Daraxonrasib: pancreatic cancer drug shows promise

10 MAY 2026

In 1988, a landmark paper in Cell said that in around 95% of pancreatic cancers, a gene called KRAScarried mutations at a particular location.
It was one of the first demonstrations of a mutation with near-universal frequency identified in a cancer.

Cancer

Cancer is uncontrolled cell division.
In a healthy individual, cells grow and divide in a tightly controlled cycle, with specific signals telling the cell when to divide or not.
If something goes amiss in this process, cells can repair themselves or undergo programmed cell death.
In cancer, this balance is disturbed, causing unregulated cell division. As a result, mistakes tend to accumulate in the DNA, leading to tumours that can invade surrounding tissues and spread to other organs.
Pancreatic cancer is particularly deadly because it is usually detected late, when the disease has already spread to neighbouring tissues.
There are very few surgical options; even after surgery, recurrence is common. Standard chemotherapy is also not very effective.

KRAS

The 1988 Cell paper showed the KRAS gene acts as a switch, regulating whether a cell divides.
The KRAS protein — the product of the gene — exists in either an ‘off’ state, which suppresses cell division or an ‘on’ state that promotes it.
The mutations reported in the study locked KRAS in its ‘on’ state, driving uncontrolled cell division, leading to pancreatic, colorectal, and lung cancers.
For decades, the medical fraternity considered KRAS to be an attractive drug target.
However, it proved exceptionally difficult to inhibit because most small-molecule drugs work by fitting into well-defined pockets or grooves on a protein’s surface, blocking its activity, whereas KRAS has a relatively smooth, compact surface with few binding sites.
Despite this difficulty, several research groups attempted to target the KRAS gene, but nearly all efforts fared poorly in clinical trials. As a result, KRAS was long labelled “undruggable”.

Daraxonrasib

In June 2024, a California-based company called Revolution Medicines reported a molecule later called daraxonrasib. It works by targeting a range of the RAS family of proteins, including KRAS, when they are in their ‘on’ state and signalling the cell to divide.
Daraxonrasib first binds to another protein called cyclophilin-A, then locking it with KRAS into a nonfunctional state.
The clinical trial findings suggested daraxonrasib may be more effective than previous treatments for pancreatic cancer. In 51% of patients, it reduced the size of tumours, and in 97% it caused their cancers to either shrink or not grow further.
However, daraxonrasib also had many side effects. Nearly all patients experienced mild to moderate effects, including skin rash, diarrhoea, mouth sores, nausea, and fatigue.
However, importantly, no life-threatening side-effects were reported in any patients.

“National Priority Voucher” status

The strong clinical results have also led the U.S. Food and Drug Administration (FDA) to include daraxonrasib among eight other therapies in the first-ever group of drugs to receive “National Priority Voucher” status.
The FDA created this designation for highly promising drug candidates that address urgent national health needs.
The voucher also allows the FDA to shorten what would typically be a year-long review process to just one or two months.
The results of the FDA review are awaited as well, and there is growing optimism that it will be positive.