mebendazole

P=N/A, N=46, Recruiting, Tanta University | Not yet recruiting --> Recruiting | Trial completion date: May 2025 --> May 2026 | Trial primary completion date: Apr 2025 --> Apr 2026

Mebendazole inhibited the viability of HCC827 and A549 cells with diminished expression of PELI3 and increased expression of TRADD. PELI3 can function as an E3 ubiquitin ligase to ubiquitinate TRADD, and Mebendazole might be a promising drug to affect PELI3 expression in NSCLC.

The combination of mebendazole and gefitinib effectively suppresses tumor cell viability and modulates key pathways involved in cancer progression. By targeting cytoskeletal integrity and EGFR signaling, it may disrupt cytokine and tumor-microenvironment interactions, supporting further exploration as a strategy to overcome resistance in lung and breast cancers.

Finally, one pair of ONC201-sensitive and ONC201-resistant DMG cell lines with acquired resistance showed same responsiveness to MBZ with similar values of IC50 and Emax. In conclusion, MBZ demonstrates high growth-inhibitory/proapoptotic activity, chemosensitization property to ONC201 and the ability to overcome ONC201 resistance in DMG cell cultures, proposing as a new low-toxicity therapeutic for DMG, with a potential to be used in second-line treatment and/or in combination protocols.

An IDH-mutant xenograft model subjected to mebendazole plus RT showed improved survival compared to either therapy alone. Mebendazole plus RT increased apoptosis and provided a survival benefit in the IDH-mutant mouse model, supporting future clinical testing.

Histopathological examination revealed that Cs@MBZ400.ZnO and Cs@MBZ200.ZnO NCP restored up to 90% of normal tissue architecture. In conclusion, chitosan and zinc oxide nanocomposites enhanced the therapeutic ability of mebendazole against T. spiralis muscular stage as these nanocomposites had the highest effect on reducing parasite burden, improving blood biochemical, decreasing cytokines levels and restoring normal histological architecture.

These results highlight the remarkable clinical translational potential of MBD, providing new potential medicine for AML patients. In addition, TUBA1A can be used potential novel therapeutic target in tumors with abnormal TUBA1A expression.

Mebendazole (MBZ), a broad-spectrum anthelmintic drug, transcriptionally inhibits USP5 expression, and then promotes EphA2 ubiquitination degradation in the NPC cells...Moreover, the levels of USP5 and EphA2 are significantly higher in the radioresistant NPCs than those in the radiosensitive NPCs, and both proteins for predicting patient prognosis are superior to individual protein. These findings suggest that USP5 binds and stabilizes EphA2 by ubiquitin proteasome pathway to promote NPC radioresistance, and MBZ increases NPC radiosensitivity by targeting USP5/EphA2 axis, and is a potential radiosensitizer in NPC and perhaps in other cancers.

P3, N=315, Not yet recruiting, Swiss Tropical & Public Health Institute

Mechanistic studies revealed a significant downregulation of Girdin, an Akt modulator, along with reduced p-Akt, p-IKKα/β, and p-NF-κB, indicating MBZ's novel mechanism of action through the Girdin-mediated Akt/IKKα/β/NF-κB signaling axis. Thus, by targeting Girdin, MBZ presents a promising repurposed therapeutic strategy to inhibit cancer cell proliferation and metastasis in ovarian cancer.

P3, N=315, Not yet recruiting, Swiss Tropical & Public Health Institute

Both MBZ and paclitaxel treatments inhibited of cell proliferation and microtubule formation by reducing the PI3K/AKT pathway in CAL-27 and UM-SCC-1 cells, with the combination demonstrating synergistic effects. Our study suggests MBZ and paclitaxel as potential agents for the treatment of OTSCC.