Why pancreatic cancer trial monitoring matters
Pancreatic ductal adenocarcinoma (PDAC) carries the worst five-year survival rate of any major solid tumor — approximately 12% across all stages, and under 3% for patients diagnosed with metastatic disease. Only three therapeutic regimens hold meaningful approval: gemcitabine plus nab-paclitaxel, FOLFIRINOX, and olaparib for the subset of patients with germline BRCA mutations. That narrow approval landscape, combined with an exceptionally immunosuppressive tumor microenvironment and late-stage diagnosis patterns, has made PDAC one of the highest-priority unmet needs in oncology and one of the most active areas of early-phase clinical development.
With roughly 24 recruiting trials actively enrolling patients and dozens more in startup or follow-up phases, systematic monitoring of ClinicalTrials.gov is essential for oncologists, pharma BD teams, and biotech investors tracking this rapidly evolving space. Key signals to watch:
- KRAS G12D inhibitors (MRTX1133, HRS-4642) entering Phase 1/2 dose-escalation and expansion cohorts
- KRAS G12C inhibitors (sotorasib, adagrasib) in PDAC cohorts within broader solid tumor basket trials
- mRNA neoantigen cancer vaccines (mRNA-5671/V941, individualized neoantigen therapies) in combination with checkpoint inhibitors
- Stroma-targeting agents (anti-IL-4Rα antibodies, losartan, PEGPH20 successors) to improve drug delivery
- CTLA-4 plus PD-1 combinations and novel checkpoint pairs in PDAC
- CAR-T and adoptive cell therapy programs targeting mesothelin, HER2, and CEACAM5
- PARP inhibitor maintenance and combination strategies for BRCA/ATM-mutant PDAC
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Our pipeline pulls directly from the ClinicalTrials.gov API every day. For a pancreatic cancer watch profile, you can configure:
- Condition keywords: "pancreatic cancer", "PDAC", "pancreatic adenocarcinoma", "pancreatic ductal adenocarcinoma", "pancreatic neuroendocrine tumor", "pNET", "pancreatic carcinoma"
- Phase filter: Phase 1 only, Phase 2/3, or all phases
- Sponsor filter: Industry-sponsored only (for competitive intelligence) or all sponsors
- Status filter: Recruiting only, all active studies, or any status
The pancreatic cancer treatment landscape in 2026
KRAS-targeted therapy enters Phase 3 in PDAC — two trials launched in early 2026
KRAS is mutated in approximately 90% of PDAC cases — predominantly G12D (~40%), G12V (~30%), and G12R (~15%). For decades, KRAS was considered undruggable. The 2021 approval of sotorasib for KRAS G12C NSCLC opened the structural biology door, and by 2026 KRAS-targeted therapy has reached Phase 3 in PDAC for the first time. Two Phase 3 trials launched in early 2026:
- Daraxonrasib (Revolution Medicines, NCT07491445, started March 2026): A Phase 3 studying daraxonrasib alone and in combination with gemcitabine plus nab-paclitaxel (GnP) as first-line treatment in metastatic PDAC. Daraxonrasib (RMC-6236) is a multi-selective RAS inhibitor designed to target multiple common KRAS mutations in their active GTP-bound state — a mechanism distinct from mutation-specific inhibitors. Phase 1 data in PDAC generated some of the strongest early-phase response rates seen in this indication.
- Setidegrasib (Astellas, NCT07409272, started February 2026): A Phase 3 evaluating setidegrasib with either mFOLFIRINOX or NALIRIFOX chemotherapy in pancreatic cancer patients. Setidegrasib is a KRAS G12D-selective inhibitor — targeting the most prevalent KRAS mutation in PDAC. Moving a G12D-selective inhibitor into Phase 3 with backbone chemotherapy is the test of whether KRAS G12D inhibition delivers on the clinical promise suggested by Phase 1/2 data.
The simultaneous launch of two KRAS Phase 3 trials in early 2026 marks a threshold moment in PDAC oncology — the point at which a historically undruggable driver becomes an actively contested Phase 3 competitive space.
