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.

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

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

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

Furthermore, functional assays confirmed that rosuvastatin addition significantly enhanced T cell cytotoxicity against leukemia cells. Collectively, our findings suggest that adding rosuvastatin to venetoclax-azacitidine shows preliminary clinical activity and acceptable safety, possibly by reducing T-cell exhaustion, thus supporting further study of this triple regimen in older/unfit AML patients.

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

By suppressing PLK1 expression, rosuvastatin inhibited cancer cell proliferation, migration, and invasion. These findings support the potential of rosuvastatin as a therapeutic agent for lung cancer, although further studies are needed to confirm its clinical utility.

P=N/A, N=242, Completed, Seoul National University Hospital | Unknown status --> Completed

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

P1, N=18, Recruiting, University of California, Irvine