‘The undruggable became druggable’: a gamechanging treatment for the world’s deadliest cancer

Summary

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Science Weekly (The Guardian)

Episode: ‘The undruggable became druggable’: a breakthrough cancer treatment
Date: June 11, 2026
Host: Madeline Findlay
Guest: Professor Noreen Starling, Consultant Medical Oncologist and Director of the Royal Marsden Clinical Trials Unit

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Episode Overview

This episode delves into a landmark breakthrough in the treatment of pancreatic cancer: the development of the drug Daraxon Rasib, an oral medication that has, for the first time, shown the ability to double survival in advanced pancreatic cancer. Host Madeline Findlay and guest Professor Noreen Starling discuss why pancreatic cancer has resisted progress for so long, what makes the new treatment so revolutionary, and its potential implications for cancer treatment as a whole.

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Key Discussion Points & Insights

1. Current State of Pancreatic Cancer Treatment

• Late Diagnosis is Common: Most pancreatic cancer patients present at an advanced stage where surgery is rarely an option.
• Chemotherapy is the Mainstay—But Not a Cure:
  • Average survival for advanced cases is about a year, sometimes more, sometimes less.
  • Treatments can help patients live “longer and better,” but are not curative.

  “The majority of patients… present with advanced pancreatic cancer that has already spread, where surgery doesn't really have a role.” – Prof. Noreen Starling (03:51)

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2. Why Pancreatic Cancer is So Difficult to Treat

• Late and Aggressive Spread: Even early, operable cancers often have already begun to spread microscopically, leading to high relapse rates (04:49).
• Genetic Barrier—The KRAS Gene:
  • 90% of pancreatic tumors have a mutation in the KRAS gene—the central driver of tumor growth and division.

  “This gene that drives the cancer to grow and develop has been considered undruggable.” – Prof. Noreen Starling (05:14)

• RAS Protein Challenge:
  • RAS proteins, produced by KRAS, lack the “deep pockets” that drugs usually bind to—making them incredibly hard to target with conventional therapies.

  “The protein is pretty smooth… good drug targets often have these deep pockets… but these pockets are pretty shallow and smooth.” – Prof. Noreen Starling (06:07)

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3. Turning the ‘Undruggable’ Druggable: The Major Breakthrough

• Scientific Milestone:
  • Recent decades of research have resulted in drugs that can finally target and inhibit RAS proteins, leading to unprecedented results presented at the American Society of Clinical Oncology (ASCO) 2026 meeting.
• The “Spine-Tingling” Presentation & Standing Ovation:

  "It was a spine tingling moment… the results were so stunning that the presenter received a standing ovation as he was presenting the data…” – Prof. Noreen Starling (07:08)

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4. How Daraxon Rasib Works

• Clinical Trial Design & Results:
  • Patients with advanced, previously treated pancreatic cancer were randomized to receive either chemotherapy or the new oral tablet.
  • Daraxon Rasib doubled median survival from 6 to 13 months.
  • Over 30% of patients on the tablet had tumor shrinkage (compared to 10% for chemotherapy).
  • Patients also reported less pain and improved quality of life.

  “The results were just jaw dropping… survival was doubled… Tumors shrink… and, really importantly… not only were they living longer, but they felt better.” – Prof. Noreen Starling (07:42)

• Novel Mechanism – Molecular Glue:
  • Unlike traditional inhibitors, the drug binds to cyclophilin A, a chaperone protein, forming a complex that “glues” and inactivates the RAS protein.

  “It binds to a chaperone protein… and then that doublet… blocks the activated state of RAS. It's forming a kind of molecular glue to shut RAS down…” – Prof. Noreen Starling (08:34)

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5. What’s Next: Expanding the Impact and Ongoing Questions

• Work Ahead in Pancreatic Cancer:

  • Current trial focused on patients who failed prior chemotherapy.
  • Upcoming trials will assess effectiveness as first-line treatment and in earlier (operable) disease.
  • Combinatorial approaches and new drugs are in the pipeline.

  “For me, this is really the key that unlocks the transformative treatment potential… we’ve been looking for that in pancreatic cancer for such a long time. I think it's a triumph for science and it's a triumph for patients.” – Prof. Noreen Starling (09:30)

• Regulatory Pathway & Patient Access:

  • Approval and access depend on regional regulatory review and reimbursement decisions.
  • UK “NICE” assessment pending; hope is for rapid approval, possibly within one to two years due to the significance of results.

