Spanish scientist develops treatment that eliminates pancreatic cancer in laboratory mice

A Spanish research team has completely eliminated pancreatic cancer in laboratory mice using a 3-drug combination with no resistance developing for over 200 days after treatment ended. The study, led by Dr. Mariano Barbacid at Spain’s National Cancer Research Centre (CNIO), was published in Proceedings of the National Academy of Sciences (PNAS) in late 2025. The results are preclinical; the therapy has not yet been tested in humans, but experts call it one of the strongest signals yet that pancreatic cancer may be defeatable.

Pancreatic cancer kills roughly 9 in every 10 patients within 5 years of diagnosis. It is the third-leading cause of cancer death in the United States. Standard chemotherapy stops working within months because tumours evolve and find new ways to grow. That is why this result stands out.

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What Is Pancreatic Cancer and Why Is It So Hard to Treat?

Pancreatic ductal adenocarcinoma (PDAC) is the most common form of pancreatic cancer, accounting for more than 90% of all cases. The pancreas sits behind the stomach and controls both digestion and blood sugar regulation through insulin production. Because the organ is deep inside the body, tumours grow silently. By the time most patients receive a diagnosis, the cancer has already spread.

3 key reasons pancreatic cancer is so deadly: it is usually detected late, spreads quickly to surrounding organs, and resists almost every existing treatment. Chemotherapy regimens like FOLFIRINOX and gemcitabine can extend survival by months, but they rarely produce lasting remission. Surgery is only possible in around 20% of patients.

In Spain alone, more than 10,300 people receive a pancreatic cancer diagnosis every year. In the US, approximately 66,000 new cases are diagnosed annually. Globally, this cancer claims around 500,000 lives per year.

The KRAS Problem: Why Previous Treatments Keep Failing

At the centre of nearly every pancreatic cancer is a mutated gene called KRAS. This oncogene continuously sends growth signals to cancer cells, telling them to multiply without stopping. KRAS mutations appear in more than 90% of PDAC cases, making it the single most important driver of this disease.

For decades, KRAS was considered “undruggable” scientists could not block it effectively. The first KRAS-targeting drugs were only approved in 2021, more than 50 years after the gene was first linked to cancer. Dr. Barbacid himself played a foundational role in KRAS research, isolating the first human oncogene HRAS back in 1982.

Even with newer KRAS inhibitors, tumours find escape routes. Block one growth pathway and the cancer activates alternative survival routes through EGFR, HER2, or STAT3 signalling and starts growing again within months. This adaptability is the central obstacle researchers have struggled to overcome.

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How the CNIO Triple-Drug Therapy Works

Dr. Barbacid’s team took a fundamentally different approach. Instead of targeting one survival pathway, the therapy attacks 3 pathways simultaneously, giving cancer cells no viable escape route.

Drug	Target	Role in Therapy
Daraxonrasib (RMC-6236)	Mutant KRAS signalling	Cuts the main engine driving tumour growth
Afatinib	EGFR and HER2 receptors	Seals the primary escape routes used when KRAS is blocked
SD36 (protein degrader)	STAT3 survival pathway	Disables the emergency backup that keeps cancer cells alive

Daraxonrasib (also known as RMC-6236) was developed by Revolution Medicines and is currently awaiting regulatory approval for other cancer types. Afatinib is already approved for certain lung adenocarcinomas. SD36 is an experimental compound that selectively degrades STAT3 in cancer cells.

Together, the 3 drugs block the tumour’s growth engine, seal its escape routes, and destroy the emergency system it uses to survive treatment. The team described the logic as similar to fixing a beam to the ceiling at three points rather than one it becomes far harder to break.

The Results: What Happened in the Laboratory

The research team tested the triple therapy in 3 different experimental systems to verify the results were real and repeatable.

• Genetically engineered mouse models (GEMMs): Mice were engineered to develop PDAC that closely mimics the human disease. Tumours disappeared completely and did not return for more than 200 days after treatment stopped.
• Orthotopic models: Tumours were grown directly in the pancreas of mice. The therapy produced complete and durable regression the gold standard test for cancer treatments.
• Patient-derived tumour xenografts (PDXs): Actual tumour tissue taken from human pancreatic cancer patients was grown in mice and then treated. The same pattern of elimination was observed.

