atorvastatin

To investigate this possibility, publicly available transcriptomic, proteomic, and phosphoproteomic datasets derived from colorectal cancer models treated with atorvastatin or lovastatin were systematically analyzed...Integrated multi-omics analysis revealed coordinated perturbation of tumor protein p53 (TP53)-centered DNA repair signaling, including pathways involved in TP53 regulation and double-strand break repair. Taken together, these findings suggest that statin-induced alteration of TP53-mediated DNA repair signaling may promote the persistence of DNA damage, thereby increasing the sensitivity of tumor cells to chemotherapy and potentially mitigating resistance mechanisms in colorectal cancer.

P1, N=40, Recruiting, AstraZeneca | Not yet recruiting --> Recruiting

P=N/A, N=60, Completed, Riphah International University

P1, N=12, Recruiting, Merck Sharp & Dohme LLC | Not yet recruiting --> Recruiting

P3, N=31, Terminated, Columbia University | Completed --> Terminated; The study was terminated early due to recruitment limitations, particularly difficulty enrolling statin-naïve patients

P1, N=50, Active, not recruiting, Joaquina Baranda | Trial completion date: Aug 2025 --> Aug 2026

In cervical cancer cisplatin-resistant cell lines (SiHa-DDP and C33a-DDP) constructed from their parental cells, the effects of seven statins (simvastatin, fluvastatin, pitavastatin, lovastatin, atorvastatin, rosuvastatin, and pravastatin) on cell viability in cisplatin-resistant cells and corresponding parental cells were assessed using the CCK-8 assay...In all, simvastatin enhanced cisplatin sensitivity by suppressing the CAV1-mediated PI3K/AKT pathway involvement in the development of cisplatin resistance in cervical cancer cells. These findings reveal a novel mechanism in cervical cancer cells resistant to cisplatin by which simvastatin may serve as a potential adjuvant to improve the therapeutic efficacy of cisplatin-based chemotherapy.

P4, N=105, Recruiting, Seoul National University Bundang Hospital | Trial primary completion date: Dec 2025 --> Dec 2026

Anti-inflammatory agents, including pentoxifylline, atorvastatin, trans-caryophyllene, azilsartan, recombinant human IL-11, and low-level laser therapy have been shown in preclinical models to reduce cytokine levels and promote mucosal healing. Similarly, microbiome-targeted approaches, such as oral microbiota transplantation and multi-strain probiotic formulations, have demonstrated potential in restoring microbial balance and attenuating CRIOM severity, with current evidence including both preclinical and clinical studies. Overall, current findings highlight cytokine toxicity and dysbiosis as synergistic drivers of CRIOM and support anti-inflammatory and microbiome-modulating strategies as promising adjunctive approaches; however, further well-designed clinical studies are required to validate their efficacy and guide clinical translation.

P=N/A, N=120, Recruiting, Taipei Veterans General Hospital, Taiwan | Not yet recruiting --> Recruiting

P4, N=320, Terminated, Seoul National University Hospital | Unknown status --> Terminated; The study was terminated early due to slow recruitment and the Principal Investigator's retirement.

P4, N=100, Recruiting, General Hospital of Shenyang Military Region | Trial completion date: Nov 2026 --> Nov 2027 | Trial primary completion date: Nov 2026 --> Nov 2027