lovastatin

PPH reverses PTX resistance by targeting cholesterol-lipid rafts to inhibit multiple ABC transporters. This offers a safer adjuvant for PTX-based breast cancer therapy and a translational framework for other drug-resistant malignancies.

In combination with αPD-1, the gel system suppresses tumor growth and metastasis, establishes durable immune memory, and effectively prevents local and distant tumor recurrence postsurgery. Collectively, these findings present an approach for translating high-dose AA therapy into practice and provide evidence for the integration of ferroptosis induction with immunotherapy for enhanced cancer treatment.

MFSD9 is a potential biomarker and therapeutic target in LUAD, with significant implications for prognosis and treatment response. Future studies should focus on functional validation and clinical application.

P2, N=120, Active, not recruiting, Vanderbilt University | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Jan 2027 | Trial primary completion date: May 2026 --> Jan 2027

Our approach prioritized 140 high-confidence drug candidates that consistently reverse TB-associated gene expression changes, successfully recovering known HDTs, including statins (atorvastatin, lovastatin, fluvastatin) and vitamin D receptor agonists (calcitriol). We identified promising novel candidates such as niclosamide and tamoxifen, both recently validated in experimental TB models, and revealed enrichment for therapeutically relevant mechanisms, e.g., cholesterol metabolism inhibition and immune modulation pathways...This work establishes transcriptome-based connectivity mapping as a viable approach for systematic HDT discovery in bacterial infections and provides a robust computational framework applicable to other infectious diseases. Our findings offer immediate opportunities for experimental validation of prioritized drug candidates and mechanistic investigation of identified druggable targets in TB pathogenesis.

Clinical relevance was demonstrated through bioinformatic analysis and immunohistochemistry, revealing that elevated Survivin expression in TNBC tissues correlated with poor prognosis and is significantly upregulated in TNBC versus non-TNBC tissues. Our findings identify the USP14-Survivin axis as a potential therapeutic target and highlight LV as a promising candidate for TNBC treatment.

The findings suggest low-dose statins can enhance innate immunity in breast cancer by degrading mutant p53, offering new treatment possibilities. Caution is advised, and further research is needed to address limitations and provide solid evidence for clinical use.

This work demonstrates the therapeutic enhancement of T-DM1 using combination therapy with lovastatin/neratinib in gastric cancer. The treatment can be successfully monitored through PET/CT imaging.

Inhibition of lipid metabolism combined with standard chemotherapy is a promising strategy that reduces CRC cell viability and allows for the use of a lower drug dose. The combination of 5-FU and Avasimibe has the greatest therapeutic potential among studied compounds.

P=N/A, N=5, Completed, University of Coimbra

P2, N=28, Recruiting, Emory University | Not yet recruiting --> Recruiting

In human RD and RH30 lines, treatment with 0.01-1 μM doses of fatostatin (SREBP2 inhibitor), lovastatin and simvastatin (HMGCR inhibitors), and zoledronic acid (FDPS inhibitor) impaired cell growth and migration, which were conversely stimulated by 50-100 μM cholesterol (CHO) supplementation. Treatment of RMS lines with higher doses of SREBP2 and MVP inhibitors (5-50 μM) promoted oxidative cell death and chemosensitization in combination with actinomycin D. Administration of lovastatin or fatostatin to RD and RH30 cells produced a rapid attenuation of Erk1/2 and Akt1 phosphorylation, detectable after 4 hours of treatment...Taken together, these data suggest that the axis formed by Akt1, SREBP2 and MVP is critical for RMS tumor growth, migration, and oxidative stress protection mainly through the maintenance of CHO levels that ensure proper intracellular signaling. Therefore, targeting CHO levels by SREBP2 and MVP inhibition may represent a viable option to improve the combination therapy protocol in RMS.