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Health3 days ago· 1 min read

Experimental Pancreatic Cancer Drug Doubles Survival Time in Major Trial

A new experimental drug called daraxonrasib has been hailed as a "game changer" for pancreatic cancer after doubling survival time in clinical trials by targeting a previously undruggable mutation.

A Breakthrough Against One of Cancer's Deadliest Forms

An experimental drug that doubles survival time for people with pancreatic cancer is being hailed as a breakthrough for combating one of the world's deadliest cancers. Pancreatic cancer has long resisted treatment innovations that have transformed outcomes for other malignancies, making this development particularly significant.

How Daraxonrasib Works

Daraxonrasib works by targeting a faulty protein that leads to unchecked tumour growth. More than nine in 10 pancreatic cancer cases are driven by a mutation in the KRAS gene, which acts as an on-off switch for cells. The mutation produces an abnormal version of the KRAS protein, which remains stuck in "on" mode, sending never-ending signals for cells to grow and multiply.

Trial Results and Expert Reaction

A Phase 3, 500-person trial pitted the once-a-day pill against standard chemotherapy in patients who had already gone through one unsuccessful round of traditional cancer treatment. Dr. Jennifer Knox, a medical oncologist specializing in pancreatic cancer at the Princess Margaret Cancer Centre in Toronto, said: "It is the biggest breakthrough for pancreatic cancer ever... We haven't seen an improvement like this with any other treatments. There's been a lot of really exciting breakthroughs across oncology; none of them worked in pancreatic cancer. And so this is the game changer."

Decades of Research Finally Bearing Fruit

Daraxonrasib is the first in a new class of drugs called RAS(ON) inhibitors, which target various members of the RAS family of genes and their corresponding proteins. The KRAS gene had been studied for decades, like 50 to 60 years, and it was thought to be undruggable. This success opens the door to similar treatments for other cancers driven by RAS mutations.

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