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A cancer drug currently being tested in patients may have entered clinical trials based on an incorrect understanding of how it works, according to a new study led by the University of Sydney in collaboration with Goethe University, Oxford University and the Institute of Cancer Research, London.

Published in Nature Chemical Biology, the study found that the experimental drug zavondemstat and a closely related research compound, QC6352—developed to treat cancers such as colorectal, pancreatic and prostate cancer—do not primarily target KDM4, a family of proteins that can help cancer cells grow and spread when overactive. Instead, both compounds largely work by blocking DHODH, an enzyme cancer cells rely on to produce the molecules needed for rapid growth.

Lead author Professor Lenka Munoz from the University of Sydney School of Medical Sciences and Charles Perkins Center said, "We can think of DHODH as a machine producing bricks needed to build new DNA. If you switch off the machine, the cell starts running out of bricks and can no longer efficiently copy its DNA and keep dividing."

These findings could affect the interpretation of previous studies around the world that used the research compound (QC6352) to investigate the biology of the cancer protein and may have implications for the ongoing clinical development of zavondemstat.

The discovery emerged from research investigating whether zavondemstat and QC6352 could be repurposed for glioblastoma, the most common and aggressive form of brain cancer.

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