200 days of tumour-free survival in mice is scientifically significant. In comparable terms, this would represent years of remission in humans. No previous therapy has achieved this outcome in PDAC preclinical models without the tumour finding resistance mechanisms.

Crucially, the combination showed low toxicity in all animal models. Blood cell counts remained normal, animals maintained body weight, and tissue integrity was preserved throughout treatment. This matters enormously: many aggressive combination therapies fail in human trials not because they don’t work, but because they are too toxic for patients to tolerate.

What This Means And What It Does Not Mean

This is not a cure for pancreatic cancer in humans. That point is non-negotiable. Dr. Barbacid was direct in his own statement: “We are not yet in a position to carry out clinical trials with this triple therapy.”

Many treatments that eliminate cancer in mouse models fail during human trials. The biology of human cancer is more complex, immune systems differ, and drug metabolism in people produces effects that cannot be fully predicted in animals. This is why the path from a preclinical result to an approved treatment typically takes 10 to 15 years.

What the study does demonstrate is a clear proof-of-concept: pancreatic cancer is vulnerable to a precisely designed multi-target approach. The study also identifies 3 specific molecular targets, KRAS, EGFR/HER2, and STAT3, as the critical combination to pursue in future human trials.

The 6 years of research behind this result, including an earlier 2019 finding where blocking EGFR and RAF1 showed limited effectiveness, reflect how systematically Barbacid’s team has built toward this breakthrough. The discovery that STAT3 completes the combination was the key final piece.

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What Happens Next: The Road to Human Trials

Dr. Barbacid estimates that human clinical trials could begin within 3 years but only if the necessary funding and regulatory approvals move at the right pace. The process requires 5 stages before patients can be enrolled.

• Stage 1 Extended animal studies: Testing across additional mouse models with different genetic alterations and studying metastatic spread.
• Stage 2 Dosing optimisation: Determining the exact dosing ratios and schedules for the 3-drug combination in preparation for human biology.
• Stage 3 Toxicology and safety reviews: Comprehensive assessments of how each drug and the combination affect healthy tissues.
• Stage 4 Regulatory approval: Submissions to agencies like the European Medicines Agency (EMA) and the US Food and Drug Administration (FDA) to authorise early-phase human trials.
• Stage 5 Phase I/II clinical trials: First human testing, focused primarily on safety and early effectiveness in a small group of patients.

Funding is the immediate bottleneck. Moving from preclinical results to a Phase I human trial requires an estimated €30 million (approximately $32.5 million / £25.7 million). Following the publication of the study, a public fundraising campaign through the CRIS Against Cancer Foundation drew more than 18,000 donors who contributed over €841,000 in under 24 hours a sign of how urgently people want this research to proceed.

Daraxonrasib, the KRAS inhibitor at the core of the therapy, could receive broader regulatory authorisation later in 2026. That approval would significantly lower one of the practical barriers to advancing the combination therapy into trials.

Who is Dr Mariano Barbacid?

Dr. Mariano Barbacid is one of the most influential figures in modern cancer biology. As head of the Experimental Oncology Group at CNIO, he is best known for isolating the first human oncogene HRAS in 1982. That discovery transformed the scientific understanding of what causes cancer at the genetic level.

In 2020, Barbacid received the Echegaray Medal, Spain’s highest scientific honour, awarded by the Royal Academy of Exact, Physical and Natural Sciences. He has spent more than four decades arguing that pancreatic cancer cannot be defeated with a single-drug approach, and this latest study represents the strongest validation yet of that position.

The study’s co-lead author is Carmen Guerra, with Vasiliki Liaki and Sara Barrambana as first authors. The research was funded by the European Research Council, the Spanish State Research Agency, and the CRIS Against Cancer Foundation.

Where This Stands Among Pancreatic Cancer Research in 2026

Pancreatic cancer research has seen 4 significant directions in recent years: KRAS inhibitors, immunotherapy (checkpoint inhibitors), PARP inhibitors for BRCA-mutated cases, and stroma-targeting therapies. Each has shown partial promise but failed to produce durable remission in PDAC.

Checkpoint inhibitors, which work well in lung cancer, melanoma, and certain other tumours, have largely failed against pancreatic cancer because PDAC creates an immunosuppressive environment. The tumour surrounds itself with dense stromal tissue that blocks immune cells and drug molecules alike.

