Mebendazole is a plausible cancer-repurposing candidate in humans, but the human evidence is still early and does not yet show clear, consistent clinical efficacy. Preclinical studies repeatedly show antitumor activity across several cancer types, and early clinical studies suggest that the drug can be given safely at substantial doses
What mechanisms of mebendazole were reported in ovarian cancer models?
Reported mechanisms in ovarian cancer models
In the ovarian cancer models cited in the conversation, mebendazole was reported to act mainly by disrupting AKT/NF-κB signaling, with broader downstream effects on proliferation, migration, invasion, colony formation, stemness, cell-cycle progression, and apoptosis. A second ovarian-cancer report framed mebendazole as part of a combinatorial strategy in which Girdin silencing enhances mebendazole-mediated anticancer activity, and noted reduced tumor growth in vivo with low toxicity.
Supporting detail
Mechanistic signals reported
Girdin-mediated inhibition of the AKT/IKKα/β/NF-κB axis was explicitly identified in ovarian cancer cell lines.
The same study also reported G2/M arrest and apoptosis, along with reduced proliferation, migration, invasion, colony formation, and stemness.
The later combinatorial ovarian-cancer paper described mebendazole as inhibiting proliferation, apoptosis, migration, and invasion, and reported that Girdin silencing enhanced this activity.
What this means
Taken together, the ovarian-cancer evidence in the conversation points to mebendazole acting through a signaling-pathway + cell-fate mechanism: interference with the AKT/IKKα/β/NF-κB pathway and consequent suppression of tumor-like behaviors, especially when paired with Girdin targeting.
References
Gupta, R., Roy, D., Ghosh, A., (...), Swarnakar, S. (2025) Mebendazole Exerts Anticancer Activity in Ovarian Cancer Cell Lines via Novel Girdin-Mediated AKT/IKKα/β/NF-κB Signaling Axis. Cells. https://doi.org/10.3390/cells14020113