New Therapy Identified That Blocks Pancreatic Cancer Drug Resistance by Inhibiting Fatty Acid Oxidation

A Korean research team has identified a new therapeutic mechanism that could overturn drug resistance, the greatest challenge in pancreatic cancer treatment, drawing attention from the international cancer research community.

Suyul Kim, Senior Researcher at the Department of Cancer Biology, National Cancer Center (left), and Sangmyung Woo, Director of the Hepatobiliary and Pancreatic Cancer Center, National Cancer Center. National Cancer Center

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The National Cancer Center announced on April 21 that a team led by Dr. Suyul Kim of the Cancer Biology Research Department-who is also CEO of New Cancer Cure Bio-and the clinical team of Professor Sangmyeong Woo, Director of the Hepatobiliary and Pancreatic Cancer Center, presented these findings at the American Association for Cancer Research (AACR 2026) conference in San Diego, USA.

The research team discovered that the key reason cancer cells survive even after chemotherapy attacks lies in their ability to supply energy through fatty acid oxidation. They demonstrated that blocking this process can completely reverse drug resistance in cancer cells.

The biggest obstacle in cancer therapy is 'recurrence,' where cancer cells withstand toxicity and regrow. When faced with nutrient deprivation or external assaults like chemotherapy, cancer cells survive through 'autophagy,' a process in which they digest parts of their own cells to generate energy.

While many attempts have been made to suppress early-stage autophagy to inhibit cancer drug resistance, cancer cells soon activate an alternative pathway known as 'late-stage autophagy,' leading to new forms of resistance. The research team was the first in the world to discover that the JNK1 protein, which activates when cancer cells are energy-deprived, induces this late-stage autophagy, and that fatty acid oxidation (FAO) is absolutely essential to this process.

This breakthrough is rooted in Dr. Kim's 'Kim Effect' theory, which posits that the primary energy source for cancer cells is not glucose but fatty acids. When chemotherapy drugs are administered, cancer cells experience an energy shortage and rapidly increase fatty acid oxidation to compensate. The team found that the energy generated through this process reactivates growth signals, enabling cancer cells to survive despite chemotherapy.

The researchers confirmed that, in first-line chemotherapy, combining a fatty acid oxidation inhibitor interrupted this connection, causing autophagy-which induces drug resistance in cancer cells-to stop, and resulting in complete cell death.

Additionally, the team developed a new drug candidate, 'KN510713,' which addresses the issue of liver toxicity that arises when fatty acid oxidation is suppressed. This compound selectively inhibits fatty acid oxidation in cancer cells without causing fat to accumulate in the liver. KN510713 has already successfully completed Phase 1 clinical trials and is currently undergoing Phase 2 trials as the world’s only pancreatic cancer therapy targeting fatty acid oxidation.

Dr. Kim stated, "This study is significant because it targets the energy metabolism common to all cancer cells, rather than specific genetic mutations. It provides a powerful weapon to address drug resistance not only in pancreatic cancer but also in various solid tumors and rare or intractable cancers with no existing treatments, and is expected to greatly improve survival rates for cancer patients."

The results of the study were published in the April online edition of 'Cancer Research' (IF 16.6), a world-renowned journal in the field of cancer research.

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