The Barbacid approach is different because it does not rely on the immune system. It targets the molecular machinery inside tumour cells. By simultaneously disabling 3 survival systems: KRAS downstream signalling, EGFR/HER2 escape pathways, and STAT3 stress response, the therapy does not give cancer cells any viable route to adapt and survive.

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Pancreatic Cancer: 6 Critical Facts You Should Know

• Survival rate is roughly 12%: Only about 12% of pancreatic cancer patients in the US survive 5 years after diagnosis, according to the Huntsman Cancer Institute.
• KRAS mutation is nearly universal: More than 90% of PDAC cases carry a KRAS mutation, making it the most consistent drug target across cancer types.
• Late detection drives poor outcomes: Around 80–85% of patients are diagnosed at a stage when surgery is no longer possible.
• It is the third-leading cause of cancer death in the US: Pancreatic cancer kills more Americans than any other cancer except lung and colorectal.
• Risk factors include 5 main categories: smoking, obesity, type 2 diabetes, chronic pancreatitis, and a family history of the disease.
• No approved early-detection test exists: Unlike breast or colon cancer, there is currently no standard screening method that catches pancreatic cancer early in the general population.

External Sources

• Official CNIO press release on the Barbacid triple therapy study
• Original research paper in PNAS: Liaki et al., 2025
• Newsweek: What to know about the pancreatic cancer breakthrough

Frequently Asked Questions

Q1. Has pancreatic cancer been cured in humans?

No. The Barbacid study is preclinical, meaning the results come from laboratory mice and patient-derived tumour tissue grown in animals. The therapy has not been tested in humans. Clinical trials, if they proceed, are expected to begin within 3 years pending funding and regulatory approvals.

Q2. What are the 3 drugs used in the CNIO triple therapy?

The 3 drugs are: daraxonrasib (RMC-6236), a KRAS inhibitor developed by Revolution Medicines; afatinib, an approved EGFR/HER2 blocker; and SD36, an experimental compound that degrades the STAT3 protein inside cancer cells. Together, they block the 3 main survival systems pancreatic tumours rely on.

Q3. Why does pancreatic cancer resist treatment so effectively?

Pancreatic cancer carries a mutated KRAS gene that drives constant cell growth. When one treatment pathway is blocked, the tumour activates alternative routes, such as EGFR, HER2, or STAT3, to keep growing. This adaptability has repeatedly made single-drug approaches fail. The new triple-drug strategy addresses this by blocking all 3 routes simultaneously.

Q4. What is the 5-year survival rate for pancreatic cancer?

Approximately 10–12% of pancreatic cancer patients survive 5 years after diagnosis in the US and UK. The rate is so low because the disease is usually discovered at an advanced stage when it has already spread to other organs.

Q5. What is KRAS and why does it matter for cancer?

KRAS is a gene that, when mutated, acts as a permanently switched-on growth signal inside cancer cells. It is mutated in more than 90% of pancreatic cancer cases, around 40% of colorectal cancers, and 25–30% of lung adenocarcinomas. Blocking KRAS is one of the top priorities in modern oncology research.

Q6. How much funding is needed to move this therapy into human trials?

An estimated €30 million (approximately $32.5 million / £25.7 million) is needed to advance the triple therapy to Phase I human clinical trials. Following the study’s publication, a public fundraising campaign raised over €841,000 from 18,000+ donors in under 24 hours through the CRIS Against Cancer Foundation.

Q7. Is this different from standard chemotherapy?

Yes. Standard chemotherapy drugs like gemcitabine and FOLFIRINOX attack all rapidly dividing cells throughout the body, which causes severe side effects and only slows PDAC growth temporarily. The CNIO triple therapy is targeted, specifically blocking molecular pathways within tumour cells, and has shown low toxicity in animal models.

The Bottom Line

Pancreatic cancer has not been cured. But for the first time in decades of research, scientists have demonstrated complete and durable elimination of PDAC tumours in multiple preclinical models with no resistance developing and no significant toxicity. That has never been achieved in this disease before.

The Barbacid triple therapy works by blocking KRAS signalling, sealing escape routes through EGFR/HER2, and disabling the STAT3 survival backup simultaneously. It is a multi-front strategy against a cancer that has always found ways to adapt to single-front attacks.

The next 3 years will determine whether this translates to human patients. Funding, regulatory timelines, and the outcome of further animal studies will all play a role. What the science shows right now is the clearest direction yet toward making pancreatic cancer beatable.