mebendazole

Combination treatment with mebendazole and oxaliplatin significantly enhanced chemosensitivity in ESCC cells. Collectively, these findings establish the USP5-IMPDH2-guanine axis as a critical driver of ESCC progression and highlight its potential as a promising therapeutic target for ESCC.

This multi-cancer investigation identifies ENOX2-MMP2 signaling as a functional driver of invasion and metastasis and demonstrates that mebendazole reprograms oncogenic-tumor suppressor networks. By integrating biomarker profiling with drug repurposing, our study highlights the translational potential of mebendazole as a cost-effective anticancer agent and supports the development of multi-gene biomarkers for diagnosis and therapy in aggressive malignancies.

MBZ holds significant potential for reshaping immunotherapy by exerting a profound impact on dendritic cells. By comprehending the intricate interaction between MBZ and dendritic cell function, innovative interventions can be developed.

Our findings suggest that MBZ modulates nucleotide synthesis pathways, contributing to its selective antiproliferative effects in GC cells. This study highlights potential new pharmacological targets for drug repurposing and further investigation into the broader therapeutic applications of MBZ.

P3, N=2500, Completed, Cornell University | Active, not recruiting --> Completed

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.