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Ivermectin, a macrolide antiparasitic drug, was discovered in the 1970s by Satoshi Ōmura and William Campbell, who isolated it from Streptomyces avermitilis bacteria in Japan. Approved in 1981 for human use against parasitic diseases like river blindness, its developers earned the 2015 Nobel Prize in Medicine for its global health impact.
Preclinical studies show ivermectin inhibits cancer cell proliferation, metastasis, and angiogenesis, while promoting programmed cell death, with potential to shrink tumors in animal models, though human clinical evidence remains limited.
Based on preclinical research, ivermectin has shown potential effects against the following cancers. Note that these findings are preliminary and lack confirmation from human clinical trials:
Ivermectin binds to glutamate-gated chloride channels in parasite nerve and muscle cells, causing paralysis and death by hyperpolarizing the cells, a mechanism highly effective against a range of parasitic worms and insects.
In cancer cells, ivermectin regulates PAK1 kinase pathways, disrupting Wnt/TCF and Akt/mTOR signaling, which are critical for cancer cell survival and proliferation, leading to growth inhibition in preclinical models.
Ivermectin increases reactive oxygen species (ROS) production and disrupts mitochondrial function in cancer cells, triggering apoptosis and autophagy via pathways like caspase activation, effectively killing malignant cells in vitro.
By inhibiting P-glycoprotein (P-gp) efflux pumps and enhancing T-cell infiltration into tumors, ivermectin reverses multidrug resistance and turns "cold" tumors "hot," improving chemotherapy efficacy and immune response in experimental studies.