Pancreatic Adenocarcinoma

P2, N=80, Recruiting, Corcept Therapeutics | N=60 --> 80

P1/2, N=22, Completed, University of Virginia | Trial completion date: Jun 2025 --> Apr 2026 | Active, not recruiting --> Completed

Peroxisomes act as pivotal regulators of digestive cancer progression by modulating signaling pathways, the TIME, therapeutic resistance, and lipid metabolism. Targeting peroxisomal function, particularly in high-risk subgroups of HCC and CRC, warrants further exploration as a promising therapeutic strategy.

P1, N=46, Recruiting, University of Illinois at Chicago | Trial completion date: Jan 2026 --> Jan 2028 | Trial primary completion date: Nov 2025 --> Nov 2027

We found that CLCA1 modulates the SIRT1/HIF-1α pathway, suppressing tumor proliferation, and might enhance gemcitabine sensitivity in pancreatic cancer cells. This investigation points to CLCA1 as a viable therapeutic target for tackling hypoxia-induced chemoresistance and enhancing treatment success in PDAC. Further exploration of CLCA1-based therapies could offer new opportunities for clinical translation.

P1, N=15, Not yet recruiting, University of Washington

Combined MEK and autophagy inhibition showed limited tolerability in human PDAC. Divergent efficacy between preclinical and clinical settings likely reflects differences in tumor cell state heterogeneity between models. Integration of diverse, representative preclinical models is critical to guide development of effective therapies in PDAC.

Targeting CSF1R might be a PAAD treatment. Inhibiting CSF1R activity or TGF-β binding to CSF1R inhibits tumour growth and immune escape. Investigating the link between CSF1R, TGF-β, and the immune system opens new opportunities for combining targeted medicines with immunotherapy.

P=N/A, N=48, Completed, University Health Network, Toronto | N=30 --> 48

Sulforaphane-mediated enhancement occurred without restoration of connexin 43 expression or coordinated reversal of epithelial-to-mesenchymal transition markers, and treatments did not induce N-cadherin upregulation or suggest acquisition of invasive characteristics. Together, these findings support NTP + TPZ as a potent combinatorial strategy for pancreatic adenocarcinoma and identify sulforaphane as an effective adjunct that enhances cytotoxic efficacy through mechanisms that remain to be fully elucidated.

P1/2, N=30, Active, not recruiting, University Health Network, Toronto | Trial completion date: Jan 2026 --> Dec 2026

P1/2, N=20, Not yet recruiting, University of Arkansas | Trial completion date: Mar 2028 --> Aug 2028 | Initiation date: Apr 2026 --> Aug 2026 | Trial primary completion date: Mar 2028 --> Aug 2028