The drug, based on a modified cold virus, was designed to work against cancers caused by mutations in the p53 tumor suppressor gene - but also works when there are defects in another gene, p14 ARF, according a report in this month's Nature Medicine.
The research team at the University of California, San Francisco, USA, studied, in culture, colorectal cancer cells that responded to the drug even though the p53 gene was healthy.
Onyx-015 is under trial for colorectal and pancreatic cancer.
They found that defects in p14 ARF could block the action of p53. When this happened, Onyx-015 was able to replicate in cancer cells.
The drug is currently undergoing phase II trials in colorectal and pancreatic cancer. Its developers, Onyx Pharmaceuticals, said a response to therapy had been observed in trials.
The inventors of Onyx-015 made ingenious use of a property of the adenovirus. The virus normally dismantles the p53 gene when it invades cells. In the modified virus from which the drug was created, the ability to block p53 was neutralized. This means that the modified virus should only be able to attack cells where the p53 gene is already inactivated.
The latest research was prompted by the discovery that the new drug was attacking a wider range of cancer cells than expected.
The company's co-founder, Dr Frank McCormick, who is also director of the University's Cancer Center, said: "This solves a big puzzle about the drug's mechanism of action."
Report Copyright: Englemed Health News at http://www.internationalmedicalnews.com