Pancreatic cancer sucks and its an absolute biotech graveyard. It’s essentially where drugs go to die.
As a result, five-year survival is still around 13%.
The chemotherapy backbone — mFOLFIRINOX — has barely changed in a decade. Almost every targeted therapy that works in other solid tumors just doesn’t in PDAC. The microenvironment is dense, immunosuppressive, and actively hostile to almost everything we throw at it.
So when a Phase 1b readout in locally advanced pancreatic cancer gets published in Nature, you pay attention.
NETRIS Pharma, a private French biotech out of Lyon, just did exactly that. Their lead asset, NP137, is a first-in-class monoclonal antibody that targets netrin-1 … a protein most people know as a neural axon guidance cue from embryology textbooks.
Turns out netrin-1 also drives epithelial-to-mesenchymal transition in cancer, helping tumor cells survive, migrate, and resist treatment.
Block it, and you potentially make chemo work better.
That’s the LAPNET-01 trial thesis. And the numbers they published are legitimately compelling.
LAPNET-01 Phase 1b: NP137 + mFOLFIRINOX in locally advanced PDAC
MEDIAN PROGRESSION-FREE SURVIVAL (MONTHS)
10.85 mo
15.65 mo
CONVERSION TO SURGERY (%)
23%
40%
Source: LAPNET-01 Phase 1b, published in Nature (April 2026)
Context: the median OS for locally advanced PDAC on standard mFOLFIRINOX is roughly 13-16 months, depending on the series. Conversion-to-surgery rates vary widely, but 10-20% is typical. NP137 plus mFOLFIRINOX hit 16.43 months median OS overall, and in the neogenin-high subgroup, the conversion rate jumped to 40%.
Getting a pancreatic cancer patient to surgery is the game. It’s the only path to long-term survival. Doubling the conversion rate in a biomarker-enriched subgroup is the kind of finding that actually changes how you design the next trial.
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Speaking of the biomarker, neogenin is one of netrin-1’s receptors.
High neogenin expression basically identifies the tumors that are most dependent on the netrin-1 signaling axis NP137 is blocking. Classic mechanism-meets-patient-selection story, and it’s the kind of predictive biomarker that can make the difference between a “mixed” readout and a regulatory-enabling one.
The PDAC field has been a graveyard for new mechanisms lately. Revolution Medicines has daraxonrasib — their pan-RAS inhibitor — in Phase 3 RASolute 303 in first-line metastatic PDAC. Kestrel cleared IND for their pan-KRAS inhibitor KST-6051 earlier this year. And today, BlossomHill Therapeutics dropped preclinical data on a pan-KRAS inhibitor with a 54-hour residence time.
Different mechanism, same target disease. Netrin-1 is upstream of the whole EMT program. It’s a different kind of shot, and the fact that it appears to work synergistically with chemo rather than replacing it is honestly the more pragmatic path to approval in this indication.
NETRIS has been quiet for a private French biotech. There’s been no big funding headlines in the past year, no flashy platform claims. They just ran a Phase 1b, got clinical activity, enriched for the right biomarker, and put the data in Nature.
Regulatory discussions in the US and Europe are next. Phase 2 trial design becomes the whole story from here. The smart play is a neogenin-stratified registration-enabling study in locally advanced disease, with surgical conversion as a co-primary endpoint.
If they run that trial well, this becomes a real drug. In pancreatic cancer. That’s a sentence you don’t get to write often.
