gemcitabine

P3, N=53, Completed, Ferring Ventures Limited | Active, not recruiting --> Completed

P2, N=20, Not yet recruiting, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest

P2, N=47, Not yet recruiting, Swiss Cancer Institute | Trial completion date: Mar 2029 --> Jul 2029 | Initiation date: Mar 2026 --> Jul 2026 | Trial primary completion date: Mar 2028 --> Jul 2028

Notably, these nanoparticles effectively reversed hypoxia-induced resistance to gemcitabine, acting as a powerful chemosensitizer. Collectively, this platform not only establishes a physiologically relevant "hypoxia-on-a-chip" model for preclinical drug evaluation but also accelerates the optimization of nanoparticle-based strategies for hypoxia-targeted therapy.

Both siRNA and high-payload nucleoside-analogues were incorporated onto a single micelle, which remained stable during in vivo circulation, rather than individual RNA nanoparticles, thus generating this advantageous synergistic cancer regression. This platform provides a powerful therapeutic tool to address colorectal cancer lung metastasis, a currently serious, lethal disease that has a very poor prognosis following diagnosis.

Gemcitabine-based chemotherapy regimens have shown limited antitumor effects for PDAC, and combination targets are urgently needed to restrict chemoresistance. Mechanistically, the focal adhesion kinase (FAK) inhibitor (IN10018) could restrict chemoresistance to Gem of PDAC by targeting SLC7A11-mediated ferroptosis through PI3K-Akt signaling pathway. For tumor microenvironment, IN10018 reduced the abundance of mesenchymal components and enhanced CD8+ T cell infiltration.

P2, N=56, Recruiting, The Lymphoma Academic Research Organisation | Trial completion date: Jan 2028 --> Apr 2028 | Trial primary completion date: Jan 2026 --> Apr 2028

P3, N=442, Not yet recruiting, Sun Yat-sen University

P2, N=129, Active, not recruiting, Canadian Cancer Trials Group | Trial primary completion date: Mar 2026 --> Jun 2026

P1, N=330, Recruiting, Pfizer | Trial completion date: Sep 2028 --> Jan 2029 | Trial primary completion date: Sep 2027 --> Jan 2028

We identified cytarabine and methotrexate as significantly more effective in the 9p21 compromised BLCA cells. Analysis of morphological alterations further supported a genotype-specific activity of nucleoside analogs, nominating gemcitabine as a drug with greater efficacy in this context...Synergy between cytarabine and inhibitors of PRMT5 (MRTX1719) and MAT2A (AG-270) was mediated by a differential activation of DNA damage and replication stress markers, suggesting an exploitable vulnerability. In fact, rational drug combinations with ATR/CHK1 pathway inhibitors increased efficacy while maintaining 9p21-specificity. Finally, we confirmed the effectiveness of these combinations in cell models of pancreatic adenocarcinoma and pleural mesothelioma, two tumor types with high prevalence of MTAP loss and, most notably, in bladder cancer patient-derived organoids, underscoring the strong translational potential of our findings.

P2/3, N=150, Recruiting, Amsterdam UMC, location VUmc | Not yet recruiting --> Recruiting