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Add as preferred source Cancer cells have a voracious appetite for sugar—using it to fuel their rapid growth. This is why many scientists have tried to develop drugs that block cancer cells' metabolism by cutting off their sugar supply.
Now a team led by researchers at The University of Texas at Austin report in Nature Chemical Biology that they have found a completely different approach. Instead of starving cancer cells, they trick them into consuming even more sugar than usual. At the same time, the drug blocks their backup fuel source—fat.
"I like to think of this technology like a two-headed dragon," said Xiaolu (Lulu) Lim Ang Cambronne, an associate professor of molecular biosciences at UT and co-corresponding author. "We are putting one part of the cell into overdrive while simultaneously weakening another part. It appears to be extremely potent."
In lab experiments, the drug was effective against several types of human cancer cells, including melanoma, leukemia, breast cancer, lung cancer, liver cancer and neuroblastoma. In mice with melanoma, most cancer cells died, while noncancerous cells were much less affected.
Drugs that attack cancer with this kind of one-two punch are not entirely new. A growing class of compounds called antibody-drug conjugates (ADCs) use an antibody to target cancer cells, then deliver a payload of chemotherapy directly to the tumor. But ADCs have many limitations.
"Antibodies are difficult to make, and because they're so large, they're only able to target proteins on the surface of cancer cells," said Ken Hsu, an associate professor of chemistry at UT and co-corresponding author. "We think of this new compound as a fully chemical counterpart to ADCs. They are much easier to manufacture. And because they are smaller, they are able to target even proteins that are inside cells."
The drug has two parts. The targeting agent, a molecule called XJ-4-85, acts on an enzyme called PFKL, speeding up glycolysis (the breakdown of sugar) inside cancer cells. After XJ-4-85 binds, it releases its payload, a compound that acts on another enzyme called CPT2. CPT2 normally helps cells break down fatty acids for energy. By disrupting both of the cells' major energy sources at the same time, it shuts down cancer growth.
"The way this drug works was totally unexpected," said Xiaoding Jiang, a postdoctoral fellow in the Hsu Lab, who designed the molecule. "A lot of research was required to figure out what it was doing on the molecular level. We were also surprised to see how selectively it binds to cancer cells."
The research is still in its early stages. Although the results are promising, much more laboratory testing is needed before the drug can be studied in people.
Beyond this particular drug, the researchers say the research also illustrates a broader approach for designing these two-part medicines, which they call "electrophile-drug conjugates" or EDCs. "They have the potential to be useful beyond cancer, for other kinds of diseases as well," Cambronne said.
The team members emphasize the importance of collaboration in making this discovery possible, bringing together experts from across UT—and beyond. "This project took a village," Hsu said.
A Covalent PFKL Activator Suppresses Tumor Growth, Nature Chemical Biology (2026). DOI: 10.1038/s41589-026-02289-9
Journal information: Nature Chemical Biology
Provided by University of Texas at Austin
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