MTAP deletion: precision approach in ~15% of PDAC
Approximately 15% of PDAC tumors carry a homozygous deletion of the MTAP gene — a co-deletion that occurs with the neighboring CDKN2A tumor suppressor. MTAP deletion creates metabolic vulnerability: these tumors rely on MAT2A and PRMT5 for methionine metabolism, making them susceptible to PRMT5 inhibitors. Bristol-Myers Squibb's MountainTAP-30 trial (NCT07076121, Phase 2/3, started October 2025) tests BMS-986504 combined with nab-paclitaxel and gemcitabine specifically in patients with untreated metastatic PDAC with homozygous MTAP deletion. This is a biomarker-selected precision oncology approach in a disease where biomarker-driven treatment has historically been limited to the ~5–8% BRCA-mutant subset. MTAP testing is not yet standard of care — a positive trial result would make it standard.
KRAS G12C inhibitors: basket trial cohorts in PDAC
Although KRAS G12C accounts for only about 1–2% of PDAC cases, the availability of approved KRAS G12C inhibitors — sotorasib (Lumakras, Amgen) and adagrasib (Krazati, Mirati/BMS) — has generated PDAC-specific cohorts within larger solid tumor basket trials. Multiple pan-KRAS or mutation-specific programs also include PDAC cohorts: BeiGene's BGB-53038 (pan-KRAS, NCT06585488, Phase 1, started November 2024) and BridgeBio's BBO-11818 (NCT06917079, Phase 1, KRAS-mutant cancers, started March 2025) are among the newer additions to the KRAS-targeted Phase 1 landscape.
Actively recruiting PDAC and pancreatic cancer trials (2026)
| NCT ID | Sponsor | Phase | Focus | Start |
|---|---|---|---|---|
| NCT07491445 | Revolution Medicines | Phase 3 | 1L PDAC — Daraxonrasib ± GnP | Mar 2026 |
| NCT07409272 | Astellas | Phase 3 | KRAS G12D — Setidegrasib + chemo | Feb 2026 |
| NCT07076121 | Bristol-Myers Squibb | Phase 2/3 | MTAP-deleted PDAC — BMS-986504 + GnP | Oct 2025 |
| NCT06989437 | Pfizer | Phase 2/3 | Metastatic PDAC cachexia — Ponsegromab | Oct 2025 |
| NCT07480928 | Beijing Biotech | Phase 1/2 | PDAC — CAR-NK (MSLN + MUC1) | Feb 2026 |
| NCT06585488 | BeiGene | Phase 1 | KRAS-mutant — BGB-53038 pan-KRAS | Nov 2024 |
| NCT06917079 | BridgeBio Oncology | Phase 1 | KRAS-mutant — BBO-11818 | Mar 2025 |
mRNA cancer vaccines: neoantigen and shared antigen approaches
The clinical success of mRNA-4157/V940 (Moderna/Merck) in melanoma has accelerated interest in mRNA-based cancer vaccines for solid tumors with high mutational burden or shared neoantigens. mRNA-5671/V941, a fixed neoantigen vaccine targeting the four most common KRAS mutations (G12D, G12V, G12C, G13D), has entered clinical evaluation in combination with pembrolizumab in PDAC and other KRAS-driven tumors. Individualized neoantigen vaccine programs from Gritstone Bio, BioNTech, and Neon Therapeutics are also generating PDAC cohort data. These programs represent a convergence of KRAS biology and mRNA platform technology that is being watched closely across oncology.
Stroma targeting: unlocking drug delivery in PDAC
One reason PDAC responds poorly to chemotherapy and immunotherapy is its exceptionally dense desmoplastic stroma, which physically barriers drug penetration and creates an immunosuppressive microenvironment. Multiple stroma-targeting strategies are in clinical development: anti-IL-4Rα antibodies to repolarize tumor-associated macrophages, losartan (angiotensin receptor blockade) to reduce collagen deposition, and hyaluronidase-based approaches (successors to PEGPH20) to degrade the hyaluronan matrix. Trials combining stroma modulation with standard chemotherapy or checkpoint inhibitors are actively registering, and their results will inform combination design for the next generation of PDAC trials.