  “…I would hope that we can see progress within this next year, or certainly within the next couple of years. But it’s such an important breakthrough, I would hope the system can move quickly.” – Prof. Noreen Starling (11:16)

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6. Could This Approach Work for Other Cancers?

• RAS Mutations in Other Cancers:
  • Non-small cell lung and colorectal cancers frequently have RAS mutations.
  • RAS is present in up to 50-60% of colorectal cancers.
• Challenges Remain:
  • The pathway’s complexity means other cancers may prove less responsive.
  • Drug resistance ("whack-a-mole") is a persistent concern with targeted therapies.

  “RAS is not the same in every disease… what we sometimes see with these targeted drugs is it's a bit like whack a mole. You press one thing down and another thing pops up in terms of resistance.” – Prof. Noreen Starling (14:12)

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7. Marking a New Era in Cancer Therapy

• Comparison with Immunotherapy Progress in Melanoma:
  • Just as immunotherapy revolutionized melanoma, this breakthrough could do the same for pancreatic and other “hard-to-treat” cancers.

  “It’s historic—that the undruggable became druggable… If RAS can be unlocked and druggable, I think that shifts our thinking. Is no target undruggable?... I think it gives our patients and their families a lot of hope.” – Prof. Noreen Starling (15:34)

• A Moment of Hope for Patients and Medicine:
  • The excitement is palpable—for researchers, clinicians, and patients alike.

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Notable Quotes & Memorable Moments

• On patient impact:

  “The fact that in this trial, patients saw a doubling of survival time, which is just, it's so huge when you’re faced with having to think about how long you might have left.” — Madeline Findlay (10:45)

• On the atmosphere at ASCO:

  “It was a spine-tingling moment… standing ovation as he was presenting the data…” — Prof. Noreen Starling (07:08)

• On the future of cancer research:

  “Honestly, I think it’s one of the most exciting times to be in clinical trials and cancer research, and I think it gives me a lot and I’m hoping it gives our patients and their families a lot of hope.” – Prof. Noreen Starling (15:34)

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Timestamps for Key Segments

• [03:51] – Why pancreatic cancer is so difficult to treat
• [05:14] – The dominance and “undruggability” of KRAS mutations
• [07:08] – Reaction to Daraxon Rasib trial results at ASCO
• [07:42] – Summary of phase three trial findings
• [08:34] – Explanation of the drug’s “molecular glue” mechanism
• [09:30] – Next questions in research; clinical trial future
• [11:16] – Regulatory pathway and access to the new drug
• [14:12] – Potential for targeting RAS in other cancers
• [15:34] – Historic shift: the “undruggable” becomes druggable

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Conclusion

This episode of Science Weekly captures a momentous development—the first compelling evidence that a once “undruggable” cancer driver can be successfully targeted, marking the start of a potentially transformative era in cancer therapy. While challenges remain and full clinical rollout will take some time, the results for Daraxon Rasib offer genuine hope not only to pancreatic cancer patients but to the wider cancer research community.

As Professor Starling sums up:

“If RAS can be unlocked and druggable, I think that shifts our thinking. Is no target undruggable?” (15:34)

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Transcript

[Professor Noreen Starling]

This is the Guardian.

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[Madeline Findlay]

Each May, the American Society of Clinical Oncology annual meeting is held in Chicago. Cancer researchers from around the world gather together to share the latest advances. And 2026 was a bit of a blockbuster year. One study pointed the finger at poor sleep in fuelling the global rise in cancer diagnoses in the under 50s. Another shared a groundbreaking genomic test that could spare millions of breast cancer patients Chemotherapy. Then there was a cancer jab that eradicated entire tumors. But there was one presentation with results so striking that the audience got to their feet and cheered. A clinical trial of a daily pill for the world's deadliest cancer found it doubled survival times. To date, pancreatic cancer has proved extremely hard to treat. But this drug could herald a new era for patients. So today, a game changing moment for pancreatic cancer. From the Guardian I'm Madeline Findlay and this is Science Weekly. Professor Noreen Starling. You're a consultant medical oncologist and director of the Royal Marsden Clinical Trials Unit and one of Your specialisms is pancreatic cancer. So what kind of treatment options are available right now for pancreatic cancer? And how effective effective are they?

