In vitro experiments confirmed the cytotoxicity and induction of methuosis in GBM cells by AP@CM-Ang, accompanied by the release of immune-stimulatory factors. In vivo experiments demonstrated that the nanodrug significantly enhanced tumor targeting, effectively inhibited tumor growth, and increased immune cell activation, validating its potential as a promising and safe strategy for GBM treatment.

A subcutaneous transplant tumor model was used to verify the inhibitory effect of fluvastatin (FLU) on NKTCL cells in vivo. Lastly, FLU and gemcitabine demonstrated satisfactory synergistic effects in tumor suppression and pyroptosis activation. Our data suggest that FLU represses NKTCL growth by promoting pyroptosis via the MVA-GGPP pathway.

P1, N=60, Not yet recruiting, International Vaccine Institute | Trial completion date: Mar 2026 --> Jul 2027 | Initiation date: Dec 2025 --> Jan 2027 | Trial primary completion date: Mar 2026 --> Jul 2027

P2/3, N=46, Not yet recruiting, Tanta University

P4, N=15, Completed, Children's Hospital of Fudan University | Recruiting --> Completed | N=10 --> 15

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.

Rosuvastatin reduces inflammation by lowering TNF-α, IL-1β, IL-6, CRP while increasing neo-angiogenesis, fibroblast reactions and microenvironmental protection in burn wounds. These effects promote repair and positively impact burn wound healing.

P1, N=32, Active, not recruiting, Genentech Inc. | Recruiting --> Active, not recruiting

P3, N=103, Not yet recruiting, Daiichi Sankyo Europe, GmbH, a Daiichi Sankyo Company

P2, N=150, Active, not recruiting, OHSU Knight Cancer Institute | Recruiting --> Active, not recruiting

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.