Visudyne (verteporfin)

The YAP inhibitor Verteporfin blunted MELK-driven PASMC proliferation and migration, underscoring the central role of YAP/TAZ signaling. Finally, in vivo pharmacological inhibition of MELK by OTS167 markedly reduced right ventricular systolic pressure, hypertrophy, and pulmonary vascular remodeling in Su/H mice, confirming the therapeutic relevance of MELK targeting in PAH. Collectively, these findings identify MELK as a novel regulator of PASMC pathobiology in PAH and suggest that it may represent a potential therapeutic target.

cDVPMA was constructed by encapsulating the stimulator of interferon genes (STING) agonist 2'3'-cGAMP in the aqueous core of a tertiary ammonium group-containing polymersome, while embedding both the photosensitizer verteporfin-phospholipid (VL) and thrombin inhibitor dabigatran etexilate within the hydrophobic layer. In a 4T1 mouse breast cancer model, cDVPMA combined with near-infrared (NIR) laser irradiation elicited robust antitumor immunity, significantly suppressing primary tumor growth and metastasis, while establishing durable immune memory that prevented tumor recurrence. This study provides valuable insights into the development of nanomedicines for immunotherapy targeting tumors in a hypercoagulable state.

While photoactivation of verteporfin (VP), a photosensitizer, has demonstrated success for overcoming MDR through direct protein aggregation upon photoactivation and through adenosine triphosphate (ATP) depletion, the impact of VP's formulation on P-gp function and cellular energetics has not been fully characterized in this context...Photodynamic priming with NanoVP at sub-cytotoxic light doses enhanced P-gp substrate retention within the cells without damaging P-gp protein, indicating ATP depletion as the primary mode of functional inhibition. These findings highlighted NanoVP's clinical potential to enhance chemotherapeutic efficacy via photoactivation-based modulation of P-gp's function in multidrug-resistant cancers.

In vivo experiments also demonstrated that verteporfin inhibited the in-situ tumor progression and ivonescimab enhanced the efficacy of immunotherapy in MS4A1 low tumor-bearing mouse. The MS4A1/M1 macrophage axis was identified as a crucial regulator of malignancy in LUAD, indicating MS4A1 as a promising novel therapeutic target for advanced LUAD treatment.

Treatment with verteporfin reversed the alleviating effects of YES1 overexpression on neuronal DNA damage and exacerbated POCD in mice. In conclusion, bupivacaine induces POCD by suppressing YES1 expression and YAP1 phosphorylation, leading to DNA damage.

This study demonstrates that FOXM1/NEDD4L axis impairs EGFR proteasomal degradation, thus contributing to EGFR-driven LUAD growth and osimertinib resistance. Combination therapy incorporating NEDD4L activation may represent a new valued therapeutic strategy for EGFR-driven LUAD and osimertinib resistance.

In conclusion, the anticancer property of verteporfin was highlighted. This finding can improve the efficacy of related PDT.

Moreover, treatment with a YAP inhibitor Verteporfin significantly attenuated the PPM1G-induced chemoresistance both in vitro and in vivo. Overall, our study elucidated a role of the PPM1G/NDR1/YAP axis in TNBC chemoresistance. We proposed that PPM1G may serve as a predictive biomarker for the treatment response of TNBC to YAP inhibitor.

Accordingly, we evaluated the sensitivity of the organoids to the Sonic Hedgehog inhibitor vismodegib and Yes-associated protein 1 inhibitor verteporfin, both of which demonstrated potent in vitro antitumor activity in organoid cultures. This model offers a valuable preclinical platform for investigating the molecular pathology of this rare malignancy and accelerating the development of targeted therapies.

TEAD specific inhibitors (and not verteporfin which is a highly non-specific inhibitor) synergize with immune checkpoint blockade in in vivo model system by promoting increased CD8⁺ T cell infiltration and prolonged survival in the melanoma mouse model. Collectively, these findings reveal a chromatin-centric vulnerability in BRAF/MEK inhibitor-resistant melanoma and propose TEAD specific inhibitors as a promising dual strategy to overcome resistance and reinvigorate the immune response, offering a novel therapeutic avenue for patients.

This study identifies NCAPH as a novel oncogenic factor in BC. NCAPH interacts with YAP1, promoting its nuclear translocation and enhancing BCSC traits and malignancy. Critically, YAP1 inhibition reverses NCAPH-driven effects, validating the NCAPH as a promising therapeutic target.

Simultaneous loss of Brg1 and Pten in pancreatic ductal cells results in ITPN formation via the activation of the YAP/TAZ pathway in the mouse model. The YAP/TAZ pathway is a key driver of ITPN formation and is a potential therapeutic target for ITPN and ITPN-derived PDAC.