designed to help the immune system recognize and attack tumors. While these therapies have changed cancer care, their effectiveness remains limited. Rachel Newsome, study author and a cancer immunology researcher at the University of Florida College of Medicine, said most patients do not respond to these drugs, making any safe method to improve outcomes highly significant. 

The findings build on several years of research into the gut microbiome, the vast network of microorganisms living in the digestive system that plays a critical role in immune function. Christian Jobin, a professor of medicine and microbiome science at the University of Florida, explained that earlier work showed a strong link between gut bacteria and immunotherapy success, but identifying a precise therapeutic target remained elusive. 

That changed after researchers gained access to preserved stool samples from cancer patients enrolled in immunotherapy trials. When gut microbes from patients who responded well to treatment were transferred into mice that previously showed resistance, the animals began responding to therapy and exhibited a 50% drop in tumor growth. This result confirmed that microbial factors were actively shaping treatment effectiveness. 

To narrow down the cause, the team isolated individual bacterial strains from the complex microbial mix. Out of more than 180 candidates, six consistently boosted immunotherapy performance in mice with lung tumors. Further analysis revealed that all six produced the same metabolite, Bac429, pointing to a single driver behind the improved response. 

Administering the molecule alongside immunotherapy led to substantially slower tumor growth in mice with highly resistant cancers. Newsome said the difference was dramatic and suggested the compound could replicate the benefits of the bacteria without the logistical challenges of microbial therapies. However, using live bacteria or fecal transplants as treatments presents major hurdles, including safety, consistency, and scalability. 

But a drug derived from a naturally occurring microbial molecule could be standardized, tested, and deployed far more easily. The research team is now refining Bac429 into drug candidates and studying how it activates immune cells, likely beginning in the gut before triggering effects throughout the body. Although the study specifically targeted lung cancer, the researchers believe the approach could apply to other cancers with low immunotherapy response rates. 

Ongoing work is also examining whether diet influences how the molecule functions, raising the possibility of combining drug therapy with targeted nutritional strategies. If successful in humans, the discovery could mark a shift in cancer treatment, turning insights from gut bacteria into tools that make existing therapies work for far more patients. 

It remains to be seen what other players in the immune-oncology R&D field like Calidi Biotherapeutics Inc. (NYSE American: CLDI) make of this new discovery and how it could potentially be incorporated in other immunotherapy protocols. 

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