[Professor Noreen Starling]

So, currently, the majority of patients we see in the UK and worldwide with pancreatic cancer present with advanced pancreas, cancer that has already spread, where surgery doesn't really have a role. Maybe we see 1 in 10 or slightly more patients who present with operable pancreatic cancer. So for the majority of patients with advanced disease today, and for really the last couple of decades, chemotherapy drug treatment has been the mainstay of our treatment approach. But these aren't curative treatments. They help us to help patients live longer and better with pancreatic cancer. But this is one of the most challenging cancers to treat. The average survival for patients with advanced pancreatic cancer is about a year, sometimes more, sometimes less.

[Madeline Findlay]

And why is pancreatic cancer so hard to treat?

[Professor Noreen Starling]

It presents often late at an advanced stage. And even for the patients who have operable disease, at a microscopic level, the cancer's already managed to break off, which is why we see so much relapse, even after surgery and chemotherapy.

[Madeline Findlay]

But there's another factor that makes pancreatic cancer so difficult to treat, and it's to do with mutations in a gene called Krasnohe.

[Professor Noreen Starling]

So 90% of patients with pancreatic cancer, so 9 out of 10 patients have a mutation in Kras, and this mutation really is the dominant driver of pancreatic cancer. This gene that drives the cancer to grow and develop has been considered undruggable.

[Madeline Findlay]

The KRAS gene is part of the RAS family of genes. These provide the instructions to make RAS proteins, which act as on and off switches for cell growth and division. Genetic mutations can mean RAS proteins get stuck in the on mode, leading to overactive cell growth and division, and ultimately cancer. Scientists spent decades trying to develop drugs to switch off RAS proteins. But there's something about them that makes them difficult to target.

[Professor Noreen Starling]

The RAS protein is tricky because the protein is pretty smooth. Now, you might think, why does that make it challenging to drug? Well, good drug targets often have these deep pockets that you can design a drug to fit and nestle into that pocket and by doing so, switch off the protein and switch off that signal. But these pockets are pretty shallow and smooth.

[Madeline Findlay]

Scientists had to look for other, more circuitous ways to get around these shallow, smooth pockets and bind their drugs to RAS proteins. But after decades of work, they did it and proved KRAS and the rest of the RAS proteins could be switched off. And last week, the next Big breakthrough was announced at the annual meeting of the American Society of Clinical Oncology in Chicago.

[Professor Noreen Starling]

Honestly, it was a spine tingling moment. I was in the room, thousands of listeners in the room as the data were presented. What we saw was a major breakthrough for the treatment of pancreatic cancer. And the results were so stunning that the presenter received a standing ovation as he was presenting the data, not even at the end of the presentation.

[Madeline Findlay]

This excitement was sparked by the results from a phase three randomised control trial of a drug called Daraxan Rasib, a tablet the patients take once a day.

[Professor Noreen Starling]

So half of the patients received another chemotherapy and half of the patients received the oral tablet therapy. And the results were just jaw dropping. So in this group of patients, survival was doubled, going for an average of about six months to over 13 months. We saw tumors shrink in the patients who had the Duraxon Rasib tablets. A good shrinkage of over 30% of patients compared to about 10% of patients with chemotherapy. And really importantly for patients, not only were they living longer, but they felt better. There was a reduction in pain and improvement in symptoms for a good amount of time.

[Madeline Findlay]

So this drug has had incredible results. But Noreen, how exactly does it work?

[Professor Noreen Starling]

The way it works is very clever and it's quite different to sort of the traditional drug inhibitor. So a drug interacts with the protein that you want and shuts it down. It does it in a more sneaky way. So it binds to a chaperone protein called cyclophenol A and forms a bond with that. And then that doublet, if you like, blocks the activated state of ras. It's forming a kind of molecular glue to shut ras down and stop it, providing the signal for the cancer cell to grow.

[Madeline Findlay]

So this drug uses another protein to form a molecular glue that grabs and shuts down Kras and and the other members of the Ras family. It's exciting science. And this clinical trial is just the beginning of exploring how it could be used to help patients.

