Visudyne (verteporfin)

Verteporfin reversed these effects...MMRN1 acts as a tumor suppressor in TC by activating the Hippo pathway and modulating oxidative stress and ferroptosis. These findings highlight MMRN1 as a potential therapeutic target for TC treatment.

P2, N=24, Active, not recruiting, Mayo Clinic | Trial completion date: Dec 2029 --> Mar 2031 | Trial primary completion date: Dec 2029 --> Mar 2028 | Recruiting --> Active, not recruiting

Increased NDUFB3 expression in RANBP1-overexpressing cells was reversed by YAP1 inhibitor verteporfin treatment or knocking down YAP1. RANBP1 enhances a more invasive microenvironment of OSCC.

The significantly differentially expressed genes (DEGs) from the Gene Expression Omnibus (GEO) database, which discriminate AGS and MKN45 cells in the presence of DMSO and verteporfin (a chemotherapy reagent), are determined...MKN45 was highlighted as more invasive cancer cell relative to AGS cells. PLOD2 was pointed out as a suitable target in the chemotherapy of gastric cancer.

This study identified a novel CAF-exosome-YAP-USP8-HER2 signaling axis that drives trastuzumab insensitivity in HER2-positive breast cancer. Intervening in this pathway may represent a potential treatment approach to counteract microenvironment-induced chemoresistance.

P1/2, N=12, Not yet recruiting, Odense University Hospital

In an immune-cold syngeneic mouse PDAC model, 690 nm light activation of SM-102-containing liposomes slowed tumor growth by up to 56% and extended survival by 40%. Together, these findings suggest that integrating SM-102 into light-activated liposomes is a simple and robust strategy to enhance photochemical ICD and may improve therapeutic outcomes in immunotherapy-based combinations that utilize liposomal drug delivery systems.

P1/2, N=66, Recruiting, SpectraCure AB | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Jul 2027

Targeted and molecular therapies in EWS show significant promise, particularly in rational combinations that exploit the tumor's dependence on EWS-FLI1-driven transcriptional dysregulation, DNA damage repair deficiencies, or survival signaling. Future research must prioritize biomarker-driven patient selection, integration of multiomics approaches, and multicenter prospective trials to translate these strategies into clinically meaningful improvements in EWS survival.

Knockdown of ZNF143/SAV1 signaling impaired the therapeutic effect of HWM, and treatment with verteporfin, pharmacological inhibition of YAP/TAZ, reversed the effects of knockdown of SAV1. Therefore, HWM might offer a potent strategy for managing TNBC effectively.

P2, N=12, Not yet recruiting, Odense University Hospital

To mitigate the off-target toxicity of verteporfin, a YAP1 inhibitor, we develop macrophage-membrane-camouflaged hollow mesoporous silica nanoparticles (M@O-VNPs) co-loaded with verteporfin and oxaliplatin...By inducing immunogenic cell death, M@O-VNPs remodel the tumor microenvironment and enhance ICB efficacy while minimizing systemic toxicity. The therapeutic potential of this strategy is supported by synergistic antitumor effects of M@O-VNPs combined with anti-PD-1 therapy in genetically engineered and syngeneic GC models.