Loading
Everything in development, the medicines held by this cancer's subtypes, the open problems and what is being done about them, the roadmaps, and what changed on this record.
What is in development for Pancreatic ductal adenocarcinoma, drawn from the whole corpus: 381 items. Drugs are grouped by the most advanced trial phase they have reached anywhere; approved treatments sit under standard of care. Technologies are the methods being tested for this cancer, trials are the studies recorded here, and ideas are proposals not yet in a trial.
10 medicines on record are linked to one of the types below rather than to Pancreatic ductal adenocarcinoma itself. Grouped by the type that holds them; each list opens that type's own page.
Resistance to RAS(ON) inhibitors: secondary RAS mutations, RTK bypass, and adaptive feedback are already described; combination strategies are unproven in phase 3.
Background: Circulating tumour DNA (ctDNA), Mutational signature. Also on OnCo: Resistance: how tumours escape each drug class · Lines of therapy.
Half of patients are too frail for FOLFIRINOX-class regimens; RAS inhibitors may change this but toxicity (rash, stomatitis) is not trivial.
Also on OnCo: Side effects by symptom · Checkpoint side effects by organ · Side effect rates across a drug class · Survivorship planner.
No population screening; MCED sensitivity for stage I PDAC is low and PPV in average-risk adults is poor.
Background: CA 19-9, Positive predictive value (PPV), Stage shift. Also on OnCo: Symptoms and red flags · Early detection roadmap.
Immune exclusion: every checkpoint inhibitor trial has failed outside MSI-H disease; vaccines must overcome a cold microenvironment.
The dense stroma blocks drug delivery, yet stripping it out made tumours more aggressive in mice and hyaluronidase failed in phase 3 (HALO-301); reprogramming rather than depleting the stroma is unproven in patients.
Access: RAS inhibitors and TTFields will be expensive; global disparities will widen.
Also on OnCo: Financial help · Coverage by country · Funding verdicts by country.
Emergency presentation: 45 percent of English cases (2019) and 60.9 percent of US Veterans Affairs cases (2026) are diagnosed as emergencies, with more advanced stage and higher mortality; the symptom-based referral rules (NG12) catch a minority.
Enzyme replacement reaches a minority: only 21.7 percent of 4,554 UK patients in primary care records received pancreatic enzyme replacement therapy, and supplies were disrupted in 2024 (NG85 note), although it is a NICE recommendation for every unresectable patient.
The 1 mm margin rule is not used everywhere, so R0 and R1 rates and their survival differences are not comparable between series or trials (Strobel 2017).
Surveillance of mutation-negative familial kindreds found no cancers in the Dutch programme and few in EUROPAC, while carriers of CDKN2A and other genes have substantial yields; who to watch, and when to stop, is unresolved.
Neither the new-onset diabetes score (3.6 percent prevalence among high scorers) nor carrier surveillance (7 of 9 CAPS5 cancers at stage I) has been tested prospectively at population scale, and CA 19-9 cannot be read in the Lewis-negative tenth of patients; four in five patients still present with disease that cannot be removed.
Two perioperative trials (PREOPANC-3, Alliance A021806) are the only ones comparing chemotherapy before and after surgery with the current adjuvant standard; until they read out, neoadjuvant treatment for clearly resectable disease rests on secondary endpoints.
Enzyme replacement reached 21.7 percent of UK patients in primary care data and cachexia has a mechanism-based drug in phase 2 but no phase 3; both determine whether combination chemotherapy is delivered, and both sit outside the trials that set the standards.
Whether chemotherapy should be given before surgery for clearly resectable tumours is still unanswered after NORPACT-1, PREOPANC-2, SWOG S1505 and NEONAX; Alliance A021806 (primary completion December 2028) and PREOPANC-3 are the only trials comparing perioperative chemotherapy with the current adjuvant standard, and until they read out neoadjuvant treatment for clearly resectable disease rests on secondary endpoints.
Radiotherapy has improved local control (LAP07) and R0 rates (CONKO-007) without lengthening life, and stereotactic radiotherapy and irreversible electroporation were equivalent in CROSSFIRE; no trial has shown that local ablation after chemotherapy extends survival in locally advanced disease.
Background: Circulating tumour DNA (ctDNA), Epithelial-mesenchymal transition & drug efflux, Minimal / molecular residual disease (MRD), Stage shift. Also on OnCo: Atlas of advanced disease · How cancer spreads: the metastasis stages.
Daraxonrasib is approved in the United States only after first-line chemotherapy; RASolute 303 (first line, six UK sites) and RASolute 304 (adjuvant, six UK sites) will show whether it belongs earlier, and no European regulator or NICE decision existed on 24 September 2026.
In England the newest options (NALIRIFOX, olaparib maintenance, daraxonrasib, zenocutuzumab, tumour treating fields) have no NICE recommendation (the olaparib and NALIRIFOX appraisals, TA750 and TA1052, were terminated when the companies made no submission; the rest have not been appraised) and liposomal irinotecan after gemcitabine is not recommended, so the funded pathway is FOLFIRINOX, gemcitabine combinations and gemcitabine plus capecitabine after surgery.
Supportive treatments that most patients need, enzyme replacement, coeliac plexus block, stents and cachexia drugs, rest on small or observational studies; the one randomised trial of enzyme replacement was negative on its primary endpoint, cachexia has a mechanism-based drug (ponsegromab) in phase 2 but no phase 3, and both sit outside the trials that set the standards even though they decide whether combination chemotherapy is delivered.
Homologous recombination deficiency in pancreatic cancer is wider than germline BRCA (somatic, PALB2 and signature-defined cases all respond to platinum) yet the only PARP inhibitor label is germline BRCA after platinum, and no genomic instability score has a pancreatic threshold.
Transcriptional subtype predicts chemotherapy response retrospectively and a GATA6 stain can call it, but no prospective subtype-directed trial has changed a guideline and basal-like patients still receive the regimen they resist.
Background: Circulating tumour DNA (ctDNA), Mutational signature. Also on OnCo: Resistance: how tumours escape each drug class · Lines of therapy.
Mutant KRAS allele and copy number change prognosis and drug choice, but routine reporting is often 'KRAS mutant' without the allele, and plasma assays that read only codons 12, 13 and 61 miss the wild-type minority in which the actionable fusions live.
CA 19-9 cannot be produced by about a tenth of patients, whose outlook is as poor as the highest-marker group, so a normal marker is a false reassurance that no guideline yet corrects with Lewis genotyping.
Dated changes read from the records linked to this cancer: approvals, regulatory steps, reported trials, guideline versions and milestones. Newest first; no date is inferred.
On EdgeAll 142 changes by month →When this page itself was last checked or edited.
FDA Molecular and Clinical Genetics Panel meeting
NDA 220910 approved as Rasonque: adults with metastatic pancreatic adenocarcinoma who have received at least one prior systemic therapy or who are not candidates for multiagent systemic therapy
Optune Pax, locally advanced pancreatic cancer with chemotherapy (PANOVA-3)
Final PMA module submitted
Metastatic pancreatic adenocarcinoma after at least one prior systemic therapy, or in adults who are not candidates for multiagent systemic therapy