[Professor Noreen Starling]

There are so many more important questions now for our patients with pancreatic cancer. So the trial is very specifically for the group of patients who have had chemotherapy previously and it has stopped working. One of the next important questions is, okay, what about the patients who've just been diagnosed with advanced stage 4 pancreatic cancer? Does Daraxon Rasib, this oral therapy, work for those patients? Does it improve survival and symptoms and how patients feel as the first line of treatment? But then going back to how do we actually prevent pancreatic cancer becoming advanced? What about those patients with operable pancreatic cancer. But it doesn't stop there. There are many other questions about what are the other combinations of this sort of drug, Duraxon, racib, but indeed other drugs that are also rapidly through clinical trials. For me, this is really the key that unlocks the transformative treatment potential for pancreatic cancer. So it's going to be a really busy clinical trials landscape. That is wonderful. We've been looking for that in pancreatic cancer for such a long time. I think it's a triumph for science and it's a triumph for patients.

[Madeline Findlay]

The fact that in this trial, patients saw a doubling of survival time, which is just, it's so huge when you're faced with having to think about how long you might have left. Others in similar situations, hearing about Diracs and Rasid now will no doubt be asking themselves, well, when am I going to be able to get hold of this? So in your mind, I know this is a little bit like asking how long is a piece of string, but when do you think this could become available to patients?

[Professor Noreen Starling]

There's two answers to that. One is the length of time it takes in terms of the regulator to review the data in order to allow the drug to be available. And within every jurisdiction, there will also need to be reimbursement considerations. And for the uk, that will be a nice appraisal which looks at benefit and resource and cost. That timeline can vary. You know, I would hope that we can see progress within this next year, or certainly with within the next couple of years. But it's such an important breakthrough. I would hope the system can move quickly. In regard to this.

[Madeline Findlay]

Coming up, could the approach behind this drug work for other cancers?

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[Madeline Findlay]

Noreen do mutations in RAS genes cause other kinds of cancer? And so could this drug or the principle behind it at least be developed for other cancers?

[Professor Noreen Starling]

Absolutely. So the two main other cancers where we can see RAS mutations include non small cell lung cancer and colorectal cancer. In fact, RAS mutations might be present in about 50 to 60% of tumours of patients with colorectal cancer. So there's definitely efforts and trial coming focused on both of these diseases. There may be additional challenges. RAAS is not the same in every disease, so it's very dominant and inhibition is powerful in pancreas cancer. Colorectal cancer could be a bit more challenging because the circuitry is somewhat difficult. What we sometimes see with these targeted drugs is it's a bit like whack a mole. You press one thing down and another thing pops up in terms of resistance. And that's again a challenge to the scientists in the field for how we manage that. So, again, very evolving field.

[Madeline Findlay]

So lots still to do. But after decades of research on this, it feels like a really exciting time, not just in the field of pancreatic cancer research, but cancer research generally. Do you see this as almost marking a moment where real progress is being made on finding new kinds of effective therapies?

[Professor Noreen Starling]

It's really exciting. And I wanted to see this in my career time, you know, when I started as a consultant 12 years ago. And I thought about what the challenges were and what I would love to see in terms of transformation, much like we saw in terms of melanoma and immunotherapy transformation. And I think this is it. Melanoma was a devastating condition when patients presented with stage four disease. You know, when I was in training, patients would survive less than a year. And now we're curing well over half of the patients with immunotherapy. It does mark a real shift in time. It's historic that the undruggable became druggable. So if RAS can be unlocked and druggable. I think that shifts our thinking. Is no target undruggable? Can we target every possible molecule that is important and a driver for cancers and across all cancers? So honestly, I think it's one of the most exciting times to be in clinical trials and cancer research and I think it gives me a lot and I'm hoping it gives our patients and their families a lot of hope.

[Madeline Findlay]

Well, Noori, we'll be looking forward to seeing the results from all these clinical trials coming down the road. Thank you so much.

[Professor Noreen Starling]

Thank you for having me.

[Madeline Findlay]

And that's all from us today. You can read more about the latest advances in cancer research from health editor Andrew [e-mail] and before you go. As the World cup kicks off, the Guardian's award winning football weekly podcast is turning into World Cup Daily. Join Max Rushton, Barry Glendenning and the team as they discuss every big match and every big moment every day of the World Cup. Listen now, wherever you get this podcast or watch on YouTube. This episode was produced by Elliot Sands. The sound design was by Ross Burns and the executive producer was Ellie Burey. We'll be back on Tuesday. See you then. This is the Guardian.

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