P2, N=98, Suspended, Alliance for Clinical Trials in Oncology | Recruiting --> Suspended

In an in vivo TNBC xenograft mouse model, combination treatment with paclitaxel and compound 12 significantly increased BRCA1 stability, reduced the final tumor weight, and decreased the number of Ki-67-positive proliferative cells. Our findings suggest that combination therapy with compound 12 can enhance BRCA1 function and improve chemotherapeutic efficacy. This study highlights CTSS inhibition as a promising therapeutic strategy for TNBC patients with wild-type BRCA1.

DHMC acts as a novel natural chalcone that overcomes MDR via dual mechanisms, apoptosis induction and transporter inhibition, underscoring its importance as a potential adjuvant in cancer therapy.

P1/2, N=144, Recruiting, Engeneic Pty Limited | Not yet recruiting --> Recruiting

Pan-cancer analysis revealed the potential of ZNF184 as a prognostic and predictive biomarker for adverse clinical outcomes. Collectively, these findings reveal a previously unknown role of ZNF184 in breast cancer progression and paclitaxel resistance, providing new insights into ZNF184 as a potential therapeutic target for cancer patients.

For decades, ovarian cancer (OC) therapy has mainly relied on a regimen of tumor resection followed by treatment with cisplatin and paclitaxel. Finally, lysosomal signaling pathways disrupt various cell death mechanisms such as apoptosis, necroptosis, and ferroptosis, which allow cancer cells to evade death under chemotherapeutic stress. Targeting lysosomal biogenesis, stage-specific autophagy modulation, and lysosome-dependent metabolic vulnerabilities are promising avenues for sensitization of chemoresistant OC cells.

P1, N=28, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

P1, N=21, Active, not recruiting, City of Hope Medical Center | Trial completion date: Jan 2026 --> Dec 2026

Lowering FOLR1 expression suppressed tumor growth and boosted paclitaxel sensitivity in mice. FOLR1 plays a significant role in promoting chemoresistance of NPC cells to paclitaxel through NLRP3 signaling.

CCNL1 overexpression affects breast cancer cells' paclitaxel sensitivity through the PI3K/AKT pathway. CCNL1 activates the NF-κB signaling pathway through its interaction with DVL3; additionally, it promotes the PI3K/AKT pathway. Together, these two mechanisms enable CCNL1 to exert a regulatory role in the progression of breast cancer.

P2, N=40, Active, not recruiting, University of California, Irvine | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

Our findings elucidate the molecular mechanisms of Rg3 in the treatment of P-gp-mediated MDR in NSCLC. This study also provides a new strategy to overcome P-gp-mediated MDR by inhibiting the MDM2-IκB-α signaling axis.