P2, N=15, Enrolling by invitation, Viatris Pharmaceuticals Co., Ltd. | Not yet recruiting --> Enrolling by invitation

P1, N=6, Active, not recruiting, Viatris Innovation GmbH | Not yet recruiting --> Active, not recruiting

P1, N=6, Not yet recruiting, Viatris Innovation GmbH

Depleting CD4+ T-cells, or blocking lymphocyte egress from the lymph nodes with FTY720, rescues tumor growth in mice with conditional deletion of Dnmt1 in ECs (Dnmt1iECKO) and dramatically shortens overall survival, whereas NK cells are dispensable...Finally, immune checkpoint blockade (ICB) administered to Dnmt1iECKO mice with experimental melanoma lung metastasis reduces tumor burden, with some mice showing tumor eradication. Our findings identify endothelial Dnmt1 as a key regulator of vascular-mediated anti-tumor immunity, providing a rationale for integrating epigenetic modulation of the vasculature with cancer immunotherapy regimens.

P=N/A, N=134, Completed, Novartis Pharmaceuticals | Active, not recruiting --> Completed | Trial completion date: Jun 2026 --> Jul 2025 | Trial primary completion date: Jun 2026 --> Jul 2025

P2, N=15, Not yet recruiting, Viatris Pharmaceuticals Co., Ltd.

Our findings indicate that antigen-specific therapy with PS liposomes mimicking apoptotic bodies downregulates the MOG-specific inflammatory immune response and expands Breg and Treg cells, offering a safe, versatile, and easily applicable approach that strongly supports its potential for near-future clinical translation in MS.

This study demonstrates that adjuvants can facilitate recruitment of cDC1s to the peritoneal cavity, a feature that may contribute to the effectiveness of i.p. administration on elicitation of CD8 T cell responses. Furthermore, we demonstrate that CAF09b-induced CD8 T cell responses require BATF3-dependent cDC1 cells. Understanding cDC1 and CD8 T cell dynamics via different immunization routes may aid in the design of more effective vaccine strategies.

Mice with EC-specifically MYPT1-deficient (Mypt1ΔEC) also showed coronary endothelial hyperpermeability, and treatment with the S1PR1 agonist FTY720 failed in alleviating the pathological effects. At 1 month post-transverse aortic constriction, both Mypt1ΔEC and S1pr1ΔEC mice displayed aggravated pathological cardiac remodeling. These findings suggest that the S1PR1-MYPT1 signaling is crucial for coronary endothelial permeability and myocardial microenvironmental homeostasis under pressure overload, targeting which may offer therapeutic potential for related heart diseases.

Our research indicates that FTY720 may inhibit NSCLC via possible targets ZEB2 and S1PR1, further laying the theoretical foundation for the utilization of FTY720 in NSCLC treatment.

In vitro and in vivo experiments validated two repositioned drugs, Fingolimod and Piperlongumine, both targeting ECM components, significantly inhibited LSCC cell growth, proliferation and migration at concentrations below 10 μM. These results provide compelling evidence for the power of systems biology to identify subtype-specific therapeutic vulnerabilities. Our findings highlight a promising framework for precision oncology and underscore the potential of ECM-targeted interventions in LSCC.

P4, N=30, Recruiting, Novartis Pharmaceuticals | Trial completion date: Jan 2026 --> Sep 2027 | Trial primary completion date: Jan 2026 --> Sep 2027