Immunotherapy combinations: overcoming PDAC's immune desert
PDAC is classified as an "immune desert" — low T-cell infiltration, abundant immunosuppressive myeloid cells, and minimal PD-L1 expression — which explains why single-agent PD-1/PD-L1 inhibitors have failed broadly in unselected PDAC patients. Current clinical strategies focus on converting this cold tumor microenvironment: dual CTLA-4 plus PD-1 blockade (ipilimumab/nivolumab), CD40 agonist antibodies (APX005M, sotigalimab) to activate macrophages and dendritic cells, and CXCR2 inhibitors to reduce myeloid-derived suppressor cell trafficking. Tracking new combination immunotherapy registrations — particularly those pairing immune primers with checkpoint inhibitors — is essential for companies developing next-generation PDAC immunotherapy.
Pancreatic neuroendocrine tumors (pNET): a distinct and growing indication
Pancreatic neuroendocrine tumors share the anatomical site with PDAC but have fundamentally different biology, treatment options, and prognosis. Everolimus (Afinitor) and sunitinib (Sutent) are approved for progressive pNET, and peptide receptor radionuclide therapy (PRRT) with lutetium-177 DOTATATE has expanded treatment options. The pNET pipeline includes novel somatostatin receptor-targeted radiopharmaceuticals, PI3K/mTOR pathway inhibitors with improved selectivity, and CDK4/6 inhibitor combinations. Investors and BD teams tracking the broader pancreatic cancer space should maintain separate pNET watch profiles given the distinct regulatory and competitive dynamics.
Who uses pancreatic cancer trial monitoring
Oncologists and academic cancer centers
Gastrointestinal oncologists and pancreatic cancer specialists at major NCI-designated cancer centers track trial registrations to identify enrollment opportunities for patients who have exhausted standard options. PDAC's limited approved therapies mean that clinical trial participation is often the best available option for second-line and beyond — making systematic trial awareness a direct patient care priority. Academic oncologists also monitor new registrations to identify investigator-initiated trial opportunities and collaborative enrollment networks.
Pharma BD and competitive intelligence teams
Companies with assets in the KRAS, PARP, immunotherapy, or radiopharmaceutical spaces maintain active PDAC trial monitoring to track competitor programs entering Phase 1 and Phase 2. A new KRAS G12D inhibitor trial registration signals a company's readiness to present clinical data 12–24 months later, enabling early partnership assessment, in-licensing evaluation, and competitive response planning. BD teams at large oncology companies — Amgen, BMS, AstraZeneca, Genentech, Merck — as well as mid-size oncology biotechs all need current awareness of the PDAC trial landscape.
Biotech investors in oncology
Investors with positions in KRAS-targeted therapy, cancer vaccines, or immuno-oncology companies track PDAC trial activity as a leading indicator of clinical execution and program prioritization. Phase 1 enrollment completion, cohort expansion decisions, and combination partner announcements all begin with a trial registration or amendment on ClinicalTrials.gov — often months before any investor-facing announcement. Systematic monitoring creates an information edge for funds and analysts covering the pancreatic cancer therapeutic space.
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Start FreeFrequently asked questions
How current is the pancreatic cancer trial data?
Our pipeline fetches from ClinicalTrials.gov every morning. Studies posted or updated in the preceding 24 hours appear in that day's digest — so a new KRAS G12D inhibitor trial registered overnight will appear in your inbox the following morning.
Can I track PDAC and pNET trials separately?
Yes. On the Pro plan ($99/month), you can create multiple search profiles. You might maintain one profile for PDAC with KRAS-targeted intervention keywords, a second for pNET with somatostatin receptor and PRRT terms, and a third for pancreatic cancer immunotherapy broadly — each delivering a focused daily digest tailored to those distinct biological and commercial questions.
How is this different from ClinicalTrials.gov alerts?
ClinicalTrials.gov offers basic RSS-style alerts without phase filtering, sponsor type filtering, or organized digest formatting. DataLookout provides filtered, labeled, and organized alerts — the intelligence layer on top of the raw registry data. You can combine condition keywords like "pancreatic ductal adenocarcinoma" with intervention keywords like "KRAS G12D" or "mRNA vaccine" to receive a digest focused precisely on the programs that matter to your work.