Together, these findings reveal a novel mechanism where Riluzole promotes apoptosis through upregulation of EGR1 , which then cooperates with YAP/p73 to activate Bax expression. These insights establish Riluzole as a promising therapeutic intervention for OS treatment through modulation of the EGR1 /Yap/p73/Bax signaling axis.
P2, N=18, Completed, Jonsson Comprehensive Cancer Center | Recruiting --> Completed | Trial completion date: Nov 2026 --> Nov 2024 | Trial primary completion date: Nov 2025 --> Nov 2024
5 months ago
Trial completion • Trial completion date • Trial primary completion date
The in vivo experiments demonstrated that LD-1 significantly suppressed tumor growth (TGI = 47.64 %) at a dosage of 40 mg/kg, coupled none obvious adverse reactions were observed. Collectively, LD-1, characterized by its novel structure, high potency, and selectivity as an MST3 inhibitor, showcases substantial potential for further investigation and therapeutic development.
P2, N=51, Recruiting, University of California, Irvine | N=34 --> 51 | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2026
5 months ago
Enrollment change • Trial completion date • Trial primary completion date
Additionally, riluzole suppresses the activity of matrix metalloprotease-2 (MMP2) in most of the osteosarcoma cell lines (but not the PDX cells). These results suggest that riluzole's inhibitory effects on osteosarcoma invasion may in part be attributable to the inhibition of MMP2 activity, and that riluzole is potentially an effective agent for inhibiting growth of primary and metastatic osteosarcomas with a wide range of genetic profiles.
Ril+Met co-treatment had a positive effect in terms of GBM cell death, decreased expression of genes involved in glucose metabolism and stemness, and reduced MMP2 activation. Disadvantage of Ril+Met treatment was increased cell migration. Taken together, these drug combinations may also allow the reduction of the concentration of Dex to minimize its side effects.