Commentary | Global Ivermectin Research Hub
Ivermectin
In recent years, numerous studies have explored the potential anticancer properties of IVM, revealing its multifaceted role in cancer suppression.
Originally developed as an antiparasitic agent, IVM has attracted attention for its ability to disrupt various molecular and cellular pathways critical for cancer progression.
Several studies have demonstrated the ability of IVM to modulate key signaling pathways associated with cancer.
For example, Rabben et al. found that IVM inhibited the Wnt/β-catenin signaling pathway in gastric cancer cells, leading to inhibition of tumor growth and metastasis.
Similarly, Lee et al. demonstrated that IVM disrupted the PI3K/AKT/mTOR pathway in pancreatic cancer, resulting in increased apoptosis and decreased cell proliferation.
Furthermore, the drug has demonstrated the ability to modulate STAT3, EGFR, and other key pathways in multiple cancer types.
Experimental evidence has also revealed inhibitory effects of IVM on various cancer cell types.
Zhou et al. reported that IVM dose-dependently inhibits the growth of colon cancer cells, promotes apoptosis by activating caspases, and increases the expression of proapoptotic proteins, while simultaneously reducing antiapoptotic markers.
In ovarian and prostate cancers, IVM has demonstrated the ability to inhibit cell growth, modulate gene expression, and alter DNA repair mechanisms.
In addition to conventional cancer cells, IVM also targets cancer stem cells (CSCs), which are often associated with treatment resistance and relapse.
Dominguez et al. demonstrated that IVM selectively inhibits CSCs in breast cancer models and reduces the expression of stemness-related genes, suggesting an important role in long-term therapeutic strategies. Combination therapies involving IVM have also shown promising results.
Draganov et al. demonstrated that combining IVM with immune checkpoint inhibitors, such as anti-PD1 antibodies, enhanced the antitumor immune response and induced complete tumor regression in breast cancer models.
Similarly, Nunes et al. reported synergistic effects when IVM was combined with paclitaxel in drug-resistant ovarian cancer cell lines
