P1, N=52, Recruiting, Immunolight, LLC | N=20 --> 52

Using CRISPR/Cas9-mediated knockout and rescue experiments in EOC cell lines, we demonstrate that MED12 deficiency significantly enhances sensitivity to ferroptosis inducers (RSL3 and Erastin), as evidenced by reduced IC50 values...Pharmacological inhibition of YAP with verteporfin or siRNA-mediated TEAD1 knockdown reverses ferroptosis sensitivity in MED12-deficient cells, confirming pathway specificity. These findings establish MED12 as a modulator of the YAP-TEAD1-ferroptosis axis and suggest that targeting this pathway could overcome chemoresistance in MED12-deficient EOC. Our work provides a mechanistic foundation for exploiting ferroptosis induction as a therapeutic strategy in ovarian cancer.

This study introduces a new structural class of mitochondria-targeted KV1.3 inhibitors with enhanced solubility compared to psoralen-based analogues. The unique mechanism of action, characterized by rapid depolarization and moderate ROS dependence, underscores their potential as selective anticancer agents. These findings warrant further investigation into in vivo efficacy and potential synergy with existing therapies.

Importantly, two clinical drugs, the RhoA inhibitor simvastatin and the YAP1/TEAD inhibitor verteporfin were determined to be the disruptors of this feed-forward signaling axis, inhibiting ICC tumor growth. These findings reveal the vital function of ANLN in ICC growth and provide promising treatment strategies for ICC.

P2, N=15, Completed, Soligenix | N=47 --> 15 | Recruiting --> Completed

The GDCA and DCA exert opposing effects on CCA progression through Hippo-YAP signaling. GDCA promotes tumor growth via YAP activation, while DCA inhibits these processes. YAP-targeted interventions demonstrate therapeutic potential, providing insights into new treatment strategies for CCA.

P4, N=327, Recruiting, University of Roma La Sapienza | Not yet recruiting --> Recruiting | Trial completion date: Feb 2030 --> Dec 2031 | Trial primary completion date: Dec 2027 --> Dec 2028

P2, N=0, Withdrawn, Therakos LLC | N=30 --> 0 | Suspended --> Withdrawn

P2, N=52, Active, not recruiting, Abramson Cancer Center at Penn Medicine | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Nov 2024 --> Dec 2026

P1, N=20, Recruiting, Immunolight, LLC | Trial completion date: Mar 2026 --> Mar 2029 | Trial primary completion date: Sep 2025 --> Sep 2028

Our findings support the pathogenic role of the CHYMASE mutation in nsHGF, establish chymase deficiency and consequent YAP/TAZ activation as the underlying mechanism and propose verteporfin-loaded exosomes as a promising therapeutic strategy for nsHGF-associated gingival overgrowth.

This approach, using hyaluronic acid nanoparticle (HANP)-formulated verteporfin (HANP/VP), concurrently induced nuclear- and mitochondrial-DNA damage, promoted immunogenic cell death (ICD), and drove T-lymphocyte infiltration into the tumor microenvironment (TME)...Overall, our findings established HANP/VP as a multifunctional nanomedicine that reprogrammed the TME and elicited potent antitumor immunity through dual DNA damage and STING activation. The study highlights a promising translational strategy for overcoming immunotherapeutic resistance in UM and converting immunologically "cold" tumors into "hot" ones, thereby improving responses to immune checkpoint blockade (ICB).