P1, N=12, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Feb 2026 --> Feb 2027

Further, the uptake of HA-1 in A549 cells was suppressed following the addition of free HA, indicating that its internalization occurred through CD44-receptor-mediated endocytosis. Moreover, the HA-1 complex exhibited better photodynamic activity against CD44-overexpressing cancer cells than both poly-L-lysine-1 complex and Photofrin, underscoring its potential as a targeted photosensitizer for photodynamic therapy.

Furthermore, PSO treatment resulted in the significant downregulation of the PI3K-AKT signaling pathway-related genes, which was supported by results from transcriptomic analysis identifying 593 differentially expressed genes. The present findings offer quantitative and mechanistic evidence supporting the clinical utilization of TX in the treatment of RCC, thereby advancing its further research and development.

Using a C57BL/6 intradermal T-cell lymphoma model, we evaluated IQDMA efficacy against conventional psoralen + UV-A (PUVA) phototherapy...Kinase-substrate network analysis revealed PAK1 substrates were 4.9-fold enriched among downregulated proteins (OR = 4.91, P = 0.011), validating the PAK-STAT axis as IQDMA's primary mechanism. These findings establish a CDC42-PAK-STAT nuclear transport axis wherein IQDMA simultaneously inhibits PAK2 kinase activity and depletes its CDC42 scaffold, creating cytoplasmic pY-STAT5 retention that uncouples phosphorylation from transcriptional execution-a dual mechanism distinct from selective JAK inhibitors that warrants clinical evaluation.

The PS exhibits absorption at 665 nm (in vivo) and shows desired pharmacokinetics with limited skin phototoxicity in patients, compared to FDA-approved Photofrin...Combination of COX-2 inhibition with PDT or with BCG-immunotherapy showed an improved rate of tumor cures. Hence, HPPH-PDT in combination with COX-2 inhibitors not only reduces the expression of COX-2, IL-6, VEGF, and PGE2 but also enhances long-term tumor cure.

Representative compounds such as osthole, psoralen, isopsoralen, and fraxin have demonstrated strong anti-osteoporotic potential through distinct mechanisms: osthole enhances osteoblast differentiation via the Wnt/β-catenin and BMP2 pathways; psoralen activates estrogen receptor α signaling to promote osteogenesis and inhibit osteoclastogenesis; isopsoralen alleviates oxidative stress to support osteogenic gene expression; and fraxin suppresses osteoclast formation by inhibiting ROS/NF-κB while promoting osteoblast-mediated bone formation through the Nrf2/GPX4 pathway. Collectively, these findings highlight that NC exert multifaceted effects on bone metabolism by regulating classic pathways (OPG/RANKL/RANK, Wnt/β-catenin, BMP/Smad, NF-κB, MAPK, and estrogen signaling) as well as cellular processes such as oxidative stress, autophagy, apoptosis, and adipogenesis. By synthesizing the current body of research, this review underscores the therapeutic potential of NC and encourages further innovation in OP treatment strategies.

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.

P1, N=9, Completed, Roswell Park Cancer Institute | Active, not recruiting --> Completed | Trial completion date: Oct 2026 --> Oct 2025

Foslip-PDT was effective in reprograming M2 macrophages to tumor-killing M1 macrophages. This study opens the way to combine direct tumor damage with TME modulation.

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

P3, N=86, Completed, Shanghai Fudan-Zhangjiang Bio-Pharmaceutical Co., Ltd. | Recruiting --> Completed

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.