A new therapeutic principle that can suppress chemotherapy resistance, considered the biggest challenge in treating pancreatic cancer, has been proposed by a Korean research team.
The National Cancer Center said on the 21st that a research team led by Kim Su-yeol, Ph.D., of the Cancer Biology Research Branch, and a team led by Professor Woo Sang-myeong of the Center for Hepato-Biliary-Pancreatic Cancer identified a method to suppress chemotherapy resistance by blocking the energy metabolism of cancer cells. Kim Su-yeol is a distinguished principal researcher at the National Cancer Center and the CEO of New Cancer Cure Bio.
The biggest problem in chemotherapy is "recurrence," in which cancer cells acquire resistance to drugs and proliferate again. It is known that cancer cells survive under stress such as chemotherapy administration or nutrient deficiency through a process called "autophagy," in which they break down their own cellular components to secure energy.
Until now, treatment strategies that inhibit the early stages of autophagy have been studied, but resistance persisted as cancer cells compensated through other pathways.
The research team found that the JNK1 protein, which regulates cellular stress responses, induces activation of the late stage of autophagy and that "fatty acid oxidation" plays an essential role in this process.
Fatty acid oxidation is a metabolic process that breaks down fat to produce energy, and the researchers confirmed that when cancer cells are exposed to chemotherapy, they activate this pathway to make up for insufficient energy. The energy secured in this process then stimulates growth signals, enabling survival even in a chemotherapy environment.
The team said that when a drug that inhibits fatty acid oxidation is administered together with chemotherapy, the autophagy process is blocked and cancer cells die.
They also developed a new drug candidate, "KN510713," that addresses potential liver toxicity that may occur when inhibiting fatty acid oxidation. The compound is characterized by selectively inhibiting fatty acid oxidation in cancer cells while minimizing the side effect of fat accumulation in the liver.
According to the research team, the candidate completed phase 1 clinical trials, and phase 2 is underway in patients with pancreatic cancer. The study is based on the so-called "Kim Effect" theory proposed by Kim Su-yeol. It holds that cancer cells use fatty acids, rather than glucose, as their main energy source, an approach that differs from conventional cancer metabolism research.
Kim Su-yeol said, "This study is meaningful in that it targets an energy metabolic pathway commonly used by cancer cells rather than a specific genetic mutation," adding, "It may be used to address chemotherapy resistance in not only pancreatic cancer but also a variety of intractable solid and rare cancers."
The results were published on the 20th (local time) in the international journal "Cancer Research."
References
Cancer Research (2026), DOI: https://doi.org/10.1158/0008-5472.CAN-25-4517