Researchers at the University of California, San Francisco, have created a drug that selectively targets a cancer-driving mutation known as K-Ras G12D, which is linked to nearly half of pancreatic cancer cases. The study outlining these findings appears in Nature Chemical Biology.
Pancreatic cancer remains less common than several other cancers, yet its treatment options are often limited. To address this gap in knowledge, scientists conducted extensive experiments in mice and developed a prototype therapy that inhibits the K-Ras G12D mutation, a major contributor to pancreatic cancer in a large share of patients.
It is noted that K-Ras mutations are highly prevalent in pancreatic tumors, appearing in about 90% of cases. Roughly half of these mutations are the G12D variant, which emerges from a single amino acid substitution. This small change—glycine being replaced by aspartate—distinguishes the carcinogenic protein from its healthy counterpart and helps drive tumor growth.
Researchers emphasize that only a handful of drugs worldwide can differentiate between cancer-associated aspartate and normal glycine, and then act solely on tumor cells without harming healthy tissue. The new drug binds to and envelops the aspartate-containing protein while sparing the normal glycine-containing proteins. In tests with mice carrying G12D-positive pancreatic tumors, treatment with the compound significantly slowed tumor progression.
Efforts are now focused on strengthening the molecule so it remains effective within the human body. The study’s authors indicate that, based on these results, clinical testing of new pancreatic cancer therapies could begin within two to three years, advancing the potential for targeted, mutation-specific treatments.
It is also noted that itching can sometimes be an indicator of pancreatic dysfunction, underscoring the importance of recognizing symptoms early and seeking medical evaluation when appropriate.