simvastatin

P=N/A, N=781430, Active, not recruiting, Brigham and Women's Hospital | Trial completion date: Jul 2026 --> Sep 2027 | Trial primary completion date: Jan 2026 --> May 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.

Curcumin did not sensitize HepG2-DR cells to doxorubicin, whereas verapamil and simvastatin enhanced doxorubicin cytotoxicity only at toxic concentrations. In contrast, several TKIs, including nilotinib, tivozanib, and, to a lesser extent, cabozantinib, exhibited synergistic effects with doxorubicin in HepG2-DR cells...Third-generation MDR1 inhibitors (tariquidar, elacridar, and zosuquidar) sensitized HepG2-DR and HB-303 cells at non-toxic nanomolar concentrations in vitro...MDR1 inhibitors, such as zosuquidar, may enable dose reductions of chemotherapeutic agents, whereas the use of synergistic TKIs, such as tivozanib, may improve therapeutic outcomes and minimize adverse effects in children with HB. TG100-115, a TRPM7 kinase inhibitor, provides neuroprotection and attenuates NLRP3 inflammasome-mediated neuroinflammation in a neonatal mouse model of hypoxic-ischemic brain injury.

P=N/A, N=12, Dermatology Hospital of Southern Medical University; Dermatology Hospital of Southern Medical University

P2, N=84, Recruiting, National Cancer Institute, Naples

P2/3, N=180, Recruiting, Fundacio Institut De Recerca De L Hospital De La Santa Creu I Sant Pau | Not yet recruiting --> Recruiting

Our findings suggest that clinically significant OATP1B-mediated interactions are not anticipated with CDK4/6 inhibitors, either as victims or perpetrators, which supports ongoing clinical trials investigating the co-administration of CDK4/6 inhibitors with OATP1B substrates and inhibitors.

Further, treatments with drugs such as IFN-γ, 2-DG, and simvastatin modulate the density of PD-L1 without affecting its monomeric state...Finally, we observed that PD-L1 forms nanoclusters at cell-cell conjugation sites between breast cancer cells and T cells. Overall, these findings based on STORM extend our understanding of the nanoscale organization of PD-L1 on the membrane.

To address this limitation, we developed a lipid-prodrug nanoamplifier (SIM-SS-LA NAs), composed of disulfide-linked linoleic alcohol and simvastatin (SIM) to enhance ferroptosis...Notably, the released LA acts as an exogenous substrate, substantially increasing lipid peroxide accumulation and synergizing with SIM-mediated GPX4 inhibition to amplify ferroptosis. As expected, the lipid-prodrug nanoamplifier showed potent ferroptosis-driven antitumor activity in a 4T1 breast tumor-bearing mouse model, offering an efficient nanotherapeutic strategy for ferroptosis-based cancer therapy.

Rats were divided into five groups(n=15 each), i.e., control, model, QBPF, QBPF + nigericin(NLRP3 activator), and simvastatin groups...In conclusion, QBPF attenuates lung function decline, suppresses inflammatory responses, alleviates pulmonary vascular remodeling, and intervenes in the disease progression of COPD complicated by PH in rats. Its mechanisms may be related to modulating the NLRP3/Caspase-1/GSDMD pathway to inhibit PAAF pyroptosis.

Downregulation of RTN3 lead to stabilization of DHCR7 and elevate cholesterol concentration, activating EGFR/ERK pathway and contributes to progression of thyroid cancer, which can be rescued by HMG-CoA reductase inhibitor Simvastatin. We identified RTN3 as a tumor suppressor and a biomarker of sensitivity to MEK inhibitors and verified the role of cholesterol in drug resistance. The combination of statins provides a novel therapeutic method in patients resistant to MEK inhibitors.

P4, N=22, Completed, Kafrelsheikh University